The friend I am giving information to and not advising has Serum Folate test results of 3.3 ug/l. It is my understanding it is thought that folic acid 5mg once a day should be taken to bring folic acid into mid range and then monitored to keep the level in mid range during any B12 supplementation.
That it is not preferred to bring folic acid levels into mid range prior to B12 supplementation. That folic acid if taken without B12 is known to mask a B12 deficiency and may result in permanent neurological symptoms. That folic acid is preferred to other forms. That folic acid and B12 are dependent on each other to provide what is needed at the cellular level. That 3.3 ug/l does not meet the requirement for folic acid deficiency but may contribute to the symptoms associated with B12 deficiency.
Any comments and corrections would be greatly appreciated.
Note “A”: My folic acid levels were in the low range and I was never told.
Note “B” I know of a person who was diagnosed with pernicious anemia without B12 deficiency. They were directed to this site and are on the right track. Those than make this site happen can take a bow now!😉
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WIZARD6787
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Hey Nackkkapan, I took 5mg a day from B12.org website not .5.mg. Not the first time I have come across conflicting information nor do I expect it to be the last. 😀
“That folic acid if taken without B12 is known to mask a B12 deficiency and may result in permanent neurological symptoms.”
Yes to masking, but be clear that the neurological symptoms that may result are those that normally come from untreated PA, and are not caused, or even exacerbated, by the folic acid.
“That folic acid is preferred to other forms.”
The ideal is to gain enough naturally-occurring folate from food.
For those who cannot, and need supplementation, synthesised folic acid is a readily available folate, and it is relatively stable, so useful for industrial food supplementation.
For individual supplementation, most people who need folate can benefit from folate in the form of folic acid, but a very few cannot.
Those who peddle other forms of folate tend to be rather quiet about them being equally a synthesised product, and rather vocal about the MTHFR gene, of which we all have one variant or another, of which only a very few people have a variant that makes them unable to benefit from folic acid.
The British National Formulary explicitly uses the word "precipitate":
Cautions
Cautions For folic acid
Should never be given alone for pernicious anaemia or other megaloblastic anaemias caused by vitamin B12 deficiency (may precipitate subacute combined degeneration of the spinal cord)
Which to my mind suggests that adding folic acid in the context of low B12 can worsen the situation.
They might be wrong, of course, but at the point of care, I'd tend to go with B12 first because that appears to avoid the possibility. The downside (obviously) being a short delay in addressing the folate issue.
Thank you for that! I think the theory is that as long as both B12 and Folic Acid are given at the same time that it is believed that the subacute combined degeneration of the spinal cord will not occur. I agree with you that it seems prudent to administer B12 first as the medical field could care less if their patient experienced a little bit of subacute combined degeneration of the spinal cord.
In my personal case what happened is I was prescribed 8 weekly injections and 1mg folic acid and 1mg of cynocabalamin daily for life. My GP took it on themselves to not prescribe monthly injections of 1mg cynocabalamin monthly for life as is the standard for PA in the US. This resulted in immediate subacute combined degeneration of the spinal cord which was debilitating painful. It is not pervasive now and seems to be working itself out with correct treatment.
I in this moment see it as folic acid taken without B12 does not only mask B12 deficiency it causes subacute combined degeneration of the spinal cord in a person who is B12 deficient. The error comes from the misinterpretation of the word precipitate.
My gait ataxia has improved to the point it is not noticeable and when I sway a bit I can't tell if it is gait ataxia or just normal.
I was walking on some cobble stones about two months ago and my right foot felt weird and I was thinking this is not good and then 1/4 mile later the same thing happened in my right.
I called my daughter in tears and told her I could feel my feet!
The big test will be when I try and golf in the spring.
Did your wife lose her sense of balance completely? This happened to me about 19 years ago and it happened fairly suddenly one day (there was a trigger). I lived abroad at the time and saw a specialist, who told me that something had affected my inner ear/balance and that the only way I could relearn this was a strict movement/exercise regime. It took me about 6 months to regain my sense of balance, but it was debilitating for the first few months. Feel free to message me if you can identify with my experience, happy to pass on what I learned.
It seems to me very odd that folic acid can precipitate a condition most closely associated with B12 deficiency, other than by masking this deficiency such that the consequences of B12D progress unchecked.
And we do know that NICE are howlingly wrong about the treatment of PA; while it is nice to see them err on the side of caution here, they are just making a bald statement that I cannot find any backup for, much less any suggestion of a mechanism by which this precipitation might occur.
