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Topic: Covid Penis
https://elemental.medium.com/yes-covid-penis-is-a-thing-4a88a3843c2c
Yes, Covid Penis Is a Thing
Some men say Covid-19 is hitting them below the belt
Wudan Yan 12 hours agoWhen Steven Bell caught Covid-19 this spring, he was surprised that he didn’t have a fever. Rather, it felt like a bad sinus infection. Soon, he lost his sense of smell, and went on to develop insomnia. He felt like the virus was also affecting his circulation, and would swing his arms in circles to keep the blood flowing. Then, more bafflingly, when he and his wife were intimate, he couldn’t get an erection. “It was frustrating and infuriating for me, because I knew it wasn’t working the way it should,” said Bell, a 49-year-old from Phoenix, AZ. “My ego wouldn’t accept that I was performing like an 80-year-old in the bedroom.”
Some men who have survived Covid-19 say that the virus may have impacted their ability to get or maintain an erection. That tracks with the idea that Covid-19 is a vascular disease, which Elemental senior writer Dana Smith explained at length in May, as blood flow is important for getting or maintaining an erection. Erectile dysfunction can occur at any age — and becomes more common as men get older — and may affect up to a third of all men. In the context of Covid-19, men as young as 39 have been documented to experience erectile dysfunction as they recovered from the virus.
“In order to have really great sex, you have to be able to relax. The pandemic just makes that exceedingly difficult for many people.”
Currently, there are a handful of anecdotal reports, but no hard data nor large-scale study that documents the link, if any, between Covid-19 and erectile dysfunction. But for the men experiencing such issues, they’re convinced that the erectile dysfunction was caused by the novel coronavirus, because they never had issues with arousal or performance during sex prior to contracting the virus. Hunter Wessells, MD, a urologist at the University of Washington School of Medicine, urges other practitioners to collect this data on their patients. “It’s important to study it, because the total number of people involved may be in the millions and across all age ranges,” he says.
What’s actually causing the ED?
Figuring out the cause of erectile dysfunction would be challenging as there are so many potential causes.
No matter the cause, “[erectile dysfunction is] the final common pathway that no man wants to go to,” says William W. Li, MD, president and medical director of the Angiogenesis Foundation, a nonprofit that studies the health and disease of blood vessels.
For starters, the pandemic has introduced an immense amount of stress, says Alexandra Stockwell, a relationship and intimacy expert. “The desire for sex and intimacy is lower,” Stockwell says. “In order to have really great sex, you have to be able to relax. The pandemic just makes that exceedingly difficult for many people.”
That seemed true for Bruce (whose name has been changed to protect his privacy), a 66-year-old from Long Island, NY, who experienced erectile dysfunction after getting Covid-19 in late March. For him, the ED, which persisted for four to five weeks, was just the tip of his issues. “I just wanted to be alive,” he said. “The ED was no big deal.”
Based on what scientists know about SARS-CoV-2, the virus that causes Covid-19, it’s possible that the virus could have direct effects on erectile dysfunction. Successfully getting and maintaining an erection not only depends on mood, but also testosterone, blood flow, and nerves. In the penis, nerves are critically dependent on a fishnet of blood vessels to get an erection. SARS-CoV-2 exploits the ACE2 receptor, which is found in both nerve cells and endothelial cells lining blood vessels. ACE2 is also found in the cells of the testicles, the organ in men that makes testosterone, a hormone that fuels a man’s sex drive. Li and his colleagues have found that the virus infects testicular cells during the acute phase of Covid-19, which means the virus may be impacting testosterone production.
On top of the effects in the penis, Covid-19 affects the cardiovascular and pulmonary systems, which, in turn, are critical for sexual function, says Li.
Wessells notes that underlying health conditions, such as diabetes, obesity, hypertension, inactivity, and smoking, may predispose men to developing ED, and that at least a few of those are associated with a higher risk of contracting Covid-19 as well. Once someone contracts Covid-19, that may be the “straw that broke the camel’s back for the ED,” Wessells says.
Fortunately, for men who suffer from erectile dysfunction, many treatments, such as Viagra, should help even if Covid-19 has damaged the vasculature, says Wessells.
Some men who say Covid-19 caused their erectile dysfunction have found some reprieve.
Art (whose name has also been changed to protect his privacy), a 53-year-old from Elmira, New York, waited until marriage to have sex with his wife. Both of them got Covid-19 in the spring. During their honeymoon this summer, the sex just… didn’t happen, because he couldn’t get an erection. “We knew we wanted children, but I’m having all sorts of issues,” he said. “There’s definitely a degree of guilt. I’m convinced I’m the problem.” Doctors dismissed his concerns that the erectile dysfunction may have been caused by Covid-19. He eventually got over the stigma of talking about his sexual health and opened up to his parents, who suggested he start taking Geritol, vitamins that help with sexual dysfunction. So far, Art says, they’ve helped. “I need to make the best of it when I have it.”
