[7A] Water-soluble vitamins

Compare the amounts we need per day of vitamins to carbs or lipids

We need relatively small amounts of vitamins/day compared to carbs and lipids

(makes sense because vitamins =MICROnutrients, carbs =MACROnutrients)

Foods with high vitamin content sorted into Canada Food Guide groups: whole grains, vegetables and fruit, proteins, healthy fats

What are vitamins

ESSENTIAL (must get from diet) for homeostasis, growth, reproduction, and other metabolic processes

vitamins are ___________ compounds

Organic

means they aren’t minerals

Vitamin bioavailability varies due to (3)

• Availability of carrier proteins

• Rate and efficiency of conversion to active form

• Interactions with other dietary components, including other micronutrients

Water soluble vs fat soluble vitamins in terms of presence at toxic levels

Water soluble vitamins are less likely than fat-soluble vitamins to be present at toxic levels, because:

1. There is no water storage in the human body (unlike fat that builds up)

2. Water-soluble vitamins are easily filtered and excreted by the kidney when in excess.

Water soluble vs fat soluble vitamins in terms of being deficient, where do deficiencies first appear

Water soluble vitamins are more likely than fat-soluble vitamins to become deficient.

1. Tend to be less stable (e.g., light, heat)

2. Exposed to kidney filtration and excretion

In metabolically active or rapidly growing tissues.

List the water-soluble vitamins (9)

Thiamin (B₁)

Riboflavin (B₂)

Niacin (B₃)

Pantothenic acid (B₅)

Vitamin B₆ (pyridoxine and related vitamers)

Biotin (B₇)

Folates and folic acid (B₉)

Vitamin B₁₂

Vitamin C

Vitamins with historical names for compounds later shown to NOT be true vitamins

Vitamins B₄, B₈, B₁₀, and B₁₁ and B₁₃

Water-soluble vitamins often act as co-enzymes for (2)

E metabolism and hematopoiesis (hgb and rbcs)

B vitamins always involved in

E metabolism pathways (also have other primary roles) 

Why are vit B6, folate (B9) and Vit B12 grouped together

Work together to help metabolize homocysteine.

Low levels can increase homocysteine in the blood.

Elevated homocysteine is associated with increased cardiovascular disease (CVD) risk, including atherosclerosis

Thiamine (Vit B1) dietary sources

Whole grains and some proteins foods (pork, lentils, fish, nuts and seeds).

Added as an enrichment/fortification to foods

Thiamine (B1) how was it discovered

Identified as the deficiency that caused beriberi in chickens > White rice but not brown rice

Thiamine (Vit B1) bioavailability

Sensitive to heat, oxygen, and low-acid (basic) conditions (destroyed easily)

Destroyed by anti-thiamin factors such as heat-labile thiaminases (raw fish/shellfish) and tannins (tea, coffee). (whole diet matters not just each individual food)

Thiamine (Vit B1) 2 uses in body

1. Production of ATP from glucose (PDH, Krebs)

2. Metabolism of sugars and amino acids (RNA, ACh)

Active form of thiamine (B1) co-enzyme for

decarboxylation reactions

Does vitamin supplementation always work?

NO - only works if you are deficient (i.e. won’t see E changes if you start taking supplement unless you were deficient to start with)

Thiamine (Vit B1) deficiency what is it called and what are the symptoms

Beriberi

E lack, depression, weakness, tingling in arms and legs, paralysis (ACh lack)

Thiamine (Vit B1) effects also observed in ___ system, symptoms such as, why?

tachycardia, edema, HF (not well understood, might be due to heart being a very metabolically active tissue as well)

Like several Vit B vitamins, B1 deficiency can result from

alcohol use disorder due to impaired absorption (inflammation) and liver damage (prevents liver from activating them)

Riboflavin (vit B2) dietary sources

Protein foods (milk, cheese, animal meats) as well as some fruits, vegetables, and whole grains.

