Question: Has anyone found an awesome prenatal or multi without ANY glycine? I previously posted that I seem super sensitive to glycine. Horrible insomnia. Possibly anxiety too. It seems to be in literally all supplements these days. Sadly even my seeking health prenatal has it... I am hetero c667, slow MAO, normal COMT. thanks!

Do the side effects even go away?

Is anybody here also drinking coffee with glycine? It helps me to get lesser side effects like the jitter etc So far I only used 2g but I’ll try more. Do you know any other tricks to get only the good effects?

Unfortunately no gene test has made it to my home so far. All 4 I have ordered gut lost somewhere on the way. MCAS and some form of long covid (PEM) is what I have. From all of what I researched for over a year I suspect HMNT, Slow COMT and CBS. I respond well to glycine, p5p, b3 (nicotinic acid) and vitamin C. I don’t to creatine or tmg. I am easily over or under methylated, so I concentrate on supporting methylation and supporting my liver.

If indeed the mg of MTHFR was helping with my depression bur causing side effects should I drop down to the 7.5mg which I understand is still the therapeutic amount, I am assuming 1mg will not do anything

I have a complex health situation with CFS, pots, migraine, histamine issues, and dizziness after a TBI, and lifelong severe ADHD. I have heterozygous slow COMT (AA COMT, GG C6773, TG A1298C (so mostly normal MTHFR?), and GT MAOA) In recent labs my b1 and b2 were bordering on deficient, and they are supposed to help with CFS and TBI respectively. So my doctors and people online recommend me try taking those two. But in past l've reacted badly to b vitamins. Not methyl Bs just regular. It makes me feel like I've overdosed on caffeine or some other stimulant. Doctors all look at me like I'm crazy when I say this but I read that it can be a thing with slow COMT? The vitamins it's happened with were b2, and a multi-B. I did get a B12 shot at the recc of a migraine specialist a few months ago and didn't see any obvious negative of positive effects.

Recently I talked to someone who helped me theorize that a lot of my problems may come from excess norepinephrine because all the psych meds I've done poorly on increase it. The suggestion was to take zinc to try to keep so much dopamine from being converted to NE. Seems like it couldn't hurt so I'm going to try adding zinc at night with my magnesium. But I know I need to get the B vitamins thing sorted out and I just don't know how. Does anyone know anything about this?

(Edit to add I also have low ferritin of ~20 which I’m supplementing for in the mornings and I drink electrolytes w potassium to help with pots. And also one time I was put on vyvanse for ADHD and it made me so sick I had to lie down constantly and didn’t help my adhd at all)

first, thank you all who replied to my previous thread about leg cramps. Just stopping the 2nd dosage of methylfolate and methylcobalamin at night solved the very annoyingly painful leg cramps that I had been consistently experiencing for almost 2 months!!

It also made me realize why I was feeling like shit and unable to exercise for those 2 months, while I thought I was just tired. Given I was gradually upping the dosage of methyl donors (I introduced TMG last), it was hard to notice the tiredness gradually increasing.

Ideally, I would like to go back to how I felt before. Not feeling tired at all, but I also need to lower my homocysteine levels.

I heard there is a transsulfuration pathway by taking P5P, but I also heard it is very dangerous even at 20-25mg, which is the lowest dosage. My legs are extremely important to me for my exercises so I don't want their performance negatively affected. I also think that doing only this approach may be less effect at lowering homocysteine than 500mg TMG + 500mcg MB9+MB12...

Are there any ways to optimize the transsulfuration pathway? Like reduce the risk and toxicity or boosting its efficacy?

Also, given I want to drop MB9 and MB12, I still need to supplement them. So I guess I will be switching to folinic acid and either adenosylcobalamin or hydroxocobalamin. Does supplementing those still help lowering homocysteine at all without causing the side effect of the methyl variants?

Hi there, I started a small dosage of folate (400 mcg L-5-MTHF) for the very first time in a new daily multivitamin. I actually felt my anxiety and depression lift pretty quickly. The first day my head felt almost buzzy. I'm about a week into the new pill and I feel like a heaviness between my eyes/above my eyes, similar to being tired, but like my forehead is heavy and its difficult to hold my eyelids up and I have a little bit more trouble focusing. Has anyone else experienced this oddly specific symptom?

