Ken Sims

A decision not to fund a prostate cancer screening pilot will cause more men to die. The foundation asked for $6.4 million over 4 years National refused - but it's funding David Seymour's private school & Regulation Ministry slush fund to the tune of $200 million

@fawfulfan The VAX does NOT prevent COVID or LONG COVID. it reduces risk of hospitalization and death which is good but respirator masks are required to actually prevent COVID. COVID expected to kill over 150,000 this year. Long COVID is number 1 chronic illness. 5.8 million children.

Disturbing news. Loss of Arctic sea ice has caused an “irreversible” shift in the chemistry of the ocean that is disrupting the foundations of chain of life, a two-decade-long study has concluded. Tipping points are already here… oceanographicmagazine.com/news/arctic-oc…

Unraveling the cardiovascular burden of long COVID: symptom profiles, underlying mechanisms, and clinical management insights 🚨A peer-reviewed cardiac bombshell just AGAIN exposed the brutal reality of Long COVID HEART DAMAGE! ➡️This Chinees review synthesizes current evidence on the symptom profiles, underlying mechanisms, and clinical management of Long COVID-related cardiovascular complications. ➡️Symptom profile: - Long COVID cardiovascular sequelae affect 10–20% of survivors, with persistent symptoms (≥2 months post-3-month mark) including palpitations (68%), chest pain (53%), fatigue (63%), and dyspnoea, - POTS occurs in ~31% of cases, - Functional deficits persist up to at least 12 months: 20% drop in 6-minute walk test distance, reduced cardiac index, stroke volume, and ejection fraction (18–29%). ➡️Structural findings: - Cardiac MRI shows involvement in 78% and myocardial inflammation in 60%, - Autopsies reveal myocarditis (14%) and macrophage infiltration (86%). ➡️Mechanisms: →Multifactorial and overlapping: - Viral persistence (spike protein detectable in 60% at 12 months), - Chronic immune dysregulation (elevated IL-1/IL-6/IFN-γ/TNF-α), - Endothelial dysfunction, - Microvascular injury with microthrombi (80% in some autopsies), - Hypercoagulability, and - Autonomic dysregulation. ➡️Blood markers / biomarkers: - Persistent spike protein is detectable in blood plasma (and tissues) in ~60% of Long COVID patients at 12 months, but absent in recovered controls. This further dismantles any vaccine-causation narrative, - Inflammatory cytokines are elevated (IL-1, IL-16, IL-17, IL-22, IFN-γ, TNF-α), linked to endothelial dysfunction, platelet activation, hypercoagulability, and myocardial injury, - Cardiac troponin is often elevated as a marker of ongoing ischemia/injury. ➡️Risk modifiers: - Severe acute infection drives more structural damage, - mild cases more autonomic/functional, - Vaccination may cut risk: 30–50%, - Delta-era cases worse than Omicron. ➡️Management: →Currently symptom-driven: - Graded rehabilitation, - Lifestyle measures, - Beta-blockers, - Targeted anticoagulation, →Multidisciplinary phenotyping recommended, →No approved mechanism-specific therapies exist. ➡️Conclusions: “Based on these findings, the following clinical recommendations are proposed: (1) cardiovascular evaluation should be considered in patients with persistent post-COVID-19 symptoms, including autonomic function testing and imaging where indicated, (2) management should be phenotype-driven and multidisciplinary, incorporating tailored exercise rehabilitation, pharmacological control of heart rate and symptoms, and anticoagulation only when thromboembolic disease is confirmed, (3) vaccination should be encouraged as a preventive measure to reduce Long COVID risk; and (4) future research should prioritize mechanism-based subtyping and randomized trials of targeted interventions.” ‼️So, AGAIN, Cardiovascular Long COVID is a real, heterogeneous, and enduring burden fuelled by unresolved viral–immune–vascular damage that current symptomatic care cannot fix. Without urgent, mechanism/phenotype-targeted treatments, millions will face chronic heart impairment for years to come! PREVENTION NEEDS PRIORITY ! #AvoidSars2 #AvoidReinfections #CleanAir frontiersin.org/journals/cardi…

"Many patients with long COVID are already receiving care but are not being recognized as having the condition. These patients are not absent from clinical care; they are absent from the diagnostic code that would identify them as long COVID patients" cidrap.umn.edu/covid-19/long-…

