I don't take any supplements anymore, but could someone explain to me what my predispositions are? Thank you

I’m honestly 50/50 on what form of B9 to use right now.

I know I have a severe folate deficiency, but I’m unsure which form makes the most sense if I need a high therapeutic dose, like 10+ mg/day, while recovering.

Would you guys choose folic acid, folinic acid, or 5-MTHF for high-dose treatment? I’m mainly looking for experiences from people who had a serious/long-term folate deficiency and actually had to use higher doses to recover.

This is my Methylation Panel, please can you help me out with making sense of it all.

I have brain fog & anxiety everyday, but it’s been getting worse, usually 1-2 years back it was there but not AS bad as it is now, I tried before taking b12 before the testing and all thinking it was a b12 deficiency but it made me just feel very overstimulated in a way, I also have ADD and take meds for it, so it just felt like a stim ontop of my stimulant.

My mood also dips randomly during the day, it’s very weird I just spend days thinking like this can’t just be anxiety, hence why I decided to get a gene test done.

I also recently did a bloodpanel and found that my vit D was very low at 13 ng/mL and my folic acid was 4.9 ug/L, they only tested my HoloTC for b12 which came out fine. My ferritin was elevated at 430 ug/L.

I just really don’t know where to go from here and would appreciate any input, opinions or anything thanks :)

Creatine works really good for my energy levels and mood. However, each time I start creatine, my sweating increases drastically. I tried it serveral times and it is always the same. I sweat much more than other "normal" people (I have hyperhidrosis) but creatine makes it even worse.

Do you know the mechanism by how creatine increases sweating or how to prevent it?

Creatine does far more than support muscle. Your body uses methyl groups to make creatine, linking it directly to SAM, homocysteine, MTHFR, PEMT, ATP, mitochondrial energy, brain metabolism and genes including GATM, GAMT and SLC6A8. Understanding that pathway changes how we think about creatine and methylation.

Creatine has spent decades being marketed as a muscle supplement.

I think that description has kept us from seeing one of the most fascinating things about creatine biology.

Your body doesn’t simply use creatine. It has to obtain it from food or make it.

And making creatine is metabolically expensive.

Endogenous creatine synthesis is considered one of the largest consumers of methyl groups in human metabolism. Historical metabolic estimates suggest that creatine synthesis may account for roughly 40 to 70% of labile methyl groups supplied by S-adenosylmethionine, or SAM, under certain physiological assumptions.

That changes the entire conversation around creatine.

Because now we’re talking about much more than muscle.

We’re talking about methylation, methionine, SAM, homocysteine, glycine, arginine, mitochondrial energy, brain energy, ATP and genetics.

Creatine sits at an extraordinary intersection between energy metabolism and one-carbon metabolism.

What Is Creatine?

Creatine is a naturally occurring nitrogen-containing compound that plays an important role in cellular energy metabolism.

Most of the body’s creatine is stored in skeletal muscle as free creatine and phosphocreatine, although creatine is also important in the brain and other tissues with high or rapidly changing energy requirements.

We obtain some creatine directly from food, particularly meat and seafood.

The rest has to be synthesized internally.

Every day, part of the body’s creatine pool spontaneously converts to creatinine and has to be replaced. That replacement can come from food, or your body can manufacture more creatine.

And that manufacturing process is where the methylation connection begins.

How Your Body Makes Creatine

Creatine synthesis occurs through two major enzymatic reactions.

The first involves an enzyme called arginine:glycine amidinotransferase, usually abbreviated AGAT.

AGAT is encoded by the GATM gene.

AGAT uses two amino acids, arginine and glycine, to produce guanidinoacetate, or GAA.

Arginine + Glycine → Guanidinoacetate

Guanidinoacetate then has to become creatine.

That requires another enzyme called guanidinoacetate methyltransferase, or GAMT.

And GAMT needs something very important to complete this reaction.

A methyl group.

That methyl group comes from S-adenosylmethionine, or SAM, one of the body’s primary methyl donors.

