Multiple myeloma, a cancer of the plasma cells, is an incurable disease. Health care professionals are still not entirely sure what causes the condition, and when symptoms manifest they can be painful and put patients at significant risk for complications.
Recent studies have suggested that immunotherapies show promise for patients with multiple myeloma in boosting their immune systems against the condition, potentially improving their chances for longer-term survival. These treatments are not without risk, however. What have these studies found about boosting immunity with multiple myeloma?
Types of Immunotherapy
A March 2021 study in Cancers examined current and potential immunotherapies in the fight against multiple myeloma.¹ The researchers noted that while autologous stem cell transplantation is one of the most common treatments for young people with recently diagnosed multiple myeloma, it also carries the risk of increasing the production of inflammatory cytokines. And while allogeneic stem cell transplantation may be better for progression-free survival, it brings an elevated risk of treatment-related mortality.
The researchers believe that immunomodulators (IMIDs) like thalidomide and lenalidomide are crucial to improved treatment outcomes in multiple myeloma. They suggest that future studies may explore the effects of combining IMIDs with other multiple myeloma treatments. The investigators also note exciting potential breakthroughs such as the genetically modified T-cell chimeric antigen receptor T (CAR-T) and bi-specific T-cell engagers. In addition, they are hopeful that future innovations can help build up patient immunity. These include marrow-infiltrating lymphocytes (which are designed with the intention of entering bone marrow and exerting anti-tumor activity) and dendritic cell-based vaccines.
Another 2021 study, this one in Frontiers in Oncology, examined findings in the therapeutic benefits of attempting to restore immunity in patients with multiple myeloma.² The investigators concluded that approaches that focus on restoring immunity have great potential to improve a patient’s long-term control over their condition. However, challenges can accompany these immune-based strategies, including infection risk and blood typing interference. Like the researchers in the previous study, the investigators reiterated the importance of IMIDs like thalidomide and the potential for dendritic cell-based vaccines, as well as protein-based vaccines, peptide-based vaccines, and genetic vaccines.
Ultimately, the researchers in each study concluded that the potential for immunity-based strategies to help patients with multiple myeloma is an exciting possibility, and one that shows the greatest ability to help patients’ response to multiple myeloma while maintaining their quality of life.
One month ago, the Navajo Nation confirmed its first case of the Delta variant which is of great concern as this variant is identified as being extremely contagious with more severe symptoms. It is reported to be 60% more transmissible than the Alpha variant, and is being referred to as two to three times more transmissible.
Submitted | Mark Peterman Ethel Branch
It has a viral load 1000 times higher than previous strains, which contributes to its quick and easy spread to others.
The higher viral load contributes to more severe symptoms. This is especially problematic for unvaccinated individuals who don’t have the immunity-boosting protections of the vaccine. Indeed, more than 99% of recent deaths from COVID-19 are among the unvaccinated.
It’s so transmissible that even vaccinated individuals are contracting this strain, but vaccinated individuals only experience mild cold or flu-like symptoms, if any at all.
And it is possible that an infected vaccinated person with little to no symptoms can transmit the virus to someone else.
Sadly, our elderly (65 and over) and our immunocompromised remain at high risk because the vaccine merely boosts your existing immune response. Those with lower initial immune responses won’t have their immunity boosted as high as someone who starts with a higher immunity level.
So our elderly and immunocompromised should continue to take strong precautions like minimizing travel, social distancing, masking up and frequently hand washing/sanitizing – even if they are vaccinated.
The Delta variant is wreaking havoc nationally, driving a sharp spike in cases. More than 80% of these new cases are the Delta variant, so if you catch COVID-19 today, it’s very likely to be Delta.
So if you catch COVID-19 now, please adhere to strict precautions and isolate yourself from the broader community and your loved ones at home – especially unvaccinated children and the elderly and immunocompromised (even if they are vaccinated).
More recently, tribal nations have begun reconvening at national conferences and large gatherings in Delta variant hotspots, such as Nevada, currently a major hotspot.
This week, ’Vegas imposed a mask mandate but this is after many of our people visited unmasked last week for the RES and NIGA conferences.
The implications of this are tremendous. If you travelled to ’Vegas recently, please get tested to ensure you didn’t inadvertently bring the Delta variant home to your loved ones – even if you are vaccinated and experiencing no symptoms.
Some might ask, “Why get vaccinated if you can still get COVID?”
Quite simply, getting vaccinated could save your life. Almost all deaths from COVID-19 are among the unvaccinated.
Meanwhile, a vaccination will boost your immune system response to where you may never even realize you have COVID even if you catch it.
The pandemic is not over, despite how much we want it to be. Vaccination on Navajo has been largely successful, but there remain significant numbers of our people who remain unvaccinated. We need those folks to step forward now and vaccinate to protect our broader community.
As the U.S. stands on the verge of another devastating COVID-19 wave, we want the story of Navajo to be a story of strength and success, not another story of vulnerability and devastation. Herd immunity is critical to this success story. It can show how our community stepped up to protect our elders and immunocompromised.
Resilience to this pandemic is underscored by how quickly we are approaching herd immunity. We are currently hovering around 50% but we need to hit the 85% to 90% threshold.
To protect our communities, please try to shop locally where you are better protected with higher domestic vaccination rates. If you must shop off-reservation, consider that New Mexico has shown strong leadership and success in vaccinating their communities as compared to the other Four Corners states.
Also please refrain from traveling to Las Vegas until the uncontrolled spread of Delta is contained there and they achieve a much higher vaccination rate.
Call your loved ones to make sure they are fully vaccinated. Let’s encourage vaccination among the remaining adults who are unvaccinated and our younger people who are now eligible to be vaccinated.
A strong push to get our children vaccinated would advance our community vaccination effort tremendously.
Being fully vaccinated protects our babies, our elders, our immunocompromised and those who can’t access the vaccine. It may also save your life.
Refusing to vaccinate will only bring further devastation and we can’t afford to lose another precious Diné life to this virus. We have lost too many already.
This Delta super strain has the potential to thrust our country back into lockdown mode but the ability to mitigate the severity of this wave on Dinetah is in our hands.
Shi’ké doo shi’Diné’ doo shi’a?chini, keep your guard up. We are not through this storm yet.
Hold those you love close, make sure they are vaccinated, and continue following COVID-19 precautions.
Let’s all be good ancestors and do our part to protect our community so we as a community can continue along the beautiful path of success and wellness that we began in the spring.
Ethel Branch is interim executive director of Yee Ha’ólníi Doo, the Navajo & Hopi Families Relief Fund. She is former attorney general for the Navajo Nation.
There are several important regions on the spike protein where antibodies can bind. Many scientists have focused on the receptor-binding domain, or RBD, where the spike protein directly contacts ACE2. But antibodies can also bind elsewhere, including the fusion peptide, a region of the spike protein’s stem that helps the virus fuse with its target cell after the RBD contacts ACE2.
