Which nutrient to dampen glutamate in manufactured food, except taurine? I've got this info on my PC. Several nutrients and compounds can help dampen the effects of free glutamate(MSG) in manufactured food, primarily by blocking receptors, assisting with conversion to GABA, or reducing neuro-inflammation. Here are the key nutrients and compounds, excluding / in addition to taurine: 1. Primary Nutrients to Dampen Glutamate  Magnesium: This is considered a critical nutrient because it directly blocks the NMDA (N-methyl-D-aspartate) glutamate receptor, preventing the excitotoxicity caused by excess glutamate.  Vitamin B6 (as P5P - Pyridoxal 5'-phosphate): This is an essential cofactor for the enzyme Glutamate Decarboxylase (GAD), which converts excess glutamate into the calming neurotransmitter GABA.  Omega-3 Fatty Acids (EPA & DHA): These fatty acids, particularly DHA, are crucial for membrane health and have been shown to protect against MSG-induced neurotoxicity by supporting astrocyte function, which clears excess glutamate from the synaptic cleft.  Vitamin C : This acts as an antioxidant that attenuates NMDA receptor activity and helps increase glutamate reuptake from the synaptic cleft.  Vitamin E: As a lipid-soluble antioxidant, it helps reduce neuroinflammatory responses and increases the activity of glutamine synthetase, which breaks down excess glutamate.  Riboflavin (Vitamin B2): This supports the conversion of B6 to its active form (PLP) and helps prevent the buildup of neurotoxic homocysteine. 2. Functional Foods and Additives  Theanine: A compound found in green tea, it lowers glutamate activity in the brain by blocking receptors while also boosting GABA levels.  Ginger: Studies have shown that ginger significantly reduces MSG-induced elevated levels of glutamate, sodium, and calcium in the brain.  Curcumin (Turmeric): Known to attenuate MSG-induced neurotoxicity, reduce glutamate levels, and protect against inflammation.  Probiotics (Lactobacillus and Bifidobacterium): Specific strains express glutamate decarboxylase (GAD), which can convert ingested glutamate to GABA in the gut. 3. Other Protective Agents  N-Acetyl Cysteine (NAC): Helps the body regulate glutamate levels.  Zinc: Protective against neuronal excitotoxicity.  Coenzyme Q10: Reduces glutamate-induced cell death. Summary Table of Protective Action Nutrient/Compound Mechanism to Dampen Glutamate Magnesium: Blocks NMDA receptor Vitamin B6: Converts Glutamate to GABA Omega-3:Enhances glial uptake Theanine: Blocks receptors/boosts GABA Ginger: Normalizes glutamate levels Vitamin C/E: Reduces neuro-inflammation Sources and References Micronutrients May Be a Unique Weapon Against the Neurotoxic Triad of Excitotoxicity, Oxidative Stress and Neuroinflammation: A Perspective doi: 10.3389/fnins.2021.726457 Front Neurosci. 2021 Sep. https://pmc.ncbi.nlm.nih.gov/articles/PMC8492967/#:~:text=Riboflavin may also be able,protective function of vitamin D. Excerpt Riboflavin may also be able to directly affect excitotoxicity by inhibiting the exocytosis of glutamate vesicles in presynaptic neurons (Wang et al., 2008). Finally, riboflavin (along with PLP, folate, and vitamin B12) also has the ability to help protect against homocysteine build-up (Rozycka et al., 2013). Homocysteine has been shown to be neurotoxic via its ability to act as an agonist at the NMDA receptor (Deep et al., 2019), making riboflavin’s ability to reduce homocysteine very valuable. Riboflavin additionally has the ability to protect against neuroinflammation. First, riboflavin was shown to effectively reduce TNF-α, IL-1β, and nitric oxide (NO) in a staphylococcus infection model (Dey and Bishayi, 2016). Riboflavin also plays an indirect role for opposing inflammation through its effects on vitamin D metabolism. Multiple enzymes in the biosynthetic pathway of vitamin D are dependent on riboflavin for their action (Pinto and Cooper, 2014). Animal models have been able to induce vitamin D deficiency from riboflavin deficiency due to this effect on the internal synthesis of vitamin D (Pinto and Cooper, 2014). Since vitamin D has anti-inflammatory effects (as detailed above), riboflavin deficiency may inhibit this protective function of vitamin D. GABA: What Is It + Its Balance with Excitatory Glutamates Dr. John Gannage. Arkham Integrative Medicine Excerpt A 2020 study published in Translational Psychiatry has demonstrated that altering synaptic excitation-inhibition balance by potentiating GABA was associated with a significant reduction in ASD symptom severity (14). Interestingly, the first nutrients in the biomedical world proposed for the treatment of ASD over 50 years ago by Bernie Rimland were magnesium and B6. Magnesium blocks glutamate uptake through the NMDA receptor and B6 (pyridoxine) is a GAD co-factor for converting glutamate to GABA. The amino acid taurine is also GABAergic and commonly recommended by functional medicine practitioners for children on the autism spectrum with behavioral issues and hyperactivity. ASD = autism (stands for autism spectrum disorder => dissociative identity disorder). 3) Natural products as safeguards against monosodium glutamate-induced toxicity doi: 10.22038/IJBMS.2020.43060.10123 Iran J Basic Med Sci. 2020 Apr. Chemistry of MSG explained. Toxicity and side effects. Protective effects of plants, food, vitamins and natural compounds.

