B Vitamins

The B Vitamins--As Individuals• The B vitamins are very active in the body.

Several of the B vitamins form part of the coenzymes that assist enzymes in the release of energy.

• Other B vitamins participate in metabolism and cell multiplication.

• Recommendations for the B vitamins come from RDA, AI, and Tolerable Upper Intake Levels.

• There are deficiencies, toxicities and food sources that are unique for each vitamin.

Thiamin (vitamin B1)• Antiberiberi or antinatriuretic vitamin.• Essential for carbohydrate utilization.• Specific coenzyme form is thiamine

pyrophosphate (TPP) • TPP is intimately connected with energy

releasing reaction in carbohydrate metabolism.

Sources & RDA• Occurs mostly in all natural foods.• Important sources are: whole and enriched

grains, cereals, wheat, yeast, pulses, legumes, oilseeds & groundnut, meats (pork), milk, and eggs.

• Milk is important source for infants. • RDA (adults): From 1.2 to 1.5 mg daily

intake is recommended The RDA, which is higher with a diet high in refined carbohydrates, decreases slightly with age.

©2001 Brooks/Cole, a division of Thomson Learning, Inc. Thomson Learning™ is a trademark used herein under license. Thiamin

Pork is the richest source of thiamin, but

enriched or whole-grain

products typically make

the greatest contribution to a day’s intake because of the

quantities eaten.

Functions of Thiamin (vitamin B1)

• Thiamin pyrophosphate (TPP) is required for proper nerve transmission. TPP is the coenzyme for several key enzymes.

• a. Pyruvate and the alpha -ketoglutarate dehydrogenases (glycolysis and the citric acid cycle)

• b. Transketolase (the pentose phosphate pathway)

• c. Branched-chain keto-acid dehydrogenase (valine, leucine, and isoleucine metabolism)

Thiamin (TPP) - Vit BThiamin (TPP) - Vit B11

- involved in the- involved in theconversion of pyruvateconversion of pyruvateto acetyl-CoAto acetyl-CoA

- deficiency results- deficiency resultsin a condition knownin a condition knownas beriberias beriberi

- damage to nervous- damage to nervoussystem, brain function,system, brain function,heart and muscles.heart and muscles.

• Thiamine deficiency is seen – Classically - in people subsisting on polished

rice, – alcoholics, – cancer victims who do not eat, – women with extreme vomiting of pregnancy, – children and adults who have been starved.

• Deficiency leads to beriberi• Biochemically - Carbohydrate metabolism is

impaired so that pyruvate accumulates in the tissue. Plasma pyruvate concentration rises and it is also excreted in urine.

• There is also accumulation of lactic acid in body fluids. Accumulation of pyruvate in the brain is responsible for the polyneuritis seen in beriberi.

• Clinically - impairment of the cardiovascular, nervous, and gastrointestinal systems.

• Beriberi occurs in three stages:• a. Early: loss of appetite, constipation and

nausea, peripheral neuropathy, irritability, and fatigue

• b. Moderately severe: Wernicke-Korsakoff syndrome (seen in chronic alcoholics), which includes mental confusion, ataxia (unsteady gait, poor coordination), and ophthalmoplegia (loss of eye coordination)

Wernicke-Korsakoff syndrome• Wernicke’s Encephalopathy• Most common CNS-related neurological problem

in alcoholics. Seen in chronic alcoholics as body demand for thiamine is increased in them.

• Characterised by loss of memory, rhythmical to & fro motion of the eyeball.

• Wernicke syndrome responds dramatically to thiamine administration.

• Thiamine has also been successfully used to treat depression.

• Wernicke syndrome – Gait disturbance- ataxia of gait – Nystagmus - weakness of eye movement– Ophthalmoplegia – Mental disturbanceKorsakoff syndrome is a more advanced stage

than Wernicke syndrome – Short term memory loss– “Compensatory” confabulation

• C. Severe• (1) “Dry beriberi” includes all of the signs and

symptoms in a and b plus more advanced neurologic symptoms, with atrophy and weakness of the muscles (e.g., foot drop, wrist drop). Dry beriberi is characterised by neurological disorders - peripheral neuritis.

• (2) “Wet” beriberi includes the symptoms of dry beriberi in combination with generalized edema (as shown in the next slide) acute high-output cardiac failure, and pulmonary congestion. The dilated cardiomyopathy of wet beriberi responds promptly to thiamine administration.

