This happened to me outta no where like 2 months ago. My hairs of the right side of hair part is way thinner than left side. When i touch my right side of head i can feel the difference of density. I did my bloodwork and it showed that i have incredibly low vitamin D (it’s 4,3), B12 and folate. Now i’m taking those vitamins do you guys think that this shit happened due to vitamin deficiency? My family has no history with balding and this is the only area thinning.

Not sure what that means, or how to fix it. I am waiting on a call my from doctor office. Any insight is much appreciated. Btw, I am healthy, 39m. The only supplements I take are creatine (5g/daily) and vitamin d 1.25mg eekly.

My protocol is simple and effective: 1. 5 grams of creatine mono 2. 1 gram of Cordyceps militaris 3. Sublingual tablet(methyl folate, methyl b12 and P5-P) 4. 500mg NAC 5. Zinc Balance 6. Omega 3-higher DHA 7. 500mg Agmatine Sulfate 8. 1gram Reishi
I take creatine, cordyceps and Reishi in bulk powders so really have plenty of stash. Thorne creatine and Real Mushrooms 150 grams packages. Taking creatine and cordy first thing in morning.
In terms of methylation there is also big part of decreasing symptoms in balancing HPA axis(cordyceps and reishi does that, especially reishi so this is why this two are eqzally important as methylation supps). There is no doubt that in cca 90% of poisers orgasm deplete methyl groups. Try taking before pmo sublingual tablet with agmatine and after 1gram reishi. Sublingual tablet will bum up methyls, agmatine balance nmda and glutamate and afterwards reishi balance hpa axis and hormones(especially cortisol).
Also mushroom extracts fix gut microbiome and destroy biofilms of candida and ebv. Part of POIS is also viral so beta glucans are heavy hitters.
This also fixed many other issues I had as a kid(brain fog, ehlers syndrome, gilbert syndrome, neuropathy, mild adhd, ocd etc). My POIS symptoms were neurological and mood swings.
Only thing in daily supplementation with methyl B would increase iron stores(ferritin) but NAC chelate metals and iron so NAC is also a valuable supplement in both departments. B vitamins are water soluble except B6 that has very long half life like 3weeks. Small dose P5-P is reccomended(like 1.5-2mg) because accumulation of it create neuropathy symptoms. I plan to continue taking this stack daily. If it works, don't fix it. I have slightly elevated folate and b12 but dont care. Homocysteine is perfect 8. Copper is important on histamine clearence(DAO enzyme) so Zinc Balance is also important(was having low serum copper).

This is the second time ive been diagnosed with clinical folate deficiency. They keep just giving me 5mg folic acid for 4 months, then it ends up dropping again, and quite fast. I found out I have MTHFR mutation homozygous A1298C. I have anxiety and mental health issues which are currently being investigated. My question is I don't know if this 5mg folic is going to help my deficiency and I cannot afford to get my homocysteine tested and the doctors won't do it. I dont want my level to drop again. What form do I take? I've heard methylfolate is actually worse for anxiety and folic acid is better despite folate appearing better for mthfr. What dosage and form to maintain once the levels up and stop becoming deficient? Do I need it with b12? My active b12 is in normal range and my serum is 437. My ferritin is 50. Vitamin D is low but GP says its not, 53nmol is not so good. Do I use a multivitamin or are individual vitamins tailored to my needs enough? Thanks....

Originally contacted my Dr regarding extreme fatigue and increase in widespread joint pain. Several investigations turned up general inflammation, including high CRP and ESR but nothing else. Finally tested b12 and folate and got the above results back - 120ng/l for b12. I know it takes a long time for b12 to deplete so significantly but I feel I've had a huge spike in type and intensity of symptoms over the last few weeks. Is this possible or is it all in my head? Looking back over the last few years, I could probably attribute most of the things I've needed to go to the Dr for to b12 deficiency.
Side note - how should I expect a Dr to treat this in the UK? I'm expecting a call today and would like to know we're on the right track.