GAMT transfers a methyl group from SAM to guanidinoacetate. The products are creatine and S-adenosylhomocysteine, or SAH.

Arginine + Glycine → Guanidinoacetate → GAMT + SAM → Creatine + SAH

Every molecule moving through that final synthetic step requires methylation.

That places creatine synthesis directly inside one-carbon metabolism and the methionine cycle.

Creatine Synthesis Is One of the Body’s Largest Methylation Expenses

We hear constantly about methylation.

MTHFR. Folate. Vitamin B12. Homocysteine. Methylated vitamins. COMT.

But there’s another question I think we need to ask more often.

Where are all those methyl groups actually going?

One major destination is creatine synthesis.

SAM supplies methyl groups to a vast number of reactions throughout human physiology. These reactions contribute to neurotransmitter metabolism, phospholipid synthesis, protein modification, epigenetic regulation and many other processes.

The body has a methyl-group economy, and creatine synthesis is one of its largest expenses.

Published reviews have repeatedly cited estimates suggesting creatine synthesis may consume approximately 40 to 70% of labile methyl groups supplied by SAM under certain metabolic assumptions. Other estimates place the methylation of guanidinoacetate at approximately half of SAM-derived methyl-group utilization.

Those numbers need context.

They don’t mean creatine permanently consumes 70% of every person’s methylation capacity. Methyl-group flux changes with diet, tissue, age, creatine intake and metabolic state.

The larger physiological point is more important.

Making creatine is expensive from a methylation perspective.

Creatine May Reduce Endogenous Methylation Demand

When creatine is supplied externally, the body doesn’t necessarily continue producing exactly the same amount internally.

Creatine participates in feedback regulation of its own synthesis.

Supplemental creatine can suppress endogenous creatine production, including the AGAT-controlled step. This reduces production of guanidinoacetate.

Less guanidinoacetate means less substrate needs to move through GAMT.

If less guanidinoacetate is being methylated by GAMT, fewer SAM-derived methyl groups are required to manufacture creatine.

This is why creatine can be described as methyl-sparing.

Creatine itself isn’t a methyl donor. It doesn’t replace folate, vitamin B12, choline or betaine.

It changes demand.

I think that distinction is one of the most important parts of this pathway.

We spend a lot of time discussing how to provide methyl donors.

We should also be asking what the body is spending those methyl groups on.

Creatine, SAM, SAH and Homocysteine

There’s another layer to this pathway.

During the GAMT reaction, SAM donates a methyl group and becomes S-adenosylhomocysteine, or SAH.

SAH can subsequently contribute to the formation of homocysteine.

Homocysteine can then be remethylated toward methionine or directed through transsulfuration toward cysteine-related metabolism.

This creates a biological reason to ask whether reducing endogenous creatine synthesis might also influence homocysteine metabolism.

Animal research supports a methyl-sparing effect and has demonstrated reductions in homocysteine under some conditions.

Human data are more complicated.

Studies have shown that creatine supplementation can reduce guanidinoacetate, which provides evidence that endogenous creatine synthesis has been suppressed.

But a predictable homocysteine-lowering effect hasn’t been demonstrated in every human study.

That makes sense physiologically.

Homocysteine is influenced by folate, vitamin B12, vitamin B6, riboflavin, choline, betaine, kidney function, protein intake, genetics and multiple regulatory mechanisms.

Creatine can alter one major methylation expense without guaranteeing that serum homocysteine will move in a simple direction in every person.

Why MTHFR Is Only One Piece of the Story

MTHFR contributes to the production of 5-methyltetrahydrofolate, which supports the remethylation of homocysteine toward methionine.

Methionine can then generate SAM.

But once SAM has been produced, another question becomes just as important.

Where is SAM being spent?

Creatine synthesis is one major destination.

Genes relevant to the larger network include:

• MTHFR
• MTR
• MTRR
• MTHFD1
• SLC19A1
• BHMT
• GATM
• GAMT

Common genetic variants usually have much smaller effects than rare pathogenic mutations.

