Has anyone here tried this SS-31 yet? It's available as a peptide for injection from the usual suppliers. Essentially, it repairs/rescues impaired, dysfunctional mitochondria. People online write to run SS-31 before trying to induce any mitochondrial fission/proliferation by e.g. MOTS-C, or even to tun SS-31 first before blasting NAD+ or other stimulators of the ETC which would require properly functioning mitochondria in the first place.

@Mauritio Psychedelics Promote Structural and Functional Neural Plasticity, 2018 7,8-DHF rather than Dihexa may be a less controversial thing to take in order to attain the same kind of nootropic effect. It looks really good indeed overall for synaptogenesis (top), even in comparison to dimethoxy-4-iodoamphetamine (DOI), LSD or DMT (bottom): [image: 1778511807611-dhf.jpg] [image: 1778511809606-dimethoxy-4-iodoamphetamine-lsd-dmt.jpg]

"Here, we demonstrate that β-klotho (KLB)-expressing neurons in the hindbrain, specifically the nucleus of the solitary tract (NTS) and area postrema (AP), are both necessary and sufficient for FGF21's effect on energy expenditure and weight loss. " https://pubmed.ncbi.nlm.nih.gov/41920739/

@Mauritio said: @yerrag said: These essentials that contain esters that are generally antifungal: petit grain, lavender, ylang ylang, clary sage, geranium, roman chamomile Aren't some/ most of them estrogenic? Yes, they are. But they're for therapeutic use. Antibiotics can be harmful, but we take them because usage is limited. Usage of these is not a lifestyle choice.

