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In this zithromax 250mg cost edition Open enrollment continues in 11 states, Washington, DCAlthough open enrollment for 2021 individual and family health insurance ended last week in most states, and ended last night in Minnesota, open enrollment is still ongoing in 11 states and Washington, DC, with the following enrollment deadlines. Enrollment up 6.6% for 2021 in states that use HealthCare.govLast Friday, CMS published preliminary enrollment data for the 36 states that used HealthCare.gov during the open enrollment zithromax 250mg cost period that ended last week. Across those 36 states, a total of 8.23 million people enrolled in private plans through HealthCare.gov.

As Charles zithromax 250mg cost Gaba notes, that’s a 6.6 percent increase over last year, after we account for the fact that Pennsylvania and New Jersey are now running their own exchange platforms and will report their enrollment numbers separately. (Both also have ongoing enrollment periods, as noted above.)As detailed by Andrew Sprung, private-plan enrollment via the exchange in states that have not expanded Medicaid is about 10 percent higher for 2021 than it was for 2020, while enrollment is slightly lower in states that have expanded Medicaid. Sprung offers several explanations for this, including the fact that many zithromax 250mg cost who lost their incomes in 2020 have transitioned to Medicaid, which is more likely to be an available option in states that have expanded Medicaid.

Sprung has also tracked the significant increase in the number of people covered by Medicaid this year.Trump administration finalizes rule changes for grandfathered group plansEarlier this month, the Trump administration finalized new rules for grandfathered group health plans. The rule change is essentially the same as the changes that the administration zithromax 250mg cost proposed in July, but the effective date has been pushed out to mid-June 2021, as opposed to the originally proposed effective date of 30 days after the rules were finalized.Under the new rules, grandfathered group plans that are HSA-qualified will be able to make cost-sharing increases necessary to retain their HSA-qualified status, even if the increases exceed the limits that would otherwise have applied to grandfathered plans. (This situation has not yet arisen, but if it does in the future, the rule change will allow these plans to keep both their HSA-qualified status and their grandfathered status.) And the new rules will also allow grandfathered group plans to increase their cost-sharing amounts by a larger threshold than previously permitted, with allowable cost-sharing expected to be about 3 percentage points higher under the new rule.Congress passes legislation to protect consumers from surprise balance billingThe surprise balance billing legislation that we told you about last week was included in the Consolidated Appropriations Act, 2021, which passed earlier this week with strong bipartisan support in both the House and Senate.

President Trump zithromax 250mg cost was widely expected to sign it as soon as it reached his desk, but he cast doubt on that via Twitter on Tuesday night, expressing displeasure at some aspects of the legislation. Trump didn’t say that he would veto the bill, but the video he shared on Twitter indicated that the current bill is no longer a sure thing.In its current form, the massive bill includes government funding for the first three quarters of 2021, extensive buy antibiotics relief, and numerous other provisions, including strong zithromax 250mg cost consumer protections against surprise balance billing that will take effect in January 2022. As the Kaiser Family Foundation’s Larry Levitt explains in this Twitter thread, the new legislation provides strong consumer protections, and – assuming it does get signed into law – will result in consumers having to pay just their normal in-network cost-sharing when they receive emergency care or unknowingly receive care from an out-of-network provider at an in-network facility.Protections against surprise balance billing for ground ambulance charges are not included in the legislation, despite the fact that ambulance rides often result in surprise balance billing.

But the legislation does call for a commission zithromax 250mg cost that will study ground ambulance charges in hopes of incorporating additional consumer protections in a future piece of legislation.Congresses passes legislation to make health insurers subject to federal antitrust lawsThe Competitive Health Insurance Reform Act of 2020 – H.R.1418 – passed in the Senate last night and is now headed to President Trump’s desk (it was passed by the House in September). Under the terms of this legislation, health insurance companies will be subject to federal antitrust laws, reversing a 75-year-old exemption that was granted in 1945 via the McCarran-Ferguson Act.Sens. Steve Daines (R-Montana) and Patrick Leahy (D-Vermont) shepherded the bipartisan bill zithromax 250mg cost through the Senate.

In announcing the passage of the bill, Daines noted that it “will ensure that health insurance issuers are subject to the same federal antitrust laws prohibiting unfair trade practices, such as price-fixing and collusion, as virtually every other industry in our economy.” The rest of the McCarran-Ferguson Act – which gives states the right to regulate their insurance markets — is unchanged by H.R.1418.Ohio enacts legislation to end ‘fail first’ drug requirements for stage 4 cancer treatmentThis week, Ohio Gov. Mike DeWine signed a new law prohibiting Ohio health insurance plans from imposing “fail zithromax 250mg cost first” requirements on drug coverage for people with stage 4 cancer. S.B.252 prohibits insurers from requiring these patients to try a cheaper medication first and then only cover another medication if the first did not work.

These “fail first” requirements are often imposed on newer, cutting-edge therapies that tend to be more expensive than older medications, but Ohio’s legislation stems from the fact that time zithromax 250mg cost is of the essence with metastatic cancer.Delaware proposal calls for increased investment in primary careDelaware’s Insurance Commissioner, Trinidad Navarro, and the state’s Office of Value-Based Health Care Delivery have published a report that outlines proposals for improving access to primary care in the state without increasing healthcare costs. The report calls for health insurers in Delaware to increase their investments in primary care while decreasing price growth for some other services, including hospital care, and to transition to a value-based payment model instead of a fee-for-service model. The state is accepting public comments on the report until January 25, 2021.Louise Norris is an individual health insurance zithromax 250mg cost broker who has been writing about health insurance and health reform since 2006.

She has written dozens of opinions and educational pieces about the Affordable Care Act zithromax 250mg cost for healthinsurance.org. Her state health exchange updates are regularly cited by media who cover health reform and by other health insurance experts.Q. Under the ACA, my insurance premium subsidy is zithromax 250mg cost dependent on adjusted gross income (AGI).

But, for a self-employed person, AGI is dependent on the insurance premium, since premiums are deductible for the self-employed.For example, my husband and I have an AGI of $77,000 before accounting for health insurance. That’s too high for a subsidy for a household zithromax 250mg cost of two in 2021, so our tax-deductible self-employed health insurance premiums (line 16 of the Schedule 1 for the 1040) would be $10,952, which is the full cost of our health plan. Subtracting $10,952 from $77,000, our new AGI is at $66,048.

Now, since zithromax 250mg cost our AGI would be less than $68,960 (for 2021 coverage, that’s the upper limit for subsidy eligibility for two people), we qualify for the subsidy. So our after-subsidy annual premium for the benchmark plan would be $6,493 (9.83 percent of our MAGI, which applies in 2021 for households with income beween 300 and 400 percent of the poverty level). But if $6,493 is what we should put in line 16 zithromax 250mg cost of the Schedule 1, our AGI (and ACA-specific MAGI) would be $70,507 (that’s $77,000 minus $6,493).

And since that’s higher than $68,980, zithromax 250mg cost we would no longer be eligible for the subsidy!. Help!. !.

A. This can be a complex situation, and our answer is intended to serve as an overview of how the subsidy calculation works. Always seek help from a qualified tax professional if you have questions about your specific situation.[Note that in the example above, we’ve included subsidy thresholds and income percentages for 2021.

These numbers change from one year to the next, and poverty level numbers will be from the year before the year in question (eg. 2020 poverty level numbers are used to determine subsidy amounts for 2021 coverage).]In July 2014, the IRS released 26 CFR 601.105, in which they acknowledged the circular relationship between self-employed health insurance premium deductions, AGI, and premium tax credits:“… the amount of the [self-employed health insurance premium] deduction is based on the amount of the … premium tax credit, and the amount of the credit is based on the amount of the deduction – a circular relationship. Consequently, a taxpayer eligible for both a … deduction for premiums paid for qualified health plans and a … premium tax credit may have difficulty determining the amounts of those items.”In the regulation, the IRS provides two methods that self-employed taxpayers can use to calculate their deduction and their subsidy.

The iterative calculation will result in a more exact answer, but it is a little more time-consuming to compute. The alternative calculation is less exact (and appears to favor the IRS just slightly), but less time-consuming and easier to calculate. You have your choice of which one you want to use, and tax software should have the calculations built in, which would make them both simple to use.In a nutshell, both methods have you do the calculations repeatedly, getting ever-closer to the correct answer (that’s what iteration means).

But while the iterative calculation has you keep going until the difference between successive answers is less than $1, the alternative calculation lets you stop sooner.The easiest way to understand how the two calculations work is to start on page 9 of the regulation and work through the examples the IRS has provided. When they mention the “limitation on additional tax,” they’re just referencing the caps on how much you have to pay back when you file your taxes if it turns out that your advance subsidy (the amount sent to your health insurance company each month) was overpaid because your income ended up being higher than projected. So in example 1 on page 9, the IRS uses $2,500 as the limitation on additional tax, because the family’s household income is between 300 and 400 percent of poverty (these limits vary by year.

For the 2020 tax year, it’s grown to $2,700).[Note that the caps on repayment of excess subsidies are listed in Table 5 on the IRS instructions for Form 8962 (the form that’s used to claim or reconcile the ACA’s premium tax credit), and they depend on your income. The more you earn, the more you potentially have to pay back if your premium subsidy was overpaid during the year, and if you end up with income over 400 percent of the poverty level and are thus not eligible for the subsidy at all, you have to pay it all back.]In addressing the question of the circular relationship between AGI and premium subsidies for self-employed people, the examples the IRS provides cover scenarios where the filers took advance premium tax credits as well as scenarios where they did not, since you can pay your own premiums in full each month and then claim your total credit for the year when you file your taxes. The examples make the calculations relatively straightforward, although the standard advice applies.

If in doubt at all, contact a tax professional for assistance.Louise Norris is an individual health insurance broker who has been writing about health insurance and health reform since 2006. She has written dozens of opinions and educational pieces about the Affordable Care Act for healthinsurance.org. Her state health exchange updates are regularly cited by media who cover health reform and by other health insurance experts..

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Cardiovascular disease (CVD) is the leading cause of how to get zithromax in the us death in women https://kompatech.de/buy-generic-levitra/ in high-income countries. Most CVD events in women occur after menopause and there is a clear relationship between earlier age at menopause and increased CVD risk. Thus, it seems biologically plausible that the decrease in hormone levels after menopause how to get zithromax in the us might be related to CVD risk (figure 1).

Yet, the potential role of post-menopausal hormone therapy (MHT) in reducing CVD risk in women remains controversial. In this issue of Heart, Gersh et al1 summarise the pros and cons of MHT how to get zithromax in the us and provide a historical overview of MHT studies, highlighting limitations such as inclusion of women with pre-existing heart disease, and the type, dose and timing of MHT. They argue that ‘Human-identical hormones initiated early in menopause appear safe to be continued indefinitely, under close supervision, offering post-menopausal women greater potential for long-term CV health and improved quality of life.’ Of course, ‘Individualised decision-making is a key component of all MHT conversations.

Standard CVD how to get zithromax in the us risk reduction must be included in all therapeutic plans.’Age-dependent shift in oestrogen levels. Levels of oestrogen decline with age and result in increased visceral fat, higher rates of insulin resistance and an increase in cardiovascular disease." data-icon-position data-hide-link-title="0">Figure 1 Age-dependent shift in oestrogen levels. Levels of oestrogen decline with age and result in increased visceral fat, higher rates of insulin resistance and an increase in cardiovascular disease.In an editorial counterpoint, Thamman2 disagrees with this approach because of the lack of hard clinical CVD endpoints in the more recent data.

She concludes how to get zithromax in the us. €˜Age at menopause should be taken into account as part of CVD risk stratification. However, using cardioprevention as the justification how to get zithromax in the us for MHT is not advisable.’ On the other hand, a recent scientific statement from the American Heart Association leans toward MHT for CVD risk reduction when started within 10 years of menopause, especially in younger women.3 It is more than disappointing that in 2021 there is inadequate scientific evidence to make clear recommendations about CVD risk for a life-stage that all women experience.

Surely those studies are long overdue.Controversy persists regarding the optimal P2Y12 receptor inhibitor for patients treated with percutaneous coronary intervention (PCI) for acute myocardial infarction (MI). Venetsanos and colleagues4 found no difference in major adverse cardiovascular events at 1 year (adjusted HR 1.03, 95% CI 0.86 to 1.24) or in bleeding risk (2.5% vs 3.2%, adjusted HR 0.92, 95% CI 0.69 to 1.22) comparing 2073 patients treated with prasugrel compared with 35 917 treated with ticagrelor after PCI for MI in the SWEDEHEART (Swedish Web-system for enhancement and development of evidence-based care in heart disease how to get zithromax in the us evaluated according to recommended therapies) registry4 (figure 2).Cumulative rate of adverse events stratified by treatment. Kaplan-Meier curves present the cumulative rates of major adverse cardiac and cerebrovascular events (MACCE) and net adverse cardiac and cerebrovascular events (NACCE), stratified by treatment." data-icon-position data-hide-link-title="0">Figure 2 Cumulative rate of adverse events stratified by treatment.