unless you’re on the bioenergetic forum

@ilovethesea said in Healthy alternative to chips: I buy authentic Mexican nixtamalized corn tortillas. Cut into 4s, bake in oven around 400F for about 10 min until crispy. Eat with salsa, yogurt or whatever dip you like. I do exactly this. Though, the recipe I follow says to bake them at 475F. No wonder it's always a small window between being done and burning! I also find most corn tortillas have softeners in them, e.g., gums. I'm hoping to find one without.

More details on this link: Relation entre potassium et insuline https://mirzoune-ciboulette.forumactif.org/t2175-relation-entre-potassium-et-insuline#30640 Blood glucose management – the essential trio – with potassium playing a key role as an often-overlooked facilitator and magnesium ensuring stability. See graph at the end of the post.

I was looking more into this recently and it appears as though it could be DHT triggering osteoblasts in the skull bones to grow more. However, that would mean the most direct fix is to reduce DHT, which is horrible (as we all know by know). This does not actually mean that skull expansion is the cause of hair loss though because it merely puts more strain on the scalp and then decreases blood flow. So, the underlying cause of all hair loss is still the same: bad metabolism. The big question would be how to best increase blood or nutrient flow and like Peat said there are many ways to do it.

I love the Tintin movie (2011) : bingeflix.tv/movie/17578

has anyone ever considered scar gels for hair loss? there is a lot of overlap with healing the skin and TGFb-1 many of them contain interesting ingredients that would stop inflammation in the scalp

https://www.youtube.com/watch?v=MZIvg4GbJUs [image: 1771462772188-it_never_did.png]

@haidut There are many ways to deplete GSH in cancer cells e.g. arsenic AI Arsenic exposure causes significant glutathione (GSH) depletion by increasing reactive oxygen species (ROS) and directly binding to sulfhydryl groups, leading to oxidative stress and reduced antioxidant capacity in blood and tissues. Depletion of GSH sensitizes cells to arsenic-induced apoptosis, frequently utilized in cancer therapies (e.g., leukemia) to enhance the efficacy of arsenic trioxide. Mechanisms of Arsenic-Induced Glutathione Depletion Oxidative Stress: Arsenic exposure increases ROS, which consumes GSH, a crucial cellular antioxidant. Direct Binding: Arsenic binds directly to glutathione and other thiol-containing proteins. Inhibition of Synthesis: Exposure can reduce essential raw materials for GSH synthesis, such as cysteine and glutamate. Enzyme Activity: While glutathione-S-transferase (GST) activity might increase in response to stress, it often results in a net decline of the GSH pool. Significance of GSH Depletion Increased Toxicity: Lowered GSH levels render cells more vulnerable to arsenic toxicity. Cancer Therapy: GSH depletion (e.g., via Buthionine sulfoximine, BSO) enhances arsenic trioxide's ability to kill cancer cells, as shown in leukemia studies. Reduced Detoxification: Impaired GSH levels impair the body's ability to methylate and excrete arsenic. Consequences and Mitigation Oxidative Damage: Depletion causes significant decreases in brain and blood protective enzymes like superoxide dismutase (SOD) and glutathione peroxidase (GPx). Therapeutic Approaches: Antioxidants or chelators, such as MiADMSA, have been shown to be effective in restoring GSH levels and reducing ROS induced by arsenic. gold nano-particles https://www.sciencedirect.com/science/article/abs/pii/S138589472501232X auranofin -indirectly https://pmc.ncbi.nlm.nih.gov/articles/PMC8777575/ silver nano-particles https://www.sciencedirect.com/science/article/abs/pii/S0378427410017984 https://thesilveredge.com/clinicalstudies/ selenite and selenate https://pubmed.ncbi.nlm.nih.gov/10406889/

