In case you did not see it, this week the suicide of 21 year old student Georgina Owen, likely due to B12 deficiency causing delusions, was reported after the coroner’s verdict.
This is tragic on so many levels, and so utterly preventable.
Let’s take a look at how B12 affects mental health and brain function.
B12 holds a key role in 2 vital enzymes in METHYLATION and in KREBS cycle for energy.
Key to understand that the NHS is obsessed with B12 in relation to anaemia, which may be a cause of fatigue.
But this is late stage feature and patients with functionally low (low intracellular levels), will be tired years before anaemia arrives.
And often it never arrives as taking folate can mask the anaemia of B12 deficiency – this is why we must always see an actual value of B12 serum, and not rely on an indirect test for B12 such as looking for haemoglobin to be low (anaemia) or mean cell volume (MCV) to be high (macrocytosis).
This is explicitly stated in NICE guidance.
This is a real issue given the fortification of foods with folic acid. If your patient with low B12 is taking cereal, bread or other foods with added folic acid, this might cover up their anaemia.
As B12 drops, its role in krebs cycle (totally unrelated to making haemoglobin for oxygen delivery), means people can get very tired.
Close up, MM CoA converts to the Kreb intermediary Succinyl-CoA, but only with B12.
This will create fatigue long before anaemia arrives, if it ever does.
And FYI, persistent fatigue is often misdiagnosed as depression.
But it is METHYLATION where B12 really affects mental health.
Methylation is simply adding a CH3 to molecules, but this is profound and occurs millions of times a second, turning some neurotransmitters on and some off.
Yes, you need to make neurotransmitters and, yes, you need to break them down or convert them, it is the balance that is the key.
It also allows us to make MYELIN, which is why low B12 also often presents with lowered pain thresholds = persistent pain, tingling, numbness and pins and needles.
So, is B12 causing mental health and psychosis a fringe idea?
Far from it.
From the NICE guidance once again:
And the from the literature:
“Psychiatric symptoms may occur in the absence of characteristic hematologic or neurologic symptoms suggestive of B12 deficiency. Because psychiatric symptoms can occur in low-to-moderate “normal” vitamin B12 levels, homocysteine or methylmalonic acid levels should also be checked in those with psychiatric symptoms. Importantly, dementia or cognitive decline become irreversible if not treated promptly. Psychosis appears to respond to vitamin B12 replacement, even after prolonged periods of a B12-deficient state, again pointing out the need to check for B12 deficiency in the elderly with psychosis”
“Within an average of 2 months, full amelioration was thus obtained in 75% of the cases and partial amelioration in the remaining 25%.”
The challenge with B12 is the diagnosis.
The NHS currently will diagnose blood levels under 133 pmol/L or 180 ng/L. Note this varies between labs and is a lower level than previously.
However, they are now explicit in saying there is an intermediate grey zone of B12 level that, if symptoms are suggestive, should trigger a trial of B12 therapy.
Specifically, they reference, 180-350 ng/L or 133 pmol/L to 258 pmol/L.
However, the labs do not reference this grey zone and have GP’s read the guidance?
My experience is no.
From our point of view, if a patient has symptoms that are suggestive and a B12 level under 677 ng/L or 500 pmol/L we are going to recommend a trial of liposomal hydroxocobalamin plus supporting B vitamins (One a day mutli or methyl B Hero).
Why under 677 ng/L or 500 pmol/L?
Re-read:
“Methods: We enrolled 231 healthy elderly volunteers (median age 71.2 years old) with a median B12 blood concentration of 414.8 pmol/L. We performed multifocal visual evoked potential testing, processing speed testing, and magnetic resonance imaging to assess neurological status. Moreover, we measured serum biomarkers of neuro-axonal injury, astrocyte involvement, and amyloid pathology.”
The results: Low B12, was associated with visual evoked potential latency delay, processing speed impairment (in an age-dependent manner; standardized, and larger volumes of white matter hyperintensities on MRI.
Let’s be 100% clear on the significance of this – people with levels well above the NHS Cut off or even grey zone has MRI finding consistent with evolving brain damage that could lead to dementia.
Please do not use cyanocobalamin (ever)
Consider why they might be low:
The most common is:
- Not eating it via ultraprocessed foods, or beign vegan and using low dose poor form B12
- Not absorbing it due to gut issues (gluten, IBS, IBD, low stomach acid via aging, or PPI or auto-immune gastritis)
- Not absorbing it due to metformin
Regardless of the cause, you must treat and you must FOLLOW THE B12 PROTOCOL.
Webinar here on that:
https://billings.krtra.com/c/SDgjYbzN7doQ/x86A
Or read it here:
https://academyofchiropracticnutrition.com/new-b12-protocol-keeping-it-simple/
Remember also, as part of protocol to assess iron stores via FERRITIN.
Ferritin should be at least 50, but in patients with symptoms at 100 ng/ml.
If your patient has not had that done on the NHS, OPTIMAL TESTING can.
