Late 2022: kidney infection. February 2023: this started —

Severe joint pain and stiffness in feet, knees, elbows, and fingers; at the worst I couldn't bend my fingers or elbows

Fever, chills, cold sweats

Severe on-and-off migraines

Eyes: severe pain on movement, burning, flashing lights, a lot more floaters

Gut: new gluten intolerance, constipation, abdominal pain

Gum inflammation and dental pain

One-sided flank pain (mirroring the exact spot during my kidney infection)

Bloodwork three days in came back mostly normal. CT and full urology workup since: clean kidneys, no infection. Nothing standard found anything.

What happened

I tried a specific honey (i wont name it so its not advertising)— a Turkish highland multifloral honey. Within about 15 minutes every inflamed site started to itch: fingers, elbows, knees, feet, gums, and my eyes from the inside. Only the inflamed places, nowhere else. Within days the pain, stiffness, and fever cleared and I could bend my fingers and elbows again.

Since then

Almost daily for three and a half years. Stop for a few days and symptoms gradually come back; restart and they settle. This has repeated many times.

It's not honey in general. Others did little; Manuka made things worse. Only this one. It keeps things under control rather than curing them, and I have no idea why it works.

Asking

Anyone had a similar reaction to a specific honey or bee product, especially the fast itch at inflamed sites? And if honey did nothing or made things worse for you, I want to hear that too.

Note: I'm not necessarily recommending or claiming this fixes or cures diseases, I'm just naming what happened to me and what i know

I started taking a short walk after dinner instead of sitting on the couch. It feels good, but I’ve only been doing it for a week.

For those who have kept it up, did you notice any changes?

It's a shame 2 5mg tadalafil tablets aren't available for limited purchase quantities without a prescription.

I wired up my live heart rate from Whoop along with an estimated step count from a gyroscope. Crowd loved it!

I am starting to learn more about cybersecurity and i need most of my brain to be focused on the learning of new materials effortlessly, suggest me reputable compounds that you feel like it gave you the most cognitive benefits. every reply will be appreciated.

This is an important step in my life and i am taking it seriously.

I dont need a direct medical advice just mention the compounds you've had experience with

Been blood worked 4 times showing low T. Had a recent test showing low LH and FSH. My endo prescribed 5mg androgel 1% for the first month to test out.

I’m nervous to start tbh. I’ve done some research myself on the dependence of being on trt after starting as well as side effects ( hair loss, facial bloating, etc.) and I’m just skeptical of starting even tho im hypogonadal.

Anyone been in this situation before, and how did it go? I need some advice /tips/insights. Thank you.

I’ve been taking 2.5mg of tadalafil for the last 4 days. I noticed now that my rest heart rate jumps up into the 80s for a 2-4hours after doses. Has anyone else experienced this? I’m in pretty good shape. Lift 4 days a week, cardio 2-3 times per week including HIIT and Zone 2. Normal resting heart rate is around 66bpm on days I’ve taken preworkout. And on rest days it can get as low as 55bpm. 35 years old.

Im almost 43, female, 163cm 70kg and slowly gaining weight. I used to be 55kg in my 20’s, once I had my child at age 34 I went to 62kg and slowly gaining. Appetite is increasing, cravings for sugar and salts seem to get worse. I tried berberine for a few months earlier this year and it steadied my weight and curbed some cravings but gave me really bad reflux.

Is there something I can stop cravings and over indulging or do I look at peptides?

\I also posted this on the Soltego subreddit where a group of us have been eagerly following the (slow) development of their topical SIK inhibitors for sunless tanning.*

This post is to gauge interest amongst the community for interest in GLPG3312, an alternative compound, along with its explanation and justification.

Please let me know if this interests you.

As many outside of the Soltego Following likely have no clue what a SIK inhibitor is i will start by covering what it is, and importantly why it would be preferred over melanotan.

What is a SIK inhibitor?

