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New research from Washington University School amoxil street price of click to investigate Medicine in St. Louis suggests that radiation therapy can reprogram heart muscle cells to what appears to be a younger state, fixing electrical problems that cause a life-threatening arrhythmia without the need for a long-used, invasive procedure.In that invasive procedure -- catheter ablation -- a catheter is threaded into the heart, and the tissue that triggers the life-threatening irregular heart rhythm -- ventricular tachycardia -- is burned, creating scars that block the errant signals. The new amoxil street price study, however, shows that noninvasive radiation therapy normally used to treat cancer can reprogram the heart muscle cells to a younger and perhaps healthier state, fixing the electrical problem in the cells themselves without needing scar tissue to block the overactive circuits.

The study also suggests that the same cellular reprogramming effect could be achieved with lower doses of radiation, opening the door to the possibility of wider uses for radiation therapy in different types of cardiac arrhythmias.The study appears Sept. 24 in the journal Nature Communications.Physician-scientists at Washington University showed in 2017 that radiation therapy typically reserved for cancer treatment could be directed at the heart to treat ventricular tachycardia.In theory, radiation therapy could reproduce the scar tissue usually created through catheter ablation but with a much shorter and amoxil street price totally noninvasive procedure, making the treatment available to more severely ill patients. Surprisingly, the doctors found that patients experienced large improvements in their arrhythmias a few days to weeks after radiation therapy, much quicker than the months it can take scar tissue to form after radiation therapy, suggesting that a single dose of radiation reduces the arrhythmia without forming scar tissue.

The data indicated amoxil street price that radiation treatment worked just as well, if not better, than catheter ablation for certain patients with ventricular tachycardia but in a different and unknown way."Traditionally, catheter ablation creates scar tissue to block the electrical circuits that are causing ventricular tachycardia," said senior author and cardiologist Stacey L. Rentschler, MD, PhD, an associate professor of medicine, of developmental biology and of biomedical engineering. "To help us understand whether the same thing was happening with radiation therapy, some of the first patients to have this new treatment gave us permission to study their amoxil street price heart tissue -- following heart transplantation or if they had passed away for another reason, for example.

We saw that scar tissue alone could not explain the remarkable clinical effects, suggesting that radiation improves the arrhythmia in some other way, so we delved into the details of that."The scientists found that radiation treatment triggered heart muscle cells to begin expressing different genes. They measured increased activity in a signaling pathway called Notch, which is known for its vital role in early development, including in forming the heart's electrical conduction system. advertisement Notch is amoxil street price usually switched off in adult heart muscle cells.

But the researchers found that a single dose of radiation temporarily activates Notch signaling, leading to a long-term increase in sodium ion channels in the heart muscle, a key physiologic change that can reduce arrhythmias."Arrhythmias are associated with slow electrical conduction speeds," Rentschler said. "Radiation therapy seems to kick amoxil street price up the speed faster by activating early developmental pathways that revert the heart tissue back into a healthier state."The researchers studied these effects in mice and in donated human hearts. In the human heart samples, the researchers found that these changes in heart muscle cells were only present in areas of the heart that received the targeted radiation dose."Radiation does cause a type of injury, but it's different from catheter ablation," said co-author and radiation oncologist Julie K.

Schwarz, MD, PhD, a professor of radiation oncology and director of the Cancer Biology Division in the Department amoxil street price of Radiation Oncology. "As part of the body's response to that injury, cells in the injured portion of the heart appear to turn on some of these early developmental programs to repair themselves. It's important to understand how this works because, with that knowledge, we can improve the way we're treating these patients and then apply it to other diseases."The researchers also found that the beneficial amoxil street price effects of radiation continued for at least two years in surviving patients.

And importantly, they were able to demonstrate in mice that a lower dose of the radiation produced the same effect. A lower radiation dose could minimize amoxil street price long-term side effects and open the door to this type of treatment in other types of heart arrhythmias. And while Notch was a big player in these effects, Schwarz said it's not the only pathway involved.

The researchers are continuing to investigate how radiation triggers heart cells to revert to a healthier state.Added first author David M. Zhang, an amoxil street price MD/PhD student in Rentschler's lab. "This was an exciting collaboration not only between basic scientists and clinicians but also cardiologists and radiation oncologists.

Historically, radiation oncologists are focused on cancer and try to avoid irradiating the heart, so this study opens up a whole new area of research and collaboration between these two fields."This work was supported by the National Institutes of Health (NIH), amoxil street price grant numbers T32 HL134635, T32 GM07200, R01 HL130212, UH3 HL141800 and S10 OD020136. This study received seed funding from the Department of Radiation Oncology, Cancer Biology Division, at Washington University. Schwarz holds a Female Investigator Award from amoxil street price AACR-Bristol Meyers Squibb and funding from the Radiological Society of North America.

Rentschler holds a Career Award for Medical Scientists from the Burroughs Wellcome Fund and funding from The Foundation for Barnes-Jewish Hospital that directly supported this work.Washington University co-authors Clifford Robinson, MD, and Phillip Cuculich, MD, have filed two institution-owned patents. Noninvasive Imaging and Treatment System for Cardiac Arrhythmias that relates to overall methods for amoxil street price delivery of cardiac radiation in patient. And System and Method for Determining Segments for Ablation that relates to use of cardiac segments for cardiac radiation targeting.

They also provide consulting services to Varian, which produces linear accelerators for radiation treatment delivery..

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How to cite this article:Singh is amoxil safe in pregnancy O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J is amoxil safe in pregnancy Psychiatry 2020;62:337-8Celebrity suicide is one of the highly publicized events in our country.

Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, the media went into a frenzy as newspapers, is amoxil safe in pregnancy news channels, and social media were full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor.

All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media is amoxil safe in pregnancy. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident.

Psychiatrists suddenly started getting distress calls from their patients in despair is amoxil safe in pregnancy with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph is amoxil safe in pregnancy of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide.

A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental condition and illness is amoxil safe in pregnancy and also his relationships and finances.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the is amoxil safe in pregnancy grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident.

Many psychiatrists and mental health professionals were called by media houses to comment on is amoxil safe in pregnancy the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so. There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist.

These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry and are is amoxil safe in pregnancy detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature is amoxil safe in pregnancy of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have guidelines and resource books for interacting with media, and psychiatrists should is amoxil safe in pregnancy familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion.

It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should is amoxil safe in pregnancy be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - is amoxil safe in pregnancy 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI.

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

This narrative review aims to provide an update of the evidence with regard to whether the practice of ECT is associated with damage to the brain. An accepted definition of brain damage remains elusive. There are also ethical and technical problems in designing studies that look at this question specifically.

Thus, even though there are newer technological tools and innovations, any review attempting to answer this question would have to take recourse to indirect methods. These include structural, functional, and metabolic neuroimaging. Body fluid biochemical marker studies.

And follow-up studies of cognitive impairment and incidence of dementia in people who have received ECT among others. The review of literature and present evidence suggests that ECT has a demonstrable impact on the structure and function of the brain. However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords.

Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update.

Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al. In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies.

The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time. Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness.

However, there are obvious ethical issues in designing human studies that are designed to answer this specific question. Therefore, one must necessarily take recourse to indirect evidences available through studies that have been designed to answer other research questions. These studies have employed the following methods:Structural neuroimaging studiesFunctional neuroimaging studiesMetabolic neuroimaging studiesBody fluid biochemical marker studiesCognitive impairment studies.While the early studies tended to focus more on establishing the safety of ECT and finding out whether ECT causes gross microscopic brain damage, the later studies especially since the advent of advanced neuroimaging techniques have been focusing more on a mechanistic understanding of ECT.

Hence, the primary objective of the later neuroimaging studies has been to look for structural and functional brain changes which might explain how ECT acts rather than evidence of gross structural damage per se. However, put together, all these studies would enable us to answer our titular question to some satisfaction. [Table 1] and [Table 2] provide an overview of the evidence base in this area.

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

In the absence of baseline neuroimaging, it would be very difficult to attribute any structural brain changes to ECT. In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today. The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain.

The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes. A single study by Coffey et al.

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

Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al.

Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al. That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies.

In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al. In a follow-up study showed that though there was a significant increase in the volume of the hippocampus 1 week after a course of ECT, the hippocampal volume returned to the baseline after 6 months.[19] Two other studies in 2013 showed that in addition to the hippocampus, the amygdala also showed significant volume increase following ECT.[20],[21] A series of structural neuroimaging studies after that have expanded on these findings and as of now, gray matter volume increase following ECT has been demonstrated in the hippocampus, amygdala, anterior temporal pole, subgenual cortex,[21] right caudate nucleus, and the whole of the medial temporal lobe (MTL) consisting of the hippocampus, amygdala, insula, and the posterosuperior temporal cortex,[24] para hippocampi, right subgenual anterior cingulate gyrus, and right anterior cingulate gyrus,[25] left cerebellar area VIIa crus I,[29] putamen, caudate nucleus, and nucleus acumbens [31] and clusters of increased cortical thickness involving the temporal pole, middle and superior temporal cortex, insula, and inferior temporal cortex.[27] However, the most consistently reported and replicated finding has been the bilateral increase in the volume of the hippocampus and amygdala.

In light of these findings, it has been tentatively suggested that ECT acts by inducing neuronal regeneration in the hippocampus – amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study – Nordanskog et al., 2014 – has followed study patients for a long term – 6 months in their case. And significantly, the authors found out that after increasing immediately following ECT, the hippocampal volume returns back to baseline by 6 months.[19] This, however, was not associated with the relapse of depressive symptoms.

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

In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression. It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus.

The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe. It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al.

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

The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al.

In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered. Furthermore, bilateral (B/L) ECT was associated with an equal increase in volume in both right and left hippocampus, whereas right unilateral ECT was associated with greater volume increase in the right hippocampus. Finally, contrary to expectation, clinical improvement was found to be negatively correlated with hippocampal volume.Thus, a review of the current evidence amply demonstrates that from looking for ECT-related brain damage – and finding none, we have now moved ahead to looking for a mechanistic understanding of the effect of ECT.

In this regard, it has been found that ECT does induce structural changes in the brain – a fact which has been seized upon by some to claim that ECT causes brain damage.[46] Such statements should, however, be weighed against the definition of damage as understood by the scientific medical community and patient population. Neuroanatomical changes associated with effective ECT can be better described as ECT-induced brain neuroplasticity or ECT-induced brain neuromodulation rather than ECT-induced brain damage. Metabolic Neuroimaging Studies.

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

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

The regions which have been most widely studied in MRSI studies include the bilateral hippocampus and amygdala, dorsolateral prefrontal cortex (DLPFC), and ACC.Till date, five MRSI studies have measured NAA concentration in the hippocampus before and after ECT. Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite.

However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies. It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations. The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis.

Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

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

Thus, we are led to the hypothesis that the same mechanism which drives clinical improvement with ECT is also responsible for the cognitive impairment following ECT. Whether this is a purely neuroinflammatory response or a neuroplastic response or a neuroinflammatory response leading to some form of neuroplasticity is a critical question, which remains to be answered.[40]Studies which have analyzed NAA concentration change in other brain areas have also produced conflicting results. The ACC is another area which has been studied in some detail utilizing the MRSI technique.

In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT. This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al.

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

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

In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al. In 2015 failed to replicate the same finding.[33],[38] Cho levels have also been studied in the amygdala, ACC, and the DLPFC. However, none of these studies showed a significant increase or decrease in Cho levels before and after ECT in the respective brain regions studied.

In addition, no significant difference was seen in the pre-ECT Cho levels of patients compared to healthy controls.[34],[36],[37]In review, we must admit that MRSI studies are still at a preliminary stage with significant heterogeneity in ECT protocols, patient population, and regions of the brain studied. At this stage, it is difficult to draw any firm conclusions except to acknowledge the fact that the more recent studies – Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 – have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] – as opposed to the earlier studies by Ende et al.[33] The view offered by the more recent studies is one of a neuroinflammatory models of action of ECT, probably driving neuroplasticity in the hippocampus. This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT.

However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development.

The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect. It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT.

Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder. The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration.

However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory. Objective memory can be roughly defined as the ability to retrieve stored information and can be measured by various standardized neuropsychological tests.

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

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

In 1994 since which time our understanding of ECT has grown substantially, helped particularly by the advent of modern-day neuroimaging techniques which we have reviewed in detail. And, what these studies reveal is rather than damaging the brain, ECT has a neuromodulatory effect on the brain. The various lines of evidence – structural neuroimaging studies, functional neuroimaging studies, neurochemical and metabolic studies, and serum BDNF studies all point toward this.

These neuromodulatory changes have been localized to the hippocampus, amygdala, and certain other parts of the limbic system. How exactly these changes mediate the improvement of depressive symptoms is a question that remains unanswered. However, there is little by way of evidence from neuroimaging studies which indicates that ECT causes destruction or degeneration of neurons.

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

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

Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question. However, in light of enduring ECT survivor accounts, there is a need to design studies that specifically answer this question.Financial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Payne NA, Prudic J.

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Correspondence Address:Dr. Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].

How to cite this amoxil street price article:Singh Cheap symbicort online canada O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the highly publicized events in amoxil street price our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, the media went into a frenzy as newspapers, news channels, and social media were full of stories amoxil street price providing minute details of the suicidal act.

Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor. All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast amoxil street price and discussed on electronic, print, and social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started getting distress amoxil street price calls from their patients in despair with increased suicidal ideation.

This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 amoxil street price (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide. A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental condition and illness and amoxil street price also his relationships and finances.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave amoxil street price impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists and mental health professionals were called by media houses to comment on amoxil street price the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so.

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

Many professional societies have guidelines and resource books for interacting with media, and psychiatrists should familiarize themselves with these amoxil street price documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion. It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to amoxil street price be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, amoxil street price West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment.

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

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

Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update. Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al.

In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies. The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time. Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness. However, there are obvious ethical issues in designing human studies that are designed to answer this specific question.

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

Structural and Functional Neuroimaging Studies Devanand et al. Reviewed 16 structural neuroimaging studies on the effect of ECT on the brain.[4] Of these, two were pneumoencephalography studies, nine were computed tomography (CT) scan studies, and five were magnetic resonance imaging (MRI) studies. However, most of these studies were retrospective in design, with neuroimaging being done in patients who had received ECT in the past. In the absence of baseline neuroimaging, it would be very difficult to attribute any structural brain changes to ECT. In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today.

The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain. The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes. A single study by Coffey et al. Followed up the patients for a duration of 6 months and repeated neuroimaging again at 6 months in order to capture any long-term changes following ECT.[10]The most important conclusion which emerged from this early series of studies was that there was no evidence of cortical atrophy, change in ventricle size, or increase in white matter hyperintensities.[4] The next major conclusion was that there appeared to be an increase in the T1 and T2 relaxation time immediately following ECT, which returned to normal within 24 h.

This supported the theory that immediately following ECT, there appears to be a temporary breakdown of the blood–brain barrier, leading to water influx into the brain tissue.[11] The last significant observation by Coffey et al. In 1991 was that there was no significant temporal changes in the total volumes of the frontal lobes, temporal lobes, or amygdala–hippocampal complex.[10] This was, however, something which would later be refuted by high-resolution MRI studies. Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al.

Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al. That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies. In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al.

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

Though almost all studies demonstrate a significant increase in hippocampal volume following ECT, a majority of studies failed to demonstrate a correlation between symptom improvement and hippocampal volume increase.[19],[20],[22],[24],[28] However, a significant minority of volumetric studies have demonstrated correlation between increase in hippocampal and/or amygdala volume and improvement of symptoms.[21],[25],[30]Another set of studies have used diffusion tensor imaging, functional MRI (fMRI), anatomical connectome, and structural network analysis to study the effect of ECT on the brain. The first of these studies by Abbott et al. In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression. It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus.

The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe. It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al. Used a source-based morphometry approach to study the structural networks in patients with depression and schizophrenia and the effect of ECT on the same. It was found that the medial prefrontal cortex/anterior cingulate cortex (ACC/MPFC) network, MTL network, bilateral thalamus, and left cerebellar regions/precuneus exhibited significant difference between healthy controls and the patient population.

It was also demonstrated that administration of ECT leads to significant increase in the network strength of the ACC/MPFC network and the MTL network though the increase in network strength and symptom amelioration were not correlated.[32]Building on these studies, a recently published meta-analysis has attempted a quantitative synthesis of brain volume changes – focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder. The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al. In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered.