• (3) Infantile form

• Infantile beriberi• Infants under 6 months of age receiving

inadequate thiamine in milk.• In acute form, - dyspnea and cyanosis death

from cardiac failure.• Aphonia may be present and the infant may

appear to be crying without emitting much sound.

• Diarrhea, wasting, vomiting and edema may be present

• There is NO known toxicity for this vitamin.

• Oxidative decarboxylation of α-keto acids

• Transketolase reaction

THIAMINE PYROPHOSPHATE

THIAMINE PYROPHOSPHATEDEFICIENCY (BERIBERI)

EARLIEST SYMPTOMS• Constipation• Appetite

suppression• Nausea• Mental depression• Peripheral

neuropathy• Fatigue

CHRONIC DEFICIENCY• Severe neurological

symptoms• Ataxia• Mental confusion• Loss of eye

coordination• Cardiomegaly• Cardiac failure• Musculature defects

WERNICKE-KORSAKOFF SYNDROME•Amnesia •Encephalopathy

Riboflavin (Vit B2) Riboflavin Coenzymes:

– Flavin mononucleotide (FMN) and – Flavin adenine dinucleotide (FAD)

• Play important role in maintaining integrity of mucocutaneous structure.

• Have a fundamental role in cellular oxidation.

Sources & RDA• Rich food sources include liver, kidney, meat,

eggs, green leafy vegetables, milk, enriched and whole grain breads and cereals.

• Richest natural source are milk, egg,, & green leafy vegetables

• Meat & fish contain small amounts.• RDA (adults): 1.1 to 1.3 mg• The allowance recommended for adults is 0.6

mg /per 1000 kcal and not less than 1 mg per day to maintain tissue saturation.

• 1.2-1.7mg/day for adults & higher intakes for pregnancy & lactation.

• Function. • Riboflavin is converted to the oxidation—

reduction coenzymes flavin aclenine dinucleotide (FAD) and flavin adenine mononucleotide (FMN).

Deficiency signs and symptoms• Deficiency - usually deficiency of B-complex.• Ocular symptoms- eye strain and fatigue, itching, burning,

and sensitivity to light may precede other symptoms. • Angular stomatitis and cheilosis/ cheilitis (inflammation

and cracking at the corners of the mouth or at the corners of the lips.)

• Glossitis, or a red and swollen tongue• Scaly dermatitis, particularly at the nasolabial folds and

around the scrotum• Localized seborrheic dermatitis of the face, hands (glove

dermatitis) • Behavioral changes have been reported• There is NO known toxicity for this vitamin.

B2 - FLAVIN NUCLEOTIDESThey are derivatives of riboflavin or vitamin B2

• Flavin Mononucleotide (FMN)• Flavin Adenine Dinucleotide (FAD)

Riboflavin (B2)Riboflavin (B2)

FMN - FLAVIN MONONUCLEOTIDE

• FMN• Riboflavin• Dehydrogenation of

two consecutive carbon atoms

• Dehydrogenation of NAD+ in Electron Transport Chain

Riboflavin (B2)FMN

FAD - FLAVIN ADENINE DINUCLEOTIDE

• FAD• Riboflavin• Dehydrogenation

of two consecutive carbon atoms

AriboflavinosisRiboflavin (B2)FMNFAD

B2 - ARIBOFLAVINOSIS•Glossitis•Seborrhea•Angular stomatitis•Cheilosis•Photophobia

•It is rare in USA and other developed countries due to the presence of adequate amounts of the vitamin in the diet.

•It is often seen in chronic alcoholics

•Riboflavin decomposes when exposed to visible light. This characteristic can lead to a deficiency in newborns treated for hyperbilirubinemia by phototherapy.

• Vitamin B6 (pyridoxine, pyridoxamine, and pyridoxal)

• The term Vitamin B6 is used to collectively represent 3 compounds namely-

i) Pyridoxineii) Pyridoxaliii) Pyridoxamine

Sources & RDA• Vitamin B-6 is widespread in nature.• Rich sources include yeast, whole grain cereals,

whole wheat, legumes, nuts and seeds, vegetables, liver, lean meat, fish, corn, egg yolk, and milk.

