😊

@BenBikmanPhD That’s adaptation, not preference. Cahill showed fuel switching for survival, not that ketones are the brain’s preferred fuel.”

@WilsonCrypto You’re changing the disagreement. And you’re the one who used the word “misinformation”. When given equal access to glucose and ketones, the brain shifts to ketones. Are you aware of evidence that refutes that?

Glucose is such a fickle fuel. No other nutrient experiences the swings glucose does, rising and falling dramatically throughout the day. And the brain appears to suffer the most, undergoing periods of feeding frenzies and starvation within hours of each other. pubmed.ncbi.nlm.nih.gov/39044609/ Give your brain a break. Controlling carbs not only stabilizes glucose availability, but also introduces ketones. Ketones, incidentally, are the brain's preferred fuel. If given equal access to glucose and ketones, the brain selects ketones at about 2/3 the rate of glucose.

@BenBikmanPhD Not shifting anything, correcting the physiology. The brain doesn’t choose ketones when glucose is equally available. In a fed state, glucose is prioritised, ketone use rises when glucose and insulin drop (fasting).

@BenBikmanPhD Glucose is the preferred fuel in a fed state, carbs support performance and insulin sensitivity (Himsworth). Ketones are a survival backup, Cahill showed they take over when fasting. Humans are metabolically flexible. Calling carbs ‘misinformation’ is ignoring basic physiology.

@BenBikmanPhD No, preferred fuel is glucose, stop with this misinformation

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@Helios_Movement Thanks to chat gpt 😅