Kaplan-Meier curves present the cumulative rates of major how to get zithromax in the us adverse cardiac and cerebrovascular events (MACCE) and net adverse cardiac and cerebrovascular events (NACCE), stratified by treatment.In the accompanying editorial, Professor Storey5 provides a detailed comparison of the properties of prasugrel and ticagrelor, reminding us that these agents are preferable to clopidogrel. He then goes on to discuss potential reasons for the conflicting results reported from the ISAR-REACT-5 (Intracoronary Stenting and Antithrombotic Regimen. Rapid Early Action for Coronary Treatment-5) trial, suggesting that ‘the most likely explanations for the superior outcomes [in ISAR-REACT-5] in the prasugrel group are (1) worse treatment adherence in patients without diabetes in the ticagrelor group and (2) by chance, numerically fewer non-cardiovascular deaths in the prasugrel group.’ He concludes that the current data from the SWEDEHEART registry ‘provide reassurance about the continued place of ticagrelor in first-line management of patients with ACS managed with PCI.’Also in this issue of Heart is a post hoc analysis from the Cardiovascular Outcomes for People Using Anticoagulation Strategies trial which was discontinued early due to a beneficial effect of rivaroxaban in addition to aspirin in patients with chronic coronary or peripheral artery disease.6 After early termination of the study, the benefit of therapy for incident myocardial infarction and cardiovascular death were lost and there was a higher stroke rate after switching to aspirin alone for participants who originally had been randomised to rivaroxaban in addition to aspirin (figure 3).Outcomes from the time of switching to non-study aspirin until final contact in participants who took study antithrombotic drugs until early stopping (n=14 086).

(A) Composite how to get zithromax in the us outcome panel. (B) cardiovascular death. (C) MI how to get zithromax in the us.

(D) stroke. ASA, aspirin how to get zithromax in the us. MI, myocardial infarction.

RIVA, rivaroxaban." data-icon-position data-hide-link-title="0">Figure 3 Outcomes from the time of switching to non-study aspirin until final contact in participants who took study antithrombotic how to get zithromax in the us drugs until early stopping (n=14 086). (A) Composite outcome panel. (B) cardiovascular death.

(C) MI how to get zithromax in the us. (D) stroke. ASA, aspirin how to get zithromax in the us.

MI, myocardial infarction. RIVA, rivaroxaban.Darmon and Ducrocq7 address the medical, ethical and regulatory challenges when a study is how to get zithromax in the us terminated before approval for continuation of study medication (if effective) has been obtained. As they conclude.

€˜The study by Dagenais et al6 sheds light how to get zithromax in the us on the various serious consequences of discontinuing study treatments that were proven effective in randomised clinical trials. It should be seen as a call for developing strategies for management of patients after trial completion, whether it is earlier than expected or scheduled.’The Education in Heart article in this issue summarises the cardiovascular manifestations of systemic inflammatory diseases.8 Advanced cardiac imaging approaches have greatly expanded our understanding of the frequency, type and extent of cardiac involvement in patients with conditions such as systemic lupus erythematosus, antiphospholipid syndrome, systemic sclerosis, autoimmune myositis and the vasculitides. A detailed summary table will be invaluable to clinicians, along with imaging examples of cardiac involvement (figure 4).Cardiovascular magnetic resonance from a patient who was 13 weeks into her first pregnancy and presented with chest pain, ECG changes and an elevated troponin.

An angiogram showed how to get zithromax in the us unobstructed coronary arteries. The figure shows T2 mapping in panel (A), with high signal (inflammation) in the mid-inferolateral wall. Panel (B) shows the cause of this to be a localised myocardial infarction how to get zithromax in the us.

The patient went on to have a positive antiphospholipid screen and was started on anticoagulation." data-icon-position data-hide-link-title="0">Figure 4 Cardiovascular magnetic resonance from a patient who was 13 weeks into her first pregnancy and presented with chest pain, ECG changes and an elevated troponin. An angiogram showed unobstructed coronary how to get zithromax in the us arteries. The figure shows T2 mapping in panel (A), with high signal (inflammation) in the mid-inferolateral wall.

Panel (B) how to get zithromax in the us shows the cause of this to be a localised myocardial infarction. The patient went on to have a positive antiphospholipid screen and was started on anticoagulation.The Cardiology-in-Focus article in this issue9 provides a concise guide to minimising risk for women, such as cardiology trainees and consultants, who work with radiation during pregnancy and points out that. €˜A better awareness of radiation protection—with more use of low-dose techniques and protective equipment—would benefit all operators and not just those who are pregnant.’Ethics statementsPatient consent for publicationNot required..

Cardiovascular disease (CVD) is the leading cause of death in women in high-income countries zithromax 250mg cost. Most CVD events in women occur after menopause and there is a clear relationship between earlier age at menopause and increased CVD risk. Thus, it zithromax 250mg cost seems biologically plausible that the decrease in hormone levels after menopause might be related to CVD risk (figure 1). Yet, the potential role of post-menopausal hormone therapy (MHT) in reducing CVD risk in women remains controversial.

In this issue of Heart, Gersh et al1 summarise the pros and cons of MHT and provide a historical overview of MHT studies, highlighting limitations such as inclusion of women with pre-existing heart disease, and the type, dose and timing of zithromax 250mg cost MHT. They argue that ‘Human-identical hormones initiated early in menopause appear safe to be continued indefinitely, under close supervision, offering post-menopausal women greater potential for long-term CV health and improved quality of life.’ Of course, ‘Individualised decision-making is a key component of all MHT conversations. Standard CVD risk reduction must zithromax 250mg cost be included in all therapeutic plans.’Age-dependent shift in oestrogen levels. Levels of oestrogen decline with age and result in increased visceral fat, higher rates of insulin resistance and an increase in cardiovascular disease." data-icon-position data-hide-link-title="0">Figure 1 Age-dependent shift in oestrogen levels.

Levels of oestrogen decline with age and result in increased visceral fat, higher rates of insulin resistance and an increase in cardiovascular disease.In an editorial counterpoint, Thamman2 disagrees with this approach because of the lack of hard clinical CVD endpoints in the more recent data. She concludes zithromax 250mg cost. €˜Age at menopause should be taken into account as part of CVD risk stratification. However, using cardioprevention as the justification for MHT is not advisable.’ On zithromax 250mg cost the other hand, a recent scientific statement from the American Heart Association leans toward MHT for CVD risk reduction when started within 10 years of menopause, especially in younger women.3 It is more than disappointing that in 2021 there is inadequate scientific evidence to make clear recommendations about CVD risk for a life-stage that all women experience.

Surely those studies are long overdue.Controversy persists regarding the optimal P2Y12 receptor inhibitor for patients treated with percutaneous coronary intervention (PCI) for acute myocardial infarction (MI). Venetsanos and zithromax 250mg cost colleagues4 found no difference in major adverse cardiovascular events at 1 year (adjusted HR 1.03, 95% CI 0.86 to 1.24) or in bleeding risk (2.5% vs 3.2%, adjusted HR 0.92, 95% CI 0.69 to 1.22) comparing 2073 patients treated with prasugrel compared with 35 917 treated with ticagrelor after PCI for MI in the SWEDEHEART (Swedish Web-system for enhancement and development of evidence-based care in heart disease evaluated according to recommended therapies) registry4 (figure 2).Cumulative rate of adverse events stratified by treatment. Kaplan-Meier curves present the cumulative rates of major adverse cardiac and cerebrovascular events (MACCE) and net adverse cardiac and cerebrovascular events (NACCE), stratified by treatment." data-icon-position data-hide-link-title="0">Figure 2 Cumulative rate of adverse events stratified by treatment. Kaplan-Meier curves present the cumulative rates of major adverse cardiac and cerebrovascular events (MACCE) and net adverse cardiac and cerebrovascular events (NACCE), stratified by treatment.In zithromax 250mg cost the accompanying editorial, Professor Storey5 provides a detailed comparison of the properties of prasugrel and ticagrelor, reminding us that these agents are preferable to clopidogrel.

He then goes on to discuss potential reasons for the conflicting results reported from the ISAR-REACT-5 (Intracoronary Stenting and Antithrombotic Regimen. Rapid Early Action for Coronary Treatment-5) trial, suggesting that ‘the most likely explanations for the superior outcomes [in ISAR-REACT-5] in the prasugrel group are (1) worse treatment adherence in patients without diabetes in the ticagrelor group and (2) by chance, numerically fewer non-cardiovascular deaths in the prasugrel group.’ He concludes that the current data from the SWEDEHEART registry ‘provide reassurance about the continued place of ticagrelor in first-line management of patients with ACS managed with PCI.’Also in this issue of Heart is a post hoc analysis from the Cardiovascular Outcomes for People Using Anticoagulation Strategies trial which was discontinued early due to a beneficial effect of rivaroxaban in addition to aspirin in patients with chronic coronary or peripheral artery disease.6 After early termination of the study, the benefit of therapy for incident myocardial infarction and cardiovascular death were lost and there was a higher stroke rate after switching to aspirin alone for participants who originally had been randomised to rivaroxaban in addition to aspirin (figure 3).Outcomes from the time of switching to non-study aspirin until final contact in participants who took study antithrombotic drugs until early stopping (n=14 086). (A) Composite outcome zithromax 250mg cost panel. (B) cardiovascular death.

(C) MI zithromax 250mg cost. (D) stroke. ASA, aspirin zithromax 250mg cost. MI, myocardial infarction.

RIVA, rivaroxaban." data-icon-position data-hide-link-title="0">Figure 3 Outcomes from the time of switching to non-study aspirin until final contact in zithromax 250mg cost participants who took study antithrombotic drugs until early stopping (n=14 086). (A) Composite outcome panel. (B) cardiovascular death. (C) MI zithromax 250mg cost.

(D) stroke. ASA, aspirin zithromax 250mg cost. MI, myocardial infarction. RIVA, rivaroxaban.Darmon and Ducrocq7 address the medical, ethical and regulatory challenges when a study is terminated before approval for continuation of study medication zithromax 250mg cost (if effective) has been obtained.

As they conclude. €˜The study by Dagenais et al6 sheds light on the various serious consequences of discontinuing study treatments that were zithromax 250mg cost proven effective in randomised clinical trials. It should be seen as a call for developing strategies for management of patients after trial completion, whether it is earlier than expected or scheduled.’The Education in Heart article in this issue summarises the cardiovascular manifestations of systemic inflammatory diseases.8 Advanced cardiac imaging approaches have greatly expanded our understanding of the frequency, type and extent of cardiac involvement in patients with conditions such as systemic lupus erythematosus, antiphospholipid syndrome, systemic sclerosis, autoimmune myositis and the vasculitides. A detailed summary table will be invaluable to clinicians, along with imaging examples of cardiac involvement (figure 4).Cardiovascular magnetic resonance from a patient who was 13 weeks into her first pregnancy and presented with chest pain, ECG changes and an elevated troponin.

An angiogram showed zithromax 250mg cost unobstructed coronary arteries. The figure shows T2 mapping in panel (A), with high signal (inflammation) in the mid-inferolateral wall. Panel (B) shows the cause of zithromax 250mg cost this to be a localised myocardial infarction. The patient went on to have a positive antiphospholipid screen and was started on anticoagulation." data-icon-position data-hide-link-title="0">Figure 4 Cardiovascular magnetic resonance from a patient who was 13 weeks into her first pregnancy and presented with chest pain, ECG changes and an elevated troponin.

An angiogram showed unobstructed coronary arteries zithromax 250mg cost. The figure shows T2 mapping in panel (A), with high signal (inflammation) in the mid-inferolateral wall. Panel (B) shows the cause of this to be zithromax 250mg cost a localised myocardial infarction. The patient went on to have a positive antiphospholipid screen and was started on anticoagulation.The Cardiology-in-Focus article in this issue9 provides a concise guide to minimising risk for women, such as cardiology trainees and consultants, who work with radiation during pregnancy and points out that.

€˜A better awareness of radiation protection—with more use of low-dose techniques and protective equipment—would benefit all operators and not just those who are pregnant.’Ethics statementsPatient consent for publicationNot required..

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How to zithromax otc alternative cite this article:Singh 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 our zithromax otc alternative 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 zithromax otc alternative 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 zithromax otc alternative were freely and blatantly broadcast and discussed on electronic, print, and social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident.

Psychiatrists suddenly started getting distress calls from their patients in despair with zithromax otc alternative 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 zithromax otc alternative 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 zithromax otc alternative condition and illness and also his relationships and finances.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric Society has written to the Press Council of India underlining this zithromax otc alternative concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more 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 zithromax otc alternative media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so. There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist.

These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry and are zithromax otc alternative 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 zithromax otc alternative the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have guidelines and zithromax otc alternative resource books for interacting with media, and psychiatrists should 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 be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should zithromax otc alternative 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, West zithromax otc alternative 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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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.

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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.