• RDA (adults): 1.3 to 1.7 mg • Recommended daily requirement for adults is

about 2-2.2mg per day. • Pregnancy,lactation & old age: 2.5mg/day.• The drugs isoniazid and penicillamine increase

the requirement for vitamin B6.• Toxicity in humans has been described when

taken at extremely high doses.

Function of Vitamin B6 (pyridoxine, pyridoxamine, and pyridoxal)

• Pyridoxal phosphate and pyridoxamine phosphate are coenzymes

• Pyridoxal phosphate is the coenzyme involved in transamination and other reactions of amino acid metabolism.

• Biochemical functions promoted is amino-group transfer. • synthesis and catabolism of amino acids,• synthesis of neurotransmitters, porphyrins and niacin.• PLP enzyme catalyzes transaminations, decarboxylations,

deaminations, racemizations and aldol cleavages and condensations, transsulfuration.

• Clinical usefulness. High doses of vitamin B6 are used to treat homocystinuria resulting from defective cystathionine ~3-synthase.

• Prolonged high intake (> 500 mg/day) (except as in 5.) may lead to vitamin B6 toxicity with sensory neuropathy.

• Deficiency is manifested by 3 different types of symptoms.

• neuropathic: due to insufficient neurotransmitter synthesis.

• anemic: due to low porphyrin synthesis• pellagrous: due to low endogenous niacin

synthesis. (Clinical symptoms similar to B2)

• Deficiency: Peripheral neuritis.

Deficiency • a. Mild: irritability, nervousness, and

depression• b. Severe: peripheral neuropathy and

convulsions, with occasional sideroblastic anemia

• c. Other symptoms: eczema and seborrheic dermatitis around the ears, nose, and mouth; chapped lips; glossitis; and angular stomatitis

PYRIDOXAL AND PYRIDOXAMINE

PHOSPHATE

• Glycogenolysis• METABOLISM OF AMINO ACIDS

RacemizationTransaminationNon-oxidative deamination

• DISEASE: NeuritisIsoniazid (to rx TB)Penicillamine

Pyridoxol

Pyridoxal

Pyridoxamine

Pyridoxal Phosphate

Pyridoxamine Phosphate

• Pyridoxine (Vit B6)

PANTOTHENIC ACID• Source: very widespread in food• Adequate intake (adults): 5 mg/d• Function. Pantothenic acid is an essential

component of coenzyme A (CoA) and the phosphopantetheine of fatty acid synthase

• Deficiency (very rare), with vague presentation that is of little concern to humans

COENZYME A

• Transfer of acyl groupsPantothenic acid

CoA-SH

• NO DISEASE

Niacin (nicotinic acid) and niacinamide (nicotinamide)

Niacin (Vitamin B-3, nicotinic acid)

• Coenzymes: – nicotinamide adenine dinucleotide (NADH) – nicotinamide adenine dinucleotide phosphate

(NADPH)

Sources & RDA• Whole grain and enriched breads and cereals, milk,

meats (liver, kidney, poultry) fish, legumes, groundnuts, and peanuts.

• Synthesized from dietary tryptophan.• Part of the niacin requirement is met by synthesis of

niacin from tryptophan. Corn is poor in niacin and tryptophan

• RDA: 14 to 16 mg of niacin or its equivalent (60 mg tryptophan = 1 mg niacin)

• Adults: 15-20mg/day• Children: 10-15mg/day

Niacin• Niacin is converted to the oxidation—reduction

coenzymes nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP).

• NAD+, NADH is an essential enzyme systems concerned with oxidation and reduction in living cells.

• Essential for carbohydrate, protein & fat metabolism.• Essential for normal functioning of skin, intestinal &

nervous system.• Niacin or nicotinic acid is known as pellagra

preventive(PP) factor.

• Mild deficiency results in glossitis of the tongue.• Severe deficiency or pellagra • involves the skin (photosensitivity), gastrointestinal

tract and central nervous system • is characterized by the three Ds: dermatitis, diarrhea,

and dementia and rarely the 4th D = Death • Endemic in the southern US (corn belt) and many

other parts of the world in the early 1900s, particularly among children.

• Pellagra was carried to Europe in the years following Columbus' discovery of the new world as maize (corn) was discovered and became the staple for Europe's poor.