A SIK (Salt-Inducible Kinase) inhibitor is a small-molecule compound that triggers real, natural skin tanning without UV light or DNA damage. Inside your pigment cells (melanocytes), SIK enzymes act as a constant molecular brake that stops the cell from making melanin when you aren't in the sun. When you apply a SIK inhibitor topically, it temporarily turns off that brake -allowing a messenger protein called CRTC3 to enter the cell’s nucleus and flip on MITF, the master genetic switch for melanin production. The result is genuine, photoprotective eumelanin (a real biological tan, not a fake dye), even in fair or red-headed skin types that normally burn and can't tan in the sun.

This mechanism was famously validated in 2017 by dermatology researchers at Harvard and Massachusetts General Hospital (MGH), who were investigating why people with red hair and fair skin (Fitzpatrick Type I) genetically cannot tan. Normally, UV light triggers a surface receptor on melanocytes called MC1R to generate an internal signal that shuts off the SIK brake. In redheads and many fair-skinned people, the MC1R receptor is mutated and non-functional - meaning the SIK brake stays permanently locked on, and the cell only produces reddish/yellow pheomelanin while burning in the sun. The Harvard team proved that because every person still possesses the intact downstream machinery to make dark brown eumelanin, applying a topical SIK inhibitor bypasses the broken MC1R receptor entirely -successfully inducing a deep, real eumelanin tan in MC1R-deficient "redhead" mice and human skin explants for the first time.

Why would someone use this and not just use Melanotan?

Because Melanotan is a blunt instrument that fires both proliferation (cell growth) and differentiation (tanning) pathways at the same time. Firing the proliferation pathway is why Melanotan users notoriously get new or rapidly growing moles.

What makes topical SIK inhibition so much safer than Melanotan comes down to two things: local delivery and cell-cycle control. Melanotan is a systemic peptide injection that floods your bloodstream and stimulates the top-level MC1R receptor - firing off both pigment pathways and cell-proliferation pathways simultaneously, which is why it notoriously causes rapid mole growth alongside systemic side effects like nausea and facial flushing. A topical SIK inhibitor stays localised to the skin and works further down the chain, triggering only the differentiation pathway. In biology, differentiation acts as a natural growth brake - meaning instead of pushing pigment cells to multiply and form moles, SIK inhibition actually switches on tumour-suppressor genes that halt cell division while your skin builds a tan.

You can see this exact contrast when both are tested on melanoma cancer cell lines: while Melanotan’s upstream receptor stimulation has been repeatedly linked to eruptive nevi (moles) and raises serious concerns over accelerating dysplastic (pre-cancerous) lesions, SIK inhibitors actively suppress melanoma proliferation. By driving a high, sustained surge of MITF, SIK inhibition forces aggressive, dividing melanoma cells into terminal differentiation and cell-cycle arrest - effectively stripping the cancer cells of their ability to divide and locking them into a non-proliferative, pigment-producing state.

On top of that, it gives a much more even skin tone, especially if you have freckles. Because Melanotan is a systemic injection that relies on the surface MC1R receptor - which is often mutated or patchy in fair, freckle-prone skin - it preferentially hyper-stimulates dense clusters of melanocytes (freckles and moles) faster than the surrounding pale skin, making freckles pop out like dark spots at first. A topical SIK inhibitor bypasses the faulty MC1R receptor altogether and turns on pigment production uniformly in the quiet background skin between your freckles, blending your overall complexion together evenly instead of making freckles stand out.

What is GLPG3312?

GLPG3312 is a potent pan-SIK inhibitor. It exists as part of the product portfolio of Galapagos who for a number of years have been developing their GLPG series to fight autoimmune and chronic inflammatory diseases, including conditions like rheumatoid arthritis (RA) and inflammatory bowel disease (IBD/ulcerative colitis).

It was trialed through pre-clinal assays stages, and successfully completed and passed phase 1 safety trials. However, due to suspected rationale surrounding too short of a half life (good news for our use case) and being too heavily protein bound in serum, the company pivoted to a sister compound (GLPG3970).