Greaney found that though people do make a mixture of antibodies (known as polyclonal antibodies), many coronavirus-blocking antibodies from previously infected people cluster at one region on RBD — a region that was quickly changing in the beta and gamma variants that began picking up steam early this year.
In contrast, she saw that antibodies generated by the Moderna vaccine had a broader binding pattern across the RBD.
Meghan Garrett, a graduate student in Hutch HIV expert Dr. Julie Overbaugh’s group, focused her attention on the segment of the spike protein that lies between its root and the RBD at its tip, a section that includes the fusion peptide.
She found that most polyclonal antibodies homed in on just a couple of sites; one in the fusion peptide and one in a linker region along the spike’s stem. But individual immune responses varied.
“Most people had responses to one site or the other, some had responses to both — but overall, the response was not uniform,” Overbaugh said.
Most people in Garrett’s study also had antibody targets sites that were unique to them as individuals, and not seen in other patients.
The findings illustrate how antibodies can target a variety of locations on the spike protein, Starr noted. Vaccine designs that prompt broad, not too-focused, antibody response may be harder for the virus to escape than those that generate strong, but overly focused immunity.
How long does immunity last?
How long immunity lasts will determine how often we’ll need to be re-vaccinated against SARS-CoV-2. Immunity’s “lifespan” depends on several factors, including the strength of the original immune response and how well the virus can evolve to evade it.
The coronaviruses that cause the common cold capitalize on mutation to reinfect us every three to five years. Rachel Eguia, a technician in Bloom’s lab, looked to the history of CoV-229E, one of the coronaviruses that causes the common cold, for insight into SARS-CoV-2. She traced the evolutionary tree of CoV-229E’s RBD back to the 1970s, showing that every few years, a dominant variant “wins” out and displaces other CoV-229E mutants.
Will her findings extend to the pandemic coronavirus?
“Although we can’t be certain, it is likely that new variants [of SARS-CoV-2] will sweep away old ones,” Bloom said. “That has already happened once in SARS-CoV-2 with the D614G mutation [now present in all variants of concern], and may now be in the process of happening again with the Delta variant.”
Those dynamics are not necessarily bad news, he noted.
“In some ways, these dynamics make vaccine updates easier than if all the variants are maintained,” Bloom said.
This is because if specific variants sweep old ones away, there’s a lot of similarity among viruses found around the world, which would make designing a vaccine that would be effective globally much less challenging. This is the case for influenza, but not HIV, Bloom said. The extreme diversity of HIV at any given moment is one reason that developing a vaccine for that virus has been so hard, he said.
Work from Kathryn Kistler, a graduate student in the lab of Hutch evolutionary biologist Dr. Trevor Bedford, found that the way that RBDs from CoV-229E and another common coronavirus, CoV-OC43, evolve suggests that they are being shaped by our immunity. According to the study, reinfection may be partly due to changes that make variants harder for our antibodies to recognize.
Eguia looked at the effects of viral mutation on immune recognition from a different angle. She tested the neutralization capability of plasma collected from people over the years to block variants of CoV-229E that arose at different points in time. She found that plasma was best at binding to CoV-229E variants that circulated shortly before the plasma was collected but became less and less potent when tested against CoV-229E variants that arose years or decades later. She also found that some individuals’ neutralization ability dropped sharply over time, while in others it ebbed slowly.
Some common coronaviruses can reinfect us because they just don’t trigger a particularly robust response to begin with. After a few years, our immunity fizzles and they can waltz back in. This timeframe may be accelerated if the variant is more virulent and able to infect more easily, which could be contributing to the success of delta and other variants of concern, Overbaugh said.
Scientists are still studying this question in SARS-CoV-2. It will take time to know how long-lasting our immune responses to natural infection or vaccination will be. Results are currently mixed — some studies report quick immune decay, while others report a normal amount (immunity always falls to some degree after an infection has been vanquished).
“I think the jury’s out. People are definitely looking and following the cohorts [of COVID-19 patients and vaccinated people] is going to be super critical,” Overbaugh said.
How do variants arise and escape the immune response?
But the persistence of our own immune response provides only one part of the answer to the question of our immunity to SARS-CoV-2 in years to come. The other part comes from the virus, and its natural ability to change over time.
When coronavirus’ genetic material is copied inside our cells, it’s not perfect — every so often the wrong genetic “letter” gets included. If this change helps the virus, it will get passed along as the virus is transmitted to new hosts. A few transmissions and a few varied letters later, and the virus can collect mutations that work together to help it.
The delta variant is a perfect example. It’s acquired mutations that are boosting its transmissibility and speeding its transit around the globe.
Viral mutations can also make it harder for the immune systems of vaccinated or previously infected people to recognize the virus. If the changes happen at key sites that our antibodies recognize, they could be enable a variant to slip past our protection. The good news is that even though the delta variant makes vaccine protection somewhat less robust, most vaccines still provide a lot of protection against severe disease, as well as symptomatic disease, from delta.
However, people — and our immune responses — vary, too. Our ability to meet viral variability with our own immunological variability could be good news as the vaccinated and previously infected are confronted with new SARS-CoV-2 variants. Because people tend to produce a slightly different complement of antibodies that target slightly different regions of the virus, a given variant’s path to escape will likely differ in different people, Overbaugh said.
“It actually means that if one virus takes hold, it may or may not actually be able to escape in everybody,” Overbaugh said.
The factors that shape how viral variants arise are complex. The fact that a virus mutates is only the first step. SARS-CoV-2 actually mutates at a slower rate than influenza, so it’s likely that its variants are arising from a combination of mutation and opportunity.
“People think that a lot of the really optimized variants, these variants of concern, happen in immunosuppressed people where the virus kept replicating,” Overbaugh said. “If it starts becoming like HIV, where it’s a persistent, replicating virus, it can adapt with the immune system. Then you start having this escape problem.”
If a person’s immune response shuts down their infection quickly, the virus has little opportunity to evolve. Hosts who can’t mount an effective defense allow the virus to incubate long enough to throw out new variants that may help the virus transmit better or cause more severe disease. In these instances, SARS-CoV-2 gets the same opportunity that HIV usually gets: a place to hunker down and continually spit out new mutants — some of which could give it the ability to escape antibody defenses.
This means that the virus has more opportunities to morph into a variant that can re-infect previously infected or vaccinated people as it continues to jump between never-infected, unvaccinated hosts.
There are a couple of factors, including how a virus interacts with the immune system, which help determine whether it will produce successful variants, said Greaney. In some cases, mutations that would allow a virus to escape immunity harm it too much in other ways. Measles is a case in point: it also mutates, but these mutations don’t allow it to escape our immunity. We’ve had the same measles vaccine for more than 60 years. The influenza vaccine, in contrast, must be updated yearly to accommodate that virus’ rapidly shifting proteins.
Determining how quickly SARS-CoV-2 escapes immunity will be key to determining how often boosters are needed. It’s too soon to say whether COVID updates will occur on a yearly basis, like flu shots, or on a longer timescale.
So how could various mutations in SARS-CoV-2 help it escape antibodies or immunity triggered by infection or a vaccine? By studying this question, scientists can reveal strategies that might make vaccine less susceptible to viral escape.
