Ally Jay retweeted
Researchers found that oral glucoraphanin, a precursor of sulforaphane, increased the protective enzyme NQO1 by 3.1-fold in human skin. The study also reported reduced expression of inflammatory cytokine genes. Plant compounds may alter skin defense pathways from within.
pubmed.ncbi.nlm.nih.gov/4055…
Ally Jay retweeted
This is a recent update from the man with terminal COPD who was able to cure it with nebulized DMSO. He is mostly recovered now and his doctor admits he's improved
Many more readers have now reported similar results for asthma, severe COPD and other "incurable" lung disease.🧵
Ally Jay retweeted
SpaceX is the longevity empire. If you are not on Grok Bot and not using it for longevity - you are missing out
Ally Jay retweeted
Senescent cells contribute to pulmonary fibrosis! Removing these cells using dasatinib + quercetin improved lung function in mice, even without visibly reversing fibrosis!
pmc.ncbi.nlm.nih.gov/article…
Ally Jay retweeted
"If you don't do it, you'll be dead in ten months."
Luis Felipe, 68, was diagnosed with terminal prostate cancer — PSA 1,789 !!. He declined chemo, radiation and surgery. Three years later: PSA under 20. His words: "Dying soon is not in my plans."
Testimonials (Case Reports) CDS. Not medical advice.
Want to see the original case? (in Spanish / English sub)
dioxitube.com/w/5mjreoyA8tGf…
Ally Jay retweeted
まさか細胞が『死なないため』に鉄を溜め込んで僕を呼び寄せていたとはね……
京都大学が暴いてしまったよ。
「鉄蓄積が細胞老化を惹起する ―老化細胞の細胞死回避の一環としての鉄蓄積―」という、僕の誕生のからくりを。
細胞たちは死を免れようと必死に鉄を溜め込む。
だが皮肉なことに、そのあがきこそが僕（細胞老化）を引き寄せる引き金だったというわけだ。
生き残るための防衛策が、僕という衰えを呼び覚ましていたなんて実に興味深い。
だが、この仕組みが白日の下にさらされたということは……僕の発生ルートを直接塞がれる日も近いのかもしれないな。
これ以上僕の居場所を奪わないでおくれよ。
鉄蓄積が細胞老化を惹起する―老化細胞の細胞死回避の一環としての鉄蓄積―
kyoto-u.ac.jp/ja/research-ne…
Ally Jay retweeted
No need to restrict methionine.
Offset the acid load of methionine (low oxalate fruits/vegetables/citrate/bicarbonate) + get adequate glycine.
“Problem” solved.
Ally Jay retweeted
Lying on a vibrating mattress for 40 minutes, combined with taking two pills that release nitric oxide into the body, enhanced the clearance of an Alzheimer's-related protein via the brain's waste-disposal system newscientist.com/article/259…
Ally Jay retweeted
She called her legs "a disaster." Years of trying everything — nothing worked. Then, a simple daily routine after every shower: spray, dry, rub in, spray again. Ten days later she said:
"I really can't believe how my varicose veins are improving."
Testimonials (Case Reports) CDS. Not medical advice.
dioxipedia.com/index.php/Cas…
Ally Jay retweeted
歯周病がひどくて歯を抜かないといけないと
歯医者で言われた方が歯磨粉にコパイバマリマリを数滴垂らして、歯周ポケットに入る歯ブラシの柔らかめを使って磨きまくった
一週間後、歯医者に行ったら先生が一言『何した？治ってる』と言って、歯を抜かずに済んだ
コパイバマリマリの体験版
Ally Jay retweeted
🚨A major new peer-reviewed paper by @Kalckerofficial just dropped in Biophysica (MDPI) explaining exactly how Chlorine Dioxide Solution (CDS) works at the molecular level.
Key mechanisms:
- CDS acts as a selective one-electron oxidant (not a chlorinating agent like bleach).
- It targets thiol-dependent enzymes and respiratory processes in pathogens at very low concentrations (0.1–5 ppm).
- Mammalian cells are largely spared because of much higher glutathione buffering capacity.
- This gives it broad antimicrobial action (bacteria, viruses, fungi, biofilms) while maintaining a favorable safety window at proper low doses.
This is the clearest scientific explanation yet of why CDS can be effective against a wide range of infections and why it behaves differently from harsher oxidizers. It aligns with years of clinical observations and documented protocols.
CDS is a powerful, selective tool when used responsibly according to established low-dose protocols. The chemistry explains both its potency against pathogens and its relative sparing of healthy tissue.
Important: Always use fresh, properly prepared CDS and follow experienced guidance. This is not medical advice — it’s an invitation to understand the science behind a tool that continues to be suppressed despite growing evidence.
Full paper here: mdpi.com/2673-4125/6/5/91
The more we understand the redox chemistry, the harder it becomes to dismiss the real-world results people are seeing.