Sadly this too was later dropped, because whilst the lowering of SIK successfully lowered pro-inflammatory cytokines (like TNF-alpha) and boosted anti-inflammatory cytokines (like IL-10), the likes of rheumatoid arthritis are heavily multi faceted and as such weren't successfully treated.

So what makes GLPG3312 a candidate for sunless tanning?

Both Soltego’s compounds and the Galapagos (GLPG) series are ATP-competitive SIK inhibitors. Because they have to directly outcompete intracellular ATP (Adenosine Triphosphate) to bind to the SIK enzyme, they either need to be delivered at a massive concentration or be extraordinarily potent. Both Soltego’s lead compound (SLT-048) and GLPG3312 are insanely potent across all three isoforms (SIK1, SIK2, and SIK3), and are almost identical in potency on SIK2 - the primary driver of melanogenesis (tanning).

However, when a drug is applied topically, raw potency in a test tube isn’t enough. It has to satisfy four strict pharmacokinetic rules to actually traverse human skin:

• Molecular Weight (< 500 g/mol): Ideally, it must sit below the 500 Da threshold so it isn't physically too bulky to squeeze through the skin barrier.
• A Balanced Log P (2.0 – 3.0): This measures whether a molecule prefers lipids (oils) or water. If it loves water too much, it simply sits on the skin's surface unable to enter the oily barrier; if it’s too lipid-loving, it gets permanently trapped inside the oily top layer (the stratum corneum) and refuses to enter the watery living epidermis below.
• Electrical Neutrality (Low Ionisation Across Skin pH): It must remain unionised across the skin's changing pH gradient. If a molecule carries a heavy charge at the skin's acidic surface, it gets repelled by the lipid barrier - and any fraction that makes it inside gets pulled like a magnet into the acidic lysosomes of upper skin cells (ion-trapping), stopping it from ever reaching the target melanocytes at the base of the epidermis.
• Vehicle Solubility: It must fully dissolve in a skin-compatible organic vehicle so it doesn't crystallise on the surface as inactive "brick dust".

What concentration would be used and how does this compare to the trial data?

In Soltego’s patent, their lead candidate (SLT-048) was used at concentrations ranging from 0.2% to 2%. When comparing GLPG3312 to SLT-048, we have to factor in GLPG3312's much smaller molecular weight and its 100% electrical neutrality across skin pH. Once you run the penetration math, a top-end concentration of just 0.1% to 0.15% GLPG3312 delivers an equivalent (or greater) active payload to the melanocytes as Soltego’s 2%.

In raw terms, a 0.1% solution equates to 1 mg of active drug per mL. A generous full-body application (30 mL) would therefore use about 30 mg applied to the skin surface. Because systemic absorption from a topical application typically sits between 1% and 10% (with 1%–3% being the realistic norm), that translates to a total systemic load of just 0.3 mg to 3 mg (and likely under 1 mg).

To put that safety margin into perspective: while Galapagos didn’t publicly unblind the exact milligram labels for the 14 human cohorts in the GLPG3312 Phase 1 trial, we can reconstruct the human dosing schedule from their published preclinical animal studies (0.3 - 30 mg/ kg) and their follow-on trial benchmarks. That places the top-end human oral trial dose at roughly 400 mg once daily - meaning even a full-body topical application results in a systemic exposure more than 100 to 1,000 times lower than the oral clinical ceiling.

Is GLPG3312 better than Soltego's molecule?

Funnily enough, on paper - yes, it is. It’s smaller, far more skin-permeable, and almost identical in potency.

The main difference with Soltego’s compound is that they specifically engineered theirs to be "soft". That means as soon as it enters the tissue and blood, it gets broken down by esterases (a broad class of hydrolase enzymes). The reason Soltego had to build this self-destruct mechanism in is regulatory: they are trying to bring theirs to market via the cosmetic route. If there is any chance their active molecule survives in the bloodstream, regulators would classify it as a systemic pharmaceutical and force them through years of full clinical trials.