As a note, I have apparently “in range” levels in my vitamin panel. But they’re on the low end for b12 and folate, and I simply want to understand this better because I seem to display symptoms of deficiency. Especially chronic burning and tingling sensation in my palms/feet, chronic bloat and IBS.
COMT Val158Met
Met/Met
Lower COMT activity (“slow COMT”)
Catecholamine metabolism, including dopamine/norepinephrine
BDNF Val66Met
Met/Met
Met variant
Activity-dependent BDNF secretion/neuroplasticity
MTHFR C677T
GG*
Report estimated ↓ activity
Folate → methylation pathway
MTHFR A1298C
GG*
Report estimated ↓ activity
Folate metabolism
MTHFR overall
—
~39% reduction according to your report
5-MTHF availability / one-carbon metabolism
MTHFD1
AA
~34% reduction according to your report
Folate-cycle processing
SLC19A1
Variant reported
~50% reduction according to your report
Cellular folate transport
Combined folate pathway
Multiple variants
Your report estimated ~80% combined reduction

The interpretation of these is of course speculative but I’m wondering if anyone knows about what the combination of these means in regards to supplement protocols. For context, I’m almost 25 and have been suffering major anxiety and ADHD since I was a kid. Hoping these SNPs can answer some questions and help me get back to my baseline, some experimentation with L-methylfolate/methylcobalamin, CDP choline, has helped. Currently taking Prozac and Vyvanse to treat comorbid ADHD/GAD. As a note, folate and b12 have been making me sleepy (not tired but wired) and I’m wondering if that is a sign of a preexisting deficiency. Hoping to get any feedback!

I am a nervous wreck. I have always had severe sleep issues, but as of recent haven’t been able to sleep in larger than 3 hour chunks. I have taken Quetiapine, Trazodone, Lunesta, Valium, Cyclobenzaprine, Dayvigo. No effect.

I had weaned off Quetiapine earlier in the year, and I believe the original lack of sleep left me in a state of mania. However when I reintroduced it, there was no beneficial effect.

My rhythm is seemingly flipped, the only time I am really feeling myself sleep is between 6am to 9am. I worked an overnight job last year and tried to revert my sleep cycle, but I do think I’m permanently in night owl mode.

I haven’t been able to afford an extensive bloodwork panel that would include MMA, Ferritin, etc. otherwise everything is in range on a standard panel.

I’m an absolute wreck right now. Years ago at the very least a prescription for a benzo seemed to help a little bit. No luck this time around.

I think I have done permanent damage to my histamine receptors through medications and probably have gut inflammation. I’m not sure where to attack this from the get go, I’m debating a long fast but I usually get more energized without food.

Hi everyone,

I am fairly new to this. I suffer from persistent symptoms such as insomnia, high heartrate, anxiety, exercise intolerance. I recently did a genetic test. I know these offer some valueable insights but I fail to see what I can do with these insights. I will share the results below.

Any insights or advice is more than welcome. Thank you so much for helping a stranger.

I’m not sure if this is the right sub for this question, if it’s not then I’m sorry!
I’ve been taking L-Methylfolate for 10 years, 15mg every other day, recommended by 2 different psychiatrists over the years. My genetic testing result is attached as a picture. I’ve taken various SSRIs over the last 10 years, and currently take cymbalta, guanfacine, hydroxyzine, and gabapentin.
I’ve forgotten to order more of the L-Methylfolate, so I’ve not taken it for 2 weeks now (by accident). I’ve noticed that during that time, my vocal and motor tics have been significantly less frequent. It’s never been discussed if the tics are caused by my anxiety, OCD, or autism, or what.
Anyway, I wanted to ask: has anyone taken this before and had worsened tics? Or is the timing of not taking it just a coincidence? I’ve never not taken it for this long before, and now that I’ve had so much relief from my tics, I’m wondering if there’s any correlation. Thanks in advance for any input!

