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Useful info on magnesium:
High-Dose Vitamin D Depletes Magnesium – Carolyn DEAN, MD ND.
https://mirzoune-ciboulette.forumactif.org/t2130-dynamique-entre-vitamine-d-magnesium-et-calcium#30339

Excerpt 1:
Magnesium expert Andrea Rosanoff, Ph.D., is one of the few people who understands the dynamic between vitamin D, magnesium, and calcium. She makes it the subject of her 2016 article, “Essential Nutrient Interactions: Does Low or Suboptimal Magnesium Status Interact with Vitamin D and/or Calcium Status?”

Excerpt 2:
Magnesium is required for many steps in vitamin D metabolism, including its conversion from its storage form (which is also the supplement form) to its active form. This means that taking extremely high doses of vitamin D can lead to magnesium deficiency without anyone realizing it.

I've ordered cytomel from clubsdiscountshop today

Sources and References
0. Inspired by my reading from Jean-Marie Defossez in a health magazine. Who is Jean-Marie Defossez?
A speaker, author, and facilitator of breathing courses and workshops, Jean-Marie Defossez holds a doctorate in animal biology and specializes in physiology. Trained in numerous therapeutic breathing techniques, notably in the USA, he founded the breathing coach in 2014.
He is notably the author of “Grand Guide du nerf vague” and “Être en bonne santé grâce au nerf vague” (The Great Guide to the Vagus Nerve, and “Being Healthy Thanks to the Vagus Nerve”, published by Jouvence Editions).
NB: His guide / site is a bit too commercial. Not everything is 100% in line with RP, but it's a good start to explore further (if you have time to lose) 😉

Short video of Relaxation and Pranayama – for Shavasana technique
https://youtu.be/1VYlOKUdylM (1.06’’)
sedinfrance.org: Vagus nerve stimulation (In French)
Chronic stress affects the functioning of the vagus nerve. Excessive or constant stimulation can lead to desensitization. An over-stimulated vagus nerve can become weakened or dysfunctional, leading to a variety of symptoms such as digestive upset, anxiety, chronic fatigue, and difficulty recovering physically and emotionally. When the nerve is constantly stimulated, it can lose its ability to function properly, affecting the balance of the autonomic nervous system and leading to dysfunction. The vagus nerve also plays an important role in regulating inflammation.
apoticaria.com le-nerf-vague-sentinelle-du-bien-être (in French)
=> When properly activated, the vagus nerve has a positive effect on regulating inflammation. Through acetylcholine, it sends a signal to immune cells (especially those in the intestine) to reduce inflammation as soon as it is no longer necessary.
How is the vagus nerve affecting acetylcholine? Indirectly through microbiota on cortisol and serotonin hormones? The vagus nerve does not directly cause the microbiota to produce acetylcholine. However …
The Role of Serotonin and Cortisol
• Microbiota influence on serotonin:
The gut microbiota affects tryptophan metabolism, a precursor to serotonin, and can produce serotonin itself, influencing the neurotransmitter levels in the body and brain.
• Microbiota's impact on cortisol:
The microbiota-gut-brain axis is involved in regulating the stress response, which includes the production of hormones like cortisol.
How It Connects
a. Microbiota influence neurotransmitter levels: Gut bacteria influence the production of neurotransmitters like serotonin.
b. Vagus nerve activation by microbial products: These microbial products, including acetylcholine and others, can directly or indirectly activate the vagus nerve, which connects the gut to the brain.
c. Influence on hormonal regulation: The vagus nerve's signals influence brain regions that modulate mood, stress, and emotion, which are linked to hormones such as cortisol and serotonin.
d. Bidirectional communication: This creates a bidirectional relationship where the microbiota influences brain function via the vagus nerve, and brain activity also influences the gut microbiota. Neurotransmitter modulation: The vagus nerve helps with stress management.
eleasante.com / le-lien-entre-le-nerf-vague-et-le-sommeil-implications-conséquences-et-pistes-thérapeutiques (in French) (The-link-between-the-vagus-nerve-and-sleep-implications-consequences-and-therapeutic-avenues)
When the vagus nerve is activated, it induces a state of relaxation and calms physiological stress reactions.
The vagus nerve modulates the production of cortisol via acetylcholine by promoting a state of relaxation and regulating the parasympathetic nervous system, which calms the body's stress response. Acetylcholine, the main neurotransmitter of the vagus nerve, has anti-inflammatory effects too and improves mood, particularly nervous system activity, which is linked to increased cortisol production. Music Use for Mood Regulation: Self-Awareness and Conscious Listening Choices in Young People with Tendencies to Depression.
https://www.frontiersin.org/journals/psychology/articles/10.3389/fpsyg.2019.01199/full Technique of Shavasana or Savasana
Vidéo (avancez jusque 45’’) : Relaxation et Pranayama - Viloma en Savasana
https://youtu.be/H4PJz-hFd54 (en français) 15’
=> You gradually and fairly slowly move through the contact points of the body parts in contact with the ground, starting from the head, i.e., the top of the skull. You imagine that you are "exhaling" the load, the tension. You feel the tension, imagine the weight of the limbs, and you gradually release them, moving through the other limbs. You feel the weight of the body leaving you. Some people will not be able to directly use this technique until they have released excess stress through a fairly energy-intensive physical activity. Jogging, for example (or whatever physical activity suits you best).