Greaney and Starr examined the effects of viral mutations on binding by both monoclonal antibodies — single antibodies that bind just one place on the virus — and polyclonal convalescent plasma, containing whatever mixture of antibodies were produced by a person infected with SARS-CoV-2. They tested mutations that aren’t yet found in prominent viral lineages, but could theoretically arise as the virus continues evolving.
(Neither Bloom’s nor Overbaugh’s groups work with whole viruses. Instead, they employ zoomed-in approaches that allow them to produce specific regions of the spike protein. Starr developed a system to cause yeast to produce the RBD, while Overbaugh’s lab looks at other areas of the spike protein produced by viruses that infect bacteria. Both teams use a technique called deep mutational scanning to introduce different mutations in their spike protein regions of interest.)
Greaney and Starr found that how much an RBD mutation affected antibody binding varied among patients. Even so, a few spots on the RBD grabbed most of the immune system’s attention — including a rapidly changing location called E484. This result was “a bit worrying,” Greaney said, because changes here were most likely to affect how well polyclonal plasma bound RBD — and it had already mutated in the novel coronavirus’ beta and gamma variants.
Garrett found less consistency among mutations that conferred antibody escape along the stem of the spike protein. These areas are less changeable among viral variants, which means they may be attractive additions to future vaccines designed to provide people with broader protection against many different variants, Overbaugh said.
If a variant is too different from its original strain, an updated vaccine may not boost prior immunity — instead, it may start a new immune response from scratch.
“That’s why we’ve been so interested in regions that are more [evolutionarily] constrained to add into the mix,” Overbaugh said. Among vaccine developers “there is interest in this idea for really a conserved target, maybe optimizing how the immune system responds.”
Both Overbaugh’s and Bloom’s groups have also begun asking similar questions of antibodies generated after vaccination against COVID-10. Garrett’s early results looking at the fusion peptide and linker region on the spike protein’s stem suggest that vaccines may elicit more-consistent immunity, but also direct antibodies to focus on a couple new sites.
Consistent with her findings that vaccination generates a broader antibody response against the RBD than infection, Greaney found that single viral mutations had less of an effect on neutralization by polyclonal antibodies from vaccinated people than from previously infected people. But a couple of mutations seen in variants of concern, including E484K in beta and gamma variants, and the L425R mutation seen in the delta variant, did reduce neutralization by vaccine-elicited antibodies by a modest-to-moderate amount, she said.
But vaccines aren’t the only anti-coronavirus strategy that are vulnerable to viral mutations. Therapeutic antibodies have been developed to treat COVID-19 patients in the hopes of lessening their disease. So far, five monoclonal antibodies have received emergency use authorization to be used as COVID-19 treatments, either individually or in two-antibody mixtures.
Greaney and Starr had begun their work on SARS-CoV-2 in 2020 by examining how SARS-CoV-2 mutations could affect neutralization by monoclonal antibodies. They’d found that many individual antibodies have different escape mutations, underlining how two-antibody mixtures could limit the potential for viral escape.
Unfortunately, Starr said, variants such as beta and gamma have arisen that combine two mutations that knock off both antibodies in one of the first authorized therapeutic antibody mixtures. And as evidenced by Greaney’s and his work, the same mutations that help SARS-CoV-2 shrug off natural immunity also help it dodge commercial antibodies. This means that some genetic changes could give the virus a two-for-one deal by rendering vaccines less effective and therapeutic antibodies ineffective in one evolutionary swoop.
Part of the reason that commercial antibodies may be so vulnerable to escape is due to how they were selected and developed, Starr noted. In the desperate rush to develop therapeutics that could help treat COVID-19, some companies chose the most potent to bring to the clinic. So far, some of the most potently neutralizing antibodies have also been those that target the virus’ most fast-changing regions. Apparently the RBD can change a lot while retaining its ability to connect with ACE2 (as Starr and Greaney showed in a separate study mapping mutations that affect how RBD interacts with ACE2).
How might we limit the coronavirus’s powers to escape immunity?
Starr wanted to seek out the antibodies and epitopes that could limit viral escape. (Epitopes are the structures to which antibodies bind.) Are there antibodies that can neutralize a broad swath of SARS-CoV-2 variants? If so, what epitopes would they bind, and how can we better identify these antibodies for therapeutic development?
To do this, he teamed up with researchers at San Francisco, California-based Vir Biotechnology, who had been studying coronaviruses since SARS-CoV-1 emerged in 2002. Starr established assays that would allow him to map which mutations allowed SARS-CoV-2 RBD to escape when pitted against 12 monoclonal antibodies. To study how well the antibodies retained their ability to neutralize across extremely divergent SARS-related coronaviruses, he also tested the antibodies against an array of RBDs from 45 SARS-related coronaviruses, including some isolated from bats and pangolins.
For the most part, Starr saw that antibodies traded potency for breadth: Those that neutralized SARS-CoV-2 RBD very effectively were less able to recognize RBD from more distantly related viruses. But included in the 12-antibody panel was one that bucked this trend.
This antibody, dubbed S2H97, had been isolated by VIR scientists from a patient who’d contracted SARS-CoV-2. And it was a standout, Starr said. Though the RBDs they tested ranged from 95% similarity to SARS-CoV-2, to just 60% similarity, and were separated by sometimes hundreds of years of evolution, this antibody bound them all. This included a divergent group of RBDs from bat coronavirus that have never spilled over into humans.
The key may be in what S2H97 targets, a so-called cryptic epitope: deeply hidden within the closed RBD, only accessible when RBD opens as it contacts ACE2.
Though rarely recognized by our immune system, this epitope is incredibly similar across SARS-related coronaviruses, Starr said. If an antibody binds this site, it can block a wide range of those viruses.
There are other antibodies that neutralize SARS-CoV-2 more potently than S2H97, but none that can neutralize so broadly. And S2H97’s potency is nothing to sneeze at: Starr and his collaborators at Vir showed that it protects hamsters against SARS-CoV-2 infection.
Starr hopes that findings like this inform future vaccine design by highlighting immune targets that could trigger broad, hard-to-escape immunity.
“If you know all the antibodies that are out there and what kinds you want, that can help you be a little bit more principled in designing vaccines that give you that type of antibody response [you’re looking for],” he said. “And we don’t know where SARS-3 will come from. If we can make antibodies or vaccines that can protect against the diversity of these SARS-related coronaviruses, that could be a long-term solution to preventing future spillovers.”
The findings could also be used to improve strategies for developing therapeutic antibodies for COVID-19 — whether or not you’re bearing future pandemics in mind, Starr said.
“Even if you only care about SARS-CoV-2, it can help to identify these epitopes that are not changing over moderate to long-term evolution,” he said. “They’re probably not going to change in short term evolution as well.”
Several of the antibody-binding spike regions that Garrett and Overbaugh identified fit this bill, and they’re now working to isolate the antibodies that bind at those sites.
