water soluble vitamins (b1, b2, b3, b5, b6, b7, b9, b12, c) and COQ10 Flashcards
B1 Thiamin
Function: TDP, TPP, Glycolysis, Energy metabolism, CHO metabolism, growth, wound function, mitochondria, neurologic, cardiac,
oxidative decarboxylation , can not generate cellular pathway without.
oxidative decarboxylation of pyruvate, alpha-ketoglutarate and 3 branched-chain amino acids (pyruvate from glycolysis to Acetyl-CoA), the in TCA cycle, also a role in the pentose phosphate pathway,
glycolysis, and branched amino acid catabolic pathway (into TCA cycle)
Antoagonists/Agonists:
Vitamin C prevents B1 oxidation
-fish, coffee, tea, berries, brussel sprouts & cabbage can destroy B1
-alcohol can decrease absorption
Other:
Agonist: Citric Acid.
Antagonist: Mg, Ca, Cu, Zn, Mn, Fe, Alcohol (ethanol).
Enhancers: Lipoic acid
Deficiencies: Beriberi, symptoms of muscle weakness, anorexia, tachardia, enlarged heart, edema,
Wernicke’s encephalopathy (often with alcoholics),
severe deficiency causes congestive heart failure (wet beriberi), peripheral neuropathy (dry beriberi), and Korsakoff syndrome (an often irreversible memory loss and dementia that can follow).
Absorption: needs some acidity, absorbed by the small intestine, brush border enzymes important.
Partners that help with absorption: Gluten sensitvity can reduce, diaminaces (raw fish, sushi) deficiency, Black teas (deficiency)
Storage: Do not store much , find it in the liver, muscles.
Excreted: Urine
Diagnostic: ETK
No toxicity
Therapy ranges: 2 mg-500 mg
Symptoms of excess: headache, seizure, ARrhythmia
Avoid: High histamine, anxiety
sources: meat, legumes, wheat germ, yeast.
RDA: Ch. .2-No UL
Adults: 1.0 mg - no UP
jumps in adolescents, males need more, no change in need from adolescent to old age.
Sources: Meat, legumes, wheat germ, yeast. Pork, Fish, muscles, blue fin tuna, Nuts, soymilk, sunflower seeds, flax seed.
supplement: thiamine HCL : 5-30 mg up to 500mg,
multivitamin or B complex.
Method of assessment in NFPE:
Hair, nails, wound healing, ataxia (clumsy movement)
coenzyme for energy
B2 Riboflavin
Function:-coenzymes FAD and FMN
-energy metabolism (redox reactions)
-metabolism of folate, Vitamin A, niacin, Vitamin B6, and Vitamin K
-neurotransmitter metabolism
-DNA synthesis
Metabolic pathway: Electron Transport Chain (hydrogen transfer reactions),
-Oxidative decarboxylation of pyruvate, and TCA cycle
-fatty acid beta oxidation
Immune system (as flavoprotein)
* Used by immunoglobulins to activate oxidation pathway that converts O2 into H2O2 to destroy pathogens
Energy transformation
* Acts as intermediate electron carrier when pyruvate dehydrogenase complex converts pyruvate to acetyl CoA and -ketoglutarate dehydrogenase complex converts -ketoglutarate to succinyl coA
* Reducing agent in TCA to convert succinate to fumarate
* Transfers electrons in electron transport chain.
Fatty acid beta oxidation (as flavoprotein)
* Acyl CoA dehydrogenases require FAD
Activating AND synthesizing other vitamins ***
* Vitamin B6 metabolism requires FMN for conversion to primary coenzyme form, pyridoxal phosphate (PLP)
* Synthesis of active folate form, 5-methyl-THF requires FADH2, enzyme is 5, 10-Methylenetetrahydrofolate reductase (MTHFR) (folate req’d to form methionine from homocysteine )
* Synthesis of niacin from tryptophan
* Deficiency alters iron metabolism but mechanism unclear
Neurotransmitters (dopamine) and amines (tyramine, histamine) (as flavoprotein)
* Require FAD-dependent monoamine oxidase
Protein structure and folding
* FAD dependent oxidases (Ero1 and sulfhydryl oxidases) form disulfide bonds in folding of secretory proteins, impaired folding with B2 deficiency
DNA synthesis (as flavoprotein)
* Acts as reducing agent in conversion reaction of ribonucleotides to deoxyribonucleotides
anatagonist: -can be destroyed with exposure to sunlight,Heating, alcohol, caffeine, fever, drugs, stress, processing, oral contraceptives, Tetracycline, Thyroid discord.
