Homesteading: Mason Jars Mania

By JGM:There are a few inventions that quietly change the trajectory of how people actually live, not in some abstract, technological sense, but in the very practical question of whether you are going to eat well in February. The plow is one. Indoor plumbing ranks pretty high, especially if you have ever hauled water in the cold and had an existential conversation with yourself about your life choices. And then there is the lowly Mason jar, which looks so simple it almost feels like it should not count, except that once you have lived with a collection of Mason jars, you realize that you may not be able to function without them.Before 1858, preserving food was less a system and more an act of faith. People used wax, corks, cloth, and a fair amount of optimism. Sometimes it worked. Sometimes it very much did not. You could do everything right and still open a jar months later to discover that nature had taken a different view of your plans. When your winter food supply depends on that jar, this is not a minor inconvenience. This is the difference between comfort and scarcity, between a full pantry and the anxious recalculation of how long the remaining potatoes will last.Into that world stepped John Landis Mason, a New Jersey tinsmith who, in 1858, patented what now seems almost embarrassingly obvious. A threaded glass jar with a screw-on lid that could actually seal. That was it. No grand industrial system, no complicated mechanism, just a better way to keep air out and food preserved. It is the kind of idea that makes you wonder why it took so long to arrive, which is usually a good sign that it is both simple and transformative. Once that seal became reliable, everything else followed. Food could be stored with confidence. Households could plan ahead.As the country expanded and refrigeration was still a distant luxury, the Mason jar moved from clever invention to absolute necessity. Homesteaders, farmers, and anyone living even slightly removed from regular markets depended on it. This was not about aesthetics or hobby canning. This was about taking a seasonal glut and turning it into a year-round food supply. The jar became a kind of multiplier. It allowed you to grow more than you could immediately eat and trust that the excess would not be wasted. On a working farm, that is the difference between abundance and loss.By the late nineteenth century, companies began to recognize what Mason had started, and none more effectively than the Ball Corporation. They did not invent the jar, but they scaled it, standardized it, and put it into the hands of ordinary households across the country. They refined the design, moved away from zinc lids and unreliable gaskets, and eventually settled on the two-piece lid system we still use today. It is one of those rare cases where a design reaches a point of near-perfection and then simply stays there. If you have ever stood in a quiet kitchen listening for that small metallic ping as a lid seals, you know that this is not just a sound. It is a signal that the work you just did will hold, that the food you put up will be there when you need it.Pressure canning (using jars under pressure) really took off in the 1910s–1940s, but theidea of routinely putting mason jars inside pressure cookersbecame more widespread among home users in the mid-20th century, especially in the 1930s–1960s, when home pressure canners became common.The importance of the Mason jar became even more obvious during the World Wars, when households were encouraged to plant Victory Gardens and preserve what they grew. This was not framed as a quaint domestic activity. It was positioned by the US government as a national resilience strategy. They even had programs to teach America how to can, and pressure cookers became a mainstay. Millions of families participated, producing and storing a meaningful portion of their own food. Shelves filled with jars were not decorative. They were a distributed, decentralized food system that reduced pressure on supply chains and increased stability at the household level. It is a lesson that tends to get rediscovered every time systems become strained.There is another benefit to the simple mason jar. The home canning and drying of food generally misses some of the “greatest hits” of the industrialized chemical food world listed below:Sodium benzoatePotassium sorbateCalcium propionateSodium nitriteBHT / BHA / TBHQEDTAFast forward to the present, and despite all of our modern conveniences, the basic design has not changed. We have larger refrigerators, global logistics networks, and more ways to outsource our food than at any point in history, and yet the same glass jar with a simple lid still does its job better than almost anything else.On our farm, jars are not a novelty. They are part of the operating system. Tomatoes line up on shelves in late summer; berries and apples are freeze-dried and air-dried; cucumbers become pickles; chopped vegetables and berries are placed in mason jars and frozen; dry goods are transferred into mason jars to keep microplastics away, and raw milk and iced tea are stored in half-gallon jars, which take up the refrigerator shelves. There is a rhythm to it that does not change much from year to year. Plant, grow, harvest, preserve, repeat.What no one really explains at the beginning is that jars have a way of multiplying. You start with a reasonable number, which feels entirely under control. Then you realize that “a reasonable number” is not actually enough. Then you begin acquiring them in cases, then in whatever quantity happens to be available when you find them.Every glass jar that enters the house becomes a candidate for reuse. Store-bought pasta sauce suddenly looks less like dinner and more like future infrastructure. And if someone offers you a box of old blue Ball jars from a relative’s basement, you will accept them with a level of enthusiasm that might concern people who do not understand what they are looking at.There is also the matter of labeling; if you are not careful, it will begin with admirable discipline and end in something closer to educated guesswork. Early in the season, everything is clearly marked, dated, and organized. By mid-summer, you are writing notes on lids in whatever marker happens to be nearby. By winter, you are opening jars with a mixture of curiosity and caution, trying to remember whether this particular batch of something was from last year or the year before. It is a small reminder that even the most well-intentioned systems have a way of drifting.A few years back, I discovered chalkboard labels, and those have worked well for me. They are reusable, although not if exposed to the rigors of a dishwasher.Food PreservationMore than anything, jars force a certain relationship with time. You cannot rush the process. You cannot decide that preserving food would be more convenient next week. The work happens when the food is ready, which is often when it is hot, busy, and you would rather be doing almost anything else. And yet, months later, standing in a cold kitchen in the middle of winter, opening a jar that you filled yourself, there is a clarity to the system that makes perfect sense. This is what it looks like to move effort forward in time. This is what it looks like to turn a moment of abundance into a period of stability.So yes, at one level, it is just a jar. But it is also a tool that quietly shifts the balance of control back toward the household. It allows you to step slightly outside the system's constant churn and build a small buffer of your own. A shelf full of jars is not just visually satisfying. It is a record of work done, of planning carried through, of a season captured and held for later use.  It is a jar of saved resources, both grown and store-bought. It says, in a very understated way, that you are just a little bit independent of the outside world.Glass, a lid, and a seal. It is hard to imagine anything simpler. It is even harder to overstate how much difference that simplicity has made.Malone News is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.Thanks for reading Malone News! This post is public so feel free to share it.ShareThe “maintenance-free” gardenIt has been a busy March on the farm, which is to say everything needs fixing at once and yet I am somehow behind on my gardening - yet planting has hardly started.When we built the Valley House, where we live, we had a brilliant idea. Take the 14 x 55 strip outside the front of the house and make it “maintenance free.” You already know where this is going.First came the dirt. Fifty to seventy five tractor bucket loads of compost and soil to build the grade up against a four foot foundation. Days of work. The kind that makes you question your life choices while reaching for coffee with arms that no longer function properly.Then came the “solution.” Heavy duty landscaping cloth, seventy five blue rug junipers, and a thick layer of mulch. Permanent ground cover. No mowing. Clean. Tidy. We even added dwarf blueberries to make it more than just a pretty face.It has been a disaster.The junipers have chosen not to participate. Too hot, too dry, wrong pH, or perhaps a general objection to the entire plan. Meanwhile the mulch turned into soil, the cloth turned out not to be a barrier, and the weeds moved in like they had been invited.And not polite weeds. Aggressive, enthusiastic weeds. The kind that make eye contact while you pull them and promise to return.I swear that I have spent more time weeding that “maintenance free” strip than the entire farm combined.So, over the winter, we came to a simple conclusion. If I am going to weed anyway, I would at least like to eat the results.We are turning it into a no till kitchen garden.Step one has been removing the landscaping cloth, which is now fused to a network of roots underneath it. This involves digging, cutting, and wrestling out massive sections like some kind of agricultural CrossFit. I have gone through an entire pack of razor blades just trying to cut the stuff into pieces I can move. One dump run down, one more to go.Sadly, local labor seems non-existent or at least not willing to get into digging in the dirt in a meaningful way. So, “my project - my back”, time will tell whether the trade-off is worth it.Next comes twenty tons of compost and old river sand, carefully worked into a space that our tractor barely fits into. Then raking. Then planting.There will still be weeds. Of course there will be weeds. But now there will also be tomatoes.The plan is clover between rows, vetch in the fall, and slowly building an actual living system instead of whatever that previous experiment was supposed to be.In other words, after years of trying to eliminate maintenance, we have decided to farm it instead. Progress.And not everything else is perfect either. Some of the fencing looks like the horses have been politely but firmly leaning on it to reach greener grass. The roads, once gravel, are again aspiring to be dirt. Fortunately, road grading is one of Robert’s domains, a skill I have wisely avoided acquiring.So that is March. Things break, plans fail, weeds soon will outsmart us again come May, and we try again.But this time, at least, the failure might come with dinner.Next week, we will be in Dallas at CPAC.But I, at least, am home on the farm today.  Robert left at 3:45 AM to catch an early jet to go to Scottsdale, AZ to be on Aaron Siri’s podcast.  He will be flying home tomorrow.  I already miss him and it isn’t even 11:00 AM yet.So, today is a cold, nasty day in Virginia, hopefully one of the last of this winter.  I am heading over our office across the yard to do more writing and hang out with the dogs. Mostly, so that I can get a fire going in the woodstore. Later, I plan to make butter and yogurt - and this week, I started liming eggs (preserving eggs in lime water for future use).  Putting up eggs is little early for next winter, but the girls are in production mode. And guess what, those big half gallon mason jars are perfect for preserving eggs!EECKK!  I need to buy more mason jars!Stay warm everyone!

Summary: and "maintenance-free" gardening


Is Omitting Data from a COVID-19 Study Conclusion a Lie?

