There IS evidence that COVID shots affect your heart

This subject could get me in trouble but it's the truth. There is a very small number of people who get heart inflammation (myocarditis) after COVID immunization.  But I have test (Multifunction Cardiogram) that has shown low levels on heart inflammation in patients who shouldn't have that, but they've had the SHOT.  

As I've said time and again every medical intervention needs to be considered in context - the individual matters.  

Assessment of Myocardial 18F-FDG Uptake at PET/CT in Asymptomatic SARS-CoV-2–vaccinated and Nonvaccinated Patients

Abstract

Background

Patients who developed myocarditis after SARS-CoV-2 vaccination show abnormalities on cardiac MRI scans. However, whether myocardial changes occur in asymptomatic individuals after vaccination is not well established.

Purpose

To assess myocardial fluorine 18 (18F) fluorodeoxyglucose (FDG) uptake on PET/CT images in asymptomatic patients vaccinated against SARS-CoV-2 compared with nonvaccinated patients.

Materials and Methods

This retrospective study included patients who underwent 18F-FDG PET/CT for indications unrelated to myocarditis during the period before (November 1, 2020, to February 16, 2021) and after (February 17, 2021, to March 31, 2022) SARS-CoV-2 vaccines were available. Myocardial and axillary 18F-FDG uptake were quantitatively assessed using maximum standardized uptake value (SUVmax). The SUVmax in all patients and in patients stratified by sex (male or female), age (<40 years, 41–60 years, >60 years), and interval between vaccination and PET/CT were compared using the Mann-Whitney U test or the Kruskal-Wallis test with post ad hoc Dwass-Steel-Critchlow-Fligner multiple comparison analysis.

Results

The study included 303 nonvaccinated patients (mean age, 52.9 years ± 14.9 [SD]; 157 female, 146 male) and 700 vaccinated patients (mean age, 56.8 years ± 13.7; 344 female, 356 male). Vaccinated patients had overall higher myocardial 18F-FDG uptake compared with nonvaccinated patients (median SUVmax, 4.8 g/mL [IQR, 3.0–8.5 g/mL] vs 3.3 g/mL [IQR, 2.5–6.2 g/mL]; P < .001). Myocardial SUVmax was higher in vaccinated patients regardless of patient sex (median range, 4.7–4.9 g/mL [IQR, 2.9–8.6 g/mL]) or age (median range, 4.7–5.6 g/mL [IQR, 2.9–8.6 g/mL]) compared with corresponding nonvaccinated groups (sex: median range, 3.2–3.9 g/mL [IQR, 2.4–7.2 g/mL]; age: median range, 3.3–3.3 g/mL [IQR, 2.3–6.1 g/mL]; P < .001 to P = .015). Furthermore, increased myocardial 18F-FDG uptake was observed in patients imaged 1–30, 31–60, 61–120, or 121–180 days after their second vaccination (median SUVmax range, 4.6–5.1 g/mL [IQR, 2.9–8.6 g/mL]) (P < .001 to P = .001), and increased ipsilateral axillary uptake was observed in patients imaged 1–30, 31–60, and 61–120 days after their second vaccination (median SUVmax range, 1.5–2.0 g/mL [IQR, 1.2–3.4 g/mL]) compared with the nonvaccinated patients (P < .001 to P < .001).

Conclusion

When compared with nonvaccinated patients, asymptomatic patients who received their second vaccination 1–180 days prior to imaging showed increased myocardial 18F-FDG uptake on PET/CT scans.

Source: https://pubs.rsna.org/doi/10.1148/radiol.2...

Don't get stuck holding the bill!

Everybody should have some form of health insurance.  Unfortunately, coverage is very often not what people want it to be.  Regularly there are copays, co-insurance and just plain non-covered situations, so being surprised is not an uncommon occurrence.  

The story attached is a another one of those surprises.  A very expensive drug has often been dosed in an office, but over time, more people decided to do the injection themselves.  So Medicare decided that everyone should inject themselves.  The guy in the story has Parkinson’s making self-injection very difficult, and potentially impossible.  Now he’s stuck with the bill (unless the class action suit wins).  

The morale is that you need to know your responsibilities.  My practice is almost entirely cash – there really aren’t surprises.  Insurance is designed to make sure that really big ticket items will be covered.  Of course, many of those items come with a 20% copay….  

Maybe the best thing to do is make sure you get ahead of your health.  Don’t wait for the problem.  Be proactive!  We can help.

FROM MEDPAGE TODAY / BY CHERYL CLARK

A 'SAD' Story: Patient Stuck With $176K Bill After Medicare Policy Switch

— CMS abruptly decided patients can self-administer Stelara -- even those with Parkinson's

For 5 years, retiree George Beitzel went to a Sacramento-area clinic every 2 months so a nurse could give him an injection of the costly drug ustekinumab (Stelara), which his doctors prescribed for his Crohn's disease.

To have a licensed professional give the shots was especially important for Beitzel, now 84, because he has Parkinson's disease.

"I shake like a bug," making it impossible to safely give himself the injections, Beitzel told MedPage Today.

Even though Stelara is among the most expensive drugs on the market, costing upwards of $40,000 per dose, Medicare had always paid for his injections under Part B, which covers drugs delivered by a doctor's office or a clinic. With his co-payments covered by his supplemental plan, "I never had to pay a thing," he said.

But all of that changed on October 15, 2021, unbeknownst to Beitzel and the clinic that continued administering his injections for another 7 months. That's according to a class-action lawsuitopens in a new tab or window filed last week by the non-profit Center for Medicare Advocacy (CMA) on behalf of Beitzel and another patient, in U.S. District Court, Eastern District of California, against HHS Secretary Xavier Becerra.

What CMS quietly and abruptly did that day was alter its payment policy on Stelara, said CMA's Litigation Director Alice Bers. It decided -- based on Medicare claims data whose use for this purpose is controversial -- that since more than 50% of Stelara users inject the drug themselves, to reclassify the drug as a "SAD," or a self-administered drugopens in a new tab or window, for everyone, and would no longer cover it when administered in an outpatient setting.