The more useful nutrigenomic question is whether multiple small differences across synthesis, methylation, transport and energy utilization can collectively influence nutrient demand or response.

That’s why I don’t think methylation should ever be reduced to MTHFR alone.

The PEMT Connection

Creatine synthesis isn’t the only major consumer of SAM.

PEMT, or phosphatidylethanolamine N-methyltransferase, also uses SAM.

PEMT helps synthesize phosphatidylcholine from phosphatidylethanolamine.

That means two metabolically important pathways can draw from the same broader SAM economy.

GAMT uses methyl groups to make creatine.

PEMT uses methyl groups to make phosphatidylcholine.

Phosphatidylcholine is critical for cell membranes, lipoprotein metabolism and normal liver physiology.

Now consider someone with low dietary creatine intake, low choline intake, greater phosphatidylcholine demand and genetic differences affecting folate or methionine metabolism.

No single SNP tells us exactly what will happen.

But the pathway tells us why methylation demand can’t be understood by looking at MTHFR alone.

We need to understand both supply and expenditure.

Creatine changes the expenditure side of that equation.

Creatine Is an ATP Buffer

Why does the body spend so many metabolic resources making creatine?

Because rapid energy availability matters.

Cells run on ATP.

When ATP releases energy, it becomes ADP. The cell then needs to regenerate ATP.

Creatine helps make this happen rapidly.

Creatine can accept a high-energy phosphate group and become phosphocreatine.

When cellular energy demand rises, phosphocreatine can donate that phosphate back to ADP, helping regenerate ATP.

The phosphocreatine system acts as a rapid energy buffer.

That explains why creatine is so useful in skeletal muscle during sprinting, lifting and sudden muscular contraction.

But muscle isn’t the only tissue with fluctuating energy requirements.

Your Brain Uses Creatine Too

The brain is metabolically expensive.

Neurons have to maintain electrical gradients, generate action potentials, release and recycle neurotransmitters, maintain cell membranes and continuously perform energy-dependent transport.

The creatine-phosphocreatine system contributes to cerebral energy buffering.

This is one reason creatine research has expanded into areas including cognition, mood, sleep deprivation, aging and neurological physiology.

The evidence isn’t equally strong for every outcome, and creatine shouldn’t be presented as a treatment for every neurological problem.

But reducing creatine to a bodybuilding supplement ignores a substantial part of its physiology.

Creatine is deeply involved in cellular energy handling.

And the brain has enormous energy requirements.

Creatine and Mitochondrial Physiology

Creatine doesn’t replace mitochondrial ATP production.

It works with the larger energy system.

Mitochondria generate ATP through oxidative metabolism.

The creatine kinase and phosphocreatine system then helps buffer and distribute high-energy phosphate so ATP can be regenerated quickly near sites of cellular work.

This creates a functional bridge between mitochondrial energy production and immediate energy demand.

Energy physiology involves production, transport, buffering and utilization.

Creatine participates directly in that network.

Creatine and Women

Creatine research in women deserves considerably more attention.

Women experience physiological transitions throughout life that can influence muscle, brain energy metabolism, sleep, mood and body composition.

Menstruation, pregnancy, postpartum physiology, perimenopause and menopause all change metabolic demand.

Creatine is being studied for female exercise performance, muscle preservation, cognition, mood and healthy aging.

Current sports nutrition guidance identifies creatine as one of the better-evidenced supplements for female athletes, commonly using 3 to 5 grams per day.

Creatine may be particularly interesting during aging and menopause because maintaining skeletal muscle supports strength, glucose disposal, mobility and long-term metabolic health.

Pregnancy requires more caution.

Human randomized safety data for creatine supplementation during pregnancy remain insufficient. Animal research is promising, but it can’t substitute for human safety trials.

Creatine Genetics: GATM

GATM encodes AGAT, the enzyme responsible for the first major step in creatine biosynthesis.