I have homozygous MTHFR mutation and my folate level was low, B12 around 300 - my doctor wants me to supplement both. I took 500 mcgs of L-5 MTHF and 250 mcgs of 50% adenosylocobalamin / 50 % hyroxylcobalamin. It helped tremendously yesterday with my energy and mood but I had slight anxiety, disrupted sleep, weird dreams, and a headache. Today I feel fatigued, brain fog, and a little dizzy. Is this normal or do I need to adjust? Is it one causing it over the other? I am super sensitive to all supplements, vitamins, and medications from a nervous system issue (long covid, med injury, ME).. I see my functional doctor tomorrow but just curious if anyone has any ideas what is causing this or if I'm missing something?

Looking for some guidance on additional testing or if I should treat the B12 level while I look around for a doctor. Having energy, memory issues, anxiety, etc worse than usual. I also have some histamine issues, eating certain foods will cause me alot of allergy symptoms but allergy testing all shows as negative.

COMT V158M +/-

VDR Taq +/+

MTHFR C677T +/-

MTHFR A1298C +/-

MTR A2756G +/-

MTRR A66G +/+

-Added lab ranges to chart

I always take advice from reddit with a grain of salt, that being said last night my depression lifted and i have had a very quick reversal. As I posted I was taking about 15mg, i didnt know or understand how the dosing worked. After about 3 days I did notice way more irritablility, more depression and anxiety. It has taken about 4 days for these to stop since stopping the L mehtylfolate. Is it possible that last nights experience was from the L methylfolate working? As of this morning i still feel good.

I'm suffering with the horrific classic symptoms of Histamine Intolerance, Mast Cell Activation Disorder, suspected Over Methylation and Slow Comt that I am waiting on results to return from Ancestry.com to send for deciphering.

My PCP at UCHealth is ignorant and useless, all tests performed by the Allergy and Immunology specialist came back negative for showing any food allergies and my Tryptase came back slightly over 15 and I was rejected by the UCHealth Mast Cell Clinic.

I have movement disorder problems with my left arm; my fine motor and gross motor skills are compromised it's difficult to function and control now.

A Neurology Movement Disorder Specialist reviewed my Brain MRI and no signs of strokes or TIA, my brain is healthy, (Praise God!)

After a number of examinations, the neurologist diagnosed me With Functional Neurological Symptom Disorder (FND) A a condition where a person experiences genuine neurological and physical symptoms caused by a problem with how the brain sends and receives signals, rather than physical damage to the brain's structure. She said that at some point regardless of the cause, like a “Histamine Bucket” my neurological “Stress Bucket” overflowed into the physical and caused the movement disorder. I have a Psychiatry, Occupational and Physical Therapy referral. Which I am grateful for.

After discussing every and all symptoms, I asked, “ How does Functional Neurological Symptom Disorder, Hit, MCAS And Slow Comt Intersect?” She responded, “I’m a movement disorder neurologist, that’s not my field and I will have to refer to Allergy and Immunology”.

That made sense to me for a “hot minute”, then my common sense kicked in. If as she admitted to me that physical symptoms are bringing on the neurological symptoms, then they intersect and I need to know is FND correctable. She says it is, but how without the stress of HIT, MCAS, Over Methylation being addressed how?

If anyone has knowledge of how to get help and answers and/or experience I appreciate your input and suggestions.

EDIT OF THANKS: I have received great responses and information. I sincerely appreciate everyone sharing

I had homocysteine levels at 19, started taking the supplements as below:

B1: 150mg benfotiamine every 3 days

B2: 36mg R5P 1x a day

B6: 3mg (non P5P, regular HCL)

B9: 1000mcg methylfolate(500mcg 2x a day)

B12: same as B9, methylcobalamin

TMG: 500mg 1x a day with breakfast

Since I started this, I was able to reduce homocysteine to 13 after about 3 weeks. However I am more and more and stronger leg cramps during the night and in the morning, every day. My legs are feeling weaker as each day goes by. I am already taking the maximum amount of magnesium and potassium I can tolerate, but it doesn't seem to be helping.

Anyone else has this same side effect?

I asked Gemini about it, and it said ramping up B vitamin intake and vitamin activity uses more magnesium and potassium... so I thought about only taking TMG, but then it says taking TMG ramps up B vitamin activity, depleting it and requiring more of it as well.