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

Magnetic Resonance Spectroscopic Imaging Magnetic resonance spectroscopic imaging (MRSI) uses a phase-encoding procedure to map the spatial distribution of magnetic resonance (MR) signals of different molecules. The crucial difference, however, is that while MRI maps the MR signals of water molecules, MRSI maps the MR signals generated by different metabolites – such as N-acetyl aspartate (NAA) and choline-containing compounds. However, the concentration of these metabolites is at least 10,000 times lower than water molecules and hence the signal strength generated would also be correspondingly lower. However, MRSI offers us the unique advantage of studying in vivo the change in the concentration of brain metabolites, which has been of great significance in fields such as psychiatry, neurology, and basic neuroscience research.[47]MRSI studies on ECT in patients with depression have focused largely on four metabolites in the human brain – NAA, choline-containing compounds (Cho) which include majorly cell membrane compounds such as glycerophosphocholine, phosphocholine and a miniscule contribution from acetylcholine, creatinine (Cr) and glutamine and glutamate together (Glx). NAA is located exclusively in the neurons, and is suggested to be a marker of neuronal viability and functionality.[48] Choline-containing compounds (Cho) mainly include the membrane compounds, and an increase in Cho would be suggestive of increased membrane turnover.

Cr serves as a marker of cellular energy metabolism, and its levels are usually expected to remain stable. The regions which have been most widely studied in MRSI studies include the bilateral hippocampus and amygdala, dorsolateral prefrontal cortex (DLPFC), and ACC.Till date, five MRSI studies have measured NAA concentration in the hippocampus before and after ECT. Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite. However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies.

It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations. The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis. Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

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

The ACC is another area which has been studied in some detail utilizing the MRSI technique. In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT. This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al. In 2011, who demonstrated that NAA levels were significantly reduced in the left ACC in patients with depression and that these levels were significantly elevated following ECT.[37] This again is contested by Njau et al.

Who showed that NAA levels are significantly reduced following ECT in the left dorsal ACC.[39] A direct comparison of these three studies is complicated by the different ECT and imaging parameters used and hence, no firm conclusion can be made on this point at this stage. In addition to this, one study had demonstrated increased NAA levels in the amygdala following administration of ECT,[34] with a trend level increase in Cho levels, which again is suggestive of neurogenesis and/or neuroplasticity. A review of studies on the DLPFC reveals a similarly confusing picture with one study, each showing no change, reduction, and elevation of concentration of NAA following ECT.[35],[37],[39] Here, again, a direct comparison of the three studies is made difficult by the heterogeneous imaging and ECT protocols followed by them.A total of five studies have analyzed the concentration of choline-containing compounds (Cho) in patients undergoing ECT. Conceptually, an increase in Cho signals is indicative of increased membrane turnover, which is postulated to be associated with synaptogenesis, neurogenesis, and maturation of neurons.[31] Of these, two studies measured Cho concentration in the B/L hippocampus, with contrasting results. Ende et al.

In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al. In 2015 failed to replicate the same finding.[33],[38] Cho levels have also been studied in the amygdala, ACC, and the DLPFC. However, none of these studies showed a significant increase or decrease in Cho levels before and after ECT in the respective brain regions studied. In addition, no significant difference was seen in the pre-ECT Cho levels of patients compared to healthy controls.[34],[36],[37]In review, we must admit that MRSI studies are still at a preliminary stage with significant heterogeneity in ECT protocols, patient population, and regions of the brain studied. At this stage, it is difficult to draw any firm conclusions except to acknowledge the fact that the more recent studies – Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 – have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] – as opposed to the earlier studies by Ende et al.[33] The view offered by the more recent studies is one of a neuroinflammatory models of action of ECT, probably driving neuroplasticity in the hippocampus.

This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT. However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development. The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect.

It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT. Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder. The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration.

However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory. Objective memory can be roughly defined as the ability to retrieve stored information and can be measured by various standardized neuropsychological tests. Subjective memory or meta-memory, on the other hand, refers to the ability to make judgments about one's ability to retrieve stored information.[58] As described previously, it has been conclusively demonstrated that anterograde memory impairment does not persist beyond 2 weeks after ECT.[57] However, one of the major limitations of this meta-analysis was the lack of evidence on retrograde amnesia following ECT. This is particularly unfortunate considering that it is memory impairment – particularly retrograde amnesia which has received the most attention.[59] In addition, reports of catastrophic retrograde amnesia have been repeatedly held up as sensational evidence of the lasting brain damage produced by ECT.[59] Admittedly, studies on retrograde amnesia are fewer and less conclusive than on anterograde amnesia.[60],[61] At present, the results are conflicting, with some studies finding some impairment in retrograde memory – particularly autobiographical retrograde memory up to 6 months after ECT.[62],[63],[64],[65] However, more recent studies have failed to support this finding.[66],[67] While they do demonstrate an impairment in retrograde memory immediately after ECT, it was seen that this deficit returned to pre-ECT levels within a span of 1–2 months and improved beyond baseline performance at 6 months post ECT.[66] Adding to the confusion are numerous factors which confound the assessment of retrograde amnesia.

It has been shown that depressive symptoms can produce significant impairment of retrograde memory.[68],[69] It has also been demonstrated that sine-wave ECT produces significantly more impairment of retrograde memory as compared to brief-pulse ECT.[70] However, from the 1990s onward, sine-wave ECT has been completely replaced by brief-pulse ECT, and it is unclear as to the implications of cognitive impairment from the sine-wave era in contemporary ECT practice.Another area of concern are reports of subjective memory impairment following ECT. One of the pioneers of research into subjective memory impairment were Squire and Chace who published a series of studies in the 1970s demonstrating the adverse effect of bilateral ECT on subjective assessment of memory.[62],[63],[64],[65] However, most of the studies conducted post 1980 – from when sine-wave ECT was replaced by brief-pulse ECT report a general improvement in subjective memory assessments following ECT.[71] In addition, most of the recent studies have failed to find a significant association between measures of subjective and objective memory.[63],[66],[70],[72],[73],[74] It has also been shown that subjective memory impairment is strongly associated with the severity of depressive symptoms.[75] In light of these facts, the validity and value of measures of subjective memory impairment as a marker of cognitive impairment and brain damage following ECT have been questioned. However, concerns regarding subjective memory impairment and catastrophic retrograde amnesia continue to persist, with significant dissonance between the findings of different research groups and patient self-reports in various media.[57]Some studies reported the possibility of ECT being associated with the development of subsequent dementia.[76],[77] However, a recent large, well-controlled prospective Danish study found that the use of ECT was not associated with elevated incidence of dementia.[78] Conclusion Our titular question is whether ECT leads to brain damage, where damage indicates destruction or degeneration of nerves or nerve tracts in the brain, which leads to loss of function. This issue was last addressed by Devanand et al. In 1994 since which time our understanding of ECT has grown substantially, helped particularly by the advent of modern-day neuroimaging techniques which we have reviewed in detail.

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

Though cognitive impairment studies do show that there is objective impairment of certain functions – particularly memory immediately after ECT, these impairments are transient with full recovery within a span of 2 weeks. Perhaps, the single-most important unaddressed concern is retrograde amnesia, which has been shown to persist for up to 2 months post ECT. In this regard, the recent neurometabolic studies have offered a tentative mechanism of action of ECT, producing a transient inflammation in the limbic cortex, which, in turn, drives neurogenesis, thereby exerting a neuromodulatory effect. This hypothesis would explain both the cognitive adverse effects of ECT – due to the transient inflammation – and the long-term improvement in mood – neurogenesis in the hippocampus. Although unproven at present, such a hypothesis would imply that cognitive impairment is tied in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.The review of literature suggests that ECT does cause at least structural and functional changes in the brain, and these are in all probability related to the effects of the ECT.

However, these cannot be construed as brain damage as is usually understood. Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question. However, in light of enduring ECT survivor accounts, there is a need to design studies that specifically answer this question.Financial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Payne NA, Prudic J. Electroconvulsive therapy.

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Acta Psychiatr Scand 2016;133:154-64. 39.Njau S, Joshi SH, Espinoza R, Leaver AM, Vasavada M, Marquina A, et al. Neurochemical correlates of rapid treatment response to electroconvulsive therapy in patients with major depression. J Psychiatry Neurosci 2017;42:6-16. 40.Cano M, Martínez-Zalacaín I, Bernabéu-Sanz Á, Contreras-Rodríguez O, Hernández-Ribas R, Via E, et al.

Brain volumetric and metabolic correlates of electroconvulsive therapy for treatment-resistant depression. A longitudinal neuroimaging study. Transl Psychiatry 2017;7:e1023. 41.Figiel GS, Krishnan KR, Doraiswamy PM. Subcortical structural changes in ECT-induced delirium.

J Geriatr Psychiatry Neurol 1990;3:172-6. 42.Rotheneichner P, Lange S, O'Sullivan A, Marschallinger J, Zaunmair P, Geretsegger C, et al. Hippocampal neurogenesis and antidepressive therapy. Shocking relations. Neural Plast 2014;2014:723915.

43.Singh A, Kar SK. How electroconvulsive therapy works?. Understanding the neurobiological mechanisms. Clin Psychopharmacol Neurosci 2017;15:210-21. 44.Gbyl K, Videbech P.

Electroconvulsive therapy increases brain volume in major depression. A systematic review and meta-analysis. Acta Psychiatr Scand 2018;138:180-95. 45.Oltedal L, Narr KL, Abbott C, Anand A, Argyelan M, Bartsch H, et al. Volume of the human hippocampus and clinical response following electroconvulsive therapy.

Biol Psychiatry 2018;84:574-81. 46.Breggin PR. Brain-Disabling Treatments in Psychiatry. Drugs, Electroshock, and the Role of the FDA. New York.

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

Principles and recent advances. J Magn Reson Imaging 2013;37:1301-25. 48.Simmons ML, Frondoza CG, Coyle JT. Immunocytochemical localization of N-acetyl-aspartate with monoclonal antibodies. Neuroscience 1991;45:37-45.

49.Obergriesser T, Ende G, Braus DF, Henn FA. Long-term follow-up of magnetic resonance-detectable choline signal changes in the hippocampus of patients treated with electroconvulsive therapy. J Clin Psychiatry 2003;64:775-80. 50.Bramham CR, Messaoudi E. BDNF function in adult synaptic plasticity.

The synaptic consolidation hypothesis. Prog Neurobiol 2005;76:99-125. 51.Duman RS, Monteggia LM. A neurotrophic model for stress-related mood disorders. Biol Psychiatry 2006;59:1116-27.

52.Bocchio-Chiavetto L, Bagnardi V, Zanardini R, Molteni R, Nielsen MG, Placentino A, et al. Serum and plasma BDNF levels in major depression. A replication study and meta-analyses. World J Biol Psychiatry 2010;11:763-73. 53.Brunoni AR, Lopes M, Fregni F.

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

A meta-analysis study. J Psychiatr Res 2016;83:47-53. 55.UK ECT Review Group. Efficacy and safety of electroconvulsive therapy in depressive disorders. A systematic review and meta-analysis.

Lancet 2003;361:799-808. 56.57.Semkovska M, McLoughlin DM. Objective cognitive performance associated with electroconvulsive therapy for depression. A systematic review and meta-analysis. Biol Psychiatry 2010;68:568-77.

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

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

J ECT 2013;29:127-33. 61.Fraser LM, O'Carroll RE, Ebmeier KP. The effect of electroconvulsive therapy on autobiographical memory. A systematic review. J ECT 2008;24:10-7.

62.Squire LR, Chace PM. Memory functions six to nine months after electroconvulsive therapy. Arch Gen Psychiatry 1975;32:1557-64. 63.Squire LR, Slater PC. Electroconvulsive therapy and complaints of memory dysfunction.

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

Arch Gen Psychiatry 1981;38:89-95. 65.Squire LR, Wetzel CD, Slater PC. Memory complaint after electroconvulsive therapy. Assessment with a new self-rating instrument. Biol Psychiatry 1979;14:791-801.

66.Calev A, Nigal D, Shapira B, Tubi N, Chazan S, Ben-Yehuda Y, et al. Early and long-term effects of electroconvulsive therapy and depression on memory and other cognitive functions. J Nerv Ment Dis 1991;179:526-33. 67.Sackeim HA, Prudic J, Devanand DP, Nobler MS, Lisanby SH, Peyser S, et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral electroconvulsive therapy at different stimulus intensities.

Arch Gen Psychiatry 2000;57:425-34. 68.Abrams R. Does brief-pulse ECT cause persistent or permanent memory impairment?. J ECT 2002;18:71-3. 69.Peretti CS, Danion JM, Grangé D, Mobarek N.

Bilateral ECT and autobiographical memory of subjective experiences related to melancholia. A pilot study. J Affect Disord 1996;41:9-15. 70.Weiner RD, Rogers HJ, Davidson JR, Squire LR. Effects of stimulus parameters on cognitive side effects.

Ann N Y Acad Sci 1986;462:315-25. 71.Prudic J, Peyser S, Sackeim HA. Subjective memory complaints. A review of patient self-assessment of memory after electroconvulsive therapy. J ECT 2000;16:121-32.

72.Sackeim HA, Prudic J, Devanand DP, Kiersky JE, Fitzsimons L, Moody BJ, et al. Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med 1993;328:839-46. 73.Frith CD, Stevens M, Johnstone EC, Deakin JF, Lawler P, Crow TJ. Effects of ECT and depression on various aspects of memory.

Br J Psychiatry 1983;142:610-7. 74.Ng C, Schweitzer I, Alexopoulos P, Celi E, Wong L, Tuckwell V, et al. Efficacy and cognitive effects of right unilateral electroconvulsive therapy. J ECT 2000;16:370-9. 75.Coleman EA, Sackeim HA, Prudic J, Devanand DP, McElhiney MC, Moody BJ.

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

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

A cohort study. Lancet Psychiatry 2018;5:348-56. Correspondence Address:Dr. Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].

What is Amoxil?

AMOXICILLIN is a penicillin antibiotic. It kills or stops the growth of some bacteria. Amoxil is used to treat many kinds of s. It will not work for colds, flu, or other viral s.

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Contact-tracing programs amoxil 500g in Visit Your URL two areas hit hardest by buy antibiotics are working. Catherine Lee, a community health representative, talks with a man at his home on the Navajo Nation. The nation has nearly 200 contact tracers spread across numerous amoxil 500g health-care agencies.Jim Thompson/Albuquerque Journal On a mild morning in April at Arizona’s Whiteriver Indian Hospital, Dr. Ryan Close tested nasal swabs from two members of an eight-person household on the Fort Apache Reservation northwest of Phoenix.

About half of the family had a runny nose and cough and had lost their sense of taste and smell — all symptoms of buy antibiotics — and, by late morning, the two tests had come back positive. Close’s contact-tracing work amoxil 500g began.For Close and his team, each day begins like this. With a list of new buy antibiotics cases — new sources that may have spread the amoxil. The 35 or so people on the team must rapidly test people, isolate the infected and visit the homes of any amoxil 500g who may have been exposed.

Again, and again. Recently, though, their cases have declined, due in part to something rare, at least in the United States. An effective amoxil 500g contact-tracing and testing plan. Both the White Mountain Apache and nearby Navajo Nation experienced some of the country’s worst rates, yet both began to curb their cases in mid-June and mid-July, respectively, due to their existing health department resources and partnerships, stringent public health orders, testing and robust contact tracing.

€œWe've seen a significant decline in amoxil 500g cases on the reservation at the same time that things were on fire for the rest of the state,” said Close, an epidemiologist and physician at Whiteriver Indian Hospital, an Indian Health Service facility. Tracing disease transmission from buy antibiotics is crucial to slowing its spread, but successful contact tracing has proven challenging for communities that lack the funds, community cooperation, personnel or supplies for rapid testing. The White Mountain Apache Tribe of Fort Apache and the Navajo Nation, however, have been growing a contact-tracing army, setting them apart from other tribes during the amoxil. As tribal communities brace for multiple waves of buy antibiotics, public health experts from the two amoxil 500g nations have already successfully adapted contact-tracing programs.

The White Mountain Apache and the Navajo Nation “were hit hardest early on, and so they have had a little bit more time and opportunity to put these systems into place,” said Laura Hammitt, director of the infectious disease and prevention program at Johns Hopkins Center for American Indian Health, which is working with the Centers for Disease Control to develop a guide for tribal governments to train and grow their own contact-tracing workforces.Across the country, tribes are employing a number of public health measures — closing reservations to nonresidents, setting curfews, providing free testing and aid to families and Indigenous language translations of public health guidelines — but few are actively contact tracing. Contact tracing requires fast and systematic amoxil 500g testing and trained personnel. In March, Close trained eight Whiteriver Indian Hospital staffers, but the number has since grown to around 35, serving some 12,000 tribal citizens and residents. The relatively small team takes advantage of the firmly closed reservation boundaries and rapid testing to find and isolate new cases.

buy antibiotics cases were dropping in Fort Apache, which stayed closed, as the state neared its caseload peak in mid-June after the governor lifted stay-at-home orders, becoming amoxil 500g one of the country’s worst antibiotics hotspots. Catherine Lee, a community health representative, talks with a man at his home on the Navajo Nation. The nation has nearly amoxil 500g 200 contact tracers spread across numerous health-care agencies.Jim Thompson/Albuquerque Journal While most contact-tracing programs rely on phone calls to learn patient history, assess symptoms, encourage isolation and trace other contacts, the Whiteriver team relies on home visits. €œI (can) come to your house to assess you, do a case investigation, or to inform you that you are a contact,” Close said.