Other:
Antagonist:CU, Zn, Fe, Mn, alcohol
Enhancers/agonists: Phosphorus, Fiber
Deficiency disease:
Risks of deficiency
* Vegans, alcoholism –low intake
* Gallbladder removed and reduced bile
* Thyroid disease, diabetes, trauma, his stress b/c thyroid hormone needed to speeds flavokinase
* Homozygous mutation
* High homocysteine b/c of MTHF???
Deficiency signs
* Chelosis
* Tongue swelling
* Edema
* Inflammatory skin
* Peripheral nerve dysfunction
* DNA damage, protein damage
TESTS
* Measure erythrocyte glutathione reductase (FAD dep)
* Levels of FMN dep. pyridoxamine phosphate oxidse
* Cellular/urinary excretion
RDA:
Men-1.3mg
Women-1.1.mg
Pregnant-1.4mg
Lactation- 1.6mg
Food sources:Good
* Milk ( & cheese
* Eggs
* Meat
* Less in legumes, green veggies
Digestion
* Bound to amino acid histidine or cysteine, proteins are degraded in digestion but still attached to residues
* Must be converted to free riboflavin by FMN phosphatase
Absorption
* By saturable, energy dependent (ATP) sodium independent carrier in small intestine
* Bile facilitates absorption
Transport
* Travels to liver to be phosphorylated to FMN (req’s ATP and flavokinase) and FAD
* Albumin, Fibrogen and globulins transport in blood
Excretion
* Most excreted in urine in free or metabolite form, fluorescent yellow
Drug nutrient interaction: Antipsychotics, chemotherapy, anticonvulsants, gluthione reduce most of the medications, Need B2 to reduce them, Glutathione reductase, help body clear them, oral contraceptives.
coenzyme for food coloring
B3 Niacin
Metabolites
N’ methyl nicotinamide
coenzyme and blood lipid regulator
Forms:Plant foods-nicotinic acid
Niacytin (complex carbs)
Niacinogens-wheat, corn, bound to peptides
Animal foods-nicotinamide
Nicotinamide nucleotides (NAD+ and NADP+)
RDA: Men-16mg
Women-14mg
Pregnant-18mg
Lactation-17mg
Niacin equivalent: (Tryptophan conversion)
1g complete protein = 10mg tryptophan
60mg tryptophan=1mg niacin
Approx 6 g complete protein = 6mg niacin
Food sources:Tuna, Halibut, Beef, Pork, Chicken, Turkey, Beef liver
Veal
***Liver can synthesize from tryptophan w/ FAD, vit B6 (PLM) and iron
Biosynthesized from tryptophan
Digestion/absorption/secretion:
Digestion
* NAD converted to free nicotinamide by hydrolyzation
Absorption
* NAD and NADP needed to enable absorption??