Even so, the emotional toll for some men persists.
“When I’m in the mood and physically reporting for duty, my anxiety has increased,” says Bell. And he’s still sometimes frustrated about the impact that Covid-19 has had on his sex life: the erectile dysfunction “crushed” his confidence during sex.
For now, he hopes that his story offers a cautionary tale. “Stay away from Covid to keep that willy up.”
Week 12: 4 Observations on the L.A. Rams’ 23-20 loss to the 49ers
* http://ramstalk.net/week12ramsloss/
The Los Angeles Rams (7-4) suffered a heartbreaking 23-20 loss to the San Francisco 49ers (5-6) at SoFi Stadium on Sunday, November 29. Rams quarterback Jared Goff completed 19 of 31 passes for 198 yards, two interceptions and a fumble lost in the defeat.
Here are four observations on the game:
TIME FOR JARED GOFF TO GROW UP
I’ve defended Goff for much of his career for good reason. The Rams put him in a poor position with former head coach Jeff Fisher as a rookie, and he’s played under multiple offensive coordinators and quarterback coaches. However, the Rams traded a bounty to select him as the No. 1 overall pick of the 2016 NFL Draft to be their franchise quarterback. They later paid him $134 million over four years ($110 million guaranteed) believing that he was ready to lead the franchise. What we saw today from Goff is far below any bar set for a fifth-year franchise quarterback. In truth, Goff’s performance put him nowhere near the value of what the Rams are paying for.
Goff will enter next week’s game against the Arizona Cardinals with the highest completion percentage of his career (67.25%). He’s already over 3,000 passing yards with an improved touchdown to interception ratio (16-10) over last season. Yet the inconsistent play that began in late 2018 has continued well into this season. Goff struggles under pressure and often fails to read opposing defenses. He possesses elite raw talent, but Goff’s decision-making often hurts his team at the worst times.
The Rams’ defense led the comeback against the 49ers, saving Goff from taking full responsibility for the team’s loss. Still, his mistakes buried the Rams for much of the game. There are no more excuses for Jared Goff. His offensive line didn’t perform well, and head coach Sean McVay certainly deserves to be questioned for his playcalling, but Goff is paid to lead this franchise on the field. It’s time he acted like it.
SEAN MCVAY’S FAILURE EVIDENT
I’ve said it time and time again on the Rams Talk Radio podcast: John Lynch built the 49ers to beat the Rams. However, that doesn’t mean the Rams cannot match up with them. The 49ers feature a strong pass rush and a fast front seven. Defensive coordinator Robert Saleh continually gameplans well for the Rams by constantly pressuring Goff and shutting down the edge against the running game.
Sean McVay failed to adjust for his offensive line’s rough performance against the 49ers pass rush for much of the first 35 minutes of the game. Keeping Goff in the pocket against that pass rush proved costly time and time again. Couple that with his failure to establish the running game and McVay hamstrung his quarterback. The 49ers’ speed stymied the Rams running game on the outside, so the obvious answer would be to attack that speed by going in between the tackles. Unfortunately, McVay failed to do that until later in the game.
McVay remains one of the brightest young minds in the game. However, he won’t win a Super Bowl until he learns to get out of his own way. Right now, McVay tends to get impatient when things don’t go his way, especially with the running game. Sometimes it’s a matter of patience, especially when facing athletic defenses. McVay could go down in history as one of the greatest coaches in the NFL. I truly believe that. However, it’s not going to happen if he doesn’t get out of his own head more.
THE OFFENSIVE LINE IS A CONCERN
The Rams offensive line protected Goff well against Tampa Bay last week, but it struggled against the aggressive 49ers front seven. Add in the Rams’ issues running the ball in the last two weeks, and there is reason for concern. The unit simply isn’t getting enough push at the line with left tackle Andrew Whitworth out of the lineup. Los Angeles is at its best when it physically controls the game. The Rams aren’t doing that, and with the Arizona Cardinals’ Kyler Murray up next, a power running game is essential for their chances. It’s time for this entire unit to step up both in pass protection and in the running game. The Rams won’t make it far without the big men showing what they are made of up front.
THE BRIGHT SPOT
Fortunately, defensive coordinator Brandon Staley’s unit kept the Rams in the game despite four turnovers from the offense. Defensive lineman Aaron Donald reaffirmed his place among the best in the league with a dominant performance in the second half, culminating in a forced fumble returned for a touchdown by defensive back Troy Hill. There will be those that are critical of the defense’s performance on the last drive of the game. Yet it seems idiotic to point the blame at a unit that pulled the Rams back from the brink. The tired defense proved unable to make one more stop, but a nine-minute time of possession difference points to the offense, which failed to carry its weight. If Goff and the offense can figure it out, the Rams have a chance at a deep playoff run.
https://www.usatoday.com/story/sports/nfl/titans/2020/10/08/tennessee-titans-buffalo-bills-game-postponed-covid-19-coronavirus/5922306002/
Why the NFL needs to immediately end the Titans’ 2020 season
Since last week, the NFL and NFLPA have had representatives in Nashville, investigating why the Tennessee Titans have by far the most positive COVID tests of any NFL team. The organization has had …
touchdownwire.usatoday.comThe Titans’ season should be cancelled. Part of the reason guys like A’Shawn aren’t coming back is because of the positive tests. The rest of the NFL has done amazing.