Added as an enrichment/fortification

Riboflavin (vit B2) bioavailability

sensitive to light > opaque milk containers (often sold in darker containers to help reserve riboflavin)

Riboflavin (vit B2) use in body (2)

1. Mitochondrial metabolism (FAD and FMN) (ETC)

• FAD involved in critic acid cycle and fatty acid metabolism

• FAD and FNM act as e carriers in transport system

2. Activates other vitamins

Since riboflavin (vit b2) activates other vitamins, what can this cause if someone is deficient

They would be deficient in the other vitamins that b2 activates

What other vitamins does riboflavin (b2) activate (6)

Folate, niacin, vitamins B3, B6, B9, K

Riboflavin (B2) deficiency called? symptoms?

Ariboflavinosis

Poor wound healing (due to inability of new cells to replace damaged ones

inflammation (eyes, lips, mouth, tongue)

cracking of tissue in corners of the mouth, scaly and greasy skin eruptions

confusion (related to brain E metabolism)

Riboflavin (B2) deficiency occurs first in

rapidly-growing tissues such as skin, linings of the eyes, mouth, and tongue

Niacin (B3) toxicity signs (4) (has UL)

Flushing, nausea, rash, tingling extremities

Niacin (B3) dietary sources

Protein foods (peanuts, lentils, animal meats) as well as whole grains and some fruits and vegetables

Niacin (B3) identified how

during study of pellagra when deficiency was associated with diets that relied on corn (niacin very low in corn)

Niacin (B3) bioavailability

Can be synthesized from tryptophan, but only when amino acid levels are in excess of protein needs (+ requires B6)

Niacin (B3) use in body, how

Aerobic respiration

Niacin forms NAD+ and NADH (Glycolysis, beta oxidation, krebs impacted)

Niacin (B3) deficiency called and best known for which symptoms

Pellagra

three D’s: dermatitis (sunburn like damage), diarrhea, dementia

Early symptoms of pellagra (B3 deficiency) (3)

fatigue, decreased appetite, and indigestion

Other GI symptoms of pellagra (B3 deficiency) (3)

bright-red tongue, vomiting, constipation

Mental symptoms of pellagra, why

begin with irritability, headaches, loss of memory, insomnia, and emotional instability; progresses to psychosis and acute delirium.

All of these rely heavily on E systems

Pantothenic acid (B5) deficiency

very rare (widely available)

Pantothenic acid (B5) dietary sources

Protein foods (milk, seeds, nuts, lentils, animal meats) as well as some whole grains

Pantothenic acid (B5) bioavailability

Sensitive to heat and extremes of pH such as low-acid (basic) and high-acid (acidic) conditions

Pantothenic acid (B5) use in the body (2)

1. Part of coenzyme A, part of acetyl-CoA (glycolysis, beta-oxidation, ketogenic amino acids à Krebs Cycle)

2. Lipids metabolism  need carriers

Pantothenic acid is also needed to produce acyl carrier protein needed for the synthesis of cholesterol and fatty acids

Pantothenic acid (B5) deficiency is rare but can occur how

as part of multiple B vitamin deficiency resulting from malnutrition or chronic alcoholism

Biotin (B7) dietary sources

Protein foods (cooked eggs, animal meats)

Identified in animal studies with rats fed protein from raw egg

One time where adding heat makes nutrient more available to you

Biotin (B7) bioavailability

Biotin is also produced by bacteria in the GI tract, which can be absorbed into the body as another source

Raw eggs contain avidin protein, which binds to biotin very tightly and make it unavailable for absorption

Biotin (B7) use in body

E metabolism (for carboxylase enzymes) (krebs, acetyl-coa)

Coenzyme for keratin production hair and nails (supplements in hair and skin products)

Biotin (B7) deficiency is

rare (nutritional requirements low), can be obtained from intestinal bacteria and diff foods

signs and symptoms of biotin (B7 deficiency)

scaly, red rash near openings such as the eye, nose, or mouth, thinning hair (alopecia), brittle nails, conjunctivitis (“pink eye”).

Neurological effects include depression, lethargy, hallucinations, paresthesia (pins and needles/tingling) of the extremities, and numbness.

