Blood

Health
Tyhisha Melhado
Blood and Its Importance
Blood is a fluid that transports oxygen, carbon dioxide,
nutrients, and waste products through the body’s blood
vessels (arteries, veins, and capillaries). Blood also delivers
immune cells to fight infections and contains components
that form a plug in a damaged blood vessel to prevent blood
loss.
• Other Functions: hormone transport as well as the regulation of pH,
body temperature, and water content of cells
Components of Blood

– Plasma
– Suspended in plasma:
- Erythrocytes (red blood cells)
- Leukocytes (white blood cells)
- Lymphocytes
- Monocytes
- Eosinophils
- Basophils
- Neutrophils
- Thrombocytes (platelets)
 The Origin of Blood
– Blood cells develop from hematopoietic
stem cells formed in the bone marrow. This
highly regulated process is known as
hematopoiesis
– Brief overview: Unspecialized stem cell → Cell
Multiplication → Precursor cell → Cell Division
→ Mature cell
– Some precursor cells stay in the marrow to
mature. Others travel to other parts of the
body to develop into mature, functioning
blood cells
– Other organs and systems that help
regulate blood cells (production,
destruction, and differentiation): lymph
nodes, spleen, and liver
Vitamins/Minerals for Blood Health

–Fat Soluble Vitamins: E, K

–Water Soluble Vitamins: B6, Folate, B12
–Minerals: Iron, Calcium, Copper
Vitamin E
– Integral part of the body’s antioxidant network which also
includes glutathione peroxidase (requires selenium), catalase
(requires iron), superoxidase dismutase (various forms require
copper, zinc, and manganese), and various carotenoids
– Antioxidant: regulates free radical activity and thus reduces oxidative
stress such as destruction of cell membranes and DNA

– Requires vitamin C for the electron regeneration for continued

function
– Prevents clots in blood vessels
Vitamin E Deficiency

– Deficiency may be a result of increased beta carotene intake

– Results in damaged cell membranes and key components needed to
repair the cell
– If deficiency persists, patients can develop hemolytic anemia
– Signs and symptoms: weakness, numbness and pain usually in the hands
and feet, abnormal eye movements, impaired immune function and
premature breakdown of red blood cells (hemolysis)
Vitamin E Toxicity
– UL: 1000mg (1500 IUs) from natural sources and 1100 IUs from synthetic
sources
– Excessive amounts can interfere with the role of vitamin K in blood clotting
– Results in a hemorrhage

– Aspirin or anticoagulation medications such as warfarin (Coumadin ©)

also prevent blood clotting
– Megadoses of Vitamin E therefore results in severe hemorrhaging in these
individuals
– Signs and symptoms: gastrointestinal distress and possible increased
severity of respiratory infections
 Vitamin K
– Functions as a coenzyme for the synthesis of blood clotting
factors by the liver
– Involved in the conversion of preprothrombin to the blood
clotting factor, prothrombin, by carboxylation of glutamic
acid
– All vitamin K-dependent proteins contain the Gla
(gammacarboxyglutamic acid) residues, which are needed
to bind calcium and form clots
– The vitamin K-dependent blood clotting proteins are Factor II
(prothrombin), VII, IX, X while Proteins C,S, Z function to inhibit
coagulation

– Vitamin K is converted to an inactive form once it has

activated the clotting factors. It must then be reactivated
for its biological action to persist
– Known as Epoxide Cycle
Vitamin K Interactions
– Anticoagulation medications such as warfarin (Coumadin
©) inhibit blood clotting.
– Patients need to maintain a consistent dietary regimen and
avoid supplementation to prevent interactions
– Excessive intake of vitamin A and E interferes with vitamin
K absorption
– Excessive vitamin A interferes with the absorption of vitamin K
from the small intestine
– Excessive vitamin E leads into a decrease in vitamin K
dependent clotting factors and an increased bleeding tendency.
Vitamin K Deficiency
& Toxicity
- Deficiency: May be a result of prolonged
antibiotic use or impaired fat absorption
- As a result, hemorrhaging occurs.
- Populations at risk: Newborns
- Signs and symptoms: Ecchymosis
- Toxicity: Although, there is no upper-level
set for vitamin K, injections of synthetic
vitamin K (menadione) can cause
hemolytic anemia, jaundice, and death in
newborns
Vitamin B6
– The primary coenzyme of vitamin B6, pyridoxal phosphate (PLP), is
required for folate metabolism (converts homocysteine → cysteine)
and the synthesis of heme

– Supports normal immune function

– Synthesis of PLP requires the riboflavin (vitamin B2) coenzyme, flavin
mononucleotide (FMN)
Vitamin B6 Deficiency