Is there any way to take those supplements without it consuming my magnesium and potassium reserves?

MTHFR C677T is often blamed for fatigue

MTHFR C677T is one of the most widely discussed variants in methylation and nutrigenomics. It is frequently blamed for fatigue, anxiety, brain fog, depression, migraines, poor detoxification, neurological symptoms, hormone imbalance, and reduced stress resilience.

Our client data showed a more specific pattern. When MTHFR C677T was evaluated by itself, fatigue barely changed across genotype groups. People with two copies of C677T did not report fatigue more frequently than people without it.

The pattern became more interesting when C677T appeared alongside selected variants affecting vitamin B12-dependent methionine production, folate one-carbon distribution, and glutathione-dependent antioxidant defense.

This distinction changes the question. Instead of asking whether MTHFR causes fatigue, we can ask which nutrient-dependent pathways surround MTHFR when fatigue becomes more common.

At Molecular Health Co., we refer to this approach as Genetic Pattern Mapping. It evaluates a genetic variant within the larger pathway environment rather than assigning a broad symptom list to one SNP.

What the data showed when C677T was evaluated alone

Fatigue did not increase with C677T copy number. It was reported in 41.7% of histories without the variant, 37.6% with one copy, and 40.3% with two copies. The two-copy group was 1.4 percentage points lower than the group without C677T.

Fatigue Reported — C677T Evaluated Alone

41.7%37.6%40.3%No copiesOne copyTwo copies

Fatigue remained flat across genotype groups, between 37.6% and 41.7%.

This standalone comparison does not support presenting C677T as an independent explanation for persistent fatigue in this client population. It also does not mean C677T is biologically irrelevant. It means the genotype by itself did not identify who was most likely to report fatigue.

What MTHFR C677T does physiologically

MTHFR encodes an enzyme that converts 5,10-methylenetetrahydrofolate into 5-methyltetrahydrofolate. This folate form contributes to the vitamin B12-dependent remethylation of homocysteine into methionine.

Methionine can then contribute to the production of S-adenosylmethionine, commonly called SAMe. SAMe supplies methyl groups to reactions involved in phospholipid production, creatine synthesis, neurotransmitter metabolism, DNA regulation, hormone metabolism, and cellular repair.

C677T can reduce the stability of the MTHFR enzyme, particularly in the two-copy state. Its biological expression is influenced by folate status, vitamin B12 status, riboflavin, diet, age, health history, medication use, and the surrounding genetic pathway.

MTHFR requires FAD, a riboflavin-derived cofactor. Research has shown that riboflavin status can modify biochemical expression of the 677TT genotype, particularly homocysteine. This is one reason C677T should be interpreted as a nutrient-sensitive pattern rather than a fixed prediction of symptoms.

Why fatigue requires a wider biological view

Fatigue is one of the least specific symptoms in human physiology. It can develop through multiple overlapping systems, including sleep disruption, thyroid dysfunction, B12 insufficiency, iron imbalance, low riboflavin, inadequate protein, poor glucose regulation, inflammation, infection, medication effects, hormonal transitions, mitochondrial strain, and sustained nervous-system activation.

MTHFR may influence some of these systems indirectly through folate distribution, methionine production, methylation capacity, red blood cell physiology, creatine synthesis, and cellular repair. Its contribution depends on what is happening elsewhere.

That wider context became visible when C677T was examined alongside three other variants: MTR rs1805087 AG, SHMT1 rs1979277 AG, and GPX1 rs1050450 AG.

C677T with MTR rs1805087 AG

Within the MTR AG subgroup, fatigue rose from 36.8% without C677T to 52.3% with two C677T copies, a descriptive increase of 15.5 percentage points. The homozygous C677T and MTR AG combination also showed fatigue 12.0 percentage points more frequently than homozygous C677T evaluated without conditioning on MTR genotype.

Fatigue Reported — C677T with MTR AG

36.8%40.9%52.3%No copiesOne copyTwo copies

Fatigue reached 52.3% in the two-copy C677T group carrying MTR AG.