“OpenSAFELY: Effectiveness of COVID-19 Vaccination in Children and Adolescents”Epidemiology37(1):p 141-151, January 2026Everyso often, a study comes along that is held up as proof of something big. Safety. Effectiveness. Consensus. “The science is settled,” as they like to say, right before quietly updating the footnotes.The Study, the Fine Print, and the Part Nobody Talks About:This one is a large OpenSAFELY cohort study out of England looking at COVID-19 vaccination in children. Big dataset. Clean methods. Peer-reviewed. The kind of thing that gets cited with confidence and read… well… less carefully.¹So let’s read it carefully.Because like most things in modern medicine, the story isn’t in the headline. It’s in the middle. And sometimes, it’s hiding down near the bottom where the tables live.First, the Big Picture (and the Timeline That Matters)The study evaluates children aged 5 to 11 and adolescents aged 12 to 15 who received the Pfizer vaccine, comparing them to unvaccinated peers across outcomes like infection, emergency visits, hospitalization, and safety signals.¹But here’s the part that tends to get lost.This data comes from an earlier phase of the pandemic.A time when:Population immunity was lowerVariants were differentPublic health systems were still operating under elevated concernEven in that earlier window, the results were striking in their smallness.Across all analyses:No COVID-19-related deathsFewer than seven critical care admissions¹In a national dataset, that’s not just low risk. That’s vanishingly rare, as in non-existent, given that critical care admissions are almost universally in children with severe pre-existing conditions.Vaccination showed:Very modest, short-term protection against infectionSome reduction in ER visits and hospitalizations¹But these benefits are layered on top of outcomes that were already uncommon.Now fast forward to today.We have:Widespread prior infectionHybrid immunity across much of the populationVariants that tend to produceless severe disease in children²Which means the already low baseline risk seen in this study has likely declined even further.So when we talk about benefit, we have to ask an uncomfortable but necessary question.Benefit relative to what, and when?Now We Get to the Part That Lives in the TablesThis is where things get more interesting.Because while the benefits are modest and contextual, the safety signal is concrete.From the paper:Myocarditis and pericarditis occurred only in vaccinated individuals.Rates were:27 cases per million after the first dose10 cases per million after the second dose¹These are rare events. No question. But they are measurable. And they are not randomly distributed.All cases occurred in the vaccinated group.In any other setting, that pattern would prompt deeper scrutiny, not quieter placement.The Broader Context They Don’t EmphasizeAnd importantly, this finding does not stand alone.Across multiple studies and surveillance systems, a consistent pattern has emerged:Myocarditis israre, but realAlmost universally,  it occurs after mRNA vaccination, but not in unvaccinated populationsIt is most common inyounger males, particularly after the second dose³So this paper isn’t introducing a new signal.It is quietly confirming an existing one, in a population where the underlying disease risk is already very low.Furthermore, there is also a subtle shift in tone when you move from the results into the discussion. The authors cite studies suggesting that children can experience illness as severe as adults, which is technically true in isolated cases, but sits awkwardly next to the vast numbers of studies that show differently, that they don’t cite, and their own data showing no deaths and almost no critical illness.At the same time, cardiac inflammation following vaccination is described as “mostly mild,” which redirects attention away from the more basic observation that these events occurred in the vaccinated group.We are repeatedly told that myocarditis following mRNA vaccination in children is “mild.” That word does a lot of work. Yes, many of these kids are discharged from the hospital within a few days, and yes, they generally survive the acute event. But when you actually read the recent peer-reviewed science, a different story emerges.Recent peer-reviewed studies show that a substantial proportion of these children do not simply bounce back to baseline. In the MACiV multicenter cohort study, cardiac MRI evidence of myocardial injury was present in the vast majority at diagnosis and persisted in a significant fraction months later (4). The German MYKKE/PedMYCVAC study found that nearly half of pediatric patients still had objective cardiac abnormalities at follow-up, even when symptoms had resolved (5).Other smaller series report the same pattern: clinically “recovered” children with lingering signs of myocardial injury on imaging (6). So while the initial presentation is often described as mild, the biology suggests something less reassuring.Calling this uniformly mild glosses over persistent myocardial involvement that we do not yet fully understand, and it substitutes a short hospital stay for a long-term answer that, at this point, simply does not exist.It is a familiar pattern. Potential harms are softened by language, while potential disease severity is emphasized through selective citation. Neither statement is false, but together they shape a narrative that feels more certain than the underlying data actually supports.So, Why Isn’t This in the Conclusion?At this point, you start to see the difference between reporting data and telling a story.There are a few reasons this doesn’t make the headline.And this is the part you only notice after reading enough of these papers: the study is framed within a population-level benefit model rooted in an earlier pandemic context.When that is your anchor, that these vaccines are “safe and effective,”  the narrative naturally emphasizes even small reductions in disease and treats rare harms as secondary. When the peer-review process requires that you emphasize safety of the vaccine over data, you end up with results being buried - deep in the data tables.So the myocarditis signal ends up exactly where you would expect:In the data.But not in the conclusion.What This Study Actually Tells Us (Then vs Now)If you strip away the framing, the picture becomes clearer.During the study period:Severe COVID outcomes in children were already extremely rareVaccination offered modest, temporary protectionIn today’s environment:Baseline risk is even lowerPopulation immunity is higherThe marginal benefit is likely smaller than what was measuredAnd across both periods:A measurable signal of cardiac inflammation appears in the vaccinated group only, consistent with broader literatureThis is not a dramatic conclusion. It’s a balanced one.Which may be why it doesn’t get emphasized.But then, this is also a paper that manages to get the words “safely” and “Effectiveness” (you know the drill by now, (“safe and effective”) into the very title.  That phrase is ingrained in the reader's brain from years of propaganda. Biasing them before they even read a single sentence.ConclusionThis study does not show what many in the medical and scientific communities assume it does.It shows a pediatric population with an already low risk of COVID-19, a modest and very short-lived vaccine benefit when COVID-19 was at its most virulent, and a measurable rate of cardiac inflammation associated with vaccination.It also shows how easily context can shift the interpretation.When the baseline risk declines, the relative importance of rare adverse events increases. Because vaccines are given out universally - without question or hesitation by medical health professionals, pharmacies, and clinics, such adverse events change the risk/benefit ratio completely.Because states all over the United States are still insisting that mRNA COVID-10 injections be injected into the arms of children universally. And they justify this by citing peer-reviewed literature such as this, which hides the data in plain sight.The question, and I think we all know the answer, is no longer simply whether something works. But what are the real risks, and are they being evaluated correctly by public health officials, particularly in the “blue” states, where tribalism has been substituted for public health?It is about whether it meaningfully changes outcomes in a population where serious results from the virus are almost nonexistent, and whether we are willing to discuss both sides of that equation with equal clarity.Especially the parts that don’t make it into the conclusion.Malone News is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.Thanks for reading Malone News! This post is public so feel free to share it.ShareReferencesOpenSAFELY Collaborative. “Safety and Effectiveness of BNT162b2 COVID-19 Vaccination in Children and Adolescents.”PMC(2025).https://pmc.ncbi.nlm.nih.gov/articles/PMC12643559/Zimmermann, Petra, and Nigel Curtis. “Why Is COVID-19 Less Severe in Children? A Review of the Evidence.”Pediatric Infectious Disease Journal39, no. 12 (2020): 1103–1105. (and subsequent updates on variant severity trends)Patone, Martina, et al. “Risks of Myocarditis Following COVID-19 Vaccination or SARS-CoV-2 Infection.”Nature Medicine28 (2022): 410–422.Truong DT, Dionne A, Muniz JC, et al.Clinically suspected myocarditis temporally related to COVID-19 vaccination in adolescents and young adults: the MACiV multicenter study.EClinicalMedicine. 2024; (details include persistent late gadolinium enhancement on follow-up cardiac MRI).Knöchelmann A, et al.Course of myocarditis after COVID-19 vaccination in children and adolescents: results from the MYKKE/PedMYCVAC study.American Heart Journal. 2024.Dionisi-Vici C, et al.Short-term follow-up of myocarditis after COVID-19 vaccination in pediatric patients.Pediatric Infectious Disease Journal. 2023.By: JGM

Summary: or just an oversight? You decide...