New here. I could use some advice. I'm having severe symptoms: Constant Pins and Needles arms/hands/legs/feet/face, extreme fatigue, internal vibration, shaking, extreme insomnia, brain fog, cognitive issues....
All of this started 3 weekend ago after I got an I infusion of vitamins which included Methylcobalamin B12, on 3 days different days.
I later found out I am COMT slow and Methylcobalamin is bad for me. After the infusions I got instantly jittery, had insomnia, and the neuropathy started and is getting worse. I stopped the infusions 2 weeks ago and symptoms are not getting better. Dr who gave them said he's never seen this reaction.
I also visited many Dr's and the ER and they are clueless saying my B12 is fine (over 2000). Before this I was just taking a multivitamin.
Here are my numbers: B12: OVER 2000 (out of range) Folate: Over 20 (out of range) MMM: 99 Potassium : 4.1 Magnesium : 2.2 Vit D Hydroxy: 47
I suspect I am overmethylating from the wrong B12, but could I also be deficient? All Dr's say no.
I did take a PPI several months ago for 8 week and had similar symptoms but those resolved after about 8 weeks after stopping.
Anyone have insight?

How much b12 should i take with 5 mg of methylfolate? I have a folate deficiency and my b12 it is just on range.
Thanks

I have my B12 in the 800s but my folate is deficient. But I still have the low B12 extreme fatigue Tingling in face and weird sensations in my arms and legs as well as headaches/tension headaches sometimes. Usually when I wake up before I take my Folic acid pills. I’m unsure if this is normal. HELP!!

Sharing my story in hopes of finding anyone else who could advise me (or had a similar experience). I do have a CT scan in about 4 weeks from now, but in the meantime, I have no idea how to improve up until then.
About 5 weeks ago, out of nowhere, I was bending over head down towards the passenger cabin of my Mom's truck helping her with groceries. For some reason, I instantly felt severe pain radiating from the right side of my brain. When I got up, my world was spinning and my head was in so much pain. I sat down until things calmed down. A week later, I went to see my Primary and he said I seem fine and my bloodwork looked fine (except for slightly high tryglicerides count).
Fast forward to today, I've been trying my best to keep a balanced diet (cut out lots of sugar, processed food, dairy, and gluten). I also have been intaking a good amout of Vitamins (B6, B12, D), folate, magnesium, and iron.
Yet, to this day, I still struggle. Every day (some days more severe than others), I get intermittent brain pressure (on the top of my head usually). Some times, they are intense and feel stabby. I also have a feeling of brain fog (where I feel like I'm not there, even though I know I'm physically there). Occasionally, maybe every other day instead of every day, I get really heavy eyes where it feels like I'm sleepy or tired although I'm well-rested (I've been getting about 7.5 hours of sleep on average the past few weeks). I don't really have balance issues (although they were present during the initial "event" 5 weeks ago).
Comments, suggestions?
*Before this "event," I wasn't suffering from any depression or anxiety or whatever. I've always been generally very confident and happy go-lucky. This still hasn't change today, although I will say that it has "slightly" gone downward since all these symptoms started manifesting without any days of being symptom free.

I am symptomatic of both anemia and low b12 but my levels are- B12- 332 Ferritin-33 Folate-7.3 The GP said this is all fine, but I’m so unwell and feel reading that these are all borderline results. Thanks

To preface, I have CFS, so fatigue is my normal every day life. I’ve had that since I was 16 (diagnosed at 19). At 18, I was diagnosed with hypothyroidism. Been on medication ever since (I’m now 31) and over the years, I have been very low in:
Vitamin D (needed prescription twice, now take a daily supplement, though it’s still on the low end of normal)
B12 (not diet related, did the intrinsic factor test, which came back negative, but it’s not always accurate. I get an injection every 12 weeks)
Folic acid (after a recent bout of worsening fatigue, I had all the bloods done, and I’m deficient in folic acid, for which I now have a 4 month course of tablets)
I obviously went googling to figure out why I could be low in folic acid. I don’t exclude anything from my diet, I eat all my greens etc. So malabsorption seemed the most logical explanation, and that’s when coeliac disease kept popping up. Apparently, because I have a thyroid disorder as well as low B12 and folates, I should get tested. But I feel like a bit of a fraud for asking the GP for this. I don’t have any severe bowel issues, I don’t notice a big difference after eating gluten. I do have always had some bloating after eating, and I had IBS symptoms when I was younger. I would say I’ve had more bloating recently, to the point that some clothes don’t fit well anymore, but I usually just shrug that off as “oh well, one of those things”. I guess when you’ve been told so many times that nothing is wrong, when your body feels wrong, you don’t think anything of a symptom anymore!
I guess I’m just wondering whether I should ask to get tested? Part of me thinks “what if this has been the reason for the fatigue all these years” but another part of me thinks that can’t be right, because I don’t feel like I ‘react’ to gluten. Can it really be causing ‘just’ the deficiencies and fatigue? I would love to hear from anyone who might have had the same symptoms, or who has any kind of advice!