pizotifen might be a better option for people who can't handle cypro

@GreekDemiGod amazing stuff

You asked for the bioenergetic approach, and I was hoping someone more knowledgeable than me would respond with that but no one has, so I will try.

I imagine that the same Peaty substances that help with depression, autism, and social withdrawal would help you.

Perhaps you don't need to focus on treating the dysphoria with anything specific to that, and it will resolve as you treat the depression or any other symptoms that you have (see below). Maybe dysphoria is just part of how you personally manifest the same high serotonin, low thyroid "syndrome" as others who have depression or autism without dysphoria.

It would be useful to know:

what other symptoms you have? (for example: gut distress, acne, brain fog, ADHD, overweight, struggle to make friends, night sweats, etc) lab work to see if anything stands out (TSH, Prolactin, Cortisol, CRP, heavy metals, mold, gut dysfunction, lots of others.) what you've tried (diet, supps, medicines) and what the results were (for all your symptoms, not just dysphoria) what is your current diet and lifestyle (do you sleep well? do you have any big micronutrient deficiencies? Etc)

Basic bioenergetic ideas to help any mental issue would be:

Take high dose Thiamine, Thyroid hormones, eat more sugar, salt, and protein in order to Increase your metabolic rate to the correct level (as measured by your morning waking temperature) and to lower the stress system (cortisol, adrenaline, serotonin, estrogen) Lower serotonin by eating a gut-friendly diet, using carrot salad, taking substances like cyproheptadine. Lowering serotonin may be very helpful for you as it is implicated in autism, and I've heard that autism and gender dysphoria are often related. Also your depression and the feelings that you describe sound like what I've read Peaters blame on serotonin.

I think it's likely that gender dysphoria is a result of childhood vaccine induced mild brain damage. I say that because it overlaps a lot with autism (widely regarded in our "alternative health" circles as vaccine induced) and because it has the same huge, inexplicable increase in prevalence across recent generations that autism shows (both were pretty rare before childhood vaccination went into overdrive).

I know of two pathways for vaccine damage:

mild brain damage from inflammation (the adjuvants in the vaccines attacking the brain at the time of vaccination) - this would have to be treated with the things that are healing to the brain. Some ideas: Thyroid hormones, Thiamine, Niacinamide, Pregnenolone, Progesterone (maybe you specifically should proceed with caution with that one as it is feminizing - perhaps haidut's Androsterone instead? I don't know), and anti-stress substances that block cortisol's brain damaging effects. heavy metal accumulation in your body: the adjuvants in the vaccines - mercury and aluminum. People have proposed various ways of removing these metals. Chelation therapy is apparently very dangerous if you don't know what you're doing, and Ray Peat recommended gentler approaches. Ray advised gently and slowly removing metals over time and said that orange juice and coffee could do that. Another idea is Silica-rich mineral water (like Fiji water) which can apparently remove aluminum over time.

