The Protein Burner
Vitamin B6 was discovered in the 1930s. Vitamin B6 occurs in several forms, all of which can be converted to the most active coenzyme form, Pyridoxal Phosphate (PLP). PLP has a vital role in catalyzing dozens of hemical reactions in the body.
Vitamin B6 is unusual as a B vitamin in that it is so extensively stored in muscle tissue. Glucose is stored as glycogen in muscle tissue to provide energy on-site and when it is first needed. PLP is a coenzyme to the enzyme glycogen phosphorylase, which catalyzes the release of glucose from glycogen,
Figure -14 Vitamin B6 (pyridoxine) assists energy production from protein and carbohydrates.
Vitamin B6 Coenzyme form is: Pyridoxal Phosphate (PLP)
Many important neurotransmitters are synthesized using PLP-dependent enzymes. Serotonin is synthesized from tryptophan in the brain with the help of PLP. Other neurotransmitters that are synthesized using PLP-dependent enzymes are dopamine, gamma-aminobutyric acid (GABA), and norepinephrine. In the discussion of niacin, it was noted that tryptophan can be converted to niacin. The vitamin B6 coenzyme PLP is needed to convert tryptophan to niacin. This is another example of how all of the B vitamins work together.
PLP can help transfer amino groups from one amino acid to another in a process called transamination moving amino acids). In this way PLP can help make nonessential amino acids in the body. Along with other nutrients, PLP also functions in the synthesis of heme, a part of hemoglobin. Some forms of vitamin B6 help hemoglobin pick up and release oxygen.
PLP from vitamin B6 serves as a coenzyme in the synthesis of nucleic acids such as DNA (deoxyribonucleic acid) and RNA, (ribonucleic acid).
Vitamin B6 is depleted by alcohol drinking. Alcohol is broken down to acetaldehyde in the body. Acetaldehyde breaks the PLP coenzymes loose from their enzymes and the PLP is lost. Some drugs, such as isonicotinic acid hydrazide (INH) also deplete the body of vitamin B6. INH is a drug used to treat tuberculosis and supplemental vitamin B6 must be given during treatment.
Elevated homocysteine in the blood is an indicator that there is increased risk of cardiovascular disease. Vitamin B6 is needed to remove homocysteine from the blood by converting homocysteine to cysteine, as seen in Figure -15. In another process, folate and vitamin B12 remove homocysteine from the blood by converting homocysteine to methionine
Summary for Pyridoxine—Vitamin B6
Main function: building amino acids and fatty acids.
RDA: men, 1.7 mg; women, 1.5 mg.
Tolerable upper intake level is set at 100 mg daily.
No toxicity reported from food or below 200 mg per day.
Healthy food sources: Bananas, potatoes, and spinach.
Degradation: easily destroyed by heat and can be leached out into cooking water.
Coenzyme form: Pyridoxal Phosphate (PLP).
Figure -15 Vitamin B6, folate, and vitamin B12 convert the undesirable homocysteine to the useful amino acids cysteine and methionine.
Adults need about 1.3 mg to 1.7 mg of vitamin B6 to meet the RDAs. Severe deficiency is uncommon because vitamin B6 is found in many foods and fortified in refined grains; please refer to Graph -5. Alcoholics are at risk of deficiency.
Increased protein intake increases the need for vitamin B6. Dietary intake of vitamin B6 in the United States averages about 2 mg/day for men and 1.5 mg/day for women, thus meeting the RDAs. Bananas, fortified cereal, spinach, chicken, salmon, and potatoes are high in vitamin B6. Vitamin B6 is easily destroyed by heat, as shown in Figure -16.
Vitamin B6 is not toxic when supplied by food in the diet. Supplemental forms are usually in the form of pyridoxine hydrochloride. The upper limit for adults set by the Institute of Medicine is 100 mg; 100 mg per day is certainly a safe limit, well below the level that might bring on neurological problems. Vitamin B6 deficiency causes depression and confusion, and, in extreme deficiency, brain wave abnormalities and convulsions.