Starr also argued that assessing potential antibodies using breadth in addition to potency could help companies identify more robust antibodies.
The emerging picture of how our immune systems interact with SARS-CoV-2 could help us develop better COVID-19 immunotherapies and better vaccines. Enduring antibody responses that target more than a few areas and focus on parts of SARS-CoV-2 that the virus can’t afford to modify may be the key to reducing how often we update vaccines and get booster shots. Such vaccines, combined with therapeutic antibodies that block a range of variants yet to come, could help make SARS-CoV-2 less of a threat in future years.
“We need a lot more antibodies,” Starr said. “The way that this virus is going to continue to evolve — you don’t know. … We need to develop a diverse arsenal of antibodies to target many epitopes.”
The projects discussed in this story were funded by a combination of federal grants, awards from private foundations and philanthropic donations.
There are over 200 different types of cancer, and all have different signs and symptoms. Cancer treatments vary depending on the type of cancer, but mainly include the use of surgery, radiation, medications to shrink and stop the progression of tumours.
However, researchers have discovered a new way to boost the immune cells that detect and destroy the disease.
Researchers at the University of Southampton have identified a potentially groundbreaking treatment that could strengthen the immune system’s ability to seek out and destroy cancer cells.
The findings shows that by restricting a group of cells known to impede immune responses, the treatment frees up other immune cells that go on to attack tumours and cancer cells.
Nulling Divecha, professor of Cell Signalling at the University of Southampton, said: “A patient’s immune system is more than able to detect and remove cancer cells and immunotherapy has recently emerged as a novel therapy for many different types of cancers.”
“However, cancer cells can generate a microenvironment within the tumour that stops the immune system from working thereby limiting the general use and success of immunotherapy.”
According to the researchers, Teffector cells (Teffs) in the immune system detect and kill cancer cells.
However, the efficiency of Teffs depends partially on another immune cell called T-regulatory cells (Tregs).
Tregs interact with Teffs and prevent them from performing to the best of their ability.
Professor Divecha explains: “Tregs carry out an important function in the human body because without them, the immune system can run out of control and attack normal cells of the body.
“However, in cancer patients, we need to the the Teff cells more freedom to carry out their job.”
While scientists have explored different avenues in their quest to find ways to inhibit Treg cells, they’ve noted that due to similarities in Teff and Treg cells, such efforts often lead to disruptions of both immune cell varieties.
However, from their study, the team found that inhibiting a family of enzymes in cells called PIP4K may successfully restrict Tregs without doing the same to Teffs.
The researchers isolated Tregs from healthy donors, then suppressed PIP4K protein in the cells using genetic technology.
They observed that when the cells lost their PIP4K protein, they stopped growing, responding to immune distress or causing disruption to the Teff cells.
Doctor Alessandro Poli, co-author of the study, noted: “This was surprising because PIP4Ks are in both types of T cells in similar concentrations, but out study shows that they seem to have a more important function for Tregs than Teffectors.
“Towards this end, we show that treatment with a drug like inhibitor of PIP4K could enable the immune system to function more strongly and be better equipped to destroy tumour cells.”
The people who live in the five Blue Zone regions have been found to be some of the longest-living people on the planet. In these areas, people not only regularly live into the triple digits, but their minds and bodies are both still working well. There are many lifestyle factors that Blue Zones founder, Dan Buettner, has found are shared by people in these regions—including low levels of stress, moving throughout the day, and having a sense of purpose. However, a significant amount of the research on longevity comes back to healthy dietary habits. The meals most frequently consumed in the Blue Zones aren’t loaded with processed ingredients or added sugars; rather, they consist of whole foods, particularly plants. This includes an array of healthy herbs, spices, and alliums shown to lower risk of disease and promote longevity.
Herbs in particular offer a one-two punch. They pack anti-microbial and antioxidant properties that boost heart health, immunity, and healing, plus they add flavor to food without any nutritional drawbacks (read: using herbs as a flavoring agent lowers your temptation to reach for the salt shaker again or to slather on a sugary sauce). While there is a lot of overlap—and all of these herbs are pretty common across the board within these five regions—some of them are particularly popular in the meals of the people that reside in each distinct zone.
Here are five herbs that are prevalent in the diets of the Blue Zone regions. Incorporating them into your cooking on the reg will give you a heart-healthy, antioxidant-rich boost linked to longevity. And in the shorter term, they’re guaranteed to make whatever you’re eating taste better, too.
5 Blue Zones herbs to add to your pantry for longevity (and flavor-boosting) benefits
Fennel can be used three different ways: the bulb is used as a vegetable, the fronds as an herb, and the seeds as a spice. Talk about an overachiever. “Fennel is rich in vitamins A, B, and C, packs plenty of fiber, plus it can act like a diuretic and helps to manage blood pressure,” says Lauren Harris-Pincus, MS, RDN, author of The Protein-Packed Breakfast Club. Both the bulb and seeds of the fennel plant contain the mineral manganese, too, which is important for enzyme activation, cellular protection, bone development, blood sugar regulation, and wound healing. Fennel also offers other minerals that are important for bone health (such as potassium, magnesium, and calcium) and has dozens of plant compounds that act as a potent antioxidant and anti-inflammatory agent.
When it comes to cooking, fennel is incredibly versatile—remember the three distinct and delicious edible parts mentioned above? You can serve fennel as a roasted veggie side dish, slice it raw into salads, or toast the fronts and/or seeds and puree them into dips and spreads. It also tastes delicious in soups and in pasta—just like they do in the Blue Zone of Sardinia. “Fennel is used in a Sardinian minestrone soup that is a lunch staple there. It’s made from seasonal vegetables, herbs, and beans,” Harris-Pincus adds. That’ll give you a nice dose of fiber and protein in addition to those immune-boosting properties.
“Oregano is rich in antioxidants and compounds proven to help fight bacteria,” says Harris-Pincus. The antioxidants can help prevent cellular damage by neutralizing disease-causing free radicals in the body and reducing inflammation. And on the antibacterial front, one study actually found that oregano was effective against 23 species of bacteria.
In addition to offering its own array of health benefits, oregano will boost the flavor of other nutrient-packed dishes, making plant-based foods like veggies and beans even more inviting. “This herb enhances the flavor of any tomato-based dish, vegetarian chili, fish, or beans.” Oregano’s rich, herbal flavor pairs perfectly with seafood, Greek salads, or in soups, moussaka, or whole grain pastas.
Sage is another option, which is similar in its properties to that of oregano. “There are properties in sage that may strengthen bones and play a role in lower rates of Alzheimer’s and dementia,” Harris-Pincus says. Try sage with turkey, chicken, or roasted mushrooms to enhance flavor. “Sage is a beautiful accompaniment to poultry, any bread dishes like stuffing, sauces, marinades, and even tea,” Harris-Pincus adds. Herbal tea is incredibly popular in the Blue Zone region of Ikaria, Greece, where locals drink it daily.