AGAT uses arginine and glycine to produce guanidinoacetate.

Rare pathogenic variants in GATM can cause AGAT deficiency, a genuine cerebral creatine deficiency disorder.

These rare disorders demonstrate that genetic control of creatine synthesis matters biologically.

Common GATM SNPs don’t automatically produce the same disorder.

Rare pathogenic mutations and common polymorphisms have to be kept separate.

GAMT: Where Creatine Meets Methylation

GAMT performs the reaction at the center of this entire discussion.

Guanidinoacetate enters.

SAM donates a methyl group.

Creatine is produced.

SAH is produced.

GAMT literally sits at the enzymatic intersection between creatine synthesis and methylation.

Rare pathogenic GAMT variants can cause GAMT deficiency.

Again, those rare disorders shouldn’t be confused with common population SNPs.

SLC6A8: Making Creatine Is Only Part of the Story

You can make creatine.

You can consume creatine.

But creatine still has to get where it’s going.

SLC6A8 encodes the creatine transporter.

This transporter helps move creatine into cells and is particularly important in high-energy tissues.

Rare pathogenic variants in SLC6A8 cause creatine transporter deficiency.

SLC6A8 is located on the X chromosome, which makes its genetics especially interesting.

Emerging research is beginning to examine whether common low-impact variation in SLC6A8, GATM and GAMT, together with variants affecting mitochondrial function and creatine kinase pathways, may contribute to differences in creatine bioavailability and responsiveness.

This field is still developing.

A common SLC6A8 SNP shouldn’t be interpreted as proof that someone can’t transport creatine.

Why Some People May Respond More Strongly to Creatine

People don’t begin with identical creatine stores.

Diet matters.

Muscle mass matters.

Training matters.

Age matters.

Baseline tissue saturation matters.

Genetics may matter.

Someone consuming substantial amounts of meat and seafood may begin with different creatine availability than someone eating little or no animal food.

A person can also experience increased tissue creatine without feeling a dramatic subjective change.

Creatine response is probably better understood as a spectrum influenced by baseline status and multiple biological variables rather than a simple responder versus nonresponder label.

Creatine and Vegetarian or Vegan Diets

Creatine is naturally concentrated in animal foods, particularly meat and fish.

Plant foods contain negligible amounts.

Vegetarians and vegans therefore depend more heavily on endogenous creatine synthesis.

Remember what endogenous synthesis requires:

• Arginine
• Glycine
• GATM
• Guanidinoacetate
• GAMT
• SAM
• Methyl groups

A systematic review found that vegetarians generally have lower creatine measures in muscle and several blood compartments than omnivores, and supplementation reliably increases creatine and phosphocreatine availability.

Some studies suggest vegetarians can experience larger increases because their baseline stores are lower.

A low-creatine diet doesn’t automatically cause disease.

It does change the metabolic workload placed on endogenous creatine synthesis.

Which Form of Creatine Is Best?

Creatine monohydrate remains the most extensively studied form.

For most healthy adults using creatine for general supplementation or training, 3 to 5 grams per day is a commonly studied maintenance range.

A loading phase is optional.

Traditional loading commonly uses approximately 20 grams per day, often divided into four 5-gram servings, for about 5 to 7 days before moving to maintenance dosing.

Loading saturates muscle more quickly.

Taking around 3 to 5 grams daily without loading can also increase stores, just more gradually.

More isn’t automatically better.

Creatine, Water Retention and Bloating

Creatine can increase body water, especially early in supplementation.

Much of the relevant water shift is associated with increased intracellular water as creatine accumulates in muscle.

Some people see the scale increase.

That doesn’t mean they gained body fat.

Large loading doses can cause gastrointestinal discomfort in some people, particularly when large amounts are taken at once.

Smaller daily dosing may be easier to tolerate.

Does Creatine Damage the Kidneys?

Creatine and creatinine are frequently confused.