Malone Busted: his Anemol Farm Message to the World

Following the turmoil of the recent injunction against the CDC’s Advisory Committee on Immunization Practices (ACIP), and hisresignation from that body, Dr. Robert Malone’s Substack was uncharacteristically silent on the affair. Instead, he penned an article entitled “Homesteading: The Great Unlearning:We all must tend the garden”which concludes:“If there is a way forward, it is not new. It is a return. A return to keeping the ground covered. To feeding the soil, not just the plant. To use living roots as the primary tool. And to accept that this is not a project with an end date.”Malone News is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.Astute readers will realize that “Malone” is an anagram for “Anemol.” Was there a hidden message. We asked venice.ai this question:“Read the article at https://www.newser.com/story/386079/cdc-vaccine-adviser-quits-over-too-much-drama.html about Robert Malone and then read his recent substack at https://www.malone.news/p/homesteading-the-great-unlearning. Consult other works written by or about him. Explore the hypothesis that his article on tending the garden is his allegorical manifesto, a la Animal Farm, on how the science, business and politics of medicine must be reformed, not only from the perspective of his erstwhile opponents, but also his allies, some of whom he appears to differ with now. Present your discussion by parsing Malone’s garden piece into its major verbatim themes with a side-by-side summary of what he actually says and your presumed allegorical interpretation.”Venice Response:Based on my analysis of the provided articles and Robert Malone’s broader body of work, I’ll explore the hypothesis that his homesteading piece serves as an allegorical manifesto for reforming medicine, science, and politics. Here’s my side-by-side parsing of the major themes:Theme 1: The Problem of Degraded SystemsWhat Malone Actually Says:“The problem with regenerative gardening or farming is that results don’t happen overnight. Building soil that can truly sustain life takes time. Years, sometimes decades, especially if you are trying to restore many acres.”Allegorical Interpretation:Malone is describing the collapse of our medical and scientific institutions. Like degraded soil, our healthcare system has been stripped of its foundational nutrients through industrialization, commercialization, and the pursuit of quick fixes. The restoration of trustworthy institutions requires decades of patient rebuilding, not overnight revolutionary change. His reference to “many acres” suggests the systemic nature of the problem across multiple domains - research, regulation, clinical practice, and public health.Theme 2: The Great Unlearning of WisdomWhat Malone Actually Says:“Much of that knowledge has since faded from common use, like the topsoil that once blew across our Great Plains. This is a kind of modern unknowing. Knowledge not entirely lost, but set aside. Forgotten by practice if not by record.”Allegorical Interpretation:This directly parallels the loss of medical wisdom and scientific integrity. Malone references Darwin’s work on earthworms - a nod to how foundational scientific principles have been abandoned. The “modern unknowing” represents how institutional memory has been erased, replaced by pharmaceutical-driven paradigms. The “paid experts” and “commercialism” he mentions mirror the capture of medicine by industry interests, where time-tested practices are discarded in favor of profitable interventions.Theme 3: The Failure of Quick FixesWhat Malone Actually Says:“Bagged mulch and compost line the shelves of home improvement stores, marketed as cure-alls for soils long stripped of life... Then come the supplements. Algae extracts, fish emulsions, and more, sold as quick fixes for soil regeneration.”Allegorical Interpretation:This is a direct critique of modern medicine’s approach to health. The “bagged products” represent pharmaceutical interventions and supplements marketed as solutions to health problems caused by systemic failures. Malone is arguing that just as soil can’t be fixed with products in bags, human health can’t be restored through pills and procedures alone. The “organic pesticides, which in the end, are still pesticides” line suggests that even “natural” or “alternative” approaches miss the point if they don’t address root causes.Theme 4: The Need for Diverse, Integrated SolutionsWhat Malone Actually Says:“No single cover crop does everything. The old farmers knew this. They mixed them. A grass for structure. A legume for nitrogen. A root crop to break the soil. Something edible, because why waste the ground?”Allegorical Interpretation:Malone is advocating for a pluralistic approach to medicine and science. Different “cover crops” represent different modalities - conventional medicine, alternative approaches, nutritional interventions, lifestyle changes. His emphasis on mixing them suggests integration rather than tribal warfare between medical paradigms. The “something edible” component points to the practical necessity that solutions should serve multiple purposes and be accessible to ordinary people.Theme 5: Critique of Both Industrial and Alternative ComplexitiesWhat Malone Actually Says:“The tried and true methods of the past are often wrapped in layers of jargon and complexity. Carbon sequestration, microbial amendments, branded systems, and organic pesticides, which in the end, are still pesticides. Enough to turn away all but the most devoted.”Allegorical Interpretation:Here Malone distances himself from both mainstream and alternative medical establishments. The “jargon and complexity” applies equally to pharmaceutical companies with their proprietary drugs and alternative medicine with its branded protocols and expensive supplements. He’s suggesting that both have created barriers to entry that exclude ordinary people from healthcare wisdom.Theme 6: The Long Game vs. Quick ResultsWhat Malone Actually Says:“Restoring soil is not a one-and-done proposition. It is something gardeners and farmers must tend year after year. There is no cure-all. This is a long game. A commitment for life.”Allegorical Interpretation:This directly challenges the medical establishment’s promise of quick cures and miracle drugs. Malone is advocating for a preventive, maintenance-based approach to health rather than intervention-only medicine. The “commitment for life” suggests that health, like soil, requires ongoing stewardship rather than episodic treatment.Theme 7: The Practice of Letting Things BeWhat Malone Actually Says:“Leaving last year’s vegetation, like sweet potato vines, in place is essentially a form of no-till. You are keeping the soil covered, feeding the microbial life, and avoiding disturbance.”Allegorical Interpretation:This may be Malone’s most subtle critique of medical overreach. The “no-till” approach suggests that sometimes the best intervention is no intervention - letting the body’s natural processes work without constant medical disruption. His caution about tomato vines carrying “disease load” could be read as a nuanced take on when intervention is necessary versus when it’s harmful.Contextual AnalysisThe timing of this piece - immediately after Malone’s resignation from the CDC vaccine panel - is significant. His frustration with “hundreds of hours of uncompensated labor, incredible hate from many quarters, hostile press, internal bickering, weaponized leaking, sabotage” aligns perfectly with the garden metaphor of dealing with poor soil, weeds, and pests.Malone appears to be positioning himself as someone who has moved beyond the institutional battles to focus on fundamental rebuilding. His emphasis on “old farmers’ wisdom” suggests he sees himself as preserving traditional knowledge that both mainstream and alternative medicine have abandoned.The allegorical reading reveals Malone’s evolution from institutional critic to something more akin to a philosophical reformer. He’s not just arguing against specific policies or products but advocating for an entirely different paradigm - one based on patience, diversity, integration, and respect for natural processes.This positions Malone uniquely in the medical freedom movement - not as an anti-vaccine activist per se, but as someone advocating for a fundamental rethinking of how we approach health, science, and medicine. His garden metaphor suggests that the problems run deeper than any single policy or product and require a complete paradigm shift rather than piecemeal reforms.The piece can be read as Malone’s manifesto for moving beyond the culture wars into something more constructive - a vision of healthcare that serves people rather than systems, that values wisdom over expertise, and that recognizes health as a lifelong practice rather than a series of interventions.When asked to comment, Dr. Malone just smiled wryly, surveyed his farm for a few seconds, and inhaled the aroma of one of his vibrant roses.Thanks for reading Malone News! This post is public so feel free to share it.Share

Summary: A meditation on Being There. By Benjamin Boxer


Friday Funnies: Ding, Dong...

We have all owned this dog at one time or another…Malone News is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.Thanks for reading Malone News! This post is public so feel free to share it.ShareThe section below is for my friends in Virginia -GET OUT AND VOTE NO FOR REDISTRICTING!Early ballots are available now at:Yourlocal General Registrar’s Office(always available)Plussatellite sites(libraries, community centers, government buildings) depending on the countyNever forget how the Democrats and MSM play bait and switch... this image is from the WSJ in Sept. 2025.  And look where we are now  - Virginia.Within two months of Spanberger becoming governor, xtreme tax measures, xtreme gerrymandering, second amendment gun rights removed, blocking (ICE) programs, and more.If wishes were fishes…On a personal note, I am at CPAC today and will be speaking with Mike Benz this afternoon on The Censorship Industrial ComplexOur talk will be streaming at 3:25 – 3:45 PMand most likely will also be available as a rocording at some point.JGM

Summary: If wishes were fishes...


