How Will the COVID Pills Change the Pandemic?

In March, 2020, researchers at Emory University published a paper about a molecule called NHC/EIDD-2801. At the time, there were no treatments available for the coronavirus. But NHC/EIDD-2801, the researchers wrote, possessed “potency against multiple coronaviruses,” and could become “an effective antiviral against SARS-CoV-2.” A few days later, Emory licensed the molecule to Ridgeback Biotherapeutics, a Miami-based biotechnology company which had previously developed a monoclonal antibody for Ebola.

Ridgeback partnered with the pharmaceutical giant Merck to accelerate its development.The Emory researchers named their drug molnupiravir, after Mjölnir—the hammer of Thor. It turns out that this was not hyperbole. Last month, Merck and Ridgeback announced that molnupiravir could reduce by half the chances that a person infected by the coronavirus would need to be hospitalized. The drug was so overwhelmingly effective that an independent committee asked the researchers to stop their Phase III trial early—it would have been unethical to continue giving participants placebos.

None of the nearly four hundred patients who received molnupiravir in the trial went on to die, and the drug had no major side effects. On November 4th, the U.K. became the first country to approve molnupiravir; many observers expect that an emergency-use authorization will come from the U.S. Food and Drug Administration in December.

Oral antivirals like molnupiravir could transform the treatment of COVID-19, and of the pandemic more generally. Currently, treatments aimed at fighting COVID—mainly monoclonal antibodies and antiviral drugs like remdesivir—are given through infusion or injection, usually in clinics or hospitals. By the time people manage to arrange a visit, they are often too sick to receive much benefit. Molnupiravir, however, is a little orange pill.

A person might wake up, feel unwell, get a rapid COVID test, and head to the pharmacy around the corner to pick up a pack. A full course, which needs to start within five days of the appearance of symptoms, consists of forty pills—four capsules taken twice a day, for five days. Merck is now testing whether molnupiravir can prevent not just hospitalization after infection but also infection after exposure.

If that’s the case, then the drug might be taken prophylactically—you could get a prescription when someone in your household tests positive, even if you haven’t.Molnupiravir is—and is likely to remain—effective against all the major coronavirus variants. In fact, at least in the lab, it works against any number of RNA viruses besides SARS-CoV-2, including Ebola, hepatitis C, R.S.V., and norovirus. Instead of targeting the coronavirus’s spike protein, as vaccine-generated antibodies do, molnupiravir attacks the virus’s basic replication machinery. The spike protein mutates over time, but the replication machinery is mostly set in stone, and compromising that would make it hard for the virus to evolve resistance.

Once it’s inside the body, molnupiravir breaks down into a molecule called NHC. As my colleague Matthew Hutson explained, in a piece about antiviral drugs published last year, NHC is similar to cytosine, one of the four “bases” from which viral RNA is constructed; when the coronavirus’s RNA begins to copy itself, it slips into cytosine’s spot, in a kind of “Freaky Friday” swap. The molecule evades the virus’s genetic proofreading mechanisms and wreaks havoc, pairing with other bases, introducing a bevy of errors, and ultimately crashing the system.

A drug that’s so good at messing with viral RNA has led some to ask whether it messes with human DNA, too. (Merck’s trial excluded pregnant and breast-feeding women, and women of childbearing age had to be on contraceptives.) This is a long-standing concern about antiviral drugs that introduce genomic errors. A recent study suggests that molnupiravir, taken at high doses and for extended periods, can, in fact, introduce mutations into DNA. But, as the biochemist Derek Lowe noted, in a blog post for Science, these findings probably don’t apply directly to the real-world use of molnupiravir in COVID patients. The study was conducted in cells, not live animals or humans.

The cells were exposed to the drug for more than a month; even at the highest doses, it caused fewer mutations than were created by a brief exposure to ultraviolet light. Meanwhile, Merck has run a battery of tests—both in the lab and in animal models—and found no evidence that molnupiravir causes problematic mutations at the dose and duration at which it will be prescribed.With winter approaching, America is entering another precarious moment in the pandemic. Coronavirus cases have spiked in many European countries—including some with higher vaccination rates than the U.S.—and some American hospitals are already starting to buckle under the weight of a new wave. Nearly fifty thousand Americans are currently hospitalized with COVID-19.