€œThe benefit of that is that, if you were ill-appearing, they can evaluate you right there.” Tracers can also determine whether other household members are symptomatic, checking temperatures and oxygen saturation, while health-care providers can check breathing with a stethoscope. The Whiteriver Hospital can turn around a buy antibiotics test in a single day, a process that takes days or weeks at other public health institutions.“We’re not just trying to amoxil 500g flatten the curve. We’re trying to actually completely contain this amoxil.”The Navajo Nation has succeeded in slowing the spread of the new antibiotics, even though the reservation spans three states — New Mexico, Arizona and Utah — so teams must coordinate across several jurisdictions. The nation amoxil 500g has nearly 200 contact tracers spread across numerous health-care agencies.

With scores of Indigenous communities to monitor over a huge geographic area, phone calls are its primary investigative tool. The Navajo Nation is setting its sights high. €œWe’re not just trying to flatten the curve,” said Sonya Shin, who leads tracing investigations amoxil 500g for the Nation, “We’re trying to actually completely contain this amoxil.”Still, critics say it is not enough. The most effective tracing relies on mass testing to catch asymptomatic people as well as those with symptoms.

Due to a limited supply amoxil 500g of tests, most tribes, like most states, can only test symptomatic people, so the number of cases is inevitably undercounted. €œContact tracing does not mean a damn thing unless you have really good tests, and you’re testing everybody,” said Rudolf Rÿser (Cree/Oneida), executive director of the Center for World Indigenous Studies. €œNot just the people showing the symptoms, but everybody, whether they are Indian or non-Indian, in your area — you have to catch them all.”Kalen Goodluck is a contributing editor at High Country News. Email him at [email protected] or submit a letter to the editor.Follow @kalengoodluck Get our Indigenous Affairs newsletter ↓ Thank you for signing up for Indian Country News, an HCN newsletter service amoxil 500g.

Look for it in your email each month. Read more More from buy antibiotics19.

Contact-tracing programs in two areas amoxil street price hit hardest by buy antibiotics are more tips here working. Catherine Lee, a community health representative, talks with a man at his home on the Navajo Nation. The nation has nearly 200 amoxil street price contact tracers spread across numerous health-care agencies.Jim Thompson/Albuquerque Journal On a mild morning in April at Arizona’s Whiteriver Indian Hospital, Dr.

Ryan Close tested nasal swabs from two members of an eight-person household on the Fort Apache Reservation northwest of Phoenix. About half of the family had a runny nose and cough and had lost their sense of taste and smell — all symptoms of buy antibiotics — and, by late morning, the two tests had come back positive. Close’s contact-tracing work began.For Close and his team, each amoxil street price day begins like this.

With a list of new buy antibiotics cases — new sources that may have spread the amoxil. The 35 or so people on the team must rapidly test people, isolate the infected and visit the homes of amoxil street price any who may have been exposed. Again, and again.

Recently, though, their cases have declined, due in part to something rare, at least in the United States. An effective contact-tracing and amoxil street price testing plan. Both the White Mountain Apache and nearby Navajo Nation experienced some of the country’s worst rates, yet both began to curb their cases in mid-June and mid-July, respectively, due to their existing health department resources and partnerships, stringent public health orders, testing and robust contact tracing.

€œWe've seen a significant decline in cases on the reservation at the same time that things were on fire for the rest of the state,” said Close, an epidemiologist and physician at Whiteriver Indian Hospital, amoxil street price an Indian Health Service facility. Tracing disease transmission from buy antibiotics is crucial to slowing its spread, but successful contact tracing has proven challenging for communities that lack the funds, community cooperation, personnel or supplies for rapid testing. The White Mountain Apache Tribe of Fort Apache and the Navajo Nation, however, have been growing a contact-tracing army, setting them apart from other tribes during the amoxil.

As tribal amoxil street price communities brace for multiple waves of buy antibiotics, public health experts from the two nations have already successfully adapted contact-tracing programs. The White Mountain Apache and the Navajo Nation “were hit hardest early on, and so they have had a little bit more time and opportunity to put these systems into place,” said Laura Hammitt, director of the infectious disease and prevention program at Johns Hopkins Center for American Indian Health, which is working with the Centers for Disease Control to develop a guide for tribal governments to train and grow their own contact-tracing workforces.Across the country, tribes are employing a number of public health measures — closing reservations to nonresidents, setting curfews, providing free testing and aid to families and Indigenous language translations of public health guidelines — but few are actively contact tracing. Contact tracing requires amoxil street price fast and systematic testing and trained personnel.

In March, Close trained eight Whiteriver Indian Hospital staffers, but the number has since grown to around 35, serving some 12,000 tribal citizens and residents. The relatively small team takes advantage of the firmly closed reservation boundaries and rapid testing to find and isolate new cases. buy antibiotics cases were dropping in Fort Apache, amoxil street price which stayed closed, as the state neared its caseload peak in mid-June after the governor lifted stay-at-home orders, becoming one of the country’s worst antibiotics hotspots.

Catherine Lee, a community health representative, talks with a man at his home on the Navajo Nation. The nation has nearly 200 contact tracers spread across numerous health-care agencies.Jim Thompson/Albuquerque Journal While most contact-tracing programs rely on phone calls to learn patient history, assess symptoms, encourage isolation and trace other contacts, the Whiteriver team relies on home visits amoxil street price. €œI (can) come to your house to assess you, do a case investigation, or to inform you that you are a contact,” Close said.

€œThe benefit of that is that, if you were ill-appearing, they can evaluate you right there.” Tracers can also determine whether other household members are symptomatic, checking temperatures and oxygen saturation, while health-care providers can check breathing with a stethoscope. The Whiteriver Hospital can turn around a buy antibiotics test in a single day, a process that takes days or weeks at other public health institutions.“We’re amoxil street price not just trying to flatten the curve. We’re trying to actually completely contain this amoxil.”The Navajo Nation has succeeded in slowing the spread of the new antibiotics, even though the reservation spans three states — New Mexico, Arizona and Utah — so teams must coordinate across several jurisdictions.

The nation amoxil street price has nearly 200 contact tracers spread across numerous health-care agencies. With scores of Indigenous communities to monitor over a huge geographic area, phone calls are its primary investigative tool. The Navajo Nation is setting its sights high.

€œWe’re not just trying to flatten the curve,” said Sonya Shin, who leads tracing investigations for the Nation, “We’re trying to actually completely contain this amoxil.”Still, critics say it is not amoxil street price enough. The most effective tracing relies on mass testing to catch asymptomatic people as well as those with symptoms. Due to a limited supply of tests, most tribes, like most states, can only test symptomatic people, so the number of cases is inevitably amoxil street price undercounted.

€œContact tracing does not mean a damn thing unless you have really good tests, and you’re testing everybody,” said Rudolf Rÿser (Cree/Oneida), executive director of the Center for World Indigenous Studies. €œNot just the people showing the symptoms, but everybody, whether they are Indian or non-Indian, in your area — you have to catch them all.”Kalen Goodluck is a contributing editor at High Country News. Email him at [email protected] or submit a letter to the editor.Follow @kalengoodluck Get our Indigenous Affairs newsletter ↓ Thank you for signing up for Indian Country News, an HCN newsletter service.

Look for it in your email each month. Read more More from buy antibiotics19.

How to get amoxil without a doctor

On November 5, 2021, the Centers for Medicare and Medicaid Services (CMS) published regulations that establish the how to get amoxil without a doctor more helpful hints first ever federal vaccination requirements for health care provider staff. Drawing on how to get amoxil without a doctor its authority to establish patient health and safety standards, CMS is requiring health care providers that participate in the Medicare and/or Medicaid programs to ensure that their staff are fully vaccinated against buy antibiotics. The new rule applies to staff who provide any care, treatment, or other services for providers or patients, including contractors and volunteers.CMS says it is now requiring health care staff to be vaccinated because its earlier efforts to simply encourage vaccination have been “insufficient” to protect patient health and safety. CMS cites data showing that buy antibiotics cases in nursing homes surged with the rise of the Delta how to get amoxil without a doctor variant. The nursing home staff vaccination rate is nearly 73 % nationally as of October 2021, with substantial variation by region.

CMS concluded that standard federal requirements across provider types are needed because the existing “patchwork” of state and how to get amoxil without a doctor employer requirements has not been enough to bring the amoxil under control in health care settings. CMS notes that the treatments are safe and highly effective at preventing severe illness and death, and unvaccinated staff can strain the health care system by transmitting buy antibiotics to patients and having to miss work if they are recovering from buy antibiotics or quarantining after exposure.The new rule applies to Medicare and Medicaid how to get amoxil without a doctor providers that are directly regulated by CMS and therefore does not reach all Medicaid providers, such as certain home and community-based services (HCBS) providers. The rule applies to nursing homes, hospitals, outpatient rehab facilities, federally qualified health centers, rural health centers, and home health agencies, among other provider types. Residents and staff of other HCBS providers, such as group homes, assisted living facilities, and day habilitation programs, face increased risk of serious how to get amoxil without a doctor illness or death from buy antibiotics, similar to nursing homes. But, because states (and not CMS) license and regulate these providers, CMS has not required them to comply with the new rule.

States or individual providers could adopt staff vaccination mandates, and providers how to get amoxil without a doctor may be subject to other rules such as the Occupational Safety and Health Administration requirement for large employers (which has been put on hold by the courts) or state or local requirements.The new rule raises many important issues to watch:Will providers have enough lead time to implement the new rule?. Staff must have received their first treatment dose by December 6, 2021, and must be fully vaccinated by January 4, 2022, or have been granted an exemption (based on disability or sincere religious belief) or temporary how to get amoxil without a doctor delay (based on CDC clinical guidelines). Decisions about whether to grant exemptions will be made by providers. The rule does not require staff to receive booster shots, though providers must track staff who have received a CDC-recommended how to get amoxil without a doctor booster. Providers also must implement “additional precautions” to mitigate buy antibiotics transmission and adopt contingency plans to address staff who are not fully vaccinated.How will the new rule affect health care staffing levels?.

An October 2021 KFF tracking how to get amoxil without a doctor poll found that 1 in 5 adults continue to say that they definitely will not get the buy antibiotics treatment or will do so only if required. When asked what they would do if their employer required the buy antibiotics treatment without an option for regular testing, 72% of unvaccinated workers (9% how to get amoxil without a doctor of all adults) say they would leave their jobs. The same poll found that just 5% of unvaccinated adults said they have left a job because an employer required them to get vaccinated. CMS acknowledges how to get amoxil without a doctor that some staff may leave their jobs because they do not want to receive the treatment. It remains to be seen whether the new rule will exacerbate existing staffing shortages or whether these effects may vary by region.

CMS cites examples of treatment mandates adopted by health systems in Texas and Detroit and a long-term care parent corporation with 250 facilities as well as the New York state health care worker mandate, all of which resulted in high rates of compliance and few employee resignations.Will efforts to monitor how to get amoxil without a doctor and enforce the new rule be sufficient?. CMS says that provider compliance with the new rule will be part of the existing how to get amoxil without a doctor oversight process through which state or federal inspectors review all Medicare and Medicaid program requirements. CMS envisions that inspectors will review facility policies and records and conduct staff interviews to verify vaccination status. CMS will provide guidance about oversight as well as penalties for noncompliance, which could include civil monetary penalties, how to get amoxil without a doctor denial of payment for new long-term care facility admissions, or termination of Medicare and/or Medicaid program participation.How long will the new rule be in place?. CMS will determine whether to make the new rule permanent based on public comments (due January 4, 2022) and the future course of the amoxil.

The new rule is not tied to the duration of the buy antibiotics public health emergency (PHE), and CMS expects that it will “remain relevant for how to get amoxil without a doctor some time beyond” the PHE end. Medicare interim final rules expire after three years how to get amoxil without a doctor unless they are finalized. In the near term, the new rule already has been challenged in a lawsuit filed by 10 state attorneys general in Missouri federal district court, which could delay or prevent implementation of the rule.Congress is considering a broad package of health, social, and environmental programs supported by President Biden, called the Build Back Better Act. The total cost of the original package had been pegged at $3.5 trillion (much of which would be offset by savings and new revenue), though the legislation has since changed in ways that will likely how to get amoxil without a doctor reduce the total. This brief summarizes major health provisions as of the bill reported to the House Rules Committee on November 3, 2021, which, at the time of publication, has not yet received a CBO score.

Negotiations are ongoing how to get amoxil without a doctor and there may be future changes.Here, we walk through 10 of the major health coverage and financing provisions of the Build Back Better Act, with discussion of the potential implications for people and the federal budget. We summarize provisions relating to the following areas and provide data on the people most directly affected by each provision and the potential costs or savings to the federal government.ACA Marketplace SubsidiesNew Medicare Hearing BenefitLowering Prescription Drug Prices and SpendingMedicare Part D Benefit RedesignMedicaid Coverage GapMaternal Care and Postpartum CoverageOther Medicaid / Children’s Health Insurance Changes CHIP ChangesOther Medicaid Financing and Benefit ChangesMedicaid Home and Community Based Services and the Direct Care WorkforcePaid Family and Medical LeaveA recent KFF poll how to get amoxil without a doctor found broad support for many of these provisions, though it did not probe on the costs or trade-offs associated with them. The poll also found that the vast majority of the public supports allowing the federal government to negotiate drug prices, after hearing arguments made by proponents and opponents.Major Provisions of the Build Back Better Act and their Potential Costs and Impact1. ACA Marketplace SubsidiesBackgroundUnder the Affordable Care Act, people purchasing Marketplace coverage could only qualify for subsidies if they met other eligibility requirements and had incomes between how to get amoxil without a doctor one and four times the federal poverty level. People eligible for subsidies would have to contribute a sliding-scale percentage of their income toward a benchmark premium, ranging from 2.07% to 9.83%.

Once income passed 400% FPL, subsidies stopped and many individuals and families were unable to afford coverage.In 2021, the American Rescue Plan Act (ARPA) temporarily expanded eligibility for subsidies by removing the upper how to get amoxil without a doctor income threshold. It also temporarily increased the dollar value of premium subsidies across the board, meaning nearly everyone on the Marketplace paid lower premiums, and the lowest income how to get amoxil without a doctor people pay zero premium for coverage with very low deductibles. The ARPA also made people who received unemployment insurance (UI) benefits during 2021 eligible for zero-premium, low-deductible plans.However, the ARPA provisions removing the upper income threshold and increasing tax credit amounts are only in effect for 2021 and 2022. The unemployment provision is only in effect for 2021.Provision DescriptionSection 137301 of The Build Back Better Act would extend the ARPA subsidy changes that eliminate the income eligibility cap and increase the amount of APTC for individuals across the board through the end of 2025.Additionally, Section 30605 of The Build Back Better Act would extend the special Marketplace subsidy rule for individuals receiving UI benefits for an additional 4 years, through the end of 2025.Section 137303 of the Act would, for purposes of determining eligibility for how to get amoxil without a doctor premium tax credits, disregard any lump sum Social Security benefit payments in a year. This provision would be permanent and effective starting in the 2022 tax year.

Starting in 2026, people would have the option to have the lump sum benefit how to get amoxil without a doctor included in their income for purposes of determining tax credit eligibility.Finally, Section 137302 modifies the affordability test for employer-sponsored health coverage. The ACA makes people ineligible for marketplace subsidies if they have an offer of affordable coverage from an employer, currently defined as requiring an employee contribution how to get amoxil without a doctor of no more than 9.61% of household income in 2022. The Build Back Better Act would reduce this affordability threshold to 8.5% of income, bringing it in line with the maximum contribution required to enroll in the benchmark marketplace plan. This provision how to get amoxil without a doctor would take effect for tax years starting in 2022 through 2025. Thereafter the affordability threshold would be set at 9.5% of household income with no indexing.People AffectedCBO projects that, under Section 137051, subsidized ACA Marketplace enrollment would increase by 3.6 million people (relative to the number of people who would be enrolled in the absence of these provisions).

CBO expects 1.4 million of these enrollees would otherwise be uninsured, while 600,000 would otherwise be covered by an how to get amoxil without a doctor unsubsidized individual market plan and 1.6 million would otherwise have employer coverage.Additionally, CBO expects the enhanced subsidies for people receiving unemployment insurance (Section 137507) would result in 500,000 people newly enrolling, on average per year during the 2022-2025 period. Most of these new enrollees would otherwise be uninsured.As of August 2021, 12.2 million people were how to get amoxil without a doctor actively enrolled in Marketplace plans – an 8% increase from 11.2 million people enrollees as of the close of Open Enrollment for the 2021 plan year. HealthCare.gov and all state Marketplaces reopened for a special enrollment period of at least 6 months in 2021, enrolling 2.8 million people (not all of whom were necessarily previously uninsured). Of these, 44% selected plans with monthly premiums of $10 or less.The US Department of Health and Human Services (HHS) reports that ARPA reduced Marketplace premiums for the 8 how to get amoxil without a doctor million existing Healthcare.gov enrollees by $67 per month, on average. If the ARPA subsidies are allowed to expire, these enrollees will likely see their premium payments double.HHS also reports that between July 1 and August 15, more than 280,000 individuals received enhanced subsidies due to the ARPA UI provisions.