Earlier this summer, the Summit supercomputer at Oak Ridge National Lab in Tennessee set about crunching data on more than 40,000 genes from 17,000 genetic samples in an effort to better understand Covid-19. Summit is the second-fastest computer in the world, but the process — which involved analyzing 2.5 billion genetic combinations — still took more than a week.
When Summit was done, researchers analyzed the results. It was, in the words of Dr. Daniel Jacobson, lead researcher and chief scientist for computational systems biology at Oak Ridge, a “eureka moment.” The computer had revealed a new theory about how Covid-19 impacts the body: the bradykinin hypothesis. The hypothesis provides a model that explains many aspects of Covid-19, including some of its most bizarre symptoms. It also suggests 10-plus potential treatments, many of which are already FDA approved. Jacobson’s group published their results in a paper in the journal eLife in early July.
According to the team’s findings, a Covid-19 infection generally begins when the virus enters the body through ACE2 receptors in the nose, (The receptors, which the virus is known to target, are abundant there.) The virus then proceeds through the body, entering cells in other places where ACE2 is also present: the intestines, kidneys, and heart. This likely accounts for at least some of the disease’s cardiac and GI symptoms.
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But once Covid-19 has established itself in the body, things start to get really interesting. According to Jacobson’s group, the data Summit analyzed shows that Covid-19 isn’t content to simply infect cells that already express lots of ACE2 receptors. Instead, it actively hijacks the body’s own systems, tricking it into upregulating ACE2 receptors in places where they’re usually expressed at low or medium levels, including the lungs.
In this sense, Covid-19 is like a burglar who slips in your unlocked second-floor window and starts to ransack your house. Once inside, though, they don’t just take your stuff — they also throw open all your doors and windows so their accomplices can rush in and help pillage more efficiently.
The renin–angiotensin system (RAS) controls many aspects of the circulatory system, including the body’s levels of a chemical called bradykinin, which normally helps to regulate blood pressure. According to the team’s analysis, when the virus tweaks the RAS, it causes the body’s mechanisms for regulating bradykinin to go haywire. Bradykinin receptors are resensitized, and the body also stops effectively breaking down bradykinin. (ACE normally degrades bradykinin, but when the virus downregulates it, it can’t do this as effectively.)
The end result, the researchers say, is to release a bradykinin storm — a massive, runaway buildup of bradykinin in the body. According to the bradykinin hypothesis, it’s this storm that is ultimately responsible for many of Covid-19’s deadly effects. Jacobson’s team says in their paper that “the pathology of Covid-19 is likely the result of Bradykinin Storms rather than cytokine storms,” which had been previously identified in Covid-19 patients, but that “the two may be intricately linked.” Other papers had previously identified bradykinin storms as a possible cause of Covid-19’s pathologies.
Covid-19 is like a burglar who slips in your unlocked second-floor window and starts to ransack your house.
As bradykinin builds up in the body, it dramatically increases vascular permeability. In short, it makes your blood vessels leaky. This aligns with recent clinical data, which increasingly views Covid-19 primarily as a vascular disease, rather than a respiratory one. But Covid-19 still has a massive effect on the lungs. As blood vessels start to leak due to a bradykinin storm, the researchers say, the lungs can fill with fluid. Immune cells also leak out into the lungs, Jacobson’s team found, causing inflammation.
Coronavirus May Be a Blood Vessel Disease, Which Explains Everything
Many of the infection’s bizarre symptoms have one thing in common
elemental.medium.comAnd Covid-19 has another especially insidious trick. Through another pathway, the team’s data shows, it increases production of hyaluronic acid (HLA) in the lungs. HLA is often used in soaps and lotions for its ability to absorb more than 1,000 times its weight in fluid. When it combines with fluid leaking into the lungs, the results are disastrous: It forms a hydrogel, which can fill the lungs in some patients. According to Jacobson, once this happens, “it’s like trying to breathe through Jell-O.”
This may explain why ventilators have proven less effective in treating advanced Covid-19 than doctors originally expected, based on experiences with other viruses. “It reaches a point where regardless of how much oxygen you pump in, it doesn’t matter, because the alveoli in the lungs are filled with this hydrogel,” Jacobson says. “The lungs become like a water balloon.” Patients can suffocate even while receiving full breathing support.
