Cyber Platos @lightbender77

mastic gum KILLS the bacteria found in 9 out of 10 Alzheimer’s brains forgetting names? losing focus? brain fog? that’s not aging — that’s P. gingivalis. from your bleeding gums. and it’s: – crossing into your brain – shredding neurons like scissors – triggering plaque your brain can’t stop they infected HEALTHY mice with it. normal brains. the mice developed Alzheimer’s. blocked it? damage REVERSED. (Dominy 2019 — Science Advances) every Alzheimer’s drug targeting amyloid has FAILED. billions spent. zero cures. what if we’ve been destroying the barricade while the bacteria kept eating? mastic gum KILLED it (PMID: 16822220) → zero resistance. 3,000 years. → penetrates biofilms toothbrushes can’t your gums bled this morning. and that’s JUST one bacteria… it also kills bacteria linked to stomach cancer, colorectal cancer, and tooth decay. 🧵 every bacteria it kills in the comments ↓

I miss when "The News" was just a guy in a suit telling you what happened, instead of a 24 hour panic machine designed to make you hate your neighbor so you don't notice your rent went up 30%.

Medical history is full of "imaginary" illnesses that turned out to be real. Ulcers. MS. Long Covid. And patients were right all along. So if you're healthy, one ask: When someone tells you they're sick, the first instinct should be to believe them.

Do go on.

Spencer Pratt @spencerpratt

4 days ago

You can tell a lot about a person by how they react when someone dies.

7K 7K 87K 5.3M 907

The causal role of gum disease bacteria in cancer. It … ‘is now undeniable: bacteria such as P.gingivalis have a role to play in certain cancers…’ 👇 Role of Porphyromonas gingivalis in oral and orodigestive squamous cell carcinoma Lamont et al 2022 bit.ly/45rxdMa

You don’t like my posts about Trump? Just ignore them like you ignore the fact that he’s a rapist and a pedophile.

Microclots are larger and more numerous in those with Long COVID compared to healthy controls. A recent pre-print from the same research group also found microclots in those with POTS. We reveal the key differences between microclots found in those with: 1. POTS only 2. Long COVID only 3. POTS and Long COVID Read more here: buff.ly/94aOTkz

Magnesium has the ability to shrink arterial plaques, demonstrated by some incredible clinical trials. The first study came out in 2008. They gave people magnesium citrate, just under 100 mg elemental magnesium per day. This is a puny dose, magnesium RDA is 4X that and people often supplement even more than that. These studies are all in hemodialysis patients, and that's mainly because these people develop heart disease at a much quicker rate due to toxin accumulation and altered mineral balance. Magnesium reduced plaque burden within 2 months. Carotid intima median thickness (cIMT) is the literal thickness of the inner part of the arteries. It's a direct measurement of plaque buildup. This was decreased on both the left and right sides, while plaque sizes tended to INCREASE without it. There was also a decent correlation between serum magnesium levels and plaque size. More magnesium = less plaque. Serum magnesium is not the best overall measure, and it mainly becomes low in severe depletion. The second paper came out in 2013. This time patients were given 440 mg of magnesium oxide 3x per week for 6 months. Magnesium oxide is a terrible form of magnesium, with as little as 4% of it getting absorbed in the gut. So really, this is a small, small amount of magnesium. Even still, after 6 months, people taking the magnesium showed improvements in plaque thickness. Both the left and right thicknesses were decreased, resulting in a total drop of plaque size. Meanwhile, the placebo group saw plaques grow once again. Another study published in 2019 showed even better effects. Again, the poorly absorbed magnesium oxide, at just 150 mg of elemental magnesium per day, showed beneficial effects across the board. Vascular: ↓ Mean left CIMT ↓ Maximum left CIMT ↓ Mean right CIMT Glycemic / Insulin sensitivity: ↓ Insulin ↓ HOMA-IR ↑ QUICKI (insulin sensitivity) ↓ HbA1c Lipids: ↓ Total cholesterol ↓ LDL cholesterol Inflammation & oxidative stress: ↓ hs-CRP ↑ Total antioxidant capacity (TAC) ↓ MDA (lipid peroxidation marker) How is magnesium so effective for heart disease? Countless reasons, really, but a few of the most important. 1. Anti-inflammatory properties. Magnesium has been shown to alleviate various inflammatory conditions, and heart disease is no exception. The entire plaque formation process is an active construction by the immune system, not just a passive building up of lipids. 2. Metabolism. Magnesium is probably the single most important nutrient for the mitochondria, being involved in countless reactions in energy metabolism and needed for ATP synthesis. Mitochondrial function is needed to stop the inflammatory process and facilitate the export of cholesterol from the arteries. 3. Antioxidant properties. The core initiating event in atherosclerosis is oxidative stress that damages lipoproteins. Magnesium is critical in maintaining antioxidant defenses. 4. NO synthesis / endothelial function. Magnesium is incredibly important for this layer of cells in the arteries. When endothelial cells do not function correctly, they become more permeable to cholesterol entering the arteries. 5. Lipid lowering. Magnesium also has shown the ability to directly lower cholesterol and other lipids, through various mechanisms. Without enough magnesium, cholesterol cannot be cleared from the blood, metabolized or have its synthesis shut off properly.