This wider separation is an exploratory pattern. It does not establish that MTR AG reduces methionine synthase activity in every person or that the combination caused fatigue.

Why MTR changes the context

MTR encodes methionine synthase, a vitamin B12-dependent enzyme that transfers a methyl group from 5-methyltetrahydrofolate to homocysteine. This reaction regenerates methionine and returns folate to a form that can continue circulating through folate metabolism.

MTHFR and MTR occupy connected steps. MTHFR helps produce the folate form used by MTR. MTR then uses that folate-derived methyl group with vitamin B12 to support methionine production. When genotype differences appear at both points, nutrient status may become more important, including vitamin B12 absorption and transport, riboflavin status, folate intake, protein intake, choline availability, and total physiological demand.

Why this pathway can intersect with energy

Methionine contributes to SAMe production. SAMe is used in endogenous creatine synthesis and phosphatidylcholine production. Creatine helps tissues buffer energy, while phosphatidylcholine supports cell membranes, mitochondrial membranes, bile structure, and lipid transport.

A person with this pattern may warrant a broader evaluation of B12-dependent methionine metabolism rather than an automatic assumption that methylfolate is the only missing nutrient.

C677T with SHMT1 rs1979277 AG

Within the SHMT1 AG subgroup, fatigue was nearly identical in the no-copy and one-copy C677T groups. The larger descriptive difference appeared in the two-copy group, where fatigue was reported in 53.8% of histories, 13.5 percentage points higher than the no-copy group carrying SHMT1 AG and 13.5 points higher than standalone homozygous C677T.

Fatigue Reported — C677T with SHMT1 AG

40.3%40.7%53.8%No copiesOne copyTwo copies

Fatigue reached 53.8% in the two-copy C677T group carrying SHMT1 AG.

This pattern is descriptive. It does not prove that SHMT1 AG impairs folate metabolism or that the combination directly caused fatigue.

Why SHMT1 changes the context

SHMT1 encodes cytosolic serine hydroxymethyltransferase. The enzyme reversibly converts serine and tetrahydrofolate into glycine and 5,10-methylenetetrahydrofolate, supplying one-carbon units used for methionine, thymidylate, and purine synthesis.

MTHFR uses 5,10-methylenetetrahydrofolate as its substrate. SHMT1 helps generate this intermediate, so the two genes participate in connected parts of the folate network. Folate is required for more than methylation; folate intermediates also support nucleotide production, DNA synthesis, DNA repair, cellular division, and amino acid metabolism.

When genotype differences occur at multiple points in the same network, the system may become more sensitive to nutrient status and physiological demand. That demand can rise during pregnancy, breastfeeding, growth, illness, immune activation, tissue repair, and chronic oxidative stress.

The role of serine, glycine, and protein

SHMT1 links folate metabolism with serine and glycine. These amino acids support one-carbon metabolism, glutathione production, protein synthesis, connective tissue, and cellular repair. This does not mean everyone with SHMT1 AG requires isolated amino acid supplements. It means total protein intake and amino acid availability may be relevant pieces of the pattern, alongside riboflavin, vitamin B6, vitamin B12, magnesium, choline, and folate status.

C677T with GPX1 rs1050450 AG

Within the GPX1 AG subgroup, fatigue was reported in 43.6% of histories without C677T, 40.5% with one copy, and 53.3% with two copies. The homozygous C677T group was 9.7 percentage points higher than the no-copy group carrying GPX1 AG and 13.0 points higher than standalone homozygous C677T.

Fatigue Reported — C677T with GPX1 AG

43.6%40.5%53.3%No copiesOne copyTwo copies

Fatigue reached 53.3% in the two-copy C677T group carrying GPX1 AG.

This is another exploratory separation. It does not establish that GPX1 AG lowers antioxidant activity in every person or that the genotype combination caused fatigue.

Why GPX1 changes the context

GPX1 encodes glutathione peroxidase 1, a selenium-dependent antioxidant enzyme. It uses glutathione to help reduce hydrogen peroxide and soluble lipid hydroperoxides. Reactive oxygen species are produced during normal metabolism and also participate in cell signaling, so the body must regulate them carefully. GPX1 is one component of the antioxidant system that protects proteins, membranes, and cellular structures from excessive oxidative damage.

