Folic Acid: Don't Be Without It!

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Folic Acid: Don't Be Without It!

 

by Hans R. Larsen, MSc ChE

 

 

 

Health starts with the individual cells of our body. If our cells are healthy so

are we. Healthy cells, in turn, depend on the continued, faultless replication

of our DNA. DNA can be seriously damaged through attacks by free radicals so an

adequate antioxidant status is essential to cell health.

 

It is now becoming clear though that antioxidants alone are not enough to

protect our DNA; more and more research points to the B vitamin folic acid as

being equally or perhaps even more important in ensuring proper DNA replication.

 

It is not surprising that a folic acid deficiency has been implicated in a wide

variety of disorders from Alzheimer's disease to atherosclerosis, heart attack,

stroke, osteoporosis, cervical and colon cancer, depression, dementia, cleft lip

and palate, hearing loss, and of course, neural tube defects. The list of

conditions involving a folic acid deficiency is growing day-by-day, as is

clinical evidence that most of these conditions can be reversed by

supplementation.

 

Folic acid (folinic acid, folacin, pteroylglutamic acid) was first isolated from

spinach leaves (its name derives from the Latin folium meaning " leaf " ) in 1964

and early on was found to be essential in the prevention of anemia in animals.

Later it was discovered that ensuring that mothers had adequate folic acid

levels could prevent neural tube defects in human babies.

 

Folic acid is essential for the synthesis of adenine and thymine, two of the

four nucleic acids that make up our genes, DNA and chromosomes.

 

It is now also clear that folic acid is required for the proper metabolism of

the essential amino acid methionine that is found primarily in animal proteins.

Methionine is converted to homocysteine in the body. Homocysteine, in turn, may

be converted back to methionine in a process requiring folic acid

(tetrahydrofolate) and vitamin-B12 (cobalamin) as a catalyst or it may be

metabolized into cysteine in a process catalyzed by vitamin-B6 (pyridoxine).

Cysteine is a vital link in the synthesis of glutathione, one of our most

important antioxidants. A high blood level of homocysteine has been found to be

highly detrimental to health and is invariably accompanied by a low level of

folic acid(1,2).

 

Homocysteine and heart disease

The idea that homocysteine may be a potent risk factor for coronary heart

disease (CAD) was first advanced in 1986(3). Since then numerous studies have

confirmed that high homocysteine levels not only increase the risk of CAD, but

also increase the risk of heart attacks, strokes, and peripheral vascular

disease (e.g. intermittent claudication)(2,4-12). The average blood level of

homocysteine in adults is about 10 micromol/L. Men with a level of 15 micromol/L

increase their risk for CAD by 60 per cent and women by 80 per cent.

 

The risk of a stroke at the 15 micromol/L level is two to five times higher

than at the 10 micromol/L level in both men and women and the risk of peripheral

vascular disease is seven times higher among people with elevated levels(5).

Researchers at the Harvard Medical School report that a homocysteine level of

more than 11.2 micromol/L confers a five-fold increase in heart attack risk as

compared to the risk at 7.2 micromol/L or less(9).

 

There is rare, unanimous consent within the medical community that homocysteine

levels in North America are too high. One study estimates that 56,000 lives

could be saved every year if average levels could be lowered by just 5

micromol/L(10,11). Fortunately, lowering your homocysteine level is simple by

supplementing with folic acid and vitamins B12 and B6(2,4,5,9-13).

 

Although most research into the harmful effects of homocysteine has centered on

heart disease there is growing evidence that high homocysteine levels (or low

folate levels) are involved in many other disorders.

 

Folic acid protects the brain

A low or deficient blood level of folate (folic acid) has been detected in 15 to

38 per cent of adults suffering from depression. There is now increasing

evidence that supplementation with therapeutic amounts of folate can

significantly improve the condition of depressed patients. In a recent trial

involving 20 elderly patients with depressive disorders, treatment with 50

mg/day of methylfolate was associated with an 81 per cent response rate within

six weeks. Folate supplementation (15 mg/day of methylfolate) has also been

found to markedly improve the effect of treatment with standard antidepressants.