I want to say I don't have experience with most of this, nor am I a Peaty expert at all. There's no one size fits all protocol, for example pregnenolone gives me terrible insomnia and is therefore counterproductive for me, even though it's great for other people.

@lobotomize-me con you please give more details on oj acting as anti thyroid? I never thought of it and I wonder whether now I feel better and less bloated as oranges are not in season and I can't get on. Thanks!

Pharmacological dosage of vitamin A as supplement
Inhibitors of retinol
We will assume that we are not dealing with vitamin A inhibitors. Mind when combining 2 or several factors: Alcohol (> 1 glass wine or beer a day), excessive coffee (more than 2-3 cups), cortisone, excess iron (>240; ideal ferritin level at 120 ng/ml), high amount of vegetable oils (> 5 g PUFA), smoking, anti-acid supplement, aspirin 500 mg without making staples (impact on platelets), …
Works synergistically with: Calcium, Phosphorus, Zinc, C, D, E*, Choline, Vitamin B* complex, EFA.

Too much of a good thing is bad.

Optimal range
There is no consensus about the ratio between HD A1 and D3.
Ratio 1:1 to 3:1 for retinol / Vit D3 is optimal when taking a supplement. For Chris Masterjohn
Ratio 4:1 to 8:1 for Dr. Lindsay. More vitamin A than vitamin D. In studies examining the protective effects of cod liver oil against upper respiratory tract infections, Dr. Lindsay and her colleagues used A-to-D ratios between 5:1 and 8:1.
Let’s say we should target 35 ng/mL 25(OH)D levels to limit immune problems. Target 45 ng is optimal
Chris Masterjohn has discussed the importance of maintaining a healthy balance between vitamins A and D, rather than focusing on high levels of either.
• 30 ng/mL as a minimum:
Many experts consider 25(OH)D levels of 30 ng/mL (75 nmol/L) and above to be sufficient for most adults to maintain bone health and potentially reduce the risk of some diseases.
• 40-60 ng/mL for potential benefits:
Some research suggests that higher levels within the 40-60 ng/mL (100-150 nmol/L) range may offer additional benefits, potentially reducing the risk of certain cancers, autoimmune diseases, and other conditions.
Note: When you reach a ceiling below 40 ng/mL Vit D, you must be careful not to exceed 420 mg of elemental magnesium. Has to be confirmed with practical guidance.

Optimal vitamin D level
There is some good evidence that 25(OH)D levels should be at least 30-35 ng/ mL (75-88 nmol/L). Much higher levels may be better, or they could start causing harm, especially in the absence of adequate vitamins A and K2. Once we leave the land of 30-35 ng/mL, however, we enter the land of speculation.
Sources:
Chris Masterjohn – Westonprice.org 2010.
https://pmc.ncbi.nlm.nih.gov/articles/PMC8003866

Synergism between Vitamin A and Vitamin D but Excess Vitamin A causes Bone Problems
A study from NIH has shown that Vitamin A, specifically retinoic acid (RA), can increase Vitamin D Receptor (VDR) expression by up to 3-fold in certain cell types. This increase is observed in various tissues and cell types, including T cells and muscle cells, when treated with RA. The study also suggests that RA-induced VDR expression can be affected by Vitamin D, and vice versa, highlighting a complex interplay between these two important nutrients.
The dose from research was less than 5000 IU of Vitamin A (1500mcg) that get best benefits.
However, an increased VDR expression due to high level of retinoic acid (RA) can influence the downstream effects of both Vitamin A and Vitamin D signaling pathways.
doi: 10.3389/fimmu.2021.684015 Fatima A H Al-Jaberi et al. 2021. Front Immunol.