This article might answer some of the questions regarding the possible role of folate in subacute combined spinal cord degeneration:
[Start]
The tolerable upper intake level for folic acid
There is no UL for natural reduced folates found in foods.8 The UL for the provitamin folic acid was established to avoid a delayed diagnosis of vitamin B12 deficiency, as assessed by hematological indices, and thereby minimize the risk of neurological complications in vitamin B12-deficient individuals. The IOM stated, “The weight of the limited but suggestive evidence that excessive folate intake may precipitate or exacerbate neuropathy in vitamin B12-deficient individuals justifies the selection of this end point as the critical end point for the development of a UL for folate.”8 The IOM was careful to note that there was not sufficient evidence to establish a UL on the basis of a no-observed-adverse-effect level (NOAEL) but rather on the basis of a lowest-observed-adverse-effect level (LOAEL).8 The LOAEL was set at 5 mg/day on the basis of several case reports and small observational studies showing that, at doses of 5 mg/day folic acid and above, there were more than 100 reported cases (from more than 20 studies) of neurological progression in patients with pernicious anemia, compared with fewer than eight cases in studies administering less than 5 mg/day oral folic acid.8 As stated by the IOM, “The LOAEL of 5 mg/day of folate was divided by an uncertainty factor of 5 to obtain the UL for adults of 1 mg/day or 1000 μg/day of folate from supplements or fortified food. A UL of 1000 μg/day is set for all adults rather than just for the elderly because of (1) the devastating and irreversible nature of the neurological consequences of a delayed diagnosis and treatment of a vitamin B12 deficiency, (2) data suggesting that pernicious anemia may develop at a younger age in some racial or ethnic groups,20 and (3) uncertainty about the occurrence of vitamin B12 deficiency in younger age groups.” According to the IOM, “the prevalence of vitamin B12 deficiency in females in the childbearing years is very low and the consumption of supplemental folate at or above the UL in this subgroup is unlikely to produce adverse effects,”8 although exceptions might include vegetarians, subsets of the population that have low dietary meat intake, and chronic users of proton pump inhibitors. Hematological indices are not commonly used to assess vitamin B12 deficiency, as they have been replaced with the use of serum biomarkers;21 hence, the basis for the UL for folic acid, which is based on hematological assessment of vitamin B12 deficiency, is less meaningful today relative to when it was established nearly 20 years ago.
But it goes on to say “There are no proposed biological premises or suggested mechanisms whereby elevated folic acid intake exacerbates vitamin B12 deficiency at the level of metabolism, cellular physiology, or human pathogenesis.”
But perhaps I shouldn’t be asking for a mechanism here. After all, they don’t even know why or how folic acid prevents or reduces the incidence of NTDs, just they know that it does.
However, if you plough through the passage above, and what follows it in the link, they don’t really know if folic acid exacerbates or precipitates decline in patients with low B12; they just have some inconclusive studies, and anecdotal evidence that indicates it might,
So they are being super-careful, as well they might when fortifying foodstuffs with folic acid which are then eaten by the general population to no beneficial effect, except to those women who are pregnant at the time, and those with B12 deficiency who are being supplemented with enough B12. Which those of us with PA generally aren’t, unless we have taken matters into our own hands 😢
"it is also noteworthy that >95% of the 155 cases in which folic acid supplementation was reported to precipitate neurologic manifestations occurred before 1963, during which time the FDA recommended dosage was 5–20 mg folic acid"
from Knowledge gaps in understanding the metabolic and clinical effects of excess folates/folic acid: a summary, and perspectives, from an NIH workshop, 202p
Thanks for that. As I read more it seems to me that health professionals often do not differentiate between treating the patient and trying to treat the world. I am an environmental scientist. Two biologists discovered that DDT pesticides caused the eggs in birds to weaken and this reduced the population of birds. The food chain theory was applied, the biologists became famous and DDT is banned throughout the world.
Current science is that raptor eggs that eat the grain in open silos that are heavily treated with DDT are thinner than they would be if the raptors did not feed on the grain. The food chain theory has not been proven.
People are dying in undeveloped countries from malaria due to the politics of environment science.
Ah - found this strand now. Re my last message to you, WIZARD6787.
My doctor suggested 400mcg once a week and one SI once a week (this is not the NHS, but the Nuffield iron clinic who diagnosed me finally). I found I was struggling with that (as I also have Longhaul Covid and PA for 2 years) and am injecting 0.5 daily and taking 800mcg twice a week at the moment.
And it's never really clear how long once should be taking the folate. Or the B12 for that matter - though I'd guess for the rest of my life.
All guesswork really, and mercifully, guidance from the forum.
All guesswork really, and mercifully, guidance from the forum. I really do not think the medical personal that I have dealt with are capable of ever treating B12 deficiency. It is too complex complex. The guidelines available are excellent only as a starting point.
Conclusions We report an association of increased risk for COVID-19 diagnosis and COVID-19-related death in people prescribed folic acid supplementation. Our results also suggest that methotrexate might attenuate these associations.
[Stop]
The study does not indicate a correlation between folate acid and Covid, but rather draws a correlation between folate acid precipitation and Covid.
In other words, as I read the article, in situations when doctors prescribe folic acid, if exposure to Covid is expected, it might be prudent to also prescribe methotrexate.
I am not medically trained and invite correction if I am in error.
Thank you all for replying! I conclude that the risk of waiting until folic acid levels are in mid range until starting B12 injections outweighs any potential benefit according to current knowledge. Not going to buy trouble with reading about folic anemia.
Wondering if the guidelines are lawsuit driven that someone was treated for folic anemia and ended up with permanent neurological symptoms because they were not also treated for B12 deficiency,
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