 

Researchers at the Harvard Medical School point out that chronic diseases (e.g.

rheumatoid arthritis), certain cancer treatments, alcoholism, and a poor diet

can all lead to a folate deficiency and the potential for depression(14,15).

 

Research has also shown that many drugs such as methotrexate, levopoda, niacin,

phenytoin (Dilantin), carbamazepine, and theophylline can markedly reduce folate

levels(2,10,11). Researchers at Oxford University recently reported that

Alzheimer's patients have substantially lower levels of folic acid and vitamin

B12 than do normal people of the same age.

 

They also found that a high homocysteine level is a potent risk factor for AD;

study participants with a level above 14 micromol/L had an almost five times

higher risk than participants with levels below 11 micromol/L. Participants with

low folate and vitamin B12 levels had a three to four times higher risk of AD

than did people with normal levels(16).

 

Folic acid is especially important for women

It is now firmly established that women can reduce their risk of giving birth to

a baby with neural tube defects (e.g. spina bifida) by supplementing with folic

acid prior to conception and during pregnancy(10,11,17). Perhaps less well known

is the finding that women can also markedly reduce their risk of giving birth to

a child with a cleft lip or palate by supplementing daily with a multivitamin

containing 0.4 to 0.8 mg of folic acid(1.

 

These findings are particularly important in view of the fact that oral

contraceptives reduce folate levels significantly. Women who have been " on the

pill " need to boost their folate status if they are planning a pregnancy(19-21).

 

Low folate levels are also heavily implicated in the development of cervical

cancer. Cervical dysplasia is the precursor of cervical cancer and is usually

first detected through a routine Pap smear.

 

Fortunately, folate supplementation (0.8-3.0 mg/day) is very effective in

reversing cervical dysplasia and preventing the cancer(22-24). Researchers at

the Harvard Medical School recently reported that women who supplemented with

folic acid (0.4 mg/day or more for at least 15 years) had a four times lower

risk of developing colon cancer than did women with a daily intake of 0.2 mg/day

or less (the daily contribution of a typical North American diet)(25-27).

 

Many postmenopausal women have increased homocysteine levels that are believed

to contribute to the risk of osteoporosis; folate supplementation can reverse

these high levels(2.

 

And the list goes on

There is no question that folic acid is extremely important to health and

wellbeing. Not only is it important for heart health, mental health and women's

health, but it is now also clear that it affects many other facets of health and

disease.

 

Researchers at the Cleveland Clinic Foundation have found that patients with

end- stage renal disease have extremely high homocysteine levels and can be

protected from cardiovascular events by supplementing with folic acid, vitamins

B6 and B12(29).

 

Diabetes patients tend to have high homocysteine levels and folate is especially

important for them(30). Recent research has also shown that low folate levels

(high homocysteine levels) are implicated in age-related hearing loss,

psoriasis, and restless leg syndrome(31-33).

 

It is indeed astounding that one single vitamin, folic acid, can have such a

profound effect on our health and yet perhaps it is not so surprising when one

considers its vital role in DNA synthesis and homocysteine metabolism.

 

So how much is enough

It is estimated that 88 per cent of all North Americans suffer from a folate

deficiency(5,. Obviously, the standard diet is not supplying what we need. This

has led to the fortification of cereals and other foodstuffs with folic acid to

try to ensure a minimum daily intake of 0.4 mg/day. Although beans and green

vegetables like spinach and kale are good sources of folates, relatively few

people eat lots of vegetables and cooking destroys most of the folate anyway(.