The bradykinin hypothesis also extends to many of Covid-19’s effects on the heart. About one in five hospitalized Covid-19 patients have damage to their hearts, even if they never had cardiac issues before. Some of this is likely due to the virus infecting the heart directly through its ACE2 receptors. But the RAS also controls aspects of cardiac contractions and blood pressure. According to the researchers, bradykinin storms could create arrhythmias and low blood pressure, which are often seen in Covid-19 patients.
The bradykinin hypothesis also accounts for Covid-19’s neurological effects, which are some of the most surprising and concerning elements of the disease. These symptoms (which include dizziness, seizures, delirium, and stroke) are present in as many as half of hospitalized Covid-19 patients. According to Jacobson and his team, MRI studies in France revealed that many Covid-19 patients have evidence of leaky blood vessels in their brains.
Bradykinin — especially at high doses — can also lead to a breakdown of the blood-brain barrier. Under normal circumstances, this barrier acts as a filter between your brain and the rest of your circulatory system. It lets in the nutrients and small molecules that the brain needs to function, while keeping out toxins and pathogens and keeping the brain’s internal environment tightly regulated.
If bradykinin storms cause the blood-brain barrier to break down, this could allow harmful cells and compounds into the brain, leading to inflammation, potential brain damage, and many of the neurological symptoms Covid-19 patients experience. Jacobson told me, “It is a reasonable hypothesis that many of the neurological symptoms in Covid-19 could be due to an excess of bradykinin. It has been reported that bradykinin would indeed be likely to increase the permeability of the blood-brain barrier. In addition, similar neurological symptoms have been observed in other diseases that result from an excess of bradykinin.”
Increased bradykinin levels could also account for other common Covid-19 symptoms. ACE inhibitors — a class of drugs used to treat high blood pressure — have a similar effect on the RAS system as Covid-19, increasing bradykinin levels. In fact, Jacobson and his team note in their paper that “the virus… acts pharmacologically as an ACE inhibitor” — almost directly mirroring the actions of these drugs.
Medium Coronavirus Blog
A real-time resource for Covid-19 news, advice, and commentary.
coronavirus.medium.comBy acting like a natural ACE inhibitor, Covid-19 may be causing the same effects that hypertensive patients sometimes get when they take blood pressure–lowering drugs. ACE inhibitors are known to cause a dry cough and fatigue, two textbook symptoms of Covid-19. And they can potentially increase blood potassium levels, which has also been observed in Covid-19 patients. The similarities between ACE inhibitor side effects and Covid-19 symptoms strengthen the bradykinin hypothesis, the researchers say.
ACE inhibitors are also known to cause a loss of taste and smell. Jacobson stresses, though, that this symptom is more likely due to the virus “affecting the cells surrounding olfactory nerve cells” than the direct effects of bradykinin.
Though still an emerging theory, the bradykinin hypothesis explains several other of Covid-19’s seemingly bizarre symptoms. Jacobson and his team speculate that leaky vasculature caused by bradykinin storms could be responsible for “Covid toes,” a condition involving swollen, bruised toes that some Covid-19 patients experience. Bradykinin can also mess with the thyroid gland, which could produce the thyroid symptoms recently observed in some patients.
The bradykinin hypothesis could also explain some of the broader demographic patterns of the disease’s spread. The researchers note that some aspects of the RAS system are sex-linked, with proteins for several receptors (such as one called TMSB4X) located on the X chromosome. This means that “women… would have twice the levels of this protein than men,” a result borne out by the researchers’ data. In their paper, Jacobson’s team concludes that this “could explain the lower incidence of Covid-19 induced mortality in women.” A genetic quirk of the RAS could be giving women extra protection against the disease.
The bradykinin hypothesis provides a model that “contributes to a better understanding of Covid-19” and “adds novelty to the existing literature,” according to scientists Frank van de Veerdonk, Jos WM van der Meer, and Roger Little, who peer-reviewed the team’s paper. It predicts nearly all the disease’s symptoms, even ones (like bruises on the toes) that at first appear random, and further suggests new treatments for the disease.
As Jacobson and team point out, several drugs target aspects of the RAS and are already FDA approved to treat other conditions. They could arguably be applied to treating Covid-19 as well. Several, like danazol, stanozolol, and ecallantide, reduce bradykinin production and could potentially stop a deadly bradykinin storm. Others, like icatibant, reduce bradykinin signaling and could blunt its effects once it’s already in the body.
Interestingly, Jacobson’s team also suggests vitamin D as a potentially useful Covid-19 drug. The vitamin is involved in the RAS system and could prove helpful by reducing levels of another compound, known as REN. Again, this could stop potentially deadly bradykinin storms from forming. The researchers note that vitamin D has already been shown to help those with Covid-19. The vitamin is readily available over the counter, and around 20% of the population is deficient. If indeed the vitamin proves effective at reducing the severity of bradykinin storms, it could be an easy, relatively safe way to reduce the severity of the virus.
