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Vitamin D is a group of fat-soluble Pro-hormones , the two major forms of which are
:
Vitamin D2 or Ergocaciferol -1
Vit. D2 is derived from Fungal and Plant sources, and is not produced by the human
.body
vitamin D3 or Cholecalciferol-2
Vitamin D3 is derived from animal sources and is produced in skin exposed to sunlight,
.Specifecally UVB Radiation
.Vitamin D plays an important role in the maintenance of Organ System
Vitamin D regulates the Calcium and Phosphorus levels in the Blood by promoting
their absorption in the intestines, and by promoting re-absorption of calcium in the
Kidneys, which enables normal mineralization of bones and prevents hypocalcemic
.Tetany
Vitamin D is an essential hormone for bone growth and development in
children and promotes skeletal health in adults. Currently, an adequate
daily intake of 200 IUs of vitamin D for children is recommended. This is
also the recommendation from the AAP. These levels, however, may not
be adequate for bone growth and musculoskeletal health in children and
adolescents
.It is also needed for bone growth and bone remodeling by osteoblasts and osteoclasts
.Vitamin D can promote soft tissue calcification•
.It inhibits Parathyroid Hormone secretion from the Parathyroid gland•
Vitamin D affects the immune System by promoting, phagocytosis , anti-tumor•
.activity, and immunomodulatory functions
(1(
Vitamin D deficiency
is a growing problem around the world, including in
developed countries where children spend little time outside.
Questions have existed for some time regarding the adequacy of the
current RDA, particularly for older children and adolescents, who
undergo a great deal of bone growth. As the researchers of this study
note, Vitamin D levels during adolescence have bearing on a child’s
.future bone density and risk for other diseases
Vit.D and RDA for Children
Science Daily (May 28, 2008) — The current (RDA) of vitamin D for
children is 200 IU, but new research reveals that children may need and
can safely take 10-times that amount. According to new research this
order-of-magnitude increase could improve the bone health of children
.worldwide and may have other long-term health benefits
Study 1 : New research published in the Journal of Clinical Endocrinology and Metabolism
suggests that the current children’s RDA for Vitamin D (200 IUs( does not sufficiently
support the “bone growth and musculoskeletal health of children and adolescents.”The RDA
value for children was set at 200 IUs because, unlike testing for adults’ dosage, there wasn’t
.adequate research into the benefits of higher amounts
For this placebo-controlled study, researchers gave children various doses of vitamin D at
various intervals and measured the impact this had on serum levels of 25-OHD. For the
short-term study, 25 students (15 boys and 10 girls( received one-weekly, 14,000 IU doses of
vitamin D for eight weeks. Serum levels of 25-OHD were then measured for an additional
eight weeks. This portion of the test was conducted during the summer and early fall, when
the highest natural levels of vitamin D are reached. For the long-term, one-year study, 340
students (172 boys and 168 girls( received either a low dose of vitamin D (1,400 IUs each
.(week( or a high dose (14,000 IUs each week
The study notes that previous research has indicated no difference between daily and weekly
supplementation of Vitamin D. To ensure full compliance, the researchers required weekly,
.on-site administration of the supplement
At the end of the study periods, only those children who had received the “high” dosage
of vitamin D had the recommended optimum serum (blood) levels as they are defined
for adults. (There is less agreement about an ideal serum level for children.( Other benefits
were seen in those who received the higher dose. Researchers observed “substantial
increments in lean mass, bone area and bone mass” particularly in girls. Their observations
from the study caused them to suggest that serum OHD-25 (vitamin D( levels in the mid-
thirties (ng/ml( may be a reasonable and beneficial target for this age group. The researchers
noted that adolescents would be less likely candidates for toxicity because of their body’s
use of the vitamin for constant growth.Our research reveals that vitamin D, at doses
equivalent to 2,000 IUs a day, is not only safe for adolescents, but it is actually necessary for
",achieving desirable vitamin D levels
(2(
Vitamin D3 is one of the most common forms of vitamin D, and is easily converted to 25-
.OHD (25-hydroxyvitamin(, which is the active form of vitamin D found in the blood
For this placebo-controlled study, researchers gave children various doses of vitamin D at
.various intervals and measured the impact this had on serum levels of 25-OHD
For the short-term study, 25 students (15 boys and 10 girls( received one-weekly, 14,000 IU
doses of vitamin D for eight weeks. Serum levels of 25-OHD were then measured for an
additional eight weeks. This portion of the test was conducted during the summer and early
.fall, when the highest natural levels of vitamin D are reached
For the long-term, one-year study, 340 students (172 boys and 168 girls( received either a
.(low dose of vitamin D (1,400 IUs each week( or a high dose (14,000 IUs each week
Only children given the equivalent of 2,000 IUs a day of vitamin D increased 25-OHD
levels from the mid-teens to the mid-thirties (ng/ml(--the level considered optimal for adults.
