Folate in food is predominantly a mixture of 2 forms -
5-methyl-H4 folate and 10-formyl-H4 folate
(http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=405403)

The synthetic one is "PGA", pteroylmonoglutamic acid. It has higher
bio-availability and is converted to the 5-methyl-H4 form by the body,
but the reaction is saturated at doses higher than 400 mcg
(http://pmid.us/15738964) so it's probably better to take it in
divided doses.

Below some clippings from my old folate/folic acid notes:

From
<http://www.cce.cornell.edu/food/expfiles/topics/stover/folicqanda.html>:

  "Q. What's the difference between the terms folic acid and
   folate?
   
   A. In cells, folic acid exists in many chemical forms with
   respect to its oxidation state, one-carbon substitutions and
   number of glutamate residues. In general, the term folates,
   when used in the generic sense, refers to all chemical forms
   of folic acid. The term folic acid refers to the oxidized,
   monoglutamate form of folate otherwise known as
   pteroylglutamic acid.
   
   Q. Is there a difference in bioavailability between folic
   acid in foods versus supplements?
   
   A. The bioavailability of food folate is difficult to
   predict. In general, the oxidized, monoglutamate form of
   folate, the form found in supplements and the form used to
   fortify foods, has a much greater bioavailability than food
   folate which tends to be in a chemically reduced and in a
   polyglutamated form. The absorption of supplement folate
   during fasting is near 100%. Prior to absorption, folate
   polyglutamates must be enzymatically converted to folate
   monoglutamates, and the efficiency of this reaction varies
   depending upon the food source of folate. Therefore, while
   all sources are important, more folate is absorbed from
   fortified foods and supplements. Folic acid supplements are
   even more bioavailable if taken between meals."

From
<http://europa.eu.int/comm/food/fs/sc/scf/out80e_en.pdf>:

   "Folate is the generic name for a number of compounds having
   a similar activity as folic acid (pteroylglutamic acid,
   PGA), i.e. being involved in single carbon (C1-) transfer
   reactions. Folic acid (PGA) is a synthetic folate compound
   used in food supplements and in food fortification because
   of its stability, and becomes biologically active after
   reduction. Natural (dietary) folates are mostly reduced
   folates, i.e. derivatives of tetrahydrofolate (THF), such as
   5-methyl- THF (5-MTHF), 5- formyl-THF and 5,10-methylene-
   THF, and exist mainly as pteroylpolyglutamates, with up to
   nine additional glutamate molecules attached to the
   pteridine ring.

   [...]

   Food folates, mainly present as polyglutamates, have to be
   hydrolysed by a (brush border associated) deconjugase enzyme
   in the gut before absorption can occur. Folate absorption
   from natural food is generally lower than synthetic forms
   (e.g. folic acid) contained in supplements, due to matrix
   effects and the presence of inhibitors of the conjugase
   enzyme in some foods. Folic acid (PGA) enters the folate
   cycle after reduction by a (dihydro-)folate reductase. This
   enzyme is present in the intestinal mucosal cell, but also
   in other tissues, such as liver and kidney. Reduction of PGA
   may be a slow process in some subjects and at higher intake
   levels (> ca 260 µg) PGA may appear unchanged in the
   circulation (i.e. in the postprandial state after supplement
   use (Kelly et al., 1997). Under normal conditions 5-MTHF (as
   monoglutamate) is the only form present in plasma, mainly
   protein-bound. Tissue uptake is carrier-mediated and/or
   through folate binding proteins. In tissues folates are
   retained as polyglutamates and the folate coenzymes can be
   interconverted in numerous (de-)methylation reactions, such
   as in DNA synthesis (formation of thymidilate from
   deoxyuridine), amino acid interconversions, such as the
   remethylation of homocysteine to methionine. In this latter
   methionine synthase (MS) reaction vitamin B12 is also
   involved as a cofactor. About 50% of the folate body store,
   estimated to be 13-28 mg, is considered to be present in the
   liver (for review see Report of the Standing Committee on
   the scientific evaluation of dietary reference intakes
   (DRIs) and its panel on folate and other B-vitamins and
   choline. Food and Nutrition Board, Institute of Medicine,
   1998)."

From
<http://users.umassmed.edu/martin.marinus/Mph200/FolicAcidMetabolism.pdf>:

   "DHF and THF from natural sources are polyglutamated and
   need to be enzymatically converted to the monoglutamate for
   absorption from the small intestine."