It seems like molnupiravir is arriving just when we need it.It isn’t the only antiviral COVID pill, either. A day after the U.K. authorized Merck’s drug, Pfizer announced that its antiviral, Paxlovid, was also staggeringly effective at preventing the progression of COVID-19 in high-risk patients. The drug, when taken within three days of the onset of symptoms, reduced the risk of hospitalization by nearly ninety per cent. Only three of the nearly four hundred people who took Paxlovid were hospitalized, and no one died; in the placebo group, there were twenty-seven hospitalizations and seven deaths. Paxlovid is administered along with another antiviral medication called ritonavir, which slows the rate at which the former drug is broken down by the body.

Like Merck, Pfizer is now examining whether Paxlovid can also be used to prevent infections after an exposure. Results are expected early in 2022. (It’s not yet known how much of a difference the drugs will make for vaccinated individuals suffering from breakthrough infections; Merck’s and Pfizer’s trials included only unvaccinated people with risk factors for severe disease, such as obesity, diabetes, or older age. Vaccinated individuals are already much less likely to be hospitalized or die of COVID-19.)

Living in an Age of ExtinctionPaxlovid interrupts the virus’s replication not by messing with its genetic code but by disrupting the way its proteins are constructed. When a virus gets into our cells, its RNA is translated into proteins, which do the virus’s dirty work. But the proteins are first built as long strings called polypeptides; an enzyme called protease then slices them into the fragments from which proteins are assembled.
If you can’t cut the plywood, you can’t build the table, and Paxlovid blunts the blade. Because they employ separate mechanisms to defeat the virus, Paxlovid and molnupiravir could, in theory, be taken together. Some viruses that lead to chronic infections, including H.I.V. and hepatitis C, are treated with drug cocktails to prevent them from evolving resistance against a single line of attack. This approach is less common with respiratory viruses, which don’t generally persist in the body for long periods.
But combination antiviral therapy against the coronavirus could be a subject of study in the coming months, especially among immunocompromised patients, in whom the virus often lingers, allowing it the time and opportunity to generate mutations.

Merck will be producing a lot of molnupiravir. John McGrath, the company’s senior vice-president of manufacturing, told me that Merck began bolstering its manufacturing capacity long before the Phase III trial confirmed how well the drug worked. Normally, a company assesses demand for a product, then brings plants online slowly. For molnupiravir, Merck has already set up seventeen plants in eight countries across three continents. It now has the capacity to produce ten million courses of treatment by the end of this year, and at least another twenty million next year.

It expects molnupiravir to generate five to seven billion dollars in revenue by the end of 2022.How much will all these pills soften the looming winter surge? As has been true throughout the pandemic, the answer depends on many factors beyond their effectiveness. The F.D.A. could authorize molnupiravir within weeks, and Paxlovid soon afterward. But medications only work if they make their way into the body. Timing is critical. The drugs should be taken immediately after symptoms start—ideally, within three to five days. Whether people can benefit from them depends partly on the public-health infrastructure where they live. In Europe, rapid at-home COVID tests are widely available.

Twenty months into the pandemic, this is not the case in much of the U.S., and many Americans also lack ready access to affordable testing labs that can process PCR results quickly.Consider one likely scenario. On Monday, a man feels tired but thinks little of it. On Tuesday, he wakes up with a headache and, in the afternoon, develops a fever. He schedules a COVID test for the following morning. Two days later, he receives an e-mail informing him that he has tested positive. By now, it’s Friday afternoon. He calls his doctor’s office; someone picks up and asks the on-call physician to write a prescription. The man rushes to the pharmacy to get the drug within the five-day symptom-to-pill window.

Envision how the week might have unfolded for someone who’s uninsured, elderly, isolated, homeless, or food insecure, or who doesn’t speak English. Taking full advantage of the new drugs will require vigilance, energy, and access.Antivirals could be especially valuable in places like Africa, where only six per cent of the population is fully vaccinated. As they did with the vaccines, wealthy countries, including the U.S. and the U.K., have already locked in huge contracts for the pills; still, Merck has taken steps to expand access to the developing world.

It recently granted royalty-free licenses to the Medicines Patent Pool, a U.N.-backed nonprofit, which will allow manufacturers to produce generic versions of the drug for more than a hundred low- and middle-income countries. (Pfizer has reached a similar agreement with the Patent Pool; the company also announced that it will forgo royalties for Paxlovid in low-income countries, both during and after the pandemic.) As a result, a full course of molnupiravir could cost as little as twenty dollars in developing countries, compared with around seven hundred in the U.S. “Our goal was to bring this product to high-, middle-, and low-income countries at fundamentally the same time,” Paul Schaper, Merck’s executive director of global pharmaceutical policy, told me.