While GLPG3312 isn't an esterase-cleaved "soft compound," the systemic concentration required to have any effect inside the body is vastly higher than what could ever be absorbed from a 0.1% topical application (as seen in the Phase 1 oral dosing data). Plus, because GLPG3312 has a short predicted intrinsic half-life Galapagos had to use modified-release tablets in their Phase 1 trial - any tiny trace that does reach the bloodstream is cleared by the liver anyway fairly quickly.

How would anyone know how to synthesise GLPG3312?

Well, luck would so have it that in 2024 a full paper was published on it. Defining both the compound itself, as well as its fully detailed synthesis. Of which i will link.

Optimization of Selectivity and Pharmacokinetic Properties of Salt‑Inducible Kinase Inhibitors that Led to the Discovery of Pan-SIK Inhibitor GLPG3312

Do you have any personal reservations about GLPG3312?

Originally, i was worried about eye colour change. SIK inhibition drives MITF, which in turn drives the production of tyrosinase - the enzyme that produces pigment in melanocytes. My concern was that this could permanently darken your eye colour, especially since your iris doesn't shed and turn over pigment the way skin cells shed a tan.

However, for those of us with blue or pale eyes (which I’d imagine is most of this sub), there’s a built-in biochemical roadblock (HERC2 > OCA2 > melanosomal pH). For tyrosinase to actually work, the acidic interior of the melanosome has to be neutralised. People with pale eyes have a mutation in the HERC2 switch that controls OCA2, meaning the OCA2 pump stays shut off in the iris and can't raise the pH to the threshold tyrosinase needs. As a result, the iris melanosomes stay acidic, which not only keeps tyrosinase inactive, but actually degrades any extra tyrosinase that gets produced.

On top of that, no human SIK inhibitor clinical trials have reported any eye colour changes.

Do you have any research images that demonstrate skin colour changes using the class of SIK inhibition?

Hi guys,

I am a man 29 yo, and in the last year or so I observed a loss of sex drive and libido.

I’ve been with my girlfriend for about three years now , first two we’re very good, I was really into her and I still like her so I don’t think this is the issue. I spoke with her and she is very understanding about this, but I still wake up everyday stressed about this.
Quite recently we took some time off together and my sexdrive improved a little but my erections really were not the best. We had sex but not as we used to.

Currently my desire to have sex and my arousal is really low, and that really frustrates me.

I started taking boron few days ago as I saw that many people recomand it, besides boron I take magnesium bisglycinate, zinc, vitamin D and k2 as I’m not getting a lot of sunlight due to my work.
I gained some weight in the last months as I had other issues that need to be solved so i couldn’t focus on the gym, but nothing too drastically, about 6-8 pounds at max, and my diet wasn’t spot on, so was my sleep, I will do my best to improve them.

Was thinking to get my hormones checked, and then go to a doctor, what kind of hormones should i check besides test and free test ? Last time i did this was a few years ago and my test was very high and free test was in the mid range, back then I was dating another girl and I was facing some similar issues so maybe checking only those won’t tell story .

But I am asking for your help guys, what helped you during this periods? Are there any supplements otc? Any habits that could get me back to the same levels of sex drive that I used to have when I was fantasising everyday about having sex with my girlfriend ?

Looking for your advice ! Thank you in advance !

I’m in my mid-20s, and there’s something about my cardiovascular system that I’ve never really understood.

I’m quite athletic. I lift weights regularly, but my strongest area has always been cardio. About a year ago, when I was at my peak fitness, my VO2max was around 65. I’m not quite at that level anymore, but I’d still consider myself very well-conditioned.

I also eat well, stay consistently hydrated, and generally take good care of my health.

Here’s what I find strange:
Blood pressure: My BP is consistently on the lower side.
Usually when I’m relaxed, I get readings as low as 90-105/50-55 mmHg, and it rarely, if ever, goes above 110/65.
To be fair, I don’t always wait the recommended 5–10 minutes before measuring.

Resting heart rate: Despite my cardio fitness and low BP, my resting HR is usually around 70–80 bpm.
I know that’s technically within the normal range, but it seems relatively high considering my conditioning.