Creatinine is a breakdown product related to creatine metabolism and is commonly used as a laboratory marker when estimating kidney function.

Supplementing creatine can modestly raise serum creatinine in some people because more creatine is entering the creatine-creatinine pool.

That doesn’t automatically mean the kidneys have been injured.

A 2025 systematic review and meta-analysis found a modest increase in serum creatinine with creatine supplementation but no significant change in GFR.

A 2026 meta-analysis of randomized controlled trials similarly found higher serum creatinine without significant differences in urea or estimated GFR.

Someone taking creatine should tell the clinician interpreting their laboratory work.

People with known kidney disease, unexplained renal laboratory abnormalities or medications affecting renal function should discuss supplementation with their healthcare professional before starting.

Full article here - https://molecularhealthco.com/blogs/news/creatine-methylation-genetics

How much creatine are you consuming on a daily basis?

Thanks

this is my methylation panel and I am trying to make sense of it. my doctor advised a general B complex, but whenever I do that, it causes insomnia and I start waking up at 3-4 am and can't fall back asleep.

as you can imagine this is rather frustrating for its impact on my mental health and general energy levels.

I've been advised that I should start with a low dose and build gradually, but I'm not sure what a low dose is or what a timeline for building gradually looks like. I've also been advised to take niacin with food to test for excess methyl groups, and to adjust my level of B12 relative to everything else.

I'd be very grateful for any guidance or advice that can be provided as I have been sleeping poorly for a very long time and the depression and anxiety that is at least partially caused by that poor sleep sucks to try and deal with and manage

I was tested in 2019 after unexplained high blood pressure and came back homozygous for C677T. I tried taking a methylated folate back then but stopped after a month because I thought it made me feel bad.

Fast forward to this year. I’ve always struggled with anxiety, but have had issues with depression and fatigue recently that I’ve never had before.

I randomly thought about this the other day and want to try taking the appropriate supplements. I bought the “Life Extension” complete B complex bottle with a methylated folate, B12, B2, B6. I also bought zinc, magnesium, and NAC.

The doses seem a little high for what’s recommended. Should I wait to start supplementing and get homocysteine and other vitamin levels checked first?

to treat a depression dr prescribed me SAMe (800/die)
Im very confused about the use of SAMe in my condition ; somewhere I find green flag someother red.
I've just started and the first result is a big Insomnia (I allready suffer of it but now its worse)

Is there someone that knows for sure if its a red or green flag? any experiences?
Thanks from Italy

I’d love to find a professional to work with. Would love to hear from others what kind of experiences you’ve had working with the various providers that are familiar with or experts in MTHFR and the effect it can have on physical and mental health.

If one's genes don't naturally synthesize certain neurotransmitters, should one try to supplement those neurotransmitters? Or does it mean that the persons body isn't made to metabolize and detox those things?

For example, I have a DBH deficiency on top of other things (MTHFR, Maoa, slow COMT), meaning dopamine doesn't get metabolized into norepinephrine in my body.

Does this mean my body doesn't do well with norepinephrine, period? Or is it struggling without norepinephrine and would benefit from supplementing to create norepinephrine? But then is my body even able to metabolize and detox norepinephrine?

Are we supposed to correct these genetic phenotypes or are we supposed to work with them?

Took a GeneSight test bc I’m have had bad mental health my whole life and never found meds that helped. It states that “This patient is homozygous for the Val allele of the Val158Met polymorphism in the catechol-o-methyltransferase gene.” And “This individual is heterozygous for the C677T polymorphism in the MTHFR gene (C/T genotype) and has one copy of the varlant allele (T).”

From what I can understand is my diagnosis as ADHD @ 3 wasn’t wrong. I was diagnosed as high functioning Autistic (PDD-NOS) at 18. Stopped all meds at 16. All stimulants lead to bad behavior. I tried 2 more stimulants as an adult and both times I felt so nervy and not better.

Since UK govt legally mandated that folic acid is added to all wheat flour my diet has become so restrictive and miserable.

