Burning Blade

@SteakhouseFi You guys cooked with this one. I love the synergy with @makinafi too.

@PolitlcsGlobal @BryptoQ @lemondefr FRANCE IS WILD 🤡

🚨🇫🇷 NEW: The location of the French aircraft carrier, FS Charles de Gaulle, has been given away by a sailor using Strava whilst jogging on the ship deck [@lemondefr]

@omgcorn @Schlagonia If there is a team that can break the gloom and doom vanity fair we have become of late, it is Yearn. 🤪 Long Live the King.

@makbags After the first deposit, time to celebrate.

COOKINGGGGGGG 🥩🥩🥩🥩

@Ceazor7 @yearnfi there goes my deposit to the OG of OGs.

Today I launch a Referral Deposit User Interface for @yearnfi The purpose of this is to help support my content as a anonymous supporter. All this does is build deposit transactions to official yearn vaults and pass my referral address to them. You still get ALL your yield. They simply share their fees with me. Your funds never touch any contracts other then official Yearn contracts. You can deposit via my site here secretsandwich.xyz/vaults Then monitor your positions and withdraw them on the yearn site when you want to. Yearn has long been my favorite project in DeFi, and I have a long long history of sharing this project with people. I feel more than comfortable sharing this with my followers. That said, do some due diligence on which vaults you feel safe depositing into . If I don't have a deposit UI for a vault you want. DM me and I will add it

The Steakhouse USD Machine is live on @MakinaFi. Our first deployment on Makina, a DeFi execution engine for onchain strategies. One deposit, automated yield aggregation across our vault portfolio, trustless NAV accounting. The Kitchen is open 🥩 app.makina.finance/strategy/usdsh…

@0xLeonis @makinafi 🤌 Diversification 🤌 And the good thing of this Steakhouse vault is that pretty much is a Vault of Vaults and they will route you through the most performant of their strategies at that moment 👇

@makinafi just checked the yield that steakhouse USD gives and it looks good I'll probably diversify my holdings between it and DUSD to get as much yield and rewards from both machines

@makinafi This is art! Whole Makina infrastructure and their main features ( Calibers, atomic unwinding) at work. And by no other than the King of Kings of vault curators 🤌

@SteakhouseFi @makinafi Nice one ! The ultimate Steakhouse vault to allow routing through all other vaults. Love it.

@bitrefill Very comprehensive post-mortem. Glad to know it was nothing serious guys 🫡

March 1st incident report On March 1, 2026, Bitrefill was the target of a cyberattack. Based on indicators observed during the investigation - including the modus operandi, the malware used, on-chain tracing and reused IP + email addresses (!) - we find many similarities between this attack and past cyberattacks by the DPRK Lazarus / Bluenoroff group against other companies in the crypto industries. The initial access originated through a compromised employee laptop, from which a legacy credential was exfiltrated. That credential provided access to a snapshot containing production secrets. From there, the attackers were able to escalate their access to our broader infrastructure, including parts of our database and certain cryptocurrency wallets. We first detected the incident after noticing suspicious purchasing patterns with certain suppliers. We realized that our gift card stock and supply lines were being exploited. At the same time we found some of our hot wallets being drained and funds transferred to attacker-controlled wallets. The moment we identified the breach, we took all of our systems offline as part of our containment response. Bitrefill operates a global e-commerce business with dozens of suppliers, thousands of products, and multiple payment methods across many countries. Safely switching all these things off and bringing them back online is not trivial. Since the incident, our team has been working closely with top industry security researchers, incident response specialists, on-chain analysts and law enforcement to understand what happened and how we can prevent it from happening again. A sincere thank you to @zeroshadow_io, @SEAL_Org, @RecoverisTeam and @fearsoff for their rapid response and support throughout this ordeal. What about your data Based on our investigation and our logs we don’t have reason to think that customer data was the target of this breach. There is no evidence that they extracted our entire database, only that the attackers ran a limited number of queries consistent with probing to understand what there was to steal, including cryptocurrency and Bitrefill gift card inventory. Bitrefill was designed to store very little personal data. We are a store, not a crypto service provider. We don’t require mandatory KYC. When a customer chooses to verify their account - e.g. to access higher purchasing tiers or certain products - that data is kept exclusively with our external KYC provider, with no backups in our system. Still, based on database logs, we know that a subset of purchase records was accessed and we want to be transparent about that. Around 18,500 purchase records were accessed by the attackers. Those records contained limited customer information, such as email addresses, crypto payment address, and metadata including IP address. For approximately 1,000 purchases, specific products required customers to provide a name. That information is encrypted in our database. However, since the attackers may have gotten access to the encryption keys, we are treating this data as potentially accessed. Customers in this category have already been notified directly by email. At this time, based on the information currently available, we do not believe customers need to take specific action. As a precaution, we recommend remaining cautious of any unexpected communications related to Bitrefill or crypto. If this assessment changes, we will of course immediately inform those affected. What we are doing We have already significantly improved our cybersecurity practices, but vow to continue to draw learnings from this experience to make sure user and company balances and data remain maximally safe. Specifically we’re: -Continuing thorough cybersecurity reviews and pentests with multiple external experts and implementing recommendations; -Further tightening internal access controls; -Further improving logging and monitoring for faster detection and more effective response; and -Continuing to refine and test our incident response procedures and automated shutdown procedures. The bottom line Getting hit by a sophisticated attack sucks (a lot). We’ve been in business for over 10 years and it’s the first time we’ve been hit this hard. But we survived. Bitrefill was designed to limit the impact if something like this ever happened. Bitrefill remains well funded, has been profitable for several years and will absorb these losses from our operational capital. Almost everything is back to normal: payments, stock, accounts. Sales volumes are also back to normal, and we are eternally thankful to our customers for your continued confidence in us. We will continue to do our best to continue deserving your trust. Thank you!