More than fifty companies around the world have already contacted the Patent Pool to obtain a sublicense to produce the drug, and the Gates Foundation has pledged a hundred and twenty million dollars to support generic-drug makers. Charles Gore, the Patent Pool’s executive director, recently said that, “for large parts of the world that have not got good vaccine coverage, this is really a godsend.” Of course, the same challenges of testing and distribution will apply everywhere.

Last spring, as a doctor caring for COVID patients, I was often dismayed by how little we had to offer. We tried hydroxychloroquine, blood thinners, and various oxygen-delivery devices and ventilator maneuvers; mostly, we watched as patients got better or got worse on their own. In the evenings, as I walked the city’s deserted streets, I often asked myself what kinds of treatment I wished we had. The best thing, I thought, would be a pill that people could take at home, shortly after infection, to halt the cascade of biological processes that sends them to the hospital, the I.C.U., or worse.

We will soon have not one but two such treatments. Outside of the vaccines, the new antiviral drugs are the most important pharmacologic advance of the pandemic. As the coronavirus becomes endemic, we’ll need additional tools to treat the inevitable infections that will continue to strike both vaccinated and unvaccinated people. These drugs will do that, reducing the damage that the coronavirus can inflict and, possibly, cordoning off avenues through which it can spread. Still, insuring that they are meaningfully and equitably used will require strength in the areas in which the U.S. has struggled: early and accessible testing; communication and coördination across health-care providers; fighting misinformation and building trust in rapid scientific advances. Just as vaccines don’t help without shots in arms, antivirals can’t work without pills in people.

 

Source: https://www.newyorker.com/

More on the Coronavirus

Covid Surge Worse Than Anything We’ve Seen

German Chancellor Angela Merkel said boosting vaccination rates will not be enough to contain soaring coronavirus infections across the country, Bloomberg reported, calling for tough action as countries across Europe come down hard on the unvaccinated and prepare drastic measures to smother the outbreak.

Key Facts

Merkel reportedly told officials from her conservative party on Monday that many Germans don’t appear to understand how severe the country’s outbreak is, according to Bloomberg, calling on individual German states to implement tougher restrictions this week.

The measures would exceed new restrictions barring unvaccinated people from public transport and many areas of public life—which apply in areas where hospitalized Covid-19 patients exceed a certain threshold—and health minister Jens Spahn said he could not rule out another nationwide lockdown.

Some politicians in Germany are debating following neighboring Austria—which went back into full lockdown Monday after a more targeted, unvaccinated-only lockdown—in requiring everyone to get vaccinated against Covid-19.

From February next year, Austrians refusing the jab will face fines of up to €3,600 ($4,000), with smaller penalties for those refusing booster shots.

Czechia and Slovakia have also started to make life harder for vaccine holdouts—Slovak Prime Minister Eduard Heger reportedly called the measures a “lockdown for the unvaccinated”—barring them from using various services, entering restaurants and public events.

Crucial Quote

By spring, “pretty much everyone in Germany… will be vaccinated, cured or dead,” Spahn said at a news conference Monday. “With the very contagious delta variant, it is very, very likely … that anyone who is not vaccinated will over the next few months become infected.”

Key Background

Europe has, again, become the center of the pandemic. Cases and deaths have been rising there even as they mostly fell around the world. The World Health Organization said it is “very worried” about the situation, warning that an additional 500,000 deaths could be recorded by March if sufficient steps aren’t taken.

Many countries, particularly in Central and Eastern Europe, are facing dramatic surges and infections are at record-breaking levels. Slovakia, Slovenia, Austria, Czechia, Germany and the Netherlands are all at, or have hit, new highs and cases are rapidly rising in other countries.

Violent protests against new lockdowns and other restrictions have erupted across the bloc as governments scramble to contain rising cases. Many of these measures explicitly target the unvaccinated, who experts and officials warn are undoubtedly driving the new wave by refusing provably safe and effective vaccines.

Follow me on Twitter. Send me a secure tip.