@haidut Metformin lowers iron, copper (could be good) ,influences zinc, magnesium, B9, B12, B1, chromium but restores Randle cycle to burn glucose zinc could lower demand on metformin metals and gallstones https://www.sciencedirect.com/science/article/pii/S1015958424011527 The roles of metal ions in gallstones formation Author links open overlay panelKuinan Tong 1, Chao Jing 1, Tingting Wang, Kun Liu, Wei Guo, Zhongtao Zhang https://doi.org/10.1016/j.asjsur.2024.05.243 https://ars.els-cdn.com/content/image/1-s2.0-S1015958424011527-gr1.jpg https://ars.els-cdn.com/content/image/1-s2.0-S1015958424011527-gr2.jpg AI Metformin disrupts the Randle cycle (glucose-fatty acid cycle) by inhibiting fatty acid oxidation and reducing free fatty acid (FFA) levels, thereby promoting glucose utilization over fats. By inhibiting this cycle, metformin reduces insulin resistance, decreases hepatic glucose production, and restores the body’s ability to utilize glucose efficiently. Key Aspects of Metformin and the Randle Cycle:Randle Cycle Overview: The Randle cycle is the competition between glucose and fatty acids for energy oxidation, where high fat levels inhibit glucose uptake and oxidation, promoting insulin resistance. Mechanism of Action: Metformin reduces the oxidation of long-chain fatty acids, specifically in red muscle, which restores glucose oxidation and reduces the reliance on fat as a primary fuel source. Impact on Diabetes: By inhibiting this cycle, metformin helps lower elevated blood glucose levels and reduces hypertriglyceridemia, which are common in type 2 diabetes. Insulin Sensitivity: Metformin-induced inhibition of the Randle cycle improves overall metabolic flexibility and improves insulin sensitivity, enhancing muscle and peripheral uptake of glucose. Energy Balance: The drug helps reverse the overactive Randle cycle that occurs in obese or diabetic patients, improving the balance between glucose and fat utilization. Both metformin and zinc appear to have protective effects against gallstones, often through improving metabolic health and reducing gallbladder inflammation. While they are frequently used together for diabetes management, their individual roles in gallbladder health are distinct. Metformin and Gallstones **Reduced Risk: Long-term use of metformin is associated with a significantly lower risk of developing gallstones in diabetic patients. Mechanism: Metformin helps by improving insulin sensitivity and gallbladder motility, which prevents the "stasis" of bile that leads to stone formation.** Animal Research Warning: In some mouse studies, while metformin prevented stones, it was also linked to porcelain gallbladder (mucosal calcification), though it is unclear if this occurs in humans. Zinc and Gallstones Zinc Deficiency Connection: Patients with gallstone disease often have significantly lower serum zinc levels. Protective Properties: Zinc may help prevent gallstones by reducing free radical formation and protecting against oxidative stress in the liver and gallbladder. Bile Flow: Supplementation has been shown in animal models to suppress liver fibrosis and improve the composition of bile, potentially aiding in stone prevention. Taking Zinc and Metformin TogetherSynergy: For diabetic patients, combining zinc and metformin can be more effective than metformin alone for overall metabolic health. Safety: There are no known direct drug interactions between zinc supplements and metformin. Metabolic Benefit: Both substances help lower HbA1c levels and improve lipid profiles (cholesterol/triglycerides), both of which are key risk factors for gallstone formation. Zinc deficiency causes significant muscle loss (muscle atrophy), reduced muscle strength, and impaired muscle repair, as zinc is essential for protein synthesis, cell growth, and tissue regeneration. Severe deficiency increases muscle protein breakdown (catabolism), reduces muscle mass, and is an independent factor for sarcopenia. Zinc Deficiency and Muscle Loss Mechanisms:Reduced Protein Synthesis & Regeneration: Low zinc levels restrict muscle regeneration by slowing down myogenesis (muscle cell formation) and impairing muscle cell activation. Increased Breakdown: Deficiency disrupts skeletal muscle proteostasis, activating the ubiquitin-proteasome system, which breaks down muscle proteins. Mitochondrial Dysfunction: Zinc is crucial for mitochondrial health; its lack can lead to impaired mitochondrial function, reducing energy supply (ATP) for muscle cells. Hormonal Imbalance: Zinc deficiency can lead to lower levels of testosterone and growth hormone, which are essential for maintaining muscle mass .Chronic Diseases & Aging: In patients with chronic liver disease, zinc deficiency is an independent predictor of sarcopenia (age-dependent loss of muscle). Zinc acts as a modulator of AMPK (AMP-activated protein kinase), a key cellular energy sensor, influencing its activity in ways that can be beneficial or harmful depending on the context. It helps maintain metabolic homeostasis and is crucial for muscle protein synthesis, with zinc deficiency often increasing susceptibility to muscle atrophy via AMPK. Key Aspects of Zinc-AMPK Interaction:Muscle Metabolism: AICAR (an AMPK activator) increases intracellular zinc levels, and zinc-depleted conditions lead to greater muscle atrophy under stress. Neural Protection: Zinc can regulate glucose metabolism in spinal cord neurons via the AMPK signaling pathway. It has been shown to induce autophagy and protect against neuronal apoptosis following injury. Neurotoxicity Mechanism: Excessive free zinc (zinc excitotoxicity) can trigger neuronal death by overactivating the LKB1-AMPK-Bim cascade, leading to ATP depletion. Metabolic Regulation: Zinc affects the AMPK pathway by modifying the Thr172 phosphorylation of AMPK, which in turn regulates downstream targets like ACC (acetyl-CoA carboxylase).Cellular Energy: Studies suggest zinc exposure can influence energy metabolism by activating the AMPK pathway. In summary, zinc helps regulate AMPK activity, with appropriate levels aiding in energy management and tissue health, while excessive free zinc can trigger toxic, AMPK-dependent cell death. Signs of Zinc-Related Muscle Issues: Difficulty gaining or maintaining muscle mass.Reduced endurance and increased muscle fatigue.Slow recovery after exercise.Slow wound healing. Important Context:Athletes: Athletes are susceptible to zinc loss through excessive sweating and elevated metabolic demand, necessitating adequate intake to avoid muscle performance decline. Cancer Cachexia: Interestingly, excess zinc accumulation in muscles—driven by a protein called ZIP14 during severe illnesses like cancer—can also lead to severe muscle wasting, not just deficiency. Ensuring adequate zinc intake through diet (meat, shellfish, legumes, nuts) is key to preventing this type of muscle loss. Insulin-degrading enzyme (IDE), or insulinase, is a zinc-dependent metalloproteinase (~110 kDa) that breaks down insulin, amylin, and other small polypeptides. It plays a crucial role in regulating insulin levels and is a key target in diabetes research. It is often found in the cytoplasm of human cells and acts with a unique (HXXEH) zinc-binding motif. Key Details About Zinc Insulinase (IDE):Function: Degrades insulin, amylin, glucagon, and amyloid (\beta ) (A(\beta )). Structure: It belongs to the M16 metalloprotease family and requires zinc as a cofactor for activity. Location: Found in mammalian cytosol, peroxisomes, and endosomes. Alternative Names: Insulysin, insulin protease, or bacterial protease III (in E. coli). Medical Relevance: Because it degrades insulin, IDE is studied for its impact on insulin resistance and type 2 diabetes. Key Characteristics:Active Site: Unlike many zinc proteases, it uses an "inverted" (HXXEH) motif to bind zinc. pH Stability: The enzyme has an optimal pH around (7.0).Inhibitors: Its activity can be inhibited by endogenous factors or specific compounds.