Although he was unaware of it at the time, each injection he received at the clinic after October 15 will now cost Beitzel $43,543.47, or as much as $176,000. Medicare has told him as much in numerous letters denying his appeals.

"Some of the denial letters said Mr. Beitzel should have been aware that Stelara was not covered because he could have read it in his 2021 Medicare & You handbook," Bers said.

"That's ridiculous and added insult to injury," she said. Not only did the over 100-page handbook, which came out in the fall of 2020, not mention Stelara, she said. It had buried and vague wording that did not tell him Medicare would reclassify the drug a year later: "Part B doesn't cover other types of drugs in a hospital outpatient setting (sometimes called 'self-administered drugs' or drugs you'd normally take on your own)."

A CMS spokesperson said the agency does not comment on pending litigation.

Beitzel sought help from Melissa Brown, an attorney with McGeorge School of Law's Elder Law Clinic in Sacramento, which is co-counsel in the lawsuit.

Their request for injunctive relief is Beitzel's last effort in the year-long, paperwork- and stress-laden battle against Medicare's multi-layered and complicated appeals process, which has been fraught with frustrating, confusing, and contradictory rulings along the way, Bers said.

Now, to get SAD drugs covered, Medicare beneficiaries -- including those with frailty, movement, or seizure disorders -- must get them from their Part D drug plan pharmacies, most of which require high co-pays, if they cover expensive drugs like Stelara at all. Then they must inject it themselves or find a qualified person who could safely do it for them. Otherwise, the Stelara and other SAD drugs are no longer covered outpatient benefits.

Stelara, used by 22,000 beneficiaries in the year ending May 2023, is so expensive, costing the Medicare program nearly $2.7 billion during that period, it is one of the 10 drugs earmarkedopens in a new tab or window in August for negotiation under the Biden Administration's Inflation Reduction Act.

Since May 2022, Beitzel has stopped going to the clinic for injections. He pays his drug plan $1,390 in cost-sharing for every Stelara dose, and has a retired health provider friend give him the injections.

What's perhaps equally difficult to understand, Bers said, is that the agency says its rules don't require it or providers to give advance notice to beneficiaries that the drug is no longer covered under Part B, leaving patients to find out about the change only when the shocking bills come in the mail months later.

And because he didn't know, and the clinic either didn't know or didn't understand, Beitzel continued receiving four injections at the clinic after the policy change -- in October and December of 2021, and February and April of 2022.

Beitzel only learned something might be wrong when he received a Medicare Summary Notice (MSN) dated March 1 that his October and December doses were "non-covered," and that he may be billed $43,543,47 for each of them. It didn't say why.

"I almost fell over because I've been doing this for 5 years and it didn't cost anything and nobody ever said anything," Beitzel told MedPage Today in a call with the center's attorneys on the line. He said the infusion center's billing department told him it was a "paper mistake" and not to worry about it.

Months later, he received another MSN denial dated June 10. It said he owed another $89,438.28 for the third and fourth doses. The infusion center appealed but was denied, but for the first time provided a reason: "We find that the above services are deemed self-administered drugs. Therefore ... no payment can be made," the lawsuit said.

"I still feel distressed and stressful," Beitzel told MedPage Today as he mentioned the foot-high stack of paperwork on his case. "And when you have Crohn's, stress is not a good thing to have. Every time I read this stuff it upsets me."

The class action also names another plaintiff, identified as K.K., a 72-year-old psoriasis patient in Darien, Connecticut with a rare form of painful arthritis that damages bones in one's hands and feet. Since 2016, she also has received Stelara injections, every 3 months, all covered by Medicare's Part B. That is, until October 15, 2021, when the regional Connecticut Medicare Administrative Contractor (MAC) changed the policy the same way.

Like Beitzel, she wasn't told about the change and continued receiving injections from a nearby hospital outpatient department.

Now, in notices she received months later, Medicare says she owes more than $116,000 for two of the doses. She appealed, and during one appeal process, was told verbally by an administrative law judge that she wouldn't be responsible for the payments. But in the ruling, the judge's decision was reversed, saying, "I am not able to ignore Medicare policy and guidance."

The lawsuit said "Ms. K. experienced and continues to experience distress, anxiety, and outrage about the termination of Part B coverage for Stelara without notice and Medicare's decisions finding that she is financially liable for the cost of the injections she received at the hospital."

The lawsuit said she had to stop taking the drug because her Part D plan requires such a high cost for it. And she suffered pain and a serious rash that "looks like a third degree burn," and covered about "50% of her body and tormenting her with itching with no relief." Now, she is back on the drug through the manufacturer.

In addition to asking the court to certify the case as a class action, the lawsuit wants the court to issue a permanent injunction requiring Becerra to ensure notice is provided when a drug changes status to self-administered; waive patients' liability for the costs; and modify the program so people with medical conditions who can't inject themselves can get them administered by a healthcare professional.

Bers said the lawsuit was filed on behalf of potentially thousands of Medicare beneficiaries who could and are finding themselves with similarly outrageous amounts of debt because of surprise SAD drug policies, and not just those taking Stelara.

Medicare contractors moved three rheumatology drugs to the SAD list a decade ago, also without warning, but efforts by the American College of Rheumatology persuadedopens in a new tab or window them to move them back to Part B, the lawsuit said. But as of August, two of the three drugs, Simponi and Orencia, are back on the list.

The lawsuit also mentions that several regional MACs have proposed SAD change decisions on other drugs covered under Part B, such as the injectable biologic for psoriasis, tezepelumab-ekko (Tezspire). But effortsopens in a new tab or window by the American College of Allergy, Asthma & Immunology have thwartedopens in a new tab or window that.

Bers said her review of the 12 regional MAC decisions on Stelara consistently categorize it now as a SAD drug, but some appear to be inconsistent in their reasons for it.

To Beitzel, the Medicare agency's actions are not just hurtful and heartless, they're dangerous.