Graph 5 Vitamin B6 amounts in some common foods
Figure 16 Vitamin B6 is easily destroyed by heat and lost to cooking water.
Folate—the DNA Creator
In 1945 folic acid was isolated from spinach. The name folate is derived from the word foliage. The terms folate and folic acid are both used for this water-soluble B vitamin. Folic acid is the form normally used in vitamin supplements and in fortifying food. Folic acid is readily converted to folate in the body. Folic acid is
rarely found in food or in the human body. On the other hand, folates are found in food in many naturally-occurring forms. Folates are the metabolically active forms in the human body.
FOLATE ENZYMES
The primary coenzyme form of folate is TetraHydroFolate (THF). THF is needed to transfer one-carbon units. These one-carbon units contain a single carbon atom, which may be added to a compound being biosynthesized. Folate coenzymes act as acceptors and donors of one-carbon units in a variety of reactions needed in the metabolism of amino acids (shown in Figure -17) and also nucleic acids.
Folate Coenzyme form is: TetraHydroFolate (THF)
Figure -17 Folate is needed in the metabolism of amino acids.
One of the main roles of folate in the body is assisting in the metabolism of nucleic acids (DNA and RNA). Synthesis of DNA is dependent on folate coenzymes. Synthesis of DNA is especially important in rapidly-growing cells, such as red blood cells.
FOLATE AND HOMOCYSTEINE
Folate, along with vitamin B12, is needed in the synthesis of methionine. Methionine is needed to synthesize S-adenosylmethionine (SAMe), as seen in Figure -18 SAMe is used as a methyl donor at many sites within both DNA and RNA. A methyl donor is any substance that can transfer a methyl group (CH3) to another substance. These methyl groups can protect DNA against the changes that might lead to cancer. This synthesis of methionine from homocysteine is also important to prevent a buildup of homocysteine in the blood.
Deficiency of folates in the blood results in increased homocysteine levels. These increased homocysteine levels increase the risk of fatal heart disease. Slightly elevated levels of homocysteine in the blood have been associated with thickening of arterial walls, arterial wall deterioration, and blood clot forma-tion. Vitamin B6 and vitamin B12 are also needed to lower homocysteine levels in the blood.
Figure -18 Folate and vitamin B12 lower homocysteine levels and lead to the formation of SAMe, which donates methyl groups .
Elevated homocysteine levels in the blood have been associated with thickening of arterial walls, arterial wall deterioration, and blood clot formation.
BIOAVAILABILIT Y OF FOLATE AND FOLIC ACID
Synthetic folic acid commonly found in fortified food and in supplements has a higher bioavailability than the naturally occurring folates. It is unusual for synthetic vitamin to be more potent that a naturally-occurring vitamin. For folates, 100 mcg (micrograms) is also 100 mcg of Dietary Folate Equivalent (DFE).
However, for folic acid, 100 mcg is considered to be 170 mcg of DFE, if eaten with food. When eaten between meals, 100 mcg of folic acid is considered to be 200 mcg of DFE. So, to calculate the total amount of folates, one must add the DFE from folates to the DFE from folic acid supplementation (normally using the multiplication factor 1.7).
ASSIMILATION OF FOLATE
Folate in food is normally bound to a string of amino acids; this is called the polyglutamate form. For intestinal absorption, it is necessary for folate to be bound to only one amino acid; this is called the monoglutamate form and is shown in Figure -19. Digestive enzymes on the surface of intestinal cells hydrolyze
Figure -19 Assimilation of folate
(split) the polyglutamate into one monoglutamate and several glutamates. A methyl group attaches to this monoglutamate to enable the transport of folate to the blood, liver, and other cells. This methyl group is needed for transport, but the methyl group needs to be removed for folate coenzymes to function. Vitamin B12 is part of the enzyme system that removes this methyl group from folate, thus activating the folate.