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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 zithromax 250mg cost this article:Singh O P. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the zithromax 250mg cost 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 zithromax 250mg cost media went into a frenzy as newspapers, 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 zithromax 250mg cost freely and blatantly broadcast and discussed on electronic, print, and social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident.

Psychiatrists suddenly started zithromax 250mg cost getting distress calls from their patients in despair with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 zithromax 250mg cost (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 zithromax 250mg cost full of speculations about the person's mental condition and illness and also his relationships and finances.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them zithromax 250mg cost aware of the 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 zithromax 250mg cost comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so. There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist.

These types of viewpoints perpetuate stigma, myths, and “misleading concepts” zithromax 250mg cost 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” zithromax 250mg cost by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional zithromax 250mg cost societies have guidelines and resource books for interacting with media, and psychiatrists should 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 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 zithromax 250mg cost 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 zithromax 250mg cost - 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].

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The International Journal of Tuberculosis and Lung Disease publishes articles on all aspects zithromax 250mg cost of lung health, including public health-related issues such as training programmes, cost-benefit analysis, legislation, epidemiology, intervention studies and health systems research. The IJTLD is dedicated to the continuing education of physicians and health personnel and the dissemination of information on lung health world-wide. To share scientific research of immediate concern as rapidly as possible, The Union is fast-tracking the publication of certain articles from the IJTLD and publishing them on The Union website, prior to their publication in the Journal.

Read fast-track articles.Certain IJTLD zithromax 250mg cost articles are also selected for translation into French, Spanish, Chinese or Russian. These are available on the Union website.Editorial BoardInformation for AuthorsSubscribe to this TitleInternational Journal of Tuberculosis and Lung DiseasePublic Health ActionIngenta Connect is not responsible for the content or availability of external websitesDownload Article. Download (PDF 53.5 kb) No AbstractNo Reference information available - sign in for access.

No Supplementary Data.No Article zithromax 250mg cost MediaNo MetricsDocument Type. EditorialAffiliations:1. University of Sydney, Faculty of Medicine and Health, School of Pharmacy, Sydney, NSW, Australia, Westmead Hospital, Sydney, NSW, Australia, Marie Bashir Institute of Infectious Diseases and Biosecurity, University of Sydney, Sydney, Australia 2.

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The IJTLD is dedicated to the continuing education of physicians and health personnel and the dissemination of zithromax 250mg cost information on lung health world-wide. To share scientific research of immediate concern as rapidly as possible, The Union is fast-tracking the publication of certain articles from the IJTLD and publishing them on The Union website, prior to their publication in the Journal. Read fast-track articles.Certain IJTLD articles are also selected for translation into French, Spanish, Chinese or Russian.

What does zithromax cure

This article appeared in the September/October 2021 issue of Discover what does zithromax cure magazine as "Frontline Fatigue." Become a have a peek at this website subscriber for unlimited access to our archive.In February 1945, U.S. Navy nurse Dorothy Still was a prisoner of war in the Japanese-occupied Philippines. Along with 11 other Navy nurses, Nurse Still provided care for civilian inmates in what does zithromax cure a prison camp where food was scarce and guards were brutal. Few inmates weighed more than 100 pounds, and most were dying from malnutrition.

On the night of Feb. 22, Nurse Still and the other inmates watched as their captors set up guns around the perimeter of what does zithromax cure the camp and turned the barrels inward. Other guards dug shallow graves. The inmates had long suspected the camp commander planned to massacre them all, and it seemed the rumors were coming true.

Yet Nurse what does zithromax cure Still and another Navy nurse reported to the infirmary for the night shift. They had little medicine or food to offer their patients. Comfort and kindness were all they had left to give. Nurse Still what does zithromax cure heard gunfire the next morning at dawn and assumed the massacre had begun.

She steeled herself to glance out the infirmary window and saw parachutes gliding to the ground. Liberation had come just in time!. U.S what does zithromax cure. And Filipino forces swiftly evacuated the 2,400 inmates to safety.

But that wasn’t the end of Nurse Still’s journey. She was haunted by the horrors she what does zithromax cure witnessed in the prison camp, and the trauma stuck with her for the rest of her life. Now nursing leaders and advocates are saying the problem of not addressing nurses’ mental health needs has again reached a critical point. Nurses have been on the front lines of the buy antibiotics crisis, but most aren’t receiving comprehensive mental health screening or treatment.

Nursing advocacy groups and scholars who study PTSD in nursing warn that leaving nurses’ mental health needs untreated could lead to a nursing shortage, much as it did after World War II.Taken as prisoners of war in 1942, Dorothy Still and 11 other Navy nurses what does zithromax cure provided medical care in the midst of brutal suffering at Los Baños Internment Camp. (Credit. Courtesy of Bureau of Medicine and Surgery) Suffering in Silence Back in the States, Nurse Still was tasked with speaking at war bond drives about the three years what does zithromax cure she was a prisoner of war. She found the experience troubling and requested a transfer to Panama, but her memories followed her to her new post.

At times, she was depressed. Other times, she couldn’t stop thinking about all she what does zithromax cure had endured. She sometimes cried without provocation and struggled to stop crying once she had started. On advice of her fiancé, she booked an appointment with a naval physician.

During her what does zithromax cure appointment, Nurse Still told the physician she had been a prisoner of war for more than three years, and asked for a medical discharge based on the trauma she was experiencing. The doctor asked when Nurse Still was liberated. The date was the same as the raising of the flag at Iwo Jima. The physician what does zithromax cure said those men were heroes, but Nurse Still was a woman and a nurse, and therefore, did not suffer.

Denied treatment, Nurse Still left the appointment shaking. She vowed she would keep her pain to herself. The Navy what does zithromax cure nurses weren’t the only medical care providers taken prisoner during WWII. Sixty-six U.S.

Army nurses as well as hundreds of physicians, pharmacists, and medical assistants were also held captive in the South Pacific. But at the end of what does zithromax cure the war, as the U.S. Prepared to welcome home millions of men and women who served their country, mental health treatment was limited — and reserved for men. Nurses, it was assumed, did not suffer.

At the time, the what does zithromax cure U.S. Military was the largest employer of nurses, and it had established an expected code of silence regarding how nurses responded to their own trauma. In 1947, an article in the American Journal of Psychiatry claimed a military hospital was a controlled environment that insulated nurses from the brutality of war. The study’s author claimed that nurses’ mental health needs were “less complex,” and what does zithromax cure that nursing fulfilled women by catering to their natural instinct to care for men.

€œThey were supplying a service which gratified the passive needs of men. And which identified these women with the mother, the wife, or the sweetheart back home.”Many nurses, including Nurse Still, responded to the lack of mental health treatment by leaving both what does zithromax cure the military and nursing. The late 1940s saw a shortage in nurses at time when hospital admissions rose by 26 percent. The shortage persisted until the late 1960s when wages began to increase.After three years as POWs, the Navy nurses were liberated in 1945.

Here, they what does zithromax cure speak with Admiral Thomas C. Kinkaid after their release, and are shown next to the aircraft that brought them from the South Pacific to Hawaii. (Credit. U.S.

Navy Bureau of Medicine and Surgery)A Looming Crisis The buy antibiotics zithromax has meant that for the first time since WWII, the vast majority of U.S. Nurses are embroiled in fighting a common enemy. It’s a demanding and emotional battle that advocates say adds a deeper stress to an already taxing job.Across the country, nurses have been caring for patients dying from buy antibiotics who do not have the support of family at their bedside due to visitor restrictions. €œThe nurses are often the ones who are serving as the loved one and helping the patient navigate the end-of-life journey,” says Holly Carpenter, a senior policy advisor with the American Nurses Association.

In addition to caring for dying buy antibiotics patients, Carpenter says, many nurses were not properly equipped at the height of the zithromax with the personal protection equipment needed to avoid . These nurses lived in fear of being infected or transmitting the zithromax to loved ones at home. And on top of these stressors, nurses are also still coping with the usual demands of the job. €œThere are the things that have always been there — long shifts, sometimes mandatory overtime, a workload that’s heavier than you’re comfortable with, having to work through breaks or lunchtime, having to come in early and stay late,” Carpenter says.

Prior to the zithromax, studies estimated that as many as half of critical-care nurses experienced post-traumatic stress disorder (PTSD). Since the zithromax began, researchers have found the crisis has amplified symptoms of mental health problems. A 2020 study in General Hospital Psychiatry found that 64 percent of nurses in a New York City medical center reported experiencing acute stress. €œAcute stress included symptoms like nightmares, inability to stop thinking about buy antibiotics, and feeling numb, detached, and on guard,” says study leader Marwah Abdalla, a clinical cardiologist and assistant professor of medicine at Columbia University Medical Center.

€œThis is concerning. We know that if these symptoms persist for more than a month, it can lead to PTSD.” Some nurses experienced PTSD before buy antibiotics, but the conditions of the zithromax have amplified mental health problems. (Credit. Eldar Nurkovic/Shutterstock)A person is diagnosed with PTSD if they meet criteria outlined by the DSM-5, the psychiatric profession’s official manual.

Criteria include experiencing, witnessing or learning about a traumatic event (such as death, serious injury, or sexual violence). Intrusive symptoms like dreams and flashbacks. Avoidance of reminders of the event. Negative changes in thoughts and moods.

And behavioral changes. A person can also develop PTSD if they are repeatedly exposed to details of a traumatic event. Suffering from undiagnosed or untreated PTSD is a life-altering condition with diverse ramifications, and may lead a nurse to leave health care. €œWe’re potentially setting up an occupational health care crisis,” Abdalla says.

€œThis has long-term implications for the health care industry and our ability to deliver adequate health care for our patients.” Carpenter says health care organizations must be proactive with screening nurses for symptoms related to anxiety, depression, and PTSD. Such screenings must be confidential and come with the assurance that a nurse’s license or job will not be compromised. Organizations also need to work to destigmatize mental health diagnosis and treatment. €œHistorically, nurses are always looked upon as the healers and the helpers,” Carpenter says.

€œThey feel they need to be strong for other people. What do you do when the hero needs help?. €For Nurse Still, help never came. She left the Navy and nursing, married, and had three children.

She returned to nursing in the late 1950s after her husband died suddenly and she needed to support her family.Only in the 1990s did she begin speaking about her experiences in interviews with oral historians and documentary producers. She also wrote a memoir, but kept the story light and did not disclose her extensive suffering.The profession has advanced since Nurse Still’s 1940s appeal for mental health support was rejected. €œWe do recognize the full PTSD, compassion fatigue, and burnout of nurses. It’s been chronicled now and we understand it,” Carpenter says.

Now the challenge is encouraging each nurse to seek and receive help. Otherwise, advocates warn, their health and wellbeing will continue to decline, and history may repeat as stressed nurses leave a strained profession. Emilie Le Beau Lucchesi is a journalist in the Chicago area and the author of This is Really War. The Incredible True Story of a Navy Nurse POW in the Occupied Philippines.It’s pretty obvious when a dog is sad.

It might whine or whimper, knit its brow, or turn its big, imploring eyes upward at you. But it would be another thing entirely to see a big tear rolling down your canine companion’s face.Animals simply don’t cry. Or at least, they don’t shed emotional tears. The only creatures who have evolved to do so, it turns out, are humans.

We snivel at sad movies, well up at weddings and blink away hot tears of frustration during arguments. €œWe appear to be the only animal that sheds tears for emotional reasons,” says Randolph Cornelius, a professor of psychological science at Vassar College in New York and an expert on human emotion.There are many theories on the evolution and purpose of emotional tears. Experts even have a few ideas why animals — who do experience emotions — don’t weep like we do. But why we evolved to eject liquid out of our eyes as a signal of distress, rather than some other reaction, is still far from settled.The Biology of CryingFrom a biological perspective, there are three types of tears.

One is basal tears, which our eyes create automatically to lubricate and clean our eyes. These come from our accessory lacrimal glands, located under the eyelids. Then there are reflex tears, which you’re likely acquainted with if you’ve ever cut an onion or been poked in the eye. The third is emotional tears — the only variety that we can control, to some extent.

These latter two types come from lacrimal glands on the upper outside of our eye sockets.“One argument is that [emotional crying] is almost like an emotional reflex as opposed to just a physical reflex,” says Marc Baker, a teaching fellow at the University of Portsmouth in England who researches adult emotional crying.Indeed, some have hypothesized that the purpose of crying is itself just another biological function. For example, biochemist William Frey theorized in the 1980s that crying balances levels of hormones in our body to relieve stress. He also suggested that crying clears our body of toxins, though subsequent studies have largely disproven this. English naturalist Charles Darwin, the father of evolution, believed children cried to experience physical relief from negative emotions.In these theories, crying is something that restores us to equilibrium.

It is the idea of crying as catharsis, or a way to calm ourselves in times of distress. After all, it’s not unusual for people to report feeling better after “a good cry” — but that relief may be coming from unexpected places.The Psychology of CryingPerhaps the most compelling explanation for tearful crying is that it is driven by our social needs. Crying is a distinct visual signal that something is wrong. In an instant, it communicates that someone might need help.