"I kept getting these letters from Medicare that I didn't understand, and it's just like a big bureaucracy is stepping on this little bitty hand," Beitzel told MedPage Today.

Beitzel said he would like to ask a Medicare representative if he would let Beitzel give him an injection, if he had the chance: "He'd see me, my hand shaking, and he'd say, 'No, I don't want you to get even close to me.'"

Source: https://www.medpagetoday.com/special-repor...

Treating ED reduces Alzheimer's?

The article has a clickbait title – Viagra cuts Alzheimer’s risk by 70%.  So what’s the real story?

Originally sildenafil (sold as Viagra) was researched because it increases Nitric Oxide (NO) which can be a real game changer for heart health.  As the research went on, other “things” started popping up, and the marketing machine took over from the scientists.  Now that the drug is off patent the cardiac research is showing up again.  

Since NO is huge regarding blood flow (opens vessels = vasodilates), it’s not a stretch to think that there might be first brain benefits, as well as the obvious “second brain” effects.  But this study DOESN’T PROVE ANYTHING.  It only hints at possibilities.

It’s a computer model of a biological model based off of insurance data.  Insurance data is often quite flawed, as well as a potential sampling bias in the group evaluated – maybe the folks using Viagra are less cognitively impaired than the others, so maybe the 70% is substantially overestimated.  

Could there be benefit? I think absolutely.  Is taking Viagra for this a good idea?  Probably not. Are there other things to do besides take Viagra?  Absolutely – there are numerous natural ways to improve NO levels that help all kinds of things, and it just might ward off early Alzheimer’s.  But proof?  No. 

Viagra Lowers the Risk of Alzheimer’s by Almost 70%, Study Finds

Research published recently suggests that Pfizer’s erectile dysfunction drug Viagra can decrease the risk of developing Alzheimer’s disease by up to 69 percent.

The research, which was published in Nature, found that the medication has a direct effect on brain health and significantly reduces the toxic proteins that can cause dementia.

The study’s findings are so promising that the drug may someday be used to counter dementia. A new team of experts is preparing to conduct another study that builds on this data but tests the generic version of Viagra, sildenafil, in patients suffering from early Alzheimer’s.

The team of researchers arrived at Viagra’s viability as a treatment for dementia after analyzing 1,600 approved drugs hoping to find one that could be repurposed to fight the root causes of dementia.

“Sildenafil, which has been shown to significantly improve cognition and memory in preclinical models, presented as the best drug candidate. Sildenafil may have neuroprotective effects and reduce levels of toxic tau proteins,” said Dr. Feixiong Cheng, the lead researcher on the study, which was conducted by the Cleveland Clinic.

Despite the excitement surrounding the study’s promising results, some experts are advising people to not get their hopes up quite yet, as clinical trials are still necessary.

Coffee and Viagra offer new hope in fight against Alzheimer’s

Another recent study uncovered another unlikely weapon in the fight against dementia: coffee. Research suggests that coffee consumption may significantly decrease your chances of developing the disease.

The study sheds light on the mysterious disease, for which there is no cure as of now. While coffee does not mitigate or fight Alzheimer’s like some medications do, the study found that people with no memory loss who also drank larger than average amounts of coffee were at less of a risk of developing mild cognitive impairment, which is considered a pre-stage of Alzheimer’s disease.

“With Alzheimer’s disease, there’s currently a lack of any effective disease-modifying treatments. Our research group is specifically looking at modifiable risk factors that could delay the onset of the disease, and even a five-year delay could have massive social and economic benefits,” said lead author Samantha Gardener, who is a research fellow at Edith Cowan University in Western Australia.

“Worldwide, a high proportion of adults drink coffee every day, making it one of the most popular beverages consumed,” Gardener added.

The popularity and ubiquitousness of coffee could make it a viable method of deferring the onset of Alzheimer’s disease. But she also stressed that further studies are necessary. Gardener and her team are not yet sure what ingredient in coffee itself contributes to the delaying of Alzheimer’s.

“This is, obviously, preliminary data and it needs a lot more research before being recommended, but it’s really positive, and hopefully in the future, it can be incorporated as a modifiable lifestyle factor that can delay Alzheimer’s disease onset,” Gardener said.

Source: https://greekreporter.com/2023/09/09/viagr...

Solving the cholesterol problem you never heard of

Lp(a), known as LP little “a” (Lp is lipoprotein), is an independent risk factor for cardiovascular disease.  The easiest way to think about Lp(a) is that it’s a genetically determined type of cholesterol carrier that makes the other risky cholesterols worse if it’s elevated.  

The problem has been two-fold – 

1. Lp(a) has only recently been measured by most doctors (I’ve been measuring it for about 10 years), and

2. Very little will change the Lp(a) level by much.  

As a consequence of #1, many patients who suffer “surprise” events (they have “normal” cholesterol but usual tests) are ultimately found to have elevated Lp(a). 

#2 leads to the strategy that lowering other cholesterol risks in the hope that you could avoid the consequences.  

The article attached reports the first successful attempt to meaningfully lower the Lp(a) (62%) with an oral medication, without screwing other stuff up, at least in an obvious way.  Phase I trials are small, and are testing for safety, but this one actually shows promise for efficacy as well.  For people with elevated Lp(a) this could be a real gamechanger.  It’s early, but fingers crossed.

Muvalaplin, an Oral Small Molecule Inhibitor of Lipoprotein(a) Formation

A Randomized Clinical Trial

Key Points

Question  Can muvalaplin, an orally administered small molecule inhibitor of lipoprotein(a) (Lp[a]) formation, achieve safe and tolerable plasma concentrations adequate to reduce steady-state Lp(a) levels without modulating plasminogen activity in humans?

Findings  In this first-in-human phase 1 study involving healthy participants, muvalaplin administered orally as single ascending doses ranging from 1 mg to 800 mg and as multiple ascending doses ranging from 30 mg to 800 mg for 14 days caused dose-dependent plasma concentration increases. Muvalaplin administration was not associated with concerns about safety or tolerability, and it reduced Lp(a) levels but not plasminogen activity.