@makinafi The timeline on X moves fast and updates can be easy to miss. This is your weekly reminder that you have double-digit yields on stablecoins and ETH on @makinafi.

The timeline on X moves fast and updates can be easy to miss. Subscribe to our Substack to get the latest delivered directly: makinafi.substack.com Several juicy updates are coming this month, don't miss out.

@GAmitej Well I do agree with you mostly! Ofc the 20% APR good ole' days of crypto are gone. But scalable, steady 8-12% APRs that underwrite real use-cases is the next best thing you can dream of! See you at KUSD launch.

There's a lie at the center of DeFi yield. Every serious builder knows it. Nobody talks about it.

@KelpDAO Beautiful magic quadrant I see there, Mr Intern

Where do your rewards come from? Most stablecoins make you choose: → High rewards from crypto that disappears when markets turn → Real-world backing that's stuck at 4-5% rewards sKUSD unlocks the quadrant nobody touched: High rewards from receivables, payments and settlement flows. Real economic activity. Not market cycles.

@VenusProtocol @maplefinance @BNBCHAIN 🤡 “They vault didnt just fill, it got devoured” 🤡

Turns out @BNBCHAIN users have a serious appetite for @maplefinance's syrupUSDT. Four pools. $64.9M supplied. $49.2M borrowed. 75.9% utilization. The vault didn't just fill, it got devoured. 🍁 Strong early demand. Real utilization. 🔗flux.venus.io/dashboard/56

@Helios_Movement Thanks George, I always learn something new. when supplementing Vit D, my understanding is that it does not need to be paired with magnesium in the same meal, is that right? I take vit D with lunch and magnesium (switched to treonate from bisglycinate recently) at night.

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)

Let me TLDR this for you and tell you what you should do to get the highest yield possible among all the strategies: 117% APR. (And yes, given this depressing bear market I have no alternative but to tell you this is actually financial advice 🤪) 🧵👇

OG crypto company targeted by North Korean hackers. Handled it like the chads they are. Once a Bitrefillooor, always a bitrefillooor.

@heider891 @QwQiao I think he means scaling law

@QwQiao Hitting a wall in terms of token demand or scaling law?

- dario, elon, sundar, satya, etc have all said recently that we r not hitting a wall. this is consistent with my experience as a user - there’s clearly far more demand for intelligence than supply (tsmc being a major bottleneck as they do not want to overbuild) - major ai-related stocks do not look ridiculously overpriced, and in fact some (eg msft) r trading near their lowest price multiples in a decade im now firmly in the no ai bubble camp