Functional Connectivity Issues and the Role of 5-HT2A Receptors in Low Serotonin Levels:
When serotonin (5-HT) levels are low, the brain often compensates by upregulating 5-HT2A receptors, meaning there are more receptors available or that they become more sensitive to serotonin. This upregulation results in an increased sensitivity to any available serotonin, leading to an exaggerated response even though the overall serotonin levels are reduced.
Impact on Functional Connectivity:

1. Low Serotonin Levels: Reduced serotonin availability prompts the brain to upregulate 5-HT2A receptors. This compensatory mechanism ensures that the limited serotonin can have a more pronounced effect by increasing receptor sensitivity or number.
2. Receptor Upregulation: Upregulation means there are more 5-HT2A receptors or that the existing receptors are more efficient at binding serotonin. This heightened sensitivity can disrupt normal neurotransmission and brain network interactions.
3. Functional Connectivity Issues: The increased sensitivity and number of 5-HT2A receptors can cause abnormal brain network interactions, leading to functional connectivity issues. These disruptions can affect mood, cognition, and perception, contributing to neuropsychiatric conditions like anxiety, depression, and perceptual disorders such as Visual Snow Syndrome (VSS) and Hallucinogen Persisting Perception Disorder (HPPD).

In summary, low serotonin levels lead to the upregulation of 5-HT2A receptors, resulting in increased receptor sensitivity. This heightened sensitivity can cause functional connectivity issues in the brain, affecting various cognitive and perceptual functions.
low serotonin levels and upregulated 5-HT2A receptors can contribute to a lack of inhibitory response in the brain. Benzodiazepines (benzos) can counteract this issue by enhancing GABAergic (gamma-aminobutyric acid) functioning, which promotes inhibitory signaling in the brain. Here’s how this interplay works:

Impact on GABAergic Functioning:

1. Low Serotonin and 5-HT2A Upregulation:
   • Low Serotonin Levels: When serotonin levels are low, it can disrupt the balance of excitatory and inhibitory neurotransmission in the brain.
   • Upregulation of 5-HT2A Receptors: Increased sensitivity and number of 5-HT2A receptors can lead to enhanced excitatory neurotransmission, contributing to a hyperexcitable state in the brain.
2. GABAergic Functioning:
   • GABA as an Inhibitory Neurotransmitter: GABA is the primary inhibitory neurotransmitter in the brain, responsible for reducing neuronal excitability and promoting relaxation and calmness.
   • Impact of 5-HT2A Receptor Activity on GABA: Enhanced activity of upregulated 5-HT2A receptors can interfere with GABAergic signaling. This can happen because 5-HT2A receptor activation generally promotes excitatory neurotransmission, which can counteract the inhibitory effects of GABA.

Role of Benzodiazepines:

• Mechanism of Benzodiazepines: Benzodiazepines enhance the effect of GABA by binding to GABA_A receptors and increasing the frequency of chloride channel opening. This hyperpolarizes the neuron, making it less likely to fire and promoting an overall inhibitory effect.
• Counteracting Hyperexcitability: By enhancing GABAergic inhibition, benzodiazepines can counteract the hyperexcitability caused by upregulated 5-HT2A receptors. This helps restore the balance between excitatory and inhibitory neurotransmission in the brain.