Meaning  The observed safety, tolerability, pharmacokinetics, and exploratory pharmacodynamics of muvalaplin in healthy participants support further clinical evaluation in patients with elevated Lp(a) levels.

Abstract

Importance  Lipoprotein(a) (Lp[a]) is associated with atherosclerotic disease and aortic stenosis. Lp(a) forms by bonding between apolipoprotein(a) (apo[a]) and apo B100. Muvalaplin is an orally administered small molecule that inhibits Lp(a) formation by blocking the apo(a)-apo B100 interaction while avoiding interaction with a homologous protein, plasminogen.

Objective  To determine the safety, tolerability, pharmacokinetics, and pharmacodynamic effects of muvalaplin.

Design, Setting, and Participants  This phase 1 randomized, double-blind, parallel-design study enrolled 114 participants (55 assigned to a single-ascending dose; 59 assigned to a multiple-ascending dose group) at 1 site in the Netherlands.

Interventions  The single ascending dose treatment evaluated the effect of a single dose of muvalaplin ranging from 1 mg to 800 mg or placebo taken by healthy participants with any Lp(a) level. The multiple ascending dose treatment evaluated the effect of taking daily doses of muvalaplin (30 mg to 800 mg) or placebo for 14 days in patients with Lp(a) levels of 30 mg/dL or higher.

Main Outcomes and Measures  Outcomes included safety, tolerability, pharmacokinetics, and exploratory pharmacodynamic biomarkers.

Results  Among 114 randomized (55 in the single ascending dose group: mean [SD] age, 29 [10] years, 35 females [64%], 2 American Indian or Alaska Native [4%], 50 White [91%], 3 multiracial [5%]; 59 in the multiple ascending dose group: mean [SD] age 32 [15] years; 34 females [58%]; 3 American Indian or Alaska Native [5%], 6 Black [10%], 47 White [80%], 3 multiracial [5%]), 105 completed the trial. Muvalaplin was not associated with tolerability concerns or clinically significant adverse effects. Oral doses of 30 mg to 800 mg for 14 days resulted in increasing muvalaplin plasma concentrations and half-life ranging from 70 to 414 hours. Muvalaplin lowered Lp(a) plasma levels within 24 hours after the first dose, with further Lp(a) reduction on repeated dosing. Maximum placebo-adjusted Lp(a) reduction was 63% to 65%, resulting in Lp(a) plasma levels less than 50 mg/dL in 93% of participants, with similar effects at daily doses of 100 mg or more. No clinically significant changes in plasminogen levels or activity were observed.

Conclusion  Muvalaplin, a selective small molecule inhibitor of Lp(a) formation, was not associated with tolerability concerns and lowered Lp(a) levels up to 65% following daily administration for 14 days. Longer and larger trials will be required to further evaluate safety, tolerability, and effect of muvalaplin on Lp(a) levels and cardiovascular outcomes.

Source: https://jamanetwork.com/journals/jama/arti...

Long COVID continues to be a COMPLICATED story

Most people know somebody who’s had COVID and then has suffered for a long time as a consequence – just never quite right yet.  Those are the “usual” Long COVID people.  Unfortunately, many have not gotten connected with folks who can help them, and thus, their suffering persists longer than may be necessary (we can help those people).  Now, though, there’s another bunch of patients who might be getting Long COVID MONTHS after seemingly being “cured”.  

Most Long COVID patients (86%) tend to improve after a year (doesn’t that sound like a really long time? It does to me.).  But “it (was) common for symptoms to resolve then re-emerge months later.”

Yikes.  

Interestingly, when they compared COVID vs non-COVID groups for symptoms, there really wasn’t a significant difference (18.3% vs 16.1%).  That means that 1 in every 5 or 6 people is walking around every day with symptoms that fall into the Long COVID-type buckets, whether or not they ever had COVID.  This seems like the basic issue – lots of people are walking around with “stuff” that’s not being handled (we can help those people, too.)

Oh, and by the way, the CDC reports that Long COVID has fallen to only 6% of the population. Heck, nothing to worry about – it’s ONLY 20 million people!

Long COVID Symptoms May Emerge Months After Infection

— Fewer Americans have long COVID but many have significant activity limitations, CDC data show

Long COVID symptoms may emerge months after SARS-CoV-2 infection, data from the prospective multicenter INSPIRE study suggested.

Symptom prevalence decreased over 1 year among long COVID patients, but persisted or emerged at different time points in some cases, reported Sharon Saydah, PhD, of the CDC's National Center for Immunization and Respiratory Diseases, and co-authors in the Morbidity and Mortality Weekly Report.

For about 16% of study participants, symptoms lasted 12 months after their initial SARS-CoV-2 test. At 3, 6, 9, and 12 months after testing, some people had ongoing symptoms, while others had emerging symptoms not reported previously.

"It was common for symptoms to resolve then re-emerge months later," noted co-author Juan Carlos Montoy, MD, PhD, of the University of California San Francisco.

"A lot of prior research has focused on symptoms at one or two points in time, but we were able to describe symptom trajectory with greater clarity and nuance," Montoy said in a statement. "It suggests that measurements at a single point in time could underestimate or mischaracterizes the true burden of disease."

INSPIRE was designed to assess long-term symptoms and outcomes among people with COVID-like illness who had a positive or negative SARS-CoV-2 test result at study enrollment. Participants who completed baseline and 3-, 6-, 9-, and 12-month surveys were included to identify emerging and ongoing symptoms.

A total of 1,741 people completed all quarterly surveys through 12 months, including 1,288 COVID test-positive and 453 COVID test-negative participants. Most participants were female.

Outcomes included self-reported symptoms in eight categories: extreme fatigue; cognitive difficulties; cardiovascular; pulmonary; musculoskeletal; gastrointestinal; constitutional; or head, eyes, ears, nose, and throat.