Homesteading: The Great Unlearning

By JGMThe problemwith regenerative gardening or farming is that results don’t happen overnight. Building soil that can truly sustain life takes time. Years, sometimes decades, especially if you are trying to restore many acres.This is why, for the home gardener, raised beds with clear borders are such a gift. You are, in effect, creating a controlled system where soil can be built faster while being protected fromOn older farms, trees and hedgerows along the edges of pastures and cropland served a similar purpose. They acted as windbreaks and slowed water, reducing both erosion and the loss of topsoil downstream. Farmers working hillsides often terraced them when gardening intensively, another practical way to hold soil in place.There were other simple, time-tested methods. Shallow basins to catch and hold water. Soil berms to slow runoff. All designed to keep water where it falls, and soil where it belongs.And beneath it all, the real work was biological. Organic matter anchored into the soil. Bacteria and mycelial networks threading through it, helping bind structure and retain nutrients. Even earthworms, quietly tunneling, improving aggregation, aeration, and water infiltration, stitching the soil together from below.The Great UnlearningAt the turn of the 20th century, scientific interest in soil biology was near its peak. There were volumes written about earthworms. Their lifecycle, how they transform soil into a living system, and how to harness their quiet labor. This was not fringe science. Charles Darwin himself published a major work on earthworms in 1881, helping to spark broader scientific study of soil organisms. One could walk into a library and find entire shelves devoted to the subject.Much of that knowledge has since faded from common use, like the topsoil that once blew across our Great Plains. This is a kind of modern unknowing. Knowledge not entirely lost, but set aside. Forgotten by practice if not by record. Left to gather dust alongside the hardbound journals and books of another era. Some of those old manuscripts have been lost over time, as libraries deaccessioned collections in the march toward modernization.Likewise, the study of zoology, once broad and immersive, has narrowed in our institutions. It once encompassed the full sweep of animal life, from vertebrates down to the smallest visible creatures. Today, much of that hands-on, whole-organism study has faded from view.No longer do rows of specimens in jars line the shelves of the biology classroom. The old, tactile way of learning the natural world has largely been replaced.And those sweeping, popular works on the lifecycle of the earth, once a staple of science education, have mostly slipped from everyday reading.Now, bagged mulch and compost line the shelves of home improvement stores, marketed as cure-alls for soils long stripped of life in suburban backyards across America. Then come the supplements. Algae extracts, fish emulsions, and more, sold as quick fixes for soil regeneration.Meanwhile, the tried and true methods of the past are often wrapped in layers of jargon and complexity. Carbon sequestration, microbial amendments, branded systems, and organic pesticides, which in the end, are still pesticides. Enough to turn away all but the most devoted.The no-nonsense ways of the past have been crowded out by a mix of commercialism, input-driven agriculture, and a growing class of paid experts. Too often, what gets lost is the simple truth. Restoring soil is not a one-and-done proposition. It is something gardeners and farmers must tend year after year.There is no cure-all. This is a long game. A commitment for life.Cover CropsCover crops have long been used to hold soil and water, and to build a living community beneath the surface. Winter rye, collards, and mustard greens in more temperate regions, along with vetch, clover, daikon radishes, and turnips, are all commonly used.In the South, where we used to live, planting collards in the fall was almost a ritual among the old-timers. Kitchen gardens and small truck farms would come alive with a swath of green by November. These same farms might grow peanuts through the summer, with a roadside stand out front selling boiled peanuts, a Southern staple. Even today, this remains common practice in parts of rural Georgia and across the South.There are cover crops suited for summer and others for winter. Knowing how and when to use them is critical to building healthy soil and a resilient garden. Many of these cover crops are paired with each other. Grasses for structure, tubers for soil-busting capabilities, and legumes for nitrogen fixing.Below is a run-down on some of the more common cover crops:Winter RyeWinter rye is one of the workhorses. It germinates in cool soil, grows when little else will, and puts down a dense root system that holds soil in place through winter rains. Come spring, it produces a heavy biomass that can be cut and left as mulch. It is not edible in the garden sense, but it does real work. It scavenges leftover nutrients, suppresses weeds, and builds organic matter fastCollardsCollards are the old Southern standby. Planted in the fall, they carry through winter with very little complaint. You get food for the table, forage for animals, and a living cover on the soil. Their root system is not as aggressive as grasses, but they still help hold soil and cycle nutrients. They are a gardener’s winter cover crop, practical and useful.Mustard GreensMustards grow fast and do not wait around. They cover bare ground quickly and are known for helping suppress certain soil pests and diseases. Young leaves are edible, but their real value is speed and biological activity. When chopped and turned in, they break down quickly and feed the soil. It is a cool-season crop in the south, often paired with rye or clover or vetch, which fix nitrogen.Hairy VetchHairy vetch is one of the best nitrogen fixers available to the small farmer. It grows through winter and explodes in spring, putting nitrogen back into the soil for the next crop. It does require some management. It can get ahead of you if you let it go to seed, but used properly, it replaces a surprising amount of fertilizer.Clover (Crimson, White, Red)Clover is steady and dependable. It fixes nitrogen, protects the soil, and supports pollinators when it blooms. Crimson clover is common in the South for winter cover, while white clover works well as a living ground cover. It does not produce the biomass of rye, but it quietly improves soil year after year.Daikon Radish (Tillage Radish)Daikon radish is the soil breaker. It drives a deep taproot into compacted ground, opening channels for water and air. When it winter-kills, that root rots in place, leaving behind a natural pathway into the soil. The greens and roots are edible when young, but its real job is below ground.TurnipsTurnips do double duty. The greens feed people and livestock, and the roots help loosen soil and add organic matter. They establish quickly and provide good ground cover. In many Southern systems, they are part of a grazing mix as well as a garden crop.Austrian Winter PeasThese are another nitrogen fixer, similar to vetch but easier to manage. They produce tender shoots that are even edible, and they mix well with grains like rye or oats. A good choice if you want nitrogen without quite as much tangling growth.Oats (Fall Oats)Oats are often used as a winter cover that will winter-kill in colder snaps. That makes them easy. No need to terminate in spring. They leave behind a soft mulch layer and help hold soil through the fall and early winter.Buckwheat (Summer)Buckwheat is the quick fix for summer. It germinates in poor soil, grows fast, and shades out weeds. It also helps mobilize phosphorus in the soil. Not frost tolerant, but very effective in warm months when beds would otherwise sit bare.Sorghum-Sudangrass (Summer)This is the biomass king for summer. It grows tall, produces a massive amount of organic matter, and has deep roots that improve soil structure. Often used when trying to rehabilitate worn-out ground.Field Peas / Cowpeas (Southern Peas)In the South, cowpeas are a natural fit. They handle heat, fix nitrogen, and produce a usable crop at the same time. Black-eyed peas fall into this category. Good for soil, good for the table.The Lazy WayLeaving last year’s vegetation, like sweet potato vines, in place is essentially a form of no-till. You are keeping the soil covered, feeding the microbial life, and avoiding disturbance. As those vines break down, they add organic matter, hold moisture, and give earthworms something to work on. But by itself, it is usually not enough, especially on heavier soils.The layer is often too thin and breaks down too quickly to fully suppress weeds or carry the soil through the season. Where it really begins to work is when you treat that residue as a base, not the whole system. Leave it, knock it down, and then plant right into it with a mix of cover crops. Now you have both residue and living roots working together. That is when no-till stops being a concept and starts acting like a system.Note that not all of last year’s vegetable crops are suitable for cover cropping in this manner. For instance, leaving tomato vines can work in a similar way, but it is a more conditional choice. They will add organic matter and provide some light cover if you leave them in place, but tomato vines tend to be stringy, slow to break down, and they do not form a dense mulch like sweet potato vines.More importantly, tomatoes carry a higher disease load. Fungal issues like early blight, septoria, and others can overwinter on that residue and come right back next season. For that reason, most growers either remove or compost tomato vines rather than leaving them in place. If you do leave them, it is best to do so in a rotation where tomatoes are not going back into that bed the following year, and ideally with a cover crop planted into the residue. So yes, it can be done, but it is not as clean or forgiving a no-till option as something like sweet potato vines.Hay and mulch can also work to protect the soil if one hasn’t planted a cover crop. And many people leave tree leaves where they fall, as an easy way to cover and protect the soil.What hasn’t been discussed here and is important is that if one is dealing with more than a raised bed, animal manure is the best way to fertilize and regenerate soil. But that is a whole nother discussion.The simple truthNo single cover crop does everything. The old farmers knew this. They mixed them.A grass for structure.A legume for nitrogen.A root crop to break the soil.Something edible, because why waste the ground?That is how you build soil. Not with a product in a bag, but with time, living roots, and a little common sense.So, most of the seeds for these plants can be bought cheaply in bulk online or in a farm store.  Learning whether these cover crops are appropriate for your region, and when and where to plant them, is an individualized process.  A process that must be learned through trial and error.Putting this togetherPutting this all together, the lesson is not complicated, even if we have managed to make it so. Soil is not an input. It is not something you buy in a bag, fix with a supplement, or correct with a single season of effort. It is a living system that responds to what you do, and just as importantly, to what you stop doing.The old farmers understood this, even if they did not use the language we use today. They planted to protect the ground. They rotated crops. They let roots do the work. They paid attention to water, to slope, to season. And they stayed with it.We have, in many ways, unlearned those habits. Replaced them with products, prescriptions, and the expectation of quick results. But the soil does not care about any of that. It responds to time, biology, and stewardship.If there is a way forward, it is not new. It is a return. A return to keeping the ground covered. To feeding the soil, not just the plant. To use living roots as the primary tool. And to accept that this is not a project with an end date.It is a practice.Season after season. Year after year.Malone News is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.Thanks for reading Malone News! This post is public so feel free to share it.Share