All of us here are pro-sunlight. But it takes approximately 380,000–400,000 IU of vitamin D3 (cholecalciferol) to reach the oral LD50 (50% lethality) in a typical half-pound rat. Translating this to a human-equivalent dose (HED) we have 19 million IU. Not thousand, not tens of thousands but million. Ideally you want a vitamin D lamp in case the UVB index is low where you live but supplements are not entirely useless. To understand how true this is, we will take a niche example of autoimmune diseases. Now first and foremost vitamin D is a secosteroid (a type of steroid with a “broken” ring (it has a rupture in the 9,10 carbon-carbon bond of the “B” ring)) and prohormone (a substance that is a precursor to an active hormone) which is metabolized in various tissues to the active vitamin D hormone 1,25(OH)2D3 /calcitriol/1,25-dihydroxyvitamin d3. It is not only involved in bone remodeling, through the regulation of calcium reabsorption from bone and the intestine, but it also regulates approximately 1000+ genes based on some research (*) in the human body through its active metabolite, influencing cellular differentiation and proliferation, immune system regulation, neural function, the cardiovascular system, and much more. (*)After all, vitamin D receptors have been found to modulate the transcription of about 3% of human genes. Now let’s move on to how we obtain this precious molecule. But first, we need to briefly mention: Vitamin D binding protein (DBP) Vitamin D receptor (VDR) DBP, also known as Gc-globulin (from “group-specific component”) is the primary carrier protein for vitamin D metabolites in the blood. It plays a central role not only in vitamin D transport but also in its bioavailability, activation and clearance. It’s a 58 kDa glycoprotein belonging to the albumin family (structurally related to albumin and alpha-fetoprotein) that’s produced mainly in the liver (also minor synthesis in other tissues like kidney and adipose) and its circulating concentration is quite high at ~4–8 μM. It binds multiple ligands with high affinity: 25(OH)D (calcidiol, the main circulating form): strongest affinity. 1,25(OH)₂D (calcitriol): lower affinity but still significant. Vitamin D₂/D₃: weaker binding. Actin (G-actin): a unique non-vitamin D role.DBP binds G-actin released during tissue injury or cell death → forms DBP-actin complexes → cleared by the liver. It basivally prevents actin polymerization into harmful filaments that could obstruct microcirculation. This “actin clearance” role is critical in acute inflammation and tissue damage. Now DBP binds 85–90% of circulating 25(OH)D and 1,25(OH)₂D to prevent rapid clearance and protect them from degradation. The DBP-vitamin D complex has a long half-life of 2–3 weeks for 25(OH)D. Of course, only the free (unbound) fraction of 25(OH)D and 1,25(OH)₂D is biologically active and can enter cells to bind the vitamin D receptor (VDR). DBP acts as a reservoir, releasing vitamin D metabolites to target tissues whether that’s called kidney for activation by 1α-hydroxylase or immune cells for local immunomodulation. In the kidney for example, DBP-bound 25(OH)D is taken up via megalin and cubilin receptors (endocytosis), gets internalized and converted to 1,25(OH)₂D by CYP27B1. This is especially important in immune cells (macrophages, dendritic cells, T cells) that express CYP27B1 → produce local 1,25(OH)₂D for autocrine/paracrine immune regulation. Also, DBP itself has direct immunomodulatory effects and even modulates neutrophil and monocyte migration for example. If all these were too complicated, simply keep in mind that vitamin D3 metabolites, including 1,25(OH)2D3, are carried by serum vitamin D binding protein for now. Moving on to the vitamin D receptor. The Vitamin D Receptor (VDR) is a ligand-activated transcription factor that belongs to the steroid/thyroid hormone receptor superfamily. When bound to its active ligand (1,25-dihydroxyvitamin D / calcitriol), VDR directly regulates gene expression by binding to specific DNA sequences called vitamin D response elements (VDREs). This allows vitamin D to influence thousands of genes involved in things we discussed such as immune regulation, inflammation control, barrier function, cell growth, calcium homeostasis, and more. Now, in the inactive state (no ligand bound) VDR is primarily located in the cytoplasm, often associated with chaperone proteins that keep it stable and prevent premature activation. Upon ligand binding, VDR undergoes a conformational change, dissociates from chaperones, forms a heterodimer with the retinoid X receptor (RXR), translocates to the nucleus, and binds VDREs to regulate target genes. Some VDR is constitutively nuclear in certain cell types such as immune cells and keratinocytes. VDR is one of the most widely distributed nuclear receptors expressed in nearly every cell type in the human body. There’s particularly high expression in: Immune cells (the highest density is found here). Epithelial cells such as: Intestinal epithelial cells (gut mucosa) Keratinocytes (skin) Alveolar epithelial cells (lung) Renal tubular cells (kidney) Bone cells Neurons Microglia Muscle (skeletal and smooth) Pancreas (beta cells) Thyroid Parathyroid Adrenal glands Adipose tissue Liver Cardiovascular endothelium And pretty much everywhere. Now here’s why this widespread expression matters in autoimmunity. High VDR in immune cells allows vitamin D to directly suppress autoreactive T/B cells, promote Tregs, and dampen inflammation (↓ Th1/Th17, ↓ NF-κB, ↑ IL-10/TGF-β). VDR in epithelial cells strengthens barriers (gut, skin, lung) → reduces antigen leakage and systemic immune activation. In autoimmune diseases, VDR expression is often downregulated in affected tissues or immune cells (synovial fibroblasts in RA, thyroid cells in Hashimoto’s, beta cells in T1D, CNS cells in MS for example), usually due to chronic inflammation (TNF-α, IFN-γ, IL-6) or genetic/epigenetic factors → weakened protective effects even when vitamin D levels are adequate. This makes VDR function a key bottleneck: raising blood vitamin D levels is only part of the solution, where preserving or restoring VDR expression and signaling (via reducing inflammation, correcting magnesium, managing stress) is equally important. Also, here’s how the VDR works in a nutshell: Vitamin D enters the cell The biologically active form is 1,25-dihydroxyvitamin D (calcitriol) produced locally in many tissues (immune cells, gut epithelium, skin) via the enzyme CYP27B1 (1α-hydroxylase) from circulating 25(OH)D. Calcitriol is lipophilic → freely diffuses across the cell membrane into the cytoplasm. Calcitriol binds to the