Fuck! The Paris agreement was meant to stop the planet breaching 1.5C by 2100. The worlds leading climate scientist says well now see 2C by the 2030’s!!!!!! Almost no media is telling you climate change is accelerating!! @piersmorgan @mrjamesob @TomSwarbrick1 @vicderbyshire @jonsopel @maitlis @Emmabarnett @tombradby @WilfredFrost @CliveMyrieBBC @amolrajan @SophyRidgeSky @TVNaga01 @OborneTweets @JohnSimpsonNews @richardpbacon @rickedwards1 @MickBooker @MartinDaubney @PatrickChristys @MichelleDewbs @MrNickKnowles @bbcvickiyoung @KamaliMelbourne @BBCsarahsmith @kirstiemallsopp @krishgm @tombradby @skynews @itvnews @ITNProductions @esmewren @adamboultonTABB @KayBurley @alexberesfordTV @kayeadams @janem @rickygervais @rachelburden @bbcnews @skynews @NickyAACampbell @ShelaghFogarty @BenKentish @bbcnickrobinson @tomhfh @susannareid100 @alexberesfordTV

The study highlights that pediatric long COVID can be significantly disabling, even when the child does not outwardly appear seriously ill. As a result, children often face misunderstanding from schools, parents, healthcare professionals. The authors also show that the measured symptom burden in these patients was, in some domains, worse than that reported in other pediatric chronic conditions, including chronic pain, active cancer treatment, type 1 diabetes, sickle cell disease, asthma, and autism. Millions of children globally. Unnecessarily. A public health disgrace. @vlvalek @adamvojtech86 @strakovka

This is where I’m at psychologically: I speak up every day because if I stayed silent, I honestly couldn’t live with myself. At the same time, I’m painfully aware that most of it barely moves the needle. People with Long Covid have largely been left behind. Governments, institutions, media ecosystems, and powerful financial interests have effectively separated the reality of Long Covid from the ongoing risks of infection itself. Now another airborne virus is emerging into a population that is exhausted, misinformed, cognitively overloaded, and psychologically conditioned to normalize illness. A huge percentage of people genuinely believe COVID is “over,” that masking is pointless, and that repeated infections are basically just colds you can power through with supplements, exercise, and positive thinking. Meanwhile, the information environment is flooded with influencers, wellness grifters, disinformation, outrage algorithms, and people monetizing confusion. I don’t know what else to say other than this: Be honest with yourself. Protect your health. Protect the people you love. And don’t let the world gaslight you out of your own ability to observe reality. And everyone once in awhile, you're allowed to tell the asshole minimizing deadline biohazards to go fuck himself.

You ever wonder how Covid enters cells? This animation shows you. Some amazing science in the thread it came from. Link in next tweet.

A heart attack after COVID may not look like the classic heart attack we usually imagine. A new core-lab study of patients with NSTEMI + COVID-19 suggests something more diffuse. Not just one blocked artery, but a blood-clotting and vessel inflammation problem🧵

Steady under pressure, firm on principle: what Dame Jacinda Ardern’s leadership showed, and what’s at stake now The contrasts in this clip from Prime Minister show a telling story of leadership that becomes tested under pressure, in front of the world, when every word carries weight. In the opening shot, Dame Jacinda Ardern holds her composure as emotion rises to the surface. Her eyes are glassy, her expression tight, but controlled showing restraint. A leader absorbing the moment, carrying the burden, and choosing not to let anything spill over. That composure carries into a visit to New York in 2018. Inside the United Nations General Assembly, Donald Trump delivers his address. Ardern listens without reaction but she does not mirror the tone in the room. Studying the moment. She was dressed in black attire, seated among delegates, hand resting against her chin, eyes fixed forward. She is fully engaged, analysing, weighing New Zealand’s place in a rapidly shifting global landscape. It is a picture of deliberate leadership. Not reactive, not performative, but anchored in thought and purpose. When she went out of her way to face the media, that clarity of her strengthen as a leader on the world stage sharpened. She refused to engage in personality politics. She redirected every question back to one point. She was there to represent New Zealand. Nothing more, nothing less. Her approach defined her government. Under Ardern, New Zealand maintained a strong, independent foreign policy. It was willing to differ from major powers, to speak to its own values, and to take positions that reflected national interest rather than global pressure. That independence allowed New Zealand to contribute meaningfully on the world stage, from diplomacy to climate and security, without being seen as an extension of any larger power. Now, that footing is being questioned. The coalition government of New Zealand National Party, ACT New Zealand, and New Zealand First faces growing criticism over the direction of foreign policy and resource decisions. It is argued that Winston Peters is drawing New Zealand closer to the United States, while Shane Jones is advancing policies that open the country’s natural resources to greater overseas extraction. One era projected a confident, independent voice, willing to stand apart when needed. The current trajectory risks narrowing that independence in favour of alignment and economic trade-offs. Those images of Ardern, steady, focused, and unmoved by external pressure, now land with added weight. This clip is just a reminder of what independent leadership looked like, and a benchmark against which today’s decisions are increasingly being judged. *Courtesy of Magnolia Pictures, CNN Films, HBO Documentary Films *This footage has been republished for the purposes of educational news reporting and public interest, in accordance with New Zealand’s fair dealing provisions under the Copyright Act 1994. #nzpol

🔥"Take‑home message: Long COVID is not a single disease but a complex, multisystem condition." ➡️Excellent new summary work/🧵👇 Thanks @DrMark_Faghy et al.