Summary: We all must tend the garden


Immune Imprinting, Immunosenescence, and the Limits of Universal Seasonal Influenza Vaccination: A Critical Review of Two Decades of Vaccine Effectiveness Surveillance Data in the United StatesWhat Is Already Known About This Topic?Seasonal influenza vaccination is universally recommended for all persons aged >=6 months in the United States. Standard-dose inactivated vaccines have demonstrated variable overall vaccine effectiveness (VE) ranging from 10% to 60% since systematic monitoring began in 2004.What Is Added by This Report?This report synthesizes two decades of VE surveillance data with mechanistic evidence for immune imprinting and immunosenescence, demonstrating that host immune factors -- particularly childhood influenza-subtype exposure and age-related immune decline -- substantially modify VE in ways not accounted for by current universal vaccination policy.What Are the Implications for Public Health Practice?Universal seasonal influenza vaccination policies may benefit from reassessment in light of evidence that repeat vaccination attenuates VE, particularly for influenza A(H3N2), and that standard-dose vaccines provide suboptimal protection in older adults. Risk-stratified or platform-stratified approaches warrant evaluation.Malone News is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.AbstractUniversal seasonal influenza vaccination has been recommended for all persons aged >=6 months in the United States since 2010. However, two decades of vaccine effectiveness (VE) surveillance demonstrate that overall adjusted VE has ranged from 10% to 60%, with a mean near 40%, reflecting persistent and largely unexplained variation. Emerging evidence implicates two host immunological phenomena --immune imprinting(the lifelong bias in immune response imposed by the first influenza subtype encountered in childhood) andimmunosenescence(the age-related deterioration of innate and adaptive immune function) -- as major, underappreciated determinants of VE that are not addressed by current universal vaccination policy. This report synthesizes two decades of CDC Influenza Vaccine Effectiveness Network data alongside mechanistic and epidemiological evidence for both phenomena. The data suggest that (1) repeat annual vaccination attenuates VE, particularly against influenza A(H3N2), through back-boosting of outdated immune memory; (2) childhood subtype imprinting shapes adult susceptibility in ways that are independent of vaccine strain match; and (3) standard-dose vaccines provide demonstrably inferior immunogenicity and clinical protection in adults aged >=65 years due to multifaceted immune decline. Taken together, these findings raise substantive questions about the adequacy and uniformity of the current one-dose-fits-all vaccination framework and suggest that risk-stratified, platform-differentiated, and immunomodulatory approaches deserve rigorous evaluation.IntroductionSeasonal influenza remains a major cause of morbidity and mortality in the United States, contributing an estimated 9 to 45 million illnesses, up to 810,000 hospitalizations, and 12,000 to 61,000 deaths annually (1). Annual vaccination of all persons aged >=6 months has been recommended by the Advisory Committee on Immunization Practices (ACIP) since 2010, predicated on the assumption that vaccination confers consistent and additive benefit across all age groups and vaccination histories (2).The scientific foundation for this universal recommendation, however, rests primarily on aggregate VE estimates that obscure considerable heterogeneity by age, subtype, and prior vaccination history. Since 2004, the CDC Influenza Vaccine Effectiveness Networks have estimated adjusted overall VE annually using test-negative case-control designs at sentinel sites across the United States (3). These data reveal that VE has rarely exceeded 60%, has fallen below 20% in at least two seasons, and shows a persistent pattern of lower effectiveness against influenza A(H3N2) compared with A(H1N1) (3,4).Two host immunological mechanisms have emerged as plausible explanations for this variability: immune imprinting, the phenomenon by which the first influenza exposure in childhood establishes a lifelong immunodominant bias toward that subtype’s antigens (5); and immunosenescence, the progressive, multifactorial deterioration of immune function with aging that reduces both the quantity and quality of adaptive immune responses to vaccination (6). Neither phenomenon is adequately accounted for in current vaccination policy design, recommendations for general populations, or VE communication to clinicians and the public.This report critically examines both phenomena, evaluates the epidemiological evidence for their influence on measured VE, and considers implications for the premise that universal annual influenza vaccination confers reliably additive public health benefit for all individuals under the current standard-dose inactivated vaccine paradigm.MethodsWe conducted a narrative synthesis of published VE estimates from CDC Influenza Vaccine Effectiveness Networks for the 2004-05 through 2024-25 influenza seasons (3), supplemented by a review of mechanistic and epidemiological literature concerning immune imprinting and immunosenescence published through March 2026. Source databases included PubMed/MEDLINE, CDC MMWR and FluView archives, and the Eurosurveillance sentinel network. Studies were selected for relevance to the specific mechanisms examined; no formal systematic review or meta-analytic protocol was applied. This report reflects the authors’ synthesis and interpretation of publicly available data.ResultsTwo Decades of VE Surveillance: Persistent UnderperformanceTable 1 summarizes adjusted overall VE estimates from the 2004-05 through 2024-25 influenza seasons. The unweighted mean VE across 20 estimable seasons is approximately 40%, with a range of 10% (2004-05) to 60% (2010-11). No season has achieved VE >=60%, the lower bound of the target range implied by vaccine development standards. The 2020-21 season produced no estimate due to suppressed influenza circulation during the COVID-19 pandemic.A consistent pattern is evident: seasons dominated by influenza A(H3N2) are associated with lower VE (unweighted mean approximately 35%) compared with seasons dominated by A(H1N1) (unweighted mean approximately 52%). This differential cannot be fully explained by antigenic mismatch alone and is consistent with the hypothesis that immunological factors specific to H3N2 -- including the difficulty of generating broadly neutralizing antibodies against its rapidly evolving hemagglutinin head domain and the influence of birth-cohort imprinting -- systematically depress effectiveness against this subtype (7,8).Immune Imprinting: Mechanistic Evidence and VE ConsequencesThe doctrine of original antigenic sin, described by Francis in 1960, proposed that antibody responses to influenza throughout life are dominated by the subtype first encountered in childhood (5). Contemporary immunology has refined this concept intoimmune imprinting: a lifelong bias in memory B cell and T follicular helper (Tfh) cell repertoires toward the antigens of the first influenza subtype exposure, which preferentially recalls existing memory at the expense of de novo responses to antigenically novel epitopes on drifted strains (9).The mechanistic basis involves competitive activation dynamics: antigen-experienced memory B cells exhibit higher precursor frequencies, possess enhanced survival programming, and have lower B cell receptor activation thresholds than naive B cells. When a vaccine or infection presents antigens that are structurally similar to the imprinted subtype, memory B cells are preferentially expanded, generating high-titer antibodies against conserved (often suboptimally neutralizing) epitopes and suppressing de novo responses to the strain-specific head epitopes that are the primary neutralization targets (9,10).Epidemiological evidence for VE-relevant imprinting is substantial. The 2009 A(H1N1) pandemic provided a natural experiment: adults aged >=65 years -- imprinted on H1N1 strains circulating before 1957 -- showed markedly lower infection and mortality rates than younger cohorts imprinted on H3N2 strains, with approximately two thirds demonstrating pre-existing serologic cross-reactivity (11). Conversely, birth cohorts imprinted on H3N2 (born after 1968) experienced disproportionately more severe disease during H1N1-predominant seasons after 2009 (12).For seasonal VE, the most consistent finding concerns repeat vaccination and H3N2. Skowronski and colleagues, using Canada’s Sentinel Practitioner Surveillance Network with test-negative designs, documented that in the 2014-15 season -- characterized by both an antigenically drifted H3N2 circulating strain and an unchanged vaccine composition from the prior season -- VE in persons with no prior vaccination history was approximately 52%, compared with -32% in those vaccinated in the prior year only and approximately -54% in those vaccinated each year since 2012-13 (13). The investigators described this as a ‘perfect storm’ of antigenic drift, unchanged vaccine composition, and repeat-vaccination immune interference (13).A subsequent meta-analysis and systematic review by Jones-Gray and colleagues, encompassing 83 studies and 43 meta-analyses, confirmed that consecutive influenza vaccination was associated with attenuated VE for influenza A and B compared with current-season-only vaccination, though the effects were characterized as not severe enough to recommend against annual vaccination (14). A separate Lancet Respiratory Medicine meta-analysis of 41 studies found that vaccination in both the current and prior seasons was associated with lower protection than current-season vaccination alone: delta VE of -9% for A(H1N1), -18% for A(H3N2), and -7% for B (15). The H3N2 attenuation is of particular concern, given that H3N2 already generates the lowest absolute VE values in matched seasons.The mechanistic framework that unifies these observations -- the antigenic distance