Interaction and Proposed Ratios
Chris Masterjohn describes a dynamic synergy: Vitamin A and vitamin D each mitigate the other’s toxicity, but when one is excessive relative to the other, metabolic harm may occur—such as bone loss (from too much A alone) or soft tissue calcification (from too much D alone). Vitamin K₂ is essential to activate key Gla proteins like osteocalcin and matrix Gla protein, helping ensure calcium goes into bone rather than soft tissues and articulations.
Source: mountaindogdiet.com interview with Chris Masterjohn: Dynamic synergy between vitamin A and vitamin D.
According to the gosling study (poultry nutrition), overly high A relative to D impaired growth—even moderate A antagonized D at low D levels. Growth was optimized with ratios closer to ~3.5:1 or lower.

Addressing Thyroid Status according to Ray Peat Considerations
I’ve noted Ray Peat’s concept of reducing retinoic acid when hypothyroid. In those cases, it may make sense to lean toward a lower A:D ratio, perhaps closer to 1:1, or even shift toward more D if RA synthesis slows. Evidence from community reports aligns: hypothyroid individuals frequently struggle to raise 25(OH)D even with doses alone, but see improvement when vitamin A is added—but only in appropriate ratios.
Thus, especially if hypothyroid, starting with ~1,000 IU A with ~1,000 IU D₃ may be more effective, slowly titrating both up while testing 25(OH)D serum, and watching for signs of imbalance.

Adressing the balance for liposoluble vitamins
Talk with ChatGPT. My final target (based on known data), making things reachable
• To reach 35 ng/mL 25(OH)D, ~2,000–3,000 IU D₃/day may be needed for most adults (see meta analysis: European adults ~2,500 IU/d → ~75 nmol/L, i.e. ~30 ng/mL) pubmed.ncbi.nlm.nih.gov.
• To maintain a sane A:D ratio between ~1:1 and 3:1, vitamin A intake at ~2,000–6,000 IU depending on your chosen D dose is reasonable.
• Your 1 mg K₂ MK 4 aligns well with vitamin K needs to activate the Gla proteins.
• Start perhaps with a mid point: 3,000 IU A in morning, 2,500 IU D₃ evening, and keep K₂ midday with fat. Check serum 25(OH)D and adjust.

Summary
 Chris Masterjohn strongly advocates balanced A:D ratios (~1:1 to 3:1); 5:1 is higher than typical guidance and risks antagonism.
 To reach 35 ng/mL D, I likely need 2,000–3,000 IU D daily.
 Therefore 2,000–6,000 IU vitamin A, paired with your 1 mg MK‑4, would better align with balance principles.
 And if hypothyroid, sticking closer to 1:1 may be safer.
 All doses remain below toxicity thresholds (UL for A ≈ 10,000 IU/day; for D ≈ 4,000 IU/day) but we’re in pharmacologic range—monitor labs.
If you want more Vit A, start perhaps with a mid point: 3,000 IU A in morning, 2,500 IU D₃ evening, and keep K₂ midday with fat at 1 mg. Check serum 25(OH)D and adjust.

Supporting Chris Masterjohn Sources
• He emphasizes the necessity to balance A and D (synergistic moderation), and cautions that excess of one can poison the other’s benefits; optimal functioning requires balanced intake plus adequate K₂ to activate key proteins
• Balance extra 500 µg K₂ with 3,000 IU A and 900 IU D offers a template to scale up proportionally as doses rise.

@wester130 Not sure, I don't wear glasses.

@Luke europe

I like to pamper myself and have cream in my coffee. It is delicious.

*) Suspicion of FUT2 deficiency
If there is a metabolic deficiency (FUT2 gene), the mucus layer is defective/insufficient.
In the presence of insufficient mucus, the small intestine is not properly protected by the thickness of the mucosa. Mucus also serves to trap unwanted organisms and push them towards the colonic flora (microbiota), which serves as food for the good bacteria. There is then a risk of stagnation and the creation of a gastro-resistant biofilm, a future pothole, where friendly or unfriendly colonies may form.
At the beginning of the process, the friendly strains that develop in the small intestine are no longer friendly at all and will proliferate "live," benefiting from 100% of the nutrition (to the detriment of their host) and forming colonies that will ultimately be pathogenic and impervious to antibiotics. So, yes, at the beginning, we will have good feelings, then after 1 to 2 months it will start to go wrong without us understanding where it comes from.