Rosemary not only tastes delicious in a wide array of dishes, but it is also a great source of iron, calcium, and vitamin B6. The herb has also been shown to boost cognitive health, increase memory retention, and help your immune system function at its best. This is because rosemary contains an ingredient called carnosic acid, which can fight off damage by free radicals in the brain, but it’s also due to its delicious (and potent) aroma. According to research outlined in Therapeutic Advances in Psychopharmacology, the scent of rosemary has the potential to improve your concentration, performance, speed, and accuracy and, to a lesser extent, your mood.
“Rosemary is a rich source of antioxidants, which can also help fight against aging and can help boost your immune system,” says Ilyse Schapiro MS, RD, CDN. “Try drinking rosemary tea or sprinkling rosemary on top of grilled vegetables,” says Schapiro. You can also use it in chicken, lamb, and salmon recipes with a squeeze of citrus.
“In addition, cilantro can aid digestion, help lower blood sugar levels, and reduce your risk of cardiovascular disease,” says Harris-Pincus. “Plus it is amazing in salsa, bean salads, and even in place of basil in a pesto.” It also tastes delicious on tacos, salads, enchiladas, grain bowls, in egg dishes, and so much more.
For centuries, garlic has been known to have medicinal properties, which make sense since it’s a staple in all of the Blue Zones regions, particularly Okinawa, Japan. While it isn’t technically an herb—garlic is a plant in the Allium (onion) family—it is used as a similar health-boosting flavoring agent in cooking. “Garlic has been shown time and again to help boost your immune system and fight against the common cold. It also can help reduce blood pressure and LDL cholesterol levels,” says Schapiro. In one study, 600 mg to 1,500 mg of aged garlic extract was shown to be as effective as the drug Atenolol at reducing blood pressure over a six month period.
Clearly, this ingredient is linked to longevity. Try adding garlic to some sautéed spinach and brown rice. Infuse it into olive oil and marinades, or use it in stir-fry recipes, as a seasoning for dips, or with roasted fish.
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WITH a deadly virus circulating the past year and a half, many people have been wondering how they can boost their immunity.
Masturbating is sometimes touted as a way to give the immune system a kickstart.
When Covid first started causing chaos in the Western world in March 2020, Google searches for “can masurbation boost immunity” went wild as people searched for ways to protect themselves.
Dr Jennifer Landa, a specialist in hormone therapy, suggests that indulging in some self-love might be exactly what you need to strengthen your body’s natural defence forces.
“Masturbation can produce the right environment for a strengthened immune system,” she said, according to Men’s Health.
But is there any evidence behind it?
One small but promising study of 11 men – who were awkwardly told to masturbate while researchers took blood tests – suggests so.
Published in 2004, it showed masturbation caused a temporary spike in immune cells, including killer cells that fight viruses.
An example is lymphocytes – white blood cells that fight foreign invaders, including the coronavirus.
The effect lasted for around 45 minutes after orgasm, according to the study by the Department of Medical Psychology, University Clinic of Essen, Germany.
The researchers wrote: “These findings demonstrate that components of the innate immune system are activated by sexual arousal and orgasm.”
It suggests getting friendly with your own hand could be the difference between catching a bug or not.
But Dr Jagdish Khubchandani, a professor of public health at New Mexico State University, told Medical News Today the size of the study was “not good enough” to be reliable.
And all the volunteers were young and fit men, meaning it can’t be applied to a general population who have varying degrees of health.
Other than that almost 20-year old study, there really is a lack of information on how masturbation impacts immunity, especially in women.
But experts say masturbation may be generally good for immunity through its indirect effects on the body.
Components of the innate immune system are activated by sexual arousal and orgasm
Researchers at University Clinic of Essen, Germany
Dr Khubchandani said it’s not easy to determine if masturbation causes a surge of immune cells itself, or if it’s due to a reduction in stress.
Orgasms in general help you relax, reduce stress, elevate mood and help you sleep better, all of which could arguably be key for keeping immunity prime.
In one study, published in the Frontiers in Public Health, almost half of men and women who masturbated before bed said they either got better sleep quality, or fell asleep quicker.
Meanwhile, research has shown orgasms trigger the release of oxytocin, also known as the “love hormone”.
It in turn can decrease levels of the stress hormone cortisol, which although has some benefits, such as fighting inflammation, is never good in high amounts.
Stress is thought to suppress the immune system, says Harvard Health, which can increase susceptibility to colds and other illnesses, potentially Covid.
Dr Felice Gersh, a gynaecologist and obstetrician who specialises in women’s health, said masturbation every day won’t prevent Covid.
“But you can say ‘It’s certainly not going to create harm’”, she told Mashable.
“I think the takeaway message is that there are no negatives from it,” she said.
Other studies have shown that masturbation can stave off prostate cancer in men and infections in women, likely due to how the genitals physically react to orgasm rather than because it bolsters immunity.
The immune system is a complex network with multiple lines of defences.
It’s strength varies from person to person, with factors like age, medication and diet largely contributing.
With all that said, if you want your immune system firing the way it should, you could try the following tricks:
Eat a healthy and balanced diet with plenty of fruit and veg
Exercise – the NHS says try and do 150 minutes of intense activity a week
Stop smoking and cut back on drinking
Minimize stress and maximise sleep
Take extra precautions like washing your hands regularly
Researchers headed by a team at the Perelman School of Medicine, University of Pennsylvania, have demonstrated how treating obese mice with a cytokine called thymic stromal lymphopoietin (TSLP) triggers significant abdominal fat and weight loss. The team’s studies found that, unexpectedly, the fat loss was notassociated with decreased food intake or faster metabolism. Rather, administering a viral vector that expressed the TSLP gene stimulated the immune system to release lipids through the skin’s oil-producing sebaceous glands.
“This was a completely unforeseen finding, but we’ve demonstrated that fat loss can be achieved by secreting calories from the skin in the form of energy-rich sebum,” said principal investigator Taku Kambayashi, MD, PhD, an associate professor of pathology and laboratory medicine at Penn, who led the study with fourth-year medical student Ruth Choa, PhD. “We believe that we are the first group to show a non-hormonal way to induce this process, highlighting an unexpected role for the body’s immune system.” The animal model findings, Kambayashi said, support the possibility that increasing sebum production via the immune system could be a strategy for treating obesity in people.
Obesity is a serious public health concern, and globally, more than 40% of adults are overweight or obese, the authors explained. Obese individuals face up to a sevenfold increased risk of associated chronic diseases, such as type II diabetes, fatty liver disease, heart disease, and certain cancers. Interestingly, recent studies have indicated that the immune system can regulate adipose tissue and its metabolic function. TSLP is a cytokine—a type of immune system protein—that plays a role in asthma and other allergic diseases. The Kambayashi research group has been investigating the expanded role of this cytokine in the activation of type 2 immune cells and expansion of T regulatory cells. Past studies have indicated that these cells can regulate energy metabolism, and the researchers hypothesized that treating overweight mice using TSLP could stimulate an immune response, which could subsequently offset some of the harmful effects of obesity. “We hypothesized that TSLP could counteract obesity and its associated complications by expanding type 2 immune cells and Treg cells,” they wrote.