I am a London-based reporter for Forbes covering breaking news. Previously, I have worked as a reporter for a specialist legal publication covering big data and as a freelance journalist and policy analyst covering science, tech and health. I have a master’s degree in Biological Natural Sciences and a master’s degree in the History and Philosophy of Science from the University of Cambridge. Follow me on Twitter @theroberthart or email me at rhart@forbes.com

Source: Covid Surge ‘Worse Than Anything We’ve Seen’: Germany Mulls Tough Restrictions As Europe Targets Unvaccinated With Lockdown, Compulsory Shots

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Further Reading

Czechs, Slovaks target unvaccinated people in step behind Austria (Reuters)

Not Just Austria—Here Are The Countries Making Covid-19 Vaccination Compulsory For Everyone (Forbes)

Europe’s Carrot vs. Stick Approach to COVID-19 Vaccination (Atlantic)

Austria Sends Unvaccinated Into Lockdown—Here’s How Other Nations Are Limiting People Who Don’t Get Covid-19 Shots (Forbes)

Merkel Says Covid Spike ‘Worse Than Anything We’ve Seen’ (Bloomberg)

‘We Have To Face Reality’: Austria Announces Nationwide Vaccine Mandate, Full-Scale Covid-19 Lockdown (Forbes)

Lockdown And Restrictions Resurface In Europe As Continent Battles Another Covid Surge (Forbes)

How Connected Life Sciences Devices Lead To Continuous Care

With connected medical devices, apps and data, life sciences organizations can bridge long-standing gaps in healthcare and deliver a more continuous care experience, says Brian Williams, Cognizant’s Chief Digital Officer for Life Sciences.

Global health systems have traditionally delivered services episodically, by focusing on acute, critical care rather than individual health and well-being. It should come as no surprise, then, that life sciences companies often deliver their solutions following that same model of care.

Sadly, this leads to gaps in data and service alignment, not to mention significant disconnects with the broader healthcare ecosystem. Consumer devices and wellness apps, for example, often exist within their own individual siloes — causing organizations to miss out on valuable data that could inform patient diagnosis, management and treatment.

This lack of orchestration produces sub-optimal outcomes at significant expense to providers, payers and patients alike. It is also at direct odds with patients’ increasing digital expectations when using medical devices and when taking drugs and therapies. Whether they are participating in a clinical trial, living with a chronic condition or recovering from a procedure, patients expect to be informed and cared for with seamless digital experiences on par with what they receive when shopping or banking online.

However, the emergence of integrated, connected devices, apps and data has opened new possibilities for treatments and clinical trials. This new level of connectivity helps bridge a longstanding gap in wellness: the disconnect between an individual’s everyday health behavior and their episodic healthcare. These experiences generate valuable data insights, creating new commercial opportunities and the promise of better patient outcomes.

The impact of life sciences connectivity

Drawing from our recent series on healthcare IoT, here are three stakeholder groups within the healthcare and life sciences ecosystem that stand to benefit greatly from this new level of connectivity and the more continuous, predictive and preventive care it enables.

  • Patients with chronic conditions. Chronic diseases are often accompanied by additional conditions, such as depression, that can impede effective treatment. Consequently, information about an individual’s behavioral health status has become increasingly important in treatment decisions, as has information about the individual’s relationships with the people around them.
  • Wearable IoT devices that monitor fitness and health conditions can pair with an ever-growing set of apps for health, wellness and nutrition monitoring. Over time, a baseline of physiological indicators such as an individual’s heart rate and blood pressure, as well as activity, diet and sleep patterns, will develop. When additional data from clinical encounters, including diagnostic imaging, lab tests, genomics, stress tests and physician notes, is integrated with that baseline, it increases the ability to predict how an individual may respond to any particular treatment.
  • Elderly patients. Quite often, the most effective tools for early detection of a developing condition in elderly patients are not implants or biometric monitors, but devices that monitor changes in activities of daily living (ADL).
  • For example, the onset of congestive heart failure can be detected through reduced use of the bed, as patients with trouble breathing when lying down switch to sleeping semi-upright in a recliner. Changes in toilet flushes, meanwhile, can detect a urinary tract infection or incipient dehydration. Moreover, while one in four Americans over 65 falls each year, only half tell their doctor.
  • Passive infrared motion detectors, pressure sensors in beds and chairs, sensors for CO2 concentration, sound (vibration) and video — anonymized as necessary for privacy — can all be used to first establish a baseline of normal variability, and then be applied to detect significant deviations from that baseline. This continuous and nearly invisible sensing can be surprisingly effective in assisting in care.
  • Hospital clinicians and support staff. Healthcare is increasingly a team enterprise — including not only physicians, nurses, allied health staff and technicians but also AI-enabled equipment. The point of care is also expanding, with shortened hospital stays and more care delivered in outpatient facilities and in-home settings.
  • Connected sensors enable every member of the team to access to real-time data relevant to their task. Smart hospitals with a real-time health system (RTHS) can leverage sensors to collect data widely, distill and analyze it — and then quickly distribute curated findings to users. When captured remotely, this eases the transition in care from the hospital to other settings, allowing a more continuous and participatory level of care that extends long past a patient’s physical stay in a healthcare facility.
  • An RTHS can improve operations, clinical tasks and patient experience. For example, providers that boost operational effectiveness typically rely on a wide range of IoT-enabled asset management solutions that locate mobile assets, monitor equipment operating conditions and track inventories of consumables, pharmaceuticals and medical devices. This optimizes equipment utilization, reduces waste, increases equipment uptime and ensures optimal inventories.
  • Once clinicians and support staff can view how long various steps take in their workflows, where delays occur and what patients experience as a result, they can then evolve solutions based on a combination of their intimate day-to-day knowledge and data on how that workflow interacts with or is used by other functions.

