Vitamin B9
 

Folic Acid Introduction

Also referenced as: Vitamin B9, Folate, folic acid, folacin

A significant member in the family of B-complex vitamins is folate, or as it is most commonly known, folic acid. Folate occurs naturally in a variety of foods. Vitamin supplements, enrichment processes, and the consumption of fortified foods (mainly cereal grains) make Vitamin B9 readily available for utilization. These food processing standards have brought folate (particularly folic acid) supplementation into mainstream consciousness. The modern inclusion of folic acid into dietary sources may prove to be one of the most important links in understanding the role of vitamin supplementation in chronic disease and illness prevention.

Like B12, the coenzyme form of B9 is tetrahydrofolate (THF). This important coenzyme assists the body in performing a variety of functions. By assisting in the synthesis of coenzymes purine and pyrimidine, THF is responsible for processing DNA and activating its overall mapping capabilities. Folate also assists DNA in the transmission of genetic code from cell to cell. This intricate process is critical for the formation and proper growth of various systems located throughout our bodies.

Folate, in assistance with B12, is also exceptionally important in amino acid synthesis and the development of cells; primarily red blood cells. The processes dependant on folate may be among the most complex of any relating to the B-compound family of vitamins.

Folic Acid Food Sources

A majority (50+ percent) of folate may be destroyed during food processing, preparation, and storage. Common dietary sources of folate are listed below:

FoodMicrograms Dietary Folate Equivalents%DV*
Ready to eat cereal, fortified with 100% of the DV, 3/4 c 400 100
Beef liver, cooked, braised, 3 oz 185 45
Cowpeas (blackeyes), immature, cooked, boiled, 1/2 c 105 25
Breakfast cereals, fortified with 25% of the DV, 3/4 c 100 25
Spinach, frozen, cooked, boiled, 1/2 c 100 25
Great Northern beans, boiled, 1/2 c 90 20
Asparagus, boiled, 4 spears 85 20
Wheat germ, toasted, 1/4 c 80 20
Orange juice, chilled, includes concentrate, 3/4 c 70 20
Turnip Greens, frozen, cooked, boiled, 1/2 c 65 15
Vegetarian baked beans, canned, 1 c 60 15
Spinach, raw, 1 c 60 15
Green peas, boiled, 1/2 c 50 15
Broccoli, chopped, frozen, cooked, 1/2 c 50 15
Egg noodles, cooked, enriched, 1/2 c 50 15
Rice, white, long-grain, parboiled, cooked, enriched, 1/2 c 45 10
Avocado, raw, all varieties, sliced, 1/2 c sliced 45 10
Peanuts, all types, dry roasted, 1 oz 40 10
Lettuce, Romaine, shredded, 1/2 c 40 10
Tomato Juice, canned, 6 oz 35 10
Orange, all commercial varieties, fresh, 1 small 30 8
Bread, white, enriched, 1 slice 25 6
Egg, whole, raw, fresh, 1 large 25 6
Cantaloupe, raw, 1/4 medium 25 6
Papaya, raw, 1/2 c cubes 25 6
Banana, raw, 1 medium 20 6
Broccoli, raw, 1 spear (about 5 inches long) 20 6
Lettuce, iceberg, shredded, 1/2 c 15 4
Bread, whole wheat, 1 slice 15 4

[1]

In January of 1998, the Food and Drug Administration required the mandatory fortifying of all enriched cereal grains with folic acid. These processes provide anywhere from 25 - 100% of daily values (DVs) required for folic acid.

Folic Acid Uses

In women, the most clinically studied of all applications relating to the dietary supplementation of Vitamin B9 continues to be birth defects; the majority of which are believed to be linked to deficient levels of folic acid. [2] More specifically, neural tube defects, such as malformations of the skull, brain (ancephaly), and spine (chiefly spine bifida); which have all been attributed to the improper or inadequate dietary intakes of B9. [3] When folic acid is taken in adequate amounts pre-conceptually and during early pregnancy, it has been shown to reduce the risk and occurrence of ancephaly and spine bifida by as much as fifty percent. [4, 5]

Less than one-third of all women of child bearing age properly supplement their diets with folic acid. By doing so, they may ultimately reduce the risks connected to neural tube, and other birth defects. [6, 7] This may provide some explaination into the reasoning behind pre-natal vitamins and the highlighted importance placed upon proper folic acid supplementation in women by physicians.