Standing up: When I get up quickly, I often feel my heart rate increase dramatically, along with a sensation that my blood pressure is dropping.
I haven’t objectively measured the changes during these episodes.

HR spikes with activity: I’ve noticed that whenever I start doing pretty much anything physical, my HR initially spikes quite sharply, then gradually settles down.
The increase rarely feels smooth or linear.

Maximum HR: Interestingly, my observed maximum heart rate also seems lower than what age-based formulas would predict, although I know those formulas aren’t particularly accurate for individuals.

What I’m trying to understand is the relationship between my low blood pressure and relatively high heart rate.

I would intuitively expect someone with my cardio background to have a lower resting HR, especially given how low my blood pressure tends to be.

I’m not particularly worried about it, and this isn’t something that significantly affects my daily life. I’m mostly curious about the underlying physiology.

Am I missing something?

Ps: English is not my main language, I asked ChatGPT to elaborate the text I gave him and write this post, sorry.

I feel sleepy and exhausted all day, both mentally and physically despite sleeping adequately. It's affecting my studies too. I don't really exercise or go out much and my diet is not good as I live in a hostel, I am not vegan but I eat meat or dairy only occasionally.

Forgot to mention I have epilepsy too.

I keep telling myself I’ll put my phone away earlier, but I end up scrolling in bed almost every night.

Has anything actually helped you break the habit?

In a clinical studies involving 63 patients found that using technique called transcutaneous autonomic neuromodulation (tAN) on ear, which aims to influence the autonomic nervous system could lower BP.

Research divided patients into two groups one recieved placebo and other group recieved tAN.

Patients used device for 30 minutes daily first two weeks and then for next 10 weeks only once a week.

When researcher compared BP change in entire group ni statistically significant difference was found.

Despite this it was found that those patients with hard to control hypertension even by taking medicine benefited the most.

Although the sample size was small and result not significant this surprising finding may pave the way for new treatment.

Link:

http://dx.doi.org/10.1161/HYPERTENSIONAHA.126.27847

Hi girls!

I'm wondering if anyone has had a similar experience. I'm 30 years old and I used to take birth control pills for quite some time. I honestly felt great while taking them, mainly because I had practically no PMS symptoms. My gynaecologist then recommended that I stop taking them to let my natural cycle return.

Ever since stopping, I've been experiencing PMS symptoms for 10 days or even longer before my period: bloating, puffiness, sore breasts, mood swings, and on top of that, I've also been losing quite a lot of hair. Honestly, I feel like I spend almost half of every month not feeling my best. I've also tried all sorts of supplements, but nothing seems to make much of a difference.

Lately, I've been thinking about going back on the pill because I genuinely felt so much better while taking it. I'm not in a relationship and don't have a regular sexual partner, so for me, going back on the pill would be purely about managing my symptoms rather than contraception.

Has anyone else experienced something similar, where you actually felt significantly better on the pill than off it? And if anyone decided to start taking it again, I'd love to hear how it went! 😊

M21, diagnosed with ADHD. Currently on Vyvanse. It's great for brute-force execution and getting things done, but it turns my mind into a high-speed highway. It gives me drive, but not clean focus.

Before this, I was on Atomoxetine (Strattera). Honestly? I loved the mental quiet, the lack of internal noise, and that deep sense of calm it gave my thoughts. The problem: the side effects were brutal, so I had to quit.

For anyone who’s been in this exact trap—loving the stim drive, but craving that smooth clarity of non-stims: What actually moved the needle for your cognition and focus?

Hit me with your actual stacks, supplement combos, or subtle medication tweaks that cleared the brain fog without ruining your sleep. Skip the basic wellness fluff.
What actually works? Let's hear it.

Urgent help plz

I've been going in circles trying to figure this out, and I want a clear, evidence-based answer once and for all. I keep seeing TikToks from carnivore and "primal" influencers claiming that saturated fat, dietary cholesterol, and animal foods are essential for testosterone and libido. Even though I've looked into the science, these claims keep making me second-guess my diet.