Dalton (Analyze & Optimize) @Outdoctrination

9 months ago

STOP focusing on cholesterol for heart disease. Your doctor doesn't realize it's only a small part of the process of developing heart disease. Here's a DEEP dive into how heart disease develops, what to do about it, & why focusing solely on cholesterol is a path to an early

18 93 489 1.1M 992

The Gut Symptoms Doctors Keep Missing in Long COVID youtu.be/A3Bg91bnqjY?is… via @YouTube

Fact 1: Gastritis (and gastric cancer) is in part regulated by TLR-4 -pubmed.ncbi.nlm.nih.gov/38204278/ Fact 2: TLR-4 can be modulated and turned-down by infrared light -pmc.ncbi.nlm.nih.gov/articles/PMC84… Fact 3: This precise type of light from the sun can easily penetrate to the level of the stomach (and in fact right through the whole body) nature.com/articles/s4159… This has nothing to do with vitamin D. At all.

Bryan Johnson @bryan_johnson

2 weeks ago

Much of the internet thinks: > meat will remedy my autoimmune gastritis > sunlight is the cure > the culprit is the food I consume These are unlikely. The sunlight assessment is claiming low vitamin D levels are making my immune system misfire. My vitamin D has been

1K 88 3K 1.7M 1K

From a study that investigated the differences in plasma biomarkers for intestinal permeability, "hospitalized COVID-19 patients have elevated concentrations of pro-inflammatory cytokines and microbial translocation markers, and the relationships between these biomarkers were significantly altered compared to healthy volunteers, especially those related to mucosa-associated homeostatic cytokines IL-17A and IL-23.. [These findings] highlight the importance of managing microbial translocation in COVID-19.." We cannot live healthily without continued support of microorganisms. 'Gut barrier integrity biomarkers are associated with increased inflammation and predict disease status in hospitalized COVID-19 patients' nature.com/articles/s4159…

Study: Folic acid and ... COVID-19 diagnosis and mortality "We report an association of increased risk for COVID-19 diagnosis and COVID-19-related death in people prescribed folic acid supplementation. Our results also suggest that methotrexate might attenuate these associations." BMJ Open bmjopen.bmj.com/content/12/8/e…

The Convergence Model of PEM Post-exertional malaise is the defining biological feature of myalgic encephalomyelitis. It is a delayed failure of physiological homeostasis triggered when exertional demand exceeds a patient's biological reserve and adaptive capacity.

A rare cause of Lyme disease has been identified in New York for the first time. Almost all U.S. Lyme disease cases are caused by Borrelia burgdorferi, but researchers recently confirmed a New York case caused by the much rarer Borrelia mayonii. What does this mean? 🧵 #lyme