* Nicotinamide and nicotinic acid absorbed mostly in sm. Intestine by sodium dependent carrier mediated diffusion
Transport
* In blood, nicotinic acid bound to plasma proteins
* Liver synthesizes NAD from nicotinamide
Excretion
* Degradation to ADP ribose & nicotinamide and then methylated & oxidized for excretion
nutrient drug interaction:
* Deficiency in vitamin B6 or tryptophan can cause niacin deficiency
* Anti-Tuberculosis drugs inhibit enzyme activie for niacin synthesis
Function:
NAD, coenzyme, acts reducing agent in energy transformation reactions
* Glycolysis (energy transformation)
* Oxidative decarboxylation of pyruvate to acetyl CoA (part of dehydrogenase pyruvate complex) and -ketoglutarate dehydrogenase complex converts -ketoglutarate to succinyl coA
* Citric acid cycle – oxidation of acetyl CoA
* oxidation of fatty acids
* Oxidation of ethanol
Key for catabolism and excretion of vitamin B6
NADP reduced to NADPH used in many processes:
* Fatty acid synthesis
* Cholesterol and steroid hormone synthesis
* Proline synthesis
* Deoxyribonucleiotide synthesis (DNA precursors)
* Glutathione, vitamin C and thioredox renegeration
* Folate coenzyme synthesis
Nonredox roles
* Donates adenosine diphosphate ribose for formation of cyclic ADP ribose which thought to act as second messenger and mobilization of calcium from intracellular stores, esp. in neurons
Deficiency, toxicity, tests
Deficiency – 4 D’s
* Dermatitis
* Dementia
* Diarrhea
* Death
At risk of niacin deficiency:
* Alchoholism-due to low intake
* Malabsorption like IBS, chronic diarrhea due to impaired absorption
TESTS
* Measure 1+ urinary metabolites e.g., N’ methyl nicotinamide or of N’methyl nicotinamide/ 1 g of creatine (not best due to urinary creatine excretion)
* Measure urinary N’method 2-pyridone 5-carboxamide to N’methyl nicotinamide (NMN)
* Serum or RBC– NAD concentrations in erythrocytes or plasma concentrations of phyridone
Disease symptoms: Phamacological doses of niacin used to treat high blood cholesterol BUT side effects exist
* Flushing of face
* Red burning itching
* Gi issues
* High blood glucose
Inhibitors:
Stable and minimal loss from heat and storage
Pantothenic acid
Vitamin B5
Coenzyme for fatty acids
Food
* Mostly bound as component of CoA
* Free form too
Only 50% absorbed
RDA and risks:AI
Adults-5mg
Pregnancy-6mg
Lactation-7mg
Food sources: Meats
Liver
Egg yolk
Yogurt
Legumes
Mushrooms
Broccoli
Avocados
Royal jelly from bees
Digestion
* Hydrolyzed
* Dephosphorylated to pantetheine
* Converted to pantothenic acid
Absorption
* Passive diffusion in high concentrations
* Sodium dependent transporter (SMVT) in low concentrations
Transport
* Free form in RBCs, uptake to organ cells dependent on SMVT
* Excretion
* Intact via urine
Enhancer: Vitamin C, B vitamins
Inhibitor:*
Easily destroyed with heating or freezing
* Stable when dry and in neutral pH solution
Functions:
As coenzyme A
Energy transformation – TCA cycle
* Oxidative decarboxylation of pyruvate to acetyl CoA (B5 provides CoA) (part of dehydrogenase pyruvate complex) and -ketoglutarate dehydrogenase complex converts -ketoglutarate to succinyl CoA
Synthesis of cholesterol, ketone bodies, fatty acids and steroid hormones
* Acetyl-CoA and acetoacetyl-CoA form key intermediaries
Acetylation of some proteins and sugars
* Acetylation can activate/deactivate enzymes
* Prolong life of proteins or change structure and function
As acyl carrier protein (ACP)
* Key in fatty acid synthase complex which binds ands transfers acyl groups to sulfhydryl groups in the enzyme complex
Deficiency:
* Burning feet syndrome-numbness of toes and feet, corrected with calcium pantothenate administration
At risk:
* GI absorption
* Diabetes mellitus
* IBS
* Alcoholism
TESTS:
* Urinary (best)
* Blood levels change w/ dietary intake
High dose of biotin will not absorb B5.
Drug-nutrient interaction: oral contraceptives
supplement: pantothenate or pantothenic acid.
Therapy range: 250 mg- 6000 mg
Broad range of toxicity
Excess: possible diarrhea
Avoid in : Low histamine
deficiency symptoms: and assocated conditions: fatigue, nausea, depression, anxiety, restless inflammation, poor healing, fIBS, Neuralgia, Eczema, palpitations, edema, allergy, insomnia, Hives, urticaria, burning feet, toe walking, adrenal fatigue
B7 Biotin
Hair, nails, skin, fatty acid synthesis, gene expression, helps with blood sugar regulation, neurotranmitters, DNA, RNA synthesis.