“Initially, we did not think TSLP would have any effect on obesity itself,” Kambayashi further explained. “What we wanted to find out was whether it could impact insulin resistance. We thought that the cytokine could correct type 2 diabetes, without actually causing the mice to lose any weight.”
To test the effect of TSLP on type 2 diabetes, the researchers injected high-fat diet (HFD)-fed obese mice with a TSLP-expressing viral vector—TSLP-expressing adeno-associated virus serotype 8 (TSLP-AAV)—that would increase their bodies’ TSLP levels. They found that after four weeks, the TSLP vector injections had not only impacted on the diabetes risk in treated mice, but had actually reversed the animals’ obesity. While the control group of mice continued to gain weight, the weight of the TSLP-treated mice went from 45 g down to a healthy 25 g, on average, in just 28 days. “TSLP not only prevented but also reversed obesity,” the team commented.
Most strikingly, the TSLP-treated obese mice also exhibited decreased visceral fat mass, improved blood glucose and fasting insulin levels, as well as decreased risk of fatty liver disease. Visceral fat is the white fat (or white adipose tissue; WAT) that is stored in the abdomen around major organs, which can increase diabetes, heart disease, and stroke risk. “Compared with mice administered control-AAV, mice given TSLP-AAV displayed selective WAT loss, which protected against diet-induced and genetic models of obesity, insulin resistance, and nonalcoholic steatohepatitis (NASH),” the investigators wrote in their research article summary.
Given the dramatic results, Kambayashi assumed that the TSLP was effectively causing the mice to sicken, and reducing their appetites. However, further tests indicated that the TSLP-treated mice were actually eating 20–30% more than the control mice, and had similar energy expenditures, base metabolic rates, and activity levels, when compared to their non-treated counterparts.
To explain the weight loss, Kambayashi recalled a small observation he had previously ignored. “When I looked at the coats of the TSLP-treated mice, I noticed that they glistened in the light. I always knew exactly which mice had been treated, because they were so much shinier than the others,” he said.
Kambayashi considered a far-fetched idea—was their greasy hair a sign that the mice were “sweating” out fat from their skin? To test the theory, the researchers shaved the TSLP-treated mice and the controls and then extracted oils from their fur. They found that Kambayashi’s hypothesis was correct. The shiny fur contained sebum-specific lipids. Sebum is a calorically dense substance produced by sebocytes (highly specializedepithelial cells) in the sebaceous glands, and helps to form the skin barrier.
The finding confirmed that the release of oil through the skin was responsible for the TSLP-induced fat loss. “Our findings support a model in which TSLP overexpression causes WAT loss by inducing skin T-cell migration and increasing sebum hypersecretion,” they commented. “Thus, we establish a paradigm in which adipose loss can be achieved by means of sebum hypersecretion and uncover a role for adaptive immunity in skin barrier function through sebum secretion … Our data provide a therapeutic proof of concept that adipose loss can be achieved by secreting calories from the skin in the form of energy-rich sebum.”
To examine whether TSLP could potentially play a role in the control of oil secretion in humans, the researchers then examined TSLPand a panel of 18 sebaceous gland-associated genes in a publicly available dataset. This revealed that TSLPexpression is significantly and positively correlated with sebaceous gland gene expression in healthy human skin.
The study authors concluded that, in humans, boosting sebum release could feasibly lead to the weight loss effectively through the release of fat through the skin. “… although weight is unlikely to be controlled by sebum release at homeostasis, it is feasible that the selective loss of WAT could be achieved through “sweating fat” in humans by therapeutically shifting sebum release into high gear,” they stated. Kambayashi’s group plans further study to test this hypothesis. “I don’t think we naturally control our weight by regulating sebum production, but we may be able to highjack the process and increase sebum production to cause fat loss,” Kambayashi said. “This could lead to novel therapeutic interventions that reverse obesity and lipid disorders.”
One physician in Alabama made headlines last week after having to explain to severely ill patients that COVID-19 vaccines couldn’t help them after they’d developed the disease.
The vaccines work by helping your immune system learn to identify and fight off the coronavirus.
As a result, vaccines protect you from getting and transmitting the virus that causes COVID-19.
By now, you’ve probably heard of the many amazing things the COVID-19 vaccines can do.
They help stop the transmission of the virus, they keep people out of the hospital with serious cases, and most importantly, they help save your life and the lives of those around you.
But there’s one thing the vaccines can’t do — they can’t help fight COVID-19 if you already have it.
One physician in Alabama made headlines last week after having to explain this to severely ill patients.
In a story that went viral last week, Dr. Brytney Cobia begged followers on Facebook to get the vaccine as soon as possible in the wake of seeing new patients in critical care who didn’t have the vaccine.
COVID-19 vaccines are effective. They work by helping your immune system learn how to identify and fight the coronavirus.
As a result, the vaccines help protect you from getting and transmitting the virus that causes COVID-19.
“Vaccines work by helping your body build up antibodies prior to an infection,” said Dr. Teresa Amato, chair of emergency medicine at Long Island Jewish Forest Hills in New York. “The vaccine [reaches it’s most effective state] about 10 to 14 days after completion of the injections. That time period is when your body increases production of antibodies and makes some memory cells to help fight the virus if you are exposed.”
The vaccines can also help keep you from getting seriously ill if you do develop COVID-19, because your immune system is better able to attack the virus before it spreads or becomes more serious.
It’s important to remember that the vaccines don’t mean your chances of getting COVID-19 are 0 percent, and in extremely rare cases, vaccinated people have needed to be hospitalized or died from the disease.
However, the vast majority of people who are currently becoming sick enough to need hospitalization in the United States are people who haven’t been vaccinated.
“The goal of all vaccines, including the COVID vaccines, is to stimulate the body’s immune system and antibody response if the offending virus or bacteria were to enter the person’s system,” said Dr. Theodore Strange, interim chair of medicine at Staten Island University Hospital in New York.
This can be done in multiple ways.
One of them is giving people an inactive piece of virus messenger which then stimulates the person’s immune system to create antibodies in the event of exposure to the virus, Strange explained.
Think of it like a suit of armor. The vaccines provide a suit of armor before going into battle to help protect you against an attack. If you go into battle without a suit of armor and become wounded, putting the armor on after the fact will not help you.
“Vaccines are not acute treatments of the disease,” added Strange. “It takes the body time before the immune response is built up, including the fact that more than one vaccination may be needed to attain the immunity.”
The best thing we can do to keep ourselves and others safe from COVID-19 is to get the vaccine now.
If you contract the virus, the vaccine can’t help you. The safest and most responsible choice we can make is to become vaccinated because, as Cobia has seen time and time again, once it’s too late, it’s too late.
“As a physician, it is important to be nonjudgmental when asking a patient about their COVID-19 vaccine status. However, it has become increasingly difficult to see patients critically ill with a COVID-19 infection that declined a vaccine earlier. Once a patient is infected with the virus and is ill, a vaccine is ineffective at decreasing symptoms,” said Amato.