Low serotonin levels lead to upregulation and increased sensitivity of 5-HT2A receptors, resulting in enhanced excitatory neurotransmission. This can negatively impact GABAergic functioning by reducing the overall inhibitory tone in the brain, contributing to a hyperexcitable state. Benzodiazepines counteract this by enhancing GABAergic inhibition, promoting neuronal hyperpolarization, and restoring the balance between excitation and inhibition.
Taking an SSRI (Selective Serotonin Reuptake Inhibitor) to counterbalance low serotonin levels can sometimes make things worse initially due to several factors:

1. Initial Increase in Serotonin:
   • Mechanism of SSRIs: SSRIs work by blocking the reuptake of serotonin into the presynaptic neuron, increasing its availability in the synaptic cleft and enhancing serotonergic transmission.
   • Initial Effects: The sudden increase in serotonin levels can initially overstimulate serotonin receptors, including 5-HT2A receptors, which might already be upregulated and sensitive.
2. Overstimulation of 5-HT2A Receptors:
   • Enhanced Excitatory Activity: The upregulated and sensitive 5-HT2A receptors can become overstimulated by the increased serotonin, potentially exacerbating excitatory neurotransmission and leading to increased anxiety, agitation, or other side effects.
   • Adaptation Period: The brain needs time to adjust to the increased serotonin levels. During this adaptation period, the overstimulation of 5-HT2A receptors might cause temporary worsening of symptoms.
3. Impact on GABAergic Function:
   • Disruption of Inhibitory Balance: The initial increase in excitatory activity due to 5-HT2A receptor overstimulation can further disrupt the balance between excitatory and inhibitory neurotransmission, potentially reducing the efficacy of GABAergic inhibition.
   • Potential for Increased Anxiety: This disruption can lead to symptoms such as increased anxiety, restlessness, or insomnia, especially in the early stages of SSRI treatment.
4. Time for Therapeutic Effects:
   • Delayed Onset of Benefits: The therapeutic benefits of SSRIs often take several weeks to manifest as the brain gradually adjusts to the new serotonin levels and receptor sensitivities normalize.
   • Side Effects Management: During the initial period, side effects may be more prominent, and it is crucial to work closely with a healthcare provider to manage these effects and adjust the dosage as needed.

When starting SSRI treatment to counterbalance low serotonin levels, the initial increase in serotonin can overstimulate upregulated and sensitive 5-HT2A receptors, potentially worsening symptoms temporarily. This overstimulation can disrupt the balance between excitatory and inhibitory neurotransmission, impacting GABAergic function and possibly leading to increased anxiety or other side effects. The brain needs time to adjust, and the therapeutic benefits of SSRIs typically take several weeks to become evident. Close monitoring and support from a healthcare provider can help manage these initial side effects.
SSRIs primarily work by blocking the reuptake of serotonin, thereby increasing its availability in the synaptic cleft. They do not directly increase the production of serotonin but rather enhance the efficacy of existing serotonin. Here’s a detailed explanation of how SSRIs affect serotonin levels and why discontinuation can lead to worsening symptoms:

SSRIs and Serotonin Levels:

1. Mechanism of SSRIs:
   • Reuptake Inhibition: SSRIs block the serotonin transporter (SERT), which is responsible for the reuptake of serotonin from the synaptic cleft back into the presynaptic neuron.
   • Increased Availability: By inhibiting reuptake, SSRIs increase the concentration of serotonin in the synaptic cleft, allowing for prolonged activation of serotonin receptors.
2. Indirect Effects:
   • No Direct Production Increase: SSRIs do not directly increase the synthesis of serotonin. They rely on the body’s existing serotonin stores to maintain increased levels in the synaptic cleft.
   • Receptor Modulation: Over time, the increased availability of serotonin can lead to changes in receptor sensitivity and density, such as the downregulation of 5-HT2A receptors.

Discontinuation of SSRIs:

1. Reduction in Synaptic Serotonin:
   • Resumption of Reuptake: When SSRIs are discontinued, the reuptake of serotonin resumes, leading to a reduction in the concentration of serotonin in the synaptic cleft.
   • Decreased Activation: The sudden decrease in synaptic serotonin can lead to reduced activation of serotonin receptors, which can cause a return or worsening of symptoms.
2. Withdrawal Symptoms:
   • Receptor Sensitivity: During SSRI treatment, the brain may adapt by altering receptor sensitivity and density. Discontinuation can disrupt this balance, leading to withdrawal symptoms such as anxiety, depression, irritability, and flu-like symptoms.
   • Neurochemical Imbalance: The abrupt change in serotonin levels can cause a temporary neurochemical imbalance, exacerbating symptoms until the brain readjusts.