• Largest outbreak since WW2 – refugees in Malawi

• Hartnup disease: caused by

malabsorption of tryptophan

• High doses (2 to 4 g/day) of nicotinic acid (not nicotinamide) result in vasodilation (very rapid flushing) and metabolic changes such as a decrease in blood cholesterol and low-density lipoproteins.

• Therapeutic uses of niacin:• Niacin is used as a drug to lowers cholesterol

levels i) Inhibits lipolysisii) Triacylglycerol synthesis in liver is decreased.

NIACIN (B3 or PP)

Nicotinic acid Nicotinamide

• NAD+ & NADP+

Hartnup diseaseCarcinoid syndromeIsoniazid

• Oxidation of one carbon atom

PELLAGRA• Glossitis• Dermatitis• Weight loss• Diarrhea• Depression• Dementia

Other Causes of Deficiency

NICOTINAMIDE ADENINE

DINUCLEOTIDE

• NAD+

• Oxidation of one carbon atom

• Feed the Electron Transport Chain

Hey, look at me!!!!

NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE

• NADP+

• Oxidation of one carbon atom

• Most important source of reduction equivalent for synthesis

Hey, look at me!!!!

•Biotin

• Sources and requirement:• Biotin is present in most food such as organ

meats, egg yolk, legumes, nuts, and chocolate.• It is also synthesized by the intestinal bacterial

flora. • A recommended allowance has not been

established.• Adequate intake: 30 rig/day.• Biotin supplements are required during

prolonged parenteral nutrition and in patients given long-term high-dose antibiotics.

• Biotin has no toxicity.

Function• Covalently linked biotin (biocytin) is the

prosthetic group for carboxylation enzymes (e.g. pyruvate carboxylase, acetyl CoA carboxylase).

• carrier of activated CO2 (carboxyl transfer)

• participates in conversion of pyruvate to oxaloacetate (gluconeogenesis) and in fatty acid synthesis

• Nutritional biotin deficiency is rare• a. Signs and symptoms include dermatitis, hair loss

(alopecia), atrophy of the lingual papillae, gray mucous membranes, muscle pain, paresthesia, hypercholesterolemia,and electrocardiographic abnormalities.

• b. Raw egg whites induces a biotin deficiency because it contains a protein avidin, that specifically binds biotin in a nondigestible form that prevent its absorption from the intestine.

• People who consume approximately 20 egg whites per day may develop biotin deficiency.

• Patients on long term high dose antibiotics without biotin suplementation also get biotin deficiency

ALOPECIA

BIOTIN• Biocitin• ATP dependent

carboxylation reactions• Transcarboxylation

DISEASE IS UNCOMMON

•Deficiency of biotinidase•Raw eggs (avidin)•Antibiotics

•Dermatitis•Loss of hair•Paralysis

The Hematopoietic Vitamins

Folic acid, B-12 Hematopoiesis

+ neuro’ symptoms

NO neuro’ symptoms

Folic acid (pteroylglutamic acid, folacin)

• Recommended name: FOLATE• Alternative name: FOLACIN• Coenzyme form: tetrahydrofolic acid

Important for carbohydrate metabolism

Sources & RDA• Main source is dark green leafy vegetable but also found in

liver, kidney, meat, dairy products, egg, citrus fruits & whole grain cereals, lima beans, asparagus, nuts, legumes and yeast.

• Adult: 200 mcg/day• Pregnancy: 400mcg/day• Lactation: 300 mcg/day• RDA: 400 mcg/day• The minimum need for adults is believed to be approximately

0.05 mg per day. Higher levels are recommended for children and during pregnancy.

• No toxicity has been observed

©2001 Brooks/Cole, a division of Thomson Learning, Inc. Thomson Learning™ is a trademark used herein under license. Folate(Folic Acid)

Leafy green vegetables,

legumes, liver, and

some fruits are

naturally rich in folate.

Folate (Folic acid)Folate (Folic acid)

- involved in the synthesis of DNA, - involved in the synthesis of DNA, especially in newly formed cellsespecially in newly formed cells

- deficiency results in anemia and GI - deficiency results in anemia and GI tract deteriorationtract deterioration

- in the developing fetus, neural - in the developing fetus, neural tube defects have been linked to low tube defects have been linked to low folate levelsfolate levels

• Biochemical function • Polyglutamate derivatives of

tetrahydrofolate derivatives serve as donors / coenzymes in transfer of one-carbon units

• in purine and pyrimidine biosynthesis • thymidylate synthesis • biosynthesis of aminoacids i.e conversion

of homocysteine to methionine, and serine—glycine interconversion

Deficiency occurs simply from a poor diet, Commonly found during pregnancy & lactation when the requirement increases.