Individuals eligible for these UI benefits can continue to how to get amoxil without a doctor enroll in 2021 coverage through the end of this year.The ARPA changes made people with income at or below 150% FPL eligible for zero-premium silver plans with comprehensive cost sharing subsidies. 40% of how to get amoxil without a doctor new consumers who signed up during the SEP are in a plan that covers 94% of expected costs (with average deductibles below $200). As a result of the ARPA, HHS reports the median deductible for new consumers selecting plan during the buy antibiotics-SEP decreased by more than 90% (from $750 in 2020 to $50 in 2021).With the ARPA and ACA subsidies, as well as Medicaid in states that expanded the program, we estimate that at least 46% of non-elderly uninsured people in the U.S. Are eligible for free or nearly-free health plans, often with low or no deductibles.Budgetary ImpactCBO published a score of certain provisions in the House Reconciliation legislation that affect coverage of nonelderly adults.CBO previously estimated that, over the ten year period 2022-2031, the cost of permanently extending how to get amoxil without a doctor ARPA ACA subsidies (Section 137501) would be $209.5 billion. Because the current legislation would only extend these subsidies through 2025, instead of making them permanent, the cost would be lower.

The cost of Section 137507, which extends additional tax credits for people receiving unemployment insurance, would be $10.6 how to get amoxil without a doctor billion over the ten-year period of 2022-2031. Modification of the affordability test for employer-sponsored coverage (Section 137502) would cost $10.8 billion over the ten-year period. As of the date of this publication, CBO estimates for ACA subsidy changes in how to get amoxil without a doctor effect for a shorter period of time were not yet available.(Back to top)2. New Medicare Hearing BenefitbackgroundTraditional Medicare currently does not cover hearing services, except under limited circumstances, such as cochlear how to get amoxil without a doctor implantation when beneficiaries meet certain eligibility criteria. Hearing services are typically offered by Medicare Advantage plans, and in 2021, 97% of Medicare Advantage enrollees in individual plans, or 17.1 million people, are offered some hearing benefits, but according to our analysis, the extent of that coverage and the value of these benefits varies.

Some beneficiaries in traditional Medicare may have private coverage or how to get amoxil without a doctor coverage through Medicaid for these services, but many do not.Provision DescriptionSection 30901 of the Build Back Better Act would add coverage of hearing services to Medicare Part B, beginning in 2023. Coverage for hearing care would include hearing rehabilitation and treatment services by qualified audiologists, and hearing aids. Hearing aids would be available once per ear, every 5 years, to individuals diagnosed with how to get amoxil without a doctor moderately severe, severe, or profound hearing loss. Hearing services how to get amoxil without a doctor would be subject to the Medicare Part B deductible and 20% coinsurance. Hearing aids would be covered similar to other Medicare prosthetic devices, and would also be subject to the Part B deductible and 20% coinsurance.

Payment for hearing aids would only be how to get amoxil without a doctor on an assignment-related basis. As with other Medicare-covered benefits, Medicare Advantage plans would be required to cover these hearing benefits.Effective Date. The Medicare hearing benefit provision would take effect in 2023.People AffectedAdding coverage of hearing services to traditional Medicare would benefit how to get amoxil without a doctor up to all 62 million people on Medicare, but particularly the roughly 36 million beneficiaries in traditional Medicare who currently lack coverage for these services. A new, defined Medicare Part B benefit could also lead to enhanced hearing benefits how to get amoxil without a doctor for Medicare Advantage enrollees. Because costs are often a barrier to care, adding this benefit to Medicare could increase use of these services, and contribute to better health outcomes.Coverage of hearing services under traditional Medicare also would make these services more affordable relative to what beneficiaries who use these services currently pay out-of-pocket.

Our analysis shows that beneficiaries who use hearing how to get amoxil without a doctor services can incur high out-of-pocket costs. Among beneficiaries who used hearing services in 2018, average spending was $914.BUDGETARY IMPACTCBO has not yet published budgetary estimates for this section of the Build Back Better Act.According to a CBO estimate of an earlier version of H.R.3 passed by the House of Representatives in 2019, which included a similar provision, adding coverage of hearing services to Medicare would increase federal spending by $89 billion over 10 years (2020-2029). However, a recent preliminary how to get amoxil without a doctor estimate from the White House projected the hearing benefit in the Build Back Better Act would cost $35 billion, so the final CBO estimate might be lower than previously estimated.(Back to top)3. Lowering Prescription Drug Prices and SpendingbackgroundCurrently, under the Medicare Part D program, how to get amoxil without a doctor which covers retail prescription drugs, Medicare contracts with private plan sponsors to provide a prescription drug benefit. The law that established the Part D benefit includes a provision known as the “noninterference” clause, which stipulates that the HHS Secretary “may not interfere with the negotiations between drug manufacturers and pharmacies and PDP [prescription drug plan] sponsors, and may not require a particular formulary or institute a price structure for the reimbursement of covered part D drugs.” For drugs administered by physicians that are covered under Medicare Part B, Medicare reimburses providers 106% of the Average Sales Price (ASP), which is the average price to all non-federal purchasers in the U.S, inclusive of rebates, A recent KFF Tracking Poll finds large majorities support allowing the federal government to negotiate and this support holds steady even after the public is provided the arguments being presented by parties on both sides of the legislative debate (83% total, 95% of Democrats, 82% of independents, and 71% of Republicans).In addition to the inability to negotiate drug prices under Part D, Medicare lacks the ability to limit annual price increases for drugs covered under Part B (which includes those administered by physicians) and Part D.

In contrast, how to get amoxil without a doctor Medicaid has an inflationary rebate in place. Year-to-year drug price increases exceeding inflation are not uncommon and affect people with both Medicare and private insurance. Our analysis shows that half of all covered Part D drugs had list price increases that exceeded the rate of inflation between 2018 and 2019.provision descriptionNegotiations how to get amoxil without a doctor. Sections 139001, 139002, and 139003 of the Build Back Better Act would amend the non-interference clause by adding an exception that would allow the federal government to negotiate prices with drug companies for a small number of how to get amoxil without a doctor high-cost drugs lacking generic or biosimilar competitors covered under Medicare Part B and Part D. The negotiation process would apply to no more than 10 (in 2025), 15 (in 2026 and 2027), and 20 (in 2028 and later years) single-source brand-name drugs lacking generic or biosimilar competitors, selected from among the 50 drugs with the highest total Medicare Part D spending and the 50 drugs with the highest total Medicare Part B spending (for 2027 and later years).

The negotiation process would also apply to all insulin products.The legislation exempts from negotiation drugs that are less than how to get amoxil without a doctor 9 years (for small-molecule drugs) or 13 years (for biological products, based on the Manager’s Amendment) from their FDA-approval or licensure date. The legislation also exempts “small biotech drugs” from negotiation until 2028, defined as those which account for 1% or less of Part D or Part B spending and account for 80% or more of spending under each part on that manufacturer’s drugs.The proposal establishes an upper limit for the negotiated price (the “maximum fair price”) equal to a percentage of the non-federal average manufacturer price. 75% for how to get amoxil without a doctor small-molecule drugs more than 9 years but less than 12 years beyond approval. 65% for drugs between 12 and how to get amoxil without a doctor 16 years beyond approval or licensure. And 40% for drugs more than 16 years beyond approval or licensure.

Part D drugs with prices how to get amoxil without a doctor negotiated under this proposal would be required to be covered by all Part D plans. Medicare’s payment to providers for Part B drugs with prices negotiated under this proposal would be 106% of the maximum fair price (rather than 106% of the average sales price under current law).An excise tax would be levied on drug companies that do not comply with the negotiation process, and civil monetary penalties on companies that do not offer the agreed-upon negotiated price to eligible purchasers.Effective Date. This provision would take effect in 2025, with the initial round of negotiated prices for drugs covered under Part D available that year how to get amoxil without a doctor. For drugs covered how to get amoxil without a doctor under Part B, negotiated prices would take effect in 2027.Inflation Rebates. Sections 139101 and 139102 of the Build Back Better Act would require drug manufacturers to pay a rebate to the federal government if their prices for single-source drugs and biologicals covered under Medicare Part B and nearly all covered drugs under Part D increase faster than the rate of inflation (CPI-U).

Under these how to get amoxil without a doctor provisions, price changes would be measured based on the average sales price (for Part B drugs) or the average manufacturer price (for Part D drugs). For price increase higher than inflation, manufacturers would be required to pay the difference in the form of a rebate to Medicare. The rebate amount is equal to the total number of units multiplied by the amount if any by which the how to get amoxil without a doctor manufacturer price exceeds the inflation-adjusted payment amount, including all units sold outside of Medicaid and therefore applying not only to use by Medicare beneficiaries but by privately insured individuals as well. Rebate dollars would be deposited in the Medicare Supplementary Medical Insurance (SMI) trust fund.Manufacturers that do not pay the requisite rebate amount would be required to pay a penalty equal to at least 125% of the how to get amoxil without a doctor original rebate amount. The base year for measuring price changes is 2021.Effective Date.

These provisions how to get amoxil without a doctor would take effect in 2023.Limits on Cost Sharing for Insulin Products. Sections 27001, 30604, and 139401, would require insurers, including Medicare Part D plans and private group or individual health plans, to charge no more than $35 for insulin products. Part D plans would be required to charge no more than $35 for whichever insulin products they cover for 2023 and how to get amoxil without a doctor 2024 and all insulin products beginning in 2025. Coverage of all insulin products would be required beginning in 2025 because the how to get amoxil without a doctor drug negotiation provision (described earlier) would require all Part D plans to cover all drugs that are selected for price negotiation, and all insulin products are subject to negotiation under that provision. Private group or individual plans do not have to cover all insulin products, just one of each dosage form (vial, pen) and insulin type (rapid-acting, short-acting, intermediate-acting, and long-acting) for no more than $35.Effective Date.

These provisions would take effect in how to get amoxil without a doctor 2023.treatments. Section 139402 would require that adult treatments covered under Medicare Part D that are recommended by the Advisory Committee on Immunization Practices (ACIP), such as for shingles, be covered at no cost. This would be consistent with coverage of treatments under Medicare Part B, such as the flu and buy antibiotics treatments.Effective how to get amoxil without a doctor Date. This provision would how to get amoxil without a doctor take effect in 2024.Repealing Drug Rebate Rule. Section 139301 would prohibit implementation of the November 2020 final rule issued by the Trump Administration that would have eliminated rebates negotiated between drug manufacturers and pharmacy benefit managers (PBMs) or health plan sponsors in Medicare Part D by removing the safe harbor protection currently extended to these rebate arrangements under the federal anti-kickback statute.

This rule was slated to take effect on January 1, 2022, but the Biden Administration delayed implementation to 2023 and the infrastructure legislation passed how to get amoxil without a doctor by the House and Senate includes a further delay to 2026.Effective Date. This provision would take effect in 2026.People affectedThe number of Medicare beneficiaries and privately insured individuals who would see lower out-of-pocket drug costs in any given year under these provisions would depend on how many and which drugs were subject to the negotiation process, and how many and which drugs had lower price increases, and the magnitude of price reductions relative to current prices under each provision.According to estimates from the CMS Office of the Actuary (OACT) of the drug price negotiation provision included in H.R.3 passed by the House of Representatives in 2019, allowing the federal government to negotiate drug prices would lower cost sharing for Part D enrollees by $102.6 billion in the aggregate (2020-2029) and Part D premiums for Medicare beneficiaries by $14.3 billion. Based on our analysis, premium savings for Medicare beneficiaries are projected to increase from an estimated 9% of the Part how to get amoxil without a doctor D base beneficiary premium in 2023 to 15% in 2029. The effects of the current legislation are likely to be more modest than this.While it is expected that some people would face lower cost sharing under these provisions, it is also possible that drug manufacturers could respond to how to get amoxil without a doctor the inflation rebate by increasing launch prices for new drugs. In this case, some individuals could face higher out-of-pocket costs for new drugs that come to market, with potential spillover effects on total costs incurred by payers as well.In terms of insulin costs, while formulary coverage and tier placement of insulin products vary across Medicare Part D plans, our analysis shows that in 2019, a large number of Part D plans placed insulin products on Tier 3, the preferred drug tier, which typically had a $47 copayment per prescription during the initial coverage phase.

However, once enrollees reach the coverage gap phase, they face a 25% how to get amoxil without a doctor coinsurance rate, which equates to $100 or more per prescription in out-of-pocket costs for many insulin therapies, unless they qualify for low-income subsidies. Paying a flat $35 copayment rather than 25% coinsurance could translate to meaningful savings on many insulin products.In terms of treatments, providing for coverage of adult treatments under Medicare Part D at no cost could help with treatment uptake among older adults. Our analysis shows that in 2018, Part D enrollees without low-income subsidies paid an average of $57 out-of-pocket for each dose of the shingles shot, which is free to most other people with private coverage.budgetary impactCBO has not yet published budgetary estimates for these sections how to get amoxil without a doctor of the Build Back Better Act.Negotiations. Based on earlier legislation, CBO estimated there would be over $450 billion in 10-year (2020-2029) how to get amoxil without a doctor savings from the Medicare drug price negotiation provision in drug price legislation considered in the 116th Congress (H.R. 3), including $448 billion in savings to Medicare and $12 billion in savings for subsidized plans in buy amoxil canada the ACA Marketplace and the Federal Employees Health Benefits Program.

CBO also estimated an increase in revenues of about $45 billion over 10 years resulting from lower drug prices available to employers, which would reduce premiums for how to get amoxil without a doctor employer-sponsored insurance, leading to higher compensation in the form of taxable wages.A separate CBO estimate of the same Medicare drug price negotiation provision included in another House bill in the 116th Congress (H.R. 1425, the Patient Protection and Affordable Care Enhancement Act) estimated higher 10-year (2021-2030) savings of nearly $530 billion, mainly because the Secretary would negotiate prices for a somewhat larger set of drugs in year 2 of the negotiation program under H.R. 1425.However, it is likely that the drug negotiation provision in the Build Back Better Act would generate substantially lower savings than either of these earlier proposals how to get amoxil without a doctor due to a reduction in the number and type of drugs eligible for negotiation and modifications to the upper limit for the negotiated price.Inflation Rebates. CBO estimated savings from the drug inflation rebate provisions in previous legislation (H.R. 3 and S how to get amoxil without a doctor.

2543, Senate Finance how to get amoxil without a doctor Committee legislation considered in the 116th Congress) amounting to $36 billion for H.R. 3 (2020-2029) and $82 billion for S. 2543 (2021-2030) how to get amoxil without a doctor. 10-year savings were estimated to be lower under H.R. 3 because the inflation provision would not apply to drugs subject to the government negotiation process that would be established by that bill how to get amoxil without a doctor.

This same exception applies in the how to get amoxil without a doctor Build Back Better Act. Savings are likely to differ for the inflation rebate provision in the Build Back Better Act because it applies to use by private insurers as well as Medicare and because it relies on a more recent benchmark year in calculating price increases than earlier legislative proposals.Repeal of Rebate Rule. Both CBO and Medicare’s actuaries estimated substantially higher Medicare spending how to get amoxil without a doctor over 10 years as a result of banning drug rebates – up to $170 billion higher, according to CBO, and up to $196 billion higher, according to the HHS Office of the Actuary (OACT). Because the cost of the rebate rule has been incorporated in CBO’s baseline for federal spending, repealing the rebate rule is expected to generate savings. CBO estimated $50.8 billion in savings between 2023 and 2026 associated with the three-year delay of this rule included in the Infrastructure Investment and Jobs how to get amoxil without a doctor Act.

The White House has estimated $145 billion how to get amoxil without a doctor in savings associated with the repeal of the rebate rule in the Build Back Better Act.(Back to top)4. Medicare Part D Benefit RedesignbackgroundMedicare Part D currently provides catastrophic coverage for high out-of-pocket drug costs, but there is no limit on the total amount that beneficiaries pay out-of-pocket each year. Medicare Part D enrollees with drug costs high enough to exceed the catastrophic coverage threshold are required to pay 5% of their total how to get amoxil without a doctor drug costs unless they qualify for Part D Low-Income Subsidies (LIS). Medicare pays 80% of total costs above the catastrophic threshold and plans pay 15%. Medicare’s reinsurance how to get amoxil without a doctor payments to Part D plans now account for close to half of total Part D spending (45%), up from 14% in 2006.Under the current structure of Part D, there are multiple phases, including a deductible, an initial coverage phase, a coverage gap phase, and the catastrophic phase.

