How To Build Digital Tools That Health Plan Members Will Use

According to recent Cognizant-sponsored research, to boost digital usage and member loyalty, healthcare payers need to prioritize investments in analytics, awareness, strategy and design, say Bill Shea and Jagan Ramachandran, leaders in Cognizant’s Healthcare practice.  

From our perspective, these lagging adoption rates are a result of payers underinvesting in awareness campaigns, analytics, strategy and design. Here are the steps payers can take to address these critical components of successful digital adoption.

1. Aggressively promote awareness of digital capabilities.

Our research over the last six years has shown increasing enthusiasm among members for conducting health plan transactions digitally. Yet even when health plans build desired digital features, members don’t use them. Our current survey shows that in 2020, when telehealth use was growing by 24%, 39% of plan members used telehealth capabilities — but from third-party service providers, not their health plans. At least one reason why is that 40% of members said they didn’t know their plans offered a telehealth option.

Payers must close these awareness gaps. Many do a poor job of promoting the tools they have and/or bury them several layers deep on their websites and don’t push them out to members when/where they need them most.

While payers often tell us, members don’t interact with them frequently enough to learn about their digital capabilities, the experience in the property and casualty insurance industry negates that excuse. The average consumer has far fewer property and auto claims in a year than they do healthcare claims. Yet P&C insurers enjoy much higher digital adoption rates than healthcare payers do, according to our research.

Why? P&C companies continually promote their apps and digital capabilities in their advertisements, websites, social feeds, etc. While they may use the apps infrequently, P&C customers do download them. Health insurers should similarly tout their digital capabilities in their marketing campaigns.

2. Make foundational investments in analytics.

Payers won’t get the value they expect from digital initiatives without strong analytics. Analytics and intelligence are prerequisites to anticipating member needs and prompting them to use a digital feature or other next best action in an app or on a website.

Analytics are also invaluable for learning about member needs. For example, most payers view call center deflection as a win. Analytics can help achieve that goal by learning from data about why and when members call for help so that payers can anticipate and proactively address those issues. If the data shows nine out of 10 members contacting the call center for updated deductible data after an emergency department visit, that function can be built into an app or website and advertised.

3. Adopt business-led strategy and design for each digital initiative.

Consumers today expect great digital experiences that payer tools don’t seem to deliver. However, health plan members reported unsatisfying experiences with payer tools, even when these tools offer self-service and other functions, they want most, such as provider search and cost estimation.

To avoid delivering disappointing member experiences, payers need to ensure the business, not IT, is leading these initiatives. In turn, the business must lead with in-depth strategy and design activities to ensure the digital capability meets actual member needs while creating business value.

Whereas business-led digital development follows a rigorous methodology that includes creating personas and journey maps and using outside-in analysis for examples of how other industries deliver similar solutions, IT-led development often starts with technology selection, and then fits processes to the technology’s capabilities. The business-led approach fully scopes out member needs first. These needs then drive the technology architecture design and technology selections so that the technology serves the business vision vs. defining it.

A large health plan we worked with took this approach to create new experiences for how brokers interact with members. We developed and designed personas, user journeys and eight future-state business processes before developing technology requirements.

4. Change funding mechanisms.

It’s accepted practice today to spend heavily on implementation while strategy and design efforts receive limited funds despite being prerequisites to successful outcomes. One organization we worked with was trying to build an industry-leading artificial intelligence model but lacked adequate budget to estimate ROI. Organizations must reallocate more budget to strategy and design efforts.

Advances in platform solutions that minimize customization needs support this funding shift. Organizations also must redefine how they identify OpEx and CapEx spend because many strategy and design efforts (e.g., journey maps, process models, business architecture, etc.) are critical to building required future capabilities and may be capitalized.

Our study revealed a number of immediate investment priorities for payers, including tools for estimating procedure costs, looking up benefits, searching for providers, finding plan options, reviews and features, checking on claims status, and calculating out-of-pocket expenses. But to realize high adoption and commensurate returns, payers must build these capabilities on a foundation of analytics and business-led strategy and design, followed by strong awareness campaigns.

By taking this approach, payers will set the stage for future member interactions that are more relational vs. transactional, such as health coaching, which will build loyalty and market share.

For more, read our report “Health Consumers Want Digital; It’s Time for Health Plans to Deliver,” produced in partnership with HFS Research.

Jagan Ramachandran is an Assistant Vice President and Partner in Cognizant’s Healthcare advisory practice. He leads Cognizant’s stakeholder experience management service line with over 20 years of experience at the intersection of healthcare business and technology. Jagan has executed a wide range of management consulting projects in the health plans space in the areas of digital strategy, member experience, broker experience, provider experience, establishing new lines of business, platform selection, M&A, and automation advisory. Jagan is a speaker on emerging trends in healthcare in several industry forums. He can be reached at Jagan.Ramachandran@cognizant.com

William “Bill” Shea is a Vice-President within Cognizant Consulting’s Healthcare Practice. He has over 20 years of experience in management consulting, practice development and project management in the health industry across the payer, purchaser and provider markets. Bill has significant experience in health plan strategy and operations in the areas of digital transformation, integrated health management and product development. Bill can be reached at William.Shea@cognizant.com

Source: How To Build Digital Tools That Health Plan Members Will Use

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A Little RedBull May Give You Wings, But It Probably Will Not Affect Your Tpe

“Energy drinks” (EDs) often contain high levels of caffeine and sugar, with variable levels of taurine, guarana, other “supplements,” and on occasion, vitamins. Frequently chosen by teens and young adults, the sale of EDs has enjoyed tremendous market growth. Over 4.6 billion cans of the most successful of these beverages, Red Bull, were sold in 2011. This prosperity resulted from the strong, recent worldwide annual growth, such as 11% in the United States, 35% in France, and 86% in Turkey.

Whether consumed alone or with alcohol or other drugs, EDs may have significant physical and behavioral effects (). Marketing materials for EDs often imply that these products will improve energy level, attention span, and physical and/or mental performance . Red Bull has been shown to increase heart rate and blood pressure and can reduce cerebral blood flow; these effects can be potentiated under conditions of stress . EDs were responsible for over 20,000 emergency department visits in the United States in 2011, including a doubling in the incidence between 2007 and 2011.

In this issue of the Anatolian Journal of Cardiology, Elitok et al. reported on the electrocardiographic effects of Red Bull. They had particular interest in Red Bull’s effects on ventricular repolarization. The dispersion of ventricular repolarization (DVR), as indicated by a longer interval between the T wave’s peak and end (Tpe or Tpe/QT), correlates with arrhythmic risk in multiple populations .

The healthy volunteer medical students in this investigation consumed a single can of Red Bull under controlled conditions, and the effects on heart rate, blood pressure, and electrocardiographic measurements were observed. As expected, both blood pressure and heart rate increased following Red Bull consumption. However, no change in electrocardiographic DVR was found.

Should young club-going people take this news as vindication of their next order for a “vodka and Red Bull?” Can we write off Red Bull’s cardiovascular effects as benign? Not so fast. The absence of an acute effect of a small dose of ED on one arrhythmia risk factor measured only in ECG lead V5 among a relatively small number of healthy young adults at rest does not equate to definite harmlessness. Our understanding of Red Bull’s effects remains incomplete, especially in cases wherein larger doses are consumed, especially by sicker people and under more strenuous conditions.

Would the consumption of five cans of Red Bull affect healthy subjects’ ECGs? Might only one serving of Red Bull affect ECG of a cardiomyopathy patient or ECG of a patient taking other cardiovascular active medications? Does chronic Red Bull consumption have the same or different effects as a Red Bull binge?

Elitok et al. should be congratulated for their interest in exposing potentially dangerous effects of popular EDs. More studies are required for us to declare Red Bull consumption to be harmless. For now, we can take heart in the absence of one signal of potential danger. At least this little bull is not in the proverbial china shop.

Energy drinks have the effects caffeine and sugar provide, but there is little or no evidence that the wide variety of other ingredients have any effect. Most of the effects of energy drinks on cognitive performance, such as increased attention and reaction speed, are primarily due to the presence of caffeine. Advertising for energy drinks usually features increased muscle strength and endurance, but there is little evidence to support this in the scientific literature.