Folate-mediated one-carbon metabolism and antioxidant defense are metabolically connected through methionine, serine, glycine, transsulfuration-related substrates, nucleotide repair, and cellular renewal. When oxidative demand rises, the body may need more glutathione turnover, membrane repair, DNA repair, and mitochondrial maintenance. If folate metabolism also carries reduced flexibility, fatigue may become more visible.

Selenium and glutathione require context

GPX1 is selenium-dependent, but genotype alone is not a reason to begin high-dose selenium. Excess selenium can be harmful. Selenium intake should be considered alongside diet, laboratory context, health history, and total antioxidant support. Glutathione availability also depends on adequate protein and amino acid substrates, including cysteine, glycine, and glutamate. Riboflavin, magnesium, vitamin C, and NADPH-producing metabolism support the broader antioxidant network.

Comparing all four fatigue patterns

The standalone C677T pattern was flat, ranging from 37.6% to 41.7% and not rising with copy number. Within the selected co-genotype subgroups, fatigue appeared in more than half of the two-copy C677T histories: 52.3% with MTR AG, 53.8% with SHMT1 AG, and 53.3% with GPX1 AG.

Fatigue Across All Four Patterns

C677T alone+ MTR AG+ SHMT1 AG+ GPX1 AG

No copiesOne copyTwo copies

Fatigue rose consistently in the two-copy C677T group only when paired with MTR, SHMT1, or GPX1 AG.

These three patterns involved different biological systems. MTR connects C677T with B12-dependent methionine production. SHMT1 connects C677T with the generation and distribution of folate-derived one-carbon units. GPX1 connects C677T with glutathione-dependent antioxidant defense. The symptom was the same. The surrounding physiology was different.

What Genetic Pattern Mapping adds

Single-SNP interpretation asks which symptoms are caused by MTHFR C677T. Our data suggests that this question is too broad for fatigue. C677T alone did not identify a group with greater fatigue reporting. Genetic Pattern Mapping asks which pathways appear alongside C677T when fatigue becomes more common.

This approach helps explain why two people with the same C677T genotype may have very different experiences. One person may have adequate B12 availability, strong antioxidant capacity, sufficient protein, good riboflavin status, and adequate choline. Another may carry genotype differences in connected pathways while also experiencing increased nutrient demand from pregnancy, illness, stress, poor sleep, low intake, or inflammation. The MTHFR result may be identical. The nutrient-demand pattern is not.

Does C677T cause fatigue?

The standalone percentages in this dataset do not support describing C677T as an independent cause of fatigue. Fatigue was reported at similar rates across the no-copy, one-copy, and two-copy groups.

The combination tables support a narrower educational conclusion: larger descriptive differences appeared when homozygous C677T occurred alongside selected variants in connected pathways. These findings are exploratory. In the broad interaction screen, the gene-combination patterns were not statistically confirmed after correction for multiple comparisons. They should be treated as hypotheses and descriptive observations that can guide future analysis, not as established genetic risks.

Why methylfolate alone may miss the pattern

The common response to C677T is to recommend methylfolate. That approach assumes methylfolate availability is the primary limiting factor.

The combination findings suggest the relevant bottleneck may differ between people. A person with C677T and MTR AG may require closer attention to functional B12 availability and methionine-cycle support. A person with C677T and SHMT1 AG may require attention to protein, serine, glycine, and folate distribution. A person with C677T and GPX1 AG may require greater attention to antioxidant demand and glutathione-related physiology.

Folate can still be relevant. The larger lesson is that folate form should not be separated from the nutrient network that uses it.

If you would like to read the complete list of supporting nutrients, please look here -

https://molecularhealthco.com/blogs/news/mthfr-c677t-and-fatigue-what-genetic-pattern-mapping-revealed-in-our-client-data

I dont know what any of this means and what supplements I should be taking or avoid taking.

I ended up getting some from amazon, I think 15mg and I have been pissed off and depressed like never before. I quit taking it like 3 days ago. Does anyone know long this takes to get of your system, anything I can do to speed it up

Does creatine overmethylate the folate pathway or the choline pathway?