From episodic to continuous care

Too often, the life sciences industry has delivered a one-size-fits-all approach to clinical trials and patient care that may not represent real-life, individual situations — situations that require tailored engagement that wrap therapies and interventions in end-to-end, digital solutions.

This can and should change. Device connectivity and access to data are impacting every aspect of healthcare and life sciences, moving the industry away from acute, episodic care, to a system that is more participatory and predictive.

For example, a patient may be walking a mere 24 hours after a typical hip surgery and could be discharged from the hospital a day or two after the procedure. However, that episodic care experience belies a much longer recovery and rehabilitation period spanning weeks or months.While that care experience today takes place largely outside the purview of the orthopedic surgeon, better device connectivity can enable patient monitoring — and even patient services — to be extended well beyond the length of the initial hospital visit.

Rather than relying on spotty reporting from physical therapists or the patients themselves, an orthopedist can continuously and seamlessly track a patient’s progress, and then decide when and how to intervene if things aren’t going as expected. Zimmer’s mymobility application, which supports patient engagement and monitoring outside the hospital following surgery, is a good example of what this looks like in practice.

A fully orchestrated ecosystem

Sensors and instrumentation — and the hundreds of APIs that connect them — can provide accurate and timely data about many parameters of the human condition. When this is all properly orchestrated, we can better understand how diseases progress and how bodies respond to various interventions.

That’s the intent behind our alliance with Philips and its HealthSuite Digital Platform, which is built on AWS and designed to simplify and standardize device connectivity, data access, identity management, and structured and unstructured data management within a high-trust, HIPAA and GDPR-compliant environment.

We believe that life sciences companies can derive true value from this influx of new data. Not only can the resulting insights inform new services, drugs and therapies and inspire new models of continuous engagement; they can also improve adherence to treatment and patient health.

To learn more, visit the Life Sciences section of our website.

Brian is Cognizant’s Chief Digital Officer for Life Sciences and is responsible for designing digitally enabled solutions to facilitate care access and delivery. He is also the Global Life Sciences Consulting

Source: How Connected Life Sciences Devices Lead To Continuous Care

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Related Contents:

M. Birkholz; A. Mai; C. Wenger; C. Meliani; R. Scholz (2016). “Technology modules from micro- and nano-electronics for the life sciences”. WIREs Nanomed. Nanobiotech. 8 (3): 355–377. doi:10.1002/wnan.1367. PMID 26391194

“What is Biomonitoring?” (PDF). American Chemistry Council. Archived from the origin(2005-04-08). Natural Fibers, Biopolymers, and Biocomposites. CRC Press. ISBN 978-0-203-50820-6.

National Human Genome Research Institute (2010-11-08). “FAQ About Genetic and Genomic Science”

Effects of Inadequate Sleep and Poor Sleep Quality In Athletes

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Athletes are always looking for ways to improve performance and take goals to the next level. Efforts for doing just that are often limited to waking hours: nutrition, hydration, recovery protocols, supplement routine and, of course, training itself. And despite all this, research shows that, on average, athletes neglect a critical performance tool: sleep. So how does inadequate sleep affect athletic performance? Interestingly, the oversight of sleep can impact performance, both directly and indirectly, and the effects largely differ by sport. 