hypothesis -- predicts that negative interference from prior vaccination is most likely when the same vaccine strains are used across consecutive seasons but fail to match the current circulating strain. Under these conditions, the prior season’s vaccine imprints memory responses to antigens that are neither identical to the current circulating strain nor to the current season’s vaccine, creating a three-way mismatch that compounds standard antigenic drift effects (16).A further complication is egg adaptation. Most conventional inactivated influenza vaccines are manufactured in embryonated hens’ eggs, and the hemagglutinin of the H3N2 component in particular undergoes adaptive mutations during this process that alter its antigenic properties relative to the circulating strain (17). If a child’s first influenza exposure is to an egg-adapted vaccine antigen, this imprinting event may adversely shape antibody repertoires for subsequent decades, potentially reducing VE in later life (17). This is particularly relevant now that the WHO recommends vaccination beginning at age 6 months, substantially increasing the proportion of the population whose primary influenza imprint originates from an egg-derived vaccine rather than natural infection.Immunosenescence: Mechanisms of Vaccine Failure in Older AdultsAdults aged >=65 years account for the overwhelming majority of influenza-related hospitalizations and deaths: during the 2023-24 season, this age group accounted for 51% of hospitalizations and 68% of deaths (18). Yet this is precisely the population in which the standard seasonal influenza vaccine performs most poorly. Immunosenescence -- the progressive, multifactorial deterioration of innate and adaptive immune function with aging -- is the primary biological explanation (6,19).Immunosenescence is not a single deficit but a convergence of at least five intersecting mechanisms:Thymic involution and naive T cell depletion.The thymic epithelial space begins declining from the first year of life and contracts at approximately 3% per year until middle age, then at 1% per year thereafter (20). T cell receptor excision circle (TREC) analysis demonstrates a steady three-log decline in circulating naive T cells across an 80-year lifespan (21). By age 65, TCR diversity drops precipitously. Because vaccine responses require de novo priming of naive T cells against new or drifted epitopes, the contracted naive T cell pool limits the breadth and quality of vaccine-induced immunity. Vaccination-induced germinal center Tfh cell clonal lineages have been shown to persist in lymph nodes over multiple years, potentially channeling responses toward historical rather than current antigens (22).B cell intrinsic defects.Aging reduces both the quantity and functional quality of B cells. Reductions in naive B cell numbers, B cell diversity, germinal center size and frequency in secondary lymphoid organs, and intrinsic B cell effector function all compound to reduce vaccine-induced antibody magnitude and avidity (6,23). High TNF-alpha levels in aged individuals -- a hallmark of inflammaging -- directly downregulate CD28 expression on T and B cells, reducing co-stimulatory signaling required for full B cell activation (24).Inflammaging.A chronic, sterile, low-grade systemic inflammatory state -- driven by senescent cell accumulation and their senescence-associated secretory phenotype (SASP), defective autophagy, gut dysbiosis, and persistent latent infections -- characterizes aging and is associated with elevated circulating IL-6, TNF-alpha, and CRP (25). Pre-vaccination inflammatory gene signatures are negatively predictive of antibody responses to influenza vaccination in elderly adults (26). While some inflammation is required for vaccine immunogenicity, the chronic basal inflammation of aging appears to occupy signaling pathways in ways that impair rather than augment vaccine-induced adaptive responses.Innate immune dysfunction and impaired antigen presentation.Age-related declines in toll-like receptor (TLR) engagement -- particularly TLR1/2, TLR3, TLR5, TLR8 in myeloid dendritic cells, and TLR7 and TLR9 in plasmacytoid dendritic cells -- reduce the innate immune sensing that initiates downstream T and B cell activation after vaccination (27). Elevated NK cell populations in older adults have been shown to suppress germinal center responses, providing an additional brake on vaccine-induced humoral immunity (28).CD8 cytotoxic T cell failure.Standard inactivated influenza vaccines generate a weak stimulus to the cytotoxic T lymphocyte (CTL) arm of adaptive immunity, relying primarily on re-stimulation of pre-existing CD8 memory rather than de novo priming (27). Age-related decline in CTL generation and function -- driven by impaired CD4 T helper cell co-stimulation, reduced IL-2 signaling, and exhaustion phenotypes in persisting memory cells -- directly reduces the capacity to clear influenza virus from the lower respiratory tract, which is the critical determinant of severe disease prevention (27).The aggregate consequence is that standard-dose vaccines produce demonstrably inferior immunogenicity in older adults by all conventional measures -- hemagglutinin inhibition (HAI) titers, seroconversion rates, and antibody avidity -- and that epidemiological VE estimates confirm lower protection against both outpatient illness and hospitalization (6,19). Critically, the mechanisms driving immunosenescence overlap with those through which immune imprinting operates: both involve the dominance of antigen-experienced memory cells over naive B cell responses, and both are exacerbated by repeat vaccination that back-boosts established memory while suppressing de novo antibody generation (9,22).Enhanced Vaccine Formulations: Partial Mitigation and Unresolved QuestionsThree vaccine strategies have been developed specifically to address immunosenescence in adults aged >=65 years: high-dose inactivated vaccine (HD-IIV, containing four times the standard antigen dose), MF59-adjuvanted inactivated vaccine (aIIV), and recombinant hemagglutinin vaccine (RIV). ACIP issued a preferential recommendation for these enhanced formulations over standard-dose vaccine in this age group beginning with the 2022-23 season (2).A meta-analysis of 12 influenza seasons and over 45 million individuals aged >=65 years demonstrated that HD-IIV provided significantly better protection than standard-dose vaccine against influenza-like illness, influenza-related hospitalizations, and cardiovascular outcomes (29). Real-world Kaiser Permanente data from the 2022-23 season found that, compared with standard-dose egg-based vaccine, the relative effectiveness against PCR-confirmed hospitalization was 25% for HD-IIV and 62% for aIIV (30). These represent clinically meaningful incremental gains above a low baseline.However, recent randomized controlled trial evidence complicates this picture. The DANFLU-2 trial, the largest individually randomized trial of HD versus standard-dose vaccine conducted to date (n = 332,438 Danish adults aged >=65 years across three influenza seasons, 2022-23 through 2024-25), found that HD-IIV did not result in a significantly lower incidence of hospitalization for influenza or pneumonia compared with standard-dose vaccine (relative VE 5.9%; 95% CI -2.1 to 13.4; p = 0.14) (31). The authors noted this finding was inconsistent with prior observational and randomized data, potentially reflecting contextual factors including circulating strain composition and background immunity.Pharmacological strategies targeting the hallmarks of aging prior to vaccination are an emerging frontier. Administration of the mTOR inhibitor RAD001 (everolimus) before influenza vaccination in adults aged >=65 years increased antibody titers against all three vaccine strains by more than 20% and reduced proportions of T cells expressing the exhaustion marker PD-1 (33). Metformin, which reduces circulating CRP, IL-6, and TNF-alpha, has been associated with higher post-vaccination antibody titers in diabetic patients compared with other hypoglycemics (33). These approaches remain investigational.DiscussionThe evidence reviewed in this report converges on a conclusion that is uncomfortable in its public health implications: the current universal seasonal influenza vaccination policy, premised on a standard-dose inactivated vaccine given annually to virtually the entire population, does not perform as a uniformly effective intervention. For a substantial proportion of vaccinated individuals -- particularly older adults receiving their fifth, tenth, or fifteenth consecutive annual vaccination, individuals born in birth cohorts imprinted on influenza A subtypes that diverge from the dominant circulating strain, and individuals receiving standard-dose vaccines during H3N2-predominant seasons -- the measured protection is modest at best and, in certain epidemiological configurations, may be functionally negligible.This assessment does not imply that influenza vaccination is without benefit. Even in the worst-performing seasons, vaccination is associated with reductions in ICU admission and influenza-attributable mortality compared with no vaccination (4). Enhanced formulations provide meaningful additional protection in older adults over standard-dose vaccines, though the magnitude of this benefit may be smaller and more variable than the observational literature suggested (29-31). The argument here is not against vaccination per se but against the intellectual and policy complacency embedded in a universal recommendation that has not been substantially revised to account for the immune biology of those it aims to protect.Three specific policy gaps follow from the evidence reviewed:The repeat vaccination paradox.Current policy encourages and in some contexts requires annual vaccination without regard to prior vaccination history. The evidence from multiple independent VE studies and meta-analyses indicates that prior-year vaccination attenuates VE, particularly against H3N2 in mismatch seasons, by an average of approximately 18-20% in the most rigorous estimates (14,15). This