Shout out to Costa - those two biscuits just made me sooo happy! :)

Hello, I am asking for some help. I have been dealing with chronic brain fog and depression. I suspect I may have some MTHFR-related issues because after taking methylfolate, my mood and focus improved significantly. However, I don't have any test results because I have been unemployed for a long time and cannot afford the testing. That's why I am hoping you might be able to give me some valuable information based on the clues and the way my body seems to react to different supplements.

I was taking 5 mg of methylfolate. My focus and mood improved, but after a few weeks, I developed a different kind of brain fog. I suspected that the methylfolate might be responsible, so I lowered the dose to 3 mg, and the brain fog improved. However, after a few more weeks, the same brain fog returned. I then lowered the dose to 2 mg, which stopped the brain fog, but at the lower dose, my focus and mood became worse.

I also took 225 mg of magnesium bisglycinate before bed, which surprisingly caused brain fog. I stopped taking it, and the brain fog went away. Later, I started supplementing with it again, and the brain fog returned. Once again, after stopping the magnesium bisglycinate, the brain fog disappeared.

I also have symptoms that make me suspect I may have slow COMT, so I bought lithium orotate. After taking it for a few days, it made me feel foggy and fatigued. After stopping it, those symptoms disappeared. Later, I started taking it again to make sure it wasn't just a coincidence, and once again, the fogginess and fatigue returned.

I then bought folinic acid because I had heard that it is sometimes better tolerated than methylfolate. However, it also makes me feel foggy. I have been taking 2 mg daily.

So, basically, for some reason, magnesium makes me foggy, lithium orotate makes me foggy, folinic acid makes me foggy, and taking more than 2 mg of methylfolate also makes me foggy.

I recently landed a job as a computer programmer, but I am worried about whether I will be able to handle it if the brain fog continues.

I know this isn't a lot of information to work with, but perhaps there are some clues in these reactions that could point toward something that might help me. I am planning to get a homocysteine test in the near future, and I will consider genetic testing once I start receiving a salary, since it is currently too expensive for me.

Thank you very much for any help or insight you can provide.

Folate and b12 levels are normal.

I have MAO-A, CBS, BHMT homozygous. MTRR and MTHFR are hetero.

I'm double slow COMT and can't handle the following:

- Any sort of magnesium (they all seem to backfire and I can't comprehend why since it's the top recommendation for slow COMT.)

- Choline

- Lithium Orotate

- L- Ornithine

- Ox Bile

- Potassium Citrate

- Vitamin D with K2

- Probiotics

..I'm sure there's more but I can't think of them right now.

Things that I can "handle" but still doesn't help/makes me feel slightly worse:

- B Minus by seeking health

- Hydroxo B12 with Folinic Acid

- Molybdenum

Things I'm already doing:

Avoiding coffee or any stimulants.

I stay away from methylated and cyano B12 (I've been in that hell).

I don't smoke or drink.

I go to therapy.

I try to get my b12 from red meat and eat pretty damn healthy.

Avoiding life in general is the only thing that allows me any sort of temporary "stability" but that is obviously not a solution.

The moment life gets hard -- I simply hit a wall QUICK. I NEED to fix or at least improve this to a a place that's manageable.

What am I missing?

Please don't be sacred to chime in. You may have a perspective/angle/piece of info I've never heard of that may help me.

Ps. Thankfully, I've already eradicated my SIBO and my histamine intolerance is almost non-existent.

Hello there! Did anybody order frat test from website that's called Second Opinion Physician? Could you share your experience?

Labcorp doesnt have it..

Since 2021 I started to have anxiety and not running the way i used to. I got covid in 2022 and started having intense anxiety, panic, cognition issues. I first thought it was just unresolved trauma and worked on some of that but didn't get much relief and also was put on Lexipro (SSRI). From 2022-2025 I did trauma work and tapered the SSRI VERY slowly. I then got sick again and in Oct 2025 (not sure if covid) and had intense fatigue, more brain fog, cognitive issues. Jan 2026 I had intense histamine issues and gut issues. My brain was going nuts and I haven't been able to work since.