 
The impact of sleep quality on overall health
 

Before moving into the impact of sleep on performance, it is important to understand how sleep affects overall health and wellness. Both the amount and quality of sleep impacts our mood and energy levels, our metabolism, and immune system health. Inadequate quality sleep can be linked to a variety of serious health problems, including an increased risk of depression, obesity, type II diabetes, and cardiovascular disease. It can even increase an individual’s risk for illness and infection.

Athletes as a population do not get adequate sleep, contributing to overtraining syndrome

Adequate rest and recovery are considered key components of improving athletic performance and preventing sleep disturbances commonly reported in overtraining syndrome. Sleep provides the body with an opportunity to rest from both the physiological and cognitive stressors many athletes face throughout the day. However, despite the body of evidence on the benefits of sleep in athletes (and the potential for sleep to alleviate fatigue), sleep duration and quality are often neglected by athletes.

It is well-reported that, on average, athletes do in fact get less than seven hours of sleep per night, often of poor quality. This falls below the recommended eight hours to combat the negative effects of sleep deprivation. Despite some research limitations, the British Journal of Sports Medicine consensus statement on the topic states that sleep deprivation does affect recovery, training, and performance in elite athletes and that these athletes as a population do not get enough sleep.

Athletes are, in general, a highly motivated group—the type of people who may willingly restrict sleep to fit more activities into waking hours. But even if you’re someone who ‘gets by just fine’ on a restricted sleep schedule, such a lifestyle can have immediate detrimental effects; evidence shows that restricting sleep to six hours per night for just four consecutive nights can impair cognitive performance and mood, glucose metabolism, appetite regulation, and immune function.

Effects of sleep deprivation on different types of athletes

Before we jump into the research of the effects of sleep deprivation in athletes, a disclaimer: Despite the recognized importance of sleep in athletes’ routines, the research on sleep in athletic populations is sparse at this time. The available research on this topic has specific limitations, including the underrepresentation of female subjects, inconsistent research methods across studies, and small sample size.

Now, the science. Current research does show a number of potential performance implications of poor sleep that should be considered in both endurance and power sport athletes. Among the subjects that have been studied, individual sport athletes appear to be more susceptible sleep deficiency and had poorer sleep efficiency than their team sport counterparts.

Two main detrimental effects of sleep deprivation on performance in all sport types are cognitive impairments and mood disturbances. Blumert et al. looked at the effects of just 24 hours of sleep deprivation in collegiate weightlifters (so, for a single night’s sleep). While they saw no difference in performance tasks, training load or intensity, there was a significant difference in mood state including fatigue and confusion in the sleep deprived athletes.

There are also observed direct effects of sleep deprivation on physical performance. Oliver et al. studied endurance running performance in a 24 hour sleep deprived state and found that that subjects who were sleep deprived ran fewer miles in the same amount of time as well-rested athletes but with the same perception of effort.[8] Athletes should also be mindful of the non-direct consequences of sleep deprivation on their performance including but not limited to metabolism, hormone regulation, immune health, and limiting recovery.

Much like everything related to health, wellness, and performance, each individual will have different sleep requirements. These requirements may also vary depending on phase or training season, sex, training volume, intensity, and type of sport.

Biomarkers related to sleep and performance in athletes

Adequate sleep helps to regulate cortisol levels, and inadequate sleep can cause cortisol levels to rise above optimized levels. Cortisol is a catabolic steroid hormone that breaks down muscle, so chronically-elevated cortisol can directly combat progress to become stronger or faster in our athletic performance. 

Sleep also helps to regulate testosterone levels. This hormone is anabolic, meaning it helps build muscle (the opposite of cortisol). But, as you might have guessed, insufficient sleep can reduce testosterone levels.

Research shows that sleep deprivation can also cause chronic inflammation, as indicated by high hsCRP levels. As athletes, inflammation and muscle damage are to be expected with any sort of training—after all, we need to cause slight damage to our muscles to make them stronger. But chronic inflammation, the kind that’s caused by overtraining or insufficient rest, can leave an athlete prone to poor performance, illness, and injury. 

Actions for athletes to take to improve sleep

While the benefits of adequate sleep are well-documented in healthy individuals, the research specific to athletes and different athlete types continues to emerge. That being said, there are well-established actions you can take right now to improve your sleep. Here are some actions to optimize your sleep habits:

. If you have trouble getting the recommended amount of sleep at night, consider taking regular naps.

. Begin tracking your sleep with a wearable activity tracker. While research has displayed varying accuracy of these devices for sleep management, they can help you establish a healthy and regular bedtime routine.

