I use the computer a lot (both desktop and mobile) but my eyesight has remained basically perfect and I can only really narrow down the factors to two things: 25k IU of beta carotene every day Wearing good sunglasses every minute outside Now, I can't say for sure it's due to those, but they are the only things I've done for years and not since starting Peating in December, and my vision is apparently a lot better than many other people my age.

@sunsunsun Does brown rice have more b1 then normal jasmine/bismati/white rice??? Although I heard brown rice is harder to digest then white rice which would be a no go for a sibo boy like me

@Jennifer Ty those are some really interesting suggestions!

@EPSTEIN lol this guy is so retarded its actually charming

@Maximalus I get euphoria from 2mg cyproheptadine mixed with coffee on relatively not full stomach, complete with waking dreams like in an opiate coma. it's as good or better than kratom anyways 4-6 weeks of cypro is what I would do.

silicon chelates aluminum *edit posted that b4 reading your whole post

https://www.youtube.com/watch?v=pnn6tbTp_T0

@engineer Drop everything and reassess? If it still persists it could be the testosterone, due to it's long half life

Nice, I've heard similar positive results from others using vitamin D (UV) lamps from a bad starting point like with you. Have you considered something like Pyrucet for appetite too? It works so well for me because it drastically ramps up glucose oxidation.

@alfredoolivas While a portion of OAA is indeed converted to citrate, this is actually a feature, not a bug, of its anti-lactate profile: Clearing the Bottleneck: By converting to citrate, OAA "pulls" Acetyl-CoA into the TCA cycle. Activating PDH: High levels of Acetyl-CoA normally inhibit Pyruvate Dehydrogenase (PDH). When OAA clears that Acetyl-CoA out by turning it into citrate, it "unlocks" PDH. Result: Pyruvate is now more likely to be converted into Acetyl-CoA (to feed the cycle) rather than being "shunted" into lactate. Cytoplasmic vs. Mitochondrial Activity The anti-lactate effects described in studies from exogenous OAA often occur in the cytoplasm before the OAA even reaches the mitochondria: The Redox Buffer: In the cytoplasm, OAA effectively starves the LDH enzyme of its necessary fuel as they both compete for use of nadh The Malate Shuttle: The resulting Malate then enters the mitochondria, effectively "shuttling" those electrons in for oxidative phosphorylation rather than letting them fester as "reductive stress" in the cytoplasm. Kinetic Inhibition of LDH OAA is a structural analogue of pyruvate. Because of this similarity, it can act as a competitive inhibitor of Lactate Dehydrogenase (LDH). Even if it eventually gets metabolized, its presence in the cellular pool interferes with the enzyme's ability to bind to pyruvate and create lactate. You are correct that OAA is highly unstable and metabolically "hungry." This is why OAA supplementation often requires higher doses or stabilized forms (like thermally stabilized anhydrous OAA) to ensure enough reaches the target tissues before being decarboxylated or converted. OAA's instability (spontaneous decarboxylation to pyruvate + CO2, half-life ~minutes at pH 7.4) necessitates stabilized forms like benaGene (anhydrous OAA) at 100-500mg doses for therapeutic levels, ensuring cytoplasmic delivery before mitochondrial uptake or decay. This supports the observed lactate drops in models without rapid citrate exhaustion.