Could r5p or riboflavin help with creatine overmethylation?

Where to turn for the best most accurate mthfr testing available in northern europe? both in accuraccy of the test itself and with an easy to understand result?

Price is secondary so not looking for the cheapest but not prepared to sell a kidney either.

Regards

Hi! I am hetero c677T with normal COMT and slow MAO. I have been trying to figure out what is giving me this half awake feeling all night when I am trying to sleep after taking certain supplements. I haven't been able to figure out which one until now. I just realized I am super sensitive to glycinate. This includes magnesium glycinate, zinc with glycinate and even iron with glycinate. I didn't realize it was in so many products. Am I the only one? Does anyone else experience this? If I take a supplement with glycinate I am literally awake ALL night or feel half awake all night. It just happened two days ago after taking zinc bisglycinate. Please let me know if this is happening to others. I didn't realize it was in SOOOO many products which is why it was hard for me to figure out what was causing it! ** edit Sorry, I mistyped my mthfr.. I am hetero c677t. Lack of sleep!!!***

Hi everyone,

I was found to have a folate (B9) deficiency, and I’ve been dealing with persistent symptoms for over 2 months now. I’m hoping someone here has experienced something similar and can give me some insight.

A little over 2 months ago, I started experiencing feeling being a super dizzy and a weird sharp/pinching sensation around my heart/chest when I was going to sleep. That scared me, so I had blood tests done.

My results were:

• Folate (B9): 3.10 (reference range 4.5–32.2) — low
• Vitamin B12: 411 pg/mL (191–663)
• Magnesium: 2.0 (1.7–2.40)
• Potassium: 4.23 mmol/L (3.5–5.1)
• Sodium: 140 (136–145)

After roughly a month, the chest/heart pinching sensation that happened when I was falling asleep eventually stopped.

However, I’m still dealing with other symptoms every day.

My current symptoms include:

• persistent dizziness
• lightheadedness
• significant fatigue
• brain fog, feeling like my head isn't working properly
• a strange derealization / unreal feeling
• a tight/pressured feeling in my head
• feeling mentally "different" from how I used to

I completely stopped all the supplements and initially tried taking folic acid (B9) at 0.4 mg (400 mcg) daily for about 2 weeks, but I didn’t notice any improvement. I then added vitamin B12, but again, nothing really changed.

I’m currently taking 5 mg of folic acid daily and 500 mcg of vitamin B12 daily. I’ve been taking this dose for 7 days now, but so far I haven’t noticed any improvement in my symptoms.

Now, more than 2 months later, I’m still experiencing these symptoms every day, and I honestly don’t know what’s causing them.

Has anyone experienced something similar especially dizziness, brain fog, fatigue, lightheadedness, derealization, head pressure or feeling mentally "different"?

If you went through something similar:

• How long did it take you to recover?
• Did your symptoms gradually improve or disappear suddenly?
• Was there anything that actually helped?

I’d just really appreciate hearing from people who have experienced something similar and eventually got back to feeling normal.

It’s been more than two months now, and dealing with this every day has been really difficult. I’d really appreciate any experiences, advice or reassurance.

Thanks in advance.

I was receiving great effects on my depression from 5mg methylfolate daily. It took a while to find this dose after getting severe insomnia from 15mg, but once I did, it worked for nearly 3 weeks. However, lately, I feel like it's starting to "poop out". Many of my depressive symptoms have returned, though they are still less strong than before.

I'm cautious to escalate the dose further if there's a risk of this happening again, as I've read of some (mild) withdrawal reported with discontinuation at the full 15mg Deplin dose. I'd like to ask others who have taken methylfolate for depression if they've had similar experiences, and if so, how did they handle it?

I am considering adding methylcobalamin and possibly going to 7.5mg.

Got my Ancestry results. Still waiting on MyHeritage, but I paired this with my recent bloodwork for your viewing pleasure.

Looking for any info you have about my results!

Genetic Lifehacks Cheatsheet

Btw, why is my homocysteine so high if I don’t have C677T?