Forms:Free biotin
Biotinyl peptides
Biocytin (bound to lysine, amino acid)
RDA:AI
Adults- 30 ug
Pregnant-35 ug
Lactation – 35 ug
Good sources:
Liver
Soybeans
Egg yolks
Legumes
Nuts
Canned salmon
Digestion
* Bound to protein or as biocytin
* Requires proteolysis by pepsin + intestinal proteases to release free biotin, biotinyl peptides or biocytin
Absorption
* Free absorbed in sm. Intestine via passive diffusion in low status, or sodium dependent carrier SMVT
* Synthesized by bacteria in colon, absorbed in transverse colon
Transport
* In plasma free or bound to albumin
* Small amount stored in liver, muscle, brain
Nutrient/drug interaction:* Anticonvulsant drugs can cause biotin deficiency
* Pregnancy may also produce deficiency
Function:As coenzyme in carboxylases, attached at active site
Creation of glucose/energy source
* Pyruvate catalyzed by pyruvate carboxylase to form OAA in gluconeogenesis
Fatty acid synthesis
* Acetyl CoA carboxylase is rate limiting enzyme that adds carbon to acetyl coA to form malonyl coA (requires Magnesium and ATP)
Breakdown of amino acids
* Propionyl-CoA carboxylase (mitochondria) catabolizes isoleucine, threonine and methionine into propionyl-CoA, requires ATP and Magnesium
* -methylcrontonyl CoA carboxylase catabolizes leucine
Genetic expression
* Over 200 human genes require biotin for expression, used in transcription of some genes and for translation of mRNAs
* Required for cells to progress normally through cell life
* Attaches to histones to avoid mutations???
Smoking in women
?
At risk:
* Alcoholism inhibits absorption
* IBS, GI issues due to absorption status
Genetic mutation – biotindase deficiency
* Seizures, developmental delays, dermatitis, acidosis
* cause propionyl CoA causes genetic disorder
Deficiency
* lethargy, pins and needles in extremities, reduced muscle toned, depression
* Red scaly dermatitis found around eyes nose and mouth
TESTS
* Plasma or urine concentration
interfere with B5
Biotin is bound to protein, and must be released by biotinidase (an intestinal enzyme) prior to being absorbed, colonic bacteria synthesized biotin (absorbed by colon)
excreted through urine
COQ10
a nutrient produced naturally in your body. A powerful antioxidant, it protects your brain, heart and muscles.
It’s mostly concentrated in the mitochondria, or the ‘powerhouse’ of the cell. That means it’s involved in energy production and powers biochemical reactions.” In addition, CoQ10 has anti-inflammatory properties.
Foods: Oily fish such as salmon, mackerel and sardines.
Eggs.
Nuts.
Chicken.
Organ meats, like livers, hearts or brains.
Whole grains
heart disease, cancer, diabetes and neurodegenerative diseases, like Parkinson’s or Alzheimer’s — can lead to lower levels of CoQ10.
ability to make COQ10 as you age goes down.
Migraines, Heart disease, statins
CoQ10/Ubiquinone (oxidized) + Ubiquinol (reduced)
Fat sol compound synthesized in vivo
Antioxidant
Cellular respiration, ATP production, ETC
Membrane stabilizer, Preserves myocardial NaKATPase activity
B6 Coenzyme for amino acid
extremely important in transamination or deamination in amino acids. conzyme for gaba and nuerotransmitters, Affects over >100 enzymes, homocysteine back to Methianine. B6 without being present = higher levels of kyneurinic acid.
Anemia: Microcytic
Most common
pyridoxal 5’-phosphate (PLP)
Vitamer forms
* Alchohol form
* Pyridoxine
* Aldehyde form
* Pyridoxal
* Amine form
* Pyrid-oxamine
Plants
* Pyridoxine, stablest, phosphoryl-ated form
Animal foods
* Pyridoxal
* Pyridoxamine
* Phosphorylated derivatives
Blood
* PLP
RDA
Men- 1.3 mg
51+ 1.3 mg
women 1.3 mg
51+ 1.5 mg
Pregnant 1.9mg
Lactation 2.0 mg
Food sources: fish, beans, nuts, meats, vegetables, Grains
Animal foods
* Steak
* Salmon
* Light meat chicken
Plants with high doses
* Banana
* Cooked broccoli
* Zucchini
* Raw carrots
Digestion: need alcalinity in small intestine to absorb.