@CrumblingCookie just saw you also posted about f. Prausnitzii. Nice synchronicity. For the purpose you mentioned above kestose might be beneficial. Since it increases butyrate and F. Prausnitzii.

@alfredoolivas fuck AI

Beautiful (minus the x-ray's in principal).

@Korven random question and it's not that important but just wondering, with your tortillas did you eat raw onions or not? or any other antimicrobial food with these foods and additives that have negative effects in studies due to microbial fermentation (choline, gums, proteins) I think eating antimicrobial foods with it probably lessens or ameliorates the negative effect

No evidence for prolactin’s involvement in the post-ejaculatory refractory period Prolactin is released during sexual behavior in male mice. "Baseline levels of circulating PRL in male mice were low for both strains (**BL6 0.86 ± 0.46; PWK: 2.31 ± 1.37 ng/ml; please see ref. 46 for BL6), but are significantly increased during sexual interaction (Bl6: F3,7 = 21.26, P < 0.0001; PWK: F3,8 = 17.18, P < 0.0001; RM one-way ANOVA) (Fig. 1a)." [image: 1778097373887-b12138a6-0a0b-4432-8de4-f8b9628819e8-image.jpeg] Acute prolactin release does not induce a refractory period-like state. "However, the involvement of PRL in the establishment and duration of the PERP is controversial and has not been formally tested" "The fact that PRL levels are already elevated during sexual interaction in BL6 and PWK males further suggests that PRL cannot promote by itself reduced sexual activity, at least in male mice" Mice have different prolactin responses to ejaculation then humans, but it was interesting experiment that does demonstrate how little is known about independent prolactin.