Other compounds could treat symptoms associated with bradykinin storms. Hymecromone, for example, could reduce hyaluronic acid levels, potentially stopping deadly hydrogels from forming in the lungs. And timbetasin could mimic the mechanism that the researchers believe protects women from more severe Covid-19 infections. All of these potential treatments are speculative, of course, and would need to be studied in a rigorous, controlled environment before their effectiveness could be determined and they could be used more broadly.
Covid-19 stands out for both the scale of its global impact and the apparent randomness of its many symptoms. Physicians have struggled to understand the disease and come up with a unified theory for how it works. Though as of yet unproven, the bradykinin hypothesis provides such a theory. And like all good hypotheses, it also provides specific, testable predictions — in this case, actual drugs that could provide relief to real patients.
The researchers are quick to point out that “the testing of any of these pharmaceutical interventions should be done in well-designed clinical trials.” As to the next step in the process, Jacobson is clear: “We have to get this message out.” His team’s finding won’t cure Covid-19. But if the treatments it points to pan out in the clinic, interventions guided by the bradykinin hypothesis could greatly reduce patients’ suffering — and potentially save lives.
NOTE: This article is pretty dense. I’m happy to answer any questions as best I can or make the appropriate referrals.
If these findings are verified, then it proves WHY athletes who make their living being the best by fractions of a percent are in danger of losing their careers and worse for those with undiagnosed CTE. Even the idea that some player with undiagnosed CTE could get COVID from a careless Titan and have his brain devastated is beyond the pale.
I agree that the Titans should be harshly dealt with up to and including going straight to ownership and letting them know that this is a forced sale level violation if they don’t take every drastic and immediate measure to get into and stay in compliance with all local, state, federal and league rules.
Wrt COVID19, the NFL needs to be the Not Fuckin-around League.
2020 has sucked enough. We don’t need losing football to be the shit cherry on the top of this giant shit sundae of a year…
Sports is the crucible of human virtue. The distillate remains are human vice.
A dummy’s guide to California 2020 ballot measures
By Eric Ting, SFGATE Updated 4:00 am PDT, Monday, September 21, 2020
You’ve seen the ads. But you’re not sure what any of these California ballot measures actually do.
Fear not! Here’s a handy, simple guide to each of the 12 propositions on the California ballot for the November general election. From affirmative action to overturning the highly controversial gig worker bill (AB-5), there are plenty of significant measures California residents will be voting on this fall. This guide is broken into three categories: 1. The big ones that interest groups are dumping millions of advertising dollars into, 2. The criminal justice ones, and 3. The rest.THE BIG ONES
Proposition 16
What it does: Allows the state and its public universities to discriminate or grant preferential treatment based on race, sex, ethnicity, or national origin in public employment, education, or contracting.
Major players for it: The University of California Board of Regents, Sens. Kamala Harris and Dianne Feinstein, and various Black Lives Matter-related advocacy groups.
Major players against it: A number of Asian American groups and Republicans in the California state Assembly.
Recent polling: 31% support, 47% oppose, 22% undecided (PPIC poll, Sept. 4-Sept 13.)
New poll finds shaky support for Proposition 16 to restore affirmative action in California (LA Times)
Proposition 16: Why some Asian Americans are on the front lines of the campaign against affirmative action (Mercury News)Proposition 15
What it does: Raises funds for schools and local governments by requiring commercial and industrial properties with more than $3 million in holdings to be taxed based on market value as opposed to purchase price. Does not impact homeowners.
Major players for it: Gov. Gavin Newsom, San Francisco Mayor London Breed, and the California Teacher’s Association.
Major players against it: California Chamber of Commerce, California Small Business Association and several taxpayers’ groups.
Recent polling: 51% support, 40% oppose, 9% undecided (PPIC poll, Sept. 4-Sept 13.)
Prop. 15 could raise billions for California, But who will pay? (NBC San Diego)
Governor’s endorsement of Proposition 15 disappoints Farm Bureau (Lassen County Times)Proposition 22
What it does: Classifies app-based drivers as independent contractors and not employees, which effectively kneecaps AB5.
Major players for it: Uber, Lyft, DoorDash and other similar services.
Major players against it: Sen. Kamala Harris, Attorney General Xavier Becerra, and several state Assembly Democrats.
Recent polling: 41% support, 26% oppose, 34% undecided (Redfield and Wilton poll, Aug. 9)
Uber and Lyft have poured millions of dollars into a November ballot measure to keep Calif. drivers paid as independent contractors (Business Insider)
Uber analyst expects California’s Prop. 22 to pass based on latest polling (Yahoo Finance)Proposition 21
What it does: Allows local governments to enact rent control on housing that was first occupied over 15 years ago.
Major players for it: Sen. Bernie Sanders, Democratic Socialists of America, Los Angeles chapter and various tenants’ groups.
Major players against it: Gov. Gavin Newsom, California Apartment Association and construction workers’ unions.