When enrollees reach the coverage gap benefit phase, they pay 25% of drug costs for both how to get amoxil without a doctor brand-name and generic drugs. Plan sponsors pay 5% for brands and 75% for generics. And drug manufacturers provide a 70% price discount on brands (there is no discount on how to get amoxil without a doctor generics). Under the current benefit design, beneficiaries can face different cost sharing amounts for the same medication depending on which phase of the benefit they are in, and can face significant out-of-pocket costs for high-priced drugs because of coinsurance requirements and no hard out-of-pocket cap.provision descriptionSections 139201 and 139202 of the Build Back Better Act amend the design of the Part D benefit by adding a hard cap on out-of-pocket spending set at $2,000 in 2024, increasing each year based on the rate of increase in per capita Part D costs. It also lowers beneficiaries’ share of total drug costs below the spending cap from 25% to 23% how to get amoxil without a doctor.

It also lowers Medicare’s share of total costs above the spending cap (“reinsurance”) from 80% to 20% for brand-name drugs and to 40% for generic how to get amoxil without a doctor drugs. Increases plans’ share of costs from 15% to 60% for both brands and generics. And adds a 20% manufacturer price discount on brand-name drugs how to get amoxil without a doctor. Manufacturers would also be required to provide a 10% discount on brand-name drugs in the initial coverage phase (below the annual out-of-pocket spending threshold), instead of a 70% price discount.The legislation also increases Medicare’s premium subsidy for the cost of standard drug coverage to 76.5% (from 74.5% under current law) and reduces the beneficiary’s share of the cost to 23.5% (from 25.5%). The legislation also allows beneficiaries the option of smoothing out how to get amoxil without a doctor their out-of-pocket costs over the year rather than face high out-of-pocket costs in any given month.Effective Date.

The Part D redesign and premium subsidy changes would take effect in how to get amoxil without a doctor 2024. The smoothing out-of-pocket costs provision would take effect in 2025.people affectedWhile most Part D enrollees have not had out-of-pocket costs high enough to exceed the catastrophic coverage threshold in a single year, the likelihood of a Medicare beneficiary incurring drug costs above the catastrophic threshold increases over a longer time span.Our analysis shows that in 2019, nearly 1.5 million Medicare Part D enrollees had out-of-pocket spending above the catastrophic coverage threshold. Looking over a how to get amoxil without a doctor five-year period (2015-2019), the number of Part D enrollees with out-of-pocket spending above the catastrophic threshold in at least one year increases to 2.7 million, and over a 10-year period (2010-2019), the number of enrollees increases to 3.6 million.We also find that in 2019, nearly 1 million more Part D enrollees incurred out-of-pocket costs for their medications above $2,000, the proposed out-of-pocket spending limit in the Build Back Better Act, than above $3,100, the proposed out-of-pocket spending limit in recent GOP drug legislation (H.R. 19) and a 2019 Senate Finance Committee bill (S. 2543).

Overall, 1.2 million Part D enrollees in 2019 incurred annual out-of-pocket costs for their medications above $2,000, while 0.3 million spent more than $3,100 out-of-pocket.Medicare Part D enrollees with higher-than-average out-of-pocket costs could save substantial amounts with an out-of-pocket spending cap, as our analysis shows. For example, the top 10% of beneficiaries (122,000 enrollees) with average out-of-pocket costs for their medications above $2,000 in 2019 – who spent at least $5,348 – would have saved $3,348 (63%) in out-of-pocket costs with a $2,000 cap and $2,248 (42%) with a $3,100 cap.budgetary impactCBO has not yet published budgetary estimates for these sections of the Build Back Better Act.Adding a cap on out-of-pocket drug spending under Part D could add costs to the program. However, other features of the redesign proposal could mitigate the spending impact, in particular the reduction in the percentage of total drug costs that Medicare pays above the annual out-of-pocket spending threshold and the increased liability for plans and manufacturers.(Back to top)5. Medicaid Coverage GapbackgroundThere are currently 12 states that have not adopted the ACA provision to expand Medicaid to adults with incomes through 138% of poverty. The result is a coverage gap for individuals whose below-poverty-level income is too high to qualify for Medicaid in their state, but too low to be eligible for premium subsidies in the ACA Marketplace.provision descriptionSection 137304 of the Build Back Better Act would allow people living in states that have not expanded Medicaid to purchase subsidized coverage on the ACA Marketplace for 2022 through 2025.

The federal government would fully subsidize the premium for a benchmark plan. People would also be eligible for cost sharing subsidies that would reduce their out-of-pocket costs to 1% of overall covered health expenses on average.Section 30608 includes adjustments to uncompensated care (UCC) pools and disproportionate share hospital (DSH) payments for non-expansion states. These states would not be able draw down federal matching funds for UCC amounts for individuals who could otherwise qualify for Medicaid expansion, and their DSH allotments would be reduced by 12.5% starting in 2023.Section 30609 would increase the federal match rate for states that have adopted the ACA Medicaid expansion from 90% to 93% from 2023 through 2025, designed to discourage states from dropping current expansion coverage.people affectedWe estimate that 2.2 million uninsured people with incomes under poverty fall in the “coverage gap”. Most in the coverage gap are concentrated in four states (TX, FL, GA and NC) where eligibility levels for parents in Medicaid are low, and there is no coverage pathway for adults without dependent children. Half of those in the coverage gap are working and six in 10 are people of color.An earlier CBO estimate showed that extending Marketplace subsidies to people with income below 100% of poverty over the 2022-2024 period would increase enrollment in nongroup resulting in 1.7 million fewer uninsured people on average over the period.budgetary impactAn earlier CBO estimate showed that the federal cost of extending Marketplace coverage to certain low-income people would increase federal costs by $47.4 billion in federal fiscal years 2022-2024.Federal costs could be reduced due to lower spending on uncompensated care and DSH for certain states, but there would be additional federal costs to increase the match rate for current expansion states from 90% to 93% for expansion states for 2023 through 2025.(Back to top)6.

Maternity Care and Postpartum CoveragebackgroundMedicaid currently covers almost half of births in the U.S. Federal law requires that pregnancy-related Medicaid coverage last through 60 days postpartum. After that period, some may qualify for Medicaid through another pathway, but others may not qualify, particularly in non-expansion states. In an effort to improve maternal health and coverage stability and to help address racial disparities in maternal health, a provision in the American Rescue Plan Act (ARPA) of 2021 gives states a new option to extend Medicaid postpartum coverage to 12 months. This new option takes effect on April 1, 2022 and is available to states for five years.provision descriptionSection 30721 of the Build Back Better Act would require states to extend Medicaid postpartum coverage from 60 days to 12 months, ensuring continuity of Medicaid coverage for postpartum individuals in all states.

This requirement would take effect in the first fiscal quarter beginning one year after enactment and also applies to state CHIP programs that cover pregnant individuals.Section 30722 would create a new option for states to coordinate care for Medicaid-enrolled pregnant and post-partum individuals through a maternal health home model. States that take up this option would receive a 15% increase in FMAP for care delivered through maternal health homes for the first two years. States that are interested in pursuing this new option can receive planning grants prior to implementation.Sections 31031 through 31048 of the Build Back Better Act provide federal grants to bolster other aspects of maternal health care. The funds would be used to address a wide range of issues, such as addressing social determinants of maternal health. Diversifying the perinatal nursing workforce, expanding care for maternal mental health and substance use, and supporting research and programs that promote maternal health equity.people affectedLargely in response to the new federal option, at least 26 states have taken steps to extend Medicaid postpartum coverage.

Pregnant people in non-expansion states could see the biggest change as they are more likely than those in expansion states to become uninsured after the 60-day postpartum coverage period. For example, in Alabama, the Medicaid eligibility level for pregnant individuals is 146% FPL, but only 18% FPL (approximately $4,000/year for a family of three) for parents.Some states have piloted maternal health homes and seen positive impacts on health outcomes. The federal grant provisions related to maternal health could affect care for all persons giving birth, but the focus of these proposals is on reducing racial and ethnic inequities. There were approximately 3.7 million births in 2019, and nearly half were to women of color. There are approximately 700-800 pregnancy-related deaths annually, with the rate 2-3 times higher among Black and American Indian and Alaska Native women compared to White women.

Additionally, there are stark racial and ethnic disparities in other maternal and health outcomes, including preterm birth and infant mortality.budgetary impactCBO has not yet published budgetary estimates for these sections of the Build Back Better Act.However, in June 2020, prior to the enactment of the ARPA option for postpartum coverage, CBO estimated that a proposal to require 12 month postpartum coverage in Medicaid and CHIP would have a net federal cost of $6 billion over 10 years (new costs of $12.3 billion offset by revenues).In FY 2022, $5 million is appropriated for planning grants to states for maternal health homes.Total allocations in FY 2022 for the federal grant sections in the Build Back Better Act related to maternal health care outside of the postpartum extension and maternal health homes are $1.1 billion.(Back to top)7. Other Medicaid and Children’s Health Insurance (CHIP) ChangesbackgroundUnder current law, states have the option to provide 12-months of continuous coverage for children. Under this option, states allow a child to remain enrolled for a full year unless the child ages out of coverage, moves out of state, voluntarily withdraws, or does not make premium payments. As such, 12-month continuous eligibility eliminates coverage gaps due to fluctuations in income over the course of the year.Under current law, Medicaid is the base of coverage for low-income children. CHIP complements Medicaid by covering uninsured children in families with incomes above Medicaid eligibility levels.

Unlike Medicaid, federal funding for CHIP is capped and provided as annual allotments to states. CHIP funding is authorized through September 30, 2027. While CHIP generally has bipartisan support, during the last reauthorization funding lapsed before Congress reauthorized funding.provision descriptionSection 30741 of the Build Back Better Act would require states to extend 12-month continuous coverage for children on Medicaid and CHIP.Section 30801 of the Build Back Better Act would permanently extend the CHIP program.people affectedAs of May 2021, there were 39 million children enrolled in Medicaid and CHIP (nearly half of all enrollees). As of January 2020, 34 states provide 12-month continuous eligibility to at least some children in either Medicaid or CHIP. A recent MACPAC report found that the overall mean length of coverage for children in 2018 was 11.7 months, and also that rates of churn (in which children dis-enroll and reenroll within a short period of time) were lower in states that had adopted the 12-month continuous coverage option and in states that did not conduct periodic data checks.

Another recent report shows that children with gaps in coverage during a year are more likely to be children of color with lower incomes.As of May 2021, there were 6.9 million people (mostly children) enrolled in CHIP.budgetary impactCBO has not yet published budgetary estimates for this section of the Build Back Better Act.Given that the length of coverage for children in Medicaid is already high (mean of 11.7 months), more than half of all states already have a continuous coverage policy in place, and costs for children are generally lower compared to other eligibility groups, new federal costs could be moderate. In addition, reducing churn could modestly reduce Medicaid administrative costs.Federal CHIP funding in Fiscal Year (FY) 2020 for the states was $17.0 billion. Since CHIP is authorized through FY 2027, CBO estimates would only account for costs in FY 2028 – FY 2031 (the current ten-year window). When CHIP was reauthorized through FY 2027, CBO estimated that this would result in net fiscal savings to the federal government because without CHIP, other alternatives would have higher federal costs and because of expected changes in the federal match rate back to traditional CHIP match rates.(Back to top)8. Other Medicaid Financing and Benefit ChangesbackgroundUnlike in the 50 states and D.C., annual federal funding for Medicaid in the U.S.

Territories is subject to a statutory cap and fixed matching rate. The funding caps and match rates have been increased by Congress in response to emergencies over time.To help support states and promote stability of coverage during the buy antibiotics amoxil, the Families First antibiotics Response Act (FFCRA) provides a 6.2 percentage point increase in the federal share of certain Medicaid spending, provided that states meet maintenance of eligibility (MOE) requirements that include ensuring continuous coverage for current enrollees.treatments are an optional benefit for certain adult populations, including low-income parent/caretakers, pregnant women, and persons who are eligible based on old age or a disability. For adults enrolled under the ACA’s Medicaid expansion and other populations for whom the state elects to provide an “alternative benefit plan,” their benefits are subject to certain requirements in the ACA, including coverage of treatments recommended by the Advisory Committee on Immunization Practices (ACIP) with no cost sharing.Under the Families First antibiotics Response Act, coverage of testing and treatment for buy antibiotics, including treatments, is required with no cost sharing in order for states to access temporary enhanced federal funding for Medicaid which is tied to the public health emergency. The American Rescue Plan Act (ARPA) clarified that coverage of buy antibiotics treatments and their administration, without cost sharing, is required for nearly all Medicaid enrollees, through the last day of the 1st calendar quarter beginning at least 1 year after the public health emergency ends. The ARPA also provides 100% federal financing for this coverage.provision descriptionSection 30731 of the Build Back Better Act would increase the Medicaid cap amount and match rate for the territories.

The FMAP would be permanently adjusted to 83% for the territories beginning in FY 2022, except that Puerto Rico’s match rate would be 76% in FY 2022 before increasing to 83% in FY 2023 and subsequent years. The legislation would also require a payment floor for certain physician services in Puerto Rico with a penalty for failure to establish the floor.Section 30741 of the Build Back Better Act would phase out the FFCRA enhanced federal funding to states. States would continue to receive the 6.2 percentage point increase through March 31, 2022, followed by a 3.0 percentage point increase from April 1, 2022 through June 30, 2022, and a 1.5 percentage point increase from July 1, 2022 through September 30, 2022.Section 30741 also would modify the FFCRA MOE requirement for continuous coverage. From April 1 through September 30, 2022, states could continue receiving the enhanced federal matching funds if they terminate coverage for individuals who are determined no longer eligible for Medicaid and have been enrolled at least 12 consecutive months. The legislation includes other rules for states about conducting eligibility redeterminations and when states can terminate coverage.Section 30751 of the Build Back Better Act would establish a 3.1 percentage point FMAP reduction from October 1, 2022 through December 31, 2025 for states that adopt eligibility standards, methodologies, or procedures that are more restrictive than those in place as of October 1, 2021 (except the penalty would not apply to coverage of non-pregnant, non-disabled adults with income above 133% FPL after December 31, 2022, if the state certifies that it has a budget deficit).Section 139405 of the Build Back Better Act would require state Medicaid programs to cover all approved treatments recommended by ACIP and treatment administration, without cost sharing, for categorically and medically needy adults.

States that provide adult treatment coverage without cost sharing as of the date of enactment would receive a 1 percentage point FMAP increase for 8 quarters.people affectedIn June 2019 there were approximately 1.3 million Medicaid enrollees in the territories (with 1.2 million in Puerto Rico).From February 2020 through May 2021 Medicaid and CHIP enrollment has increased by 11.5 million or 16.2% due to the economic effects of the amoxil and MOE requirements.All states provide some treatment coverage for adults enrolled in Medicaid who are not covered as part of the ACA’s Medicaid expansion, but as of 2019, only about half of states covered all ACIP-recommended treatments.budgetary impactCBO has not yet published budgetary estimates for these sections of the Build Back Better Act.With the public health emergency unwinding, states are likely to face pressures to contain growth in state spending tied to enrollment, particularly after the enhanced FMAP ends, even as they work to overcome challenges with systems and staffing to ensure that eligible individuals remain covered by Medicaid or transition to other sources of coverage.(Back to top)9. Medicaid Home and Community Based Services and the Direct Care WorkforcebackgroundMedicaid is currently the primary payer for long-term services and supports (LTSS), including home and community-based services (HCBS), that help seniors and people with disabilities with daily self-care and independent living needs. There is currently a great deal of state variation as most HCBS eligibility pathways and benefits are optional for states.PROVISION DESCRIPTIONSections 30711-30713 of the Build Back Better Act would create the HCBS Improvement Program, which would provide a permanent 6 percentage point increase in federal Medicaid matching funds for HCBS. To qualify for the enhanced funds, states would have to maintain existing HCBS eligibility, benefits, and payment rates and have an approved plan to expand HCBS access, strengthen the direct care workforce, and monitor HCBS quality. The bill includes some provisions to support family caregivers.