More info on the way how coco acts... How does coconut oil can stabilize or protect ingested PUFA from oxidation? Key ideas Coconut oil is not just resistant to oxidation but it can stabilize membranes. Coconut oil protects against the inflammation caused by endotoxins (but don’t use coco in case of a detox at the beginning of the process because it could amplify the immune reaction). SFA has an impact on enzyme expression when use in high amount (far from the ratio 2:2:1 for SFA/MUFA/PUFA). If you have a high intake of LA (omega-6), it can compete with ALA (omega-3) for the enzymes that are responsible for converting ALA into anti-inflammatory eicosanoids. SFAs like lauric acid (from coconut oil) don’t require desaturases. Thus, adding coconut oil won’t inhibit PUFA processing by competing for those enzymes, because SFAs don’t undergo desaturation. Coconut oil is 90 % SFA with 2/3 MCT oil. Adding coconut oil may help protect membranes by giving a spatial and stabilizing protection, improving membrane packing. ! Caveat: Balance is Key: Too much of a good thing is bad. How does coconut oil can stabilize or protect ingested PUFA from oxidation? Coconut’s structure, primarily consisting of saturated fats, is less susceptible to the chemical reactions that cause oxidation. Not just opposing resistance or fragility to oxidation (rancidity) but the way SFA can stabilize membranes. Coconut oil can indirectly protect PUFAs from oxidation by stabilizing the overall lipid environment and potentially influencing PUFA metabolism. (1) Saturated fat content, particularly medium-chain fatty acids (MCFAs) like lauric acid, can help to pack and stabilize cell membranes, making them less susceptible to the damaging effects of oxidation. Additionally, coconut oil's unique fatty acid profile and natural antioxidants may further contribute to its resistance to oxidative damage. When adding SCFA in a meal having some PUFA, it forms a tighter packing; when incorporated to tissues, it reduces the space available for PUFA chains to move and react with free radicals, thus stabilizing the membrane and protecting PUFAs from oxidation. Ray Peat, making a extrapolation in “Unsaturated fatty acids: Nutritionally essential, or toxic?” Question to AI How can SFA from coconut oil stabilize and thus protect incorporated fat in membrane? A clue: When incorporated to tissues, it reduces the space available for PUFA chains to move and react with free radicals, thus stabilizing the membrane and protecting PUFAs from amplifying ROS. Detailed answer on the link. https://mirzoune-ciboulette.forumactif.org/t2109-english-corner-coconut-oil-stabilizes-or-protects-ingested-pufa-from-oxidation#30204

If you want other sources: Are PUFAs toxic? Video of Chris Masterjohn 30’ https://youtu.be/WRmUzYD8l7Q CM earned a PhD in Nutritional Sciences from the University of Connecticut in 2012 and currently researches the physiological interactions between fat-soluble vitamins A, D, and K at the University of Illinois, Urbana-Champaign. https://chriskresser.com/an-update-on-omega-6-pufas/ Eat real food and balance your diet. Avoid industrial seed oils. Don’t go overboard with the nut flours. Eat pre-formed EPA and DHA (white fish). Ray Peat PhD. – Kate Deering – Dr. Rita Lee – Etc. Huile de poisson et effet sur la thyroïde http://mirzoune-ciboulette.forumactif.org/t1388-huile-de-poisson-et-effet-sur-la-thyroide#15791 Effets anti thyroïde des oméga-3 (In French, translator needed) (See translation of the excerpt below) Excerpt: Translation (« Huile de poisson et effet sur la thyroïde » => Fish oil and effect on thyroid) • ALA administration results in a 22% reduction in T3, the most potent form of thyroid hormone. T4 to T3 conversion rates decrease by 56% in response to ALA ingestion. ALA even interferes with normal T3 levels if you pre-administer T4 into the cells. (2) 2. http://www.ncbi.nlm.nih.gov/pubmed/1815532 • Animals fed a high PUFA diet compared to a high SFA diet (with corn oil or lard) experienced a significant decrease in thyroid hormone response in PUFA-fed rats. (3) http://www.jbc.org/content/256/14/7113.full.pdf+html Excerpt 1 from: Arachidonic acid causes an uncoupling effect and inhibits cellular respiration https://www.sciencedirect.com/science/article/pii/S0891584999000349 “It is shown that arachidonic acid causes an uncoupling effect under state 4 respiration of intact mitochondria as well as a marked inhibition of uncoupled respiration. Excerpt 2 from: Unsaturated Vegetable Oils: Toxic http://www.raypeat.com/articles/articles/unsaturated-oils.shtml To defend the seeds from the animals that would eat them, the [PUFA]-oils block the digestive enzymes in the animals' stomachs. Their tendency to oxidize is very great. These oxidative processes can damage enzymes and other parts of cells, and especially their ability to produce energy. The enzymes which break down proteins are inhibited by unsaturated fats, and these enzymes are needed not only for digestion, but also for production of thyroid hormones, clot removal, immunity, and the general adaptability of cells. The risks of abnormal blood clotting, inflammation, immune deficiency, shock, aging, obesity, and cancer are increased. Thyroid and progesterone are decreased. Since the unsaturated oils block protein digestion in the stomach, we can be malnourished even while "eating well." *) Useful info: more to be read on my forum. Effets anti-thyroïde des oméga-3 Effets Immunosuppressifs des omega-3 https://mirzoune-ciboulette.forumactif.org/t2042-effets-anti-thyroide-des-omega-3#29683 Excerpt: No one disputes the benefits of omega-3s for reducing inflammation and counteracting an overactive immune response. But it's all about long-term use. Not to mention that some sources of omega-3s also provide omega-6s. This leads to the storage and release of amino acids. See the details in the post "Fatty Acids for Dummies," linked below. (15) You'll find further information in the links provided below.