Recent polling: N/A
Bernie Sanders backs rent control, slams greedy landlords in new ‘yes on 21’ spot (Business Wire)
Opponents of rent control initiative say Prop. 21 backers violated Stolen Valor Act in ad (San Diego Union Tribune)THE CRIMINAL JUSTICE ONES
Proposition 25
What it does: Eliminates cash bail and gives judges the ability to determine whether a defendant should be released prior to a trial.
Major players for it: Gov. Gavin Newsom, several congressional Democrats and civil liberties groups.
Major players against it: Orange County Board of Supervisors and several groups affiliated with the bail bonds industry.
Recent polling: 39% support, 32% oppose, 29% undecided (UC Berkeley Institute of Government Studies poll, Sept. 13-Sept.18)
California’s cash bail system favors the rich. Would replacing it help people of color? (Fresno Bee)
Prop. 25 will replace cash bail with risk assessment, if passed (Daily Cal)Proposition 17
What it does: Restores voting rights to people with felony convictions who have been released from prison but remain on parole.
Major players for it: Sen. Kamala Harris, the ACLU of California and many state Assembly Democrats.
Major players against it: State Sen. Jim Nielsen (R-4) and the Election Integrity Project California.
Recent polling: N/A
LA County supervisors support proposition restoring voting rights to those on parole (CBS Los Angeles)
Alex Padilla: Why Prop. 17 will strengthen both voting rights and public safety (San Diego Union Tribune)Proposition 20
What it does: Adds several crimes to the list of violent felonies for which early parole is restricted. Would undo a series of reforms enacted between 2011 and 2016 aimed at reducing the state’s prison population.
Major players for it: Assemblyman Jim Cooper (D-9) and multiple law-enforcement-affiliated groups.
Major players against it: Former Gov. Jerry Brown, the ACLU of California and several criminal justice reform advocacy groups.
Recent polling: N/A
Grocery stores are pushing California to be tougher on crime (LA Times)
Opposition to Prop. 20 increases; opponents charge it’s a step backward for CA (Davis Vanguard)THE REST
Proposition 19
What it does: Allows homeowners over the age of 55, disabled or victims of a natural disaster to take existing, lower property tax rates to new homes anywhere in the state.
Major players for it: California Realtors Association, California Professional Firefighters and several local real estate groups.
Major players against it: Howard Jarvis Taxpayers Association.Recent polling: N/A
Links to learn more:
Prop. 19 debate: Funding for fighting wildfires or attack on Prop 13 tax protections? (CBS San Francisco)
Worried about fires? California ballot initiative could help you move to a new city (Sacramento Bee)Proposition 24
What it does: Expands the state’s consumer data privacy laws by creating a new state agency to enforce privacy laws, empowering consumers to order that businesses not sell their personal information, and increasing financial penalties on those who violate privacy laws.
Major players for it: Former Democratic presidential candidate Andrew Yang and several online privacy groups.
Major players against it: ACLU of California and the Consumer Federation of California.
Recent polling: N/A
Links to learn more:
Andrew Yang takes lead role in California data privacy campaign (Politico)
Prop. 24 seemingly seeks to expand internet privacy, critics say it won’t (Salinas Californian)Proposition 18
What it does: Allows 17-year-old Californians who will be 18 by the following general election to vote in primaries and special elections.
Major players for it: California Secretary of State Alex Padilla and Assembyman Kevin Mullin (D-22).
Major players against it: The Election Integrity Project California.
Recent polling: N/A
Links to learn more:
Alex Padilla: Vote yes on Prop. 18 to engage, energize and empower the next generation of voters (San Diego Union Tribune)
Thousands of 17-year-olds could vote in California primaries if initiative passes, study says (Sacramento Bee)Proposition 14
What it does: Issues $5.5 billion in general obligation bonds for the state’s stem cell research institute.
Major players for it: Californians for Stem Cell Research, Treatments & Cures and the University of California Board of Regents.
Major players against it: The Center for Genetics and Society
Recent polling: N/A
Link to learn more:
Prop. 14: There’s much, much more than meets the eye (Capitol Weekly)Proposition 23
What it does: Places several new regulations on dialysis clinics, including requiring an on-site physician, mandating increased reporting of dialysis-related infections, and not allowing clinics to close before obtaining consent from the state health department.
Major players for it: Californians for Kidney Dialysis Patient Protection
Major players against it: American Legion, California Medical Association and several veterans’ and health groups.
Link to learn more:
Prop. 23: Kidney dialysis clinic rules (Cal Matters)A Supercomputer Analyzed Covid-19 — and an Interesting New Theory Has Emerged
A closer look at the Bradykinin hypothesis[/b]Earlier this summer, the Summit supercomputer at Oak Ridge National Lab in Tennessee set about crunching data on more than 40,000 genes from 17,000 genetic samples in an effort to better understand Covid-19. Summit is the second-fastest computer in the world, but the process — which involved analyzing 2.5 billion genetic combinations — still took more than a week.