Storage: Liver, bone, muscle,
* Dephosphorylated requires zinc to hydrolyze phosphate form yielding free pyridoxine (PN), pyridoxal (PL) and pyridoxamine (PM)
* Absorbed in free form into portal blood
Metabolism/transport
* Liver metabolizes Unphosphorylated forms by phosphorylating using ATP in cytosol of hepatocyte
* PNP and PMP are converted to the main vitamer PLP, requires adequate riboflavin (Vit B2)
* Intracellular PLP concentrations are dependent upon availability of binding proteins
* Unbound PLP is hydrolyzed to PL, released into blood for use by other tissues
* Bound to albumin
Storage
* Mainly muscles
* Liver 5-10%
excreted in urine.
Inhibitor:
Prolonged heating, milling of refined grains and more
Antagonist: Alcohol, Diuretics, caffeine, Drugs, OCP, HRT, Flax seed meal, Hydrazines, L.dopa, Isoniadid, D-penicillaine, HIV, liver disease, cancer, niacin
Nutrient/drug interaction*
Deficiency impairs niacin synthesis from tryptophan
* Inhibits metabolism of homocysteine (b/c req’d for methionine from cysteine)
Drugs increase deficiency
* Tuberculosis drugs
* Penicillamine to treat autoimmune and wilson’s disease – inactivates the vitamin
* Corticosteroids to suppress immune system – promotes loss from body
* Anticonvulsants-inhibits activity
* Oral contraceptives
Function:
As coenzyme
Amino acid metabolism
* Transamination- PLP or PMP acts as coenzyme for aminotransferases in transamination which transfers amino group from one amino acid to an -ketoacid used in synthesis of nonessential amino acids and carbon skeletons for glucose production (PLP acts as the Schiff base during removal binding to the remaining parts of amino acid)
* Deamination- PLP acts as coenzyme in deamination which removes amino acid from compound to release as ammonia or ammonium ion
* Transulfhydration- PLP req’d by two enzymes in transulfyhydration path creating methionine from cysteine, key for metabolism of homocysteine
* Transleenation – PLP dependent enzyme cleaves selenium to generate selenide and PLP enzyme generates selenide from selenocysteine
* Cleavage – removal of a hydroxymethyl group from serine to tetra hydrofolate (THF) so glycine is formed
* Racemization – required to catalzye the converstion of D and L amino acids
* Niacin- formation of niacin from tryptophan req’d PLP enzyme
* Formation of carnitine, taurine – PLP dependent reactions
Neurotransmitter metabolism
* Decarboxylation -PLP acts as coenzyme in decarboxylation reactions (removal of COO- from amino acid or other compound (e.g., GABA from glutamate, serotonin from 5-hydroxytryptopha, histamine from histidine, dopamine from dihdroxypheylalanine from tyrosine)
RBC formation
* Synthesis of heme – necessary coenzyme in 1st step
* Glycogen degradation (used for 50% of B6) – not well understood vitamin B6 is required for glycogen phosporylase which catabolizes glycogen to form glucose 1-PO4, most B6 found in muscle is bound to glycogen phosphorylase
Noncoenzyme role
Gene expression
* Binds to DNA and modulate steroid hormone binding or transcription factor binding
deficiency and toxicity
Deficiency symptoms
* Seborrheic rash on face, neck, shoulder and buttocks
* Weakness
* Fatigue
* Cheilosis
* Angular stomachitis
* Neurological issues including confusion, seizures and convulsions
GLossitis
At risk
* Elderly with poor intake
* Elderly w/accelerated hydrolysis of PLP and oxidation of PL??
* Alcoholics impairs conversion of PN and PM to PLP
Toxicity –w/high treatment levels (TI=100mg)
* Excessive phyrdoxine (>200mg/day) causes senory and peripheral neuropathy, tingling in extremities, impaired tendon reflexes
* 2g/day+ cause numbness in hands and feet, impaired motor control
* High intakes cause degeneration of spinal cord, loss of elimation and degeneration of sensory fibers in perpipheral nerve
TESTS
* Plasma levels of P5P (best)
* Common functional test
* Urinary B6 and urinary pyrdioxic acid
* Transaminase activity before/after B6 (l.t. status)
Homocysteine
Kyneurinic/Xanthurenic
Disease symptoms:
Used to treat:
- Hyperhomocysteinemia (high chomocysteine)
- Carpal tunnel
- Morning sickness
- PMS
- Depression
- Muscular fatigue
Anemia: microcytic, Insomnia, Inflammation, Poor growth, Neuralgia, malabsorption, Poor conv tryp> niacin, Hyperpigmentation, Dermatitis
RDA: Ch: .1 mg- UL30mg
Ad: 2.0 mg-UL 100mg
stages of life cycle: men and women need the same until 50. >50 higher for men in senior years. Higher need in lactation.