Improving blood flow to the extremities (hands and feet) involves more than just "moving more." It requires a balance between the mechanical pumping of the heart and the biochemical signals that tell your blood vessels to open up (vasodilation). For someone focused on metabolic efficiency, the goal is to improve circulation without triggering excessive stress responses that can actually lead to peripheral vasoconstriction. 1. The Biochemical Trigger: The Role of CO2 Effective circulation depends on the Bohr Effect. For oxygen to leave your blood and enter your tissues (especially in the small capillaries of your fingers and toes), carbon dioxide (CO2) must be present. Vasodilation: CO2 is a powerful natural vasodilator. When your metabolic rate is high and you are producing CO2 efficiently, your blood vessels relax, allowing blood to reach the extremities. The Trap: Over-exercising to the point of "gasping for air" or hyperventilating actually flushes CO2 out of the system. This can cause the peripheral vessels to constrict, leading to cold hands and feet even while your heart rate is high. 2. Strategic Exercise Selection To optimize blood flow to the extremities, the type of movement matters. Resistance Training (Concentric Focus): Lifting weights or bodyweight movements (like squats or push-ups) creates a mechanical "pump" effect. Focus on the concentric (the lifting phase) to stimulate blood flow and metabolic demand without creating excessive tissue damage or systemic inflammation. Low-Impact Steady State (LISS): Walking at a brisk pace where you can still breathe through your nose helps maintain a high CO2 tension. This keeps the peripheral "gates" open longer than high-intensity sprinting might. Micro-Movements: If you spend long periods at a desk, simple calf raises or grip strengtheners are highly effective. The calves are often called the "second heart" because their contraction is essential for pumping venous blood back up from the feet. 3. Thermoregulation and the "Core-to-Extremity" Link Your body prioritizes keeping your internal organs warm. If your core temperature drops even slightly, the body will pull blood away from your skin and extremities to protect the center. Warmth as a Catalyst: Exercising in a warm environment or wearing adequate layers helps signal to the nervous system that it is "safe" to send blood to the periphery. Metabolic Rate: A robust oxidative metabolism keeps your internal "furnace" running. If your resting metabolic rate is low, your body will naturally be more stingy with blood flow to the fingers and toes. 4. Nutritional and Biochemical Support Circulation is also a matter of fluid dynamics and mineral balance. Magnesium and Calcium: Magnesium helps the smooth muscles of the blood vessels relax (vasodilation), while calcium helps them contract. Ensuring adequate magnesium intake can prevent the "clamping" of peripheral vessels. Sodium Balance: Adequate salt intake is necessary to maintain blood volume. Low blood volume makes it much harder for the heart to push blood all the way to the ends of the limbs. Short-Chain Fatty Acids (SCFAs): Compounds like butyrate can support mitochondrial health and gut integrity, which indirectly supports systemic blood flow by reducing the low-grade inflammation that can make vessels "stiff." Summary of Strategies Strategy Action Mechanism Nasal Breathing Breathe only through the nose during light exercise. Increases CO2 retention and vasodilation. Calf Raises Perform 20 reps every hour while sitting. Engages the "venous pump" in the lower legs. Temperature Check Keep the torso and neck warm. Prevents the "survival" vasoconstriction reflex. Mineral Balance Ensure sufficient Magnesium and Salt. Maintains blood volume and vessel flexibility.