A caffeine intake of 400 mg per day (for an adult) is considered as safe from the European Food Safety Authority (EFSA). Adverse effects associated with caffeine consumption in amounts greater than 400 mg include nervousness, irritability, sleeplessness, increased urination, abnormal heart rhythms (arrhythmia), and dyspepsia. Consumption also has been known to cause pupil dilation. Caffeine dosage is not required to be on the product label for food in the United States, unlike drugs, but most (although not all) place the caffeine content of their drinks on the label anyway, and some advocates are urging the FDA to change this practice.

Excessive consumption of energy drinks can have serious health effects resulting from high caffeine and sugar intakes, particularly in children, teens, and young adults. Excessive energy drink consumption may disrupt teens’ sleep patterns and may be associated with increased risk-taking behavior. Excessive or repeated consumption of energy drinks can lead to cardiac problems, such as arrhythmias and heart attacks, and psychiatric conditions such as anxiety and phobias.

In Europe, energy drinks containing sugar and caffeine have been associated with the deaths of athletes. Reviews have noted that caffeine content was not the only factor, and that the cocktail of other ingredients in energy drinks made them more dangerous than drinks whose only stimulant was caffeine; the studies noted that more research and government regulation were needed

By: Todd M. Rosenthal and Daniel P. Morin

Source: A little Red Bull may give you wings, but it probably will not affect your Tpe

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If You’re Still Working at 65, How To Avoid Costly Medicare Mistakes

Key Points
  • You could face lifelong late-enrollment penalties if you don’t sign up for Medicare when you’re supposed to.
  • The rules for enrollment when you already have insurance through your job depend partly on whether your employer is large or small.
  • It’s important to know that once you sign up for Medicare, even if only for Part A (hospital coverage), you can no longer contribute to a health savings account.

Workers who are nearing age 65 and have health insurance through their job may want to consider how Medicare could factor into their medical coverage.

While not everyone must sign up for Medicare at that age of eligibility, many are required to enroll — or otherwise face lifelong late-enrollment penalties.

“The biggest mistake … is to assume that you don’t need Medicare and to miss enrolling in it when you should have,” said Danielle Roberts, co-founder of insurance firm Boomer Benefits.

Roughly 10 million workers are in the 65-and-older crowd, or 17.9% of that age group, according to the Bureau of Labor Statistics.

The general rule for Medicare signup is that unless you meet an exception, you get a seven-month enrollment window that starts three months before your 65th birthday month and ends three months after it. Having qualifying insurance through your employer is one of those exceptions. Here’s what to know.

The basics

Original, or basic, Medicare consists of Part A (hospital coverage) and Part B (outpatient care coverage).

Part A has no premium as long as you have at least a 10-year work history of contributing to the program through payroll (or self-employment) taxes. Part B comes with a standard monthly premium of $148.50 for 2021, although higher-income beneficiaries pay more through monthly adjustments (see chart below).

Some 43% of individuals choose to get their Parts A and B benefits delivered through an Advantage Plan (Part C), which typically includes prescription drugs (Part D) and may or may not have a premium.

The remaining beneficiaries stick with basic Medicare and may pair it with a so-called Medigap policy and a stand-alone Part D plan. Be aware that higher-income beneficiaries pay more for drug coverage, as well (see chart below).

Remember that late-enrollment penalties last a lifetime. For Part B, that surcharge is 10% for each 12-month period you could have had it but didn’t sign up. For Part D, the penalty is 1% of the base premium ($33.06 in 2021) multiplied by the number of full, uncovered months you didn’t have Part D or creditable coverage.Working at a large company

The general rule for workers at companies with at least 20 employees is that you can delay signing up for Medicare until you lose your group insurance (i.e., you retire).

Many people with large group health insurance delay Part B but sign up for Part A because it’s free. “It doesn’t hurt you to have it,” Roberts said. However, she said, if you happen to have a health savings account paired with a high-deductible health plan through your employer, be aware that you cannot make contributions once you enroll in Medicare, even if only Part A.

Also, if you stay with your current coverage and delay all or parts of Medicare, make sure the plan is considered qualifying coverage for both Parts B and D. If you’re uncertain whether you need to sign up, it’s worth checking with your human resources department or your insurance carrier.

“I find it is always good to just confirm,” said Elizabeth Gavino, founder of Lewin & Gavino and an independent broker and general agent for Medicare plans. Some 65-year-olds with younger spouses also might want to keep their group plan. Unlike your company’s option, spouses must qualify on their own for Medicare — either by reaching age 65 or having a disability if younger than that — regardless of your own eligibility.If your employer is small

If you have health insurance through a company with fewer than 20 employees, you should sign up for Medicare at 65 regardless of whether you stay on the employer plan. If you do choose to remain on it, Medicare is your primary insurance. However, it may be more cost-effective in this situation to drop the employer coverage and pick up Medigap and a Part D plan — or, alternatively, an Advantage Plan — instead of keeping the work plan as secondary insurance.

Often, workers at small companies pay more in premiums than employees at larger firms. The average premium for single coverage through employer-sponsored health insurance is $7,470, according to the Kaiser Family Foundation. However, employees contribute an average of $1,243 — or about 17% — with their company covering the remainder.

At small firms, the employee’s share might be far higher. For example, 28% are in a plan that requires them to contribute more than half of the premium for family coverage, compared with 4% of covered workers at large firms. Original Medicare consists of Part A (hospital coverage) and Part B (outpatient care coverage). Excluding limited exceptions, there is no coverage related to dental, vision or hearing, which can lead to beneficiaries forgoing care.

“It would be a significant improvement [to provide coverage] for people who often go without needed care because they can’t afford it and for people who pay a lot for the care they need,” said Tricia Neuman, executive director for the Kaiser Family Foundation’s program on Medicare policy. Some beneficiaries get limited coverage for dental, vision and hearing if they choose to get their Parts A and B benefits delivered through an Advantage Plan (Part C), which often include those extras. About 40% of beneficiaries are enrolled in Advantage Plans.

However, Lipschutz said, the extra coverage generally is not comprehensive. On the other hand, if expanded benefits — no matter how generous — were required under original Medicare, they’d become standard in an Advantage Plan.

Source: If you’re still working at 65, how to avoid costly Medicare mistakes

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SPAC deals face mounting lawsuits and regulation risks: CNBC After Hours

The Lambda Coronavirus Variant Has Arrived In Australia Here’s What We Know So Far

We’ve seen the Alpha, Kappa and Delta variants cross our borders, but it turns out another strain of the virus that causes COVID-19 has reached our shores.

The variant, named Lambda by the World Health Organization (WHO) last month, was detected in an overseas traveller who was in hotel quarantine in New South Wales in April, according to national genomics database AusTrakka.

Some reports suggest the new variant could be fast spreading and difficult to tackle with vaccines. So what sets this variant apart from others and should we be concerned?

Here’s what we know so far.

Where did it originate?

Previously known as C.37, Lambda was first detected in Peru in December 2020. Since then, it’s spread to 29 countries, seven of which are in South America.

In April and May this year, Lambda accounted for over 80 per cent of COVID-19 cases in Peru, with a high proportion of cases also in Chile, Argentina, and Ecuador.

On 14 June, Lambda was listed as a ‘variant of interest’ by the World Health Organization due to its vast spread in South America.

Variants of interest are listed as such because they have the potential to be more infectious and severe, but haven’t yet had the devastating impact of those listed as variants of concern.

On 23 June, Public Health England classified it as a ‘variant under investigation’, after six cases were detected in the UK to date, which were all linked to overseas travel.

What makes it different from other variants?

There are now 11 official SARS-CoV-2 variants listed by the WHO.

All SARS-CoV-2 variants are distinguished from one another by mutations in their spike proteins — the components of the virus that allow it to invade human cells.

For instance, the Delta variant first detected in India has two key spike protein mutations — T478K and L452R  — that allow it to infect cells more easily and evade the body’s immune response.