Therapy dosages: 10-500 mg
P5P 10-50 mg
Excess: reversible neuropathy,
Supplements: Pyridoxine HCl, P5P
Diagnostics test:
Transamination (the transfer of amine group to synthesize AA acids, such as a-keto acid for gluconeogenesis)
Morning Sickness, Hyperhomocystenemia, carpal tunnel, PMS, depression, pyridoxine dependent epilepsy
cheilosis/inflammation of mucous membranes of lips (also b2, b3)
Glycogen Phosphorylase (rate limiting enzyme; Needs B6, – Phosphoglucomutase (PGM)…converts G1P > G6P, Debranching enzymes
B6 needed by Glycogen Phosphorylase to shorten chain
Decarboxylation (the removal of COO= from AA or other compounds, such as Glutamate > GABA)
Neurotransmitter synthesis, AA & protein metabolism
B6 req for Glycogen phosphorylase (enzyme catabolizing glycogen to Glucose-1P)
X-linked Sideroblastic anemia —- (lack ALA synthase which req’ b6)
Heme Synthesis: b6 is coenzyme for the 1st step in Heme Synthesis for ALA-Synthase enzyme (Succinyl CoA + Glycine > 5-ALA)
Transulfhydration: Remethylation of THF after MTHF form is used to methylate Homocysteine (generating THF and Methionine)
B6 decreases effects of Anticonvulsants
Has effects on very uncommon drugs (TB, Penicillamine, Epileptic, Corticosteroids)
⭐ Adequate b6 decreases the need for b3/niacin (b/c b6 is req’ for synthesis of b3/niacin FROM Tryptophan also B2, Iron), B6 needs Riboflavin (b2) to be activated
Elevated Xanthurenic acid
B6 Inhibits biosynthesis of b1
B6 Inhibitors: MAO-inhibitors, Antituberculars (inhibit enzyme action req’ b6), Leucine (antagonizes b6 functions converting tryptophan > b3), Penicillamine,
Epileptic drugs, Alcohol (increases P5P catabolism), Milling/processing, Fiber, Contraceptives, Dyes
B6 def: dermatitis, brain wave abnormalities, cheilosis, glossitis (but also b2, b3), seborrheic rash, fatigue, neuro (confusion, seizures, convulsions)
B6 Toxicity: sensory neuropathy, ataxia, degeneration of neurons, extremity tingling/tendon reflexes, impaired motor control, degen of spinal cord, peripheral nerves,
painful/disfiguring dermatological lesions, photosensitivity, GI sx (nausea/heartburn)
Stay with 100 mg per day.
**large intakes may enhance immune function, ameliorate sx of PMS, carpal tunnel/asthma, morning sickness, high homocysteine** b6/P5P Food Sources: Chicken, Liver, eggs, Chickpeas, yeast, Nuts
Can be toxic at higher forms.
Use for P5P or blend.
Wont give you side effects but there is a limit of what you should take.
Hyperemesis: Helpful B6 and active form in Unisom reduces the chances of vomiting. 100 mg per day of B6.
Upper limit should be 100 mg per day.
CBC ( some RBC changes would indicate) and CMP (AST and ALT: low, will show you that you are possibly low in B6. AST and ALT can not happen without P5P)
Drug/nutrient interactions: Alcohol, diuretics, Drugs, OCP.
B9 (folate) coenzyme for DNA synthesis
Anemia: Macrocytic (immature Red blood cells) and Megalo
DNA synthesis , RBC synthesis, directly related to cell division and cell growth. bone health and bone tissue.
Reproduction, brain development, Amino acid metabolism.
