What is a safe dose of folate, vitamin b9?

So what is a safe dose of folate? Why should you care? Because vitamin b9 controls the health of your DNA and your genes. Folate deficiency is associated with a long list of cancers, cardiovascular diseases, and other serious conditions.

You seldom hear about the other side. Where in certain situations and with certain people folate can accelerate cancer among other conditions.

After months of research I have established that no one really knows, exactly, what is the proper amount of folate to take, but in my upcoming book, Folic Acid 2006, you can get close enough to ensure your health and longevity.


Journal of Neurology Neurosurgery and Psychiatry 2002;72:567-571
Benefits and risks of folic acid to the nervous system
E H Reynolds
Institute of Epileptology, Weston Education Centre, King's College Denmark Hill Campus, Cutcombe Road, London SE5 9PJ, UK
During three decades of neurological practice I have witnessed a remarkable change in attitudes
to the benefits and risks of folic acid therapy in nervous system disorders. In the 1960s all that
was known and taught was that folic acid was harmful to the nervous system, especially in
precipitating or exacerbating the neurological complications of vitamin B12 deficiency. So
deeply held was this view that the possibility of neuropsychological benefits from this vitamin
was initially viewed with considerable scepticism.1
During the 1970s and 1980s there was gradual and increasing recognition of the benefits of the
vitamin in neuropsychiatric disorders associated with folate deficient megaloblastic anaemia.2
Furthermore, the association of neurological disorders with inborn errors of folate metabolism3
and the potential for folic acid to prevent neural tube defects4 reinforced the importance of the
vitamin in the developing brain. More contentious has been the significance of folic acid
deficiency associated with neuropsychiatric disorders in the absence of anaemia
Some of the advocates of these policies [universal fortification of food] have cast doubt on or
even dismissed the risks of folic acid to the nervous system.10,11 In 30 years we have moved
from a view of all risks and no benefits to one of all benefits and little or no risks! The
experience of a whole generation of physicians who painfully learned the risks of folic acid to
the nervous system in the 1940s and 1950s,12,13 to which the risk of aggravating epilepsy was
later added,13,14 is in danger of being overlooked, and a more balanced approach is needed.
Careful assessment shows that about two thirds of patients presenting to physicians or
haematologists with megaloblastic anaemia due to either folic acid or vitamin B12 deficiency
have nervous system complications responsive to appropriate vitamin therapy in proportion to
the severity and duration of the disorder.2 These manifestations of the two deficiency states,
including cognitive impairment, overlap considerably but peripheral nerve and spinal cord (subacute combined degeneration) disorders are commoner with vitamin B12 deficiency and depression with folate deficiency. In elderly or psychogeriatric populations the incidence of folic acid deficiency is even higher but again consistently associated with depression and cognitive decline Isolated examples of a reticulocyte response and neurological deterioration were seen with doses of folic acid as low as 0.3 to 0.5 mg daily. As in the case of the benefits of folic acid, and for the same reasons, the duration of folic acid therapy may be as important as the dose of the
vitamin. A little studied occasional side effect of folate therapy in pharmacological doses—5 mg daily or more—is increased arousal, overactivity, sleeplessness, and the rare precipitation of hypomania in predisposed persons,60 as can occur with any antidepressant drug and has also been noted with the closely related metabolite, SAM
There is evidence from open and controlled trials of replacement therapy with folic acid and
methyl folate of an effect of the vitamin on mood, arousal, cognitive, and social function. The
vitamin has significant risks in patients with vitamin B12 deficiency or epilepsy which are
related to both the dose and duration of treatment. It is difficult to define a safe dose of the
vitamin in these situations, and a low dose over many years may not be without risk. The
vitamin interferes with the natural history of both the anaemia and the neurological
complications of vitamin B12 deficiency.