According to research published last week but yet to be peer reviewed,  Lambda has seven unique spike protein mutations.

A Chilean team of scientists analysed blood samples from health workers in Santiago who had received two doses of the CoronaVac vaccine developed by Sinovac Biotech in China.

They found  the Lambda variant has a mutation called L452Q, which is similar to the L452R mutation seen in the Delta and Epsilon variants.

As the L452R mutation is thought to make Delta and Epsilon more infectious and resilient against vaccination, the team concluded that Lambda’s L452Q mutation might also help it spread far and wide.

While it’s possible that Lambda is indeed more infectious than other variants, it’s too early to know for sure, said Kirsty Short, a virologist at the University of Queensland.

“It’s very preliminary,” said Dr Short, who was not involved in the study.

“It’s a good starting point, but I certainly wouldn’t infer anything from that into the clinic.”

Are vaccines still effective against the Lambda variant?

The study also found signs that Lambda’s unique spike mutations could help it slip past the body’s immune response.

The results of the study suggested that the CoronaVac vaccine produces fewer neutralising antibodies — proteins that defend cells against infections — in response to the Lambda variant.

But according to Paul Griffin, who specialises in infectious diseases and vaccines at the University of Queensland, it’s important to remember that these antibodies are just one aspect of immunity.

“We know that [neutralizing antibodies] only tell a part of the story,” said Dr Griffin, who was not involved in the study.

“If that further immunity remains intact, then even with a reduction in neutralizing antibodies, sometimes that protection can still be enough.”

It’s also worth remembering that different vaccines work in different ways to respond to the virus and its variants.

“You can’t really extrapolate from one vaccine,” Dr Short said.

CoronaVac uses inactive versions of SARS-CoV-2 to kick the immune system into gear.

On the other hand, Pfizer contains a single strand of the genetic code that builds the virus’s spike proteins, while AstraZeneca contains a double-strand.

Dr Griffin said that more traditional inactivated vaccines like CoronaVac have proven to be less effective overall than others.

“As a broad category, the inactivated ones have been a little bit underwhelming, particularly compared to others that have such high rates of efficacy,” said Dr Griffin, who was not involved in the study.

While not much is known about how effective the Pfizer and AstraZeneca vaccines are against Lambda, their response to the Delta variant can offer clues.

A recent study from the UK found that two doses of either Pfizer or AstraZeneca are over 90 per cent effective at preventing hospitalisation due to the Delta variant.

Should Australia be worried?

While there has only been one case of Lambda recorded in hotel quarantine in Australia so far, it’s worth keeping an eye on the emergence and spread of SARS-CoV-2 variants around the world, Dr Short said.

“There’s a reason why it’s a variant that we’re watching and looking into more, but it’s certainly not at a point of panic or anything like that.”

Dr Griffin added that Lambda would need to out-compete Delta to become a major concern. “That’s certainly not what we’re seeing,” he said.  But as more people get infected, the more chance the virus has to evolve into new variants, Dr Short said.

The best way to tackle this is to focus on getting more people vaccinated, not just in Australia, but globally. “What this should emphasise to everyone is that we need global effort in the vaccination campaign,” Dr Short said.

 By: ABC Health & Wellbeing Gemma Conroy

Source: The Lambda coronavirus variant has arrived in Australia. Here’s what we know so far – ABC News

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The Symptoms of The Delta Variant Appear To Differ From Traditional COVID Symptoms. Here’s What To Look Out For

We’ve been living in a COVID world for more than 18 months now. At the outset of the pandemic, government agencies and health authorities scrambled to inform people on how to identify symptoms of the virus.

But as the virus has evolved, it seems the most common symptoms have changed too.

Emerging data suggest people infected with the Delta variant — the variant behind most of Australia’s current cases and highly prevalent around the world — are experiencing symptoms different to those we commonly associated with COVID earlier in the pandemic.


Read more: What’s the Delta COVID variant found in Melbourne? Is it more infectious and does it spread more in kids? A virologist explains

Clear explanations about the pandemic from a network of research experts

We’re all different

Humans are dynamic. With our differences come different immune systems. This means the same virus can produce different signs and symptoms in different ways.

A sign is something that’s seen, such as a rash. A symptom is something that’s felt, like a sore throat.

The way a virus causes illness is dependent on two key factors:

  • viral factors include things like speed of replication, modes of transmission, and so on. Viral factors change as the virus evolves.
  • host factors are specific to the individual. Age, gender, medications, diet, exercise, health and stress can all affect host factors.

So when we talk about the signs and symptoms of a virus, we’re referring to what is most common. To ascertain this, we have to collect information from individual cases.

It’s important to note this data is not always easy to collect or analyse to ensure there’s no bias. For example, older people may have different symptoms to younger people, and collecting data from patients in a hospital may be different to patients at a GP clinic.

So what are the common signs and symptoms of the Delta variant?

Using a self-reporting system through a mobile app, data from the United Kingdom suggest the most common COVID symptoms may have changed from those we traditionally associated with the virus.

The reports don’t take into account which COVID variant participants are infected with. But given Delta is predominating in the UK at present, it’s a safe bet the symptoms we see here reflect the Delta variant.


The Conversation, CC BY-ND

While fever and cough have always been common COVID symptoms, and headache and sore throat have traditionally presented for some people, a runny nose was rarely reported in earlier data. Meanwhile, loss of smell, which was originally quite common, now ranks ninth.

There are a few reasons we could be seeing the symptoms evolving in this way. It may be because data were originally coming mainly from patients presenting to hospital who were therefore likely to be sicker. And given the higher rates of vaccination coverage in older age groups, younger people are now accounting for a greater proportion of COVID cases, and they tend to experience milder symptoms.

It could also be because of the evolution of the virus, and the different characteristics (viral factors) of the Delta variant. But why exactly symptoms could be changing remains uncertain.


Read more: Coronavirus: how long does it take to get sick? How infectious is it? Will you always have a fever? COVID-19 basics explained


While we still have more to learn about the Delta variant, this emerging data is important because it shows us that what we might think of as just a mild winter cold — a runny nose and a sore throat — could be a case of COVID-19.

This data highlight the power of public science. At the same time, we need to remember the results haven’t yet been fully analysed or stratified. That is, “host factors” such as age, gender, other illnesses, medications and so on haven’t been accounted for, as they would in a rigorous clinical trial.

And as is the case with all self-reported data, we have to acknowledge there may be some flaws in the results.

Does vaccination affect the symptoms?

Although new viral variants can compromise the effectiveness of vaccines, for Delta, the vaccines available in Australia (Pfizer and AstraZeneca) still appear to offer good protection against symptomatic COVID-19 after two doses.



Importantly, both vaccines have been shown to offer greater than 90% protection from severe disease requiring hospital treatment.

A recent “superspreader” event in New South Wales highlighted the importance of vaccination. Of 30 people who attended this birthday party, reports indicated none of the 24 people who became infected with the Delta variant had been vaccinated. The six vaccinated people at the party did not contract COVID-19.

In some cases infection may still possible after vaccination, but it’s highly likely the viral load will be lower and symptoms much milder than they would without vaccination.

We all have a role to play

Evidence indicating Delta is more infectious compared to the original SARS-CoV-2 and other variants of the virus is building.

It’s important to understand the environment is also changing. People have become more complacent with social distancing, seasons change, vaccination rates vary — all these factors affect the data.

But scientists are becoming more confident the Delta variant represents a more transmissible SARS-CoV-2 strain.


Read more: What’s the difference between mutations, variants and strains? A guide to COVID terminology


As we face another COVID battle in Australia we’re reminded the war against COVID is not over and we all have a role to play. Get tested if you have any symptoms, even if it’s “just a sniffle”. Get vaccinated as soon as you can and follow public health advice.

By: Research Leader in Virology and Infectious Disease, Griffith University

Source: The symptoms of the Delta variant appear to differ from traditional COVID symptoms. Here’s what to look out for

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Critics:

Deltacoronavirus (Delta-CoV) is one of the four genera (Alpha-, Beta-, Gamma-, and Delta-) of coronaviruses. It is in the subfamily Orthocoronavirinae of the family Coronaviridae. They are enveloped, positive-sense, single-stranded RNA viruses. Deltacoronaviruses infect mostly birds and some mammals.

genesis

While the alpha and beta genera are derived from the bat viral gene pool, the gamma and delta genera are derived from the avian and pig viral gene pools.