Nural tube defects are due to not enough folate for cell division.
Clear catacholamines,
Digestion/absorption:
Bound up in plant matter, absorbed in Small intestine
Storage: Liver, bones,
excrete through urine:
pancreatic enzymes can reduce absorption
Help: vitamin C and riboflavin
Lifecycle stages: growth
> infancy into childhood (need more)
>adolescents to end of life (men and women need the same) 400 mcg
>pregnancy needs most (600 mcg)
>lactation 500 mcg
Transfer of 1-C unit
Primarily absorbed in Jejunum
Masks b12 deficiency (in the situation of Anemia….cannot decipher where anemia is coming from)
Drug/nutrient interactions:
1.NSAIDS (large doses impact folate)
Anticonvulsants (impairs bioavailability of folate)
2.Methotrexate (folate antagonist)
3. BCP (high dose estrogen)
Folate Def in elderly results from poor diet or use of drugs that impede folate absorption (antacids raise pH)
Food
* Folate, reduced form
Supplements + fortified foods
* Folic acid (oxidized form)
Biological tissues
* Folate, reduced from
Blood
* mono-glutamate forms: Folate, THF, 5-methyl THF, 10-formyl THF, dihyrofolate, formylated forms
RDA:
Adults – 400 ug
Pregnancy – 600 ug
Lactation – 500 ug
**Difference in bio-availability from food vs. supplements
Dietary folate equivalents
1 DFE = 1 ug of food folate = .6 of folic acid from supplement or fortified food
Food sources:Mushroom Green veggies, Spinach, Brussels, Broccoli
Peanuts, Beans, Lentils, Liver
Banana, Orange, Cantaloupe, orange juice, fortified and enriched foods.
Inhibitors:* Destroyed by heat, oxidation and exposure to U/V light
Inhibitors:
* Alcohol
* Compounds in legumes, lentils, cabbage and oranges diminish digestion enzymatic activity of polygutamate folate
-Alcohol, OCP, HRT, Phenobarbitol, Dilantin, Diuretic, Caffeine, Antacids, Tobacco, Def. Of B12, C, E
Deficiency risk:
* Alcoholism
* IBS, GI disorders due to digestion AND absorption issues
Deficiency result:
* Megloblastic macrocytic anemia –release of fewer, large, immature RBC cells
- Fatigue, weakness, shortness of breath, headaches, irritability, difficulty concentrating, neural tube defects in pregnancy. cognition changes. COMT gene relies. poor growth, fatigue, Glossitis, Neuroplathy.
You can overmethylate: hypersalivation,
Folate blend (methylated) ,
Deplin (15 mg of folate) psychiatrist, excentuates the antipsychotic meds. Antipsychotic meds use up folate fast.
Folate is a group: methylated, selenic acid,
- Treatment 1-5 mg/daily
Symptoms
TESTS:
* Give oral histidine and test FIGLU excretion, should be low if histidine converts to glutamate
* Serum + plasma level (intake effects)
* RBC concentration, better indicator (CBC lab)
* Deoxyurdine suppression – measures folate for thymidine synth.
* Plasma levels of homocysteine
Therapy: 200 mcg-10 mg
Preg: 1-3 mg
Do not dose methylated folate quickly, supplement slowly. Most people even with MTHFR gene change dont need
Nature folate, design for health blend.
Must balance out the methylated with unmethylated.
No toxic
Methotrexate(cancer or crohns), anti-epileptic
Vitamin C (ascorbic acid) antioxidant and collagen cofactor
Function: Antioxidant, Anti-histamine, immune, healing, collagen, Bone oxidation, vascular integrity, neurotransmitters function
Regenerates vitamin E , A,
REQUIRED FOR COLLAGEN
scurvy (bbreakdown of collagen)
Hair skin and nails (vitamin c with collagen) better outcome.
Amino acid makes carnetine: glycine and needs vitamin C.
Vitamin D: has to be hydroxylated, vitamin C is required for hydroxylated actions to occur.
Digestion, absorptions: small intestine, store a little in the liver, highest concentration in the adrenal glands.
Excretion: Urine
Life cycle :
Higher need in infancy than there is in childhood. higher in early teen, when you are an adult (highest)
Men need more than women, pregnant need more than nonpregnant and lactating need most.
smokers need more.