The prevalence of any symptom decreased substantially from baseline to 3-month follow-up -- from 98.4% to 48.2% for COVID-positive participants, and from 88.2% to 36.6% for COVID-negative participants.

Persistent symptoms decreased over the year. Emerging symptoms were reported for every symptom category at each follow-up period for both groups.

At 12 months, symptom prevalence was similar between groups, at 18.3% in the COVID-positive group and 16.1% in the COVID-negative group (P>0.05).

"We were surprised to see how similar the patterns were between the COVID-positive and COVID-negative groups," Montoy noted. "It shows that the burden after COVID may be high, but it might also be high for other non-COVID illnesses. We have a lot to learn about post-illness processes for COVID and other conditions."

In other research published in the Morbidity and Mortality Weekly Report, a national survey showed the prevalence of long COVID fell to 6.0%.

The survey also found that one in four people with long COVID (26.4%) had significant activity limitations, reported Nicole Ford, PhD, of the CDC's National Center for Immunization and Respiratory Diseases, and co-authors. The findings came from the Census Bureau's Household Pulse Survey from June 1-13, 2022 to June 7-19, 2023.

Among people who reported a history of previous SARS-CoV-2 infection, long COVID prevalence fell from 18.9% in 2022 to 11% in 2023. In the overall U.S. population -- irrespective of history of previous COVID-19 -- the prevalence of long COVID dropped from 7.5% to 6.0%.

Among both groups, prevalence declined from June 2022 through January 2023 before stabilizing.

The percentage of people with significant activity limitations didn't change over time, the researchers said. Only adults under age 60 experienced significant rates of decline (P<0.01).

"These findings highlight the importance of COVID prevention, including staying up to date with recommended COVID-19 vaccination, and could inform healthcare service needs planning, disability policy, and other support services for persons experiencing severe activity limitation from long COVID," Ford and colleagues wrote.

"Limited ability to carry out day-to-day activities because of long COVID symptoms can have a significant impact on quality of life, functional status, and ability to work or provide care to others," they added. "Long COVID in U.S. adults has also been associated with lower likelihood of working full time and higher likelihood of being unemployed."

Source: https://www.medpagetoday.com/neurology/lon...

The reports of (my) death are greatly exaggerated

Chat GPT agains tolls the bell of impending doom, etc.  Or not.  

The whole generative AI space is very promising, and some really interesting results have come out of evaluating the technology in the healthcare space.  This article’s title again makes the case that the computer is better than the doctor.  And for some cases, that’s true – where you might think it would be helpful.  Like in the case of some real oddities, complex collections of stuff that’s uncommon, etc.  But there continues to be issues around some stuff that the regular doc would be thinking of long before the computer got around to it.  And don’t get me started on the MSU (Make S**t Up) quotient that I’ve touched on before – it continues to be a real problem.  

The future of AI assisted healthcare is, indeed, very bright.  But don’t get ahead of yourself – it’s like consulting Dr. Google – oh, I have cancer….but it really just looks like a splinter…..

AI Beat Clinicians at Figuring Out Difficult Diagnoses

GPT-4 may help with diagnoses that have been missed by clinicians, study author says

A generative artificial intelligence (AI) program diagnosed elderly patients with extensive medical histories and long hospital stays more accurately than clinicians, suggesting the technology could help identify missed diagnoses, according to a new study.

An analysis of medical histories for six patients over the age of 65 with delayed diagnoses revealed that GPT-4 (Generative Pre-trained Transformer 4, made by OpenAI) accurately diagnosed four out of six patients, according to Yat-Fung Shea, MBBS, of the Department of Medicine at Queen Mary Hospital and University of Hong Kong, and coauthors.

By comparison, clinicians accurately diagnosed only two out of six of those same patients, according to a research letter published in JAMA Network Open.

When differential diagnoses were included, AI's accuracy improved to five out of six patient diagnoses, compared with three out of six correct patient diagnoses made by clinicians.

Differential diagnoses were also generated using a medical diagnostic decision tool known as Isabel DDx Companion. This tool accurately diagnosed none of the patients in the initial attempt, and two out of six patients when provided differential diagnosis information.

"GPT-4 may be able to provide potential diagnoses which have been missed by clinicians," Shea told MedPage Today in an email. "If a doctor encounters elderly patients, who have been admitted into hospital for work-up for at least a month but [are] still without a definite diagnosis, he/she can consider using GPT-4 to analyze the medical histories."

"GPT-4 may help clinicians to analyze clinical situations with diagnostic difficulties, especially in alerting clinicians to possible underlying malignancies or side effects of drugs," he added.

The AI program was able to successfully diagnose patients as a result of the extensive medical histories available for each of them, Shea said, including radiological and pharmacological information.

Shea noted that they chose to work with older patients because they often suffered from multiple comorbidities, which can require prolonged efforts to achieve a correct diagnosis. With GPT-4, clinicians could potentially identify diagnoses they might have otherwise missed, which would help close the time to initial diagnosis in this population.

The AI program successfully diagnosed patients with a range of conditions, including polymyalgia rheumatica (patient 2), mycobacterium tuberculosis-related hemophagocytic lymphohistiocytosis (patient 3), metronidazole-induced encephalopathy (patient 5), and lymphoma (patient 6).

Still, GPT-4 had trouble with certain aspects of diagnosing patients, including multifocal infections. The AI program failed to pinpoint the source of a recurrent infection in one patient, and it did not suggest the use of clinically relevant testing for infections in most of the patients in the study.

Shea noted that GPT-4 should be seen as a tool that can increase a clinician's confidence in a diagnosis or even offer clinicians suggestions similar to those of a specialist. This would be especially beneficial in lower-income countries that lack the wide availability of specialists to assist with consulting on older patients.

"Our results showed that GPT-4 has the potential to improve clinician responses," Shea said. "GPT-4 may alert clinicians [of] certain overlooked things in the clinical history, e.g. potential side effects of drugs or abnormal findings on imaging. These may be relevant especially when certain subspecialties are not immediately available for consultation."