Recombination appears to be common among deltacoronaviruses.Recombination occurs frequently in the viral genome region that encodes the host receptor binding protein. Recombination between different viral lineages contributes to the emergence of new viruses capable of interspecies transmission and adaptation to new animal hosts.

References

  1. Lau SKP, Wong EYM, Tsang CC, Ahmed SS, Au-Yeung RKH, Yuen KY, Wernery U, Woo PCY. Discovery and Sequence Analysis of Four Deltacoronaviruses from Birds in the Middle East Reveal Interspecies Jumping with Recombination as a Potential Mechanism for Avian-to-Avian and Avian-to-Mammalian Transmission. J Virol. 2018 Jul 17;92(15):e00265-18. doi: 10.1128/JVI.00265-18. Print 2018 Aug 1. PMID: 29769348

External links

The 5 Most Commonly Reported Covid-19 Symptoms

 

The official list of Covid-19 symptoms should be expanded as the existing one could “miss many Covid-19 cases”, experts have argued. The UK should follow other countries and include a broader range of symptoms, according to a group of scientists. Classic symptoms of Covid-19, listed on the NHS website, are a high temperature, a new continuous cough and/or a loss or change to a person’s sense of smell or taste.

But the most commonly reported symptoms by people taking part in the Office for National Statistics (ONS) Covid-19 Infection Survey are cough, headache and fatigue. The latest ONS release shows 61% of people who tested positive reported symptoms. Of these, 42% had a cough, 39% reported headache and 38% reported fatigue, according to the ONS.

Muscle ache was reported by a quarter of people and 32% reported having a sore throat. Meanwhile a third reported fever and 21% reported loss of smell and 15% reported loss of taste. A separate study – the Zoe Covid Symptom study – recently reported that a headache, sore throat and runny nose are now the most commonly reported symptoms. These are most likely symptoms of the Delta variant.

Writing in the British Medical Journal (BMJ), Dr Alex Crozier and colleagues – including Professor Calum Semple who is a member of Sage – suggest that limiting testing to only people with fever, cough and a change in taste or smell could “miss or delay identification of many Covid cases”.

They suggest this could “hamper efforts to interrupt transmission” of the virus. The group argue that increasing the symptom list could improve Britain’s pandemic response by expanding the criteria for self-isolation and eligibility for symptomatic testing.

The “narrow” case definition “limits” the early detection of contagious people, which restricts the efforts of the Test and Trace programme, they say. Non-traditional symptoms “often manifest earlier”, they added. The US Centres for Disease Control lists 11 more symptoms than the UK, and the World Health Organisation includes nine more. The testing capabilities are now able to facilitate people with a broader spectrum of symptoms, they added.

They say testing people with a single non-specific symptom could overwhelm capacity in the UK, but “combinations of symptoms could be used to help identify more cases sooner without overwhelming testing capacity”. The authors continue: “The UK’s decision to adopt a narrow case definition was based on ease of communication, avoiding confusion with other infections and preserving testing capacity.

People who had mild symptoms at first can still have long-term problems, says the NHS. The signs of long Covid vary from person to person, but the NHS now lists the following common symptoms: extreme tiredness (fatigue), shortness of breath , chest pain or tightness , problems with memory and concentration (“brain fog”), difficulty sleeping (insomnia), heart palpitations, dizziness , pins and needles ,joint pain, depression and anxiety, tinnitus, earaches, feeling sick, diarrhoea, stomach aches, loss of appetite, a high temperature, cough, headaches, sore throat, changes to sense of smell or taste and rashes.

This situation is now different — testing capacity is high. “Covid-19 is associated with a wide range of symptoms. Many patients do not experience the UK’s official case-defining symptoms, initially, or ever, and other symptoms often manifest earlier. Limiting the symptomatic testing to those with these official symptoms will miss or delay identification of many Covid-19 cases, hampering efforts to interrupt transmission.

“Expanding the clinical case definition of Covid−19, the criteria for self-isolation, and eligibility for symptomatic testing could improve the UK’s pandemic response. The Department of Health and Social Care has been approached for comment by PA Media. We will update this piece if there is a response.

The reason women might be more susceptible to long Covid might lie in differences in how our immune systems work – or that’s what scientists hypothesise, anyway. Research is needed to look into this. In a 2016 review on the differences in immune responses between males and females, professor Sabra Klein, of The Johns Hopkins Bloomberg School of Public Health, and professor Katie Flanagan, of Monash University, said females’ strong immune responses result in faster clearance of pathogens and greater vaccine efficacy compared to males. But it also contributes to females’ increased susceptibility to inflammatory and autoimmune diseases.

By:

Source: The 5 Most Commonly Reported Covid-19 Symptoms | HuffPost UK Life

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Critics:

Patients with COVID-19 can present with neurological symptoms that can be broadly divided into central nervous system involvement, such as headache, dizziness, altered mental state, and disorientation, and peripheral nervous system involvement, such as anosmia and dysgeusia. Some patients experience cognitive dysfunction called “COVID fog“, or “COVID brain fog”, involving memory loss, inattention, poor concentration or disorientation. Other neurologic manifestations include seizures, strokes, encephalitis, and Guillain–Barré syndrome (which includes loss of motor functions).

Other neurological symptoms appear to be rare, but may affect half of patients who are hospitalized with severe COVID-19. Some reported symptoms include delirium, stroke, brain hemorrhage, memory loss, psychosis, peripheral nerve damage, anxiety, and post-traumatic stress disorder.

Neurological symptoms in many cases are correlated with damage to the brain’s blood supply or encephalitis, which can progress in some cases to acute disseminated encephalomyelitis. Strokes have been reported in younger people without conventional risk factors.

As of September 2020, it was unclear whether these symptoms were due to direct infection of brain cells, or of overstimulation of the immune system. A June 2020 systematic review reported a 6–16% prevalence of vertigo or dizziness, 7–15% for confusion, and 0–2% for ataxia.

References

The Cancer Custodians Hidden Truths

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Part of Dennis Plenker’s daily job is growing cancer. And a variety of different ones, too. Depending on the day and the project, different tumors may burgeon in the petri dishes stocked in the Cold Spring Harbor Laboratory where Plenker works as a research investigator. They might be aggressive breast cancers.

They might be glioblastomas, one of the deadliest brain tumors that rob patients of their ability to speak or read as they crowd out normal cells. Or they might be pancreatic cancers, the fast and vicious slayers that can overtake a healthy person within weeks or even days.

These tiny tumor chunks are transparent and bland—they look like little droplets of hair gel that accidentally plopped into a plastic dish and took hold. But their unassuming appearance is deceptive. If they were still in the human bodies they came from, they would be sucking up nutrients, rapidly growing and dodging the immune system defenses.

But in Plenker’s hands—or rather in the CSHL’s unique facility—these notorious killers don’t kill anyone. Instead, scientists let them grow to devise the most potent ways to kill them. These tumor chunks are called organoids. They are three-dimensional assemblages of malignant growths used to study cancer behavior and vulnerability to chemotherapy and the so-called “targeted drugs”—the next generation therapies.

Scientists used to study tumors at a single-cell level, but because tumors grow as cell clusters in the body, it proved to be inefficient. The three-dimensional structures make a difference. For example, chemo might destroy the tumor’s outer cell layer, but the inner ones can develop resistance, so where single cells may die, a 3D mass will bounce back. Organoids can provide a window into these little-known mechanisms of drug resistance.

They can reveal how normal tissues turn malignant and where the cellular machinery goes off-track to allow that to happen. As their name suggests, organoids are scientists’ windows into organs, whether healthy or stricken with disease. You need to know your enemy to beat it, Plenker says, and cancer organoids offer that opportunity.