When others attend to the crier, it contributes to a collaborative social environment that is highly complex in humans.Inquiries by Cornelius support this theory of tears as a quick and effective social signal. In a number of studies, he and colleagues showed photographs of faces to participants (under the guise of another purpose) and asked them to interpret the emotion. In some of the photos, people were crying real tears. In others, they had been digitally removed.When shown the pictures with tears, almost every participant labelled the emotion as sadness or grief.

Tear-free crying faces, on the other hand, were confusing. €œWithout the tears, the emotion almost disappears,” Cornelius says. €œTheir judgments of the emotion don't tend to cluster around the ‘sad’ family of emotions — they're all over the place. And in fact, some people say there's no emotion there at all.”This indicated that crying is a strong signal to others of our immediate emotional state.

It’s hard to fake real tears. And as researchers of crying can attest, it’s hard to induce genuine emotional crying in a lab setting — one of the reasons it’s challenging to study.Solving an Evolutionary MysteryFrom an evolutionary perspective, some of our physiological reactions have a clear purpose. It makes sense that we sweat when overheated, raise our voices when angry or tense up in fear. But at a distance, our tearful tendencies are just plain weird.

Someone showing an alien around Earth would have to explain that when humans (and only humans) feel distress or even overwhelming happiness, their faces get slightly wet and puffy.Animals do have lacrimal glands, which they use for reflex tears. But in humans, something seems to have changed somewhere along the way. What started as distress calls that many animals make became connected with the production of tears, and experts still aren’t sure why. €œThere’s no answer, sorry,” Baker says.

But there are a few theories.Clinical psychologist Ad Vingerhoets has suggested that crying might have been more advantageous than other kinds of noises because it suggests submissiveness and harmlessness to would-be predators, who might then reduce their aggression. But that still doesn’t explain the tears themselves or why animals wouldn’t benefit from them in the same way.For that, researchers point toward other, seemingly unrelated hallmarks of human physiology and development that could have led to tears. For one, we walk upright — unlike bears and wolves, who, in their position closer to the ground, rely mostly on smells to signal distress. Perhaps partially because of this, we rely heavily on visual cues to communicate in social situations.

€œFrom a kind of evolutionary perspective, it makes sense that lots of our signals become visual signals, because we are just quite visual animals,” Baker says. We also position ourselves forward. Our faces, then, developed to become the most complex in the animal kingdom — especially on the top half of our face. €œOur kind of facial expressions far exceed almost every other animal, especially around the eyes,” he says.

€œWe can do much more with the top half of our face.”An intricate facial musculature arose, and with it, machinery that could induce crying. Asmir Gračanin, a professor of psychology at the University of Rijeka in Croatia, and colleagues theorized that the orbicularis oculi muscle may have evolved along with our hyper-expressive faces. This eye socket muscle could have squeezed the corneal sensory nerves that trigger the production of tears by the lacrimal gland and proved advantageous to human babies as a call for immediate help.This also fits in with the uniqueness of human babies, who are much more helpless than other baby animals that come out of the womb ready to walk and perform other basic functions. Human babies need more help, cry for assistance and comfort, and then (largely) grow out of crying as adults.But adults still do cry emotional tears — in sadness, happiness, awe or frustration.

€œIt's kind of what makes us human, almost,” says Baker, “[our] ability to share emotions very silently, with a small drop of saline solution from the eye.”The introduction of the contraceptive pill in the 1960s spurred a landmark moment for women, liberating many from the home and propelling them into the world. But this excitement overshadowed the side effects and hazards associated with the pill, which we now know may include a slightly increased risk of breast cancer.“A lot of women are unaware of the cancer risk associated with hormonal birth control because the advent of the pill freed up the lives of women to enter the workforce more effectively,” says Beverly Strassmann, a human evolutionary biologist at the University of Michigan. When radically altering the body with synthetic hormones, you can’t assume there won’t be side effects, she says. But the field hasn’t made significant progress, partly because contraceptives have provided women with tangible benefits.

Sixty years on, pharmaceutical companies are still “resting on their laurels” and need to better evaluate the association between hormonal birth control and cancer, she adds. Research has also linked the pill to depression, decreased sexual desire, anxiety and an altered ability to form emotional memories. Most physicians, however, still don’t closely follow research investigating the links between hormonal birth control and its psychological side effects, says evolutionary psychologist Sarah Hill, author of How the Pill Changes Everything. Your Brain on Birth Control.

€œMost medication doesn’t look at the full spectrum of side effects in the way people experience the world. It’s not even in physicians’ peripheral vision,” Hill says. But women want the next birth control revolution. Younger women especially seek non-hormonal options, Hill says.

€œA lot of women aren’t being served, and many are on the pill even though they don’t love it — their standards are low because there’s so few good options,” she says. In recent years, contraception apps have attracted a rise in users, which may suggest that many women no longer tolerate the impacts of hormonal birth control on their bodies. But these apps have faced criticism over their efficacy. A New Kind of PillAnother possibility.

A non-hormonal pill. Now, University of Connecticut physiologist and geneticist Jianjun Sun is wading through the unknowns to formulate it.“We know that, in humans, the ovulation process is triggered by a hormone surge, but how the egg is released is very precise. The menstrual cycle is very tightly controlled and there are a lot of unknowns in this area,” he says. Sun does know that when a person ovulates, an egg that’s contained within a follicle bursts out of the ovary and sets off down the fallopian tube, where it can be fertilized.

He’s hoping to formulate a drug that stops the follicle from rupturing and releasing the egg. Shutting off ovulation isn’t a new concept — hormonal contraception does this by tricking the body into thinking users aren’t pregnant. But he seeks a new way to halt egg release without the use of synthetic hormones. Crucially, Sun has devised a way to analyze different compounds without relying on human subjects (which would complicate the process).

He realized that fruit flies ovulate in a similar way to people, and the fly’s ovulation process resembles that within mice. As this research took off, the Gates Foundation had begun supporting scientists developing non-hormonal contraceptives. The organization has funded Sun to test compounds on flies. Now, Sun is screening up to 500 compounds daily to see which ones prevent follicles from rupturing and releasing eggs.

€œThe Gates are very excited now. They’re trying to get us to find the target, then we can study this target using genetic tools,” he says. Researchers could test the drug in humans eventually, Sun says. Unlike hormonal pills, users wouldn’t need to take it daily.

To inhibit ovulation, you only need to take it for a week or so before the process begins.While this sounds tempting, many people don’t know when exactly they ovulate — and only 10 to 15 percent of women experience 28-day cycles. And because the drug concept is so new, researchers aren’t sure what dosing might look like. €œIt’s still hypothetical in terms of how to use contraceptives targeting ovulation, since there’s no products on the market,” Sun says. A Dearth of ResearchDespite the many unknowns, experts seem receptive to any new research in hormonal birth control alternatives.

In recent years, few studies have taken on this challenge.Hormonal contraceptives dominate at a time when, researchers argue, scientific and technological advances bring unprecedented opportunities for new drugs across medical fields. If Sun’s research is fruitful, it could attract more funding for other researchers working on these alternatives, says Bethan Swift, a PhD student at the University of Oxford who studies the epidemiology of women’s health. €œOne big barrier to developing new contraception is that existing options work,” Swift says, “So there’s little demand from the pharmaceutical industry to put money into creating new compounds.” This shortage of funds places significant pressure on Sun. The Gates Foundation hopes that at least one drug will hit the market by 2026, he says.

But the bar for birth control approval is uniquely high. Because it isn’t meant to alleviate an illness, possible side effects may not be worth the trade-off versus, for example, cancer treatments. It will probably take between five and 10 years before a new drug is available, Sun says. “Developing new contraception isn’t easy because they’re going to healthy women, unlike other drugs, where it’s more accepted that there will be side effects,” Sun says.

The final drug will likely cause some side effects, but fewer than hormone-based contraceptives, he notes. However, Hill is concerned that the end product could still affect the body’s natural hormone levels.Our bodies produce most sex hormones via ovulation, and high levels of estrogen propel monthly egg maturation. After an egg is released, the empty follicle releases progesterone — so levels would fall fairly low if you prevent ovulation, she says. €œStopping ovulation sounds perfect, but if you understand that’s how the body makes hormones, you’d realize it’s not a panacea.”This article contains affiliate links to products.

Discover may receive a commission for purchases made through these links.Did you know that sleeping in a zero-gravity position may help alleviate symptoms from improve sleep disorders, relieve neck and back pain, and allow for better circulation and heart health?. An adjustable bed frame allows you to place your body in a zero-gravity position to enjoy all of these benefits and more as you sleep comfortably with optimal support throughout the night. If you’ve been considering getting an adjustable bed, you’re not alone. Many individuals are making the switch to enhance their comfort, improve their health, and, of course, to enjoy more restful sleep.

Deciding which adjustable bed frame is right for you can be challenging. The market is overflowing with options, and sorting through all these choices can be overwhelming. Fortunately, our best adjustable beds reviews below can help you focus your search, narrow down your choices, and select the right model to help you mitigate sleep disorders, to sleep more comfortably, and to wake up feeling more rested. What is Zero Gravity?.

Zero gravity refers to a specific position where the body is a state of weightlessness. NASA actually developed this term for astronauts to help them find the ideal position to keep their weight balanced and neutralized as they flew into space. Being in a zero-gravity position prevents gravity from affecting your body, which means that nothing is pulling your body down. Your body is in a zero-gravity position when.

When your body is in the zero-gravity position, it should look like a V shape. This alignment helps ensure that your weight is distributed evenly. As you can imagine, sleeping in this V-shaped position on a standard bed frame isn’t possible. However, adjustable bed frames enable you to sleep in a zero-gravity position and prevent your body’s weight from placing pressure on your hips, spine, and other joints.

Sleeping in a zero-gravity position offers a myriad of benefits. We’ll explore these benefits in the next section. Benefits of Sleeping in a Zero-Gravity Position with an Adjustable Bed Frame Adjustable beds have been used in hospitals for over a century due to their ability to properly position patients to facilitate recovery and reduce complications from surgeries and other medical procedures. If adjustable beds can protect the health of patients in a hospital, then it seems like a logical conclusion that they can also offer health benefits for individuals who use them at home.

Indeed, there are many ways switching to an adjustable bed frame and sleeping in a zero-gravity position can benefit your health. These include. While some individuals snore every night, others are more prone to it only when they are congested. Adjustable beds can also help reduce snoring caused by congestion because keeping the head elevated can allow the sinuses to drain.

Reduced sleep apnea. An adjustable bed may also reduce sleep apnea symptoms. Sleep apnea, which occurs when an individual stops breathing during sleep, is also sometimes the result of an obstructed airway. Elevating the head may open up the airway enough to prevent or lessen sleep apnea, allowing individuals get more restful sleep.

Relief from neck, back, and joint pain. Sleeping in a zero-gravity position can significantly increase your comfort and reduce your pain. The reason for this benefit is that when you’re in the zero-gravity position, your weight is evenly distributed. This improved distribution of weight takes the pressure of your back, neck, and joints, which is often the main cause of pain.

Laying on a flat mattress, on the other hand, does not allow your weight to be evenly distributed. This places unnecessary pressure on the spinal column and can result in a significant pain and discomfort. Adjustable beds may provide relief from pain caused from sciatica, fibromyalgia, arthritis, scoliosis, and other conditions. Improved circulation.

Sleeping in a zero-gravity position allows more blood to flow to the heart. This increase of blood flow reaching the heart makes its muscles work harder to pump that blood throughout the body. Increased blood circulation can improve the overall health of your heart and other vital organs. Decreased swelling.

Another benefit of improved circulation is decreased swelling. When the body lays flat, blood and other fluids may accumulate the in the lower body since the heart isn’t able to keep blood flowing effectively. This can result in inflammation or swelling. However, with the increased blood flow that results from sleeping in a zero-gravity position, fluids won’t accumulate in the extremities, and swelling may be reduced.

Improved digestion. Digestion can also be improved by sleeping on an adjustable bed frame. Sleeping flat can make it more difficult for the body to digest food properly. Sleeping flat can also aggravate acid reflux, heartburn, and GERD (gastroesophageal reflux disease.

Elevating the head about six inches can reduce these symptoms. This position removes pressure from the digestive track and makes it more difficult for stomach acids to go up into the throat. Better breathing. When you sleep in the zero-gravity position, the pressure placed on your lungs and airway is reduced.

As a result, your body can breathe more easily and can limit the impact asthma, allergies, and congestion can have on your sleep. Best Adjustable Bed Reviews Whether you’re looking for the best split king adjustable bed reviews or the best adjustable twin, queen, or full bed frames, we have you covered. We have selected some of the top models currently available that will help you stay comfortable while you sleep and will enable you to enjoy the benefits described above. Read on to discover which adjustable bed frame is right for you.