(DHF=dihydrofolic acid; THF=tetrahydrofolic acid)

From
<http://www.pdrhealth.com/drug_info/nmdrugprofiles/nutsupdrugs/fol_0110.shtml>:

   "The term folate is used in two different ways. Folate, a
   member of the B-vitamin family, is a collective term for a
   number of chemical forms which are structurally related and
   which have similar biological activity to folic acid. Folate is
   also the term which is used for the anionic form of folic acid.
   Folic acid or pteroylglutamic acid (PGA) is comprised of para-
   aminobenzoic acid linked at one end to a pteridine ring and at
   the other end to glutamic acid. The pteridine-para-aminobenzoic
   acid portion of the molecule is called the pteroyl group. Folic
   acid is a synthetic folate form which is used for food
   fortification and nutritional supplements. It is not one of the
   principal naturally occurring forms of folate, used in the
   collective sense.

   The naturally occurring forms of folate differ in the extent of
   the reduction state of the pteroyl group, the nature of the
   substituents on the pteridine ring and the number of glutamyl
   residues attached to the pteroyl group. The naturally occurring
   folates, include 5-methyltetrahydrofolate (5-MTHF), 5-
   formyltetrahydrofolate (5-formyl-THF), 10-
   formyltetrahydrofolate (10-formyl-THF), 5,10-
   methylenetetrahydrofolate (5,10-methylene-THF), 5,10-
   methenyltetrahydrofolate (5,10-methenyl-THF), 5-
   formiminotetrahydrofolate (5-formimino-THF), 5,6,7,8-
   tetrahydrofolate (THF) and dihydrofolate (DHF). Most naturally
   occurring folates are pteroylpolyglutamates, containing two to
   seven glutamates joined in amide (peptide) linkages to the
   gamma-carboxyl of glutamate. The principal intracellular
   folates are pteroylpentaglutamates, while the principal
   extracellular folates are pteroylmonoglutamates.
   Pteroylpolyglutamates with up to 11 glutamic acid residues
   exist naturally.

   [...]
 
   PHARMACOKINETICS

   Folic acid or pteroylglutamic acid (PGA) is the form of
   folate used in food fortification and the principal form of
   folate found in nutritional supplements. Natural food
   folates are pteroylpolyglutamate derivatives.
   Pteroylpolyglutamate derivatives are hydrolyzed to
   pteroylmonoglutamate forms prior to absorption from the
   small intestine. The enzyme that catalyzes the cleavage is
   called folate conjugase or gamma-glutamylhydrolase. The
   monoglutamate forms of folate, including folic acid, are
   transported across the proximal small intestine via a
   saturable pH-dependent process. Higher doses of the
   pteroylmonoglutamates, including folic acid, are absorbed
   via a nonsaturable passive diffusion process. The efficiency
   of absorption of the pteroylmonoglutamates is greater than
   that of the pteroylpolyglutamates.

   Because of the difference in absorption efficiency between
   natural food folate and folic acid, the concept of dietary
   folate equivalents (DFEs) has been introduced. Folic acid
   taken on an empty stomach is twice as available as food
   folate. Folic acid taken with food is 1.7 times as available
   as food folate. For example, 400 micrograms of folic acid
   taken on an empty stomach is equivalent to 470 micrograms of
   folic acid taken with food and is equivalent to 800
   micrograms of food folate. DFEs can be calculated as
   follows:

   1 microgram of DFEs = 1 microgram of food folate = 0.5
   micrograms of folic acid taken on an empty stomach = 0.6
   micrograms of folic acid taken with meals.

   Following absorption of physiological amounts of folic acid
   into the enterocytes, a certain percentage undergoes
   reduction. Reduced folate is transported to the liver via
   the portal circulation. Much of a pharmacological dose of
   folic acid is transported to the liver as such, without
   first undergoing metabolism in the enterocytes. The various
   natural pteroylmonoglutamate forms undergo some metabolism
   in the enterocytes to pteroylpolyglutamate forms, but for
   the most part are also transported as their unmetabolized
   forms via the portal circulation to the liver. The folates
   are taken up by the liver and metabolized to polyglutamate
   derivatives (principally pteroylpentaglutamates), via the
   action of folylpolyglutamate synthase. Folates are stored in
   tissue in their polyglutamate forms. Folate is metabolized
   to its various metabolic forms in the liver. The various
   pteroylpolyglutamate forms are the active cellular cofactor
   forms of folate. Folate polyglutamates are released from the
   liver to the systemic circulation and to the bile. When
   released from the liver into the circulation, the
   polyglutamate forms are hydrolyzed by gamma-
   glutamylhydrolase and reconverted to the monoglutamate
   forms.

   The principal folate in the plasma is 5-
   methyltetrahydrofolate in its monoglutate form. 5-
   Methyltetrahydrofolate circulates in erythrocytes in its
   polyglutamate form. Approximately two-thirds of folate in
   plasma is protein bound. All tissue forms of folate are
   polyglutamates, while circulating forms of folate are
   monoglutamates. When pharmacological doses of folic acid are
   administered, a significant amount of unchanged folic acid
   is found in the plasma. The liver contains approximately 50%
   of the body stores of folate, or about 6 to 14 milligrams.
   The total body store of folate is about 12 to 28 milligrams.