When Summit was done, researchers analyzed the results. It was, in the words of Dr. Daniel Jacobson, lead researcher and chief scientist for computational systems biology at Oak Ridge, a “eureka moment.” The computer had revealed a new theory about how Covid-19 impacts the body: the bradykinin hypothesis. The hypothesis provides a model that explains many aspects of Covid-19, including some of its most bizarre symptoms. It also suggests 10-plus potential treatments, many of which are already FDA approved. Jacobson’s group published their results in a paper in the journal eLife in early July.
According to the team’s findings, a Covid-19 infection generally begins when the virus enters the body through ACE2 receptors in the nose, (The receptors, which the virus is known to target, are abundant there.) The virus then proceeds through the body, entering cells in other places where ACE2 is also present: the intestines, kidneys, and heart. This likely accounts for at least some of the disease’s cardiac and GI symptoms.But once Covid-19 has established itself in the body, things start to get really interesting. According to Jacobson’s group, the data Summit analyzed shows that Covid-19 isn’t content to simply infect cells that already express lots of ACE2 receptors. Instead, it actively hijacks the body’s own systems, tricking it into upregulating ACE2 receptors in places where they’re usually expressed at low or medium levels, including the lungs.
In this sense, Covid-19 is like a burglar who slips in your unlocked second-floor window and starts to ransack your house. Once inside, though, they don’t just take your stuff — they also throw open all your doors and windows so their accomplices can rush in and help pillage more efficiently.
The renin–angiotensin system (RAS) controls many aspects of the circulatory system, including the body’s levels of a chemical called bradykinin, which normally helps to regulate blood pressure. According to the team’s analysis, when the virus tweaks the RAS, it causes the body’s mechanisms for regulating bradykinin to go haywire. Bradykinin receptors are resensitized, and the body also stops effectively breaking down bradykinin. (ACE normally degrades bradykinin, but when the virus downregulates it, it can’t do this as effectively.)
The end result, the researchers say, is to release a bradykinin storm — a massive, runaway buildup of bradykinin in the body. According to the bradykinin hypothesis, it’s this storm that is ultimately responsible for many of Covid-19’s deadly effects. Jacobson’s team says in their paper that “the pathology of Covid-19 is likely the result of Bradykinin Storms rather than cytokine storms,” which had been previously identified in Covid-19 patients, but that “the two may be intricately linked.” Other papers had previously identified bradykinin storms as a possible cause of Covid-19’s pathologies.
As bradykinin builds up in the body, it dramatically increases vascular permeability. In short, it makes your blood vessels leaky. This aligns with recent clinical data, which increasingly views Covid-19 primarily as a vascular disease, rather than a respiratory one. But Covid-19 still has a massive effect on the lungs. As blood vessels start to leak due to a bradykinin storm, the researchers say, the lungs can fill with fluid. Immune cells also leak out into the lungs, Jacobson’s team found, causing inflammation.
And Covid-19 has another especially insidious trick. Through another pathway, the team’s data shows, it increases production of hyaluronic acid (HLA) in the lungs. HLA is often used in soaps and lotions for its ability to absorb more than 1,000 times its weight in fluid. When it combines with fluid leaking into the lungs, the results are disastrous: It forms a hydrogel, which can fill the lungs in some patients. According to Jacobson, once this happens, “it’s like trying to breathe through Jell-O.”
This may explain why ventilators have proven less effective in treating advanced Covid-19 than doctors originally expected, based on experiences with other viruses. “It reaches a point where regardless of how much oxygen you pump in, it doesn’t matter, because the alveoli in the lungs are filled with this hydrogel,” Jacobson says. “The lungs become like a water balloon.” Patients can suffocate even while receiving full breathing support.
The bradykinin hypothesis also extends to many of Covid-19’s effects on the heart. About one in five hospitalized Covid-19 patients have damage to their hearts, even if they never had cardiac issues before. Some of this is likely due to the virus infecting the heart directly through its ACE2 receptors. But the RAS also controls aspects of cardiac contractions and blood pressure. According to the researchers, bradykinin storms could create arrhythmias and low blood pressure, which are often seen in Covid-19 patients.
The bradykinin hypothesis also accounts for Covid-19’s neurological effects, which are some of the most surprising and concerning elements of the disease. These symptoms (which include dizziness, seizures, delirium, and stroke) are present in as many as half of hospitalized Covid-19 patients. According to Jacobson and his team, MRI studies in France revealed that many Covid-19 patients have evidence of leaky blood vessels in their brains.
Bradykinin — especially at high doses — can also lead to a breakdown of the blood-brain barrier. Under normal circumstances, this barrier acts as a filter between your brain and the rest of your circulatory system. It lets in the nutrients and small molecules that the brain needs to function, while keeping out toxins and pathogens and keeping the brain’s internal environment tightly regulated.