GhostBed Adjustable Base If you’re looking for an adjustable bed frame with luxury features for a budget-friendly price, consider the GhostBed Adjustable Base. This fully-adjustable frame allows you to customize your position for ultimate comfort. The fully adjustable head and foot sections allow for an unlimited number of options, including a zero-gravity position. This bed frame also offers 15 head and foot massage modes to deliver additional comfort and relaxation.

Furthermore, it is equipped with two USB ports on each side to allow for easy charging and convenient access to electronic devices. Under-bed LED lights are also integrated into the design to provide soft lighting if you wake up in the middle of the night. The included backlit remote makes it easy to adjust the bed to the ideal position for sleeping or relaxing. Use the foot and head up/down buttons to move the frame to the exact position you desire.

The remote can also save your favorite position for sleeping and return you to it with just a press of a button. Additionally, the remote offers preset positions for zero-gravity, watching TV, and lounging. With the remote, you can even control the under-bed lighting and turn on the head or foot massage and adjust their intensity. The GhostBed Adjustable Base features a sturdy steel frame.

It also has a retainer bar and non-skid surface to ensure the mattress stays in place. This adjustable bed frame is available in twin XL, queen, and split king sizes. Split king adjustable beds offer the added benefit of allowing each partner to customize their own position. All orders include free shipping and a limited lifetime warranty.

Puffy Adjustable Base Premium The Adjustable Base Premium from Puffy Sleep is another top contender when you’re looking for the best adjustable bed frame. The head on this model adjusts up to 60 degrees and the legs adjust up to 45 degrees to help each individual find their most comfortable sleeping position. The adjustable bed frame from Puffy Sleep is available in twin, twin XL, full, queen, king, and split-king sizes. Use the included remote to customize your position whether reading a book in bed, watching TV, or drifting off to dreamland.

The remote also has a memory feature that can save your favorite position. Some of the other remote settings include zero gravity, watching TV, and anti-snore. Puffy Sleep has some of the best split king adjustable beds reviews. With the split king adjustable frame, you and a partner can each set the bed to the position that is most comfortable for you.

This can help ensure that each of you get the restorative sleep that need. For a nominal additional fee, you can upgrade the Puffy Sleep Adjustable Base to include head and food massage features and dual USB ports for charging electronic devices. This adjustable frame is constructed from coated metal for lasting durability. Each purchase is protected by a 10-year warranty and includes free shipping.

Layla Adjustable Base Plus This motorized and fully adjustable base from Layla Sleep also has a lot to offer users. It is available in twin XL, queen, king, and split king sizes. A wireless remote is included with the frame for easy operation. The remote includes preset buttons for moving the frame to zero-gravity, anti-snore, or flat positions.

You can also set the remote to remember up to three of your preferred positions. A mobile app is available for controlling the bed frame with a smartphone or tablet, and the frame is even compatible with Amazon’s Alexa and the Google Assistant for voice command operations. Layla Sleep incorporated some upgraded features into the design of this frame. The frame features dual-zone vibrating massage motors at the head and foot of the frame.

There are three massage intensities to choose from, as well as an auto-shutoff timer to stop the vibrations at a set time. Each side of the frame features two ports to keep your devices charged and within easy reach. Some of the other notable features of this adjustable bed frame include the under-bed lighting and wall-hugging technology that keeps the head of the bed at the same distance from the wall regardless of the incline angle. Layla Sleep backs this bed frame with a 10-year warranty.

They also offer free-shipping and a 30-night money-back guarantee. Sweet Night Tranquil Adjustable Bed Frame Last, but certainly not least, we also think you’ll love the Tranquil Adjustable Bed Frame from Sweet Night. Available in twin XL, full, queen, and split California king sizes, this bed frame delivers the ability to tailor your position for enhanced comfort. Adjust the head incline between 0 and 60 degrees and the foot incline between 0 and 40 degrees for a nearly endless number of positioning options.

The Tranquil Adjustable Bed Frame from Sweet Night can be controlled using the included wireless remote or with an app on your smartphone or tablet. Use the remote or app to adjust the head and foot inclines or to select one of the preset positions including anti-snore, zero gravity, watching TV, or lying down flat. In addition to allowing you to adjust your position, this bed frame includes some other helpful and impressive features. Each side of the frame offers dual USB ports for charging your phone, tablet, or other devices.

There is also a pocket on each side to hold a smartphone and keep it within easy reach. Remote-controlled LED under-bed lights, provide low lighting if needed at night or in the morning. The frame is made using a sturdy aluminum alloy that can support up to 705 pounds. All orders include free shipping and free returns.

Adjustable Bed Frame Buying Guide If you’re interested in taking advantage of all the benefits associated with using an adjustable bed frame, it is imperative to note that each model is slightly different. There are a number of important considerations to keep in mind as you shop for an adjustable bed frame. Read through our buying guide below to learn more about these considerations and choose the best adjustable bed frame to match your needs. Mattress Compatibility If you’re planning to use your existing mattress, the first thing you should do is to confirm compatibility.

Most adjustable bed frames are designed to be compatible with different mattress brands, but some manufacturers recommend only using their mattresses on their proprietary frames. Keep in mind that most innerspring mattresses are too inflexible to work well with an adjustable frame. Hybrid, foam, or latex mattresses are more flexible and will work best. Size After determining if your current mattress is compatible with the bed frame or if you need to purchase a new mattress with your new bed frame, then you will need to evaluate if each model is available in your desired sire.

Obviously, the bed frame must match the size of the mattress you are planning to use on it, so you won’t want to waste your time looking at a model that isn’t even available in your preferred size. Settings and Operation Before making a purchase, look at the range of motion of each bed frame. Some adjustable bed frames offer more adjustability than others. This flexibility, or lack of it, could certainly make one model more appealing than another.

The head can often be elevated between 60 and 80 degrees, while the range of motion for the lower portion of the mattress is typically between 30 and 40 degrees. If there is a specific angle you’d prefer, then confirm it is possible with each bed frame you’re considering. Next, look at how easy it will be to adjust the bed frame. Does it include a remote control?.

Are there any preset positions or memory features?. Can you download an app to control the bed frame using a smart device?. Additional Features Some manufacturers include additional features to make their adjustable bed frames more user-friendly. These features may include heat and massage functions, under-bed lighting, USB charging ports, and built-in speakers.

If any of these features are important to you, look for a manufacturer that integrates them into their design of their adjustable bed frame. Frequently Asked Questions Can you use a regular mattress on an adjustable bed frame?. Yes, most regular mattresses can be used on an adjustable bed frame. Many frames are compatible with latex, foam, and hybrid mattresses.

Unfortunately, most innerspring mattresses are too rigid to move with an adjustable frame. What is a split king adjustable bed?. Split king adjustable beds allow the right and left sides to adjust independently of one another. This means that each partner can elevate their head and feet to their exact comfort level without needing to make compromises with their partner.

Are adjustable beds worth the additional cost?. This is a personal question that will come down to your priorities and financial situation. Many people find that adjustable beds are worth the additional cost due to how much better they sleep and all the other health benefits they offer, such as reduced back and neck pain, better circulation, decreased swelling, and improved digestion. Split king adjustable beds can be particularly beneficial for partners who prefer different sleeping positions or who are facing different health issues.

With a split king adjustable bed, each partner can independently adjust their own side of the bed. How can you get into a zero-gravity position with an adjustable bed?. You need to elevate your legs and feet to a higher level than your head and your heart to achieve a zero-gravity position. This position alleviates pressure placed on your joints to relieve back pain and is also beneficial for improving the body’s circulation.

How do you keep sheets on an adjustable bed?. When shopping for sheets for an adjustable bed, the first thing to do is to check the depth of the mattress and confirm that the pocket-depth of the fitted sheet is sufficient for a proper fit. Choosing a sheet that is not deep enough for your mattress will almost certainly cause the corners to slip off as the bed adjusts. When making the bed, tuck the edges of the flat sheet under the mattress.

You can also find some flat sheets that include corner straps. These corner straps grip on to the fitted sheet and will help ensure that the flat sheet stays in place. If these ideas still don’t work, sheet suspenders are another option. A sheet suspender is a large band designed to ensure a flat sheet doesn’t slip off a mattress.This article appeared in the September/October 2021 issue of Discover magazine as "Heart Ache." Become a subscriber for unlimited access to the archive.Chloe looked miserable.

She was curled up on the hospital bed, sweaty and shaking, wracked with waves of nausea, her heart racing. I gave her a cool washcloth and a basin as the nurse started her IV. I had cared for her before. Though only 16, she’d been in the hospital a dozen times already.“I think it may be another heart valve ,” I told her.

She nodded, familiar with the diagnosis, and the treatment that followed. She was at particular risk for a type of called endocarditis, where bacteria invade and infect the valves of the heart.Chloe was born with an aortic valve that had only two parts, instead of its normal three, and was unusually small and stiff. As she grew older, her valve became thicker and less pliable. Unable to open properly, her heart had to work too hard to pump out blood.

When she was 14 years old, surgeons cut through her breastbone to her heart, delicately repairing the abnormal aortic valve. Though her valve was now working normally and heart pumping well, she was still dealing with the procedure’s unwelcome consequences.As before, we followed the same routine — strong antibiotics to kill the bacteria in her heart and bloodstream, fluids and medications to quell her nausea and dehydration. She settled into her hospital room with magazines and movies, expecting a long stay.The Night ShiftTwo days later, I stopped to check on Chloe at the beginning of my night shift. Her thin frame was tangled in the sheets, shaking and agitated, unable to find a comfortable position.

Her nurse told me Chloe seemed no better — and perhaps worse — than when she’d arrived. The usual medicines did not seem to relieve her nausea, and she had started having diarrhea.I wondered if something more was going on. Could it be a more aggressive or resistant bacteria causing her endocarditis, or an entirely new intestinal caused by her antibiotics?. But blood tests showed the same common bacteria that had caused her previous heart s, and which her antibiotic should kill.

Stool tests sent that day showed no dangerous bacteria. Perhaps she just needed more time to improve on her current treatment.As I sat by her bedside, I noticed a few other odd symptoms. Her pupils were as wide as saucers, her nose was running, and her skin was damp with sweat and covered with goosebumps. This constellation of findings pointed in a surprising direction that I had seen before in my adult medicine rotations as a student — opiate withdrawal.I looked in Chloe’s chart, reviewing the medications she took routinely at home and those we had given her in the hospital.

While she had needed opiate pain medicines such as morphine, hydrocodone and fentanyl in the past, we had not given her any this time, nor did she have any recent prescriptions for them.Returning to her bedside with another cool washcloth, I approached Chloe gently. I asked her to be honest with me, explaining that I truly needed to know everything that was going on so I could help her out of this misery.Tearfully, she began to whisper about her struggle with opiates, which had started shortly after her surgery. Despite trying, she had been unable to wean off the pain medications, finding herself dependent on the high they provided. She started buying oxycodone pills from a schoolmate at first, but when this got too expensive, she turned to a cheaper and riskier alternative.

Heroin. At first, she snorted or smoked it, but in the last several months had turned to injecting it. I realized this was likely what caused her endocarditis. The unclean needles introduced bacteria into the bloodstream, where they could nestle into her healing heart valve.

Her days in the hospital restricted her access to opiates, sending her plummeting into withdrawal.(Credit. Kellie Jaeger/Discover)While not fatal, opiate withdrawal feels awful. Taking opiates generally slows things down, making you sleepy, constipated and slowing your heart and breathing rates. But withdrawing from them speeds things up, making you more agitated, with a faster heart rate and overactive bowels.

For chronic opiate users, the first few hours without the drug are marked by cravings, anxiety and restlessness. Within a day, the body is wracked with tremors, insomnia, runny nose, profuse sweating, belly cramping, vomiting and diarrhea.Now we knew we didn’t just have to treat Chloe’s endocarditis, but address her opiate dependence, as well.An Ongoing EpidemicChloe was not alone. Teens in the United States are using opiates at concerning levels. Between 2001 and 2014, opiate-use disorders among youth aged 13 to 25 soared nearly sixfold.

Although their use has since started to decline, hundreds of thousands of adolescents still misused pain relievers each year between 2015 and 2019, according to a national survey from the U.S. Substance Abuse and Mental Health Services Administration.About a third of people over age 12 get their drugs from healthcare providers, at least initially. Opiates such as morphine and fentanyl can be immensely helpful for the acute, severe pain caused by surgeries like Chloe’s heart valve repair. These medications take advantage of our body’s natural pain response system.

Under stress, our body can create its own pain management hormones, commonly called endorphins, sending chemical messengers that connect with opiate receptors in organs all across the body. The opiates we take as medications bind to these same receptors, mimicking endorphins. When bound to receptors in the brain and nerves, opiates quell pain signals, calm stress responses by dampening our “fight or flight” hormones and stimulate our brain’s reward and pleasure centers. These intoxicating effects on the brain are what give chronic opiate use the particular potential to develop into full-blown addiction.