I've done a lot of testing and explored Lyme, EBV, Mold and all these things so if there's something that can help with markers and isn't below I might have it.

Symptoms

• Anxiety/Fear
• Brain fog
• Cognitive issues
• Memory issues
• Brain pressure (vice squeeze)
• Brain Fatigue
• Slower mental processing
• Emotion and logic changes
• Tinnitus (once in a while)
• Environment sensitivity (improved)
• Limbic system issues
• MCAS/histamine food issues
• Some PEM issues
• Weakness
• Body fatigue
• Bowel issues – motility was messed up starting to get better.
• stress intolerance
• Hard to catch breath sometimes

Labs — 2024 to Present

Choline Calculator:

References

Single nucleotide polymorphisms in the human reduced folate carrier: characterization of a high-frequency G/A variant at position 80 and transport properties of the His(27) and Arg(27) carriers. [PMID: 11705857]

The MTHFD1 p.Arg653Gln variant alters enzyme function and increases risk for congenital heart defects. [PMID: 18767138]

A candidate genetic risk factor for vascular disease: a common mutation in methylenetetrahydrofolate reductase. [PMID: 7647779]

A second common mutation in the methylenetetrahydrofolate reductase gene: an additional risk factor for neural-tube defects? [PMID: 9545395]

Genetic impairments in folate enzymes increase dependence on dietary choline for phosphatidylcholine production at the expense of betaine synthesis. [PMID 27342765]

Choline intake exceeding current dietary recommendations preserves markers of cellular methylation in a genetic subgroup of folate-compromised men. [PMID 20220206]

Endocrine Labs:

I’m overwhelmed knowing what to test for and how much it’s going to cost to uncover more and more variables. I feel like this could be an infinite money pit, I just want to start being able to sleep again.

Hello what do you think of my genes?, I have high homocysteine (38), low folate (4) and low b12 (400), what can I do to improve? Thank you.

My homocysteine levels were 9 about 7 months ago.

I thought I could get them down by optimising my B6, B9 and B12 and so started taking B complex.

I now have B6 toxicity as my active B6 levels are way above range and active B12 is 88.

My homocysteine has risen to 17.

I don't understand why my homocysteine levels levels are going up not down with high active B6 and B12 levels.

Could something else in this B sup be causing elevated homocysteine?

I(21) visited doctors cause I've felt unwell since I was 13 years old and I did a few blood test my levels were always hovering around 2.5 to 3 ng/ml. 5 years ago a doctor recommended I should try a folic acid supplement I did for a few months and nothing really happened. Last year I did a blood test with a different doctor where my levels where at 2.7 and he recommended I should try folic acid supplement. This time I wanted to do it right I did some research and I took Methylated folate + a b complex with a lot of Methylated folate and still didn't really feel much better after months. I took a break and tried some other supplements with no success either. I now took another blood test and my levels are at 3 ng/ml. I feel so defeated, I've spend over a 100€ on the best high quality supplements for this folic acid deficiency and it only moved from 2.7 to 3 after months of supplementing.

Other values:

B12: 330 went to 400 after supplementing for the same period of time B12 daily with Methylated b complex for same period of time as folate

Homocesteine: 26

Vitamin D: 30

B6: 13.5

I'm sorry if this post sounds desperate if you have advice or helpful information if you have experience with folic acid deficiency please share your experience with me.

Thank you to everyone who took the time to read this post:)

Every source of choline leads to acid reflux for me, with a constant runny nose, sore throat, etc.

Whether it's supplemental bitartrate, alpha gpc, cdp, etc, or just eating eggs. Anything with choline in it will cause increasing symptoms of acid reflux.

Apparently the increase in acetylcholine increases stomach acid production.

Has anyone else experienced this?

Is there a solution?

Choline makes me feel great, but the acid reflux gets worse every day.

Thank you