The somewhat misleadingly named folic acid is in fact one of the most important of the water soluble B complex of vitamins. In the form of folates it is found naturally in the body as well as in various common foods. As folic acid it has been extensively researched and is widely available as a food supplement.
Inadequate dietary intake of folates by pregnant women has been widely publicised as a cause of serious and even fatal birth defects. Research has also suggested a strong association between folate deficiency and an increased incidence of certain of the more common cancers.
The implications of these findings will be covered in subsequent articles in this series, but this article will focus on the role of folates and folic acid in regulating blood homocysteine, excessively high levels of which have been identified as a key risk factor for both cardiovascular disease and Alzheimer's disease.
Homocysteine is a protein formed as a perfectly normal by-product of the body's digestive processes and in optimally healthy individuals it will be removed harmlessly from the body But its effective removal is heavily dependent on the presence of adequate supplies of three B complex vitamins, B6, B12 and folic acid or folates.
The build up of excess homocysteine if these vitamins are not present in sufficient quantities can have severe consequences. A large 1997 European study of young and middle aged adults showed a more than doubled risk of cardiovascular disease and stroke for individuals whose blood homocysteine levels were in the top fifth of the normal range. In fact some sources attribute as many as 10% of heart attack fatalities and an even higher proportion of stroke deaths directly to high homocysteine levels. Since these are still two of the biggest causes of premature death and disability in the affluent Western world, such figures are particularly alarming.
The link between raised homocysteine levels and Alzheimer's disease is not quite so well established, at least in the view of orthodox medicine, but a number of studies have found a clear association. It has also been observed that sufferers from this appalling disease are more likely to be deficient in both folic acid and dietary folates. Not surprisingly perhaps, given that damage to blood vessels appears to be one of the principal effects of elevated homocysteine, it has also been strongly linked with vascular dementia.
The role of folic acid and folates in lowering blood homcysteine levels is well established, with one recent study showing 60% and 90% reductions when supplement regimes of 0.2 mg and 0.4 mg respectively were followed. And given that high homocysteine levels have been shown to increase the risk of cardiovascular disease, as well as Alzheimer's and other dementias, it might be thought self-evident that supplementation should be a powerful weapon against them.
Conventional medicine, however, continues to be cautious about recognising the link. Although there is good evidence from at least one ten year study that high levels of dietary folate can reduce heart attack risk by more than 50%, there appears not be the same direct corroboration for the effects of folic acid supplementation. Somewhat bizarrely, therefore, the profession finds itself recommending supplementation for the purpose of reducing the elevated homocysteine levels known to increase the risk of disease, but declines to recommend it as a specific protector against the disease itself. Not surprisingly, nutritional therapists show no such hesitation, and many recommend supplementation at levels far in excess of the officially Recommended Dietary Allowance (RDA) of 400 mcg (0.4 mg) a day.
But whatever the benefits of high dosage supplementation, it is clear in any case that a diet rich in folates can only be of benefit to the body's general health. This is because amongst the best and most readily available sources of folates are leafy green vegetables and orange juice which also provide a plentiful supply of valuable anti-oxidants.
A single cup of spinach or asparagus, for example, may provide as much as 130 or more micrograms (mcg) of folate; a small glass of orange juice perhaps 80 mcg. Pulses such as beans and lentils are also good sources, the latter providing around 180 mcg in just half a cup, beans between 80 and 140 mcg according to type.
Best of all, however, is fortified breakfast cereal, a single cup of which may yield between 200 and 400 mcg, reflecting the FDA's insistence on the addition of folic acid to refined grain foods, including bread.
Despite this official recognition of the importance of this nutrient, the US Food and Nutrition Board nevertheless recommends that folic acid intake should be limited to 1,000 mcg (1 mg) per day. But this is not so much because of any possible ill effects of the folic acid itself, but rather because it may cure megaloblastic (commonly known as pernicious) anaemia which is one of the symptoms of an underlying deficiency of vitamin B12. If the removal of this symptom means that the deficiency is consequently undetected and left untreated, the neurological consequences may indeed be severe.