is not a marginal finding. In a season such as 2014-15, the interaction between an unchanged vaccine composition, antigenic drift in H3N2, and repeat vaccination produced what investigators described as near-zero or negative VE in multiply vaccinated individuals (13). The mechanism -- back-boosting of outdated memory B cell responses at the expense of de novo neutralizing antibody generation -- is biologically coherent and supported by both animal model and human immunogenicity data (9,10). Public health guidance that does not acknowledge this attenuation effect misleads clinicians and patients about the expected benefit of vaccination.The immunosenescence gap.Adults aged >=65 years bear the largest absolute burden of influenza mortality yet derive the least reliable protection from standard-dose vaccines, due to thymic involution, B cell dysfunction, inflammaging, and innate immune impairment (6,19). The ACIP preferential recommendation for enhanced formulations in this age group is a recognition of the problem; however, the evidence base for the effectiveness of these formulations against severe outcomes such as hospitalization and death -- the outcomes that matter most -- remains uncertain, as the DANFLU-2 trial results demonstrate (31). Furthermore, even if enhanced vaccines modestly improve immunogenicity, the fundamental biology of immunosenescence means that seroconversion rates and HAI titers generated by senescent immune systems may not faithfully predict clinical protection in the way they do in younger adults (32). The correlates of protection may differ.The imprinting-policy disconnect.Current vaccination policy is strain-agnostic with respect to the recipient’s birth cohort and prior immune history. Yet the evidence -- from pandemic epidemiology, from birth-cohort-specific VE analyses, and from mechanistic immunology -- indicates that an individual’s first influenza exposure in childhood is a major determinant of their subsequent vaccine response for decades (5,9,11). In particular, the large proportion of the current elderly population in the United States that was imprinted on H1N1 strains circulating before 1968 faces both immunosenescence-related immune decline and imprinting-related suboptimal responses to H3N2 vaccine antigens -- a compounding of disadvantages that the current policy framework does not address.Taken together, these considerations suggest that the scientific justification for strict universal annual vaccination -- as opposed to risk-stratified, platform-differentiated, or historically informed approaches -- is weaker than is commonly represented. This does not diminish the importance of protecting high-risk populations with the best available tools. It does argue for investment in more targeted strategies: universal use of enhanced formulations in adults aged >=65 years, accelerated evaluation of mRNA vaccines and their effectiveness against severe outcomes, clinical trial evaluation of immunomodulatory pre-treatment to address inflammaging, and policy-level acknowledgment that the benefit of annual vaccination in previously multiply-vaccinated individuals in matched versus mismatched H3N2 seasons may differ substantially from the headline VE figures communicated to the public.This report has limitations. VE estimates from test-negative designs are observational and subject to confounding by indication and frailty bias, although standard adjustment procedures mitigate but do not eliminate these effects. The mechanistic evidence for immune imprinting’s effects on VE derives partly from observational birth-cohort analyses and animal models; the degree to which childhood imprinting modifies individual-level VE is not yet quantifiable with precision. The evidence base for immunosenescence mechanisms is robust in terms of cellular biology but translating cellular observations to population-level VE is imprecise. Nevertheless, the convergence of mechanistic plausibility with consistent epidemiological patterns across multiple independent surveillance systems in multiple countries provides a foundation for policy reconsideration that has been insufficiently engaged.ConclusionsTwo decades of influenza VE surveillance reveal a consistently underperforming vaccine whose limitations are substantially attributable to host immunological factors -- immune imprinting and immunosenescence -- rather than antigenic mismatch alone. Repeat annual vaccination attenuates VE against influenza A(H3N2) through immunological interference with de novo antibody responses; older adults, the primary target of influenza mortality reduction efforts, receive the least reliable protection from the standard platform recommended for the general population; and the combination of childhood subtype imprinting and age-related immune decline in the current elderly cohort creates compounding vulnerabilities that existing policy does not address. Enhanced vaccine formulations provide partial mitigation, but their superiority over standard-dose vaccines against severe outcomes is not firmly established by randomized trial evidence as of 2025. Universal seasonal influenza vaccination remains a valuable public health intervention, but the homogeneity of current policy design is misaligned with the heterogeneity of host immune biology. Risk-stratified recommendations, accelerated development and evaluation of next-generation vaccine platforms, and transparent public communication about the conditional nature of annual vaccination benefit are warranted.AcknowledgmentsThe author acknowledges the ongoing contributions of the CDC Influenza Vaccine Effectiveness Networks and their academic collaborators, who have generated the surveillance data underlying this analysis. No funding specific to this review was received.  The author formerly served as the vice chairperson of the CDC ACIP committee, but consequent to a recent court decision in the case of AAP vs HHS, no longer has any affiliation with the CDC or the ACIP.  The views expressed are those of the author alone, and do not reflect the opinions of the USG, HHS, CDC, or ACIP.Conflict of Interest StatementNo conflicts of interest are reported.Thanks for reading Malone News! 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Lancet Respir Med. 2023;11(1):27-44. https://doi.org/10.1016/S2213-2600(22)00266-115.McLean HQ, Thompson MG, Sundaram ME, et al. Impact of repeated vaccination on vaccine effectiveness against influenza A(H3N2) and B during 8 seasons. Clin Infect Dis. 2014;59(10):1375-1385. https://doi.org/10.1093/cid/ciu68016.Skowronski DM, Chambers C, De Serres G, et al. Serial vaccination and the antigenic distance hypothesis: effects on influenza vaccine effectiveness during A(H3N2) epidemics in Canada, 2010-2011 to 2014-2015. J Infect Dis. 2017;215(7):1059-1099. https://doi.org/10.1093/infdis/jiw60517.Gouma S, Anderson EM, Hensley SE. The impact of egg adaptation and immune imprinting on influenza vaccine effectiveness. Vaccine. 2025. https://doi.org/10.1016/j.vaccine.2025.12690518.Centers for Disease Control and Prevention. FluView: influenza-associated hospitalizations. Accessed March 2026. https://www.cdc.gov/flu-burden/19.Poland GA, Ovsyannikova IG, Kennedy RB. Personalized vaccinology: a review. Vaccine. 2018;36(36):5350-5357. https://doi.org/10.1016/j.vaccine.2017.07.06220.Palmer DB. The effect of age on thymic function. Front Immunol. 2013;4:316. https://doi.org/10.3389/fimmu.2013.0031621.Hakim FT, Gress RE. Thymic involution and immune reconstitution. Trends Immunol. 2009;30(7):300-306. https://doi.org/10.1016/j.it.2009.03.00822.Schattgen SA, Guion K, Crawford JC, et al. Linking T cell receptor sequence to functional phenotype at the single-cell level. Nat Immunol. 2024;25:131-144. Cited in: Herath TK, et al. Vaccination against influenza viruses annually: renewing or narrowing the protective shield? J Exp Med. 2025;222(7):e20241283.23.Frasca D, Blomberg BB. Aging and vaccines: the use of system biology approaches for developing vaccines for the aging population. Exp Gerontol. 2014;53:62-67. https://doi.org/10.1016/j.exger.2013.12.01024.Frasca D, Diaz A, Romero M, Landin AM, Blomberg BB. High TNF-alpha levels in resting B cells negatively correlate with their response. Exp Gerontol. 2014;54:116-122. https://doi.org/10.1016/j.exger.2014.01.00425.Ferrucci L, Fabbri E. Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty. Nat Rev Cardiol. 2018;15(9):505-522. https://doi.org/10.1038/s41569-018-0064-226.Nakaya HI, Wrammert J, Lee EK, et al. Systems biology of vaccination for seasonal influenza in humans. Nat Immunol. 2011;12(8):786-795. https://doi.org/10.1038/ni.206727.McElhaney JE, Andrew MK, McNeil SA. Estimating influenza vaccine effectiveness: evolution of methods to better understand the confounding effects of frailty. Vaccine. 2017;35(49 Pt B):6989-6996. https://doi.org/10.1016/j.vaccine.2017.10.01828.Cossarizza A, Ortolani C, Forti E, et al. NK cells and influenza: non-specific effectors or immunoregulators? J Leukoc Biol. 2004;76(4):791-798.29.Lee JKH, Lam GKL, Shin T, et al. High-dose influenza vaccine in older adults by age and seasonal characteristics: systematic review and meta-analysis update. Vaccine X. 2023;14:100327. https://doi.org/10.1016/j.jvacx.2023.10032730.Ku JH, Rayens E, Sy LS, et al. Comparative effectiveness of adjuvanted and high-dose versus standard-dose influenza vaccines against influenza-related medical encounters and hospitalizations in older adults, 2022-2023. Clin Infect Dis. 2024. https://doi.org/10.1093/cid/ciae40731.Johansen ND, Skaarup KG, Biering-Sorensen T, et al. High-dose influenza vaccine effectiveness against hospitalization in older adults: the DANFLU-2 randomized trial. N Engl J Med. 2025. https://doi.org/10.1056/NEJMoa250990732.Haddad F, Dokmak G, Karaman R. Humoral immune response to mRNA-based influenza vaccines in older adults: a systematic review and meta-analysis of randomized controlled trials. PMC. 2025.33.Camacho-Muñoz D, et al. Targeting the hallmarks of aging to improve influenza vaccine responses in older adults. Immun Ageing. 2023;20:22. https://doi.org/10.1186/s12979-023-00348-6