keyboard_arrow_left Previous keyboard_arrow_right Next

🌟 𝐍𝐞𝐰 𝐚𝐫𝐭𝐢𝐜𝐥𝐞: 𝐭𝐡𝐞 𝐜𝐨𝐧𝐧𝐞𝐜𝐭𝐢𝐨𝐧 𝐛𝐞𝐭𝐰𝐞𝐞𝐧 𝐋𝐨𝐧𝐠 𝐂𝐎𝐕𝐈𝐃, 𝐌𝐲𝐚𝐥𝐠𝐢𝐜 𝐄𝐧𝐜𝐞𝐩𝐡𝐚𝐥𝐨𝐦𝐲𝐞𝐥𝐢𝐭𝐢𝐬 𝐚𝐧𝐝 𝐩𝐨𝐬𝐭-𝐯𝐚𝐜𝐜𝐢𝐧𝐚𝐥 𝐬𝐲𝐧𝐝𝐫𝐨𝐦𝐞𝐬 𝐥𝐢𝐞𝐬 𝐢𝐧 𝐭𝐡𝐞 𝐝𝐞𝐯𝐞𝐥𝐨𝐩𝐦𝐞𝐧𝐭 𝐨𝐟 𝐚𝐧 𝐀𝐮𝐭𝐨𝐢𝐦𝐦𝐮𝐧𝐞 𝐇𝐲𝐩𝐨𝐜𝐨𝐫𝐭𝐢𝐬𝐨𝐥𝐞𝐦𝐢𝐜 𝐒𝐲𝐧𝐝𝐫𝐨𝐦𝐞🌟 🌐 I am excited to share with you our latest paper entitled "𝐇𝐲𝐩𝐨𝐜𝐨𝐫𝐭𝐢𝐬𝐨𝐥𝐞𝐦𝐢𝐜 𝐀𝐒𝐈𝐀: 𝐀 𝐯𝐚𝐜𝐜𝐢𝐧𝐞- 𝐚𝐧𝐝 𝐜𝐡𝐫𝐨𝐧𝐢𝐜 𝐢𝐧𝐟𝐞𝐜𝐭𝐢𝐨𝐧-𝐢𝐧𝐝𝐮𝐜𝐞𝐝 𝐬𝐲𝐧𝐝𝐫𝐨𝐦𝐞 𝐛𝐞𝐡𝐢𝐧𝐝 𝐭𝐡𝐞 𝐨𝐫𝐢𝐠𝐢𝐧 𝐨𝐟 𝐥𝐨𝐧𝐠 𝐂𝐎𝐕𝐈𝐃 𝐚𝐧𝐝 𝐦𝐲𝐚𝐥𝐠𝐢𝐜 𝐞𝐧𝐜𝐞𝐩𝐡𝐚𝐥𝐨𝐦𝐲𝐞𝐥𝐢𝐭𝐢𝐬". In this paper, we explain the links between Long COVID, Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (ME/CFS) and COVID-19 post-vaccine syndromes. 🤔 Stay reading to the end and you will also find our treatment proposal that could improve symptoms.💊 ➡️𝐋𝐢𝐧𝐤 𝐨𝐟 𝐨𝐮𝐫 𝐫𝐞𝐯𝐢𝐞𝐰 𝐚𝐫𝐭𝐢𝐜𝐥𝐞: frontiersin.org/journals/immun… 🔍 𝐀𝐛𝐬𝐭𝐫𝐚𝐜𝐭: We present a model for the development of these diseases that involves a complex interplay between immune hyperactivation, autoimmune hypophysitis or pituitary hypofunction, and immune exhaustion. We believe that the starting point is a deficient CD4 T-cell response to viral infections in genetically predisposed individuals (HLA-DRB1). This would follow from an uncontrolled immune response with hyperactivation of CD8 T cells and elevated antibody production, some of which could be directed against self-antigens, triggering autoimmune hypophysitis or direct damage to the pituitary, resulting in decreased production of pituitary hormones, such as ACTH. 🧬 🔬 𝐖𝐡𝐚𝐭'𝐬 𝐭𝐡𝐞 𝐛𝐢𝐠 𝐝𝐞𝐚𝐥? 1️⃣ 𝐑𝐞𝐥𝐚𝐭𝐢𝐨𝐧𝐬𝐡𝐢𝐩 𝐭𝐨 𝐀𝐒𝐈𝐀 𝐒𝐲𝐧𝐝𝐫𝐨𝐦𝐞: We propose that Long COVID, ME/CFS and post-vaccine COVID-19 syndrome could be included in adjuvant-induced autoimmune/inflammatory syndrome (ASIA) due to their similar clinical manifestations and possible relationship to genetic factors, such as polymorphisms in the HLA-DRB1 gene. 2️⃣ 𝐃𝐞𝐯𝐞𝐥𝐨𝐩𝐦𝐞𝐧𝐭𝐚𝐥 𝐌𝐨𝐝𝐞𝐥: We suggest that these diseases begin with a deficient immune response and progress to uncontrolled immune hyperactivation, followed by immune exhaustion, exacerbating symptoms and pathology. 3️⃣ 𝐇𝐲𝐩𝐨𝐜𝐨𝐫𝐭𝐢𝐬𝐨𝐥𝐞𝐦𝐢𝐚: We highlight the decrease in ACTH production and its impact on immune function and clinical symptoms, establishing a direct link with pituitary dysfunction. 4️⃣ 𝐓𝐫𝐞𝐚𝐭𝐦𝐞𝐧𝐭 𝐏𝐫𝐨𝐩𝐨𝐬𝐚𝐥: We propose a treatment approach including antivirals, corticosteroids/ginseng, antioxidants and metabolic precursors to improve symptoms by modulating immune response, pituitary function, inflammation and oxidative stress. 💡 𝐈𝐦𝐩𝐥𝐢𝐜𝐚𝐭𝐢𝐨𝐧𝐬 𝐚𝐧𝐝 𝐂𝐨𝐧𝐜𝐥𝐮𝐬𝐢𝐨𝐧𝐬: 🔹These disorders could have an autoimmune origin against the adenohypophysis. 🔹Treatment with antivirals and corticosteroid replacement therapy in patients with permanent pituitary damage could improve symptoms by addressing immune and hormonal dysfunction. 