Taken from patients currently undergoing cancer treatments, these tumor chunks will reveal their weaknesses so scientists can find the cancers’ Achilles’ heel and devise personalized treatments. “Organoids are essentially patients in a dish,” Plenker says. Only unlike real patients, the organoids can be subjected to all sorts of harsh experiments to zero in on the precise chemo cocktails that destroy them in the best possible way.

And they will likely provide a more realistic scenario than drug tests in mice or rats, as animal models aren’t perfect proxies for humans.

These notorious killers don’t kill anyone. Instead, scientists devise the most potent ways to kill them.

The way that cancer proliferates in the body is hard to reproduce in the lab. Stem-cell research made it possible. After scientists spent a decade understanding how various cells multiply and differentiate into other cell types based on molecular cues and nourishment, they were able to make cells grow and fuse into tissues.

To stick together like bricks in a nicely laid wall, cells need a biological scaffold that scientists call an extracellular matrix or ECM, which in the body is made from collagen and other materials. Today, the same collagen scaffolds can be mimicked with a gooey substance called Matrigel—and then seeded with specific cells, which take root and begin to multiply.

Some tissue types were easy to grow—Columbia University scientists grew viable bones as early as 2010.1 Others, like kidney cells, were trickier. They would grow into immature tissues incapable of performing their job of cleaning and filtering blood. It took scientists time to realize that these cells wanted more than scaffolding and food—they needed to “feel at home,” or be in their natural habitat. Kidney cells needed the feeling of liquid being washed over them, the Harvard University group found, when they first managed to grow functioning kidney tissue in 2018.2

Cancers have their own growth requirements. In the body, they manage to co-opt the organism’s resources, but keeping them happy in a dish means catering to their dietary preferences. Different cancers need different types of molecular chow—growth factors, hormones, oxygen and pH levels, and other nutrients. Pancreatic adenocarcinoma thrives in low-oxygen conditions with poor nutrients.3 Glioblastomas feed on fatty acids.4 These nutrients are delivered to organoids via a specific solution called growth medium, which the lab personnel regularly doles out into the dishes.

Plenker is charged with keeping this murderous menagerie alive and well. He is the one who designs the cancers’ dietary menu, a specific protocol for each type. And while his official title is facility manager and research investigator who works closely with David Tuveson, director of the CSHL’s Cancer Center, he is essentially a cancer custodian, a curator of a unique collection that aims to change the paradigm of cancer treatment.

Plenker’s research area is pancreatic cancer—one of the most notorious killers known. Often diagnosed late and resistant to treatment, it is essentially a death sentence—only 8 to 10 percent of patients remain alive five years after diagnosis. The chemo drugs used to treat it haven’t changed in 40 years, Plenker says. In the past decade, physicians tried combining multiple drugs together with relative success. Identifying winning combos can save lives, or at least prolong them—and that’s what the organoids will help clinicians do better.

In a groundbreaking clinical trial called PASS-01 (for Pancreatic Adenocarcinoma Signature Stratification for Treatment), Plenker’s team collaborates with other American and Canadian colleagues to identify the most effective chemo cocktails and to understand the individual patients’ tumor behaviors, which would lead to more personalized treatments.5

Scientists know the same cancer types behave differently in different patients. Typically, all malignancies have the so-called “driver mutation”— the cancer’s main trigger caused by a mutated gene. But tumors also often have “passenger mutations” that happen in nearby genes. These additional mutated genes can generate various proteins, which may interfere with treatment.

Or not. Scientists call these mutated gene combinations tumor mutational signatures, which can vary from one patient to the next. With some cancers, doctors already know what mutations signatures they may have, but with pancreatic cancer they don’t have good tale-telling signs, or biomarkers. “There aren’t many biomarkers to help clinicians decide which chemo may be better for which patient,” explains oncologist Grainne O’Kane, who treats pancreatic cancer patients at the Princess Margaret Hospital in Toronto, Canada.

That’s the reason O’Kane participates in the PASS-01 trial—it will give doctors a better view into the exact specifics of their patients’ malignancies. As they take their patients’ biopsies, they are sending little cancer snippets to the CSHL to be grown into organoids, which will be subjected to chemo cocktails of various combinations to design more personalized regiments for them.

The hospital treats all patients with the so-called standard of care chemotherapy, which is more of a one-size-fits-all approach. Some patients will respond to it but others won’t, so the goal is to define the second line of chemo defense in a more personalized fashion. “That’s where the biopsies we send to Tuveson’s lab might be useful,” O’Kane says. “They can help us find something to benefit patients after the first line of chemo stopped working.”

Organoids are patients in a dish. Unlike real patients, organoids can be subjected to experiments.

Scientists can try all kinds of combos on the tumorous organoids, which they can’t do in living people. “You can treat 100 organoids with 100 different compounds and see which one works, or which compound does a good job and which ones don’t work at all,” Plenker says. That would also allow scientists to define the precise amount of chemo, so doctors wouldn’t have to over-treat patients with harsh drugs that create sickening side effects. Ultimately, organoids should take a lot of guesswork out of the process.

With about 150 patients’ adenocarcinomas already collected, the team hopes to come up with some answers. O’Kane says her team already has three patients for which they were able to design the more personalized second line of defense chemo, based on what their organoids revealed. They haven’t yet tried it, because the trial has only started recently, but this would be the next step.

“Being able to piece all this information together in real time as patients are moving through their therapies can really improve the outcomes,” O’Kane says. And while they may not be able to save all of those who graciously donated their biopsy snippets to science, it will help build better treatments in the future. “Even if we won’t be able to help these specific patients we’re hoping to use this info in the future clinical trials,” O’Kane says.

Organoids can also help understand how cancer develops. This is particularly true for breast cancers, says Camilla dos Santos, associate professor and a member of the CSHL Cancer Center. She studies the inner life of human mammary glands, more commonly referred to as breasts, and is also part of the cancer custodian crew. The hormonal changes that women go through during pregnancy subsequently modify breast cancer risk, sometimes lowering it and sometimes increasing—a complex interplay of the body’s chemicals.

“We know that women who get pregnant for the first time before they turn 25 years old, have a 30 percent decrease in breast cancer incidents later in life,” dos Santos says. “When they turn 60 or 70, 30 percent of them will not develop cancer.” On the contrary, those who are pregnant past 38 have a 30 to 50 percent increase in developing aggressive breast cancer types. Clearly, some molecular switches are involved, but they are very hard to study within the body. That’s where organoids can provide a window into the surreptitious process.

Using breast organoids, scientists can model the complex life of mammary glands at various stages of a woman’s life. And while most women wouldn’t want their breasts poked and pierced when they are pregnant or breastfeeding, many donate their tissues after breast reduction surgery or prophylactic mastectomy due to high-risk mutations like the BRCA gene.

That’s where organoids shine because scientists can not only grow them, but also give them the pregnancy hormonal cues, which will make cells generate milk, stop lactating, or do it again—and study the complex cellular interactions that take place in real life.

There’s a lot to study. At birth, mammary glands are similar in both genders—just little patches of the mammary epithelium tissue. But when puberty hits, the female glands fill up with the so-called mammary tree—a system of ducts for future milk production, which fully “blooms” in pregnancy.

“When a woman becomes pregnant, the duct tree expands, growing two types of cells—luminal and myoepithelial ones,” explains Zuzana Koledova, assistant professor of Masaryk University in Czech Republic who also uses organoids in her work. When the baby is born, the luminal cells, which line the inside of the ducts, produce the proteins that comprise milk.

The myoepithelial cells reside outside the ducts and work as muscles that squeeze the ducts to push milk out. Dos Santos likens this pregnancy mammary gland growth to the changes of the seasons. The images of sprouting ducts look like blossoming trees in the spring while later they shrivel like plants do in the fall.

The body governs these processes via the molecular machinery of hormones, which stimulate breast cells growth during pregnancy, and later cause them to die out. The two pregnancy-related hormones, prolactin and oxytocin, are responsible for milk production. Prolactin induces the luminal cells to make milk while oxytocin makes the myoepithelial cells contract. Once the baby is weaned, the levels of these hormones drop, causing cells to shrink back to their non-pregnant state.