Vitamin D Receptor (VDR) VDR is a nuclear receptor protein (~50 kDa) usually found in the cytoplasm in its inactive state, bound to chaperone proteins (heat shock proteins like HSP90) that keep it stable and prevent premature activation. High-affinity binding of calcitriol to VDR causes a conformational change in the receptor → chaperones dissociate → VDR exposes its nuclear localization signal (NLS) and DNA-binding domain. VDR forms a heterodimer with RXR (retinoid X receptor) VDR rarely acts alone — it must partner with RXR (another nuclear receptor) to form a VDR-RXR heterodimer. RXR can be bound to 9-cis-retinoic acid (a vitamin A derivative), but in many cases the heterodimer forms without it. This dimerization stabilizes the complex, enhances DNA binding, and allows recruitment of co-regulators. The VDR-RXR complex binds to Vitamin D Response Elements (VDREs) VDREs are specific DNA sequences located in the promoter or enhancer regions of target genes. The VDR-RXR heterodimer recognizes and binds these elements with high specificity → anchors the complex to DNA. Recruitment of co-activators and chromatin remodeling Once bound to VDREs, the VDR-RXR complex recruits co-activators (e.g., SRC-1, SRC-2, SRC-3, p300/CBP, DRIP/TRAP complex, Mediator). These co-activators have histone acetyltransferase (HAT) activity → acetylate histones → loosen chromatin structure → make DNA more accessible to RNA polymerase II. Some genes are repressed by VDR (via co-repressors like NCoR/SMRT), so the complex can turn genes on or off depending on context and cell type. Net result: Changes in gene expression that regulate cell function The process alters the transcription of thousands of genes. Immune-related examples: Upregulation of FoxP3 1,25(OH)₂D directly induces FoxP3 expression in naïve CD4+ T cells → promotes differentiation into peripheral regulatory T cells (pTregs) and stabilizes natural Tregs (nTregs). FoxP3 is the master transcription factor for Treg identity and function → enables suppression of autoreactive T cells via IL-10, TGF-β, CTLA-4, direct contact, and IL-2 consumption (starving effector cells). Upregulation of IL-10 and TGF-β Increases IL-10 production in Tregs, macrophages, dendritic cells, and epithelial cells → potently suppresses pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-12, IFN-γ) and inhibits Th1/Th17 differentiation. Enhances TGF-β expression → drives Treg induction, IgA class-switching in B cells, and epithelial repair. Together, IL-10 and TGF-β create a tolerogenic microenvironment that dampens autoreactivity and promotes resolution of inflammation. Downregulation of IFN-γ (Th1) and IL-17 (Th17) Suppresses T-bet (Th1 master regulator) → ↓ IFN-γ production → reduces macrophage activation and cell-mediated autoimmunity (important in T1D, RA, MS). Inhibits RORγt (Th17 master regulator) → ↓ IL-17A/F and IL-22 → limits neutrophil recruitment, chemokine production (CXCL1/2/8), and tissue inflammation. Downregulation of B-cell proliferation and plasma cell differentiation Inhibits cell-cycle genes (cyclin D1) and transcription factors (Blimp-1, XBP-1) → reduces clonal expansion of autoreactive B cells and their differentiation into antibody-secreting plasma cells. Inhibition of NF-κB and other pro-inflammatory pathways VDR-RXR physically interacts with NF-κB p65 subunit → blocks its nuclear translocation and DNA binding. Suppresses STAT1 (IFN-γ signaling) and AP-1 pathways → reduces transcription of TNF-α, IL-6, IL-1β, IL-12, IL-23, chemokines (CCL2, CXCL10), and adhesion molecules. This blunts cytokine storms and tissue damage. Upregulation of anti-inflammatory pathways Increases IL-10 and TGF-β expression → promotes regulatory responses. Enhances SOCS1 (suppressor of cytokine signaling) → inhibits JAK/STAT pro-inflammatory cascades. Reduction of oxidative stress and mitochondrial dysfunction Activates Nrf2 pathway → upregulates antioxidant enzymes (HO-1, NQO1, GCLC for glutathione synthesis, SOD, catalase). Protects mitochondrial membrane potential, reduces ROS production, and restores energy metabolism in immune cells and target tissues. Upregulation of tight junction proteins Increases occludin, claudin-1/3/4, ZO-1 expression → strengthens paracellular sealing → reduces intestinal permeability (”leaky gut”). Downregulates zonulin release → prevents transient junction opening. Enhancement of mucus layer and antimicrobial defenses Stimulates MUC2 production by goblet cells → thickens protective mucus. Upregulates antimicrobial peptides (α/β-defensins, RegIIIγ) via synergy with IL-22. Now we can get vitamin D through UVB light or dietary means (food and supplements). Here’s how vitamin D is created when the sun hits our skin. Our skin in the epidermis (the upper layer of the skin and specifically the stratum spinosum and stratum basale) has a cholesterol derivative that is called 7-dehydrocholesterol. When wavelengths between 290 and 315 nanometers hit our skin, they break a chemical bond in it (the B ring), turning it into previtamin D3. This is called photolysis. But previtamin D3 is thermally unstable and has to undergo a rearrangement where a double bond shifts to a trans configuration and forms cholecalciferol. This conversion takes 8-24 hours. Then, two hydroxylations happen: -One in the liver on carbon 25 in order to get 25-hydroxyvitamin D (25(OH)D), or calcidiol (this is the circulating form measured in blood tests). *The enzyme 25-hydroxylase (primarily CYP2R1) adds a hydroxyl group (-OH) to carbon 25 of cholecalciferol, forming 25-hydroxyvitamin D (25(OH)D), or calcidiol. -One in the kidneys on carbon 1 in order to get 1,25-dihydroxyvitamin D (1,25(OH)2D), or calcitriol, the active hormonal form that binds to the vitamin D receptor (VDR). *1-alpha-hydroxylase (CYP27B1) adds another hydroxyl group to carbon 1 of 25(OH)D, producing 1,25-dihydroxyvitamin D (1,25(OH)2D). In the context of autoimmune diseases, vitamin D is important both for prevention and disease management. Here’s why, in a nutshell: Vitamin D receptors (VDR) are present on nearly every major immune cell type such as: -T cells (CD4+ and CD8+) -B cells (including plasma cells) -Dendritic cells (DCs) -Macrophages and monocytes -Natural killer (NK) cells -Innate lymphoid cells (ILCs) -Even some neutrophils and mast cells express VDR under inflammatory conditions For example, immature DCs exposed to calcitriol become tolerogenic DCs that: -Downregulate co-stimulatory molecules (CD80, CD86) and MHC class II → less effective at activating effector T cells. -Increase IL-10 and TGF-β production → favor Treg induction. Then, macrophages polarize toward an M2-like (anti-inflammatory) phenotype → ↑ IL-10, arginase-1, ↓ TNF-α, IL-6, IL-12. Active vitamin D (1,25(OH)₂D) induces regulatory T cells (Tregs) → suppresses autoreactive T cells. 