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| Complete MultiVitamins (A-Zinc) plus Ginseng |
Vitamins and Minerals:
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Vitamin C
Vitamin C, also known as ascorbic acid, is a water-soluble
vitamin. Unlike most mammals and other animals, humans do not have the ability
to make their own vitamin C. Therefore, we must obtain vitamin C through our
diet.
Function
Vitamin C is required for the synthesis of collagen, an
important structural component of blood vessels, tendons, ligaments, and bone.
Vitamin C also plays an important role in the synthesis of the
neurotransmitter, norepinephrine. Neurotransmitters are critical to brain
function and are known to affect mood. In addition, vitamin C is required for
the synthesis of carnitine, a small molecule that is essential for the
transport of fat into cellular organelles called mitochondria, where the fat is
converted to energy (1). Research also suggests that vitamin C is involved in
the metabolism of cholesterol to bile acids, which may have implications for
blood cholesterol levels and the incidence of gallstones (2).
Vitamin C is also a highly effective antioxidant. Even in
small amounts vitamin C can protect indispensable molecules in the body, such
as proteins, lipids (fats), carbohydrates, and nucleic acids (DNA and RNA),
from damage by free radicals and reactive oxygen species that can be generated
during normal metabolism as well as through exposure to toxins and pollutants
(e.g., cigarette smoke). Vitamin C may also be able to regenerate other
antioxidants such as vitamin E (1). One recent study of cigarette smokers found
that vitamin C regenerated vitamin E from its oxidized form (3).
Deficiency
Scurvy
Severe vitamin C deficiency has been known for many
centuries as the potentially fatal disease, scurvy. By the late 1700s the
British navy was aware that scurvy could be cured by eating oranges or lemons,
even though vitamin C would not be isolated until the early 1930s. Symptoms of
scurvy include bleeding and bruising easily, hair and tooth loss, and joint
pain and swelling. Such symptoms appear to be related to the weakening of blood
vessels, connective tissue, and bone, which all contain collagen. Early
symptoms of scurvy like fatigue may result from diminished levels of carnitine,
which is needed to derive energy from fat, or from decreased synthesis of the
neurotransmitter norepinephrine (see Function). Scurvy is rare in developed
countries because it can be prevented by as little as 10 mg of vitamin C daily
(4). However, cases have occurred in children and the elderly on very
restricted diets (5, 6).
Calcium
Calcium is the most common mineral in the human body. About
99% of the calcium in the body is found in bones and teeth, while the other 1%
is found in the blood and soft tissue. Calcium levels in the blood and fluid
surrounding the cells (extracellular fluid) must be maintained within a very
narrow concentration range for normal physiological functioning. The
physiological functions of calcium are so vital to survival that the body will
demineralize bone to maintain normal blood calcium levels when calcium intake
is inadequate. Thus, adequate dietary calcium is a critical factor in
maintaining a healthy skeleton (1).
Function
Structure
Calcium is a major structural element in bones and teeth.
The mineral component of bone consists mainly of hydroxyapatite
[Ca10(PO4)6(OH)2] crystals, which contain large amounts of calcium and
phosphate (2). Bone is a dynamic tissue that is remodeled throughout life. Bone
cells called osteoclasts begin the process of remodeling by dissolving or
resorbing bone. Bone-forming cells called osteoblasts then synthesize new bone
to replace the bone that was resorbed. During normal growth, bone formation
exceeds bone resorption. Osteoporosis may result when bone resorption
chronically exceeds formation (1).
Cell signaling
Calcium plays a role in mediating the constriction and
relaxation of blood vessels (vasoconstriction and vasodilation), nerve impulse
transmission, muscle contraction, and the secretion of hormones like insulin
(3). Excitable cells, such as skeletal muscle and nerve cells, contain
voltage-dependent calcium channels in their cell membranes that allow for rapid
changes in calcium concentrations. For example, when a muscle fiber receives a
nerve impulse that stimulates it to contract, calcium channels in the cell
membrane open to allow a few calcium ions into the muscle cell. These calcium
ions bind to activator proteins within the cell, which release a flood of
calcium ions from storage vesicles inside the cell. The binding of calcium to
the protein, troponin-c, initiates a series of steps that lead to muscle
contraction. The binding of calcium to the protein, calmodulin, activates
enzymes that breakdown muscle glycogen to provide energy for muscle contraction
(1).