RECYCLING OF FOLATE
When there is excess folate in the blood, the liver puts much of the extra folate into bile. This bile goes back into the intestines, where the folate may be reabsorbed. This reabsorption of folate is dependent on healthy intestines. This reabsorption of folate by the intestines is vital. If the intestines are not healthy enough to absorb folate, then this limits the ability of the body to make rapidly-growing cells. The intestinal walls are made up of rapidly-growing cells. In a vicious cycle, the lack of folate can prevent uptake of folate and other nutrients. Also, alcohol drinking can decrease the absorption of folate
NEURAL TUBE DEFECTS
Lack of folate in the diet can cause neural tube defects in an embryo of a pregnant woman. These can cause devastating and sometimes fatal birth defects. Five servings of fruits and vegetables daily will provide enough folate for normal embryonic development. However, many American women do not eat this quantity of fruits and vegetables. To be assured of adequate folate to prevent neural tube defects, women are advised to take 400 mcg (micrograms) of folic acid daily either as a dietary supplement or in fortified food. This folic acid supplementation needs to be taken from one month before conception until the end of the first trimester of pregnancy. To protect against neural tube defects, the U.S. Food and Drug Administration has mandated that folic acid be added to enriched grain products. This enrichment of grain with folate is estimated to deliver an average of 100 mcg of folic acid daily..
Folate is needed to prevent birth defects called neural tube defects.
FOLATE AND VITAMIN B12
High levels of folic acid supplementation, especially above 1000 mcg daily, can mask symptoms of vitamin B12 deficiency. The addition of folic acid to food is risky because some people may get enough folic acid to hide the terrible effects of vitamin B12 deficiency on nerves. The addition of folic acid to grains is also controversial because it only helps prevent neural tube defects about half of the time.
FOLATE DEFICIENCY
Folate deficiency signs include anemia and deterioration of the gastrointestinal tract. The anemia results from abnormal blood cell division resulting in fewer and larger red blood cells. This type of anemia is called megaloblastic anemia, referring to the large immature red blood cells. Neutrophils, a type of white blood cell,
also can be abnormal. Symptoms of folate deficiency typically take a few months to develop and may result in fatigue from lower oxygen-carrying capacity of red blood corpuscles.
Folate deficiency can be caused by inadequate absorption, inadequate consumption, or unusually high metabolic needs for this vitamin. Drugs that can interfere with folate include aspirin, anticancer drugs, antacids, and oral contraceptives.Older people tend to have higher homocysteine levels and are encouraged to meet or exceed the RDA for folate.
FOLATE IN FOOD
Leafy green vegetables are the best sources of folate. Legumes are also high in folate; please refer to Graph 6. Other sources include fruit and enriched grains.
Summary for Folate
Main function: synthesis of DNA and red blood cells.
RDA: adults, 400 mcg; pregnant women, 600 mcg.
Tolerable upper intake level: 1000 mcg.
No toxicity reported from food.
Deficiency disease: neural tube defects, anemia, and excess folates may mask vitamin B12 deficiency.
Healthy food sources: leafy green vegetables and legumes.
Degradation: easily destroyed by oxygen and heat.
The RDA for folate as expressed in DFE (Dietary Folate Equivalents) is 400 mcg per day for adults. Atolerable upper intake level of 1,000 mcg per day was established by the Food and Nutrition Board to prevent the masking of vitamin B12 deficiency. Folate and folic acid are not toxic. Folate in food can be destroyed by heat, light, and air, as shown in Figure -20. Among the various cooking techniques, microwave cooking results in the greatest losses of folate. Coenzyme form: TetraHydroFolate (THF).
Figure -20 Folate losses in storage and cooking.
Graph 6 Folate amounts in some common foods.
Vitamin B6 was discovered in the 1930s. Vitamin B6 occurs in several forms, all of which can be converted to the most active coenzyme form, Pyridoxal Phosphate (PLP). PLP has a vital role in catalyzing dozens of hemical reactions in the body.