1,25(OH)₂D directly upregulates FoxP3 (the master transcription factor for Tregs) in naïve CD4+ T cells. It promotes conversion of naïve T cells into peripheral Tregs (pTregs) and stabilizes existing natural Tregs (nTregs). Tregs suppress autoreactive T cells through multiple pathways: -Secretion of IL-10 and TGF-β (anti-inflammatory cytokines). -CTLA-4-mediated inhibition of antigen-presenting cells. -Direct cell-contact suppression. -Consumption of IL-2 (starving effector T cells). This results in fewer autoreactive T cells escaping into circulation and thus reduced risk of tissue attack. Inhibits pro-inflammatory T helper subsets such as Th1 cells (T-bet+, IFN-γ producers) and Th17 cells (RORγt+, IL-17 producers). In the first case, 1,25(OH)₂D inhibits T-bet expression and IFN-γ production → reduces macrophage activation and cell-mediated autoimmunity. In the second case: Strongly suppresses RORγt and IL-17/IL-22 production → limits neutrophil recruitment, chemokine release, and tissue inflammation. Overall, it shifts the balance from Th1/Th17 dominance → toward Treg dominance. Promotes Treg and IL-10-producing cells → enforces tolerance to self-antigens. Downregulates B-cell proliferation(*), plasma cell differentiation, and autoantibody production. (*)1,25(OH)₂D binds VDR on B cells → inhibits cell-cycle progression (↓ cyclin D1, ↑ p27) → reduces clonal expansion of autoreactive B cells. Suppresses transcription factors such as Blimp-1 and XBP-1 that are required for B cells to become antibody-secreting plasma cells. Decreases class-switch to IgG/IgM autoantibodies. Inhibits NF-κB and other pro-inflammatory pathways. The 1,25(OH)₂D-VDR complex physically interacts with the NF-κB p65 subunit for example and it prevents its nuclear translocation and DNA binding. It also suppresses STAT1 (IFN-γ signaling) and AP-1 pathways which overall results in less transcription of pro-inflammatory genes and of course, lower production of TNF-α, IL-6, IL-1β, IL-12, IL-23 and IL-17. Upregulates anti-inflammatory pathways. It increases IL-10 (from Tregs, macrophages, DCs) and TGF-β expression for example promoting regulatory responses and tissue repair but it also enhances SOCS1 (suppressor of cytokine signaling) and inhibits JAK/STAT pro-inflammatory cascades. Reduces oxidative stress and mitochondrial dysfunction. For example, it upregulates Nrf2 and thus increases antioxidant enzymes such as HO-1, NQO1, GCLC, SOD and catalase. 1,25(OH)₂D upregulates occludin, claudin-1, claudin-4, ZO-1 → strengthens paracellular sealing → reduces permeability. It also downregulates zonulin release → prevents transient junction opening. Increases MUC2 production by goblet cells → thickens protective mucus. Upregulates antimicrobial peptides (defensins, RegIIIγ) via IL-22 synergy. Favors SCFA-producing taxa such as Faecalibacterium, Roseburia and Akkermansia → higher butyrate/propionate → further barrier support and Treg induction. Reduces LPS-producing Proteobacteria → lower endotoxin load. Promotes IgA class-switching and sIgA secretion → coats commensals → prevents translocation without inflammation. Decreases class-switch recombination to IgG/IgM There’s of course, more such as that: In SLE patients, higher 25(OH)D levels correlate with lower anti-dsDNA titers and reduced disease activity (SLEDAI). In RA, vitamin D supplementation (often 50,000 IU/week) has been associated with decreased rheumatoid factor and ACPA levels in some trials. In Sjögren’s, low vitamin D is linked to higher anti-Ro/La titers and more severe glandular inflammation. Low 25(OH)D levels (<20–30 ng/mL) are common in RA, SLE, MS, T1D, Hashimoto’s, Sjögren’s, vitiligo, alopecia areata, and IBD. Lower levels correlate with higher disease activity (DAS28 in RA, SLEDAI in lupus, EDSS in MS) and more frequent flares. Large prospective cohorts show that low vitamin D in childhood/adolescence predicts higher risk of later MS, T1D, and RA (20–60% increased risk in deficient groups). 4,000 IU/day + calcium reduced T1D risk in Finnish children at genetic risk (RR ~0.2–0.4 in some cohorts). Vitamin D supplementation (2,000–10,000 IU/day) slows progression and reduces relapse rates in relapsing-remitting MS. 50,000 IU/week + methotrexate improved DAS28 scores and reduced CRP/ESR in several RCTs. 2,000–4,000 IU/day reduced thyroid antibodies (anti-TPO) and improved TSH in many studies. So overall, vitamin D is able to modulate both innate and adaptive immune functions. Note 1: Genetic variants in it like rs2282679 and rs7041 can dial down your 25(OH)D. Note 2: There are certain genetic variations in the VDR that make it less efficient that you should be aware of: -rs1544410 -rs2228570 -rs731236 Note 3: Variants in CYP2R1 or CYP27B1 like rs2060793 or rs28934607 can also slow the conversion steps. Note 4: When measuring 25(OH)D you want a 45+ ng/mL ideally. Below 20 ng/mL is a serious deficiency. Between 20-30 ng/mL is nsufficient. Between 30-45S ng/mL is decent, and between 45-70/ng/mL is great and anything past that is just excessive (and wrong) supplementation or signals that you live in a place were you are not designed to (a Swedish person living in Brazil for example). Now, here’s how you can increase your vitamin D levels. Number 1: First and foremost, get bloodwork done (serum 25D). Number 2: If your levels are low tackle the most common causes of a vitamin D deficiency, such as: -Overconsuming caffeine -Not spending time outside -Not getting enough magnesium -Low fat and low cholesterol diets -Very high fiber diets -No resistant starch or things that feed parabacteroides. -Wearing sunscreens with high SPF (>30) -Things that harm the VDR such as stress, sodium fluoride, BPA/xenoestrogens, heavy metals and being overweight (boron and curcumin help with this) The glucocorticoid receptor competes with VDR for co-activators for example. The estrogen receptor also competes with VDR for co-activators Then obesity suppresses VDR signaling and increases CYP24A1. Number 3: If your levels are still low after implementing these for 2 months, get a vitamin D lamp. Number 4: If you want to supplement : -Make sure that your kidneys work fine and that your PTH is within range -Get one in oil form and start with 8K IUs -Consume it at noon(-ish) (vitamin D opposes melatonin) -Test again after just 1 month of supplementing -Consume it with a retinol-rich meal for breakfast (eggs for example) -Supplement with vitamin K2 and magnesium as well (300mcg of MK7 and 600-800mg of magnesium glycinate)