. Work on implementing good sleep habits or a bedtime routine that reduces stress and promotes a good sleeping environment.

. Consider adjusting your exercise routine and incorporate more rest and active recovery in times of sleep deprivation or high life stress to help support your overall health and prevent injury or illness.

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Source: Effects of inadequate Sleep and Poor sleep Quality in Athletes.

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. “The effects of REM sleep deprivation on the level of sleepiness/alertness”. Sleep. 21 (6): 609–614. doi:10.1093/sleep/21.6.609. PMID9779520. Riemann D, Berger M, Voderholzer U (July–August 2001). “Sleep and depression – results from psychobiological studies: an overview”. Biological Psychology. 57 (1–3): 67–103. doi:10.1016/s0301-0511(01)00090-4. PMID11454435. S2CID31725861. Kushida (2005). Sleep deprivation. Informa Health Care. pp. 1–2. ISBN978-0-8247-5949-0. Rechtschaffen A, Bergmann B (1995). “Sleep deprivation in the rat by the disk-over-water method”. Behavioural Brain Research. 69 (1–2): 55–63. doi:10.1016/0166-4328(95)00020-T. PMID7546318. S2CID4042505. Morphy, Hannah; Dunn, Kate M.; Lewis, Martyn; Boardman, Helen F.; Croft, Peter R. (2007). “Epidemiology of Insomnia: a Longitudinal Study in a UK :<|”:<“. Sleep. 30 (3): 274–80. PMID17425223. Archived from the original on 22 December 2015. Retrieved 13 December 2015. Kim, K; Uchiyama, M; Okawa, M; Liu, X; Ogihara, R (1 February 2000). “An epidemiological study of insomnia among the Japanese general population”. Sleep. 23 (1): 41–7. doi:10.1093/sleep/23.1.1a. PMID10678464. “Dyssomnias” (PDF). WHO. pp. 7–11. Archived (PDF) from the original on 18 March 2009. Retrieved 25 January 2009. Buysse, Daniel J. (2008). “Chronic Insomnia”. Am. J. Psychiatry. 165 (6): 678–86. doi:10.1176/appi.ajp.2008.08010129. PMC2859710. PMID18519533. For this reason, the NIH conference [of 2005] commended the term “comorbid insomnia” as a preferable alternative to the term “secondary insomnia.” Erman, Milton K. (2007). “Insomnia: Comorbidities and Consequences”. Primary Psychiatry. 14 (6): 31–35. Archived from the original on 15 July 2011. Two general categories of insomnia exist, primary insomnia and comorbid insomnia. World Health Organization (2007). “Quantifying burden of disease from environmental noise” (PDF). p. 20. 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Impact Of Covid-19 Pandemic Extends To Tuberculosis And Neglected Tropical Diseases

Last month, the World Health Organization reported that for the first time in 15 years the number of people who have died from tuberculosis has increased. Worldwide, in 2020, more than 1.5 million deaths were attributed to tuberculosis; the first year-on-year increase since 2005. Multiple reasons have been cited, one of which is diversion of resources due to the Covid-19 pandemic.

And, tuberculosis is not the only diseasethat has been impacted, with disproportionately severe health burdens on the world’s poorest populations.

Since the spring of 2020, there has been acute disruption of activities, such as neglected tropical disease (NTD) control and elimination programs. Across the globe, for example, mass drug administration campaigns targeting NTDs have been postponed. NTDs are a heterogeneous group of infections which are common in developing regions of Africa, Asia, and the Americas.

These diseases – caused by a variety of pathogens, including viruses, bacteria, protozoa, and parasites – include, among others, onchocerciasis (river blindness), African trypanosomiasis, leishmaniasis, cholera, Chagas disease, and Dengue fever. Diseases are said to be neglected if they are (often) overlooked and therefore underfunded by drug developers, owing to a lack of commercial prospects.

And, while tuberculosis has also suffered from neglect, it belongs to the so-called “big three infectious diseases” – HIV/AIDS, tuberculosis,and malaria – which have generally received more media attention and research and development funding than the NTDs.

The WHO had developed an NTD roadmap that was meant to officially launch in June 2020. The roadmap included specific disease targets to control and eliminate NTDs by 2030. Not only did the Covid-19 pandemic postpone the launch of the work plan, many NTD activities that had been ongoing were suspended to prevent the risk of additional transmission of the coronavirus.