Vitamin B6 is unusual as a B vitamin in that it is so extensively stored in muscle tissue. Glucose is stored as glycogen in muscle tissue to provide energy on-site and when it is first needed. PLP is a coenzyme to the enzyme glycogen phosphorylase, which catalyzes the release of glucose from glycogen,
Figure -14 Vitamin B6 (pyridoxine) assists energy production from protein and carbohydrates.
Vitamin B6 Coenzyme form is: Pyridoxal Phosphate (PLP)
Many important neurotransmitters are synthesized using PLP-dependent enzymes. Serotonin is synthesized from tryptophan in the brain with the help of PLP. Other neurotransmitters that are synthesized using PLP-dependent enzymes are dopamine, gamma-aminobutyric acid (GABA), and norepinephrine. In the discussion of niacin, it was noted that tryptophan can be converted to niacin. The vitamin B6 coenzyme PLP is needed to convert tryptophan to niacin. This is another example of how all of the B vitamins work together.
PLP can help transfer amino groups from one amino acid to another in a process called transamination moving amino acids). In this way PLP can help make nonessential amino acids in the body. Along with other nutrients, PLP also functions in the synthesis of heme, a part of hemoglobin. Some forms of vitamin B6 help hemoglobin pick up and release oxygen.
PLP from vitamin B6 serves as a coenzyme in the synthesis of nucleic acids such as DNA (deoxyribonucleic acid) and RNA, (ribonucleic acid).
Vitamin B6 is depleted by alcohol drinking. Alcohol is broken down to acetaldehyde in the body. Acetaldehyde breaks the PLP coenzymes loose from their enzymes and the PLP is lost. Some drugs, such as isonicotinic acid hydrazide (INH) also deplete the body of vitamin B6. INH is a drug used to treat tuberculosis and supplemental vitamin B6 must be given during treatment.
Elevated homocysteine in the blood is an indicator that there is increased risk of cardiovascular disease. Vitamin B6 is needed to remove homocysteine from the blood by converting homocysteine to cysteine, as seen in Figure -15. In another process, folate and vitamin B12 remove homocysteine from the blood by converting homocysteine to methionine
Summary for Pyridoxine—Vitamin B6
Main function: building amino acids and fatty acids.
RDA: men, 1.7 mg; women, 1.5 mg.
Tolerable upper intake level is set at 100 mg daily.
No toxicity reported from food or below 200 mg per day.
Healthy food sources: Bananas, potatoes, and spinach.
Degradation: easily destroyed by heat and can be leached out into cooking water.
Coenzyme form: Pyridoxal Phosphate (PLP).
Figure -15 Vitamin B6, folate, and vitamin B12 convert the undesirable homocysteine to the useful amino acids cysteine and methionine.
Adults need about 1.3 mg to 1.7 mg of vitamin B6 to meet the RDAs. Severe deficiency is uncommon because vitamin B6 is found in many foods and fortified in refined grains; please refer to Graph -5. Alcoholics are at risk of deficiency.
Increased protein intake increases the need for vitamin B6. Dietary intake of vitamin B6 in the United States averages about 2 mg/day for men and 1.5 mg/day for women, thus meeting the RDAs. Bananas, fortified cereal, spinach, chicken, salmon, and potatoes are high in vitamin B6. Vitamin B6 is easily destroyed by heat, as shown in Figure -16.
Vitamin B6 is not toxic when supplied by food in the diet. Supplemental forms are usually in the form of pyridoxine hydrochloride. The upper limit for adults set by the Institute of Medicine is 100 mg; 100 mg per day is certainly a safe limit, well below the level that might bring on neurological problems. Vitamin B6 deficiency causes depression and confusion, and, in extreme deficiency, brain wave abnormalities and convulsions.
Graph 5 Vitamin B6 amounts in some common foods
Figure 16 Vitamin B6 is easily destroyed by heat and lost to cooking water.