– Inhibition of DNA synthesis • This leads to an arrest of cells in S phase and a

characteristic "megaloblastic" change in the size and shape of the nuclei of rapidly dividing cells (RBC precursors)

• Megaloblastic RBCs – hemolytic anemia– Often induced by anti-folate chemotherapy drugs

(aminopterin, methotrexate) – 50% and 70% of the birth defects in this country could

be eliminated if all pregnant women took folic acid supplements during pregnancy.

– The average diet includes only about half the required amount

• Deficiency signs and symptoms• a. Megaloblastic anemia, similar to that of vitamin B12

deficiency, as a consequence of blocked DNA synthesis (with glossitis, cheilosis, diarrhoea, distension & flatulence

b. Neural tube defects as a result of maternal folate deficiency (in some cases).Deficiency in pregnant women may cause neural defects in foetus.

• c. Severe folate deficiency may cause infertility & sterility. • d. Elevated blood homocysteine, which is associated with

atherosclerotic heart disease, with folate and vitamin B6 deficiency (in some cases)

• e. Several drugs can lead to folate deficiency, including methotrexate (cancer chemotherapy), trimethoprim (antibacterial), pyrimethamine (antimalarial), and diphenylhydantoin and primidone (anticonvulsants).

TETRAHYDROFOLATE

• Transfer of one carbon atom fragment with different oxidation status

• Very important in the synthesis of nucleotides

• DISEASE: Megaloblastic anemia

COFACTORS FROM TETRAHYDROFOLATE

Vitamin B12 (cobalamin)

Sources & RDA• Vitamin B12 is not found in plant foods because plants cannot

synthesize B-12 It is the only vitamin which is synthesized by micro-organisms & not by plants & animals.

• B12 comes from bacteria in animals. Intestinal bacteria can synthesize B-12 (in colon), but the site of synthesis does not allow absorption.

• Vegan Sources: nutritional yeast, fortified cereals, fortified soy milks and soy products

• Best sources meat,liver, kidney, fish, whole milk and other dairy products , eggs, oyster, shellfish, shrimp, pork and chicken.

• Only water-soluble vitamin that can be stored • Liver is main storage site of vitamin B12, enough for a 3 year

supply• Normal adults: 1 mcg/day Pregnancy: 1.5 mcg/day• Lactation: 1.5 mcg/day Infants & children: 0.2 mcg/day

• Vit B12 is also known as anti-pernicious anemia vitamin • Intrinsic factor produced in stomach facilitates transport from

gut to blood• To be utilized the B-12 must first be removed from the

protein by acid hydrolysis in the stomach or trypsin digestion in the intestine.

• It then must combine with "intrinsic factor", a glycoprotein secreted by the stomach, which carries it to the ileum for absorption.

• Patients with pernicious anemia lack the intrinsic factor. • Pernicious anemia in elderly patients may be caused by lack

of gastric acid• Deficiency of IF (can be autoimmune) can result in B12

deficiency• Possible to get deficiency if vegetarian, but rare• In food B-12 (extrinsic factor) usually occurs bound to

protein.

• Functions of Vitamin B12 (cobalamin)It has separate biochemical role, unrelated to folate, in synthesis of fatty acids in myelin.

• Catalyzes 1,2 shift of hydrogen atoms • a. Deoxyadenosyl cobalamin is the coenzyme for the

conversion (isomerisation) of methyl-malonyl CoA to succinyl CoA (methylmalonyl CoA mutase) in the metabolism of propionyl CoA.

• b.Methylcobalamin is the coenzyme for methyl group transfer between tetrahy-drofolate and methionine (homocysteine methyl transferase) in the synthesis of methionine from homocysteine.

• (Transfer of methyl-group from N5-methyl tetrahydrofolate to homocysteine to form methionine.)

• c.Formation of collagen• d.Facilitates absorbtion of iron from vegetable foods.• e.Inhibits nitrosamine formation by intestinal mucosa.