In fact, interruptions in NTD program work were experienced in at least 44% of low and middle income countries: Specifically, suspension of mass administration campaigns of vaccines and treatments, case detection, and vector control. In addition, there was disruption to supply chains and reduction in the manufacturing of active pharmaceutical ingredients. In brief, there was diversion of financial resources, which effectively meant a reassignment of NTD personnel to the Covid-19 response.

It’s not all been bad news, as a month ago the WHO endorsed the first malaria vaccine (a recombinant, protein-based agent) for use among children in at-risk areas. Malaria is a preventable disease that kills around 500,000 people a year; mostly African children.

It should be noted, however, that most of the clinical development of the malaria vaccine occurred prior to the Covid-19 pandemic. Furthermore, the vaccine – called Mosquirix – has modest efficacy, as it reduces the number of severe malaria cases by approximately 30%.

To save the most lives, African countries must continue to scale up teams of local health workers to identify and respond to cases, and increase access to mosquito nets and antimalarial drugs, such as the fixed dose combination Coartem (artemether/lumefantrine). Yet, it’s precisely in these areas that the pandemic has been the most disruptive.

Opportunity Cost

One of the core tenets of economics is that resource allocation decisions invariably involve trade-offs. As an illustration, there is an opportunity cost of allocating large amounts of resources towards the Covid-19 response. The dollars spent on combating the coronavirus can’t be used to address other diseases.

Unless the overall amount of healthcare resources is expanded, there will be forgone alternatives left unfunded. And, government budgetary constraints often prevent expansion of healthcare budgets from happening. Alternatively, it is difficult to draw down budgets in other sectors, such as defense, in order to fund healthcare sector expansion, whether domestically or for the purposes of international health aid projects.

Budget impact analyses lay bare the individuals or groups who lose out; in other words, those who bear the opportunity cost of spending resources in one area, say, Covid-19, rather than another.

This doesn’t mean that a substantial amount of resources shouldn’t have been spent (or continue to be expended) on developing and paying for coronavirus vaccines or Covid-19 treatments. It does, however, imply that policymakers be made aware of forgone alternative uses of resources, account for the extent to which society can afford to crowd out non-Covid-19 resources, and fill in the budgetary gaps where necessary.

At multiple levels – local, state, federal, and global – when a healthcare system or international program with a relatively fixed budget “overpays” in one area, it must extract resources from elsewhere in the budget, or enlarge the budget.

Early in the pandemic, it was clear that federal regulators in the U.S. were aware of the issue of opportunity cost. In reallocating resources to address the novel coronavirus, the Food and Drug Administration (FDA) stated that new drug and biologics programs were being impacted by “considerable increases in Covid-19 related work.” As a result, the agency said “it’s possible that we will not be able to sustain our current performance level in meeting goal dates.”

Of course, this wasn’t just an issue at the FDA. Other government regulators, as well as global agencies such as WHO, were faced with similar sets of problems.

With government deficits running at record levels, it’ll be extraordinarily difficult to expand budgets to sustain non-Covid-19 related work at the desired levels. But, moving forward, such expansion will have to occur in order to meet the needs of underserved populations worldwide.

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I’m an independent healthcare analyst with over 22 years of experience analyzing healthcare and pharmaceuticals. Specifically, I analyze the value (costs and benefits) of biologics and pharmaceuticals, patient access to prescription drugs, the regulatory framework for drug development and reimbursement, and ethics with respect to the distribution of healthcare resources. I have over 110 publications in peer-reviewed and trade journals, in addition to newspapers and periodicals. I have also presented my work at numerous trade, industry, and academic conferences. From 1999 to 2017 I was a research associate professor at the Tufts Center for the Study of Drug Development. Prior to my Tufts appointment, I was a post-doctoral fellow at the University of Pennsylvania, and I completed my PhD in economics at the University of Amsterdam. Before pursuing my PhD I was a management consultant at Accenture in The Hague, Netherlands. Currently, I work on freelance basis on a variety of research, teaching, and writing projects.

Source: Impact Of Covid-19 Pandemic Extends To Tuberculosis And Neglected Tropical Diseases

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Related Contents:

Njie GJ, Morris SB, Woodruff RY, Moro RN, Vernon AA, Borisov AS (August 2018). “Isoniazid-Rifapentine for Latent Tuberculosis Infection: A Systematic Review and Meta-analysis”. American Journal of Preventive Medicine. 55 (2): 244–252. doi:10.1016/j.amepre.2018.04.030. PMC 6097523. PMID 29910114.

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