Folate—the DNA Creator
In 1945 folic acid was isolated from spinach. The name folate is derived from the word foliage. The terms folate and folic acid are both used for this water-soluble B vitamin. Folic acid is the form normally used in vitamin supplements and in fortifying food. Folic acid is readily converted to folate in the body. Folic acid is
rarely found in food or in the human body. On the other hand, folates are found in food in many naturally-occurring forms. Folates are the metabolically active forms in the human body.
FOLATE ENZYMES
The primary coenzyme form of folate is TetraHydroFolate (THF). THF is needed to transfer one-carbon units. These one-carbon units contain a single carbon atom, which may be added to a compound being biosynthesized. Folate coenzymes act as acceptors and donors of one-carbon units in a variety of reactions needed in the metabolism of amino acids (shown in Figure -17) and also nucleic acids.
Folate Coenzyme form is: TetraHydroFolate (THF)
Figure -17 Folate is needed in the metabolism of amino acids.
One of the main roles of folate in the body is assisting in the metabolism of nucleic acids (DNA and RNA). Synthesis of DNA is dependent on folate coenzymes. Synthesis of DNA is especially important in rapidly-growing cells, such as red blood cells.
FOLATE AND HOMOCYSTEINE
Folate, along with vitamin B12, is needed in the synthesis of methionine. Methionine is needed to synthesize S-adenosylmethionine (SAMe), as seen in Figure -18 SAMe is used as a methyl donor at many sites within both DNA and RNA. A methyl donor is any substance that can transfer a methyl group (CH3) to another substance. These methyl groups can protect DNA against the changes that might lead to cancer. This synthesis of methionine from homocysteine is also important to prevent a buildup of homocysteine in the blood.
Deficiency of folates in the blood results in increased homocysteine levels. These increased homocysteine levels increase the risk of fatal heart disease. Slightly elevated levels of homocysteine in the blood have been associated with thickening of arterial walls, arterial wall deterioration, and blood clot forma-tion. Vitamin B6 and vitamin B12 are also needed to lower homocysteine levels in the blood.
Figure -18 Folate and vitamin B12 lower homocysteine levels and lead to the formation of SAMe, which donates methyl groups .
Elevated homocysteine levels in the blood have been associated with thickening of arterial walls, arterial wall deterioration, and blood clot formation.
BIOAVAILABILIT Y OF FOLATE AND FOLIC ACID
Synthetic folic acid commonly found in fortified food and in supplements has a higher bioavailability than the naturally occurring folates. It is unusual for synthetic vitamin to be more potent that a naturally-occurring vitamin. For folates, 100 mcg (micrograms) is also 100 mcg of Dietary Folate Equivalent (DFE).
However, for folic acid, 100 mcg is considered to be 170 mcg of DFE, if eaten with food. When eaten between meals, 100 mcg of folic acid is considered to be 200 mcg of DFE. So, to calculate the total amount of folates, one must add the DFE from folates to the DFE from folic acid supplementation (normally using the multiplication factor 1.7).
ASSIMILATION OF FOLATE
Folate in food is normally bound to a string of amino acids; this is called the polyglutamate form. For intestinal absorption, it is necessary for folate to be bound to only one amino acid; this is called the monoglutamate form and is shown in Figure -19. Digestive enzymes on the surface of intestinal cells hydrolyze
Figure -19 Assimilation of folate
(split) the polyglutamate into one monoglutamate and several glutamates. A methyl group attaches to this monoglutamate to enable the transport of folate to the blood, liver, and other cells. This methyl group is needed for transport, but the methyl group needs to be removed for folate coenzymes to function. Vitamin B12 is part of the enzyme system that removes this methyl group from folate, thus activating the folate.