Antagonists: Toxins, oxidants, tobacco, aspirin, heating, caffeine, diuretics, cortisone , stress, illness, OCP, HRT< Pregn, Inflammation.
Enhancers: Bioflavnoids, L-carnitine
Deficiency symptoms: Bruising, bleeding, immune dysfunction, poor bone, healing, capillary fagility, joint pain, cataracts, gingivitis, periodontitis, depression, anxiety, anemia, cervical dysplasia, folate deficiency.
Reducing Agent (excess copper)
Vitamin C works in tandem with Copper to help reduce Iron to reduced Ferrous state (Fe2+)
Bioflavonoids (important part of vit C, found in pulp)
Increases absorption of non-heme Iron
Increases absorption of Estrogen/BCP, Aspirin, Anticoagulants
Leading vitamin (Antioxidant) for Collagen synthesis
Carnitine Synthesis (Transports LCFA into mitochondria for energy) body builders
High doses of Vitamin C may interfere w/ lab tests (oxalates, creatinine, bilirubin)
Deficiency: Scurvy, bleeding gums, poor wound healing, Bruising, poor bone, healing, joint pain, cataracts, loose teeth, connective tissue issues,
follicular (bumps on arms)
Toxicity: Diarrhea, Nausea, not toxic, if too much at one time will become osmotic laxative.
Food sources: citrus, fruits, berries, bell pepper, broccoli, Raw veggies, Fruits, Acerola, Sprouts.
Disease from deficiency
* neural tube defects
* Increased risk of coronary heart disease with high hyperhomocysteinenmia
* Dementia risk due to homocysteine accumulation
* Colorectal cancer
Supplements: ascorbic acid, buffered, Ester,
Testing: urine panel, possible serum
Drug nutrient interactions:
Anticoagulant (warfarin), cortisone.
B12 coenzyme and metal containing
*****Most common nutrient deficiency in elderly: B12
Cofactor for Methionine synthesis
Function: Metabolism, Lipids, amino acids, RBC formation, Energy, Bone marrow, Nucleic acid, Gowth
***Digestion, absorption, storage:
Stomach: acidic (B12 comes from animal) , need intrinsic factor (generated by parietal cells) intrinsic bear hugs B12, travels out of the stomach to the ileum.
**Store: in the Liver
excretion in bile and stool
SIBO starts in the cecum and moves into the ileum, intestine surgery, can affect.
Methionine Synthase (b12 dep), catalyses conversion of 5-MTH and Homocysteine to Tetrahydrofolate/L-methionine
megaloblastic/macrocytic anemia (pernicious autoimmune disease anemia likely from lack of Intrinsic Factor)
Directly related to neuropathy. Used in the kreb cycle
b12 Def: Contributes to ATAXIA – loss of ankle knee reflex, gait abnormality, speech changes (along with E, B1), Premature graying (also Cu), Hearing Loss
Undetected b12 def for several years = Neuropsychiatric damage that may be irreversible
Common causes of b12 def: Gastritis, HIV, renal disease
**Hypothyroidism iS NOT a common cause of b12 deficiency
Stages in lifecycle
Higher need in pregnancy and higher in lactation.
Men and women are the same from teenager to end of life. Need doesnt change.
food: animal protein, Eggs, Milk
signs of deficiency:
slow growth, anemia, neuropathy, growth restriction, Memory loss, RBC hemolysis.
Supplements: cobalamin (methyl, Hydroxyl)
3000 mcg (blend, 1000, 1000, 1000)
use sublingual
OAT test: Methylmelonic acid. (MMA)
If MMA is high, will not be absorbing B12.
Forms of life:
cobalamin, chloryphyl, heme (iron)
pernicious anemia (autoimmune) attacks the intrinsic factor.
Interactions (antagonists)
PPI (antacid, Prilosec) , antibiotics, oral contraception,
If not able to determine if B12 or folate is low, give both unless you know for sure that you dont need it.
*****Most common nutrient deficiency in elderly: B12
B6, B12 or folate
How do you rule them out if homosysteine is high.
CBC (macrocytic cells) : rule out B6
B12 and folate ?
figlu is an organic acid when folate is low.