Outside the nervous system, opiates can slow down the intestines, disrupt deep sleep and blunt the body’s immune response. They can also cause the lungs to breathe slowly and irregularly, which is often the cause of death from overdose.Studies show that 5 to 7 percent of adolescents and young adults prescribed an opioid will go on to develop an opioid-use disorder. Accordingly, all who care for teens must be wary of their potential to spark dependence. They can even lead to a more dangerous road — now, more teens are transitioning from prescription opioids to heroin, which is often less expensive and easier to acquire.While adults are increasingly receiving care for opioid use disorders, for adolescents, the rate of treatment is actually declining, particularly among youth of color.

It’s often harder for teens to get successful treatment because many care facilities are uncomfortable with or inexperienced in treating them. Those that do accept teens may find it difficult to keep them in treatment. And many providers who care for adolescents are uncomfortable or unfamiliar with the use of effective medications such as naexone or buprenorphine.Thankfully, Chloe was open to treatment and had access to care from our hospital’s adolescent addiction team. She was given methadone during her hospitalization, which quickly quenched her withdrawal.

Within weeks, her endocarditis was cured, and she left the hospital with a plan for tackling for her opioid-use disorder. She started taking methadone daily to address her body’s cravings for opiates. To deal with the psychological effects of her dependence, she began attending weekly counseling and group therapy sessions. Tired of spending time in the hospital, Chloe was driven to put her surgery — and all its complications — behind her..

This article appeared in the September/October 2021 issue of Discover magazine as "Frontline Fatigue." Become a subscriber for http://mydatinghangovers.com/2012/05/facebook-friend-request/ unlimited access to our archive.In zithromax 250mg cost February 1945, U.S. Navy nurse Dorothy Still was a prisoner of war in the Japanese-occupied Philippines. Along with 11 other Navy nurses, Nurse Still provided care for civilian inmates in a prison camp where food was scarce zithromax 250mg cost and guards were brutal. Few inmates weighed more than 100 pounds, and most were dying from malnutrition. On the night of Feb.

22, Nurse Still and zithromax 250mg cost the other inmates watched as their captors set up guns around the perimeter of the camp and turned the barrels inward. Other guards dug shallow graves. The inmates had long suspected the camp commander planned to massacre them all, and it seemed the rumors were coming true. Yet Nurse Still and another Navy zithromax 250mg cost nurse reported to the infirmary for the night shift. They had little medicine or food to offer their patients.

Comfort and kindness were all they had left to give. Nurse Still zithromax 250mg cost heard gunfire the next morning at dawn and assumed the massacre had begun. She steeled herself to glance out the infirmary window and saw parachutes gliding to the ground. Liberation had come just in time!. U.S zithromax 250mg cost.

And Filipino forces swiftly evacuated the 2,400 inmates to safety. But that wasn’t the end of Nurse Still’s journey. She was haunted by the horrors she witnessed in the prison camp, and the trauma stuck with zithromax 250mg cost her for the rest of her life. Now nursing leaders and advocates are saying the problem of not addressing nurses’ mental health needs has again reached a critical point. Nurses have been on the front lines of the buy antibiotics crisis, but most aren’t receiving comprehensive mental health screening or treatment.

Nursing advocacy groups and scholars who study PTSD in nursing warn that leaving nurses’ mental health needs untreated could lead to a nursing shortage, much as it did after World War II.Taken as prisoners of war in 1942, Dorothy Still and 11 other Navy nurses provided medical care in zithromax 250mg cost the midst of brutal suffering at Los Baños Internment Camp. (Credit. Courtesy of Bureau of Medicine and Surgery) Suffering in Silence Back in the States, Nurse Still was tasked with speaking at war zithromax 250mg cost bond drives about the three years she was a prisoner of war. She found the experience troubling and requested a transfer to Panama, but her memories followed her to her new post. At times, she was depressed.

Other times, she couldn’t zithromax 250mg cost stop thinking about all she had endured. She sometimes cried without provocation and struggled to stop crying once she had started. On advice of her fiancé, she booked an appointment with a naval physician. During her appointment, Nurse Still told the physician she had been a prisoner of war for more zithromax 250mg cost than three years, and asked for a medical discharge based on the trauma she was experiencing. The doctor asked when Nurse Still was liberated.

The date was the same as the raising of the flag at Iwo Jima. The physician said those men were heroes, but Nurse Still was a woman and a nurse, and therefore, did not zithromax 250mg cost suffer. Denied treatment, Nurse Still left the appointment shaking. She vowed she would keep her pain to herself. The Navy zithromax 250mg cost nurses weren’t the only medical care providers taken prisoner during WWII.

Sixty-six U.S. Army nurses as well as hundreds of physicians, pharmacists, and medical assistants were also held captive in the South Pacific. But at zithromax 250mg cost the end of the war, as the U.S. Prepared to welcome home millions of men and women who served their country, mental health treatment was limited — and reserved for men. Nurses, it was assumed, did not suffer.

At the time, the U.S zithromax 250mg cost. Military was the largest employer of nurses, and it had established an expected code of silence regarding how nurses responded to their own trauma. In 1947, an article in the American Journal of Psychiatry claimed a military hospital was a controlled environment that insulated nurses from the brutality of war. The study’s author claimed that nurses’ mental health needs were “less complex,” and that nursing zithromax 250mg cost fulfilled women by catering to their natural instinct to care for men. €œThey were supplying a service which gratified the passive needs of men.

And which identified these women with the mother, the wife, or the zithromax 250mg cost sweetheart back home.”Many nurses, including Nurse Still, responded to the lack of mental health treatment by leaving both the military and nursing. The late 1940s saw a shortage in nurses at time when hospital admissions rose by 26 percent. The shortage persisted until the late 1960s when wages began to increase.After three years as POWs, the Navy nurses were liberated in 1945. Here, they speak with Admiral Thomas C zithromax 250mg cost. Kinkaid after their release, and are shown next to the aircraft that brought them from the South Pacific to Hawaii.

(Credit. U.S. Navy Bureau of Medicine and Surgery)A Looming Crisis The buy antibiotics zithromax has meant that for the first time since WWII, the vast majority of U.S. Nurses are embroiled in fighting a common enemy. It’s a demanding and emotional battle that advocates say adds a deeper stress to an already taxing job.Across the country, nurses have been caring for patients dying from buy antibiotics who do not have the support of family at their bedside due to visitor restrictions.

€œThe nurses are often the ones who are serving as the loved one and helping the patient navigate the end-of-life journey,” says Holly Carpenter, a senior policy advisor with the American Nurses Association. In addition to caring for dying buy antibiotics patients, Carpenter says, many nurses were not properly equipped at the height of the zithromax with the personal protection equipment needed to avoid . These nurses lived in fear of being infected or transmitting the zithromax to loved ones at home. And on top of these stressors, nurses are also still coping with the usual demands of the job. €œThere are the things that have always been there — long shifts, sometimes mandatory overtime, a workload that’s heavier than you’re comfortable with, having to work through breaks or lunchtime, having to come in early and stay late,” Carpenter says.

Prior to the zithromax, studies estimated that as many as half of critical-care nurses experienced post-traumatic stress disorder (PTSD). Since the zithromax began, researchers have found the crisis has amplified symptoms of mental health problems. A 2020 study in General Hospital Psychiatry found that 64 percent of nurses in a New York City medical center reported experiencing acute stress. €œAcute stress included symptoms like nightmares, inability to stop thinking about buy antibiotics, and feeling numb, detached, and on guard,” says study leader Marwah Abdalla, a clinical cardiologist and assistant professor of medicine at Columbia University Medical Center. €œThis is concerning.

We know that if these symptoms persist for more than a month, it can lead to PTSD.” Some nurses experienced PTSD before buy antibiotics, but the conditions of the zithromax have amplified mental health problems. (Credit. Eldar Nurkovic/Shutterstock)A person is diagnosed with PTSD if they meet criteria outlined by the DSM-5, the psychiatric profession’s official manual. Criteria include experiencing, witnessing or learning about a traumatic event (such as death, serious injury, or sexual violence). Intrusive symptoms like dreams and flashbacks.

Avoidance of reminders of the event. Negative changes in thoughts and moods. And behavioral changes. A person can also develop PTSD if they are repeatedly exposed to details of a traumatic event. Suffering from undiagnosed or untreated PTSD is a life-altering condition with diverse ramifications, and may lead a nurse to leave health care.

€œWe’re potentially setting up an occupational health care crisis,” Abdalla says. €œThis has long-term implications for the health care industry and our ability to deliver adequate health care for our patients.” Carpenter says health care organizations must be proactive with screening nurses for symptoms related to anxiety, depression, and PTSD. Such screenings must be confidential and come with the assurance that a nurse’s license or job will not be compromised. Organizations also need to work to destigmatize mental health diagnosis and treatment. €œHistorically, nurses are always looked upon as the healers and the helpers,” Carpenter says.

€œThey feel they need to be strong for other people. What do you do when the hero needs help?. €For Nurse Still, help never came. She left the Navy and nursing, married, and had three children. She returned to nursing in the late 1950s after her husband died suddenly and she needed to support her family.Only in the 1990s did she begin speaking about her experiences in interviews with oral historians and documentary producers.

She also wrote a memoir, but kept the story light and did not disclose her extensive suffering.The profession has advanced since Nurse Still’s 1940s appeal for mental health support was rejected. €œWe do recognize the full PTSD, compassion fatigue, and burnout of nurses. It’s been chronicled now and we understand it,” Carpenter says. Now the challenge is encouraging each nurse to seek and receive help. Otherwise, advocates warn, their health and wellbeing will continue to decline, and history may repeat as stressed nurses leave a strained profession.

Emilie Le Beau Lucchesi is a journalist in the Chicago area and the author of This is Really War. The Incredible True Story of a Navy Nurse POW in the Occupied Philippines.It’s pretty obvious when a dog is sad. It might whine or whimper, knit its brow, or turn its big, imploring eyes upward at you. But it would be another thing entirely to see a big tear rolling down your canine companion’s face.Animals simply don’t cry. Or at least, they don’t shed emotional tears.

The only creatures who have evolved to do so, it turns out, are humans. We snivel at sad movies, well up at weddings and blink away hot tears of frustration during arguments. €œWe appear to be the only animal that sheds tears for emotional reasons,” says Randolph Cornelius, a professor of psychological science at Vassar College in New York and an expert on human emotion.There are many theories on the evolution and purpose of emotional tears. Experts even have a few ideas why animals — who do experience emotions — don’t weep like we do. But why we evolved to eject liquid out of our eyes as a signal of distress, rather than some other reaction, is still far from settled.The Biology of CryingFrom a biological perspective, there are three types of tears.

One is basal tears, which our eyes create automatically to lubricate and clean our eyes. These come from our accessory lacrimal glands, located under the eyelids. Then there are reflex tears, which you’re likely acquainted with if you’ve ever cut an onion or been poked in the eye. The third is emotional tears — the only variety that we can control, to some extent. These latter two types come from lacrimal glands on the upper outside of our eye sockets.“One argument is that [emotional crying] is almost like an emotional reflex as opposed to just a physical reflex,” says Marc Baker, a teaching fellow at the University of Portsmouth in England who researches adult emotional crying.Indeed, some have hypothesized that the purpose of crying is itself just another biological function.

For example, biochemist William Frey theorized in the 1980s that crying balances levels of hormones in our body to relieve stress. He also suggested that crying clears our body of toxins, though subsequent studies have largely disproven this. English naturalist Charles Darwin, the father of evolution, believed children cried to experience physical relief from negative emotions.In these theories, crying is something that restores us to equilibrium. It is the idea of crying as catharsis, or a way to calm ourselves in times of distress. After all, it’s not unusual for people to report feeling better after “a good cry” — but that relief may be coming from unexpected places.The Psychology of CryingPerhaps the most compelling explanation for tearful crying is that it is driven by our social needs.

Crying is a distinct visual signal that something is wrong. In an instant, it communicates that someone might need help. When others attend to the crier, it contributes to a collaborative social environment that is highly complex in humans.Inquiries by Cornelius support this theory of tears as a quick and effective social signal. In a number of studies, he and colleagues showed photographs of faces to participants (under the guise of another purpose) and asked them to interpret the emotion. In some of the photos, people were crying real tears.

In others, they had been digitally removed.When shown the pictures with tears, almost every participant labelled the emotion as sadness or grief. Tear-free crying faces, on the other hand, were confusing. €œWithout the tears, the emotion almost disappears,” Cornelius says. €œTheir judgments of the emotion don't tend to cluster around the ‘sad’ family of emotions — they're all over the place. And in fact, some people say there's no emotion there at all.”This indicated that crying is a strong signal to others of our immediate emotional state.

It’s hard to fake real tears. And as researchers of crying can attest, it’s hard to induce genuine emotional crying in a lab setting — one of the reasons it’s challenging to study.Solving an Evolutionary MysteryFrom an evolutionary perspective, some of our physiological reactions have a clear purpose. It makes sense that we sweat when overheated, raise our voices when angry or tense up in fear. But at a distance, our tearful tendencies are just plain weird. Someone showing an alien around Earth would have to explain that when humans (and only humans) feel distress or even overwhelming happiness, their faces get slightly wet and puffy.Animals do have lacrimal glands, which they use for reflex tears.