Shea also noted that the study was limited by a very small sample size. The analysis was conducted using the medical histories for six patients (two women and four men) in a single hospital unit -- the Division of Geriatrics in the Department of Medicine at Queen Mary Hospital. All of the patients had delayed definitive diagnosis for longer than 1 month in 2022. Their histories were entered into GPT-4 chronologically starting at admission, at 1 week after admission, and before final diagnosis. The data were entered into the AI program on April 16, 2023.

The authors also cautioned that the AI program is susceptible to regurgitating wrong information based on incorrect medical histories.

They concluded that use of generative AI in diagnosing patients showed promise, especially when extensive medical histories were available, but it also presented several new challenges for clinicians.

Source: https://www.medpagetoday.com/special-repor...

Could there be anything more OBVIOUS concerning Long COVID?

DUH!  It takes an expert panel to recommend that we need to study Long COVID more.  This is specifically around cognitive issues – brain fog, trouble with executive function, stuff like that.  There’s a report from a modeling study of 1.2 million people that demonstrated that 2.2% still had issues months after being sick.  Plus the specter of long term neurodegeneration is possible in those folks, maybe even likely.  That’s 26,000 people in the study.  If we consider that 35% of Americans have been known to test positive for COVID (very much an understated number), this would translate to about ¼ of a million cognitively impaired Americans.  That’s a huge problem, still largely undefined and in conventional practices, largely unaddressed.  

If you are one of the folks who feels like things still aren’t quite right, PLEASE call – don’t expect things to improve on their own if they haven’t by now.  There is help available.

Long COVID Cognitive Research Needs an Overhaul, Task Force Says

Expert group issues recommendations for future studies

Long COVID cognitive research needs better studies, an international task force urged.

The approach to assessing cognitive dysfunction after SARS-CoV-2 infection requires an overhaul to better understand long COVID prevalence, trajectory, mechanisms, phenotypes, and psychosocial factors, said experts from the NeuroCOVID International Neuropsychology Taskforce.

"As one of the most common symptoms of post-COVID-19 condition and one for which affected individuals may seek accommodations and disability benefits in accordance with the Americans With Disabilities Act, it is imperative that we use more rigorous studies of cognitive outcomes," wrote task force member Sara Weisenbach, PhD, of McLean Hospital and Harvard Medical School in Boston, and co-authors, in a viewpoint paper published in JAMA Psychiatry.

Long COVID cognitive dysfunction, including "brain fog," can affect even relatively young people and can last for months. A modeling study based on 1.2 million COVID patients showed that 2.2% had cognitive problems lasting 3 months or longer after symptomatic infection. Moreover, data from patients with severe COVID suggested SARS-CoV-2 infection may raise the risk of subsequent neurodegeneration.

"Since the beginning of the SARS-CoV-2 pandemic, the medical community has experienced an influx of patients reporting new cognitive difficulties months after infection clearance," Weisenbach told MedPage Today.

"There is evidence in the research literature of objective cognitive impairment in some individuals following infection; however, many studies have methodological weaknesses that limit the conclusions that can be drawn and applied in clinical settings," she said.

The task force outlined three recommendations based on initial guidelines the group proposed in 2021.

The first calls for a rigorous assessment of post-COVID cognitive dysfunction. Studies relying on self-reported data early in the pandemic have skewed perceptions about the frequency of cognitive dysfunction, Weisenbach and co-authors pointed out, and objective and subjective findings often don't align with each other. Comprehensive test batteries should be used, and studies should include control groups, diverse samples, and when possible, pre-pandemic and post-pandemic data, they argued.

The group's second recommendation was for new research to identify clinical phenotypes. COVID severity, age, family history, and pre-existing cognitive or psychiatric disorders are factors to consider, the task force observed. Other phenotypes may be based on COVID-19 variants, vaccination status, or history of other viral illnesses or pre-existing autoimmune conditions.

Finally, psychosocial factors need to be assessed given the controversies surrounding post-COVID-19 cognitive dysfunction, including skepticism of its existence and disagreement on its cause, Weisenbach and co-authors said.

"This controversy is familiar to neuropsychologists, who frequently evaluate patients with similarly controversial conditions, such as myalgic encephalomyelitis, or chronic fatigue syndrome," the task force said. "Perhaps because psychiatric disorders can co-occur with these multifaceted conditions, many have dismissed these conditions as being psychosomatic with nonbiologic underpinnings."

"This broad dismissal is contrary to scientific evidence and can be harmful for patients and communities affected," the group added. It's possible that in some people, cognitive symptoms may reflect an interplay between illness and psychological and social factors, and in others it's associated with a postviral syndrome and persistent inflammation, they suggested.

Clinical studies will likely have different results than those from large cohorts, Weisenbach and colleagues noted.

"Together, these data will allow improved clarity regarding the pathophysiology of post-COVID-19 cognitive dysfunction and factors that contribute to symptom persistence," they wrote. "Ultimately, this will create opportunities for the development of effective treatment interventions using a personalized medicine approach."

Source: https://www.medpagetoday.com/neurology/lon...

What if you are NOT "Normal"? I guess you'll keep sniffling.

The FDA is now announcing that an ingredient in many cold and allergy medications, phenylephrine is no more effective than placebo.  This story gets complicated, but I know that, for myself, phenylephrine ABSOLUTELY works to combat nasal congestion.  But then again, I know I’m not normal (😊).  

If the FDA decides to pull this ingredient off the shelves, there will be essentially no appropriate pharmaceutical options for folks with colds (there are some homeopathic remedies, and other options, that of course, conventional practices won’t tell you about).  

The FDA bases their evaluations of population effects.  If you’re “not normal” (middle of the pack), you might fall outside of the usual recommendations.  FeldMed looks at the individual, not the population.  This is the basis for “Personalized Medicine” – it doesn’t have to work for everybody – it just has to work for you! 