How are B6, B9 and B12 related

Work together to help metabolize homocysteine.

Low levels can increase homocysteine in the blood.

Elevated homocysteine is associated with increased cardiovascular disease (CVD) risk, including atherosclerosis

B6 toxicity signs

numbness, n. damage

B6 dietary sources

Protein foods (milk, seeds, nuts, lentils, animal meats), whole grains, some fruits and vegetables

Added back to food as enrichment or fortification

How was B6 identified

through a deficiency syndrome that did not respond to thiamine or riboflavin (process of elimination)

B6 bioavailability

Easily destroyed by food processing, heat, light

B6 uses in body (main 2)

1. Amino acid metabolism (by transamination and deamination)

• Synthesis of non-essential amino acids by transamination

• Deamination, allows amino acids to enter energy metabolism pathways such as gluconeogenesis, Krebs cycle

2. Nervous system

• NT synthesis from amino acids

• Synthesis of myelin

B6 other uses in the body

• Synthesis of hemoglobin

• Formation of white blood cells

• Needed for the conversion of tryptophan to niacin

• May regulate homocysteine levels (should decrease CVD risk):

  • Met à homocysteine requires methyl-B12

  • B12: Methyl-B12 modulated by folate and B6

Homocystinuria describe

Genetic disorder causes chronically high levels of homocysteine; patients develop atherosclerosis at an early age

What vitamin should those with homocystinuria go above the UL for?

V B6. high amounts of B6 reduce homocysteine > reduces CVD risk

Low B6 is similar to ___ in a sense

LDL (atherosclerosis)

B6 deficiency symptoms overall (2)

neurological and microcytic anemia

Deficiency in B6 will appear more quickly in what type of diet, why

high protein due to role in amino acid metabolism (if high protein diet it is easy for you to burn through your B6)

Microcytic anemia in what deficiency

small, pale, RBCs

likely from impaired hgb synthesis

B6

Folate (B9) high intake may mask

B12 deficiency

Folate (B9) dietary sources

Protein foods (milk, seeds, nuts, lentils, animal meats), whole grains, some fruits and vegetables

added back to food as enrichment or fortification

Folate B9 identified as

group of compounds that were part of Wills Factor that cured macrocytic anemia in pregnant women

Folate (B9) bioavailability

Estimated that only ~50% of dietary folate is absorbed by the body

Synthetic folate different from folate how

Synthetic folate (“folic acid”) from supplements or as a fortification does not contain the poly-glutamate chain; it is readily absorbed by the body

Folate nutritional requirements are stated in dietary folate equivalents (DFE) to account for differences in absorption (~50% part)

Folate (B9) use in body

Co-enzyme for reactions that transfer chemical groups containing a single carbon atom

• Nucleotide synthesis (DNA replication > cell growth and division)

• Gene expression via DNA methylation to silence genes

• Metabolism of some amino acids, notably methionine

Folate (B9) deficiency most severe in

tissues with rapidly dividing cells (e.g., bone marrow), and during periods of rapid growth and development

Folate (B9) deficiency see what in infants

Neural tube defects

Neural tube doesn’t close properly > hernia tube out of back of infant

Folate moves methyl groups around >

folate deficiency can be masked due to B12 deficiency (think of both at same time)

Folate (B9) deficiency see (2)

1. Megaloblastic anemia

RBCs are unable to divide, leading to large but immature cells that cannot leave the bone marrow, have a reduced lifespan, and slowly decline in number over time due to poor replenishment.