With organoids scientists can observe these cellular dynamics at work. Koledova’s team had watched breast organoids secrete milk based on biological cues. They even recorded movies of cells pumping tiny milk droplets in the dish they were growing in. Using tiny snippets of donated breast tissue, the team grew the organoids inside the Matrigel matrix in the growth media and then added the two pregnancy hormones into the mix, explains Jakub Sumbal, a mammary gland researcher in Koledova’s group.

As they began to secret proteins that compose milk, the organoids, which looked like little domes inside the dish, changed from translucent to opaque. “At first, you can see through them, but then as they produce these proteins, they kind of darken,” Sumbal says. “And you can see them pushing out these little droplets.”

Cancer patients would no longer have to undergo chemotherapy by trial and error.

Dos Santos’s team, who also did similar work, outlined molecular changes that follow such dish-based hormonal cues in their recent study.6 In response to hormonal messages, cells produce proteins, which they display on their surfaces, like status symbols. During pregnancy the burgeoning cells prepping for milk production display the “proteins flags” that make them look important, attracting nourishment. When it’s time to die, they commit a cellular suicide.

They signal to the bypassing macrophages—immune system cleanup crew—to devour them. “They essentially say ‘come eat me!’ to the macrophages,” dos Santos says. “Because I’m no longer needed.”

The ability to mimic these processes in a dish, allows scientists to study the molecular switches that trigger breast cancer development—or minimize it. Scientists know that cancerous cells can hide from the immune system and even co-opt it into protecting themselves. They do it by displaying their own “do not eat me” protein flags on the surface and avoid destruction.

“Sometimes cancer cells can recruit specific types of immune cells to protect them,” dos Santos says. “They can not only say ‘do not eat me,’ but say ‘come hang out with me’ to the macrophages, and the macrophages will send suppressive signals to the B-cells or T-cells, the body defenders.” It is as if the cancer requests protection—a crew of guardians around it to defend against other cells that would otherwise wipe it out.

Scientists can’t telescope into the body to peek at these interactions, but they now can watch these stealth battles unfolding in a dish. “Right now we are looking at the proteins that are secreted by the organoids—the proteins that go on the surface of the organoids’ cells and what they would communicate to the immune system,” dos Santos says.

“Even when there’s no immune system surrounding them, they would still be doing that.” There’s a way to mimic the immune system, too. Scientists can add B-cells, T-cells, macrophages, and other players into the growth medium and watch the full-blown cellular warfare in action. “That’s the next step in our research,” dos Santos says.

Understanding what hormonal fluxes trigger breast cancer, and how it recruits other cells for safekeeping, can give scientists ideas for pharmaceutical intervention. “We can find drugs that pharmacologically turn off the switches that trigger cancer or interrupt its signaling for protection,” dos Santos says. “That opens novel ways to treat people.”

Can organoid research lead to a new standard of care for cancer patients? That’s the ultimate goal, researchers say. That’s why Plenker works at keeping his collection of cancer glops alive and well and thriving—he calls it a living biobank. And he keeps a stash in the cryogenic freezer, too.

He is also developing protocols that would allow commercial companies to grow organoids the same way chemical industries make reagents or mice suppliers grow rodents for research. A benefit of organoid experiments is they don’t involve animals at all.

Hospitals may one day start growing organoids from their patients’ biopsies to design and test personalized chemo cocktails for them. Once science crosses over to that reality, the entire treatment paradigm will change. Cancer patients won’t have to undergo chemotherapy by trial and error.

Instead their cancer organoids will be subjected to this process—knocked out by a gamut of drug combinations to find the winning one to use in the actual treatment. Plenker notes that once enough data is gathered about the tumors’ mutational signatures, scientists may create a database of tumor “mugshots” matching them to the chemo cocktails that beat them best.

And then just sequencing a biopsy sample would immediately inform oncologists what drug combo the patient needs. “We may be about 10 years away from that,” Plenker says, but for now there’s a lot more research to do. And a lot more cancers to grow.

By: Lina Zeldovich

Lina Zeldovich grew up in a family of Russian scientists, listening to bedtime stories about volcanoes, black holes, and intrepid explorers. She has written for The New York Times, Scientific American, Reader’s Digest, and Audubon Magazine, among other publications, and won four awards for covering the science of poop. Her book, The Other Dark Matter: The Science and Business of Turning Waste into Wealth, will be released in October 2021 by Chicago University Press. You can find her at LinaZeldovich.com and @LinaZeldovich.

Source: The Cancer Custodians – Issue 102: Hidden Truths – Nautilus

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Critics:

Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body. These contrast with benign tumors, which do not spread. Possible signs and symptoms include a lump, abnormal bleeding, prolonged cough, unexplained weight loss, and a change in bowel movements. While these symptoms may indicate cancer, they can also have other causes. Over 100 types of cancers affect humans.

Tobacco use is the cause of about 22% of cancer deaths. Another 10% are due to obesity, poor diet, lack of physical activity or excessive drinking of alcohol. Other factors include certain infections, exposure to ionizing radiation, and environmental pollutants. In the developing world, 15% of cancers are due to infections such as Helicobacter pylori, hepatitis B, hepatitis C, human papillomavirus infection, Epstein–Barr virus and human immunodeficiency virus (HIV).

These factors act, at least partly, by changing the genes of a cell. Typically, many genetic changes are required before cancer develops. Approximately 5–10% of cancers are due to inherited genetic defects. Cancer can be detected by certain signs and symptoms or screening tests. It is then typically further investigated by medical imaging and confirmed by biopsy.

Most cancers are initially recognized either because of the appearance of signs or symptoms or through screening. Neither of these leads to a definitive diagnosis, which requires the examination of a tissue sample by a pathologist. People with suspected cancer are investigated with medical tests. These commonly include blood tests, X-rays, (contrast) CT scans and endoscopy.

The tissue diagnosis from the biopsy indicates the type of cell that is proliferating, its histological grade, genetic abnormalities and other features. Together, this information is useful to evaluate the prognosis and to choose the best treatment.

Further reading

The Hidden Dangers of Protein Powders

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Adding protein powder to a glass of milk or a smoothie may seem like a simple way to boost your health. After, all, protein is essential for building and maintaining muscle, bone strength, and numerous body functions. And many older adults don’t consume enough protein because of a reduced appetite.

But be careful: a scoop of chocolate or vanilla protein powder can harbor health risks. “I don’t recommend using protein powders except in a few instances, and only with supervision,” says registered dietitian Kathy McManus, director of the Department of Nutrition at Harvard-affiliated Brigham and Women’s Hospital.

What is protein powder?

Protein powders are powdered forms of protein that come from plants (soybeans, peas, rice, potatoes, or hemp), eggs, or milk (casein or whey protein). The powders may include other ingredients such as added sugars, artificial flavoring, thickeners, vitamins, and minerals. The amount of protein per scoop can vary from 10 to 30 grams. Supplements used for building muscle contain relatively more protein, and supplements used for weight loss contain relatively less.

What are the risks?

There are numerous risks to consider when using a protein powder. Among them:

  • A protein powder is a dietary supplement. The FDA leaves it up to manufacturers to evaluate the safety and labeling of products. So, there’s no way to know if a protein powder contains what manufacturers claim.
  • We don’t know the long-term effects. “There are limited data on the possible side effects of high protein intake from supplements,” McManus says.
  • It may cause digestive distress. “People with dairy allergies or trouble digesting lactose [milk sugar] can experience gastrointestinal discomfort if they use a milk-based protein powder,” McManus points out.
  • It may be high in added sugars and calories. Some protein powders have little added sugar, and others have a lot (as much as 23 grams per scoop). Some protein powders wind up turning a glass of milk into a drink with more than 1,200 calories. The risk: weight gain and an unhealthy spike in blood sugar. The American Heart Association recommends a limit of 24 grams of added sugar per day for women and 36 grams for men.

A new risk revealed

Earlier this year, a nonprofit group called the Clean Label Project released a report about toxins in protein powders. Researchers screened 134 products for 130 types of toxins and found that many protein powders contained heavy metals (lead, arsenic, cadmium, and mercury), bisphenol-A (BPA, which is used to make plastic), pesticides, or other contaminants with links to cancer and other health conditions. Some toxins were present in significant quantities. For example, one protein powder contained 25 times the allowed limit of BPA.