• Causes of vitamin B12 deficiency• Deficiencies of B-12 are extremely rare • a. Intake of no animal products. Long-term

vegetarians (vegans) are at risk for vitamin B12 deficiency.

• b. Severe malabsorption diseases.• c. Impaired absorption [from achlorhydria (insufficient

gastric hydrochloric acid), decreased secretion of gastric intrinsic factor, impaired pancreatic function]

• d. Up to 20 percent of older people may exhibit diminished B12 absorption and require supplements due to insufficient production of intrinsic factor and/or HCl in the stomach

Deficiency: In man there are two major symptoms associated

with B-12 deficiency, hematopoietic and neurological.

– Hematopoietic – • megaloblastic anemia.

– Neurological – • progressive demyelination of nervous tissue.

Deficiency signs and symptoms• Pernicious (megaloblastic) anemia similar to

that in folate deficiency• Neuronal degeneration & demyelination of

nervous system with paresthesia (numbness and tingling of the extremities), with weakness and other neurologic changes

• Prolonged deficiency leads to irreversible nervous system damage.

• Infertility in animal species.

DISEASE:• Pernicious anemia• Megaloblastic anemia• Nerve demyelinization

Elevated urine methylmalonate levels

• Rx is B12 injections

B12 - ADENOSYL COBALAMINEREACTIONS:• Metabolism of one carbon atom fragment• Isomerization of methylmalonyl-CoA

The B Vitamins--In Concert

• The B Vitamins are interdependent. The presence of one may affect the absorption, metabolism and excretion of another.

• A deficiency of one may affect the functioning or deficiency of another.

• A variety of foods from each food group will provide an adequate supply of all the B vitamins.

The B Vitamins--In Concert

• B Vitamin Roles– Coenzymes involved directly or indirectly with

energy metabolism– Facilitate energy-releasing reactions– Build new cells to deliver oxygen and

nutrients for energy reactions

The B Vitamins--In Concert

• B Vitamin Deficiencies– Deficiencies rarely occur singly except for

beriberi and pellagra.– Can be primary or secondary causes– Glossitis and cheilosis are two symptoms

common to B vitamin deficiencies.• B vitamin toxicities can occur with

supplements.

The B Vitamins--In Concert

• B Vitamin Food Sources– Grains group provides thiamin, riboflavin,

niacin and folate.– Fruits and vegetables provide folate.– Meat group provides thiamin, niacin, vitamin

B6 and vitamin B12.– Milk group provides riboflavin and vitamin B12.

B Vitamins The B Vitamins--As IndividualsSlide 3Slide 4Slide 5Sources & RDASlide 7Slide 8Functions of Thiamin (vitamin B1) Slide 10Slide 11Slide 12Slide 13Wernicke-Korsakoff syndromeSlide 15Slide 16Slide 17Slide 18THIAMINE PYROPHOSPHATETHIAMINE PYROPHOSPHATE DEFICIENCY (BERIBERI)Slide 21Slide 22Slide 23Slide 24Deficiency signs and symptomsSlide 26B2 - FLAVIN NUCLEOTIDESFMN - FLAVIN MONONUCLEOTIDEFAD - FLAVIN ADENINE DINUCLEOTIDESlide 30B2 - ARIBOFLAVINOSISSlide 32Slide 33Function of Vitamin B6 (pyridoxine, pyridoxamine, and pyridoxal) Slide 35Slide 36Deficiency PYRIDOXAL AND PYRIDOXAMINE PHOSPHATESlide 39COENZYME ASlide 41Niacin (Vitamin B-3, nicotinic acid)Slide 43Slide 44NiacinSlide 46Slide 47Slide 48Slide 49Slide 50NIACIN (B3 or PP) NICOTINAMIDE ADENINE DINUCLEOTIDENICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATESlide 54Slide 55FunctionSlide 57Slide 58BIOTINThe Hematopoietic VitaminsSlide 61Slide 62Slide 63Slide 64Slide 65Slide 66Slide 67Slide 68Slide 69TETRAHYDROFOLATECOFACTORS FROM TETRAHYDROFOLATESlide 72Slide 73Slide 74Slide 75Slide 76Slide 77Slide 78Slide 79Slide 80Slide 81The B Vitamins--In ConcertSlide 83Slide 84Slide 85Slide 86Slide 87