2. CVD

Like B6 and B12, folate is involved in homocysteine metabolism. Low levels of folate may increase homocysteine levels and the risk of atherosclerosis

B12 dietary sources

Exclusively in animal-based protein foods (milk, cheese, pork, beef, fish, chicken) any food that has gut microbiome

B12 relation to vegetarians and vegans

nutrient of concern > must get B12 from nutritional yeast or take supplement

B12 use in body

Converted into active coenzyme forms: methylcobalamin (“methyl-B12”) and adenosylcobalamin (“adenosyl-B12”)

• Nervous system

  • Necessary of maintenance of myelin and normal nerve signal transmission

• Fatty acid metabolism

  • Adenosyl-B12 rearranges carbon atoms to allow certain products enter Krebs cycle

• Amino acid metabolism & folate regeneration

  • Methyl-B12 involved in the synthesis of methionine from homocysteine; it also regenerates the active coenzyme form of folate from its deactivated methyl-folate form

B12 bioavailability

Requires several digestive processes:

• Released from bound proteins in food by gastric acid and pepsin

• Binds to intrinsic factor in SI, forming a complex that is absorbed in the ileum

• Small amounts synthesized by microbiota, but not absorbed

  • Little vitamin B₁₂ is lost by the body, so deficiency develops very slowly

  • Alterations in any of the above processes increases risk of deficiency

B12 deficiencies common or uncommon, risk factors (3)

common

1. Pernicious anemia, autoimmune disease destroys cells that produce intrinsic factor required for B12 absorption

2. Atrophic gastritis, inflammation of stomach can > reduction in stomach acid (limits B12 extraction) and bacterial overgrowth (competes for B12 absorption)

3. Vegan and vegetarian diets

B12 deficiency see what and describe

macrocytic megaloblastic anemia

Cells very large and dark, can’t move through bones well

B12 deficiency can be masked by _______ how

folate supplement

prevent anemia onset > serious and irreversible neurological effects can progress

B12 deficiency signs and symptoms

Neurological symptoms numbness and tingling, abnormalities in gait, memory loss, and disorientation, paralysis

Cardiovascular disease

Like B6 and folate, B12 is involved in homocysteine metabolism. Low levels of B12 may increase homocysteine levels and the risk of atherosclerosis

What are the vitamins of each of these metabolic pathways: TPP, FMN and FAD, NAD and NADP, CoA, PLP, THF

TPP: Thiamin

FMN and FAD: Riboflavin

NAD and NADP: niacin

CoA: Pantothenic acid

PLP: Vitamin B6

THF: Folate

Vit C toxicity

Diarrhea, nausea, and abdominal cramps

Vit C dietary sources

Fruits and vegetables (levels are especially high in citrus fruits)

Vitamin C deficiency identified as

causative for scurvy

Vit C bioavailability

Unstable; destroyed by oxygen, light, heat, and low acid (basic) conditions

Reactive with copper or iron cooking utensils (using certain pots can decrease vit C)

Vit C use in body (3)

1. Water-soluble antioxidant

gets rid of free radicals before they react with important biomolecules

2. Collagen formation

connective tissue fibre networks to make strong protein

3. Other metabolic reactions

   hydroxylation of carnitine, which transports long-chain fatty acids into the mitochondria

   conversion of tryptophan and tyrosine into 5HT and NE

   Synthesis thyroxin, regulates metabolic rate

   Involved in synthesis of bile acids from cholesterol

   Aids in Fe absorption by reducing Fe³⁺ to Fe²⁺

Vit C deficiency and describe, symptoms

Scurvy- Collagen cannot be maintained and connective tissue degrades

BVs under skin lose integrity and break spontaneously, leading to “pinpoint” or “pinprick” bleeding around hair follicles

Vit C scurvy deficiency associated with (2)

microcytic anemia due to poor Fe absorption and depleted stores

Poor wound healing - Bad if you’re pirate raiding ships

Who has higher DRI for Vit C and recommended to take supplements

smokers (due to oxidative properties of cigarette smoke) burn through VC more quickly if you smoke

Lack of evidence on Vit C supp for

Reduced risk of CVD (antioxidant à reduced LDL; required to convert cholesterol into bile acids).

• Lack of epidemiological and human intervention trial evidence in support

Cancer prevention (inverse relationship between intake of fruits and vegetables and cancer risk).

• Difficult to separate confounding factors from vitamin C-specific effects.

Often sold as a prophylactic supplement to reduce duration of a cold, but evidence is weak and contradictory