Folate may also reduce homocysteine levels in the blood; thereby reducing the incidence of diseases associate with the heart. [8] This amino acid may be directly influenced by the dietary supplementation of B-vitamin compounds B6, folate, and B12. Furthermore, folate may reduce the damage to blood vessels, plaque build up on artery walls (atherosclerosis), and may even lessen the risk for blood clumping and clotting. [9]

Another serious concern with elevated homocysteine levels is the risk of stroke. Elevated homocysteine levels may be an independent factor for stroke occurrences. Individuals may be as much as 2.5 times more likely to suffer a stroke than those individuals who, as a result of B-vitamin supplementation, have lower homocysteine plasma levels. [10] Elevation of this amino acid may also play an integral role in formation of osteoporosis and rheumatoid arthritis.

Homocysteine has been also shown to play an important role in the health of the nervous system and may contribute to a variety of cognitive disorders, namely dementia. Alzheimer’s disease is included in this category of mental illness, and studies suggest that the condition’s onset may be directly affected by one’s dietary intake of folate. [11] Included with the supplementation of vitamins B6 and B12, folate may also assist in the symptoms associated with impaired cognitive abilities (i.e. thinking, judging, learning), especially within the elderly population. [12]

Cancer is another disease that science has targeted regarding disease occurrence and the relation to the dietary supplementation of Vitamin B9. Research has revealed that lower levels of folate in the body may increase one’s chances of developing certain forms of cancer. [13] This is thought to be the direct result of folate’s influence on DNA formation and coding. Cancers of the stomach, esophagus, breast, and colon, have been of particular interest in various clinical trials. From a cellular perspective, improper folate intake may cause damage to the DNA of particular cells; thereby exposing them to the dangers of cancer-causing agents. [14] The formation of certain cancers may be less common among those persons who have higher levels of folate intake.

Lower levels of Vitamin B9 in the blood may also be associated with cervical dysplasia. [15] This condition is characterized by certain changes of the cervix that are usually detected by pap smear. These changes take place within cellular structures of the cervix, and may prove to cancerous. Individuals at an elevated risk include women whose pap smears continually result in abnormalities (e.g. genital warts).

Depression is another area of interest concerning Vitamin B9 supplementation. Research indicates a strong relationship between folate and its role in treating the symptoms of mental illness; above all, depression. [16, 17] B-complex vitamin supplements are usually recommended for those who are genetically predisposed to this mental illness.

Finally, certain medications used in the treatment of chronic diseases may cause a malabsorption of folate and other B-vitamins (e.g. anti-convulsants). Lower levels of folic acid has been attributed to certain diseases. These include, but are not limited to, ulcerative colitis, Crohn's disease, and cancer. [18, 19]

Folic Acid Dosages

The RDA for folate was revised in 1998. Folate is expressed by the Dietary Folate Equivalent (DFE), used to distinguish between varying absorption rates from food sources of folate, folic acid, and its synthetic form. [3]

Life StageMenWomenPregnancyLactation
Ages 19+ 400 mcg 400 mcg
All ages 600 mcg 500 mcg
Dietary Folate Equivalent (DFE) is equal to 1 microgram food based folate = 0.6 micrograms of folic acid from fortified foods-Vitamin supplements consumed w/meal = 0.5 micrograms of synthetic folic acid digested in empty stomach-

It is important to note the strict standards placed upon vitamin supplements containing folic acid by the U.S. Food and Drug Administration (FDA). The FDA regulates the amount of B9 contained in a given supplement and when folic acid is wrongfully substituted for B12. This is primarily due to the significance of a dietary deficiency of B12. Folate (B9) has the ability to ‘mask’ the signs and symptoms of an underlying cobalamin deficiency.

Folic Acid Toxicities and Deficiencies

Folic Acid Deficiencies

In regards to the intake of B-compound vitamins, B9 deficiency is the most common. This is caused by improper dietary choices and our negligence in obtaining adequate amounts of proper plant food sources. Interestingly, liver is the only animal source to provide for significant levels of dietary folate in the human diet.

