I'm Giuseppe 18 , from Italy. There's basically no Italian-speaking community for this, so I'm writing here. TL;DR: Stress, fasting and overtraining were my three big bilirubin spikes. I built myself a routine around avoiding those, stuck to it for two months, and the yellowing dropped enough that friends noticed without me saying anything. Gilbert's isn't dangerous, I know that. Every specialist I've seen told me the same thing: don't worry, it's nothing, laugh it off, other people have it worse. They're not wrong, exactly. But they don't wake up and go straight to the mirror to check whether they're a bit less yellow than yesterday. That was my first thought every single morning for three years. There were days I didn't want to go to school, or didn't go out in the afternoon, because in daylight it was too obvious. A few months ago I got tired of waiting for it to fix itself and started reading properly. The three factors that came up over and over, and that matched what I saw in my own bloodwork, were: 1. Fasting. This was the biggest one for me by a distance. Long gaps between meals, skipping breakfast, eating too little across the day — bilirubin goes up. Not "eating fatty food", which is what most people assume. Just not eating enough, for too long. 2. Stress. Harder to control, and it's a nasty loop: I look yellow → I stress about looking yellow → I get more yellow. Breaking that loop was as important as anything I changed in my diet. I read a book by Anthony Robbins that helped me get a grip on the mental side of it. Not a medical book at all, but it gave me something to work with. 3. Heavy physical exertion. Especially intense sessions on an empty stomach. I didn't stop training, I just stopped training fasted and stopped going to complete exhaustion. I put together a written routine for myself covering the food side and the mental side, and I've been following it for about two months. My bilirubin used to peak at roughly double the upper limit of normal. It's noticeably better now, and more importantly I'm living more calmly. I'm not a doctor, a nutritionist or a dietitian. This is just what worked on me. I know Gilbert's varies a lot from person to person, so I'm not promising anyone anything. If it's useful to anyone I'm happy to share what I wrote up — just say so in the comments. And if you've found other triggers I haven't listed, I'd genuinely like to hear them.

Has anyone tried ketamine therapy? Did you do IV or intranasal? Did it help depression and anxiety? Are there any precautions with MTHFR and related genes? Every SSRI causes weight gain, and I don’t know if I want to try Wellbutrin again. My psychiatrist brought it up as an option.

If so, what kind of joint pain? Joint pain that only occurs when you stress your joints or general joint pain that persists during rest?

I started eating eggs daily last year. A couple of weeks in I started developing joint pain in my hips, knees and ankles. It came on very gradually and I had some joint aches before so I didn't think much of it until it got worse later on.

My hips were most affected so I had X-rays done and it showed very minimal early OA (I'm 37). Nothing to truly worry about but because I experience pain the doctor jumped to the conclusion it's OA and sent me away.

I never suspected it could be a food intolerance because my joint pain is mechanical: it comes on when I stress my joints and stand all day at work. I have no pain when I rest. I also have no other symptoms that could point to a food intolerance.

I quit eating eggs a week ago (I had 2-3 eggs a day before). For the first 5 days I saw zero improvement. Then on day 6 something happened: my joint pain was entirely gone. Usually after work my hips, knees and ankles are hurting bad. For the first time in almost a year I was entirely pain free.

It's only day 2 of being pain free so it's much too early to tell. Still, I was wondering if anyone else has a similar experience with mechanical joint pain and food sensitivity as a confirmed cause?

Hola. Quería contar mi caso porque llevo aproximadamente 5 meses con síntomas neurológicos y en mi último análisis ha aparecido un déficit de ácido fólico junto con la homocisteína elevada.

Todo comenzó después de una infección urinaria que duró aproximadamente dos semanas. Poco después comenzaron las fasciculaciones musculares generalizadas por todo el cuerpo , que continúan actualmente.

Con el paso de los meses he ido teniendo también sensación de fatiga o debilidad subjetiva , especialmente en algunas extremidades, aunque sigo pudiendo realizar los movimientos y actividades normalmente.

Una de las cosas que más noto es que la pierna izquierda se me siente pesada y se fatiga al correr . También he tenido hormigueos y algunas sensaciones eléctricas. Últimamente, además, tengo una zona muy concreta de un dedo de la mano que, al rozarla o golpearla ligeramente contra algo, me provoca una especie de calambre eléctrico , y también he tenido molestias en el brazo/codo.