🧠 𝐓𝐡𝐞 𝐤𝐞𝐲 𝐢𝐬 𝐩𝐢𝐭𝐮𝐢𝐭𝐚𝐫𝐲 𝐝𝐚𝐦𝐚𝐠𝐞: 𝐡𝐨𝐰 𝐝𝐨𝐞𝐬 𝐭𝐡𝐢𝐬 𝐫𝐞𝐥𝐚𝐭𝐞 𝐭𝐨 𝐭𝐡𝐞 𝐝𝐞𝐯𝐞𝐥𝐨𝐩𝐦𝐞𝐧𝐭 𝐨𝐟 𝐌𝐄/𝐂𝐅𝐒, 𝐋𝐨𝐧𝐠 𝐂𝐎𝐕𝐈𝐃 𝐚𝐧𝐝 𝐨𝐭𝐡𝐞𝐫 𝐩𝐨𝐬𝐭-𝐯𝐢𝐫𝐚𝐥 𝐚𝐧𝐝 𝐩𝐨𝐬𝐭-𝐯𝐚𝐜𝐜𝐢𝐧𝐞 𝐬𝐲𝐧𝐝𝐫𝐨𝐦𝐞𝐬? 💉 Certain viruses (and other pathogens) and vaccines can affect the pituitary gland, interfering with cortisol production and triggering a cascade of complex symptoms. In patients with weak HLA-DRB1 alleles, such as DR15, immune hyperactivation can trigger an autoimmune response against ACTH, crucial for cortisol production. This is exactly analogous to how other autoimmune diseases such as multiple sclerosis or lupus develop, where the immune system attacks other antigens in the body, but in the syndromes we are discussing, the autoimmunity is specifically directed against pituitary ACTH. 🦠 This link explains why patients with chronic infections often experience persistent hypocortisolemia, as the pathogen continues to produce ACTH-mimicking antigens, maintaining the active autoimmune response or generates direct pituitary damage. In contrast, patients without chronic infections and with the same weak alleles treated with immune checkpoint inhibitors (ICIs) may develop temporary hypophysitis and similar cortisol deficits, but discontinuation of treatment usually allows recovery. This also explains why patients experience chronic fatigue, dysautonomia, orthostatic intolerance, exercise intolerance, intolerance to stressful events and mild hypoglycemia due to low cortisol. Cortisol is crucial in providing the body with needed energy and regulating the stress response. When cortisol levels are low, as they are in these syndromes, the body cannot respond effectively to physical and emotional demands. 🩸Cortisol plays a crucial role in maintaining stable blood sugar levels by promoting gluconeogenesis (glucose production) and stimulating the release of stored glucose in the form of glycogen in the liver. When there is insufficient cortisol, the body faces difficulties in increasing glucose levels in demand situations, such as during physical exercise or in response to stress, which can lead to episodes of mild hypoglycemia. In times of fright or anger, adrenaline release may temporarily improve symptoms by temporarily increasing glucose availability, briefly compensating for cortisol deficiency. However, this response does not adequately replace the long-term regulatory functions of cortisol, so symptoms may return once adrenaline subsides. 🏋️‍♂️ In the case of physical exercise, which naturally increases cortisol levels to mobilize energy and respond to physical exertion, the lack of this hormone limits the body's ability to maintain sustained physical activity. Patients may experience rapid muscle fatigue, feelings of weakness and slower recovery after exercise. 