Cofactor for enzymes and proteins
Calcium is necessary to stabilize a number of proteins and
enzymes, optimizing their activities. The binding of calcium ions is required
for the activation of the seven "vitamin K-dependent" clotting
factors in the coagulation cascade (see vitamin K). The term, "coagulation
cascade," refers to a series of events, each dependent on the other that
stops bleeding through clot formation (4).
Regulation of calcium levels
Calcium concentrations in the blood and fluid that surrounds
cells are tightly controlled in order to preserve normal physiological function
(diagram). When blood calcium decreases (e.g., in the case of inadequate
calcium intake), calcium-sensing proteins in the parathyroid glands send
signals that result in the secretion of parathyroid hormone (PTH) (5). PTH
stimulates the conversion of vitamin D to its active form, calcitriol, in the
kidneys. Calcitriol increases the absorption of calcium from the small
intestine. Together with PTH, calcitriol stimulates the release of calcium from
bone by activating osteoclasts (bone resorbing cells) and decreases the urinary
excretion of calcium by increasing its reabsorption in the kidneys. When blood
calcium rises to normal levels, the parathyroid glands stop secreting PTH and
the kidneys begin to excrete any excess calcium in the urine. Although this
complex system allows for rapid and tight control of blood calcium levels, it
does so at the expense of the skeleton (1).
Deficiency
A low blood calcium level usually implies abnormal
parathyroid function and is rarely due to low dietary calcium intake since the
skeleton provides a large reserve of calcium for maintaining normal blood
levels. Other causes of abnormally low blood calcium levels include chronic
kidney failure, vitamin D deficiency, and low blood magnesium levels that occur
mainly in cases of severe alcoholism. Magnesium deficiency results in a
decrease in the responsiveness of osteoclasts to PTH. A chronically low calcium
intake in growing individuals may prevent the attainment of optimal peak bone
mass. Once peak bone mass is achieved, inadequate calcium intake may contribute
to accelerated bone loss and ultimately to the development of osteoporosis (see
Disease Prevention) (1).
Chromium: What is it?
Chromium is a mineral that humans require in trace amounts,
although its mechanisms of action in the body and the amounts needed for
optimal health are not well defined. It is found primarily in two forms: 1)
trivalent (chromium 3+), which is biologically active and found in food, and 2)
hexavalent (chromium 6+), a toxic form that results from industrial pollution.
This fact sheet focuses exclusively on trivalent (3+) chromium.
Chromium is known to enhance the action of insulin [1-3], a
hormone critical to the metabolism and storage of carbohydrate, fat, and
protein in the body [4]. In 1957, a compound in brewers' yeast was found to
prevent an age-related decline in the ability of rats to maintain normal levels
of sugar (glucose) in their blood [3]. Chromium was identified as the active
ingredient in this so-called "glucose tolerance factor" in 1959 [5].
Chromium also appears to be directly involved in
carbohydrate, fat, and protein metabolism [1-2,6-11], but more research is
needed to determine the full range of its roles in the body. The challenges to
meeting this goal include:
Defining the types
of individuals who respond to chromium supplementation;
Evaluating the
chromium content of foods and its bioavailability;
Determining if a
clinically relevant chromium-deficiency state exists in humans due to
inadequate dietary intakes; and
Developing valid
and reliable measures of chromium status .
Cobalamin (Vitamin B12)
Vitamin B12 is a water-soluble vitamin that is naturally
present in some foods, added to others, and available as a dietary supplement
and a prescription medication. Vitamin B12 exists in several forms and contains
the mineral cobalt [1-4], so compounds with vitamin B12 activity are
collectively called "cobalamins". Methylcobalamin and 5-deoxyadenosylcobalamin
are the forms of vitamin B12 that are active in human metabolism [5].
Vitamin B12 is required for proper red blood cell formation,
neurological function, and DNA synthesis [1-5]. Vitamin B12 functions as a
cofactor for methionine synthase and L-methylmalonyl-CoA mutase. Methionine
synthase catalyzes the conversion of homocysteine to methionine [5,6].
Methionine is required for the formation of S-adenosylmethionine, a universal
methyl donor for almost 100 different substrates, including DNA, RNA, hormones,
proteins, and lipids. L-methylmalonyl-CoA mutase converts L-methylmalonyl-CoA
to succinyl-CoA in the degradation of propionate [3,5,6], an essential
biochemical reaction in fat and protein metabolism. Succinyl-CoA is also
required for hemoglobin synthesis.