Whatever is happening to him, his older work is still gold and worth listening to

Youtube Video

@NoeticJuice said in Iodine as a game changer:

I've read elsewhere that vitamin C, B2, B3 and magnesium should be supplemented alongside iodine and selenium. Are these not needed?

Magnesium: For sure (preferably bisglycinate Mg). 300 mg Mg element when stressed.
80% people lack RDA (+/ 420 mg)
Vitamin C: I'd take 2 or 3 very mini pinches of powder. mind the kind (...).
Target 500 mg.
Riboflavin B2: yes but not required every day. 2 or 3X+wk.
B2 is a cofactor essential for various enzymes involved in energy production and neurotransmitter synthesis in the brain. Hypothyroidism can impair the conversion of riboflavin to its active forms, potentially leading to functional riboflavin deficiency.
B1 B2 and B3 + Biotin are often associated. We lack 50 % B1 to assimilate carbs. 2x/wk a complex B50 (co-enzymed).
If you're in the fog, or if you lack energy, a higher level of B1 could be needed. 100 mcg.
(+ glycine via collagen or bone broth). See the posts of mostlylurking.
Note: There is no proof but ... We lack thiamine, as explained. Thiamine deficiency can exacerbate symptoms like fatigue, especially in individuals with hypothyroidism, and supplementation can potentially improve these symptoms.

@Kilgore I'm sure we'll both get a lot of use out of it. This is designed much better to make it convenient to use. I hardly used the ones I bought from Redlightman.

Lack of magnesium
How does a lack of magnesium induce a deficiency in mitochondrial energy at the end of the process?
I’ve been reading a RP letter recently and I wanted afterwards to go deeper in the PKC system (Protein Kinase C) to connect the dots. (1)
Nearly every reader here knows the impact of PUFA on metabolism. And the interdependence and the ripple effect between excess estrogens and adipocyte cells (though AA cascade when we are stressed).
When we have difficulty in maintaining an adequate energy production, whatever the cause may be (e.g. diabetes, hypothyroidism, colopathy, etc.), a deficit produces an alarm state, causing increased production of adrenalin and cortisol. (2) (Derived from the "fight-or-flight" response, a protective survival process). These stress hormones trigger the release of stored energy from the liver (glycogenolysis) and fat tissue (lipolysis). Thus, adrenalin mobilizes fat from storage, and these free fatty acids are often going to create a chronic problem.
Metabolic Shift
During stress, the hormones adrenaline (epinephrine) and cortisol shift the body's energy focus from glycolysis (using glucose for energy) towards lipolysis (breaking down stored fats for energy). However, reduced reliance on glycolysis is not completely shut down; its relative importance is diminished as the body prioritizes fat breakdown for energy. Big advantage of our specie on the animal reign (enable to quickly mobilize stored energy reserves for a long time).
Estrogen and PUFA activate the PKC system
I cite RP:
“Estrogen and the polyunsaturated fatty acids (PUFA), linoleic and linolenic acid, alike activate the protein kinase C (PKC) system of cellular activation. Many of the functions of PUFA are similar to the functions of estrogen (e.g., antagonism to thyroid function, promotion of age pigment/lipofuscin), so this information showing that they both act similarly on the same basic regulatory pathway is important.
Estrogen increases secretion of growth hormone (GH; it's closely associated with prolactin, also increased by estrogen), and GH causes an increase in free fatty acids in the blood. Estrogen promotes iron retention, so it sets the stage for oxidative stress. At least in some systems, both estrogen and PUFA promote the entry of calcium into the cell.” (1)
In diabetes, there is a generalized excess activation of the PKC system (protein kinase C). (…)
Protein Kinase C system (PKC)
What is the role of PKC system and its impact on energy?
In short: PKC is a key player in cellular energy regulation, influencing mitochondrial function, energy sensing, neurotransmitter release, and other energy-related processes. By modulating these processes, PKC helps cells maintain energy balance and respond to changes in energy availability.
PKC is also intertwined with other energy-signaling processes (AMPK) and neurotransmitters.