How could protein powder contain so many contaminants? The Clean Label Project points to manufacturing processes or the existence of toxins in soil (absorbed by plants that are made into protein powders).

Not all of the protein powders that were tested contained elevated levels of toxins. You can see the results at the Clean Label Project’s website (www.cleanlabelproject.org).

Daily protein goals

Aim for the Recommended Dietary Allowance for protein intake: 46 grams per day for women and 56 grams for men. For example:

  • an egg for breakfast (6 grams)
  • 6 ounces of plain Greek yogurt at lunch (18 grams)
  • a handful of nuts for a snack (4–7 grams)
  • a cup of milk (8 grams) and 2 ounces of cooked chicken for dinner (14 grams).

What you should do

McManus says that in certain cases, chemical-free protein powders may be helpful—but only with medical supervision. Such cases could include

  • difficulty eating or an impaired appetite (as a result of cancer treatment or frailty from older age)
  • a surgical incision or a pressure wound that is not healing well (your body needs protein to repair cells and make new ones)
  • a serious condition requiring additional calories and protein in order for you to get better (such as burns).

Otherwise, get protein from whole foods: nuts, seeds, low-fat dairy products (yogurt, milk, cheese), legumes (beans, lentils), fish, poultry, eggs, and lean meat. “You’ll find,” McManus says, “that there are many ways to get protein without turning to a powder.”

Source: The hidden dangers of protein powders – Harvard Health

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Critics:

Bodybuilding supplements are dietary supplements commonly used by those involved in bodybuilding, weightlifting, mixed martial arts, and athletics for the purpose of facilitating an increase in lean body mass. The intent is to increase muscle, increase body weight, improve athletic performance, and for some sports, to simultaneously decrease percent body fat so as to create better muscle definition.

Among the most widely used are high protein drinks, pre-workout blends, branched-chain amino acids (BCAA), glutamine, arginine, essential fatty acids, creatine, HMB, whey protein, ZMA and weight loss products. Supplements are sold either as single ingredient preparations or in the form of “stacks” – proprietary blends of various supplements marketed as offering synergistic advantages.

While many bodybuilding supplements are also consumed by the general public the frequency of use will differ when used specifically by bodybuilders. One meta-analysis concluded that – for athletes participating in resistance exercise training and consuming protein supplements for an average of 13 weeks – total protein intake up to 1.6 g/kg of body weight per day would result in an increase in strength and fat-free mass, but that higher intakes would not further contribute.

In addition to being potentially harmful, some have argued that there is little evidence to indicate any benefit to using bodybuilding protein or amino acid supplements. A 2005 overview concluded that “[i]n view of the lack of compelling evidence to the contrary, no additional dietary protein is suggested for healthy adults undertaking resistance or endurance exercise”.

In dispute of this, a 2017 meta-analysis concluded that for athletes participating in resistance exercise training and consuming protein supplements for an average of 13 weeks, total protein intake up to 1.6 g per kg body weight per day would result in an increase in strength and fat-free mass, i.e. muscle, but that higher intakes would not further contribute. The muscle mass increase was statistically significant but modest – averaging 0.3 for all trials and 1.0 to 2.0 kg, for protein intake ≥ 1.6 g/kg/day.

See also

Is Patient Financing Right for Your Health Practice?

In these times of post-pandemic financial uncertainty, additional return on investment for medical providers is more welcome than ever. Patient financing — which for the purposes of this article means partnering with an external lender to provide service and procedure payments — can produce not just steady income for a practice, but help ensure that patients won’t have to put off procedures or, worse yet, abandon them altogether.

For example, Toronto Plastic Surgeons provides this facility to its patients through Medicard Patient Financing. There are also veterinary financing services for pets available through Medicard Patient Financing. What are some reasons practitioners might have employed in deciding upon this option?

No More Delays

There are, unfortunately, economic disparities when it comes to accessing healthcare services. Too often, the high-income and privileged have more access to healthcare resources than the medium- and low-income populations. Patient financing can help in reducing this imbalance, because the simple and daunting truth is that many medical problems don’t come announced, and it’s often impossible to plan for their associated expenses. With financing, patients don’t need to wait to get their accounts in order before opting for procedures — the result is, ideally, prompt and less stressful treatment.

Related: Fintech fuelling growth in Healthcare Financial Industry

Increased Patient Satisfaction

Since clients can often better manage their expenses via patient financing, they tend to be more satisfied on the whole. In part this is because they are not stressed and burdened with sudden financial decisions associated with urgent medical procedures. Better yet, they are more likely to stay loyal to a practice if they don’t have to worry as much. Compared to other practices that don’t offer this option, they are more likely to choose the former, which can mean increased business through word of mouth.

Reduced Collection Costs

When you partner with a patient financer, you receive payments on time. It also means that your team won’t spend needless hours and energy trying to collect payments.

Steady Cash Flow and Less Bad Debt

In setting up a conventional payment plan for a patient, your team is taking the responsibility of keeping tabs on payments and collecting them on time. It’s essentially extending a loan to a patient, typically without any interest. However, expenses like bills, payroll and lease/rent go on as usual. This can lead to tied up in , which will easily and quickly impact a budget. But when you opt for association with a patient financing company, the latter bears the cost of collections, including giving you the option of getting payment upfront.

Related: Healthcare is in Turmoil, But Technology Can Save Businesses Billions

Better Marketing

Association with a financing company with its own marketing arm can help promote a business — making your clinic stand out in comparison to competitors.

Which to Choose?

When it comes to financing models, three predominate. In the first, Self-Funding, you as the healthcare provider are responsible for receivables. From creating a payment schedule to collecting funds to following up with the patient, your team carries out all the tasks. In the Recourse Lending model, you work with a patient financier/lender, which will approve a patient’s loan after the business/practice passes qualifying criteria.

If the patient doesn’t pay, the lending/financing company will recover the losses from you. Among the drawbacks here is that the practice will have to bear the losses and lender’s fees. Lastly, there is the Non-Recourse Lending model. Similar to the second, you work with a lending company. Key differences are that it is the patient who has to pass the underwriting criteria (if the lender doesn’t approve the patient, no funding is provided by them), and that losses are borne by the lender. One disadvantage of this method is that the lenders charge interest from patients; when rates are high, patients might not be interested. Also, patients with a weak credit history might be rejected during the underwriting evaluation.

By : Chris Porteous / Entrepreneur Leadership Network Contributor – High Performance Growth Marketer

Source: Is Patient Financing Right for Your Health Practice?

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Critics:

Publicly funded healthcare is a form of health care financing designed to meet the cost of all or most healthcare needs from a publicly managed fund. Usually this is under some form of democratic accountability, the right of access to which are set down in rules applying to the whole population contributing to the fund or receiving benefits from it.

The fund may be a not-for-profit trust that pays out for healthcare according to common rules established by the members or by some other democratic form. In some countries, the fund is controlled directly by the government or by an agency of the government for the benefit of the entire population. That distinguishes it from other forms of private medical insurance, the rights of access to which are subject to contractual obligations between an insured person (or their sponsor) and an insurance company, which seeks to make a profit by managing the flow of funds between funders and providers of health care services.

When taxation is the primary means of financing health care and sometimes with compulsory insurance, all eligible people receive the same level of cover regardless of their financial circumstances or risk factors.

Most developed countries have partially or fully publicly funded health systems. Most western industrial countries have a system of social insurance based on the principle of social solidarity that covers eligible people from bearing the direct burden of most health care expenditure, funded by taxation during their working life.

Among countries with significant public funding of healthcare there are many different approaches to the funding and provision of medical services. Systems may be funded from general government revenues (as in Canada, United Kingdom, Brazil and India) or through a government social security system (as in Australia, France, Belgium, Japan and Germany) with a separate budget and hypothecated taxes or contributions.