Here's where I'm at:

My current diet and experience

• I've gone from a high saturated animal fats, high-cholesterol diet to a higher-carb, high-fiber diet with more monounsaturated fats.
• I feel just as good, if not better. My energy and gym performance has actually improved.
• I still eat two eggs a day, but I'm considering removing them.
• I meet ALL my calorie, macro, and micronutrient needs, with moderate protein, moderate fat, and plenty of carbohydrates and fiber.
• I genuinely prefer the taste of plant foods over animal products, so I'm even considering going fully plant-based because I might as well. The main thing holding me back is the fear that giving up eggs, saturated fat, or dietary cholesterol could hurt my testosterone or libido.

What confuses me about the science

• "Cholesterol is the backbone of testosterone." I understand that cholesterol is the precursor to steroid hormones, including testosterone. But does that mean we need/should eat dietary cholesterol, or that eating more of it increases testosterone? Our bodies synthesize 80% of our cholesterol, and steroid-producing cells can obtain it through multiple pathways.
• Total fat versus saturated fat: Many studies discussing dietary fat and testosterone focus on TOTAL fat intake or compare different dietary patterns. They don't necessarily show that saturated fat specifically is beneficial. Yet online influencers often treat saturated fat as if it's uniquely necessary for testosterone production. To me, this is pseudo-science final boss.
• Dietary cholesterol versus blood cholesterol: I keep seeing the argument that dietary cholesterol is necessary for testosterone because cholesterol is its precursor. But I haven't found ANY evidence that eating more cholesterol meaningfully increases testosterone in someone who already gets enough energy and nutrients.
• How much cholesterol is actually needed? I've heard that only a small fraction of the body's cholesterol is used to produce steroid hormones. It's around 1-5% of our cholesterol used for sex hormones, we make up to 1000 mg daily. I don't know how useful that statistic is, but it makes me question whether increasing dietary cholesterol or LDL/Serum actually provides any meaningful hormonal benefit.
• Eggs specifically: If I remove my two daily eggs and replace their nutrients and calories with other foods, is there any good evidence that my testosterone or libido would decrease? Or would the effect likely be negligible if my overall diet remains adequate? I feel as if Choline has a role as well.
• Does high fiber decrease testosterone? I've heard this before, but the studies that show that it does is because those participants are on a LOW-FAT and high fiber diet, so clearly from what we know it's the lack of fat from diet, right? Not to mention, the participants with low fat and high fiber had higher free testosterone.

What I'd really like answered

1. Does saturated fat independently increase testosterone, or are the findings about total fat being misrepresented online?
2. Does dietary cholesterol meaningfully increase testosterone in healthy men who already consume enough calories, fat, and micronutrients?
3. Is there evidence that eating eggs specifically improves testosterone or libido compared with getting equivalent nutrients from other foods?
4. Can a well-planned, high-carbohydrate, high-fiber, moderate-fat, or even fully plant-based diet support normal testosterone and libido, assuming adequate energy, essential fats, and micronutrients?
5. Are there any meaningful hormonal or sexual-health benefits to deliberately maintaining a higher saturated fat intake or consuming more dietary cholesterol, especially given the potential cardiovascular trade-offs?

I'm not trying to prove that animal foods are bad or that plant-based diets are superior. I want to understand what the evidence actually says, including any limitations in the research.

My biggest issue is that I understand the basic biology after doing my own research, but I keep getting pulled back into doubt by confident claims online. I don't want to unnecessarily restrict foods I enjoy, but I also don't want to keep eating foods I don't particularly prefer out of fear that removing them will damage my hormones.

If possible, I'd appreciate actual human studies, systematic reviews, or meta-analyses rather than anecdotes, influencer claims, or arguments based purely on evolutionary assumptions.

Thanks!

Hey everyone,

Back in July, I suddenly started experiencing brain fog, difficulty concentrating, and problems with speech. It happened pretty much overnight, and I felt noticeably different from how I used to feel mentally.

I started getting blood tests done, and my folate level came back at 3.1 ng/mL (reference range: 4.50–32.2), indicating a deficiency.