Vitamin B12, bound to protein in food, is released by the
activity of hydrochloric acid and gastric protease in the stomach [5]. When
synthetic vitamin B12 is added to fortified foods and dietary supplements, it
is already in free form and, thus, does not require this separation step. Free
vitamin B12 then combines with intrinsic factor, a glycoprotein secreted by the
stomach's parietal cells, and the resulting complex undergoes absorption within
the distal ileum by receptor-mediated endocytosis [5,7]. Approximately 56% of a
1 mcg oral dose of vitamin B12 is absorbed, but absorption decreases
drastically when the capacity of intrinsic factor is exceeded (at 1–2 mcg of
vitamin B12) [8].
Pernicious anemia is an autoimmune disease that affects the
gastric mucosa and results in gastric atrophy. This leads to the destruction of
parietal cells, achlorhydria, and failure to produce intrinsic factor,
resulting in vitamin B12 malabsorption [3,5,9-11]. If pernicious anemia is left
untreated, it causes vitamin B12 deficiency, leading to megaloblastic anemia
and neurological disorders, even in the presence of adequate dietary intake of
vitamin B12.
Vitamin B12 status is typically assessed via serum or plasma
vitamin B12 levels. Values below approximately 170–250 pg/mL (120–180
picomol/L) for adults [5] indicate a vitamin B12 deficiency. However, evidence
suggests that serum vitamin B12 concentrations might not accurately reflect
intracellular concentrations [6]. An elevated serum homocysteine level (values
>13 micromol/L) [12] might also suggest a vitamin B12 deficiency. However,
this indicator has poor specificity because it is influenced by other factors,
such as low vitamin B6 or folate levels [5]. Elevated methylmalonic acid levels
(values >0.4 micromol/L) might be a more reliable indicator of vitamin B12
status because they indicate a metabolic change that is highly specific to
vitamin B12 deficiency [5-7,12].
Folate
Folate is a water-soluble B vitamin that is naturally
present in some foods, added to others, and available as a dietary supplement.
Folate, formerly known as folacin, is the generic term for both naturally
occurring food folate and folic acid, the fully oxidized monoglutamate form of
the vitamin that is used in dietary supplements and fortified foods. Folic acid
consists of a p-aminobenzoic molecule linked to a pteridine ring and one
molecule of glutamic acid. Food folates, which exist in various forms, contain
additional glutamate residues, making them polyglutamates .
Folate functions as a coenzyme or cosubstrate in
single-carbon transfers in the synthesis of nucleic acids (DNA and RNA) and
metabolism of amino acids [1-3]. One of the most important folate-dependent
reactions is the conversion of homocysteine to methionine in the synthesis of
S-adenosyl-methionine, an important methyl donor [1-3]. Another
folate-dependent reaction, the methylation of deoxyuridylate to thymidylate in the
formation of DNA, is required for proper cell division. An impairment of this
reaction initiates a process that can lead to megaloblastic anemia, one of the
hallmarks of folate deficiency .
When consumed, food folates are hydrolyzed to the
monoglutamate form in the gut prior to absorption by active transport across
the intestinal mucosa [2]. Passive diffusion also occurs when pharmacological
doses of folic acid are consumed [2]. Before entering the bloodstream, the
monoglutamate form is reduced to tetrahydrofolate (THF) and converted to either
methyl or formyl forms [1]. The main form of folate in plasma is 5-methyl-THF.
Folic acid can also be found in the blood unaltered (known as unmetabolized
folic acid), but whether this form has any biological activity or can be used
as a biomarker of status is not known.
The total body content of folate is estimated to be 10 to 30
mg; about half of this amount is stored in the liver [1,3] and the remainder in
blood and body tissues. A serum folate concentration is commonly used to assess
folate status, with a value above 3 nanograms (ng)/mL indicating adequacy. This
indicator, however, is sensitive to recent dietary intake, so it might not
reflect long-term status. Erythrocyte folate concentration provides a longer-term
measure of folate intakes, so when day-to-day folate intakes are variable—such
as in people who are ill and whose folate intake has recently declined—it might
be a better indicator of tissue folate stores than serum folate concentration.