But to the educated layman the solution to this potential problem appears readily apparent. It is simply to ensure, through supplementation if necessary, that a generous intake of vitamin B12 is also obtained. This should present no difficulty if the standard recommendation never to take one of the B vitamins in isolation is followed. These vitamins should always be taken as part of a supplement containing the entire complex, and for maximum benefit should preferably be accompanied by a comprehensive multi-mineral
Inadequate dietary intake of folates by pregnant women has been widely publicised as a cause of serious and even fatal birth defects. Research has also suggested a strong association between folate deficiency and an increased incidence of certain of the more common cancers.
The implications of these findings will be covered in subsequent articles in this series, but this article will focus on the role of folates and folic acid in regulating blood homocysteine, excessively high levels of which have been identified as a key risk factor for both cardiovascular disease and Alzheimer's disease.
Homocysteine is a protein formed as a perfectly normal by-product of the body's digestive processes and in optimally healthy individuals it will be removed harmlessly from the body But its effective removal is heavily dependent on the presence of adequate supplies of three B complex vitamins, B6, B12 and folic acid or folates.
The build up of excess homocysteine if these vitamins are not present in sufficient quantities can have severe consequences. A large 1997 European study of young and middle aged adults showed a more than doubled risk of cardiovascular disease and stroke for individuals whose blood homocysteine levels were in the top fifth of the normal range. In fact some sources attribute as many as 10% of heart attack fatalities and an even higher proportion of stroke deaths directly to high homocysteine levels. Since these are still two of the biggest causes of premature death and disability in the affluent Western world, such figures are particularly alarming.
The link between raised homocysteine levels and Alzheimer's disease is not quite so well established, at least in the view of orthodox medicine, but a number of studies have found a clear association. It has also been observed that sufferers from this appalling disease are more likely to be deficient in both folic acid and dietary folates. Not surprisingly perhaps, given that damage to blood vessels appears to be one of the principal effects of elevated homocysteine, it has also been strongly linked with vascular dementia.
The role of folic acid and folates in lowering blood homcysteine levels is well established, with one recent study showing 60% and 90% reductions when supplement regimes of 0.2 mg and 0.4 mg respectively were followed. And given that high homocysteine levels have been shown to increase the risk of cardiovascular disease, as well as Alzheimer's and other dementias, it might be thought self-evident that supplementation should be a powerful weapon against them.
Conventional medicine, however, continues to be cautious about recognising the link. Although there is good evidence from at least one ten year study that high levels of dietary folate can reduce heart attack risk by more than 50%, there appears not be the same direct corroboration for the effects of folic acid supplementation. Somewhat bizarrely, therefore, the profession finds itself recommending supplementation for the purpose of reducing the elevated homocysteine levels known to increase the risk of disease, but declines to recommend it as a specific protector against the disease itself. Not surprisingly, nutritional therapists show no such hesitation, and many recommend supplementation at levels far in excess of the officially Recommended Dietary Allowance (RDA) of 400 mcg (0.4 mg) a day.
But whatever the benefits of high dosage supplementation, it is clear in any case that a diet rich in folates can only be of benefit to the body's general health. This is because amongst the best and most readily available sources of folates are leafy green vegetables and orange juice which also provide a plentiful supply of valuable anti-oxidants.
A single cup of spinach or asparagus, for example, may provide as much as 130 or more micrograms (mcg) of folate; a small glass of orange juice perhaps 80 mcg. Pulses such as beans and lentils are also good sources, the latter providing around 180 mcg in just half a cup, beans between 80 and 140 mcg according to type.
Best of all, however, is fortified breakfast cereal, a single cup of which may yield between 200 and 400 mcg, reflecting the FDA's insistence on the addition of folic acid to refined grain foods, including bread.
Despite this official recognition of the importance of this nutrient, the US Food and Nutrition Board nevertheless recommends that folic acid intake should be limited to 1,000 mcg (1 mg) per day. But this is not so much because of any possible ill effects of the folic acid itself, but rather because it may cure megaloblastic (commonly known as pernicious) anaemia which is one of the symptoms of an underlying deficiency of vitamin B12. If the removal of this symptom means that the deficiency is consequently undetected and left untreated, the neurological consequences may indeed be severe.
But to the educated layman the solution to this potential problem appears readily apparent. It is simply to ensure, through supplementation if necessary, that a generous intake of vitamin B12 is also obtained. This should present no difficulty if the standard recommendation never to take one of the B vitamins in isolation is followed. These vitamins should always be taken as part of a supplement containing the entire complex, and for maximum benefit should preferably be accompanied by a comprehensive multi-mineral
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