I actually just realized Yucca also has a 3:1 4:1 ratio just like the carrot salad and bok choy

@jamezb46 literally something like what you've posted in the next paragraph as counter evidence you cultured swine

COX-2 is overexpressed in advanced stages of tumors. Aspirin starts inhibiting COX-2 meaningfully after dosages of about 500mg (better would be >1g). Aspirin vindicated as an anti cancer drug. "Most solid tumors express the cyclooxygenase-2 (COX-2) protein, a target of NSAIDs. COX-2 overexpression in tumorsis considered a predictor of more advanced stage disease and of worse prognosis in a number of studies investigating solid malignancies. Therefore, NSAIDs are evaluated as anti-cancer drugs." Artificially overexpressing COX-2 makes mice more prone to developing tumors and knocking it out makes them less likely to develop tumors. "Both COX-1 and COX-2 are involved in tumor vascularization. COX inhibitors can directly affect angiogenesis [47]. " "Thus, COX-2 may be the cause of progression of estrogen-dependent breast cancer either directly by stimulating tumor cell proliferation, or indirectly by upregulating aromatase activity [60]. " "Part of the rationale for combining NSAIDs with chemotherapy involves circumvention of chemotherapy resistance mechanisms." https://pubmed.ncbi.nlm.nih.gov/16945549/ COX-2 inhibition makes chemotherapy (5-fluorouracil) more effective in vitro. https://pubmed.ncbi.nlm.nih.gov/21163769/

skin surface way is capacitive coupling https://pubmed.ncbi.nlm.nih.gov/8200888/ this showed effect i dont have the info on their approach rn. non fusing fractures for 11+ months 6/10 fused vs 0 The non-union healed in six of the ten patients who had been managed actively but in none of the patients who had been managed with the placebo unit. https://www.semanticscholar.org/paper/Capacitively-coupled-electrical-stimulation-results-Abeed-Naseer/bc78f0db97ce86d9fc64d5487b91cee839744c8d 11 of non unions unified by 15 weeks applied through steel plates on the skin - healed if the plates were within 8cm of each other The only significant factor determining the success of healing was the distance between the plates; a distance of eighty millimeters or less resulted in healing in all cases https://pubmed.ncbi.nlm.nih.gov/8458140/ partial limb regeneration https://pmc.ncbi.nlm.nih.gov/articles/PMC4683620/ https://pmc.ncbi.nlm.nih.gov/articles/PMC3495370/

@user73636 sounded like a gimmick at first but its well studied theres a lot on it, decent amount from japan , another way to get it without a machine is buying some elemental magnesium metal sticks or ribbons (safer to avoid as fine powder tho unless stored right). can add a stick or ribbon chunk to water and it will make hydrogen bubbles (added a small amount of malic acid to speed up getting past the oxide surface and a bit more hydrogen , then rinsing after drinking. i added it without malic and it still bubbled) https://bioenergetic.forum/topic/9291/hydrogen-dissolved-in-drinking-water-or-via-gastric-acid i reckon 200ug hydrogen at once would be good. trying to figure out how much a 10cm 130mg ribbon would give. max water saturation you can get is 1mg - 1.5mg per L but it reacts slow and without a lot of acid it forms a black layer. i read some papers where they dipped it for a short time and it had effect still

@LunaticRed I shave my arms and apply it there and the inside of thighs currently.