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B-VITAMINS
Working individually and in concert
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Relationship with Energy Metabolism

• Vitamins do not provide the body with fuel for energy
• However, they can work as coenzymes
• Assist enzymes with release of energy
• Without coenzyme, an enzyme cannot function
• B-vitamins assist enzymes that unlock energy from our energy-
yielding nutrients
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Function of a Coenzyme
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Thiamin
• Part of coenzyme thiamin pyrophosphate (TPP)
• Energy metabolism
• Conversion of pyruvate to acetyl CoA in glucose metabolism
• Participates in citric acid cycle in mitochondria
• Essential for nerve activity and muscle activity
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Thiamin
• Deficiency
– Malnourished and alcoholics
– Beriberi
• Dry – nervous system
• Wet – cardiovascular system

• Toxicity
– No adverse effects
• No UL

• Prolonged cooking destroys thiamin

• Leaches into water when boiling or blanching foods
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Food Sources of Thiamin

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Riboflavin
• Serves as coenzyme in energy metabolism
– Flavin mononucleotide (FMN)
– Flavin adenine dinucleotide (FAD)
• Carries hydrogen atoms and their electrons to electron transport chain
• Each time it does this, 2 molecules of ATP are generated
• Deficiency
– Inflammation of membranes
• Toxicity
– No UL
• Destruction of riboflavin
– Ultraviolet light (thus the opaque containers for milk)
– Irradiation
– Not destroyed by cooking
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Food Sources of Riboflavin

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Niacin
• Two chemical structures
• Nicotinic acid
• Nicotinamide
• Major form of niacin in blood

• Two coenzyme forms participate in metabolic reactions

• Nicotinamide adenine dinucleotide (NAD)
• Carries hydrogen atoms and their electrons to electron transport chain
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Niacin
• Deficiency
• Pellagra
• Symptoms: 3 Ds
• Diarrhea
• Dermatitis
• Dementia

 Toxicity
 Naturally occurring: no harm
 Supplements or drugs
 “Niacin flush”
 Nausea, vomiting, liver damage, glucose intolerance
 Potential health benefits of large doses of nicotinic acid: may
lower LDL cholesterol
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Food Sources of Niacin

Niacin is tolerant to heat but can be lost in cooking water

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Biotin
 Coenzyme critical in citric acid cycle
 Facilitates first step in cycle (entry point for acetyl-CoA
Participates in breakdown of fatty acids and amino
acids
 Participates in gluconeogenesis and fatty
acid synthesis
 Deficiency is very rare, no known toxicity
 Widely distributed in foods, needed in small amounts
(30 mcg/day)
 Raw egg white consumption
 Deficiency symptoms: hair loss, rash, neurological
impairment
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Pantothenic Acid
 Part of chemical structure of coenzyme A
 Entry point into many metabolic pathways
 Involved in >100 different steps in synthesis of lipids,
hormones, neurotransmitters, and hemoglobin
 Deficiency is rare, no known toxicity
 Symptoms: failure of all body systems, fatigue, GI distress,
neurological disturbances
 Food sources
 Widely available in meats, whole grains, potatoes, egg yolks,
broccoli
 Easily destroyed in food processing: freezing, canning, refining
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Vitamin B6
 Three forms
 Pyridoxal, pyridoxine, and pyridoxamine
 All converted to coenzyme pyridoxal phosphate
(PLP)
 Amino acid metabolism
 Urea metabolism
 Conversion of tryptophan to niacin or serotonin
 Synthesis of heme, nucleic acids, & lecithin
 Influences cognitive performance, hormone activity,
and immune function
 Stored extensively in muscle tissue
 Large doses do not enhance muscle performance!
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Vitamin B6
 Deficiency
 Impacts amino acid metabolism
 Abnormal compounds made from tryptophan accumulate in
brain
 Early signs: depression, confusion
 Advanced symptoms: abnormal brain wave patterns,
convulsions
 Alcohol: increases breakdown and excretion of PLP
 Isoniazid (anti-tuberculosis med): B6 antagonist
 Toxicity: only from supplements
 Can cause irreversible nerve degeneration
 In food
 Small amounts in lots of foods
 Lost when food is heated
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Food Sources of B6
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Folate
 Known as folacin or folic acid
 Primary coenzyme form – THF
(tetrahydrofolate)
 Transfers single-carbon compounds
during metabolism (methlyation)
 Converts vitamin B12 to coenzyme form
 Involved in DNA synthesis
 Needed for cell division
 Helps process amino acid homocysteine
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Folate
 Folate disposal from body
 Secretion by liver into bile
 Can be recycled via enterohepatic circulation
 Vulnerable to GI tract injuries
 Depletion occurs rapidly with alcohol abuse
 Leads to greater tissue damage, greater losses (and
impaired absorption of other nutrients, too)
 Bioavailability
 Synthetic form (folic acid) 1.7x more bioavailable than
natural form (folate)
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Folate Status and Birth Defects