The proportion of the cost of care covered also differs: in Canada, all hospital care is paid for by the government, while in Japan, patients must pay 10 to 30% of the cost of a hospital stay. Services provided by public systems vary. For example, the Belgian government pays the bulk of the fees for dental and eye care, while the Australian government covers eye care but not dental care.

Publicly funded medicine may be administered and provided by the government, as in the Nordic countries, Portugal, Spain, and Italy; in some systems, though, medicine is publicly funded but most hospital providers are private entities, as in Canada. The organization providing public health insurance is not necessarily a public administration, and its budget may be isolated from the main state budget. Some systems do not provide universal healthcare or restrict coverage to public health facilities. Some countries, such as Germany, have multiple public insurance organizations linked by a common legal framework. Some, such as the Netherlands and Switzerland, allow private for-profit insurers to participate.

See also

Taming The World’s Leading Killer: High Blood Pressure

An article published recent in in the New England Journal of Medicine reports some astounding research findings which could save millions of lives. Why did you miss it? Because there was zero media coverage (apart from a few specialty medical blogs). Zero. That tells you something. Tells you a lot, actually. So, here are the details.

High blood pressure is the world’s leading killer — and will kill more people, including more young people, than Covid-19 (and, in usual years, more than all other infectious diseases combined). High blood pressure can be prevented, mostly by reducing dietary sodium, and is effectively treated with safe, low-cost medications.

But globally, we’re doing terribly on blood pressure control. Less than 1 in 7 people with high blood pressure, an abysmal 14%, have it controlled. This is, frankly, pathetic — and is killing millions of people a year. It’s the most important health care intervention for adults to save lives, and we get it right less than 1 in 7 times (and, in the United States, with a $4 trillion dollar health care system, we get this right less than half the time, despite it being the intervention that can save more lives than any other health care intervention in the US!)

Elegant studies by University of Oxford scientists prove that, for every 20-point increase in systolic blood pressure (the larger “top” number), the death rate from cardiovascular disease doubles. What’s more, this starts at a blood pressure of 115/75 — way below the usual level at which we treat, or toward which we aim treatment. Adapted from “Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies” in The Lancet. But showing that lower is better didn’t prove that lowering more is better. That’s where the incredibly important Systolic Blood Pressure Intervention Trial (SPRINT) study, begun in 2010, comes in.

It’s one thing to prove (as Oxford’s Dr. Sarah Lewington did) that lower blood pressure correlates with lower risk of death, but quite another to prove that lowering blood pressure more saves more lives. Lower blood pressure reduces the risk of death, but how low do we need to go? That’s what’s big news about the results from the SPRINT study that were just released. They prove that lower IS better — and that setting a blood pressure goal lower than the standard treatment goal prevented many more deaths.

The SPRINT study also showed that, despite more side effects (far less dangerous than heart attack or stroke), intensive blood pressure treatment to reach the lower blood pressure goal is safe — even for older people. More intensive treatment prevented more heart attacks, strokes and deaths.Based on the SPRINT study, many guidelines now recommend that certain high-risk patients with high blood pressure aim for a systolic blood pressure below 130 rather than the standard target of 140. (SPRINT aimed for an even lower target of 120/80.)

But the bigger implication: We need to do much better at getting people to under 140/90. For years, doctors were afraid to lower their patients’ blood pressures to levels they thought would be too low, and potentially dangerous. Now, it’s proven that “overshooting” the goal of 140/90 isn’t just something that won’t hurt the patient — it could well save their life.

The death rate among people treated with a blood pressure goal of under 120/80 was 27% lower than the death rate of people treated to the usual target of 140/90. And for every death prevented, about two heart attacks are prevented in addition to strokes, kidney failure, dementia, and more. Now, it’s also true that interventions other than medication can be important. Reducing sodium, in particular, can reduce blood pressure and other health harms from our overly salty diet. Getting regular physical activity, eating a healthier diet overall, reducing air pollution, and more can make a big difference. But these interventions are best done on a societal, community-wide basis.

That’s why, although we should empower and inform patients, we shouldn’t expect them to be able to withstand the obesogenic, salty, sedentary, polluted environment we live in. And even if we could magically improve our food and overall environment, there would still be a billion people in the world in need of medications to treat their hypertension. Why are we failing to control high blood pressure? One reason is that we’ve made treatment too complicated — far more complicated than it needs to be for optimal results. For the past four years, Resolve to Save Lives has worked with our global partners to identify characteristics of high-performing hypertension control programs throughout the world.

The WHO HEARTS technical package for improving cardiovascular health simplifies hypertension treatment: standard treatment protocols that any health worker can implement, reliable supply of quality-assured medicines, team-based health care, patient-centered services and a strong health information system. This makes it more likely that patients will achieve and maintain blood pressure control. Think about it. A study came out last week that could save millions of lives. There was not a single news article about it. Though this was “just” the final report from a study whose key results had previously been released in advance (because the findings are so important), we have been slow to implement these recommendations. It shows that we still have a lot to learn about what we need to focus on to save the most lives.

Resolve To Save Lives partners with countries which implement WHO’s HEARTS package to lower blood pressure. Sodium reduction and hypertension treatment can prevent 3 million early deaths — every year. Lowering blood pressure can save millions of lives. We know what we need to do, now let’s make it happen.

By: Dr. Tom Frieden, director of the US Centers for Disease Control and Prevention during the Obama administration, when he oversaw responses to the H1N1 influenza, Ebola and Zika epidemics, is President and CEO of Resolve to Save Lives, an initiative of Vital Strategies and Senior Fellow for Global Health at the Council on Foreign Relations. Twitter: @DrTomFrieden.

Source: Taming the world’s leading killer: high blood pressure – CNN

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Hypertension or high blood pressure is a chronic medical condition in which the blood pressure in the arteries is higher than it should be. This involves the heart working harder than normal to circulate blood through the blood vessels.

The pressure in the arteries changes depending on what the heart is doing. When the heart squeezes, pumping blood into the arteries, the pressure increases. When the heart relaxes, the pressure decreases. When blood pressure is measured, the highest pressure (when the heart is squeezing) is called the systolic blood pressure. The lowest pressure (when the heart is relaxing) is called the diastolic blood pressure.

Blood pressure is written as two numbers. For example, in the picture at the right, the person’s systolic blood pressure was 158. Their diastolic blood pressure was 99. This blood pressure is written as 158/99. It is said “158 over 99.”

Hypertension Types

There are two types of hypertension, called “primary” and “secondary.” Primary hypertension means that the hypertension is not caused by any other disease or condition and it gradually develops over time with age. Secondary hypertension means that the hypertension is caused by another disease or conditions. Secondary hypertension tend to result in higher blood pressure than primary hypertension. In most cases (90-95%), hypertension is primary. Only a small amount of hypertension (5-10%) is secondary.

There are various health conditions that leads to secondary hypertension which includes: Obstructive sleep apnea, Kidney problems, Adrenal gland tumors, Thyroid problems, Certain defects you’re born with (congenital) in blood vessels, Certain medications (birth control pills, cold remedies, decongestants, over-the-counter pain relievers and some prescription drugs), Illegal drugs (cocaine and amphetamines)

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References

  • “High blood pressure (hypertension) – Symptoms and causes”. Mayo Clinic. Retrieved 2019-10-28.
  • Arguedas, JA (Jul 8, 2009). Arguedas, Jose Agustin (ed.). “Treatment blood pressure targets for hypertension”. Cochrane Database of Systematic Reviews (3): CD004349. doi:10.1002/14651858.CD004349.pub2. PMID 19588353. Unknown parameter |coauthors= ignored (|author= suggested) (help)
  • Williams, B; Poulter, NR, Brown, MJ, Davis, M, McInnes, GT, Potter, JF, Sever, PS, McG society (March 2004). “Guidelines for management of hypertension: report of the fourth working party of the British Hypertension Society, 2004-BHS IV”. Journal of Human Hypertension 18 (3): 139–85. doi:10.1038/sj.jhh.1001683. PMID 14973512 Law M, Wald N, Morris J (2003). “Lowering blood pressure to prevent myocardial infarction and stroke: a new preventive strategy”. Health Technol Assess 7 (31): 1–94. PMID 14604498.
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