Those especially at risk for a B-vitamin deficiency include; individuals with inadequate diets or eating disorders, alcoholics and persons with substance abuse issues, impoverished individuals, and pregnant women (due to the proper needs for the overall development of embryo). Deficiencies are hard to detect and effects vary from person to person. Signs and symptoms may include:

  • Loss of appetite
  • Weight loss
  • Headaches
  • Behavioral disorders
  • Bleeding gums
  • Gastrointestinal disorders
  • Birth defects
  • Palpitations of the heart
  • Megaloblastic anemia (lack of oxygen carried by red blood cells)
  • Malabsorption syndromes

Folic Acid Toxicities

Doses of folate, folic acid, or folacin consumed in excess may interfere with our abilities to absorb the mineral zinc. Megadoses of B9 have also been shown to interfere with anticonvulsant medications, chiefly in epileptics. [21]

References

1. Clinical Nutrition Service, Warren Grant Magnuson Clinical Center, National Institutes of Health (NIH), NIH. Folate. December. 9. 2002. http://www.pdrhealth.com/drug_info/nmdrugprofiles/herbaldrugs/101840.shtml

2. Shaw GM, Schaffer D, Velie EM, Morland K, Harris JA. Periconceptional vitamin use, dietary folate, and the occurrence of neural tube defects. Epidemiology 1995; 6: 219-226.

3. Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes: Thiamin, riboflavin, niacin, vitamin B6, folate, vitamin B12, pantothenic acid, biotin, and choline. National Academy Press. Washington, DC 1998.

4. Medical Research Council Vitamin Study Research Group. Prevention of neural tube defects: results of the Medical Research Council vitamin study. Lancet 1991; 338: 131-7.

5. Czeizel AE, Dudas I. Prevention of the fist occurrence of neural tube defects by periconceptual vitamin supplementation. N Engl J Med 1992; 327: 1832-5.

6. Li DK, Daling JR, Mueller BA, Hickok DE, Fantel AG, Weiss NS. Periconceptual multivitamin use in relation to the risk of congenital urinary tract anomalies. Epidemiology 1995; 6: 212-8.

7. Botto LD, Khoury MJ, Mulinare J, Erickson JD. Periconceptual multivitamin use and the occurrence of conotruncal heart defects: results from a population based, case-control study. Pediatrics 1996; 98: 911-7.

8. Eikelboom JW, Lonn E, Genest J, Hankey G, Yusuf S. Homocyst(e)ine and cardiovascular disease: Results from a cohort of US adults. Ann Epidemiol. 1998; 8: 490-496.

9. Malinow MR. Plasma homocyst(e)ine and aterial occlusive diseases: A mini-review. Clin Chem 1995; 41: 173-6.

10. Wald DS. Randomized trial of folic acid supplementation and serum homocysteine levels. Arch Intern Med. 2001.; 56: 1188-1194.

11. Wang HX. Vitamin B12 and folate in relation to the development of Alzheimer’s disease. Neurology. 2001; 161: 695-700.

12. Calvaresi E, Bryan J. B vitamins, cognition, and aging: a review. J Gerontol B Psychol Sci Soc Sci. Nov 2001; 56 (6): P327-329.

13. Freudenheim JL, Grahm S, Marshall JR, Haughey BP, Cholewinski S, Wilkinson G. Folate intake and carcinogenesis of the colon and rectum. Int J Epidemiol 1991; 20: 368-374.

14. Jennings E. Folic Acid as a cancer preventing agent. Med Hypothesis 1995; 20: 368-374.

15. Butterworth CE Jr, Hatch KD, Macaluso M, et al. Folate deficiency and cervical dysplasia. JAMA. 1992;267(4): 528-533.

16. Alpert JE, Mischoulon D, Nierenberg AA, Fava M. Nutrition and depression: focus on folate. Nutrition. 2000; 16: 544-581.

17. Alpert JE, Fava M. Nutrition and depression: the role of folate. Nutrition Rev. 1997; 5(5): 145-149.

18. Steger GG, Mader RM, Vogelsang H, Schöfl R, Lochs H, Ferenci P. Folate absorption in Crohn’s disease. Digestion. 1994;55:234-238.

19. Kamen B. Folate and antifolate pharmacology. Semin Oncol 1997; 24: S18-30-S18-39.

20. Collins CS, Bailey LB, Hillier S, Cerda JJ, Wilder BJ. Red blood cell uptake of supplemental folate in patients on anticonvulsant drug therapy. Am J Clin Nutr 1988; 48: 1445-1450.

21. Herbert, Victor. “Vitamins and Minerals Plus Antioxidant Supplements” Total Nutrition Ed. Victor Herbert, M.D., Genell J. Subak-Sharpe, M.S. New York: Saint Martin’s Griffin, 1995. 94-118.