PKC system in details
Here's a more detailed look at PKC's impact on energy:

Mitochondrial Function:
• PKC signaling can influence mitochondrial function by regulating enzymes involved in oxidative phosphorylation, the process by which mitochondria generate ATP.
• For example, PKC can regulate pyruvate dehydrogenase (PDH) and cytochrome c oxidase (Complex IV), which are critical for cellular energy production.
• PKC also plays a role in mitochondrial dynamics, which is important for maintaining healthy mitochondria and efficient energy production. Energy Sensing and Signaling:
• PKC can phosphorylate AMPK, an enzyme that is activated by cellular energy depletion.
• This phosphorylation can affect AMPK's activity, which in turn influences cellular processes that regulate energy balance.
• By interacting with AMPK, PKC can help cells respond to changes in energy levels and maintain homeostasis. Neurotransmitter Release and Energy:
• PKC is involved in regulating neurotransmitter release, which requires energy for the process of exocytosis (releasing neurotransmitters from vesicles).
• By modulating the proteins involved in synaptic vesicle exocytosis, PKC can impact the energy demands of neuronal signaling. Other Energy-Related Processes:
• PKC can influence various other cellular processes related to energy, such as the opening and closing of the mitochondrial permeability transition pore (MPTP), which affects mitochondrial function and energy production.
• PKC can also affect the activity of proteasomes, which are involved in protein degradation and cellular energy balance.
In summary: PKC is a key player in cellular energy regulation, influencing mitochondrial function, energy sensing, neurotransmitter release, and other energy-related processes. By modulating these processes, PKC helps cells maintain energy balance and respond to changes in energy availability.

Sources and References

Diabetes, scleroderma, oils and hormones”. 2006 raypeat.com The Role of Protein Kinase C During the Differentiation of Stem and Precursor Cells into Tissue Cells - doi: 10.3390/biomedicines12122735 Biomedicines 2024 AA cascade
Cascade AA Cox Lox P450 03.gif
The AA cascade explained when there is a discharge of FFA due to stress. We already know the deleterious effects of excess PUFA.
When you're stressed, your body releases certain hormones that trigger your cells to break down fats stored in the membranes. One of the fats released is called arachidonic acid (AA), which comes from a type of fat known as PUFA.
Once AA is free in the body, it acts like fuel for inflammation. It gets turned into other substances (prostaglandins) that tell the body to create swelling, pain, and heat — all part of the "inflammatory response." While this can be helpful short-term (like in healing), too much of it keeps the body in a state of constant low-level inflammation (especially from diets high in omega-6).
So, during stress, your body’s release of AA can make things worse if you already have a lot of these fats stored. That’s part of why people say excess PUFA can have harmful effects, especially over time.
Prostaglandins (PGE) and their link to excess omega-6 (ALA) in the AA cascade:
When we eat a lot of omega-6 fats — especially from things like seed, corn or soy oils — our bodies convert them into arachidonic acid (AA). This is especially true with a type of omega-6 fat called linoleic acid (LA, a type of omega-6) — not to be confused with alpha-linolenic acid (ALA, a type of omega-3).
Once there's a buildup of AA in our cells – we don't use / need much PUFA, stress can trigger the release of AA into the body. That’s where things take a turn: AA gets turned into compounds like prostaglandins (especially PGE2).
Prostaglandins (PGE) are like chemical messengers that tell the body to create inflammation. They're useful in small amounts for healing and repair, but when there’s too much AA around, you get too much PGE2, which causes chronic inflammation, swelling, and even pain.
This inflammation signals the body that something’s wrong — which ironically increases stress levels further. It becomes a vicious cycle:
More omega-6 → more AA → more PGE2 → more inflammation → more stress.
That’s one reason people are concerned about eating too much omega-6, especially from processed foods. It overloads this system and keeps your body in a kind of "fight mode" all the time.
Cascade AA & prostaglndines.jpg

Hello Ali, nice to meet you. How are you?