Realizing the poor availability from the diet many medical researchers now

advocate daily supplementation with folic acid. Because folic acid needs the

catalysts vitamins B12 and B6 to carry out its functions effectively it is usual

to supplement with a combination of the three. Dosage recommendations for folic

acid vary between 0.4 mg/day and 10 mg/day or more depending on the severity of

the deficiency and the health problem to be overcome. The RDA for adults is now

0.4 mg/day and 0.6 mg/day for pregnant women. Recommendations for vitamin B12

generally range from 0.5 to 1.0 mg/day and for vitamin-B6 from 10 to 250

mg/day(2,4,5,9,10,11,13,34-36).

 

Supplementation with folic acid and vitamins B6 and B12 costs only pennies a day

and yet it is indeed hard to imagine a better investment in protecting your

health.

 

 

 

 

 

 

 

REFERENCES

 

Lehninger, Albert L. Biochemistry, 2nd edition, 1975, NY, Worth Publishers Inc.,

pp. 345-7

Moustapha, Ali and Robinson, Killian. Homocysteine: an emerging age-related

cardiovascular risk factor. Geratrics, Vol. 54, April 1999, pp. 41-51

Kang, S.S., et al. Protein-bound homocysteine. A possible risk factor for

coronary artery disease. J. Clin. Invest., Vol. 77, 1986, pp. 1482-86

Stampfer, Meir, J. and Malinow, M. Rene. Can lowering homocysteine levels reduce

cardiovascular risk? New England Journal of Medicine, Vol. 332, February 2,

1995, pp. 328-29

Boushey, Carol J., et al. A quantitative assessment of plasma homocysteine as a

risk factor for vascular disease. Journal of the American Medical Association,

Vol. 274, October 4, 1995, pp. 1049- 57

Nygard, Ottar, et al. Total plasma homocysteine and cardiovascular risk profile.

Journal of the American Medical Association, Vol. 274, November 15, 1995, pp.

1526-33

Perry, I.J., et al. Prospective study of serum total homocysteine concentration

and risk of stroke in middle-aged British men. The Lancet, Vol. 346, November

25, 1995, pp. 1395-98

Morrison, Howard I., et al. Serum folate and risk of fatal coronary heart

disease. Journal of the American Medical Association, Vol. 275, June 26, 1996,

pp. 1893-96

Verhoef, Petra, et al. Homocysteine metabolism and risk of myocardial

infarction: relation with vitamins B-6, B-12, and folate. American Journal of

Epidemiology, Vol. 143, May 1, 1996, pp. 845-59

Moghadasian, Mohammed H., et al. Homocysteine and coronary artery disease.

Archives of Internal Medicine, Vol. 157, November 10, 1997, pp. 2299-2308

Fallest-Strobl, Patricia C., et al. Homocysteine: a new risk factor for

atherosclerosis. American Family Physician, Vol. 56, October 15, 1997, pp.

1607-12

Rimm, Eric B., et al. Folate and vitamin B-6 from diet and supplements in

relation to risk of coronary heart disease among women. Journal of the American

Medical Association, Vol. 279, February 4, 1998, pp. 359-64 and pp. 392-93

(editorial)

Lowering blood homocysteine with folic acid based supplements: meta-analysis of

randomised trials. British Medical Journal, Vol. 316, March 21, 1998, pp. 894-98

Alpert, Jonathan E. and Fava, Maurizio. Nutrition and depression: the role of

folate. Nutrition Reviews, Vol. 55, May 1997, pp. 145-49

Ebly, Erika M., et al. Folate status, vascular disease and cognition in elderly

Canadians. Age and Ageing, Vol. 27, July 1998, pp. 485-91

Clarke, Robert, et al. Folate, vitamin B12, and serum total homocysteine levels

in confirmed Alzheimer disease. Archives of Neurology, Vol. 55, November 1998,

pp. 1449-55 and pp. 1407-08 (editorial)

Palca, Joseph. Agencies split on nutrition advice. Science, Vol. 257, September

25, 1992, p. 1857

Shaw, Gary M., et al. Risks of orofacial clefts in children born to women using

multivitamins containing folic acid periconceptionally. The Lancet, Vol. 346,

August 12, 1995, pp. 393-96

Shojania, A.M. Oral contraceptives: effect of folate and vitamin B12 metabolism.