@celestialbe1ng What about it coconut milk instead of milk? Also the I see you used skimmed milk over full fat/raw milk? Why is this?

Other things I do: • B vitamins • more milk more sugar and coffee (sugary cafe lattes) more salt • red light therapy, tanning shop • progesterone (Progest E), pregnenolone • fun group exercise • D3 & K2 • fresh orange juice every couple of hours • novelty (like a spontaneous trip to the theatre) • collagen, gelatine, high doses glycine 5+grams • playing joyful music all day long • baking soda and magnesium baths • little happy rituals: doing my skincare, putting on makeup and nice clothing to feel elevated • talking to my mum • having a drink with sisters (belly laughs included) • cooking oxtail soup • tricking my brain into feeling good by dancing • activated charcoal away from food or supps • Ray Peat carrot salad • candied ginger, ginger broth (pho), ginger tea • cacao • l theanine, magnesium, aspirin • inhaling CO2 • goes without saying: ditch all PUFA, everything that impairs your digestion / transit / motility; and absolutely NO serotonergic supps like 5-HTP or ashwagandha

Whenever I notice myself spiralling into unmotivated, dissociative states; loss of edge, reduced urgency or just less emotional spark, I take 1/4 of a Periactin tablet (cyproheptadine) at bedtime and some lisuride with breakfast. It cures loser mode within 1–2 days. Serotonin antagonism and dopamine agonism are what give you your humanity back in this evil serotonergic world that’s trying to turn you into a slave-minded fearful rat. Ray Peat hasn’t been wrong once.