Why your flu shot may work differently than you thinkTwo decades of federal surveillance data reveal how immune imprinting and an aging immune system undermine flu vaccine effectiveness. Current universal vaccination policy has not caught up to the biology.Every autumn, public health authorities deliver a message that is simultaneously accurate and misleading: get your flu shot. All Americans aged six months and older are recommended to receive one. The guidance is consistent, reassuring, and considerably more complicated than it sounds.A synthesis of two decades of CDC surveillance data, which will be published separately in Malone.News makes an argument that has been quietly building in the immunology literature for years: the current one-size-fits-all approach to seasonal influenza vaccination fails to account for two fundamental features of how the immune system actually works. The first is that your first flu exposure as a child permanently shapes how you respond to every flu vaccine you will ever receive. The second is that the immune system ages in ways that make older adults both the most important target for vaccination and the least reliable responders to it.This is not a case against flu vaccination. It is a case for being honest about what the vaccine does and does not do, and for whom.  In other words, it is a case for open and transparent informed consent.Malone News is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.The track record: never reliably above 60%Before getting to the biology, it is worth establishing how variable the vaccine’s performance actually is. Since 2004, the CDC has estimated seasonal flu vaccine effectiveness every year through a network of sentinel clinics and hospitals. The results tell a different story than the usual reassuring headlines and approved narratives.Vaccine effectiveness by season (selected years)Source: CDC Influenza VE Networks, 2004-2026.A 40% average effectiveness figure means that roughly four in ten flu cases that would have occurred among unvaccinated people were prevented among vaccinated people. That is genuinely useful. But it is far below vaccines like measles (97% effective) or childhood polio (99% effective). And in bad years, it falls into territory where the protection is marginal.The culprit in most low-effectiveness years is the H3N2 subtype of influenza A. It evolves faster than the other major circulating strains, it is harder to match, and it tends to mutate in ways that are specifically worsened by the egg-based manufacturing process most flu vaccines still rely on. In H3N2-dominant years, which occur in roughly a third to half of recent seasons, effectiveness against that specific strain has sometimes fallen below 20%.These fluctuations are not random noise. They have patterns, and those patterns trace back to biology that current policy largely ignores.The ghost of flu seasons past: immune imprintingIn 1960, a virologist named Thomas Francis Jr. described something he called “original antigenic sin.” When people were vaccinated against influenza strains they had never seen before, their immune response was still dominated by the flu virus they had first encountered as children, sometimes decades earlier. Like a palimpsest (an overwritten manuscript), the old exposure kept showing through.Modern immunology has renamed thisimmune imprintingand clarified the mechanism in considerable detail. The immune system maintains a permanent library of memory cells -- B cells and T cells -- tuned to pathogens it has encountered before. These memory cells vastly outnumber naive cells; they activate faster and respond more vigorously. When a new vaccine arrives with antigens that are similar but not identical to a past exposure, the memory cells are preferentially activated. The immune system, essentially, recalls the old answer rather than generating a new one.THE 2009 PANDEMIC MADE THIS VISIBLE IN REAL TIMEWhen the H1N1 pandemic emerged in 2009, illness patterns did not follow age lines as expected. They followed birth-year lines. Adults over 65, whose childhoods occurred during a period when H1N1 strains dominated, were largely protected. About two thirds had pre-existing immunity from exposures that had occurred decades earlier. Middle-aged adults, whose early flu experiences were dominated by H3N2 strains circulating since 1968, were the most vulnerable. Their immune memory was tuned to the wrong flu family. The same vaccine given to both groups produced different levels of protection depending on what each person’s immune system had memorized as a child.The immune system tends to recall the old answer rather than generating a new one -- even when the old answer is subtly wrong.A series of Canadian surveillance studies conducted between 2012 and 2019 documented this phenomenon with striking clarity. In the 2014-15 season, a year when the dominant circulating H3N2 virus had drifted significantly from the vaccine strain while the vaccine composition remained unchanged from the prior year, people who had been vaccinated in the previous one to two years showed near-zero or even negative effectiveness against the dominant strain. A systematic review published in theLancet Respiratory Medicinein 2023, analyzing 83 studies, confirmed that consecutive annual vaccination is associated with approximately 18 to 20% lower effectiveness against H3N2 compared to vaccinating in the current season alone.The data indicate that vaccination still protected better than no vaccination. But the accumulating immune imprint from prior exposures measurably reduced the precision of the response. The immune system, having been repeatedly told to remember one answer, struggled to learn a new one.THE MECHANISMMemory cells win the competitionWhen vaccine antigens arrive, memory B cells trained on past exposures activate within hours. Naive B cells, which would generate genuinely updated antibodies, need days to weeks to respond. In an established immune system, they are effectively outcompeted. The result is a response tuned to the past rather than the present flu season.THE EGG PROBLEMManufacturing introduces another mismatchMost flu vaccines are still grown in chicken eggs. The H3N2 virus adapts to avian cells during this process, subtly shifting its surface proteins away from those that circulate in humans. A child vaccinated with an egg-adapted antigen may carry a slightly misaligned immune imprint for decades, a consequence of the production method encoded in immune memory from the very first vaccination.When the immune system ages out: immunosenescenceThe people who most need the flu vaccine -- adults over 65, who account for more than two thirds of flu deaths every year -- are also the people whose immune systems respond to it least reliably. Understanding why requires a brief look at how the immune system changes with age.Four converging changesFROM BIRTH Thymic involution: the training facility closesThe thymus, the organ where new T cells are trained and released into circulation, begins shrinking from the first year of life. By the mid-60s, T cell output has fallen by roughly 95% from its peak. The pool of naive T cells available to mount a fresh response to a new vaccine is drastically reduced. The immune system becomes increasingly dependent on its existing memory library, which, as described above, can work against precision.BY AGE 50 Inflammaging: a persistent low-grade fireAs we age, a chronic, sterile, low-grade inflammatory state develops, driven by senescent cells accumulating in tissue, gut microbiome changes, and persistent low-level infections. Blood levels of inflammatory markers like IL-6, TNF-alpha, and CRP rise. This state, called inflammaging, appears to occupy immune signaling pathways in ways that blunt vaccine responses, even as it reflects immune system activity. Some inflammation is necessary for vaccines to work, but the chronic background inflammation of aging occupies channels without providing the coordinated response that generates protection.BY AGE 65 Germinal center decline: the antibody factory closesLymph nodes contain structures called germinal centers, which are microscopic factories where B cells compete to produce better and better antibodies through a process of mutation and selection. With age, lymph nodes shrink, germinal centers become fewer and less active, and the quality of the antibodies produced decreases. Antibodies generated in older immune systems are fewer in number, bind their targets less tightly, and wane faster. This is why the same vaccine that generates robust, lasting immunity in a 30-year-old may generate a weaker, shorter-lived response in an 80-year-old.ONGOING The compounding interactionImmunosenescence and immune imprinting reinforce each other. As the naive T and B cell pool shrinks, the immune system becomes even more reliant on existing memory, which intensifies the imprinting effect. An 80-year-old’s immune response to this year’s flu vaccine is more dominated by childhood exposures than a 40-year-old’s. The two phenomena together create a compounding disadvantage that is most acute in the people who need protection most.A COUNTERINTUITIVE POINTLower side effects in older adults after a flu shot are not a sign that the vaccine is working well; often, it is the opposite. The same immune dysfunction that reduces the protective response also reduces the inflammatory response that produces arm soreness, fatigue, and low-grade fever. An 80-year-old who feels nothing after a flu shot is not necessarily better protected than a 35-year-old who feels lousy for a day. Reactogenicity is a rough proxy for immune activation, and both go down together with immunosenescence.Three gaps in current policyThe scientific review examined here identifies three specific ways that current universal vaccination policy fails to account for what the biology shows.1. The repeat vaccination paradoxCurrent policy encourages and, in some settings, effectively requires annual vaccination without any consideration of prior vaccination history. But the evidence shows that in H3N2-mismatched seasons, which occur frequently, prior-year vaccination can reduce effectiveness by an average of 18 to 20%. The mechanism involves back-boosting of outdated immune memory that crowds out a fresh response. This effect is biologically coherent and has been replicated across multiple independent surveillance systems in multiple countries. Yet patients are never informed that their vaccination history may influence how well this year’s shot works. The scientific literature acknowledges this effect; public health guidance does not.2. The immunosenescence gap in older adultsAdults over 65 bear 68% of flu deaths yet receive the least reliable protection from standard-dose vaccines. The U.S. Advisory Committee on Immunization Practices made an important step forward in 2022 by preferentially recommending enhanced formulations, specifically high-dose, MF59-adjuvanted, or recombinant vaccines, for this group. These do meaningfully produce better immune responses. But even the most rigorously conducted clinical trial testing a high-dose vaccine against a standard-dose vaccine, enrolling 332,000 older Danish adults over three seasons (DANFLU-2, published 2025), found no statistically significant difference in hospitalization rates. The fundamental biology of immunosenescence means that improving immunogenicity (the number of antibodies generated) does not automatically translate into improved clinical protection. The correlates of immunity may operate differently in aging immune systems than in younger ones.3. The imprinting-policy disconnectEvery vaccination decision is made without reference to the recipient’s birth cohort or immune history, specifically what flu strain they first encountered as a child and which family of viruses their immune system is fundamentally tuned to respond to. Yet the evidence from pandemic epidemiology, from birth-cohort-specific effectiveness analyses, and from mechanistic immunology all converge on the same conclusion: that first childhood flu exposure is a major lifelong determinant of vaccine response. The current elderly cohort in the United States was largely imprinted on H1N1 strains circulating before 1957. These individuals face not only immunosenescence but also suboptimal responses to H3N2 vaccine components, a compounding of disadvantages that the current policy framework neither acknowledges nor addresses.What this does and does not meanIt is worth being precise about the argument here. Even in years with poor effectiveness, current data indicate that vaccination reduces ICU admission and flu-attributable mortality compared to no vaccination. The benefit for adults over 75, where the number needed to vaccinate to prevent one hospitalization is approximately 390 to 540 in a well-matched season, is genuine and clinically meaningful. Enhanced formulations for older adults provide real additional benefit over standard-dose vaccines. None of this is contested.What is contested is the framing. The aggregate “40 to 60% effective” figure communicated to the public obscures genuine variation by age, birth cohort, prior vaccination history, and season type. Someone who has been vaccinated for 15 consecutive years is in a measurably different immunological position than someone being vaccinated for the first time. An 80-year-old is not in the same position as a 40-year-old, even if they receive the same product on the same day at the same pharmacy.The path forward requires two things that tend to advance together: more honest communication about what the current vaccines do and for whom, and investment in platforms capable of overcoming the biological obstacles that current vaccines cannot overcome.Cell-based and recombinant platforms already avoid the egg-adaptation problem that has contributed to H3N2 underperformance. Adjuvanted vaccines and pre-vaccination immunomodulation, including mTOR inhibitors that have shown a 20% improvement in vaccine response in older adults in clinical trials, represent a serious near-term research frontier.None of these solutions are ready to replace the existing approach tomorrow. But the existing approach has not exceeded 60% effectiveness in 20 years of tracking. At some point, describing a structural limitation as a weather problem -- an unfortunate mismatch this particular season -- becomes a way of avoiding a harder conversation about the platform itself.Thanks for reading Malone News! This post is public so feel free to share it.ShareSources and further readingCDC Influenza Vaccine Effectiveness Networks, season-by-season effectiveness estimates 2004-2026. cdc.gov/flu-vaccines-work/php/effectiveness-studies/Skowronski DM, Chambers C, Sabaiduc S, et al. A perfect storm: impact of genomic variation and serial vaccination on low influenza vaccine effectiveness during the 2014-2015 season. Clinical Infectious Diseases. 2016;63(1):21-32.Jones-Gray E, Robinson EJ, Kucharski AJ, Fox A, Sullivan SG. Does repeated influenza vaccination attenuate effectiveness? A systematic review and meta-analysis. Lancet Respiratory Medicine. 2023;11(1):27-44.Henry C, Palm AKE, Krammer F, Wilson PC. From original antigenic sin to the universal influenza virus vaccine. Trends in Immunology. 2018;39(1):70-79.Dugan HL, Henry C, Wilson PC. Aging and influenza vaccine-induced immunity. Cellular Immunology. 2020;348:103998.Herath TK, et al. Vaccination against influenza viruses annually: renewing or narrowing the protective shield? Journal of Experimental Medicine. 2025;222(7):e20241283.Gostic KM, Ambrose M, Worobey M, Lloyd-Smith JO. Potent protection against H5N1 and H7N9 influenza via childhood hemagglutinin imprinting. Science. 2016;354(6313):722-726.Johansen ND, et al. High-dose influenza vaccine effectiveness against hospitalization in older adults: the DANFLU-2 randomized trial. New England Journal of Medicine. 2025. doi:10.1056/NEJMoa2509907This article summarizes findings from a peer-reviewed-style scientific synthesis. It does not constitute medical advice. Speak with a qualified healthcare provider about your individual vaccination decisions.


Sunday Strip: An hour late!

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Summary: Nah- just the return of normalcy


Friday Funnies: Incoming

The Woke Left and the Woke Reich are birds of the same feather, that don’t flock together.The frackery continues in Virginia.This week, there was a Congressional hearing where Gov. Walz was raked over the coals about his lying and his involvement (or lack thereof) in the explosion of fraud in his state. Simultaneously, Congress released aninterim reporton the subject.Strange - how mainstream media couldn’t be bothered to write about it…True story - we once had four teenage girls do an internship on the farm one year. Having boys, we had no idea what it would be. Turns out a gaggle of girls is very different from a pack of boys.It culminated in a two-hour road trip to go to an amusement park. Frankly, the amount of squealing, singing off-key, and screeching, whelp, we were lucky we didn’t burst our eardrums.The Australian Mutton Marketing Association wins the top prize for best commercial of 2026.Malone News is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.Thanks for reading Malone News! This post is public so feel free to share it.ShareThisneverhappens in our house…

Summary: fire...