• Needs rise during pregnancy
• Closure of neural tube, from which brain and spinal cord
develop, occurs during first few weeks
• Low folate status in mother can cause brain and spinal cord
disorders, and even death of infant/fetus
• Rate of neural tube defects has declined since folate
fortification began in 1996
• Adequate folate status may also prevent cleft lip or palate
• Supplementation or careful monitoring of dietary
folate adequacy recommended for all women of
childbearing age
• To get 400 mcg/d, at least 5 servings of fruits and vegetables
recommended
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Folate
 Deficiency
 Impairs cell division and  Toxicity
protein synthesis
 Can occur from natural or
 Red blood cells and GI tract supplemental/fortified sources
cells falter
 Anemia  Primary concern: can mask B12
 GI tract deterioration
deficiency, since early signs of
B12 deficiency are usually due
 Primary deficiencies: due to to impaired folate activity
inadequate intake or
increased need  Food sources
 Secondary deficiencies: drugs  Heat and oxidation destroy
 Anti-cancer meds (folate folate
antagonists)
 Heavy use of aspirin or
antacids
 Oral contraceptives
 Smoking
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Food Sources of Folate

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Vitamin B12
 Vitamin B12 and folate depend on each
other for activation
 Very important for DNA synthesis, cell
replication
 Individual roles of vitamin B12
 Maintains myelin sheath, promotes normal
growth of nerve cells
 Involved in bone cell metabolism/activity
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Vitamin B12
 Digestion and absorption
 Stomach
 HCl acid and proteases release B12 from dietary protein
 Secretes intrinsic factor
 Small intestine
 Intrinsic factor binds to B12, absorbed as complex
 Enterohepatic pathway continuously recycles
B12
 In healthy individuals, deficiency is rare, since it is
constantly reabsorbed
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Vitamin B12
 Deficiency
 Inadequate absorption or intake
 Lack of hydrochloric acid or intrinsic factor
 Lack of animal foods
 Individuals at risk
 Older adults: atrophic gastritis
 Vegans
 Those with anemia of folate deficiency
 Symptoms of vitamin B12 deficiency
 Moderate: cognitive impairment
 Severe: creeping paralysis
 Toxicity unknown
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Anemia of B12 or Folate Deficiency

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Choline
 Manufactured from amino acid methionine in body
 When insufficient in diet, body alone cannot meet
needs
 Used to make neurotransmitter acetylcholine
 Supports neural tube closure and nervous system
development in fetus
 Common sources: milk, eggs, peanuts
 Deficiencies are rare
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B-Vitamins In Concert
 Each B-vitamin coenzyme is involved in energy
metabolism
 Some vitamins are necessary to activate others
 B12 and folate
 Riboflavin and B6
 Riboflavin, B6, and Niacin (synthesis from tryptophan)
 Deficiencies
 Single B-vitamin deficiencies seldom show up in
isolation
 Frank deficiency is rare in US, but suboptimal intake
is more common
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B-Vitamins in Concert