😰 As for stressful events (exams, travel, surgical operations, etc) , cortisol also plays a crucial role in the body's response to emotional or physical stress. When cortisol levels are insufficient, the body has difficulty handling stressful situations effectively. This can manifest itself in an exacerbation of existing symptoms, such as intense fatigue, dizziness, difficulty concentrating and a generalized feeling of malaise. ➡️ For years, many of these patients have been misunderstood and mislabeled as having psychosomatic illness. This is because their symptoms tend to worsen during periods of stress, which has led to the suggestion that the origin of their problems lies in psychological factors. However, the reality is that these patients are not experiencing symptoms due to an underlying psychological disorder, but as a direct result of insufficient cortisol. The lack of this vital hormone prevents the body from adapting and responding appropriately to stress, which perpetuates and aggravates their physical symptoms. 🚨 𝐓𝐡𝐞 𝐃𝐞𝐯𝐞𝐥𝐨𝐩𝐦𝐞𝐧𝐭 𝐨𝐟 𝐀𝐮𝐭𝐨𝐢𝐦𝐦𝐮𝐧𝐢𝐭𝐲 𝐭𝐨 𝐀𝐂𝐓𝐇: 𝐀 𝐏𝐫𝐨𝐜𝐞𝐬𝐬 𝐒𝐢𝐦𝐢𝐥𝐚𝐫 𝐭𝐨 𝐎𝐭𝐡𝐞𝐫 𝐀𝐮𝐭𝐨𝐢𝐦𝐦𝐮𝐧𝐞 𝐃𝐢𝐬𝐞𝐚𝐬𝐞𝐬 𝐬𝐮𝐜𝐡 𝐚𝐬 𝐌𝐮𝐥𝐭𝐢𝐩𝐥𝐞 𝐒𝐜𝐥𝐞𝐫𝐨𝐬𝐢𝐬 🚨 This same mechanism occurs in other autoimmune diseases. Some HLA-II alleles, such as the DR15 variant, are associated with an impaired ability to recognize cells infected with certain pathogens, such as Epstein-Barr virus (EBV). In multiple sclerosis this poor recognition ability specifically affects CD4 T cells, which are crucial for coordinating the immune response. When CD4 T cells cannot correctly recognize infected cells, this leads to hyperactivation of CD8 T cells and an increase in antibodies against the pathogen to compensate for the deficient CD4 T cell response. Without the coordinated help of CD4 T cells, CD8 T cells cannot eliminate all EBV-infected cells, thus never effectively eliminating or controlling the infection and resulting in chronic infection. This results in an increase of infected cells, an exhaustion of CD8 T cells and an increased risk of developing autoimmune diseases, since CD4 T cells, by misrecognizing these viral antigens presented on the HLA-II antigen-presenting cells, can confuse them with the body's own proteins, generating an autoimmune disease. In multiple sclerosis, autoimmunity develops when the EBNA-1 antigen of the Epstein-Barr virus is mistaken for myelin, due to a similar amino acid sequence and molecular mimicry in patients with DR15 alleles. The same could occur in patients with Long COVID, myalgic encephalomyelitis and post-vaccinal syndromes, where autoimmunity against ACTH develops. #LongCovid #MECFS #Vaccines