In addition, the Act would include funding ($130 million) for state planning grants and enhanced funding for administrative costs for certain activities (80% instead of 50%).Section 30714 of the Build Back Better Act would require states to report HCBS quality measures to HHS, beginning 2 years after the Secretary publishes HCBS quality measures as part of the Medicaid/CHIP core measures for children and adults. The bill provides states with an enhanced 80% federal matching rate for adopting and reporting these measures.Sections 30715 and 30716 of the Build Back Better Act would make the ACA HCBS spousal impoverishment protections and the Money Follows the Person (MFP) program permanent.Sections 22301 and 22302 of the Build Back Better Act would provide $1 billion in grants to states, community-based organizations, educational institutions, and other entities by the Department of Labor Secretary to develop and implement strategies for direct service workforce recruitment, retention, and/or education and training.Section 25005 of the Build Back Better Act would provide $20 million for HHS and the Administration on Community Living to establish a national technical assistance center for supporting the direct care workforce and family caregivers.Section 25006 of the Build Back Better Act would provide $40 million for the HHS Secretary to award to states, nonprofits, educational institutions, and other entities to address the behavioral health needs of unpaid caregivers of older individuals and older relative caregivers.people affectedThe majority of HCBS are provided by waivers, which served over 2.5 million enrollees in 2018. There is substantial unmet need for HCBS, which is expected to increase with the growth in the aging population in the coming years. Nearly 820,000 people in 41 states were on a Medicaid HCBS waiver waiting list in 2018. Though waiting lists alone are an incomplete measure, they are one proxy for unmet need for HCBS.

Additionally, a shortage of direct care workers predated and has been intensified by the buy antibiotics amoxil, characterized by low wages and limited opportunities for career advancement. The direct care workforce is disproportionately female and Black.A KFF survey found that, as of 2018, 14 states expected that allowing the ACA spousal impoverishment provision to expire would affect Medicaid HCBS enrollees, for example by making fewer individuals eligible for waiver services.Over 101,000 seniors and people with disabilities across 44 states and DC moved from nursing homes to the community using MFP funds from 2008-2019. A federal evaluation of MFP showed about 5,000 new participants in each six month period from December 2013 through December 2016, indicating a continuing need for the program.Budgetary ImpactCBO has not yet published budgetary estimates for these sections of the Build Back Better Act.The House Energy and Commerce Committee markup of the bill described the cost to the federal government as $190 billion. This is less than the $400 billion originally proposed by President Biden. While the program requirements are not the same, CBO previously estimated that the American Rescue Plan Act’s 10 percentage point increase in federal matching funds for Medicaid HCBS for 1 year would increase federal costs by about $12.7 billion.(Back to top)10.

Paid Family and Medical LeavebackgroundThe U.S. Is the only industrialized nation without a minimum standard of paid family or medical leave. Although six states and DC have paid family and medical leave laws in effect, and some employers voluntarily offer these benefits, this has resulted in a patchwork of policies with varying degrees of generosity and leaves many workers without a financial safety net when they need to take time off work to care for themselves or their families.provision descriptionSection 130001 of the Build Back Better Act would guarantee four weeks per year of paid family and medical leave to all workers in the U.S. Who need time off work to welcome a new child, recover from a serious illness, or care for a seriously ill family member. Annual earnings up to $15,080 would be replaced at approximately 90% of average weekly earnings, plus about 73% of average weekly earnings for annual wages between $15,080 and $32,248, capping out at 53% of average weekly earnings for annual wages between $32,248 and $62,000.

While all workers taking qualified leave would be eligible for at least some wage replacement, the progressive benefits formula means that the share of pay replaced while on qualified leave is highest for workers with lower wages. The original Act called for 12 weeks of paid leave for similar qualified reasons, plus three days of bereavement leave, and benefits began at 85% of average weekly earnings for annual wages up to $15,080 and were capped at 5% of average weekly earnings for annual wages up to $250,000.people affectedAccording to the Bureau of Labor Statistics (BLS), approximately one in four (23%) workers has access to paid family leave through their employer. Data on the share of workers with access to paid medical leave for their own longer, serious illness are limited, although BLS also reports that 40% of workers have access to short-term disability insurance.​It is estimated that 53 million adults are caregivers for a dependent child or adult and 61% of them are women. Sixty percent (60%) of caregivers reported having to take a leave of absence leave from work or cut their hours in order to care for a family member. Workers who take leave do so for different reasons.

Half (51%) reported taking leave due to their own serious illness, one-quarter (25%) for reasons related to pregnancy, childbirth, or bonding with a new child, and one-fifth (19%) to care for a seriously ill family member. In total, four in ten (42%) reported receiving their full pay while on leave, one-quarter (24%) received partial pay, and one-third (34%) received no pay.budgetary impactCBO has not yet published budgetary estimates for this section of the Build Back Better Act.The current Build Back Better Act would allocate $1.5 billion for paid family and medical leave program administration for FY 2022. The Act states that Treasury funds not otherwise appropriated shall be appropriated “as may be necessary” for paid leave benefits and grants.(Back to top).

On November 5, 2021, the Centers for Medicare and http://www.em-oberschaeffolsheim.site.ac-strasbourg.fr/?p=812 Medicaid Services (CMS) published regulations that establish the first ever federal vaccination requirements for health amoxil street price care provider staff. Drawing on its authority to establish patient health and safety standards, CMS is requiring health care providers that participate in the Medicare and/or Medicaid programs to ensure that their staff are fully amoxil street price vaccinated against buy antibiotics. The new rule applies to staff who provide any care, treatment, or other services for providers or patients, including contractors and volunteers.CMS says it is now requiring health care staff to be vaccinated because its earlier efforts to simply encourage vaccination have been “insufficient” to protect patient health and safety. CMS cites data amoxil street price showing that buy antibiotics cases in nursing homes surged with the rise of the Delta variant.

The nursing home staff vaccination rate is nearly 73 % nationally as of October 2021, with substantial variation by region. CMS concluded that standard federal requirements across provider types are needed because the amoxil street price existing “patchwork” of state and employer requirements has not been enough to bring the amoxil under control in health care settings. CMS notes that the treatments are safe and highly effective at preventing severe illness and death, and unvaccinated staff can strain the health care system by transmitting buy antibiotics to patients and having to miss work if they are recovering from buy antibiotics or quarantining after exposure.The new rule applies to Medicare and Medicaid providers amoxil street price that are directly regulated by CMS and therefore does not reach all Medicaid providers, such as certain home and community-based services (HCBS) providers. The rule applies to nursing homes, hospitals, outpatient rehab facilities, federally qualified health centers, rural health centers, and home health agencies, among other provider types.

Residents and staff of other HCBS providers, such as group homes, assisted living facilities, and day habilitation programs, face increased risk of serious illness or death amoxil street price from buy antibiotics, similar to nursing homes. But, because states (and not CMS) license and regulate these providers, CMS has not required them to comply with the new rule. States or individual providers could adopt staff vaccination mandates, and providers may be subject to other rules such as the Occupational Safety and Health Administration requirement for large employers (which has been put on hold by the courts) or state or local requirements.The new rule raises many important issues to amoxil street price watch:Will providers have enough lead time to implement the new rule?. Staff must have received their first treatment dose by December 6, 2021, and must be fully vaccinated by January 4, 2022, or have been granted an exemption (based on disability amoxil street price or sincere religious belief) or temporary delay (based on CDC clinical guidelines).

Decisions about whether to grant exemptions will be made by providers. The rule amoxil street price does not require staff to receive booster shots, though providers must track staff who have received a CDC-recommended booster. Providers also must implement “additional precautions” to mitigate buy antibiotics transmission and adopt contingency plans to address staff who are not fully vaccinated.How will the new rule affect health care staffing levels?. An October 2021 KFF tracking poll found that 1 in 5 adults continue to say that they amoxil street price definitely will not get the buy antibiotics treatment or will do so only if required.

When asked what they would do if their employer required amoxil street price the buy antibiotics treatment without an option for regular testing, 72% of unvaccinated workers (9% of all adults) say they would leave their jobs. The same poll found that just 5% of unvaccinated adults said they have left a job because an employer required them to get vaccinated. CMS acknowledges that some staff may amoxil street price leave their jobs because they do not want to receive the treatment. It remains to be seen whether the new rule will exacerbate existing staffing shortages or whether these effects may vary by region.

CMS cites examples of treatment mandates adopted by health systems in Texas and Detroit and a long-term care parent corporation with 250 facilities as well as the New York state health care worker mandate, all of which resulted in high rates of compliance and few employee resignations.Will efforts to monitor and enforce the new amoxil street price rule be sufficient?. CMS says that provider compliance with the new rule will be part of the existing oversight process through which state or federal inspectors review all amoxil street price Medicare and Medicaid program requirements. CMS envisions that inspectors will review facility policies and records and conduct staff interviews to verify vaccination status. CMS will amoxil street price provide guidance about oversight as well as penalties for noncompliance, which could include civil monetary penalties, denial of payment for new long-term care facility admissions, or termination of Medicare and/or Medicaid program participation.How long will the new rule be in place?.

CMS will determine whether to make the new rule permanent based on public comments (due January 4, 2022) and the future course of the amoxil. The new rule is not tied to the duration of the buy antibiotics public amoxil street price health emergency (PHE), and CMS expects that it will “remain relevant for some time beyond” the PHE end. Medicare interim final rules expire after three years unless they amoxil street price are finalized. In the near term, the new rule already has been challenged in a lawsuit filed by 10 state attorneys general in Missouri federal district court, which could delay or prevent implementation of the rule.Congress is considering a broad package of health, social, and environmental programs supported by President Biden, called the Build Back Better Act.

The total cost of the original package had been pegged at $3.5 trillion (much of which would be offset by savings and new revenue), though amoxil street price the legislation has since changed in ways that will likely reduce the total. This brief summarizes major health provisions as of the bill reported to the House Rules Committee on November 3, 2021, which, at the time of publication, has not yet received a CBO score. Negotiations are ongoing and there may be future changes.Here, we walk through 10 of the major health coverage amoxil street price and financing provisions of the Build Back Better Act, with discussion of the potential implications for people and the federal budget. We summarize provisions relating to the following areas and provide data on the people most directly affected by each provision and the potential costs or savings to the amoxil street price federal government.ACA Marketplace SubsidiesNew Medicare Hearing BenefitLowering Prescription Drug Prices and SpendingMedicare Part D Benefit RedesignMedicaid Coverage GapMaternal Care and Postpartum CoverageOther Medicaid / Children’s Health Insurance Changes CHIP ChangesOther Medicaid Financing and Benefit ChangesMedicaid Home and Community Based Services and the Direct Care WorkforcePaid Family and Medical LeaveA recent KFF poll found broad support for many of these provisions, though it did not probe on the costs or trade-offs associated with them.

The poll also found that the vast majority of the public supports allowing the federal government to negotiate drug prices, after hearing arguments made by proponents and opponents.Major Provisions of the Build Back Better Act and their Potential Costs and Impact1. ACA Marketplace SubsidiesBackgroundUnder the Affordable Care Act, people purchasing Marketplace coverage could only qualify for subsidies if they met other amoxil street price eligibility requirements and had incomes between one and four times the federal poverty level. People eligible for subsidies would have to contribute a sliding-scale percentage of their income toward a benchmark premium, ranging from 2.07% to 9.83%. Once income passed 400% FPL, subsidies stopped and many individuals and families were unable to afford coverage.In 2021, the American Rescue amoxil street price Plan Act (ARPA) temporarily expanded eligibility for subsidies by removing the upper income threshold.

It also temporarily increased the dollar value of premium subsidies across the board, meaning nearly everyone on the Marketplace paid lower premiums, and the lowest income people amoxil street price pay zero premium for coverage with very low deductibles. The ARPA also made people who received unemployment insurance (UI) benefits during 2021 eligible for zero-premium, low-deductible plans.However, the ARPA provisions removing the upper income threshold and increasing tax credit amounts are only in effect for 2021 and 2022. The unemployment provision is only in effect for 2021.Provision DescriptionSection 137301 of The Build Back Better Act would extend the ARPA subsidy changes that eliminate the income eligibility cap and increase the amount of APTC for individuals across the board through the end of 2025.Additionally, Section 30605 of The Build Back Better Act would extend the special Marketplace subsidy rule for individuals receiving UI benefits for an additional amoxil street price 4 years, through the end of 2025.Section 137303 of the Act would, for purposes of determining eligibility for premium tax credits, disregard any lump sum Social Security benefit payments in a year. This provision would be permanent and effective starting in the 2022 tax year.

Starting in 2026, people would have the option to have the lump sum benefit included in their income for purposes of determining tax credit eligibility.Finally, Section 137302 modifies the affordability test for employer-sponsored health coverage amoxil street price. The ACA makes people ineligible for marketplace subsidies if they have an offer of affordable coverage from an employer, amoxil street price currently defined as requiring an employee contribution of no more than 9.61% of household income in 2022. The Build Back Better Act would reduce this affordability threshold to 8.5% of income, bringing it in line with the maximum contribution required to enroll in the benchmark marketplace plan. This provision would take effect for tax years starting in amoxil street price 2022 through 2025.

Thereafter the affordability threshold would be set at 9.5% of household income with no indexing.People AffectedCBO projects that, under Section 137051, subsidized ACA Marketplace enrollment would increase by 3.6 million people (relative to the number of people who would be enrolled in the absence of these provisions). CBO expects 1.4 million of these enrollees would otherwise be uninsured, while 600,000 would otherwise be covered by an unsubsidized individual market plan and amoxil street price 1.6 million would otherwise have employer coverage.Additionally, CBO expects the enhanced subsidies for people receiving unemployment insurance (Section 137507) would result in 500,000 people newly enrolling, on average per year during the 2022-2025 period. Most of these new enrollees would otherwise be uninsured.As of August 2021, 12.2 million people were actively enrolled in Marketplace plans – an 8% increase from 11.2 million people enrollees as of the close of Open amoxil street price Enrollment for the 2021 plan year. HealthCare.gov and all state Marketplaces reopened for a special enrollment period of at least 6 months in 2021, enrolling 2.8 million people (not all of whom were necessarily previously uninsured).

Of these, 44% selected plans with monthly premiums of $10 or less.The US Department of Health and Human Services (HHS) reports that amoxil street price ARPA reduced Marketplace premiums for the 8 million existing Healthcare.gov enrollees by $67 per month, on average. If the ARPA subsidies are allowed to expire, these enrollees will likely see their premium payments double.HHS also reports that between July 1 and August 15, more than 280,000 individuals received enhanced subsidies due to the ARPA UI provisions. Individuals eligible for these UI benefits can continue to enroll in 2021 coverage through the end of amoxil street price this year.The ARPA changes made people with income at or below 150% FPL eligible for zero-premium silver plans with comprehensive cost sharing subsidies. 40% of new consumers who signed up during the SEP are in a plan that covers 94% of expected costs (with amoxil street price average deductibles below $200).

As a result of the ARPA, HHS reports the median deductible for new consumers selecting plan during the buy antibiotics-SEP decreased by more than 90% (from $750 in 2020 to $50 in 2021).With the ARPA and ACA subsidies, as well as Medicaid in states that expanded the program, we estimate that at least 46% of non-elderly uninsured people in the U.S. Are eligible for free or nearly-free health plans, often with low or no deductibles.Budgetary amoxil street price ImpactCBO published a score of certain provisions in the House Reconciliation legislation that affect coverage of nonelderly adults.CBO previously estimated that, over the ten year period 2022-2031, the cost of permanently extending ARPA ACA subsidies (Section 137501) would be $209.5 billion. Because the current legislation would only extend these subsidies through 2025, instead of making them permanent, the cost would be lower. The cost of Section 137507, which extends additional tax credits for people receiving unemployment insurance, would be $10.6 billion over amoxil street price the ten-year period of 2022-2031.

Modification of the affordability test for employer-sponsored coverage (Section 137502) would cost $10.8 billion over the ten-year period. As of amoxil street price the date of this publication, CBO estimates for ACA subsidy changes in effect for a shorter period of time were not yet available.(Back to top)2. New Medicare amoxil street price Hearing BenefitbackgroundTraditional Medicare currently does not cover hearing services, except under limited circumstances, such as cochlear implantation when beneficiaries meet certain eligibility criteria. Hearing services are typically offered by Medicare Advantage plans, and in 2021, 97% of Medicare Advantage enrollees in individual plans, or 17.1 million people, are offered some hearing benefits, but according to our analysis, the extent of that coverage and the value of these benefits varies.

Some beneficiaries in traditional Medicare may have private coverage or coverage through Medicaid for these services, but many do not.Provision DescriptionSection 30901 of the Build Back Better Act would add coverage of hearing services to Medicare Part amoxil street price B, beginning in 2023. Coverage for hearing care would include hearing rehabilitation and treatment services by qualified audiologists, and hearing aids. Hearing aids amoxil street price would be available once per ear, every 5 years, to individuals diagnosed with moderately severe, severe, or profound hearing loss. Hearing services would amoxil street price be subject to the Medicare Part B deductible and 20% coinsurance.

Hearing aids would be covered similar to other Medicare prosthetic devices, and would also be subject to the Part B deductible and 20% coinsurance. Payment for hearing amoxil street price aids would only be on an assignment-related basis. As with other Medicare-covered benefits, Medicare Advantage plans would be required to cover these hearing benefits.Effective Date. The Medicare hearing benefit provision would take effect in 2023.People AffectedAdding coverage of hearing services to traditional Medicare would benefit up to all 62 million people on Medicare, but particularly the roughly 36 million beneficiaries in traditional Medicare who currently lack amoxil street price coverage for these services.