But in humans, something seems to have changed somewhere along the way. What started as distress calls that many animals make became connected with the production of tears, and experts still aren’t sure why. €œThere’s no answer, sorry,” Baker says. But there are a few theories.Clinical psychologist Ad Vingerhoets has suggested that crying might have been more advantageous than other kinds of noises because it suggests submissiveness and harmlessness to would-be predators, who might then reduce their aggression. But that still doesn’t explain the tears themselves or why animals wouldn’t benefit from them in the same way.For that, researchers point toward other, seemingly unrelated hallmarks of human physiology and development that could have led to tears.

For one, we walk upright — unlike bears and wolves, who, in their position closer to the ground, rely mostly on smells to signal distress. Perhaps partially because of this, we rely heavily on visual cues to communicate in social situations. €œFrom a kind of evolutionary perspective, it makes sense that lots of our signals become visual signals, because we are just quite visual animals,” Baker says. We also position ourselves forward. Our faces, then, developed to become the most complex in the animal kingdom — especially on the top half of our face.

€œOur kind of facial expressions far exceed almost every other animal, especially around the eyes,” he says. €œWe can do much more with the top half of our face.”An intricate facial musculature arose, and with it, machinery that could induce crying. Asmir Gračanin, a professor of psychology at the University of Rijeka in Croatia, and colleagues theorized that the orbicularis oculi muscle may have evolved along with our hyper-expressive faces. This eye socket muscle could have squeezed the corneal sensory nerves that trigger the production of tears by the lacrimal gland and proved advantageous to human babies as a call for immediate help.This also fits in with the uniqueness of human babies, who are much more helpless than other baby animals that come out of the womb ready to walk and perform other basic functions. Human babies need more help, cry for assistance and comfort, and then (largely) grow out of crying as adults.But adults still do cry emotional tears — in sadness, happiness, awe or frustration.

€œIt's kind of what makes us human, almost,” says Baker, “[our] ability to share emotions very silently, with a small drop of saline solution from the eye.”The introduction of the contraceptive pill in the 1960s spurred a landmark moment for women, liberating many from the home and propelling them into the world. But this excitement overshadowed the side effects and hazards associated with the pill, which we now know may include a slightly increased risk of breast cancer.“A lot of women are unaware of the cancer risk associated with hormonal birth control because the advent of the pill freed up the lives of women to enter the workforce more effectively,” says Beverly Strassmann, a human evolutionary biologist at the University of Michigan. When radically altering the body with synthetic hormones, you can’t assume there won’t be side effects, she says. But the field hasn’t made significant progress, partly because contraceptives have provided women with tangible benefits. Sixty years on, pharmaceutical companies are still “resting on their laurels” and need to better evaluate the association between hormonal birth control and cancer, she adds.

Research has also linked the pill to depression, decreased sexual desire, anxiety and an altered ability to form emotional memories. Most physicians, however, still don’t closely follow research investigating the links between hormonal birth control and its psychological side effects, says evolutionary psychologist Sarah Hill, author of How the Pill Changes Everything. Your Brain on Birth Control. €œMost medication doesn’t look at the full spectrum of side effects in the way people experience the world. It’s not even in physicians’ peripheral vision,” Hill says.

But women want the next birth control revolution. Younger women especially seek non-hormonal options, Hill says. €œA lot of women aren’t being served, and many are on the pill even though they don’t love it — their standards are low because there’s so few good options,” she says. In recent years, contraception apps have attracted a rise in users, which may suggest that many women no longer tolerate the impacts of hormonal birth control on their bodies. But these apps have faced criticism over their efficacy.

A New Kind of PillAnother possibility. A non-hormonal pill. Now, University of Connecticut physiologist and geneticist Jianjun Sun is wading through the unknowns to formulate it.“We know that, in humans, the ovulation process is triggered by a hormone surge, but how the egg is released is very precise. The menstrual cycle is very tightly controlled and there are a lot of unknowns in this area,” he says. Sun does know that when a person ovulates, an egg that’s contained within a follicle bursts out of the ovary and sets off down the fallopian tube, where it can be fertilized.

He’s hoping to formulate a drug that stops the follicle from rupturing and releasing the egg. Shutting off ovulation isn’t a new concept — hormonal contraception does this by tricking the body into thinking users aren’t pregnant. But he seeks a new way to halt egg release without the use of synthetic hormones. Crucially, Sun has devised a way to analyze different compounds without relying on human subjects (which would complicate the process). He realized that fruit flies ovulate in a similar way to people, and the fly’s ovulation process resembles that within mice.

As this research took off, the Gates Foundation had begun supporting scientists developing non-hormonal contraceptives. The organization has funded Sun to test compounds on flies. Now, Sun is screening up to 500 compounds daily to see which ones prevent follicles from rupturing and releasing eggs. €œThe Gates are very excited now. They’re trying to get us to find the target, then we can study this target using genetic tools,” he says.

Researchers could test the drug in humans eventually, Sun says. Unlike hormonal pills, users wouldn’t need to take it daily. To inhibit ovulation, you only need to take it for a week or so before the process begins.While this sounds tempting, many people don’t know when exactly they ovulate — and only 10 to 15 percent of women experience 28-day cycles. And because the drug concept is so new, researchers aren’t sure what dosing might look like. €œIt’s still hypothetical in terms of how to use contraceptives targeting ovulation, since there’s no products on the market,” Sun says.

A Dearth of ResearchDespite the many unknowns, experts seem receptive to any new research in hormonal birth control alternatives. In recent years, few studies have taken on this challenge.Hormonal contraceptives dominate at a time when, researchers argue, scientific and technological advances bring unprecedented opportunities for new drugs across medical fields. If Sun’s research is fruitful, it could attract more funding for other researchers working on these alternatives, says Bethan Swift, a PhD student at the University of Oxford who studies the epidemiology of women’s health. €œOne big barrier to developing new contraception is that existing options work,” Swift says, “So there’s little demand from the pharmaceutical industry to put money into creating new compounds.” This shortage of funds places significant pressure on Sun. The Gates Foundation hopes that at least one drug will hit the market by 2026, he says.

But the bar for birth control approval is uniquely high. Because it isn’t meant to alleviate an illness, possible side effects may not be worth the trade-off versus, for example, cancer treatments. It will probably take between five and 10 years before a new drug is available, Sun says. “Developing new contraception isn’t easy because they’re going to healthy women, unlike other drugs, where it’s more accepted that there will be side effects,” Sun says. The final drug will likely cause some side effects, but fewer than hormone-based contraceptives, he notes.

However, Hill is concerned that the end product could still affect the body’s natural hormone levels.Our bodies produce most sex hormones via ovulation, and high levels of estrogen propel monthly egg maturation. After an egg is released, the empty follicle releases progesterone — so levels would fall fairly low if you prevent ovulation, she says. €œStopping ovulation sounds perfect, but if you understand that’s how the body makes hormones, you’d realize it’s not a panacea.”This article contains affiliate links to products. Discover may receive a commission for purchases made through these links.Did you know that sleeping in a zero-gravity position may help alleviate symptoms from improve sleep disorders, relieve neck and back pain, and allow for better circulation and heart health?. An adjustable bed frame allows you to place your body in a zero-gravity position to enjoy all of these benefits and more as you sleep comfortably with optimal support throughout the night.

If you’ve been considering getting an adjustable bed, you’re not alone. Many individuals are making the switch to enhance their comfort, improve their health, and, of course, to enjoy more restful sleep. Deciding which adjustable bed frame is right for you can be challenging. The market is overflowing with options, and sorting through all these choices can be overwhelming. Fortunately, our best adjustable beds reviews below can help you focus your search, narrow down your choices, and select the right model to help you mitigate sleep disorders, to sleep more comfortably, and to wake up feeling more rested.

What is Zero Gravity?. Zero gravity refers to a specific position where the body is a state of weightlessness. NASA actually developed this term for astronauts to help them find the ideal position to keep their weight balanced and neutralized as they flew into space. Being in a http://headsnap.net/services/ zero-gravity position prevents gravity from affecting your body, which means that nothing is pulling your body down. Your body is in a zero-gravity position when.

When your body is in the zero-gravity position, it should look like a V shape. This alignment helps ensure that your weight is distributed evenly. As you can imagine, sleeping in this V-shaped position on a standard bed frame isn’t possible. However, adjustable bed frames enable you to sleep in a zero-gravity position and prevent your body’s weight from placing pressure on your hips, spine, and other joints. Sleeping in a zero-gravity position offers a myriad of benefits.

We’ll explore these benefits in the next section. Benefits of Sleeping in a Zero-Gravity Position with an Adjustable Bed Frame Adjustable beds have been used in hospitals for over a century due to their ability to properly position patients to facilitate recovery and reduce complications from surgeries and other medical procedures. If adjustable beds can protect the health of patients in a hospital, then it seems like a logical conclusion that they can also offer health benefits for individuals who use them at home. Indeed, there are many ways switching to an adjustable bed frame and sleeping in a zero-gravity position can benefit your health. These include.

While some individuals snore every night, others are more prone to it only when they are congested. Adjustable beds can also help reduce snoring caused by congestion because keeping the head elevated can allow the sinuses to drain. Reduced sleep apnea. An adjustable bed may also reduce sleep apnea symptoms. Sleep apnea, which occurs when an individual stops breathing during sleep, is also sometimes the result of an obstructed airway.

Elevating the head may open up the airway enough to prevent or lessen sleep apnea, allowing individuals get more restful sleep. Relief from neck, back, and joint pain. Sleeping in a zero-gravity position can significantly increase your comfort and reduce your pain. The reason for this benefit is that when you’re in the zero-gravity position, your weight is evenly distributed. This improved distribution of weight takes the pressure of your back, neck, and joints, which is often the main cause of pain.

Laying on a flat mattress, on the other hand, does not allow your weight to be evenly distributed. This places unnecessary pressure on the spinal column and can result in a significant pain and discomfort. Adjustable beds may provide relief from pain caused from sciatica, fibromyalgia, arthritis, scoliosis, and other conditions. Improved circulation. Sleeping in a zero-gravity position allows more blood to flow to the heart.

This increase of blood flow reaching the heart makes its muscles work harder to pump that blood throughout the body. Increased blood circulation can improve the overall health of your heart and other vital organs. Decreased swelling. Another benefit of improved circulation is decreased swelling. When the body lays flat, blood and other fluids may accumulate the in the lower body since the heart isn’t able to keep blood flowing effectively.

This can result in inflammation or swelling. However, with the increased blood flow that results from sleeping in a zero-gravity position, fluids won’t accumulate in the extremities, and swelling may be reduced. Improved digestion. Digestion can also be improved by sleeping on an adjustable bed frame. Sleeping flat can make it more difficult for the body to digest food properly.

Sleeping flat can also aggravate acid reflux, heartburn, and GERD (gastroesophageal reflux disease. Elevating the head about six inches can reduce these symptoms. This position removes pressure from the digestive track and makes it more difficult for stomach acids to go up into the throat. Better breathing. When you sleep in the zero-gravity position, the pressure placed on your lungs and airway is reduced.

As a result, your body can breathe more easily and can limit the impact asthma, allergies, and congestion can have on your sleep. Best Adjustable Bed Reviews Whether you’re looking for the best split king adjustable bed reviews or the best adjustable twin, queen, or full bed frames, we have you covered. We have selected some of the top models currently available that will help you stay comfortable while you sleep and will enable you to enjoy the benefits described above. Read on to discover which adjustable bed frame is right for you. GhostBed Adjustable Base If you’re looking for an adjustable bed frame with luxury features for a budget-friendly price, consider the GhostBed Adjustable Base.

This fully-adjustable frame allows you to customize your position for ultimate comfort. The fully adjustable head and foot sections allow for an unlimited number of options, including a zero-gravity position. This bed frame also offers 15 head and foot massage modes to deliver additional comfort and relaxation. Furthermore, it is equipped with two USB ports on each side to allow for easy charging and convenient access to electronic devices. Under-bed LED lights are also integrated into the design to provide soft lighting if you wake up in the middle of the night.

The included backlit remote makes it easy to adjust the bed to the ideal position for sleeping or relaxing. Use the foot and head up/down buttons to move the frame to the exact position you desire. The remote can also save your favorite position for sleeping and return you to it with just a press of a button. Additionally, the remote offers preset positions for zero-gravity, watching TV, and lounging. With the remote, you can even control the under-bed lighting and turn on the head or foot massage and adjust their intensity.

The GhostBed Adjustable Base features a sturdy steel frame. It also has a retainer bar and non-skid surface to ensure the mattress stays in place. This adjustable bed frame is available in twin XL, queen, and split king sizes. Split king adjustable beds offer the added benefit of allowing each partner to customize their own position. All orders include free shipping and a limited lifetime warranty.