Canadian Medical Association Journal, Vol. 126, No. 3, February 1, 1982, pp.

244-47

Martinez, O. and Roe, D.A. Effect of oral contraceptives on blood folate levels

in pregnancy. American Journal of Obstetrics and Gynecology, Vol. 128, No. 3,

June 1, 1977, pp. 255-61

Pietarinen, G.J., et al. Dietary folate intake and concentration of folate in

serum and erythrocytes in women using oral contraceptives. American Journal of

Clinical Nutrition, Vol. 30, March 1977, pp. 375-80

Murray, Michael T. Encyclopedia of Nutritional Supplements, 1996, Rocklin, CA,

Prima Publishing, p. 124

Passwater, Richard A. Cancer Prevention and Nutritional Therapies, 1993, New

Canaan, CT, Keats Publishing Inc., p. 182

Butterworth, Charles E., Jr., et al. Folate-induced regression of cervical

intraepithelial neoplasia in users of oral contraceptive agents. American

Journal of Clinical Nutrition, Vol. 33, 1980, p. 926

Giovannucci, Edward, et al. Multivitamin use, folate, and colon cancer in women

in the Nurses' Health Study. Annals of Internal Medicine, Vol. 129, October 1,

1998, pp. 517-24

Kim, Young-In, et al. Colonic mucosal concentrations of folate correlate well

with blood measurements of folate status in persons with colorectal polyps.

American Journal of Clinical Nutrition, Vol. 68, October 1998, pp. 866-72 and

pp. 763-64 (editorial)

Kato, I., et al. Serum folate, homocysteine and colorectal cancer risk in women:

a nested case-control study. British Journal of Cancer, Vol. 79, No. 11/12,

April 1999, pp. 1917-21

Murray, Michael T. Encyclopedia of Nutritional Supplements, 1996, Rocklin, CA,

Prima Publishing, pp. 123-24

Robinson, Killian, et al. Hyperhomocysteinemia confers an independent increased

risk of atherosclerosis in end-stage renal disease and is closely linked to

plasma folate and pyridoxine concentrations. Circulation, Vol. 94, No. 11,

December 1, 1996, pp. 2743-48

Hultberg, B., et al. Poor metabolic control, early age at onset, marginal folate

deficiency are associated with increasing levels of plasma homocysteine in

insulin-dependent diabetes mellitus. Scand. J. Clin. Lab. Invest., Vol. 57, No.

7, November 1997, pp. 595-600

Houston, Denise K., et al. Age-related hearing loss, vitamin B-12, and folate in

elderly women. American Journal of Clinical Nutrition, Vol. 69, March 1999, pp.

564-71

Fry, L., et al. The mechanism of folate deficiency in psoriasis. British Journal

of Dermatology, Vol. 84, June 1971, pp. 539-44

Rona, Zoltan. Return to the Joy of Health, 1995, Vancouver, BC, Alive Books, p.

193

Bailey, Lynn B. Dietary reference intake for folate: the debut of dietary folate

equivalents. Nutrition Reviews, Vol. 56, October 1998, pp. 294-99

Bronstrup, Anja, et al. Effects of folic acid and combinations of folic acid and

vitamin B-12 on plasma homocysteine concentrations in healthy, young women.

American Journal of Clinical Nutrition, Vol. 68, November 1998, pp. 1104-10

Brouwer, Ingeborg A., et al. Low-dose folic acid supplementation decreases

plasma homocysteine concentrations: a randomized trial. American Journal of

Clinical Nutrition, Vol. 69, January 1999, pp. 99-104

 

 

 

This article was first published in International Health News in July 1999

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