A new, defined Medicare Part B benefit could also lead amoxil street price to enhanced hearing benefits for Medicare Advantage enrollees. Because costs are often a barrier to care, adding this benefit to Medicare could increase use of these services, and contribute to better health outcomes.Coverage of hearing services under traditional Medicare also would make these services more affordable relative to what beneficiaries who use these services currently pay out-of-pocket. Our analysis shows that beneficiaries who use hearing services amoxil street price can incur high out-of-pocket costs. Among beneficiaries who used hearing services in 2018, average spending was $914.BUDGETARY IMPACTCBO has not yet published budgetary estimates for this section of the Build Back Better Act.According to a CBO estimate of an earlier version of H.R.3 passed by the House of Representatives in 2019, which included a similar provision, adding coverage of hearing services to Medicare would increase federal spending by $89 billion over 10 years (2020-2029).

However, a recent preliminary estimate from the White House projected the hearing benefit in the Build Back Better Act would cost $35 billion, so the final CBO estimate might be lower amoxil street price than previously estimated.(Back to top)3. Lowering Prescription Drug Prices and SpendingbackgroundCurrently, under the Medicare Part D program, which covers retail prescription drugs, Medicare contracts with private amoxil street price plan sponsors to provide a prescription drug benefit. The law that established the Part D benefit includes a provision known as the “noninterference” clause, which stipulates that the HHS Secretary “may not interfere with the negotiations between drug manufacturers and pharmacies and PDP [prescription drug plan] sponsors, and may not require a particular formulary or institute a price structure for the reimbursement of covered part D drugs.” For drugs administered by physicians that are covered under Medicare Part B, Medicare reimburses providers 106% of the Average Sales Price (ASP), which is the average price to all non-federal purchasers in the U.S, inclusive of rebates, A recent KFF Tracking Poll finds large majorities support allowing the federal government to negotiate and this support holds steady even after the public is provided the arguments being presented by parties on both sides of the legislative debate (83% total, 95% of Democrats, 82% of independents, and 71% of Republicans).In addition to the inability to negotiate drug prices under Part D, Medicare lacks the ability to limit annual price increases for drugs covered under Part B (which includes those administered by physicians) and Part D. In contrast, amoxil street price Medicaid has an inflationary rebate in place.

Year-to-year drug price increases exceeding inflation are not uncommon and affect people with both Medicare and private insurance. Our analysis shows that half of all covered Part D drugs had list price increases that exceeded the rate of inflation between 2018 and 2019.provision descriptionNegotiations amoxil street price. Sections 139001, 139002, and 139003 of the Build Back Better Act would amend amoxil street price the non-interference clause by adding an exception that would allow the federal government to negotiate prices with drug companies for a small number of high-cost drugs lacking generic or biosimilar competitors covered under Medicare Part B and Part D. The negotiation process would apply to no more than 10 (in 2025), 15 (in 2026 and 2027), and 20 (in 2028 and later years) single-source brand-name drugs lacking generic or biosimilar competitors, selected from among the 50 drugs with the highest total Medicare Part D spending and the 50 drugs with the highest total Medicare Part B spending (for 2027 and later years).

The negotiation process would also apply to all insulin products.The legislation exempts from negotiation drugs that are less than 9 years (for small-molecule drugs) or 13 years (for biological products, based on the Manager’s Amendment) from their FDA-approval amoxil street price or licensure date. The legislation also exempts “small biotech drugs” from negotiation until 2028, defined as those which account for 1% or less of Part D or Part B spending and account for 80% or more of spending under each part on that manufacturer’s drugs.The proposal establishes an upper limit for the negotiated price (the “maximum fair price”) equal to a percentage of the non-federal average manufacturer price. 75% for small-molecule drugs more than 9 years but less amoxil street price than 12 years beyond approval. 65% for amoxil street price drugs between 12 and 16 years beyond approval or licensure.

And 40% for drugs more than 16 years beyond approval or licensure. Part D drugs with prices negotiated under amoxil street price this proposal would be required to be covered by all Part D plans. Medicare’s payment to providers for Part B drugs with prices negotiated under this proposal would be 106% of the maximum fair price (rather than 106% of the average sales price under current law).An excise tax would be levied on drug companies that do not comply with the negotiation process, and civil monetary penalties on companies that do not offer the agreed-upon negotiated price to eligible purchasers.Effective Date. This provision would take effect in 2025, with the initial round amoxil street price of negotiated prices for drugs covered under Part D available that year.

For drugs covered under Part amoxil street price B, negotiated prices would take effect in 2027.Inflation Rebates. Sections 139101 and 139102 of the Build Back Better Act would require drug manufacturers to pay a rebate to the federal government if their prices for single-source drugs and biologicals covered under Medicare Part B and nearly all covered drugs under Part D increase faster than the rate of inflation (CPI-U). Under these provisions, price changes would be measured based on the average sales price (for Part B drugs) or the average manufacturer price amoxil street price (for Part D drugs). For price increase higher than inflation, manufacturers would be required to pay the difference in the form of a rebate to Medicare.

The rebate amount is equal to the total number of units multiplied by the amount if any by which the manufacturer price exceeds the inflation-adjusted payment amount, including all units sold outside of amoxil street price Medicaid and therefore applying not only to use by Medicare beneficiaries but by privately insured individuals as well. Rebate dollars would be deposited in the Medicare Supplementary Medical Insurance (SMI) trust fund.Manufacturers that do not pay the amoxil street price requisite rebate amount would be required to pay a penalty equal to at least 125% of the original rebate amount. The base year for measuring price changes is 2021.Effective Date. These provisions would take effect in 2023.Limits on Cost Sharing amoxil street price for Insulin Products.

Sections 27001, 30604, and 139401, would require insurers, including Medicare Part D plans and private group or individual health plans, to charge no more than $35 for insulin products. Part D plans would be required to charge no more than $35 for whichever insulin products they cover for 2023 and 2024 and all insulin products amoxil street price beginning in 2025. Coverage of all insulin products would be required amoxil street price beginning in 2025 because the drug negotiation provision (described earlier) would require all Part D plans to cover all drugs that are selected for price negotiation, and all insulin products are subject to negotiation under that provision. Private group or individual plans do not have to cover all insulin products, just one of each dosage form (vial, pen) and insulin type (rapid-acting, short-acting, intermediate-acting, and long-acting) for no more than $35.Effective Date.

These provisions would amoxil street price take effect in 2023.treatments. Section 139402 would require that adult treatments covered under Medicare Part D that are recommended by the Advisory Committee on Immunization Practices (ACIP), such as for shingles, be covered at no cost. This would be consistent with coverage of amoxil street price treatments under Medicare Part B, such as the flu and buy antibiotics treatments.Effective Date. This provision amoxil street price would take effect in 2024.Repealing Drug Rebate Rule.

Section 139301 would prohibit implementation of the November 2020 final rule issued by the Trump Administration that would have eliminated rebates negotiated between drug manufacturers and pharmacy benefit managers (PBMs) or health plan sponsors in Medicare Part D by removing the safe harbor protection currently extended to these rebate arrangements under the federal anti-kickback statute. This rule was slated to take effect on January 1, 2022, but the Biden Administration delayed implementation to 2023 and the infrastructure legislation passed by the House and Senate includes a further delay to amoxil street price 2026.Effective Date. This provision would take effect in 2026.People affectedThe number of Medicare beneficiaries and privately insured individuals who would see lower out-of-pocket drug costs in any given year under these provisions would depend on how many and which drugs were subject to the negotiation process, and how many and which drugs had lower price increases, and the magnitude of price reductions relative to current prices under each provision.According to estimates from the CMS Office of the Actuary (OACT) of the drug price negotiation provision included in H.R.3 passed by the House of Representatives in 2019, allowing the federal government to negotiate drug prices would lower cost sharing for Part D enrollees by $102.6 billion in the aggregate (2020-2029) and Part D premiums for Medicare beneficiaries by $14.3 billion. Based on amoxil street price our analysis, premium savings for Medicare beneficiaries are projected to increase from an estimated 9% of the Part D base beneficiary premium in 2023 to 15% in 2029.

The effects of the current legislation are likely to be more modest than this.While it is expected that some people would face lower cost sharing under these provisions, it is also possible that drug amoxil street price manufacturers could respond to the inflation rebate by increasing launch prices for new drugs. In this case, some individuals could face higher out-of-pocket costs for new drugs that come to market, with potential spillover effects on total costs incurred by payers as well.In terms of insulin costs, while formulary coverage and tier placement of insulin products vary across Medicare Part D plans, our analysis shows that in 2019, a large number of Part D plans placed insulin products on Tier 3, the preferred drug tier, which typically had a $47 copayment per prescription during the initial coverage phase. However, once enrollees reach the coverage gap phase, they face a amoxil street price 25% coinsurance rate, which equates to $100 or more per prescription in out-of-pocket costs for many insulin therapies, unless they qualify for low-income subsidies. Paying a flat $35 copayment rather than 25% coinsurance could translate to meaningful savings on many insulin products.In terms of treatments, providing for coverage of adult treatments under Medicare Part D at no cost could help with treatment uptake among older adults.

Our analysis shows that in 2018, Part D amoxil street price enrollees without low-income subsidies paid an average of $57 out-of-pocket for each dose of the shingles shot, which is free to most other people with private coverage.budgetary impactCBO has not yet published budgetary estimates for these sections of the Build Back Better Act.Negotiations. Based on earlier legislation, CBO estimated there would be over $450 billion in 10-year (2020-2029) savings from the Medicare drug price negotiation provision in drug price amoxil street price legislation considered in the 116th Congress (H.R. 3), including $448 billion in savings to Medicare and $12 billion in savings for subsidized plans in the ACA Marketplace and how can i buy amoxil the Federal Employees Health Benefits Program. CBO also estimated an increase in revenues of about $45 billion over 10 years resulting from lower drug prices available to employers, which would reduce premiums for employer-sponsored insurance, leading to higher compensation in the form of taxable wages.A separate CBO estimate amoxil street price of the same Medicare drug price negotiation provision included in another House bill in the 116th Congress (H.R.

1425, the Patient Protection and Affordable Care Enhancement Act) estimated higher 10-year (2021-2030) savings of nearly $530 billion, mainly because the Secretary would negotiate prices for a somewhat larger set of drugs in year 2 of the negotiation program under H.R. 1425.However, it is likely that the drug negotiation provision in the Build Back Better Act would generate substantially lower savings than either of these amoxil street price earlier proposals due to a reduction in the number and type of drugs eligible for negotiation and modifications to the upper limit for the negotiated price.Inflation Rebates. CBO estimated savings from the drug inflation rebate provisions in previous legislation (H.R. 3 and amoxil street price S.

2543, Senate Finance Committee legislation considered in the 116th amoxil street price Congress) amounting to $36 billion for H.R. 3 (2020-2029) and $82 billion for S. 2543 (2021-2030) amoxil street price. 10-year savings were estimated to be lower under H.R.

3 because the inflation provision would not apply to drugs subject to the amoxil street price government negotiation process that would be established by that bill. This same exception applies in the amoxil street price Build Back Better Act. Savings are likely to differ for the inflation rebate provision in the Build Back Better Act because it applies to use by private insurers as well as Medicare and because it relies on a more recent benchmark year in calculating price increases than earlier legislative proposals.Repeal of Rebate Rule. Both CBO and Medicare’s actuaries estimated substantially higher Medicare spending over 10 years as a result of banning drug rebates – up to $170 billion higher, according to CBO, and up to $196 billion higher, according to the HHS Office amoxil street price of the Actuary (OACT).

Because the cost of the rebate rule has been incorporated in CBO’s baseline for federal spending, repealing the rebate rule is expected to generate savings. CBO estimated $50.8 billion in savings between 2023 and 2026 associated amoxil street price with the three-year delay of this rule included in the Infrastructure Investment and Jobs Act. The White House has estimated $145 amoxil street price billion in savings associated with the repeal of the rebate rule in the Build Back Better Act.(Back to top)4. Medicare Part D Benefit RedesignbackgroundMedicare Part D currently provides catastrophic coverage for high out-of-pocket drug costs, but there is no limit on the total amount that beneficiaries pay out-of-pocket each year.

Medicare Part D enrollees with drug costs high enough to exceed the catastrophic coverage threshold are required to pay 5% of their total drug costs unless they qualify for Part D Low-Income amoxil street price Subsidies (LIS). Medicare pays 80% of total costs above the catastrophic threshold and plans pay 15%. Medicare’s reinsurance payments to Part D plans now account for close to half of total Part D spending (45%), up amoxil street price from 14% in 2006.Under the current structure of Part D, there are multiple phases, including a deductible, an initial coverage phase, a coverage gap phase, and the catastrophic phase. When enrollees reach the coverage gap benefit phase, they pay 25% of drug costs amoxil street price for both brand-name and generic drugs.

Plan sponsors pay 5% for brands and 75% for generics. And drug manufacturers provide a 70% price discount on brands (there amoxil street price is no discount on generics). Under the current benefit design, beneficiaries can face different cost sharing amounts for the same medication depending on which phase of the benefit they are in, and can face significant out-of-pocket costs for high-priced drugs because of coinsurance requirements and no hard out-of-pocket cap.provision descriptionSections 139201 and 139202 of the Build Back Better Act amend the design of the Part D benefit by adding a hard cap on out-of-pocket spending set at $2,000 in 2024, increasing each year based on the rate of increase in per capita Part D costs. It also lowers beneficiaries’ share of total drug costs below amoxil street price the spending cap from 25% to 23%.

It also lowers Medicare’s share of total costs above the spending cap (“reinsurance”) from 80% to 20% amoxil street price for brand-name drugs and to 40% for generic drugs. Increases plans’ share of costs from 15% to 60% for both brands and generics. And adds a 20% manufacturer price amoxil street price discount on brand-name drugs. Manufacturers would also be required to provide a 10% discount on brand-name drugs in the initial coverage phase (below the annual out-of-pocket spending threshold), instead of a 70% price discount.The legislation also increases Medicare’s premium subsidy for the cost of standard drug coverage to 76.5% (from 74.5% under current law) and reduces the beneficiary’s share of the cost to 23.5% (from 25.5%).

The legislation also allows beneficiaries the option of smoothing out their out-of-pocket costs over the year rather than face high out-of-pocket amoxil street price costs in any given month.Effective Date. The Part D redesign and premium amoxil street price subsidy changes would take effect in 2024. The smoothing out-of-pocket costs provision would take effect in 2025.people affectedWhile most Part D enrollees have not had out-of-pocket costs high enough to exceed the catastrophic coverage threshold in a single year, the likelihood of a Medicare beneficiary incurring drug costs above the catastrophic threshold increases over a longer time span.Our analysis shows that in 2019, nearly 1.5 million Medicare Part D enrollees had out-of-pocket spending above the catastrophic coverage threshold. Looking over a five-year period (2015-2019), the number of Part D enrollees with out-of-pocket spending above the catastrophic threshold in at least one year increases to 2.7 million, and over a 10-year period (2010-2019), the number of enrollees increases to 3.6 million.We also find that in 2019, nearly 1 million more Part D enrollees incurred out-of-pocket costs for their medications above $2,000, the proposed out-of-pocket spending limit in the Build Back Better Act, than amoxil street price above $3,100, the proposed out-of-pocket spending limit in recent GOP drug legislation (H.R.

19) and a 2019 Senate Finance Committee bill (S. 2543). Overall, 1.2 million Part D enrollees in 2019 incurred annual out-of-pocket costs for their medications above $2,000, while 0.3 million spent more than $3,100 out-of-pocket.Medicare Part D enrollees with higher-than-average out-of-pocket costs could save substantial amounts with an out-of-pocket spending cap, as our analysis shows. For example, the top 10% of beneficiaries (122,000 enrollees) with average out-of-pocket costs for their medications above $2,000 in 2019 – who spent at least $5,348 – would have saved $3,348 (63%) in out-of-pocket costs with a $2,000 cap and $2,248 (42%) with a $3,100 cap.budgetary impactCBO has not yet published budgetary estimates for these sections of the Build Back Better Act.Adding a cap on out-of-pocket drug spending under Part D could add costs to the program.

However, other features of the redesign proposal could mitigate the spending impact, in particular the reduction in the percentage of total drug costs that Medicare pays above the annual out-of-pocket spending threshold and the increased liability for plans and manufacturers.(Back to top)5. Medicaid Coverage GapbackgroundThere are currently 12 states that have not adopted the ACA provision to expand Medicaid to adults with incomes through 138% of poverty. The result is a coverage gap for individuals whose below-poverty-level income is too high to qualify for Medicaid in their state, but too low to be eligible for premium subsidies in the ACA Marketplace.provision descriptionSection 137304 of the Build Back Better Act would allow people living in states that have not expanded Medicaid to purchase subsidized coverage on the ACA Marketplace for 2022 through 2025. The federal government would fully subsidize the premium for a benchmark plan.