“It is unfortunate that people are hesitant about the vaccine,” she added. “I have personally cared for patients infected with COVID-19 who really regret not having gotten the vaccine sooner.”
And for those who are currently fully vaccinated, the CDC has recently updated its guidelines in light of the new Delta variant, which has proven to be even more contagious than previous versions.
Lung cancer treatment options will vary according to the type of lung cancer a person has, the stage of the disease, and the person’s overall health.
Surgery is a standard treatment for the removal of a cancerous tumor, while a person may require chemotherapy and radiation therapy to kill cancerous cells. In some cases, a doctor may recommend other treatment approaches, such as targeted treatments and immunotherapy.
This article provides a list of potential treatment options for lung cancer, including complementary and alternative treatments, and ways to seek emotional support. We also outline some of the latest research into cancer treatments.
The treatments for lung cancer include surgery, chemotherapy, radiation therapy, and other options.
Surgery may be an option in small cell lung cancer if the cancer is only in one lung and nearby lymph nodes.
Some different types of lung surgery include:
Wedge resection: Surgery to remove an area of an affected lung lobe.
Lobectomy: Surgery to remove the lung lobe that contains the tumor.
Pneumonectomy: Surgery to remove the entire affected lung.
Sleeve resection: Surgery to remove part of a large airway.
Doctors may also recommend treating some early stage tumors using video-assisted thoracic surgery (VATS). Since VATS uses smaller incisions, it may lead to fewer complications and a shorter hospital stay compared to other surgeries.
Following surgery, some people may also undergo additional treatment, such as chemotherapy or radiation therapy.
Chemotherapy drugs are medications that help to kill cancer cells or stop them from dividing. This helps to stop cancers from growing or spreading to other areas of the body.
A doctor may prescribe chemotherapy as a treatment for both small cell and non-small cell lung cancers.
Doctors may recommend chemotherapy as a standalone treatment or as an adjuvant therapy. An adjuvant therapy is one that a doctor prescribes before or after a primary cancer treatment to try to kill any remaining cancer cells.
The delivery method for chemotherapy will vary depending on the type of drug and the person’s general health. Examples of delivery methods include:
taking chemotherapy drugs orally
receiving injectable chemotherapy into a vein or muscle tissue
receiving chemotherapy directly into the target organ or area
There are many chemotherapy drugs. A doctor will work closely with a person to explore the most appropriate options.
Radiation therapy uses high-energy X-rays or other sources of radiation to kill cancer cells and help prevent them from dividing.
Radiation therapy is either internal or external:
Internal radiation therapy: Involves inserting a radioactive substance directly into or near the cancer.
External radiation therapy: Involves using a machine to deliver radiation into the target area from outside the body.
A combination of radiation therapy and chemotherapy is a standard treatment for small cell lung cancer.
When treating NSCLC, a doctor may recommend radiation therapy alone or in combination with surgery or other cancer treatments.
Targeted therapies are drugs that aim to stop the growth and spread of cancer cells. They do this by interfering with molecules on cancer cells that encourage the cells to grow and increase.
Targeted therapy may be an option in cases where it is possible to identify and target changes to the cancer’s DNA.
Targeted therapies have the following characteristics that help to differentiate them from standard chemotherapy drugs:
Chemotherapy drugs destroy rapidly dividing cells, regardless of whether those cells are normal or abnormal. Targeted therapies target molecular markers specific to cancer, thereby destroying only cancer cells.
Chemotherapy drugs are cytotoxic, meaning they kill tumor cells. Targeted therapies are typically cytostatic, meaning they prevent cancer cells from increasing.
Targeted therapies may cause fewer side effects than non-targeted therapies.
However, targeted therapy may not be suitable for all types of cancer. A doctor will discuss all possible options with the person seeking treatment.
Immunotherapy is a cancer treatment that activates the body’s own immune system to engage and kill cancer cells. It may be a treatment option for certain forms of lung cancer, such as advanced or recurring cancers.
Some immunotherapy drugs work by targeting molecules on immune cells, called “immune checkpoints” (ICs). The purpose of these ICs is to help the body identify and eliminate damaged or abnormal cells. Some cancers “trick” the ICs into letting them go undetected. Drugs called “immune checkpoint inhibitors” target ICs to help them identify and eliminate cancerous cells. Doctors give these drugs via an intravenous injection.
Researchers are currently working to identify other forms of immunotherapy.
Immunotherapy may not be an appropriate treatment option for all people or all types of cancer. Doctors will discuss all treatment options with the person who is seeking treatment.
Radiofrequency ablation is a procedure where doctors use high-energy radio waves to heat the tumor and kill the cancer cells. To do this, they insert a needle-like probe into the tumor through the skin using CT scans to guide it.
This procedure typically occurs in an outpatient setting. It involves the use of local anesthesia to numb the area where the doctor inserts the probe.
Doctors may decide to use radiofrequency ablation to treat people with small NSCLC tumors situated at the outer edge of the lungs, particularly if they are unable to have surgery.
Research into treatment for lung cancer and other types of cancer is ongoing. Clinical trials may reveal new drugs or drug schedules that will help in the fight against cancer.
Developments in immunotherapy practices may also lead to new treatments. Examples include:
cancer vaccines that may help the body eliminate certain cancer-specific proteins
adoptive T-cell therapy, which alters a type of immune cell called a “T cell” to help the body fight cancer
The American Lung Association notes that research into these treatments is still underway, and the drugs are not yet FDA-approved. Future research may help explore their possible use in lung cancer treatment.
The NCI provides a search tool to explore current clinical trials by cancer type. This may be beneficial for people who have received a recent diagnosis or have not responded to standard treatments.
Complementary treatment is a type of treatment a person may use alongside standard cancer treatment. Examples include using acupuncture or dietary supplements to reduce side effects from chemotherapy or radiotherapy.
Alternative treatments are treatments a person may use instead of standard cancer treatment. Examples include:
megadoses of certain vitamins or herbal preparations
If a person is curious about complementary or alternative therapies, they should talk with their doctor for further advice. The NCI notes that researchers may not have scientifically tested many complementary and alternative treatments. As such, it is not clear whether some treatments are safe or effective, or whether they may interfere with standard cancer treatments.
A person’s individual outlook with any cancer treatment can vary according to the following factors:
their general health
the type of cancer they have
the stage of the cancer
how well the person responds to treatment
whether the person experiences side effects or other complications
Some cancers are more treatable if a person detects and treats them in their early stages. As such, it is important that people receive regular check-ups from their healthcare professional, especially if they are experiencing concerning symptoms.
According to a 2021 review of cancer statistics, new methods of cancer detection and treatment have helped improve survival rates for NSCLC. Between 2009 and 2016, 2-year survival rates increased from 34% to 42%. Small cell lung cancer survival rates remained about the same, between 14–15%.
Lung cancer can be a difficult diagnosis for a person to come to terms with. According to the NCI, some common emotions a person may experience after receiving a cancer diagnosis include:
Doctors may recommend talking therapy or support groups to help a person process the emotional impact of a cancer diagnosis. Support may also be available for the person’s family and close friends.