FROM NEWSDAY / BY LISA L. COLANGELO

A decongestant found in popular nonprescription cold medications including some types of Sudafed, DayQuil and Mucinex doesn’t work, according to a panel of experts reviewing the ingredient phenylephrine for the U.S. Food and Drug Administration.

The unanimous vote on Tuesday could lead the FDA to pull medications with phenylephrine from store shelves, if it accepts the findings. Sales of products with the ingredient were worth $1.7 billion in 2022.

“Modern studies, when well conducted, are not showing any improvement in congestion with phenylephrine,” said Dr. Mark Dykewicz, a member of the panel and an allergy specialist at the Saint Louis University School of Medicine.

Findings from recent studies as well as interpretation of older data, shows phenylephrine is not effective, said Dr. David Rosenthal, attending physician at the division of allergy/immunology at Northwell Health.

“Science progresses over time, and even though it was approved as being effective in the 1970s, it doesn’t meet the current standards for effectiveness,” he said. “This was typically used as a medication that shrank blood vessels in the nose so people would not be as congested.”

Get the latest stories every week about health and wellness, covering topics from medicine and mental health to updates on the coronavirus and new research.

Members of the FDA’s Nonprescription Drug Advisory Committee had been convened to examine data and help determine whether oral phenylephrine is an effective nasal decongestant. The review did not include nasal sprays with phenylephrine.

The debate over the effectiveness of phenylephrine has gone on for over a decade, led by some medical experts and researchers. But sales of products containing the ingredient are strong, especially during the cold and flu seasons. More than 242 million bottles/packages of over-the-counter cough, cold, allergy oral medications with phenylephrine were sold in retail stores in 2022, according to an FDA briefing document.

FDA reviewers said the research shows how quickly phenylephrine is metabolized when taken orally, leaving only trace levels that reach nasal passages to relieve congestion. The drug appears more effective when applied directly to the nose, in sprays or drops.

Rosenthal said people suffering from allergy symptoms are better off addressing symptoms with antihistamines and seeing an allergist. Cold symptoms will improve when the cold virus goes away with the help of rest, nasal saline and drinking warm liquids.

Rosenthal said preventing infections by getting vaccinated against the flu, COVID-19 and RSV is also important.

Source: https://www.newsday.com/news/health/nasal-...

Who's Trippin' Now?

I love Pink Floyd.  Complex layers, mind-bending instrumentals and  “mess with your head” lyrics.  What’s not to like.  That’s what a bunch of neuroscientists thought, too, when they used Pink Floyd as their brainwave subject matter.  The attempt to recreate the music from actual brainwaves was somewhat successful, which has all kinds of crazy implications which I’ll let your imaginations run away with! 

FROM SCIENTIFIC AMERICAN / bY LUCY TU

Neuroscientists Re-create Pink Floyd Song from Listeners’ Brain Activity

Artificial intelligence has turned the brain’s electrical signals into somewhat garbled classic rock

Researchers hope brain implants will one day help people who have lost the ability to speak to get their voice back—and maybe even to sing. Now, for the first time, scientists have demonstrated that the brain’s electrical activity can be decoded and used to reconstruct music.

A new study analyzed data from 29 people who were already being monitored for epileptic seizures using postage-stamp-size arrays of electrodes that were placed directly on the surface of their brain. As the participants listened to Pink Floyd’s 1979 song “Another Brick in the Wall, Part 1,” the electrodes captured the electrical activity of several brain regions attuned to musical elements such as tone, rhythm, harmony and lyrics. Employing machine learning, the researchers reconstructed garbled but distinctive audio of what the participants were hearing. The study results were published on Tuesday in PLOS Biology.

Neuroscientists have worked for decades to decode what people are seeing, hearing or thinking from brain activity alone. In 2012 a team that included the new study’s senior author—cognitive neuroscientist Robert Knight of the University of California, Berkeley—became the first to successfully reconstruct audio recordings of words participants heard while wearing implanted electrodes. Others have since used similar techniques to reproduce recently viewed or imagined pictures from participants’ brain scans, including human faces and landscape photographs. But the recent PLOS Biology paper by Knight and his colleagues is the first to suggest that scientists can eavesdrop on the brain to synthesize music.

“These exciting findings build on previous work to reconstruct plain speech from brain activity,” says Shailee Jain, a neuroscientist at the University of California, San Francisco, who was not involved in the new study. “Now we’re able to really dig into the brain to unearth the sustenance of sound.”

To turn brain activity data into musical sound in the study, the researchers trained an artificial intelligence model to decipher data captured from thousands of electrodes that were attached to the participants as they listened to the Pink Floyd song while undergoing surgery.

Why did the team choose Pink Floyd—and specifically “Another Brick in the Wall, Part 1”? “The scientific reason, which we mention in the paper, is that the song is very layered. It brings in complex chords, different instruments and diverse rhythms that make it interesting to analyze,” says Ludovic Bellier, a cognitive neuroscientist and the study’s lead author. “The less scientific reason might be that we just really like Pink Floyd.”

The AI model analyzed patterns in the brain’s response to various components of the song’s acoustic profile, picking apart changes in pitch, rhythm and tone. Then another AI model reassembled this disentangled composition to estimate the sounds that the patients heard. Once the brain data were fed through the model, the music returned. Its melody was roughly intact, and its lyrics were garbled but discernible if one knew what to listen for: “All in all, it was just a brick in the wall.”

The model also revealed which parts of the brain responded to different musical features of the song. The researchers found that some portions of the brain’s audio processing center—located in the superior temporal gyrus, just behind and above the ear—respond to the onset of a voice or a synthesizer, while other areas groove to sustained hums.

Although the findings focused on music, the researchers expect their results to be most useful for translating brain waves into human speech. No matter the language, speech contains melodic nuances, including tempo, stress, accents and intonation. “These elements, which we call prosody, carry meaning that we can’t communicate with words alone,” Bellier says. He hopes the model will improve brain-computer interfaces, assistive devices that record speech-associated brain waves and use algorithms to reconstruct intended messages. This technology, still in its infancy, could help people who have lost the ability to speak because of conditions such as stroke or paralysis.