If bradykinin storms cause the blood-brain barrier to break down, this could allow harmful cells and compounds into the brain, leading to inflammation, potential brain damage, and many of the neurological symptoms Covid-19 patients experience. Jacobson told me, “It is a reasonable hypothesis that many of the neurological symptoms in Covid-19 could be due to an excess of bradykinin. It has been reported that bradykinin would indeed be likely to increase the permeability of the blood-brain barrier. In addition, similar neurological symptoms have been observed in other diseases that result from an excess of bradykinin.”
Increased bradykinin levels could also account for other common Covid-19 symptoms. ACE inhibitors — a class of drugs used to treat high blood pressure — have a similar effect on the RAS system as Covid-19, increasing bradykinin levels. In fact, Jacobson and his team note in their paper that “the virus… acts pharmacologically as an ACE inhibitor” — almost directly mirroring the actions of these drugs.By acting like a natural ACE inhibitor, Covid-19 may be causing the same effects that hypertensive patients sometimes get when they take blood pressure–lowering drugs. ACE inhibitors are known to cause a dry cough and fatigue, two textbook symptoms of Covid-19. And they can potentially increase blood potassium levels, which has also been observed in Covid-19 patients. The similarities between ACE inhibitor side effects and Covid-19 symptoms strengthen the bradykinin hypothesis, the researchers say.
ACE inhibitors are also known to cause a loss of taste and smell. Jacobson stresses, though, that this symptom is more likely due to the virus “affecting the cells surrounding olfactory nerve cells” than the direct effects of bradykinin.
Though still an emerging theory, the bradykinin hypothesis explains several other of Covid-19’s seemingly bizarre symptoms. Jacobson and his team speculate that leaky vasculature caused by bradykinin storms could be responsible for “Covid toes,” a condition involving swollen, bruised toes that some Covid-19 patients experience. Bradykinin can also mess with the thyroid gland, which could produce the thyroid symptoms recently observed in some patients.
The bradykinin hypothesis could also explain some of the broader demographic patterns of the disease’s spread. The researchers note that some aspects of the RAS system are sex-linked, with proteins for several receptors (such as one called TMSB4X) located on the X chromosome. This means that “women… would have twice the levels of this protein than men,” a result borne out by the researchers’ data. In their paper, Jacobson’s team concludes that this “could explain the lower incidence of Covid-19 induced mortality in women.” A genetic quirk of the RAS could be giving women extra protection against the disease.
The bradykinin hypothesis provides a model that “contributes to a better understanding of Covid-19” and “adds novelty to the existing literature,” according to scientists Frank van de Veerdonk, Jos WM van der Meer, and Roger Little, who peer-reviewed the team’s paper. It predicts nearly all the disease’s symptoms, even ones (like bruises on the toes) that at first appear random, and further suggests new treatments for the disease.
As Jacobson and team point out, several drugs target aspects of the RAS and are already FDA approved to treat other conditions. They could arguably be applied to treating Covid-19 as well. Several, like danazol, stanozolol, and ecallantide, reduce bradykinin production and could potentially stop a deadly bradykinin storm. Others, like icatibant, reduce bradykinin signaling and could blunt its effects once it’s already in the body.
Interestingly, Jacobson’s team also suggests vitamin D as a potentially useful Covid-19 drug. The vitamin is involved in the RAS system and could prove helpful by reducing levels of another compound, known as REN. Again, this could stop potentially deadly bradykinin storms from forming. The researchers note that vitamin D has already been shown to help those with Covid-19. The vitamin is readily available over the counter, and around 20% of the population is deficient. If indeed the vitamin proves effective at reducing the severity of bradykinin storms, it could be an easy, relatively safe way to reduce the severity of the virus.
Other compounds could treat symptoms associated with bradykinin storms. Hymecromone, for example, could reduce hyaluronic acid levels, potentially stopping deadly hydrogels from forming in the lungs. And timbetasin could mimic the mechanism that the researchers believe protects women from more severe Covid-19 infections. All of these potential treatments are speculative, of course, and would need to be studied in a rigorous, controlled environment before their effectiveness could be determined and they could be used more broadly.
Covid-19 stands out for both the scale of its global impact and the apparent randomness of its many symptoms. Physicians have struggled to understand the disease and come up with a unified theory for how it works. Though as of yet unproven, the bradykinin hypothesis provides such a theory. And like all good hypotheses, it also provides specific, testable predictions — in this case, actual drugs that could provide relief to real patients.
The researchers are quick to point out that “the testing of any of these pharmaceutical interventions should be done in well-designed clinical trials.” As to the next step in the process, Jacobson is clear: “We have to get this message out.” His team’s finding won’t cure Covid-19. But if the treatments it points to pan out in the clinic, interventions guided by the bradykinin hypothesis could greatly reduce patients’ suffering — and potentially save lives.