People would also be eligible for cost sharing subsidies that would reduce their out-of-pocket costs to 1% of overall covered health expenses on average.Section 30608 includes adjustments to uncompensated care (UCC) pools and disproportionate share hospital (DSH) payments for non-expansion states. These states would not be able draw down federal matching funds for UCC amounts for individuals who could otherwise qualify for Medicaid expansion, and their DSH allotments would be reduced by 12.5% starting in 2023.Section 30609 would increase the federal match rate for states that have adopted the ACA Medicaid expansion from 90% to 93% from 2023 through 2025, designed to discourage states from dropping current expansion coverage.people affectedWe estimate that 2.2 million uninsured people with incomes under poverty fall in the “coverage gap”. Most in the coverage gap are concentrated in four states (TX, FL, GA and NC) where eligibility levels for parents in Medicaid are low, and there is no coverage pathway for adults without dependent children. Half of those in the coverage gap are working and six in 10 are people of color.An earlier CBO estimate showed that extending Marketplace subsidies to people with income below 100% of poverty over the 2022-2024 period would increase enrollment in nongroup resulting in 1.7 million fewer uninsured people on average over the period.budgetary impactAn earlier CBO estimate showed that the federal cost of extending Marketplace coverage to certain low-income people would increase federal costs by $47.4 billion in federal fiscal years 2022-2024.Federal costs could be reduced due to lower spending on uncompensated care and DSH for certain states, but there would be additional federal costs to increase the match rate for current expansion states from 90% to 93% for expansion states for 2023 through 2025.(Back to top)6.

Maternity Care and Postpartum CoveragebackgroundMedicaid currently covers almost half of births in the U.S. Federal law requires that pregnancy-related Medicaid coverage last through 60 days postpartum. After that period, some may qualify for Medicaid through another pathway, but others may not qualify, particularly in non-expansion states. In an effort to improve maternal health and coverage stability and to help address racial disparities in maternal health, a provision in the American Rescue Plan Act (ARPA) of 2021 gives states a new option to extend Medicaid postpartum coverage to 12 months.

This new option takes effect on April 1, 2022 and is available to states for five years.provision descriptionSection 30721 of the Build Back Better Act would require states to extend Medicaid postpartum coverage from 60 days to 12 months, ensuring continuity of Medicaid coverage for postpartum individuals in all states. This requirement would take effect in the first fiscal quarter beginning one year after enactment and also applies to state CHIP programs that cover pregnant individuals.Section 30722 would create a new option for states to coordinate care for Medicaid-enrolled pregnant and post-partum individuals through a maternal health home model. States that take up this option would receive a 15% increase in FMAP for care delivered through maternal health homes for the first two years. States that are interested in pursuing this new option can receive planning grants prior to implementation.Sections 31031 through 31048 of the Build Back Better Act provide federal grants to bolster other aspects of maternal health care.

The funds would be used to address a wide range of issues, such as addressing social determinants of maternal health. Diversifying the perinatal nursing workforce, expanding care for maternal mental health and substance use, and supporting research and programs that promote maternal health equity.people affectedLargely in response to the new federal option, at least 26 states have taken steps to extend Medicaid postpartum coverage. Pregnant people in non-expansion states could see the biggest change as they are more likely than those in expansion states to become uninsured after the 60-day postpartum coverage period. For example, in Alabama, the Medicaid eligibility level for pregnant individuals is 146% FPL, but only 18% FPL (approximately $4,000/year for a family of three) for parents.Some states have piloted maternal health homes and seen positive impacts on health outcomes.

The federal grant provisions related to maternal health could affect care for all persons giving birth, but the focus of these proposals is on reducing racial and ethnic inequities. There were approximately 3.7 million births in 2019, and nearly half were to women of color. There are approximately 700-800 pregnancy-related deaths annually, with the rate 2-3 times higher among Black and American Indian and Alaska Native women compared to White women. Additionally, there are stark racial and ethnic disparities in other maternal and health outcomes, including preterm birth and infant mortality.budgetary impactCBO has not yet published budgetary estimates for these sections of the Build Back Better Act.However, in June 2020, prior to the enactment of the ARPA option for postpartum coverage, CBO estimated that a proposal to require 12 month postpartum coverage in Medicaid and CHIP would have a net federal cost of $6 billion over 10 years (new costs of $12.3 billion offset by revenues).In FY 2022, $5 million is appropriated for planning grants to states for maternal health homes.Total allocations in FY 2022 for the federal grant sections in the Build Back Better Act related to maternal health care outside of the postpartum extension and maternal health homes are $1.1 billion.(Back to top)7.

Other Medicaid and Children’s Health Insurance (CHIP) ChangesbackgroundUnder current law, states have the option to provide 12-months of continuous coverage for children. Under this option, states allow a child to remain enrolled for a full year unless the child ages out of coverage, moves out of state, voluntarily withdraws, or does not make premium payments. As such, 12-month continuous eligibility eliminates coverage gaps due to fluctuations in income over the course of the year.Under current law, Medicaid is the base of coverage for low-income children. CHIP complements Medicaid by covering uninsured children in families with incomes above Medicaid eligibility levels.

Unlike Medicaid, federal funding for CHIP is capped and provided as annual allotments to states. CHIP funding is authorized through September 30, 2027. While CHIP generally has bipartisan support, during the last reauthorization funding lapsed before Congress reauthorized funding.provision descriptionSection 30741 of the Build Back Better Act would require states to extend 12-month continuous coverage for children on Medicaid and CHIP.Section 30801 of the Build Back Better Act would permanently extend the CHIP program.people affectedAs of May 2021, there were 39 million children enrolled in Medicaid and CHIP (nearly half of all enrollees). As of January 2020, 34 states provide 12-month continuous eligibility to at least some children in either Medicaid or CHIP.

A recent MACPAC report found that the overall mean length of coverage for children in 2018 was 11.7 months, and also that rates of churn (in which children dis-enroll and reenroll within a short period of time) were lower in states that had adopted the 12-month continuous coverage option and in states that did not conduct periodic data checks. Another recent report shows that children with gaps in coverage during a year are more likely to be children of color with lower incomes.As of May 2021, there were 6.9 million people (mostly children) enrolled in CHIP.budgetary impactCBO has not yet published budgetary estimates for this section of the Build Back Better Act.Given that the length of coverage for children in Medicaid is already high (mean of 11.7 months), more than half of all states already have a continuous coverage policy in place, and costs for children are generally lower compared to other eligibility groups, new federal costs could be moderate. In addition, reducing churn could modestly reduce Medicaid administrative costs.Federal CHIP funding in Fiscal Year (FY) 2020 for the states was $17.0 billion. Since CHIP is authorized through FY 2027, CBO estimates would only account for costs in FY 2028 – FY 2031 (the current ten-year window).

When CHIP was reauthorized through FY 2027, CBO estimated that this would result in net fiscal savings to the federal government because without CHIP, other alternatives would have higher federal costs and because of expected changes in the federal match rate back to traditional CHIP match rates.(Back to top)8. Other Medicaid Financing and Benefit ChangesbackgroundUnlike in the 50 states and D.C., annual federal funding for Medicaid in the U.S. Territories is subject to a statutory cap and fixed matching rate. The funding caps and match rates have been increased by Congress in response to emergencies over time.To help support states and promote stability of coverage during the buy antibiotics amoxil, the Families First antibiotics Response Act (FFCRA) provides a 6.2 percentage point increase in the federal share of certain Medicaid spending, provided that states meet maintenance of eligibility (MOE) requirements that include ensuring continuous coverage for current enrollees.treatments are an optional benefit for certain adult populations, including low-income parent/caretakers, pregnant women, and persons who are eligible based on old age or a disability.

For adults enrolled under the ACA’s Medicaid expansion and other populations for whom the state elects to provide an “alternative benefit plan,” their benefits are subject to certain requirements in the ACA, including coverage of treatments recommended by the Advisory Committee on Immunization Practices (ACIP) with no cost sharing.Under the Families First antibiotics Response Act, coverage of testing and treatment for buy antibiotics, including treatments, is required with no cost sharing in order for states to access temporary enhanced federal funding for Medicaid which is tied to the public health emergency. The American Rescue Plan Act (ARPA) clarified that coverage of buy antibiotics treatments and their administration, without cost sharing, is required for nearly all Medicaid enrollees, through the last day of the 1st calendar quarter beginning at least 1 year after the public health emergency ends. The ARPA also provides 100% federal financing for this coverage.provision descriptionSection 30731 of the Build Back Better Act would increase the Medicaid cap amount and match rate for the territories. The FMAP would be permanently adjusted to 83% for the territories beginning in FY 2022, except that Puerto Rico’s match rate would be 76% in FY 2022 before increasing to 83% in FY 2023 and subsequent years.

The legislation would also require a payment floor for certain physician services in Puerto Rico with a penalty for failure to establish the floor.Section 30741 of the Build Back Better Act would phase out the FFCRA enhanced federal funding to states. States would continue to receive the 6.2 percentage point increase through March 31, 2022, followed by a 3.0 percentage point increase from April 1, 2022 through June 30, 2022, and a 1.5 percentage point increase from July 1, 2022 through September 30, 2022.Section 30741 also would modify the FFCRA MOE requirement for continuous coverage. From April 1 through September 30, 2022, states could continue receiving the enhanced federal matching funds if they terminate coverage for individuals who are determined no longer eligible for Medicaid and have been enrolled at least 12 consecutive months. The legislation includes other rules for states about conducting eligibility redeterminations and when states can terminate coverage.Section 30751 of the Build Back Better Act would establish a 3.1 percentage point FMAP reduction from October 1, 2022 through December 31, 2025 for states that adopt eligibility standards, methodologies, or procedures that are more restrictive than those in place as of October 1, 2021 (except the penalty would not apply to coverage of non-pregnant, non-disabled adults with income above 133% FPL after December 31, 2022, if the state certifies that it has a budget deficit).Section 139405 of the Build Back Better Act would require state Medicaid programs to cover all approved treatments recommended by ACIP and treatment administration, without cost sharing, for categorically and medically needy adults.

States that provide adult treatment coverage without cost sharing as of the date of enactment would receive a 1 percentage point FMAP increase for 8 quarters.people affectedIn June 2019 there were approximately 1.3 million Medicaid enrollees in the territories (with 1.2 million in Puerto Rico).From February 2020 through May 2021 Medicaid and CHIP enrollment has increased by 11.5 million or 16.2% due to the economic effects of the amoxil and MOE requirements.All states provide some treatment coverage for adults enrolled in Medicaid who are not covered as part of the ACA’s Medicaid expansion, but as of 2019, only about half of states covered all ACIP-recommended treatments.budgetary impactCBO has not yet published budgetary estimates for these sections of the Build Back Better Act.With the public health emergency unwinding, states are likely to face pressures to contain growth in state spending tied to enrollment, particularly after the enhanced FMAP ends, even as they work to overcome challenges with systems and staffing to ensure that eligible individuals remain covered by Medicaid or transition to other sources of coverage.(Back to top)9. Medicaid Home and Community Based Services and the Direct Care WorkforcebackgroundMedicaid is currently the primary payer for long-term services and supports (LTSS), including home and community-based services (HCBS), that help seniors and people with disabilities with daily self-care and independent living needs. There is currently a great deal of state variation as most HCBS eligibility pathways and benefits are optional for states.PROVISION DESCRIPTIONSections 30711-30713 of the Build Back Better Act would create the HCBS Improvement Program, which would provide a permanent 6 percentage point increase in federal Medicaid matching funds for HCBS. To qualify for the enhanced funds, states would have to maintain existing HCBS eligibility, benefits, and payment rates and have an approved plan to expand HCBS access, strengthen the direct care workforce, and monitor HCBS quality.

The bill includes some provisions to support family caregivers. In addition, the Act would include funding ($130 million) for state planning grants and enhanced funding for administrative costs for certain activities (80% instead of 50%).Section 30714 of the Build Back Better Act would require states to report HCBS quality measures to HHS, beginning 2 years after the Secretary publishes HCBS quality measures as part of the Medicaid/CHIP core measures for children and adults. The bill provides states with an enhanced 80% federal matching rate for adopting and reporting these measures.Sections 30715 and 30716 of the Build Back Better Act would make the ACA HCBS spousal impoverishment protections and the Money Follows the Person (MFP) program permanent.Sections 22301 and 22302 of the Build Back Better Act would provide $1 billion in grants to states, community-based organizations, educational institutions, and other entities by the Department of Labor Secretary to develop and implement strategies for direct service workforce recruitment, retention, and/or education and training.Section 25005 of the Build Back Better Act would provide $20 million for HHS and the Administration on Community Living to establish a national technical assistance center for supporting the direct care workforce and family caregivers.Section 25006 of the Build Back Better Act would provide $40 million for the HHS Secretary to award to states, nonprofits, educational institutions, and other entities to address the behavioral health needs of unpaid caregivers of older individuals and older relative caregivers.people affectedThe majority of HCBS are provided by waivers, which served over 2.5 million enrollees in 2018. There is substantial unmet need for HCBS, which is expected to increase with the growth in the aging population in the coming years.

Nearly 820,000 people in 41 states were on a Medicaid HCBS waiver waiting list in 2018. Though waiting lists alone are an incomplete measure, they are one proxy for unmet need for HCBS. Additionally, a shortage of direct care workers predated and has been intensified by the buy antibiotics amoxil, characterized by low wages and limited opportunities for career advancement. The direct care workforce is disproportionately female and Black.A KFF survey found that, as of 2018, 14 states expected that allowing the ACA spousal impoverishment provision to expire would affect Medicaid HCBS enrollees, for example by making fewer individuals eligible for waiver services.Over 101,000 seniors and people with disabilities across 44 states and DC moved from nursing homes to the community using MFP funds from 2008-2019.

A federal evaluation of MFP showed about 5,000 new participants in each six month period from December 2013 through December 2016, indicating a continuing need for the program.Budgetary ImpactCBO has not yet published budgetary estimates for these sections of the Build Back Better Act.The House Energy and Commerce Committee markup of the bill described the cost to the federal government as $190 billion. This is less than the $400 billion originally proposed by President Biden. While the program requirements are not the same, CBO previously estimated that the American Rescue Plan Act’s 10 percentage point increase in federal matching funds for Medicaid HCBS for 1 year would increase federal costs by about $12.7 billion.(Back to top)10. Paid Family and Medical LeavebackgroundThe U.S.

Is the only industrialized nation without a minimum standard of paid family or medical leave. Although six states and DC have paid family and medical leave laws in effect, and some employers voluntarily offer these benefits, this has resulted in a patchwork of policies with varying degrees of generosity and leaves many workers without a financial safety net when they need to take time off work to care for themselves or their families.provision descriptionSection 130001 of the Build Back Better Act would guarantee four weeks per year of paid family and medical leave to all workers in the U.S. Who need time off work to welcome a new child, recover from a serious illness, or care for a seriously ill family member. Annual earnings up to $15,080 would be replaced at approximately 90% of average weekly earnings, plus about 73% of average weekly earnings for annual wages between $15,080 and $32,248, capping out at 53% of average weekly earnings for annual wages between $32,248 and $62,000.

While all workers taking qualified leave would be eligible for at least some wage replacement, the progressive benefits formula means that the share of pay replaced while on qualified leave is highest for workers with lower wages. The original Act called for 12 weeks of paid leave for similar qualified reasons, plus three days of bereavement leave, and benefits began at 85% of average weekly earnings for annual wages up to $15,080 and were capped at 5% of average weekly earnings for annual wages up to $250,000.people affectedAccording to the Bureau of Labor Statistics (BLS), approximately one in four (23%) workers has access to paid family leave through their employer. Data on the share of workers with access to paid medical leave for their own longer, serious illness are limited, although BLS also reports that 40% of workers have access to short-term disability insurance.​It is estimated that 53 million adults are caregivers for a dependent child or adult and 61% of them are women. Sixty percent (60%) of caregivers reported having to take a leave of absence leave from work or cut their hours in order to care for a family member.

Workers who take leave do so for different reasons. Half (51%) reported taking leave due to their own serious illness, one-quarter (25%) for reasons related to pregnancy, childbirth, or bonding with a new child, and one-fifth (19%) to care for a seriously ill family member. In total, four in ten (42%) reported receiving their full pay while on leave, one-quarter (24%) received partial pay, and one-third (34%) received no pay.budgetary impactCBO has not yet published budgetary estimates for this section of the Build Back Better Act.The current Build Back Better Act would allocate $1.5 billion for paid family and medical leave program administration for FY 2022. The Act states that Treasury funds not otherwise appropriated shall be appropriated “as may be necessary” for paid leave benefits and grants.(Back to top).