As you may know well, "analysis of biofluids and neuroimaging from PASC (post-acute sequelae of COVID-19 or long COVID) patients underline long-term changes in the proteome and CNS (central nervous system) response following the infection.. Potential disease mechanisms underlying neurological symptoms observed in severe COVID-19 are vascular and fluid-brain barrier abnormalities, chronic neuroinflammation, persistent axonal damage and protein aggregation. In PASC patients, an altered biofluid proteome with increased neuronal proteins and pro-inflammatory cytokines was observed. The pathological burden in affected brain regions may contribute to manifestations such as anosmia, memory deficits, and cerebellar ataxia." I wonder how many people remember that COVID-19 causes memory loss. 'Human brain matters: Navigating the neuropathology of COVID-19' onlinelibrary.wiley.com/doi/full/10.11…

Kind of seems like something.

Honestly, you've got to have balls of steel to publish this graph and say without evidence that Covid has nothing to do with this fall. Especially since the press release the article is based on *doesn't even say that*.

A groundbreaking study has pinpointed a microscopic culprit behind the debilitating fatigue, brain fog, and other persistent symptoms of long COVID: abnormal, sticky microclots embedded with neutrophil extracellular traps (NETs) in patients' blood. These microclots—tiny aggregates of clotting proteins—are small enough to obstruct the body's tiniest blood vessels (capillaries), restricting oxygen delivery to tissues and organs without triggering obvious large-scale clotting events. In long COVID patients, researchers observed a dramatic ~20-fold increase (median 19.7 times higher) in the number of these microclots compared to healthy controls, with the clots also tending to be larger. What sets this finding apart is the discovery that these microclots are structurally intertwined with NETs—web-like structures of DNA, enzymes (such as myeloperoxidase and neutrophil elastase), and proteins released by neutrophils (a type of white blood cell) to ensnare pathogens. Normally, NETs form temporarily and then dissolve, but in long COVID, they persist and become physically embedded within the microclots, creating highly resistant, "gummy" structures that evade the body's natural clot-breaking processes (fibrinolysis). This creates a chronic thromboinflammatory state, where blocked microcirculation and ongoing low-grade inflammation may sustain symptoms like exhaustion and cognitive impairment. The differences were so pronounced that machine learning models analyzing anonymized blood samples (via fluorescence microscopy for markers like ThT for amyloid-like structures, DNA stains, and MPO for NETs) could distinguish long COVID patients from healthy individuals with 91% accuracy—offering a potential objective biomarker for a condition that has long evaded reliable diagnosis through standard tests (e.g., normal D-dimer, PT/INR, or aPTT levels despite significant microclot burden). This work, led by teams including Prof. Etheresia Pretorius (Stellenbosch University) and Dr. Alain Thierry (Montpellier University), reframes long COVID as a tangible, blood-based disorder driven by dysregulated coagulation and innate immunity rather than vague "post-viral malaise." Targeting NETs or microclots—perhaps with therapies to degrade NETs or prevent their stabilization—could open doors to treating root causes instead of merely alleviating symptoms. [Thierry, A. R., Usher, T., Sanchez, C., Turner, S., Venter, C., Pastor, B., Waters, M., Thompson, A., Mirandola, A., Pisareva, E., Prevostel, C., Laubscher, G. J., Kell, D. B., & Pretorius, E. (2025). Circulating Microclots Are Structurally Associated With Neutrophil Extracellular Traps and Their Amounts Are Elevated in Long COVID Patients. Journal of Medical Virology, 97(10), e70613. DOI: 10.1002/jmv.70613]

A January study of essential workers (with blood samples before and after COVID infection) found those with long-term neurological symptoms had higher phosphorylated tau—a protein linked to early brain degeneration. uniladtech.com/science/resear…

Cattle H5N1 now replicates in human lung tissue. Not hypothetical. Not simulated. Direct infection of human respiratory cells confirmed. Bird flu found a mammalian amplifier. Cows are evolution engines.

“Debilitating a Generation”: Expert Warns That Long COVID May Eventually Affect Most Americans | Institute for New Economic Thinking ineteconomics.org/perspectives/b…

In the past six years we have let children, in some cases repeatedly, be infected with a disease that research shows can negatively impact the immune system. Our friends’ kids are getting pneumonia, scarlet fever, strep, whooping cough etc at rates simply not seen pre-pandemic.