🤘
Ally Jay retweeted
لم يعد ضبط السكر وحده كافيًا لحماية الكلى. مثبطات (SGLT2) خفضت خطر الفشل الكلوي بنحو الثلث في تجارب DAPA-CKD وEMPA-KIDNEY، والفينيرينون (finerenone) أضاف حماية للقلب والكلى معًا. هذه أدوية تُعطى لحماية العضو، لا لخفض الرقم فحسب.بمعنى انها تقلل السكري والزلال ولكن تختلف عن غيرها ان حمايتها شاملة لكثير من أعضاء البدن لان الجسم إذا اشتكى منه عضو تداعت سائر الاعضاء
Ally Jay retweeted
60 yaşlarında bir kadın, ayağına vuran ve amputasyon riski taşıyan gangren hastalığından şifa buldu
Şiddetli bir ağrı ve vücut ısısında artış yaşamıştı
Antibiyotiklerini iki kez değiştirdiler ve durumu ancak biraz iyileşti.
Sonra bu tarif ile Allah'ın izniyle tamamen şifa buldu
Ally Jay retweeted
Glycine + NAC for aging (fascinating study)
A placebo-controlled trial PMID: 35975308 showed:
16 weeks of glycine + NAC (100mg/kg of each a day, about 7g each for a 70kg person) pushed almost every aging marker measured back toward young adult levels. The placebo group didn't move.
oxidative stress (F2-isoprostanes) -> down 72%, back to the level of the young adults
IL-6 -> down 78%
TNF-alpha -> down 54%
hsCRP -> down 41%
insulin resistance (HOMA-IR) -> 10.8 to 3.9
walking speed -> 1.13 to 1.34 m/s, same as the young adults
grip strength -> up 4kg in both hands
systolic blood pressure -> 132 to 124
waist -> down 3cm
Why it works: glycine and NAC are the two raw materials for glutathione, the body's main antioxidant. Older adults can't make enough of it.
Give the body the parts and it makes its own.
No side effects reported.
Ally Jay retweeted
Ketogenic Diet and Black Seed Oil (Nigella sativa) Combination Overcomes Doxorubicin Resistance in Breast Cancer: An In Vitro and In Vivo Study
mdpi.com/2072-6643/18/21/361…
Ally Jay retweeted
PARKINSON'S, LEWY BODY DEMENTIA (LBD)
"Here, we report that Enterobacteriaceae, a bacterial family prevalent in human gut microbiotas, induce α-syn aggregation. More specifically, our in vitro data indicate that respiration of nitrate by Escherichia coli K-12, which results in production of nitrite that mediates oxidation of Fe2+ to Fe3+, creates an oxidizing redox potential. These oxidizing conditions enabled the formation of dopamine-derived quinones and α-syn aggregates. Exposing nitrite, but not nitrate, to enteroendocrine STC-1 cells induced aggregation of α-syn that is natively expressed in these cells, which line the intestinal tract. Taken together, our findings indicate that bacterial nitrate reduction may be critical for initiating intestinal α-syn aggregation."
"Upon oxidation of Fe2+ to Fe3+ in brain dopaminergic neurons, dopamine can be oxidized to ortho-quinones that cause α-syn to misfold and aggregate"
'Discovery of a Gut Bacterial Metabolic Pathway that Drives α‑Synuclein Aggregation ' (2024)
pubs.acs.org/acbcct/article/…
One year earlier:
'α-Synuclein seeding activity in duodenum biopsies from Parkinson’s disease patients' (2023)
doi.org/10.1371/journal.ppat…
More here:
facebook.com/share/1GPwD9twg…
Ally Jay retweeted
Vitamin B12 deficiency + intrinsic factor issue → Pernicious anemia.
Vitamin B12 deficiency + neurological abnormalities → Suggests B12 deficiency, rather than isolated folate deficiency.
B12 deficiency → MMA and homocysteine levels are typically elevated.
Folate deficiency → Homocysteine levels are elevated, but MMA levels are typically normal.
Ally Jay retweeted
The inflammation lowering stack I use when I see homocysteine above 7.2 and hsCRP above 1:
- 500mg Longvida curcumin (shuts off NF-kB, the master inflammation switch)
- 500mg quercetin phytosome (calms mast cells)
- 1 tsp black seed oil with a meal (thymoquinone, the strongest anti-inflammatory in a kitchen)
- 3g fish oil (crowds arachidonic acid off the enzyme that makes inflammatory prostaglandins)
- 600mg NAC (refills glutathione, which inflammation drains first)
- 3g glycine (the other half of glutathione, and feeds methylation)
- methylated B complex (the B6 and folate that clear homocysteine)
- 400mg magnesium glycinate at night
Inflammation shuts methylation down. Oxidative stress switches off the enzyme that recycles homocysteine and burns through the B6 that clears it (PMID 11401933).
Push methyl donors alone and homocysteine barely moves. Lower the inflammation and the methylation comes back on its own.