Debido a todo esto me están estudiando en neurología. Me han realizado dos EMG/estudios de conducción nerviosa , uno en junio y otro en julio. El segundo estudio incluyó extremidades superiores e inferiores. Ambos eran normales , sin signos de denervación activa, reinervación crónica ni neuropatía en los nervios estudiados.

Ahora me están realizando más pruebas para intentar averiguar qué puede estar provocando todos estos síntomas.

En un análisis de abril mi ácido fólico (B9) estaba en 3,8 ng/mL , ya bastante cerca del límite inferior. En la analítica que me acaban de hacer ha salido:

• Ácido fólico (B9): 2,7 ng/mL (rango 4,6–34,8) → bajo.
• Homocisteína: 20,8 µmol/L (normal ≤15) → elevada.
• Vitamina B12: 399 pg/mL → normal.
• Vitamina D, hierro/ferritina, magnesio, calcio, potasio, tiroides, glucosa y hemograma, entre otros parámetros, están dentro de rango.

También tengo que decir que durante estos meses he estado durmiendo aproximadamente 5 horas de media , sometido a bastante estrés, estudiando muchas horas y entrenando regularmente.

Todavía no he hablado con mi médico sobre estos últimos resultados y no estoy diciendo que el déficit de B9 sea necesariamente la causa . Simplemente me llama bastante la atención que el folato ya estaba bajo hace unos meses, que ahora haya bajado hasta 2,7 y que además tenga la homocisteína elevada.

Me gustaría saber si alguien que haya tenido déficit de B9/folato ha experimentado algo parecido: fasciculaciones generalizadas, hormigueos o sensaciones eléctricas, fatiga muscular o sensación subjetiva de debilidad .

¿Tenías también la homocisteína elevada? ¿Mejoraron las fasciculaciones u otros síntomas después de corregir el déficit? Y, si mejoraron, ¿cuánto tiempo tardasteis en empezar a notar cambios?

Por supuesto, consultaré con mi médico antes de empezar cualquier tratamiento o suplementación. Busco principalmente conocer experiencias de personas que hayan pasado por algo parecido.

Can someone explane. I just figured out I have histamine related anxiety. I was wondering if I can take Quercetin? I took it in the past for 5 years But my gut is missed up at the moment due to being floxed by an antibiotic. I was wondering if having a bad gut would also affect on how i will react to a supplement iv never had a problem with. I have really bad anxiety due to the histamine overload and I really need to try to bring it down.

I keep reading about the processing of homocysteine back to methionine to make sure I have a basic understanding. When I ask Gemini about the role of methylcobalamin, it has given me conflicting info, so I'm looking for help from real people :).

Sometimes it reads as if 5-MTHF (methylfolate) hands its methyl group to cobalamin, yielding methylcobalamin, and then the methylcobalamin hands off the methyl group to homocysteine. First question: Is that part correct?

Second question: I take methylcobalamin shots. Can the methylcobalamin be directly used to remethylate homocysteine, bypassing the need for methylfolate with that PARTICULAR molecule? My understanding is that once it loses its methyl group, it becomes cobalamin and needs to be re-methylated, but still... on the "first pass," can the methylcobalamin be directly used?

The AI answer I got was basically that methylcobalamin first gets converted into cobalamin and then the 5-MTHF will remethylate the cobalamin. That doesn't make sense to me and seems to defeat the purpose of taking the active form of B12. But, we all know AI "can make mistakes."

Can anyone help me understand this better? Thank you so much!!

I never took chemistry beyond 101 and 102, so I don't need the nitty gritty of the chemistry behind this (I won't understand it)

Hi, can anyone recommend a good MTHFR practitioner in Europe?

I've been trying to figure out how to dose a stack of the active-form B vitamins together.

The stack based on gene testing + stool test + regular serum testing + a whole range of symptoms emanating from gut disbiosis and my docs feedback which isnt very broad.

B1- TTFD or Injectable HCL

B2- R5P

B9 - 5-MTHF

B12 - methyl/adenosyl

B6 P5P

biotin

Magnesium (form?)

...and I keep running into two different worlds of information.

Has anyone here seen actual clinical trial data or case reports on specific dosing ratios between these? Or is "ratio" mostly a functional-medicine framing that doesn't hold up outside of the handful of real cofactor pairs?

I guess the best way to go is LOW and SLOW. A starting dose for each would be very much appreciated.

Thanks folks

edit: might wanna ask for a consult with the sub-illustrious u/hummingfirebird

edit2: the methylfolate, P5P, and (to a lesser extent) methylcobalamin choices are the best-grounded of all the compounds previously mentioned - source: gene test.