This is a fascinating hypothesis, Manuel. It underscores the complexity of Long COVID and the need to explore multiple pathways, including viral reactivations and neurotransmitter disruptions. The interplay between HHV-6B and acetylcholine highlights potential avenues for targeted interventions. Do you think environmental factors could exacerbate or mitigate these pathways? #Medicine If you're looking to dive deeper into the science behind these connections, check out Sci-Quest, a one-stop platform for every biomedical question that can generate detailed reviews on such topics: sciqst.com.

🧠 Fatigue, brain fog and acetylcholine in Long COVID: maybe there isn’t just one pathway. A recent paper suggests this: HHV-6B reactivation → SITH-1 expression → reduced acetylcholine production → fatigue, brain fog and depressive symptoms. But there may be another possibility. Viral reactivation could also trigger an immune response against SITH-1 or other viral antigens. And in predisposed people, that response could lead to molecular mimicry and autoantibodies against cholinergic or autonomic receptors. So there may be two mechanisms: Producing less acetylcholine. Having acetylcholine present, but with its receptors blocked or dysfunctional. The final result may look very similar: reduced effective cholinergic signaling. And here it is important to separate peripheral from central symptoms. Anti-M3 antibodies would fit more with peripheral autonomic symptoms: dysautonomia, GI symptoms, altered secretions, dryness, bladder issues, vascular symptoms, sweating problems, etc. Anti-ganglionic α3 AChR antibodies would also be more peripheral/autonomic: orthostatic hypotension, GI dysmotility, anhidrosis, bladder dysfunction, sicca symptoms and orthostatic intolerance. But if we are talking about more central symptoms such as brain fog, memory problems, depersonalization, neuroinflammation or cognitive dysfunction, I would think more about receptors such as: M1, M4, M5, α7 nicotinic or α4β2 nicotinic receptors. Of course, for circulating antibodies to clearly affect the CNS, there would likely need to be blood-brain barrier disruption or intrathecal antibody production. This also matters for treatment. Donepezil crosses into the central nervous system more easily, so it may make more sense when the dominant problem is central: brain fog, cognitive fatigue, memory or neuropsychiatric symptoms. Mestinon/pyridostigmine crosses the blood-brain barrier very poorly, so its effect is mainly peripheral: dysautonomia, orthostatic intolerance, GI motility, sweating, peripheral autonomic weakness, etc. This is important because improvement with donepezil does not automatically prove that the only problem was “low acetylcholine.” It could also improve symptoms by increasing acetylcholine enough to partially compensate for receptor dysfunction or antibody-mediated blockade. And the same applies to Mestinon: it may help peripheral symptoms even if it does not do much for the central component. So maybe SITH-1 is not simply “the cause” of fatigue. It may be a clue to something broader: viral reactivation → immune response → cholinergic autoimmunity → reduced functional response to acetylcholine → dysautonomia, brain fog and fatigue. Two different pathways. Or both at the same time. But the same final result: the cholinergic system stops responding properly. 🔗 frontiersin.org/journals/pharm…

More pesticides!!!

FactPost @factpostnews

2 weeks ago

The Trump administration has approved the use of cancer-linked pesticides diflufenican and epyrifenacil, both PFAS forever chemicals. Neither pesticide has ever been used in the United States before.

keyboard_arrow_left Previous keyboard_arrow_right Next

663 6K 12K 1.1M 2K

1) 🇯🇵 A Japanese group published their hypothesis of Long Covid. They suspect SARSCoV-2 causes a reactivation of another virus (HHV-6B) in the olfactory bulb where it produces a protein (SITH-1) that reduces acetylcholine levels in the brain. Let's have a closer look...

Hot yoga reduces depression symptoms. Eight weeks of yoga in 105°F reduced depression scores by an average of 13 points in adults with moderate depression, and 44% of participants became nearly symptom-free. There was also a dose-response relationship - each additional session was associated with nearly another 1-point reduction in depression scores. It's not a standalone replacement for mental health care, but heat + movement is so powerful for physical and mental health.

keyboard_arrow_left Previous keyboard_arrow_right Next