– Results in elevated levels of homocysteine and decreased

hemoglobin synthesis
– Microcytic hypochromic anemia develops
– At risk populations: women, older adults, black individuals,
smokers, users of oral contraceptive agents, those who have
alcoholism, are underweight or consume poor diets, those that
take 1-DOPA, isoniazid, or theophylline
– Signs and symptoms: angular stomatitis, cheilosis, glossitis,
seborrheic dermatitis, pallor
Folate
– Folate coenzymes are formed from a central coenzyme form called
tetrahydrofolic acid (THFA) which is critical for the synthesis and
maintenance of new cells
– Supplies methylene (CH2) from pyrimidine thymine to pyrimidine
uracil
– Required for the synthesis of purines (adenine and guanine) in DNA
– Important in amino acid metabolism, especially the interconversions
of amino acids (glycine → serine, the main source of methyl groups
for THFA as well as histidine → glutamic acid and homocysteine →
methionine)
Folate
– Vitamin C helps protect folate from
oxidative destruction
– Vitamin B12 coenzyme is required to recycle
the folate coenzyme for DNA synthesis.
– Needed for methionine synthase enzyme to
accept methyl group from 5-MTHF
– Vitamin B6 is required for the conversion of
serine → glycine and homocysteine →
cysteine
– Vitamin B2 indirectly participates in
homocysteine metabolism via FAD
dependent coenzyme 5,10-MTHFR
 Folate Deficiency
Deficiency:
– Impacts cell division by decreased production of
methionine and SAM and increased levels of
homocysteine
– At risk: pregnant women, impoverished individuals,
those with alcoholism, chronic gastrointestinal
diseases, a MTHFR mutation, and those who take
certain medications, such as some anticonvulsants
and Methotrexate
– Signs: megaloblastic (macrocytic) anemia
– Also occurs with vitamin B12 deficiency therefore may
develop from this vitamin (“functional folate
deficiency”)
– Anemia can be mediated by choline
– Other signs and symptoms: decreased immune
function, pallor, cyanosis , glossitis, atrophied papillae

Toxicity:
- Increased intake may mask a vitamin B12 deficiency
- Signs and symptoms: insomnia, malaise, irritability, GI
distress
Vitamin B12 Deficiency
– Results in megaloblastic, macrocytic anemia
– Impairs folate metabolism
– Results in pernicious anemia
– This disease can result from the inadequate production of the
intrinsic factor required for vitamin B12 absorption, malabsorption,
or use of some medications
– Results in elevated plasma homocysteine concentrations
– At risk: elderly, vegetarians/vegans, infants breastfed by
vegetarian/vegan mothers, those with a parasitic infection or
pancreatic insufficiency, as well as those taking proton pump
inhibitors, H2 blockers, or Metformin
– Signs and symptoms: pallor, cyanosis, ataxia,
numbness/tingling, glossitis, atrophied papillae, dry, dark,
and curved nails
Iron
– Essential for oxygen transport to tissues via hemoglobin in red
blood cells and storage of oxygen in the heart and skeletal muscle
via myoglobin
– Hemoglobin – four polypeptide chains that contain four heme molecules
and four iron atoms
– Myoglobin – one polypeptide chain that houses one heme molecule and
iron atom
– Required to produce lymphocytes and natural killer (NK) cells that
help prevent infections
– Factors that enhance absorption: heme iron in food, meat protein
factor (MPF), vitamin C intake, gastric acidity
Iron Deficiency
– May result from a riboflavin deficiency
– Severe deficiency progresses into microcytic, hypochromic anemia
– Factors that decrease absorption: lack of vitamin C with consumption of non heme
iron foods, phytic acid in whole grains and legumes, oxalic acid in leafy vegetables,
polyphenols/tannins in tea, coffee, red wine, and oregano, reduced gastric acidity,
excessive intake of other minerals (zinc, phosphorus, manganese, calcium),
phosvitin
– At risk: premature infants, young children, adolescent, females during childbearing
years, pregnant women, vegetarians/vegans, those that are at risk for
hemorrhaging, and those with kidney disease, steatorrhea, parasites, impaired
absorption, protein energy malnutrition (PEM), and achlorhydria
– Signs and symptoms: Shortness of breath and fatigue (especially with physical
activity and exertion), pallor, compromised immune function, delayed cognitive
development, abnormal GI tract, koilonychias, pica, pagophasia, abnormal
temperature regulation
Copper

– Involved in iron transport

– Ceruloplasmin (also called ferroxidase I)
oxides iron for incorporation into transferrin
– Supports normal immune function
– Factors that enhance absorption: low
copper status with decreased intake,
organic acids (such as vitamin C), sulfur
containing amino acids
Copper Deficiency

– Factors that decrease absorption: high copper status, antacids, phytates,

excessive intake of other minerals (zinc, iron, calcium, and phosphorus)
– Results in a decrease in ceruloplasmin
– As a result, iron deficiency anemia (microcytic, hypochromic anemia) develops
– At risk: infants (premature and milk-based formula), those on long term
total parenteral nutrition (TPN) without added copper, high zinc intake,
individuals with Menkes disease, those that consume antacids, those with
GI malabsorption disorders
– Signs and symptoms: leukopenia, hypo/depigmentation skin/hair,
corkscrew hair, osteopenia, impaired immune function, cardiovascular and
pulmonary dysfunction
Calcium

– Participates in several reactions in a cascade that leads to

the formation of fibrin, the main component of a blood clot
– Required for activation of vitamin K dependent clotting factors
– Factors that enhance absorption: calcitriol
Calcium Deficiency
– Possible cause: magnesium deficiency
– Results a hemorrhage
– Factors that decrease absorption: decreased HCl, chronic diarrhea,
phytic acid (fiber), oxalic acid, polyphenols, fat malabsorption, age,
excessive intake of other minerals (zinc, iron, magnesium)
– At risk: those that are lactose intolerant, vegetarians/vegans,
individuals with hypoparathyroidism, those on long term thiazide
diuretics, PPI/H2 blocker, glucocorticoids (prednisone)
– Signs and symptoms: tetany, bone loss and eventual development of
osteoporosis