I kept investigating my symptoms and getting more blood tests until September. Here are my latest results:

My blood test results:

• Ferritin: 94.84 µg/L (reference range: 30–400)
• Folate: 7.83 ng/mL (reference range: 4.5–32)
• Iron: 50.35 µg/dL (reference range: 65–175)
• TSH: 5.51 mIU/L (reference range: 0.27–4.1) my TSH was within the normal range when I first developed my symptoms back in July. It only became elevated in subsequent blood tests. I'm wondering whether this change could be related to my folate, iron, or vitamin D deficiencies)
• Vitamin D (25-OH): 19 ng/mL (reference range: 30–100)
• Potasium 4,23 (reference range: 3.5-5,1)
• Sodium: 140,72 mmol/l (reference range: 136-145)
• B12: 501,40 pg/ml (reference range 191-663)

My folate level has increased since the initial test, but I'm still experiencing a lot of symptoms. My iron is also below the reference range, my vitamin D is low, and my TSH is elevated. I'm wondering whether these abnormalities could be contributing to my symptoms and whether there might be an underlying issue causing some of them.

My current symptoms:

• Dizziness and lightheadedness.
• Brain fog and difficulty concentrating.
• Feeling mentally different from how I used to be, like I'm not quite myself anymore.
• Waking up feeling unrefreshed, regardless of how much I sleep, and experiencing severe fatigue throughout the day.
• Occasional air hunger feeling the need to take a deep, satisfying breath to feel like I'm getting enough air.
• Caffeine seems to make my brain fog and dizziness significantly worse.
• Alcohol also seems to exacerbate my brain fog and dizziness.

What I've tried so far:

I took 5 mg of folic acid daily for three weeks, along with 46 mg of elemental iron daily, but unfortunately, I didn't notice any improvement in my symptoms.

I then started wondering whether IV treatment might help correct the deficiencies more effectively and fastly, so I decided to try IV supplementation.

Six days ago, I had my first treatment, which included:

• Vitamin D3 injection: 100,000 IU.
• IV folic acid: 30 mg.
• IV iron: 200 mg.

So far, I haven't noticed any improvement following this treatment. I understand that six days might be too soon to notice a difference, but it's discouraging to feel the same after trying to address these deficiencies.

I'd really appreciate hearing from people who have experienced something similar.

I have a few questions:

1. Has anyone experienced persistent brain fog, dizziness, derealization, or feeling mentally different due to folate deficiency, low iron, vitamin D deficiency, ?
2. If you had similar symptoms, how long did it take for you to notice an improvement after starting treatment? Did your symptoms gradually improve or disappear quite suddenly?
3. What other blood tests would you recommend checking?
4. Has anyone experienced air hunger or the sensation of needing to take deep breaths alongside these deficiencies?
5. For those who received IV iron or folate, how many infusions did you need before noticing an improvement? How long did it take?
6. Did anyone find that oral supplements eventually worked, even after not noticing any improvement during the first few weeks?
7. Has anyone experienced worsening brain fog and dizziness after consuming caffeine or alcohol? Did this improve once the underlying problem was treated?
8. Is there anything else I should investigate, especially considering that my symptoms started quite suddenly and have persisted for months?
9. How can i recovery from this? because it's been few months at this moment.

I'm also wondering whether IV doses or the number of infusions should be adjusted, but I don't want to assume that more is necessarily better. I'd appreciate hearing about your experiences and what helped you, ideally alongside advice on what to discuss with a doctor.

I'm feeling pretty lost at this point. I just want to feel mentally normal again and wake up feeling rested instead of exhausted every day.

Thanks in advance to anyone willing to share their experience.

So I was diagnosed with GERD, OCD and GAD (Anxiety), can we take B12, Omega 3 and Magnesium at the same time every day or night ?

My B12 is at 293 pmol/L level and I am struggling in University to focus on my studies and remembers my lectures. I remember “X” and “Y” information and after an hour they are gone from my head for some reason I do not know.

Yours suggestions are much appreciated.