Propolis extract (ethanolic) Appears to have significant effects on healing of upper gastrointestinal tract mucosa (gastric & duodenal ulcers), especially as treatment enhancement of antibiotics against H. pylori, as well as for promoted healing thereafter (gastritis only slowly subsides over the course of at least 6 months up to a couple of years even after successful H. pylori eradication) Using human equivalent conversion from rat trials, generous daily propolis doses seem to be required: Ideally 3600mg. Certainly not below 1800mg. Synergistic combinations with olive leaf extract (OLE) and/or L. rhamnosus and/or L. reuteri. However, propolis monotherapy fails for H. pylori eradication. There's initial inhibition, but then the infection and bacterial evasion catches up. Propolis and Its Potential to Treat Gastrointestinal Disorders, 2018, review Propolis in the Treatment of Oral Mucositis ** Propolis shown effective. Propolis in the Therapeutic Management of Ulcerative Colitis ** "the studies developed with kaempferol, luteolin, and naringenin stood out" ** yet "these studies do not translate to human application, remaining to be explored its efficacy and safety in clinical trials." Propolis and Its Potential to Treat Gastrointestinal Cancers ** Various effects in vitro Antiulcer Activity of Propolis ** "propolis has been used in folk medicine to treat gastric ulcer" ** Dose-dependent protective effects (preventative), but also healing effects ** Effects of propolis mirrored in part by oral caffeic, ferulic, and cinnamic acids ** "100% of the tested extracts inhibited the H. pylori growth" Evaluating the Inhibitory Effects of Probiotic Bacteria and Propolis Extracts on the Growth and Histopathological Changes in Gastric Tissues of Helicobacter pylori Challenged Wistar Rats, 2024 "In vivo, the findings demonstrated that oral administrations of propolis and probiotics [L. rhamnosis, L. reuteri], either separately or in combination, led to significant increases in body weight and amelioration of histopathological changes in gastric tissue samples, particularly in terms of erosion depth, hemorrhagic inflammation, and apoptosis in the infected animals" Effects were dose-dependent and highest at 300mg/KG per day (HED = 48mg/KG, ie 3600mg@75KG). The yellow positive control received antibiotic triple therapy: [image: ijpr-23-1-148158-i001.jpg] "Propolis generally exhibits bacteriostatic properties against various bacterial genera; however, it may demonstrate bactericidal effects at elevated concentrations" "Propolis contains caffeic acid phenethyl ester (CAPE), which inhibits the enzyme peptide deformylase, a critical factor for the survival of H. pylori." "The antibacterial activities of propolis are dependent on the concentration of biologically active compounds, including phenolic acid esters and flavonoids such as pinocembrin and galangin" "During the study, a significant enhancement in the antibacterial activity was observed in the prepared propolis mixture (combination of all four propolis extracts). " "In the gastric tissue samples of the animals treated with propolis and/or probiotics, reduced bacterial load comparable to the antibiotic-treated group animals was observed. " "polyphenol compounds of propolis have significant enhancing effects on the eradication rate of H. pylori in rats with gastritis and peptic ulcers, suggesting that propolis supplementation may enhance the effectiveness of conventional H. pylori treatment" Anti-inflammatory and anti-oxidative effect of Korean propolis on Helicobacter pylori-induced gastric damage in vitro, 2020 "These findings indicate that the use of Korean propolis, which has anti-inflammatory and anti-oxidative effects, can be promising for the prevention of H. pylori-induced gastric damage. South African Propolis: Anti-Helicobacter pylori Activity, Chemistry, and Toxicity, 2025 Of 27 geographically distinct South African propolis sources tested, only 7 propolis compositions exhibited a MIC of >6.25 mg/mL against H. pylori. Many sources were as dose-effective as amoxicillin. "Propolis from northern Spain was investigated against H. pylori with ethanolic and propylene glycol extracts which were found to have MIC values ranging between 6.00 and 14.00 mg/mL" "The compounds pinocembrin, 3‐O‐acetylpinobanksin, and pinobanksin were found to be the most abundant." "Antimicrobially active South African propolis was reported to be primarily comprised of pinocembrin, galangin, and chrysin" Potential Efficacy of Propolis in Treating Helicobacter pylori Infection and Its Mechanisms of Action, 2025 "Propolis demonstrates dual functionality by inhibiting the release of inflammatory mediators and suppressing H. pylori growth" [image: nutrients-17-02803-g005.jpg] "The combined use of propolis with other natural extracts demonstrates superior efficacy. Studies indicate that propolis complexes, when used in combination with olive leaf and licorice extracts, more effectively inhibit H. pylori-induced gastric mucosal ulcers, reduce bacterial colonization, and alleviate gastric mucosal inflammation" "A trial involving 18 infected participants showed that after seven consecutive days of oral administration of Brazilian green propolis extract (3 times daily, 20 drops per dose), 50% of participants experienced a decrease of over 20% in their urea breath test values, indicating an initial inhibitory effect; However, after a 40-day treatment cycle, 83% of participants failed to achieve complete eradication of H. pylori, suggesting that while propolis monotherapy has some activity, it is insufficient for effective eradication and may require optimization of the dosing regimen, such as increasing the dose or frequency, to achieve sufficient antimicrobial concentrations."

[image: 1772102331525-47ba56e8-1e11-47ae-b195-65dfeb9c7f70-image.png]

@user73636 Quoting Wikipedia: https://en.wikipedia.org/wiki/Diisopropylamine_dichloroacetate#:~:text=DADA is formed by combining diisopropylamine with dichloroacetic acid. It is chemically related to pangamic acid (formerly known as "vitamin B15")%2C which may convert to DADA and diisopropylamine in the body.[4] Pangamic acid = ester of D-gluconic acid (the sugar-acid part) N,N-dimethylglycine (DMG) (the amino-acid part) Pangamic acid, stomach acid quickly breaks the ester bond and you get free DMG + free gluconic acid.

@ThinPicking open ai pin… ! Ass Intake of the wedgie given to wearers of the Open Ass Intake Pin. 🩲

I've seen a couple of gay peaters that seem to be relatively healthy. Nathan Hatch on fuckportioncontrol.com comes to mind as being gay but seemingly healthy. Though I think he's always been gay and did have cancer and digestive problems in the past. I do think it's more likely that someone is predispositioned to being gay if their mother has high stress or thyroid problems though.

I believe a stack of B5 + carnitine + OAA/malate High carb low fat Eating leaner meat cuts Lower bcaa intake And focusing on odd chain fats (produce less acetyl coa) would be a great way to lower the acetyl coa/coa ratio further increasing the activity of pyruvate dehydrogenase Also eat foods rich in nad precursors as the nad/nadh ratio is also important for pdh/pdk ratio malate and OAA can not only help pull acetyl-CoA into the TCA cycle (Krebs cycle) to make energy, which frees up CoA. They also help turn NADH back into usable NAD+. (TCA Cycle Pull) OAA mixes with acetyl-CoA to start the cycle, releasing free CoA each turn . Malate turns into OAA inside mitochondria, keeping OAA stocked so the cycle keeps running smoothly.

@hwisdom ur projecting here again it makes for really boring, mostly useless posts, that read like your dear diary.