RECYCLING OF FOLATE
When there is excess folate in the blood, the liver puts much of the extra folate into bile. This bile goes back into the intestines, where the folate may be reabsorbed. This reabsorption of folate is dependent on healthy intestines. This reabsorption of folate by the intestines is vital. If the intestines are not healthy enough to absorb folate, then this limits the ability of the body to make rapidly-growing cells. The intestinal walls are made up of rapidly-growing cells. In a vicious cycle, the lack of folate can prevent uptake of folate and other nutrients. Also, alcohol drinking can decrease the absorption of folate
NEURAL TUBE DEFECTS
Lack of folate in the diet can cause neural tube defects in an embryo of a pregnant woman. These can cause devastating and sometimes fatal birth defects. Five servings of fruits and vegetables daily will provide enough folate for normal embryonic development. However, many American women do not eat this quantity of fruits and vegetables. To be assured of adequate folate to prevent neural tube defects, women are advised to take 400 mcg (micrograms) of folic acid daily either as a dietary supplement or in fortified food. This folic acid supplementation needs to be taken from one month before conception until the end of the first trimester of pregnancy. To protect against neural tube defects, the U.S. Food and Drug Administration has mandated that folic acid be added to enriched grain products. This enrichment of grain with folate is estimated to deliver an average of 100 mcg of folic acid daily..
Folate is needed to prevent birth defects called neural tube defects.
FOLATE AND CANCER
Folate may also play a role in cancer prevention. Cancer is thought to arise when DNA is damaged faster than it can be repaired. Folate assists with synthesis and repair of DNA. Folate also assists with methylation by increasing the SAMe in the cell. Cancer is thought to arise from excess expression of certain genes within DNA. Methylation quiets RNA replication and can help the cells regulate excess growth. Folate may be helpful in preventing breast cancer in women who drink alcohol. Sufficient folate intake has also been associated with lower colorectal cancer riskFOLATE AND VITAMIN B12
High levels of folic acid supplementation, especially above 1000 mcg daily, can mask symptoms of vitamin B12 deficiency. The addition of folic acid to food is risky because some people may get enough folic acid to hide the terrible effects of vitamin B12 deficiency on nerves. The addition of folic acid to grains is also controversial because it only helps prevent neural tube defects about half of the time.
FOLATE DEFICIENCY
Folate deficiency signs include anemia and deterioration of the gastrointestinal tract. The anemia results from abnormal blood cell division resulting in fewer and larger red blood cells. This type of anemia is called megaloblastic anemia, referring to the large immature red blood cells. Neutrophils, a type of white blood cell,
also can be abnormal. Symptoms of folate deficiency typically take a few months to develop and may result in fatigue from lower oxygen-carrying capacity of red blood corpuscles.
Folate deficiency can be caused by inadequate absorption, inadequate consumption, or unusually high metabolic needs for this vitamin. Drugs that can interfere with folate include aspirin, anticancer drugs, antacids, and oral contraceptives.Older people tend to have higher homocysteine levels and are encouraged to meet or exceed the RDA for folate.
FOLATE IN FOOD
Leafy green vegetables are the best sources of folate. Legumes are also high in folate; please refer to Graph 6. Other sources include fruit and enriched grains.
Summary for Folate
Main function: synthesis of DNA and red blood cells.
RDA: adults, 400 mcg; pregnant women, 600 mcg.
Tolerable upper intake level: 1000 mcg.
No toxicity reported from food.
Deficiency disease: neural tube defects, anemia, and excess folates may mask vitamin B12 deficiency.
Healthy food sources: leafy green vegetables and legumes.
Degradation: easily destroyed by oxygen and heat.
The RDA for folate as expressed in DFE (Dietary Folate Equivalents) is 400 mcg per day for adults. Atolerable upper intake level of 1,000 mcg per day was established by the Food and Nutrition Board to prevent the masking of vitamin B12 deficiency. Folate and folic acid are not toxic. Folate in food can be destroyed by heat, light, and air, as shown in Figure -20. Among the various cooking techniques, microwave cooking results in the greatest losses of folate. Coenzyme form: TetraHydroFolate (THF).
Figure -20 Folate losses in storage and cooking.
Graph 6 Folate amounts in some common foods.
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