An erythrocyte folate concentration above 140 ng/mL indicates adequate folate
status , although some researchers have suggested that higher values are
optimal for preventing neural tube defects.
A combination of serum or erythrocyte concentration and
indicators of metabolic function can also be used to assess folate status.
Plasma homocysteine concentration is a commonly used functional indicator of
folate status because homocysteine levels rise when the body cannot convert
homocysteine to methionine due to a 5-methyl-THF deficiency. Homocysteine
levels, however, are not a highly specific indicator of folate status because
they can be influenced by other factors, including kidney dysfunction and
deficiencies of vitamin B12 and other micronutrients [1,3,6]. The most commonly
used cutoff value for elevated homocysteine is 16 micromoles/L, although
slightly lower values of 12 to 14 micromoles/L have also been used.
Iron
Iron: What is it?
Iron, one of the most abundant metals on Earth, is essential
to most life forms and to normal human physiology. Iron is an integral part of
many proteins and enzymes that maintain good health. In humans, iron is an
essential component of proteins involved in oxygen transport. It is also
essential for the regulation of cell growth and differentiation. A deficiency
of iron limits oxygen delivery to cells, resulting in fatigue, poor work
performance, and decreased immunity. On the other hand, excess amounts of iron
can result in toxicity and even death.
Almost two-thirds of iron in the body is found in hemoglobin,
the protein in red blood cells that carries oxygen to tissues. Smaller amounts
of iron are found in myoglobin, a protein that helps supply oxygen to muscle,
and in enzymes that assist biochemical reactions. Iron is also found in
proteins that store iron for future needs and that transport iron in blood.
Iron stores are regulated by intestinal iron absorption.
What foods provide iron?
There are two forms of dietary iron: heme and nonheme. Heme
iron is derived from hemoglobin, the protein in red blood cells that delivers
oxygen to cells. Heme iron is found in animal foods that originally contained
hemoglobin, such as red meats, fish, and poultry. Iron in plant foods such as
lentils and beans is arranged in a chemical structure called nonheme iron. This
is the form of iron added to iron-enriched and iron-fortified foods. Heme iron
is absorbed better than nonheme iron, but most dietary iron is nonheme iron. A
variety of heme and nonheme sources of iron are listed in Tables 1 and 2.
Magnesium
Magnesium, an abundant mineral in the body, is naturally
present in many foods, added to other food products, available as a dietary
supplement, and present in some medicines (such as antacids and laxatives).
Magnesium is a cofactor in more than 300 enzyme systems that regulate diverse
biochemical reactions in the body, including protein synthesis, muscle and
nerve function, blood glucose control, and blood pressure regulation [1-3].
Magnesium is required for energy production, oxidative phosphorylation, and
glycolysis. It contributes to the structural development of bone and is
required for the synthesis of DNA, RNA, and the antioxidant glutathione.
Magnesium also plays a role in the active transport of calcium and potassium
ions across cell membranes, a process that is important to nerve impulse
conduction, muscle contraction, and normal heart rhythm [3].
An adult body contains approximately 25 g magnesium, with
50% to 60% present in the bones and most of the rest in soft tissues [4]. Less
than 1% of total magnesium is in blood serum, and these levels are kept under
tight control. Normal serum magnesium concentrations range between 0.75 and
0.95 millimoles (mmol)/L [1,5]. Hypomagnesemia is defined as a serum magnesium
level less than 0.75 mmol/L [6]. Magnesium homeostasis is largely controlled by
the kidney, which typically excretes about 120 mg magnesium into the urine each
day [2]. Urinary excretion is reduced when magnesium status is low [1].
Assessing magnesium status is difficult because most
magnesium is inside cells or in bone [3]. The most commonly used and readily
available method for assessing magnesium status is measurement of serum
magnesium concentration, even though serum levels have little correlation with
total body magnesium levels or concentrations in specific tissues [6]. Other
methods for assessing magnesium status include measuring magnesium
concentrations in erythrocytes, saliva, and urine; measuring ionized magnesium
concentrations in blood, plasma, or serum; and conducting a magnesium-loading
(or "tolerance") test. No single method is considered satisfactory
[7]. Some experts [4] but not others [3] consider the tolerance test (in which
urinary magnesium is measured after parenteral infusion of a dose of magnesium)
to be the best method to assess magnesium status in adults. To comprehensively
evaluate magnesium status, both laboratory tests and a clinical assessment
might be required.