While SSRIs increase the availability of serotonin in the synaptic cleft by inhibiting reuptake, they do not directly address the underlying issue of serotonin production. Discontinuing SSRIs can lead to a reduction in synaptic serotonin, potentially causing withdrawal symptoms and a worsening of underlying conditions due to receptor and neurochemical imbalances. This is why it is crucial to taper off SSRIs gradually under medical supervision to allow the brain time to readjust to the changes in serotonin levels. Functional connectivity refers to the statistical association between the activities of different brain regions, often observed through imaging techniques like fMRI. It doesn't necessarily imply a loss of neurons. Instead, it reflects how different brain areas work together or communicate with each other, which can be influenced by factors like neuronal activity, neurotransmitter levels, and network, Functional connectivity itself doesn't directly imply a loss of specific types of neurons, such as serotoninergic (related to serotonin) or GABAergic (related to GABA, an inhibitory neurotransmitter) neurons. It's more about how these neurons or neural networks are functioning and communicating with each other
how to increase serotonin naturally
Vitamin D 1000-2000IU daily with vitamin K2-MK4 Activate folate B9 The active form of vitamin B9 is a type of folate known as 5-methyltetrahydrofolate (5-MTHF) not folic acid (best taking in conjunction with vitamin B6 (make sure B6 isn't in the 100MG and more in the lower figure of 25MG to avoid toxicity)and B12 make sure those are active forms as well Plenty of rich Tryptophan foods Lactobacillus Plantarum 299V ( https://pubmed.ncbi.nlm.nih.gov/30388595/ )
that's the best information I have for naturally increasing serotonin levels

Hey all. I recently asked my doc to check my b12 levels and they were extremely low (200). I had mistakeningly thought that when my doctor told me my regular yearly bloodwork "looks great" that included my b12 levels. But I didn't know the whole time, my b12 was never checked! Anyway I'm hit with a triple whammy of risk factors- long term vegan (please dont fault the diet. Its my fault for not properly supplementing and checking my b12.), family history of b12 deficiency (all the women in my family have had to have shots, and they ate like carnivores so its not a plant based thing) and long term on hormones.
The doc started me on daily cyanocobalamin (whatever it's called, the c one) shots daily for 1 week, then weekly for 1 month, then monthly.
I did not expect the side effects to be this bad. I read a bit on here about wake up symptoms but this is rough. Day two I could barely walk, I have horrible pain sensations in my feet and muscles all over. Near where j injected on my thigh, my whole leg hurts like hell all day. I'm starting to cough and develop a sore throat. Is this a deficiency of folate or potassium or something or could it be bad timing that I'm getting sick? It really feels a bit like covid but a little different. The muscle pain is the worst.
I have been eating bananas and taking a multi vitamin. I also ordered folate and more b12 that dissolves under the tongue.
Hoping to hear some personal anecdotes here if this is something others have experienced on the injections and does it get better with time? Thanks for reading and thanks for the very good pinned guide, it has helped me understand this so much better.

42F, fibromyalgia, migraines, chronic fatigue (all different versions of the same symtpoms really). I have these conditions which I know cause fatigue (I've been like this for 20 years). But my fatigue levels have been extreme in the last year. I've noticed that on three blood tests over the last year my MCH levels have been borderline high (33), and varying immune cells have been low (one time eosinophils, another time WBC and monocytes). Red cell width is always normal. B12 and folate have in the past tested normal. I had poor liver function 20+ years ago due to mono, but its been fine since then. The mono also triggered the chronic fatigue and fibromyalgia. Good times.
Is this just a variation of normal or should it be looked into further in case there is something else going on? It's very very hard to get an appointment with my doctor at the moment and she also always defers to "lets see how it goes" or "thats just what happens when you get older", so I don't get straight answers from her. I can't change because there is a mega shortage of GPs and no-one is taking on new patients.
I need exercise to feel less pain but struggle with doing exercise because of fatigue and pain so if theres anything that can make me feel slightly less like a sack of shit I'm keen to sort it out.

For reference, I’m 40F who is trying to prevent dementia and may try and get pregnant soon. I also take biotin, CoQ10, magnesium Glycinate, a probiotic and metformin.

When I take magnesium or b12 or folate or a multivitamin , it so obviously impacts my focus that I’m thinking ok there must have been a deficiency to begin with . Otherwise that change wouldn’t be that strong.
Then I thought ok maybe it’s something anyone experiences . But I know people who took this stuff and didn’t really feel any difference . Sometimes you see that on iherb too..
So what’s going on ?