@Mangan150 Nice, going to start with beef and fruit to drop excess weight/bloat

@WilsonCrypto No, I’m not. I’ve never done full carnivore. In my case, I wouldn’t expect incremental benefits. For some people, it’s the right move.

I'll be 71 this week. Now, I'm not going to do one of those 71 lessons for 71 years posts. But I do have one piece of advice: Get rid of limiting beliefs like "I'm too old" or "it's too late". You're not too old to get lean, fit and strong. Here's some inspiration:

@celestialbe1ng What fruit do you eat?

Ray Peat diet is so expensive can someone help me budget my weekly food shop? Oysters - £8 Liver - £3 Carrots - £2 Ox tail - £16 Milk - £10 Potatoes - £4 Orange juice - £6 Coconut oil - £3 Coca-cola - £6 Fruit - £10 Sugar - £2 Lip filler - £1200 Please help

@SamaHoole Gluconeogensis and there’s sugar (carbs) in mares milk 😅

Sometimes I forget to eat my pre-workout carbs. Then I remember that the Mongols conquered 24 million square kilometres, the largest contiguous land empire in human history, on horseback, in all weathers, eating dried meat and fermented mare's milk. No oats. No banana. No "fast-digesting carbohydrates to fuel performance." Just men who had been eating animals their entire lives and apparently had sufficient energy to defeat every army between the Pacific and the Danube. I think I can manage leg day.

@stella_chadwick 15mg zinc with 1g of copper?

DAO is the enzyme that clears histamine in the gut. It requires copper as a cofactor. Everyone is supplementing zinc. Almost nobody is checking copper. High zinc without adequate copper = suppressed DAO = histamine builds no matter how clean the diet is. #Histamine #MCAS #MastCells #PANDAS #PANS #FunctionalMedicine

@celestialbe1ng Raw milk, you don’t want pasteurized!?

Milk gives you long legs and makes you grow tall. Milk used to hold a special status, and we would convince children to drink copiously for the promise of growing tall and strong, and having unbreakable bones. We need the milk propaganda back.

@mscarnivore Zero sugar cola? Opposite of peating!

Peating at the airport after a 12 hour flight.

@nehalzzzz1 Fake

While most panic… We execute. Study. Plan. Trade. Repeat. Winners are built in red markets.

@celestialbe1ng @Nixxy_M Have purchase projest e @celestialbe1ng. With someone with endometriosis (had operation to clear over a year ago and now 7 weeks pregnant, what would you recommend dosage wise? How will this help? Thankyou

The only progesterone product I recommend is Progest E Complex by kenogen. It is of very high quality, and does not contain soyabean oil or soya proteins, even though the Vitamin E it contains is technically derived from soya. There are several undesirable substances found in whole soya beans, but they are all eliminated during the extraction of vitamin E.

Unironically aspirin and carrot salad would be much better options for estrogen dominant men than that testosterone they’re being loaded with. And for women too! Aspirin inhibits the aromatisation of estrogen and carrot can sweep the excess estrogen out. My two favourite weapons against estrogen.

@LuckSide Random?

Not a big cucumber guy, but this is surprising! The REFRESHING Cucumber Breeze Cocktail Recipe | HOW TO MAKE youtu.be/gQYRRSTYscA

@celestialbe1ng @arctic_cryx Isn’t it a neurotoxin?

@arctic_cryx Intentionally! Ideally they shouldn’t look like I had anything done. Subtle work for gentle plumping :)

I don’t know much about Clavicular but one thing I do know: a year ago Twitter crucified me for 2019 lip filler. Then I actually got them done again last month, admitted it openly…and no one blinked. The Trump gilded era killed the raw-meat LARP and brought looksmaxxing back in

@WEEX_Official Is that a Shiba inu !? 👀