Jain says future research should investigate whether these models can be expanded from music that participants have heard to imagined internal speech. “I’m hopeful that these findings would translate because similar brain regions are engaged when people imagine speaking a word, compared with physically vocalizing that word,” she says. If a brain-computer interface could re-create someone’s speech with the inherent prosody and emotional weight found in music, it could reconstruct far more than just words. “Instead of robotically saying, ‘I. Love. You,’ you can yell, ‘I love you!’” Knight says.

Several hurdles remain before we can put this technology in the hands—or brains—of patients. For one thing, the model relies on electrical recordings taken directly from the surface of the brain. As brain recording techniques improve, it may be possible to gather these data without surgical implants—perhaps using ultrasensitive electrodes attached to the scalp instead. The latter technology can be employed to identify single letters that participants imagine in their head, but the process takes about 20 seconds per letter—nowhere near the speed of natural speech, which hurries by at around 125 words per minute.

The researchers hope to make the garbled playback crisper and more comprehensible by packing the electrodes closer together on the brain’s surface, enabling an even more detailed look at the electrical symphony the brain produces. Last year a team at the University of California, San Diego, developed a densely packed electrode grid that offers brain-signal information at a resolution that is 100 times higher than that of current devices. “Today we reconstructed a song,” Knight says. “Maybe tomorrow we can reconstruct the entire Pink Floyd album.”

Source: https://www.scientificamerican.com/article...

Make your STEPS count

If you’ve been paying attention AT ALL, then you know we’ve talked about getting up and moving.  We’ve previously debunked the “you gotta get 10,000 steps”, but at the same time, more is better.  Here’s a tidy summary of lots of walking data over years that again supports the idea that doing more is better.  Simply, if you add 1000 steps to your daily routine you can expect a 15% reduction on overall mortality (that’s a population risk – we usually only get to die once), while 500 steps will buy you a 7% reduction in cardiovascular risk.  

I’m going to say it again – EXERCISE is the single most important thing you can do to improve your overall health, reduce your risk of chronic disease, and extend your life and healthspan.  I am happy to assist you in developing a specific program to directly address your specific needs.  Just give me a call and we can get started.

FROM THE EUROPEAN JOURNAL OF PREVENTIVE CARDIOLOGY / BY MACIEJ BANACH, JOANNA LEWEK, STANISŁAW SURMA, PETER E PENSON, AMIRHOSSEIN SAHEBKAR, SETH S MARTIN, GANI BAJRAKTARI, MICHAEL Y HENEIN, ŽELJKO REINER, AGATA BIELECKA-DĄBROWA, IBADETE BYTYÇI

The association between daily step count and all-cause and cardiovascular mortality: a meta-analysis


Lay Summary

  • There is strong evidence showing that sedentary life may significantly increase the risk of cardiovascular (CV) disease and shorten the lifespan. However, the optimal number of steps, both the cut-off points over which we can see health benefits, and the upper limit (if any), and their role in health are still unclear.

  • In this meta-analysis of 17 studies with almost 227 000 participants that assessed the health effects of physical activity expressed by walking measured in the number of steps, we showed that a 1000-step increment correlated with a significant reduction of all-cause mortality of 15%, and similarly, a 500-step increment correlated with a reduced risk of CV mortality of 7%. In addition, using the dose–response model, we observed a strong inverse nonlinear association between step count and all-cause mortality with significant differences between younger and older groups.

  • It is the first analysis that not only looked at age and sex but also regional differences based on the weather zones, and for the first time, it assesses the effect of up to 20 000 steps/day on outcomes (confirming the more the better), which was missed in previous analyses. The analysis also revealed that depending on the outcomes, we do not need so many steps to have health benefits starting with even 2500/4000 steps/day, which, in fact, undermines the hitherto definition of a sedentary life.

Abstract Aims

There is good evidence showing that inactivity and walking minimal steps/day increase the risk of cardiovascular (CV) disease and general ill-health. The optimal number of steps and their role in health is, however, still unclear. Therefore, in this meta-analysis, we aimed to evaluate the relationship between step count and all-cause mortality and CV mortality.

Methods and results

We systematically searched relevant electronic databases from inception until 12 June 2022. The main endpoints were all-cause mortality and CV mortality. An inverse-variance weighted random-effects model was used to calculate the number of steps/day and mortality. Seventeen cohort studies with a total of 226 889 participants (generally healthy or patients at CV risk) with a median follow-up 7.1 years were included in the meta-analysis. A 1000-step increment was associated with a 15% decreased risk of all-cause mortality [hazard ratio (HR) 0.85; 95% confidence interval (CI) 0.81–0.91; P < 0.001], while a 500-step increment was associated with a 7% decrease in CV mortality (HR 0.93; 95% CI 0.91–0.95; P < 0.001). Compared with the reference quartile with median steps/day 3967 (2500–6675), the Quartile 1 (Q1, median steps: 5537), Quartile 2 (Q2, median steps 7370), and Quartile 3 (Q3, median steps 11 529) were associated with lower risk for all-cause mortality (48, 55, and 67%, respectively; P < 0.05, for all). Similarly, compared with the lowest quartile of steps/day used as reference [median steps 2337, interquartile range 1596–4000), higher quartiles of steps/day (Q1 = 3982, Q2 = 6661, and Q3 = 10 413) were linearly associated with a reduced risk of CV mortality (16, 49, and 77%; P < 0.05, for all). Using a restricted cubic splines model, we observed a nonlinear dose–response association between step count and all-cause and CV mortality (Pnonlineraly < 0.001, for both) with a progressively lower risk of mortality with an increased step count.

Conclusion

This meta-analysis demonstrates a significant inverse association between daily step count and all-cause mortality and CV mortality with more the better over the cut-off point of 3967 steps/day for all-cause mortality and only 2337 steps for CV mortality.

FOR THE FULL STUDY CLICK HERE


Source: https://academic.oup.com/eurjpc/advance-ar...