   Folate is excreted in the urine as folate cleavage products.
   Intact folate enters the glomerulus and is reabsorbed into
   the proximal renal tubule. Very little intact folate is
   excreted in the urine. Folate is excreted in the bile and
   much of it is reabsorbed via the enterohepatic circulation."

B12 is needed to convert circulating 5-methyltetrahydrofolate
(5-methyl THFA), omce inside the cell, to THFA, the active form
participating in folate-dependent enzymatic reactions. In the
absence of B12, folate is "trapped" as 5-methyl THFA.

The dietary folate is either monoglutamate or polyglutamate.  Most is
polyglutamate and it can not be absorbed at all. All supplement folic
acid is monoglutamate and it is absorbed very well. The human gut has
a peptidase that hydrolyzes all of the glutamate off the polyglutamate
to give the monoglutamate form. This enzyme will not work
without B12. Low B12 will cause a folate deficiency unless a folic
acid supplement is used. See the page

<http://www.feinberg.northwestern.edu/nutrition/factsheets/folate.html>:

   "... Only about half of the folate consumed from food
   sources has acceptable bioavailability. Folate occurs
   naturally attached to multiple glutamic acid molecules which
   must be removed by hydrolysis prior to absorption by a
   vitamin B12-dependent enzyme to form pteroylmonoglutamate.
   In general, foods with high proportions of the monoglutamate
   form have higher folate bioavailability irrespective of the
   total amount. ..."

So B12 is needed both for the absorption of dietary folate and for the
folate metabolism inside the cell.

See also

<http://www.emedicine.com/MED/topic802.htm>:

  "Folic acid is composed of a pterin ring connected to p-
   aminobenzoic acid (PABA) and conjugated with one or more
   glutamate residues. It is distributed widely in green leafy
   vegetables, citrus fruits, and animal products. Humans do
   not generate folate endogenously because they cannot
   synthesize PABA, nor can they conjugate the first glutamate.
   
   Folates are present in natural foods and tissues as
   polyglutamates because these forms serve to keep the folates
   within cells. In plasma and urine, they are found as
   monoglutamates because this is the only form that can be
   transported across membranes. Enzymes in the lumen of the
   small intestine convert the polyglutamate form to the
   monoglutamate form of the folate, which is absorbed in the
   proximal jejunum via both active and passive transport.
   
   Within the plasma, folate is present, mostly in the 5-
   methyltetrahydrofolate (5-methyl THFA) form, and is loosely
   associated with plasma albumin in circulation. The 5-methyl
   THFA enters the cell via a diverse range of folate
   transporters with differing affinities and mechanisms (ie,
   adenosine triphosphate [ATP]–dependent H+ cotransporter or
   anion exchanger). Once inside, 5-methyl THFA may be
   demethylated to THFA, the active form participating in
   folate-dependent enzymatic reactions. Cobalamin (B-12) is
   required in this conversion, and in its absence, folate is
   "trapped" as 5-methyl THFA.
   
   From then on, folate no longer is able to participate in its
   metabolic pathways, and megaloblastic anemia results. Large
   doses of supplemental folate can bypass the folate trap, and
   megaloblastic anemia will not occur. However, the
   neurologic/psychiatric abnormalities associated with B-12
   deficiency ensue progressively.
   
   The biologically active form of folic acid is
   tetrahydrofolic acid (THFA), which is derived by the 2-step
   reduction of folate involving dihydrofolate reductase. THFA
   plays a key role in the transfer of 1-carbon units (such as
   methyl, methylene, and formyl groups) to the essential
   substrates involved in the synthesis of DNA, RNA, and
   proteins. More specifically, THFA is involved with the
   enzymatic reactions necessary to synthesis of purine,
   thymidine, and amino acid. Manifestations of folate
   deficiency thereafter, not surprisingly, would involve
   impairment of cell division, accumulation of possibly toxic
   metabolites such as homocysteine, and impairment of
   methylation reactions involved in the regulation of gene
   expression, thus increasing neoplastic risks."

From
<http://users.umassmed.edu/martin.marinus/Mph200/FolicAcidMetabolism.pdf>:

   "*Increased excretion/loss: Increased excretion of folate
   can occur subsequent to vitamin B-12 deficiency. During the
   course of vitamin B-12 deficiency, methylene THFA is known
   to accumulate in the serum, which is known as the folate
   trap phenomenon. In turn, large amounts of folate filter
   through the glomerulus, and urine excretion occurs. Another
   mechanism of excess excretion occurs in people with chronic
   alcoholism who can have increased excretion of folate into
   the bile. Patients undergoing hemodialysis also have been
   known to have excess folate loss during procedures."