If therapy or support groups are not an option, a person may benefit from reaching out to a close friend or family member. Talking to another person may help to ease the emotional load of a cancer diagnosis. Another person may also be able to offer practical support.
The NCI provides the following tips on coping with a cancer diagnosis:
Find ways to aid relaxation, such as reading or meditation.
Take part in enjoyable hobbies.
Perform gentle exercises, such as walking or yoga.
Focus on things a person can control, such as:
Lung cancer treatment can vary according to the type and stage of the cancer, as well as the person’s overall health. The way a person responds to or reacts to treatment will also play a role in the treatment options available to them in the future.
As with many cancers, detecting and treating lung cancer in its early stages may improve treatment outcomes.
Research is continually underway to explore new cancer treatments and treatment methods. Some people may be eligible to enroll in a clinical trial. People should work closely with their healthcare professional to determine the treatments that are best suited to their individual needs.
Many scientists say that vaccinated people probably won’t need booster shots anytime soon. Some are getting them anyway.
They are going to local pharmacies, other states or even other countries — anywhere where there is no record of them having been vaccinated — to get extra doses out of concern about the Delta variant or because they are worried their protection may be wearing off. The news on Thursday that Israel would give them to some older people seems likely to spur the trend.
“You can’t get enough, that’s my feeling,” said Ida Thompson, a retired geology professor who got a Pfizer shot a few weeks ago in the United States, months after receiving two doses of the AstraZeneca vaccine in Britain. “Bring it on.”
Dr. Thompson, who has six grandchildren, said that her decision to get a booster happened at the spur of the moment. While getting a coronavirus test at a pharmacy in Florida, where she was visiting family, she saw the pharmacy was offering vaccines.
When a pharmacy employee asked whether this was her first or second shot, she said first. “Since it was my first Pfizer,” Dr. Thompson said. “It was pretty clear to me that A.Z. plus Pfizer was a good idea,” she added, after reading about a study on the benefits of mixing AstraZeneca and Pfizer.
Does a booster provide extra protection?
Maybe, but it is too early to say, at least according to the U.S. Centers for Disease Control and Prevention. The C.D.C. has not authorized booster shots, but there is a growing consensus in the Biden administration that people who are 65 and older or who have compromised immune systems would benefit from a third shot.
Pfizer and BioNTech, the company that invented the vaccine and partnered with Pfizer to develop it, have reported that a third shot of their vaccine boosts the blood levels of antibodies against several versions of the coronavirus, including the highly contagious Delta variant. And some research suggests that mixing different types of vaccines could provoke a more robust immune response than a single brand alone.
Israel forged ahead on Thursday, with Prime Minister Naftali Bennett announcing that health care providers would begin giving third Pfizer shots to people 60 and older, starting on Sunday. They will need to have had their second doses more than five months ago to be eligible.
But some researchers and public health officials have cautioned that much of this data is preliminary and people should not assume boosters are necessary. Two shots of the Pfizer or Moderna offer robust and lasting protection against severe disease and death. Johnson & Johnson said the company’s data shows the vaccine was 85 percent effective against severe illness from the Delta variant and protected those who received it against hospitalization and death.
Dr. Krutika Kuppalli, an infectious-disease specialist and an assistant professor of medicine at the Medical University of South Carolina, said many of her patients who got the Johnson & Johnson vaccine have asked if they should get an additional shot. That vaccine, like AstraZeneca’s, is less effective than the mRNA vaccines.
It is not unreasonable for those patients to consider it, she tells them.
But Dr. Kuppalli said she explains to her patients that the data remains murky about potential side effects and the research is not definitive yet. “We actually want science to be driving our policies,” she said.
Terri Givens, a professor at McGill University in Quebec who received the Johnson & Johnson vaccine in March, said she was mulling a booster, but did not want to get ahead of the research.
“I don’t want to do it because it might work,” said Professor Givens, 56, who teaches political science. “I want to do it in a conscientious way where my doctor says it’s OK.”
Given the decentralized system for booking vaccines in the United States, several people said it was easy to get a booster, even though they were not technically allowed.
In its emergency authorizations of the vaccines, the Food and Drug Administration permitted only two doses of the Pfizer and Moderna vaccines and a single dose of the Johnson & Johnson vaccine. Before the C.D.C. could recommend boosters, the F.D.A. would have to change this authorization or fully approve the vaccines. If they were fully approved, then doctors would have more leeway to prescribe a booster for their patients.
In statements, Walgreens and CVS pharmacies, which have inoculated hundreds of thousands of Americans, said they were not offering booster shots.
Trevor Achilles, a 27-year-old who is vulnerable to Covid-19 because he received a kidney transplant, said he struggled to get an appointment at CVS for his third vaccine, even after his doctor recommended one in addition to the two doses of Pfizer he had already received.
He was finally able to make an appointment at a local pharmacy in Charlottesville, Va., where he lives, for a Moderna vaccine on Thursday. “I’m so excited,” said Mr. Achilles, a dishwasher. “I’m incredibly vulnerable and don’t want to take any chances as far as Delta.”
What about the ethics?
It falls into a gray area, experts said. Ideally, the leftover vaccines in wealthy countries should go to countries with lower inventory, rather than to people who want extra doses, Dr. Kuppalli said.
“Before we start talking about people getting a third dose of the vaccine, we need to make sure that everyone can get one dose of it,” she said.
Understand the State of Vaccine Mandates in the U.S.
Erin Matson, who got a Moderna shot on Sunday after having had one shot of the Johnson & Johnson vaccine, said she worried about the possibility that she could be taking a dose from someone who had not been vaccinated yet.
“I’m not taking it from somebody who would otherwise not have had a vaccine,” said Ms. Matson, 41, who lives in the Washington D.C. area. “I’m taking it from a landfill.”
Ms. Matson, the director of a nonprofit organization, said she was worried about getting the highly transmissible Delta variant and infecting her 8-year-old daughter. She got her booster shot at a pharmacy where, to her relief, no one asked her if she had already received a vaccine.
She said that anyone who got a booster shot was contributing to the ignorance about vaccine inequities.
“If I make a decision to go get a booster, I think I’m complicit in my government’s or the pharma companies’ decisions,” said Dr. Kelley, a bioethics professor at the Nuffield Department of Population Health at the University of Oxford. “I don’t think we can easily separate out the individual decisions from these kind of more policy-level decisions.”
Another bioethicist, Hon-Lam Li, the deputy director of the Chinese University of Hong Kong’s center for bioethics, said he saw a more important issue: It’s arguably unethical to avoid vaccination, because that endangers the lives of others. He said he did not see ethical issues in cases where patients were vulnerable or where physicians recommend a booster.
And what about a fourth shot? Dr. Thompson, the retired geologist in Edinburgh, said that she would consider it when she goes back to Florida in a few months.
“If I thought that would improve my immunity even more,” she said, “I would certainly do that.”