Puffy Adjustable Base Premium The Adjustable Base Premium from Puffy Sleep is another top contender when you’re looking for the best adjustable bed frame. The head on this model adjusts up to 60 degrees and the legs adjust up to 45 degrees to help each individual find their most comfortable sleeping position. The adjustable bed frame from Puffy Sleep is available in twin, twin XL, full, queen, king, and split-king sizes. Use the included remote to customize your position whether reading a book in bed, watching TV, or drifting off to dreamland. The remote also has a memory feature that can save your favorite position.

Some of the other remote settings include zero gravity, watching TV, and anti-snore. Puffy Sleep has some of the best split king adjustable beds reviews. With the split king adjustable frame, you and a partner can each set the bed to the position that is most comfortable for you. This can help ensure that each of you get the restorative sleep that need. For a nominal additional fee, you can upgrade the Puffy Sleep Adjustable Base to include head and food massage features and dual USB ports for charging electronic devices.

This adjustable frame is constructed from coated metal for lasting durability. Each purchase is protected by a 10-year warranty and includes free shipping. Layla Adjustable Base Plus This motorized and fully adjustable base from Layla Sleep also has a lot to offer users. It is available in twin XL, queen, king, and split king sizes. A wireless remote is included with the frame for easy operation.

The remote includes preset buttons for moving the frame to zero-gravity, anti-snore, or flat positions. You can also set the remote to remember up to three of your preferred positions. A mobile app is available for controlling the bed frame with a smartphone or tablet, and the frame is even compatible with Amazon’s Alexa and the Google Assistant for voice command operations. Layla Sleep incorporated some upgraded features into the design of this frame. The frame features dual-zone vibrating massage motors at the head and foot of the frame.

There are three massage intensities to choose from, as well as an auto-shutoff timer to stop the vibrations at a set time. Each side of the frame features two ports to keep your devices charged and within easy reach. Some of the other notable features of this adjustable bed frame include the under-bed lighting and wall-hugging technology that keeps the head of the bed at the same distance from the wall regardless of the incline angle. Layla Sleep backs this bed frame with a 10-year warranty. They also offer free-shipping and a 30-night money-back guarantee.

Sweet Night Tranquil Adjustable Bed Frame Last, but certainly not least, we also think you’ll love the Tranquil Adjustable Bed Frame from Sweet Night. Available in twin XL, full, queen, and split California king sizes, this bed frame delivers the ability to tailor your position for enhanced comfort. Adjust the head incline between 0 and 60 degrees and the foot incline between 0 and 40 degrees for a nearly endless number of positioning options. The Tranquil Adjustable Bed Frame from Sweet Night can be controlled using the included wireless remote or with an app on your smartphone or tablet. Use the remote or app to adjust the head and foot inclines or to select one of the preset positions including anti-snore, zero gravity, watching TV, or lying down flat.

In addition to allowing you to adjust your position, this bed frame includes some other helpful and impressive features. Each side of the frame offers dual USB ports for charging your phone, tablet, or other devices. There is also a pocket on each side to hold a smartphone and keep it within easy reach. Remote-controlled LED under-bed lights, provide low lighting if needed at night or in the morning. The frame is made using a sturdy aluminum alloy that can support up to 705 pounds.

All orders include free shipping and free returns. Adjustable Bed Frame Buying Guide If you’re interested in taking advantage of all the benefits associated with using an adjustable bed frame, it is imperative to note that each model is slightly different. There are a number of important considerations to keep in mind as you shop for an adjustable bed frame. Read through our buying guide below to learn more about these considerations and choose the best adjustable bed frame to match your needs. Mattress Compatibility If you’re planning to use your existing mattress, the first thing you should do is to confirm compatibility.

Most adjustable bed frames are designed to be compatible with different mattress brands, but some manufacturers recommend only using their mattresses on their proprietary frames. Keep in mind that most innerspring mattresses are too inflexible to work well with an adjustable frame. Hybrid, foam, or latex mattresses are more flexible and will work best. Size After determining if your current mattress is compatible with the bed frame or if you need to purchase a new mattress with your new bed frame, then you will need to evaluate if each model is available in your desired sire. Obviously, the bed frame must match the size of the mattress you are planning to use on it, so you won’t want to waste your time looking at a model that isn’t even available in your preferred size.

Settings and Operation Before making a purchase, look at the range of motion of each bed frame. Some adjustable bed frames offer more adjustability than others. This flexibility, or lack of it, could certainly make one model more appealing than another. The head can often be elevated between 60 and 80 degrees, while the range of motion for the lower portion of the mattress is typically between 30 and 40 degrees. If there is a specific angle you’d prefer, then confirm it is possible with each bed frame you’re considering.

Next, look at how easy it will be to adjust the bed frame. Does it include a remote control?. Are there any preset positions or memory features?. Can you download an app to control the bed frame using a smart device?. Additional Features Some manufacturers include additional features to make their adjustable bed frames more user-friendly.

These features may include heat and massage functions, under-bed lighting, USB charging ports, and built-in speakers. If any of these features are important to you, look for a manufacturer that integrates them into their design of their adjustable bed frame. Frequently Asked Questions Can you use a regular mattress on an adjustable bed frame?. Yes, most regular mattresses can be used on an adjustable bed frame. Many frames are compatible with latex, foam, and hybrid mattresses.

Unfortunately, most innerspring mattresses are too rigid to move with an adjustable frame. What is a split king adjustable bed?. Split king adjustable beds allow the right and left sides to adjust independently of one another. This means that each partner can elevate their head and feet to their exact comfort level without needing to make compromises with their partner. Are adjustable beds worth the additional cost?.

This is a personal question that will come down to your priorities and financial situation. Many people find that adjustable beds are worth the additional cost due to how much better they sleep and all the other health benefits they offer, such as reduced back and neck pain, better circulation, decreased swelling, and improved digestion. Split king adjustable beds can be particularly beneficial for partners who prefer different sleeping positions or who are facing different health issues. With a split king adjustable bed, each partner can independently adjust their own side of the bed. How can you get into a zero-gravity position with an adjustable bed?.

You need to elevate your legs and feet to a higher level than your head and your heart to achieve a zero-gravity position. This position alleviates pressure placed on your joints to relieve back pain and is also beneficial for improving the body’s circulation. How do you keep sheets on an adjustable bed?. When shopping for sheets for an adjustable bed, the first thing to do is to check the depth of the mattress and confirm that the pocket-depth of the fitted sheet is sufficient for a proper fit. Choosing a sheet that is not deep enough for your mattress will almost certainly cause the corners to slip off as the bed adjusts.

When making the bed, tuck the edges of the flat sheet under the mattress. You can also find some flat sheets that include corner straps. These corner straps grip on to the fitted sheet and will help ensure that the flat sheet stays in place. If these ideas still don’t work, sheet suspenders are another option. A sheet suspender is a large band designed to ensure a flat sheet doesn’t slip off a mattress.This article appeared in the September/October 2021 issue of Discover magazine as "Heart Ache." Become a subscriber for unlimited access to the archive.Chloe looked miserable.

She was curled up on the hospital bed, sweaty and shaking, wracked with waves of nausea, her heart racing. I gave her a cool washcloth and a basin as the nurse started her IV. I had cared for her before. Though only 16, she’d been in the hospital a dozen times already.“I think it may be another heart valve ,” I told her. She nodded, familiar with the diagnosis, and the treatment that followed.

She was at particular risk for a type of called endocarditis, where bacteria invade and infect the valves of the heart.Chloe was born with an aortic valve that had only two parts, instead of its normal three, and was unusually small and stiff. As she grew older, her valve became thicker and less pliable. Unable to open properly, her heart had to work too hard to pump out blood. When she was 14 years old, surgeons cut through her breastbone to her heart, delicately repairing the abnormal aortic valve. Though her valve was now working normally and heart pumping well, she was still dealing with the procedure’s unwelcome consequences.As before, we followed the same routine — strong antibiotics to kill the bacteria in her heart and bloodstream, fluids and medications to quell her nausea and dehydration.

She settled into her hospital room with magazines and movies, expecting a long stay.The Night ShiftTwo days later, I stopped to check on Chloe at the beginning of my night shift. Her thin frame was tangled in the sheets, shaking and agitated, unable to find a comfortable position. Her nurse told me Chloe seemed no better — and perhaps worse — than when she’d arrived. The usual medicines did not seem to relieve her nausea, and she had started having diarrhea.I wondered if something more was going on. Could it be a more aggressive or resistant bacteria causing her endocarditis, or an entirely new intestinal caused by her antibiotics?.

But blood tests showed the same common bacteria that had caused her previous heart s, and which her antibiotic should kill. Stool tests sent that day showed no dangerous bacteria. Perhaps she just needed more time to improve on her current treatment.As I sat by her bedside, I noticed a few other odd symptoms. Her pupils were as wide as saucers, her nose was running, and her skin was damp with sweat and covered with goosebumps. This constellation of findings pointed in a surprising direction that I had seen before in my adult medicine rotations as a student — opiate withdrawal.I looked in Chloe’s chart, reviewing the medications she took routinely at home and those we had given her in the hospital.

While she had needed opiate pain medicines such as morphine, hydrocodone and fentanyl in the past, we had not given her any this time, nor did she have any recent prescriptions for them.Returning to her bedside with another cool washcloth, I approached Chloe gently. I asked her to be honest with me, explaining that I truly needed to know everything that was going on so I could help her out of this misery.Tearfully, she began to whisper about her struggle with opiates, which had started shortly after her surgery. Despite trying, she had been unable to wean off the pain medications, finding herself dependent on the high they provided. She started buying oxycodone pills from a schoolmate at first, but when this got too expensive, she turned to a cheaper and riskier alternative. Heroin.

At first, she snorted or smoked it, but in the last several months had turned to injecting it. I realized this was likely what caused her endocarditis. The unclean needles introduced bacteria into the bloodstream, where they could nestle into her healing heart valve. Her days in the hospital restricted her access to opiates, sending her plummeting into withdrawal.(Credit. Kellie Jaeger/Discover)While not fatal, opiate withdrawal feels awful.

Taking opiates generally slows things down, making you sleepy, constipated and slowing your heart and breathing rates. But withdrawing from them speeds things up, making you more agitated, with a faster heart rate and overactive bowels. For chronic opiate users, the first few hours without the drug are marked by cravings, anxiety and restlessness. Within a day, the body is wracked with tremors, insomnia, runny nose, profuse sweating, belly cramping, vomiting and diarrhea.Now we knew we didn’t just have to treat Chloe’s endocarditis, but address her opiate dependence, as well.An Ongoing EpidemicChloe was not alone. Teens in the United States are using opiates at concerning levels.

Between 2001 and 2014, opiate-use disorders among youth aged 13 to 25 soared nearly sixfold. Although their use has since started to decline, hundreds of thousands of adolescents still misused pain relievers each year between 2015 and 2019, according to a national survey from the U.S. Substance Abuse and Mental Health Services Administration.About a third of people over age 12 get their drugs from healthcare providers, at least initially. Opiates such as morphine and fentanyl can be immensely helpful for the acute, severe pain caused by surgeries like Chloe’s heart valve repair. These medications take advantage of our body’s natural pain response system.

Under stress, our body can create its own pain management hormones, commonly called endorphins, sending chemical messengers that connect with opiate receptors in organs all across the body. The opiates we take as medications bind to these same receptors, mimicking endorphins. When bound to receptors in the brain and nerves, opiates quell pain signals, calm stress responses by dampening our “fight or flight” hormones and stimulate our brain’s reward and pleasure centers. These intoxicating effects on the brain are what give chronic opiate use the particular potential to develop into full-blown addiction. Outside the nervous system, opiates can slow down the intestines, disrupt deep sleep and blunt the body’s immune response.

They can also cause the lungs to breathe slowly and irregularly, which is often the cause of death from overdose.Studies show that 5 to 7 percent of adolescents and young adults prescribed an opioid will go on to develop an opioid-use disorder. Accordingly, all who care for teens must be wary of their potential to spark dependence. They can even lead to a more dangerous road — now, more teens are transitioning from prescription opioids to heroin, which is often less expensive and easier to acquire.While adults are increasingly receiving care for opioid use disorders, for adolescents, the rate of treatment is actually declining, particularly among youth of color. It’s often harder for teens to get successful treatment because many care facilities are uncomfortable with or inexperienced in treating them. Those that do accept teens may find it difficult to keep them in treatment.

And many providers who care for adolescents are uncomfortable or unfamiliar with the use of effective medications such as naexone or buprenorphine.Thankfully, Chloe was open to treatment and had access to care from our hospital’s adolescent addiction team. She was given methadone during her hospitalization, which quickly quenched her withdrawal. Within weeks, her endocarditis was cured, and she left the hospital with a plan for tackling for her opioid-use disorder. She started taking methadone daily to address her body’s cravings for opiates. To deal with the psychological effects of her dependence, she began attending weekly counseling and group therapy sessions.

Tired of spending time in the hospital, Chloe was driven to put her surgery — and all its complications — behind her..