@cedric good info

https://www.youtube.com/watch?v=VTchFM3wb68

@bio3nergetic We must remember that vit.A , retina/brain/LRAT require phospholipids/lecithin Lecithin forms cell mambranes and we lose it while aging Perhaps some forms of vit.A "toxicity" could be a lecithin deficiency AI Lecithin supplementation has shown potential in supporting retinal function, primarily through its role in enhancing the bioavailability of nutrients essential for eye health and as a component of specialized medical treatments. Lecithin, particularly in the form of lecithin-bound iodine (LBI) or phosphatidylcholine, is associated with improvements in retinal pigment epithelium (RPE) health, tear film stability, and the reduction of oxidative damage in the retina. Key Findings on Lecithin and Retinal Function: Retinal Pigment Epithelium (RPE) Protection: Lecithin-bound iodine (LBI) has been used in Japan to treat retinal diseases, including central serous chorioretinopathy. In studies, LBI was shown to prevent hypoxic damage to RPE cells and suppress inflammatory responses (such as CCL2 secretion), suggesting a protective effect on the retinal structure. Retinal Degeneration and Function: In animal models of retinal degeneration, a lecithin-containing diet improved retinal function, as evidenced by higher b-wave amplitude in electroretinography (ERG) tests compared to control groups. It was found to reduce the invasion of macrophages into the retina and decrease inflammatory markers. Enhancing Nutrient Absorption: Lecithin acts as an emulsifier that helps the body absorb and utilize fat-soluble vitamins, including Vitamin A, which is crucial for producing visual pigments in the retina and maintaining photoreceptor function. Exudative Age-Related Macular Degeneration (AMD): Research into the use of iodized lecithin tablets for exudative AMD indicated a potential positive impact, with studies reporting improved visual acuity and reduced retinal thickness in treated groups compared to control groups. Tear Film Stability (Dry Eye Disease): Sunflower lecithin supplementation has been shown to improve dry eye disease (DED) symptoms. As a rich source of phosphatidylcholine, it may enhance the lipid secretions from the meibomian glands, stabilizing the tear film. Retina Protection against Toxicity: Studies on rat retinas indicate that lecithin can help maintain the structural integrity of retinal proteins (specifically α-helix and β-sheet ratios) when exposed to oxidative stress, potentially reducing damage from, for example, chemotherapeutic agents like ifosfamide. Important Context: Lecithin-Retinol Acyltransferase (LRAT): Lecithin:retinol acyltransferase is an enzyme crucial for the metabolism of Vitamin A in the retina. It helps convert all-trans retinol to all-trans retinyl ester, a key step in the visual cycle. Limitations: While promising, some uses of lecithin, specifically lecithin-bound iodine, have limited clinical trials outside of Japan, and many findings are based on preclinical or older studies. In summary, lecithin supplementation, particularly when containing iodine or as a source of phosphatidylcholine, may support retinal function by improving structural integrity, reducing inflammation, and increasing the absorption of necessary nutrients, according to research.

@user73636 Vit. K3 and C can bypass Q10 to cyt.c Vit .K3 is intermediate to K2 https://pmc.ncbi.nlm.nih.gov/articles/PMC5953218/