.None of the children in either trial showed any evidence for vitamin D intoxication
Although many experts agree that a 25-OHD level of 30 ng/ml is desirable in adults, what
constitutes an optimal D level for children and adolescents is more debatable. According to
the researchers, due to rapid skeletal growth, children and adolescents are more likely to be
vitamin D deficient, and are far less likely to reach vitamin D levels that doctors would
.consider toxic
Supplementation of children and adolescents with 2,000 IUs a day of vitamin D3 is well"
tolerated and safe," said Dr. Fuleihan. "This is particularly relevant in light of the
increasingly recognized health benefits of vitamin D for adults and children
Table of Contents
Introduction
Reference Intakes
Sources of Vitamin D
Vitamin D Intakes and Status About
Vitamin D Deficiency General Sa
Groups at Risk of Vitamin D Inadequacy Advi
Vitamin D and Health Discla
Health Risks from Excessive Vitamin D
Interactions with Medications Print-friendly ver
Vitamin D and Healthful Diets
References
Introduction
Vitamin D is a fat-soluble vitamin that is naturally present in very few foods, :Posted D
added to others, and available as a dietary supplement. It is also produced 4/18/2
endogenously when ultraviolet rays from sunlight strike the skin and trigger :Upda
vitamin D synthesis [1-3]. Vitamin D obtained from sun exposure, food, and PM 1:52 12/11/2
supplements is biologically inert and must undergo two hydroxylations in the
body for activation. The first occurs in the liver and converts vitamin D to 25-
hydroxyvitamin D [25(OH)D], also known as calcidiol. The second occurs
primarily in the kidney and forms the physiologically active 1,25-
.[dihydroxyvitamin D [1,25(OH)2D], also known as calcitriol [4
Reference Intakes
Intake reference values for vitamin D and other nutrients are provided in the
Dietary Reference Intakes (DRIs) developed by the Food and Nutrition Board
(FNB) at the Institute of Medicine of The National Academies (formerly
National Academy of Sciences) [5]. DRI is the general term for a set of
reference values used to plan and assess nutrient intakes of healthy people.
:These values, which vary by age and gender [5], include
Recommended Dietary Allowance (RDA): average daily level of•
intake sufficient to meet the nutrient requirements of nearly all (97-
.98%) healthy people
Adequate Intake (AI): established when evidence is insufficient to•
develop an RDA and is set at a level assumed to ensure nutritional
.adequacy
Tolerable Upper Intake Level (UL): maximum daily intake unlikely to•
.[cause adverse health effects [5
The FNB established an AI for vitamin D that represents a daily intake that is
sufficient to maintain bone health and normal calcium metabolism in healthy
people. AIs for vitamin D are listed in both micrograms (mcg) and International
Units (IUs); the biological activity of 1 mcg is equal to 40 IU (Table 2). The AIs
for vitamin D are based on the assumption that the vitamin is not synthesized
.[by exposure to sunlight [5
Fortified foods provide most of the vitamin D in the American diet [5,22]. For
example, almost all of the U.S. milk supply is fortified with 100 IU/cup of
vitamin D (25% of the Daily Value or 50% of the AI level for ages 14-50 years).
In the 1930s, a milk fortification program was implemented in the United
States to combat rickets, then a major public health problem. This program
virtually eliminated the disorder at that time [5,14]. Other dairy products
made from milk, such as cheese and ice cream, are generally not fortified.
Ready-to-eat breakfast cereals often contain added vitamin D, as do some
brands of orange juice, yogurt, and margarine. In the United States, foods
allowed to be fortified with vitamin D include cereal flours and related
products, milk and products made from milk, and calcium-fortified fruit juices
.and drinks [22]. Maximum levels of added vitamin D are specified by law
Sun exposure
Most people meet their vitamin D needs through exposure to sunlight [6,27].
Ultraviolet (UV) B radiation with a wavelength of 290-315 nanometers
penetrates uncovered skin and converts cutaneous 7-dehydrocholesterol to
previtamin D3, which in turn becomes vitamin D3 [11,27-28]. Season,
geographic latitude, time of day, cloud cover, smog, skin melanin content, and
sunscreen are among the factors that affect UV radiation exposure and
vitamin D synthesis [28]. The UV energy above 42 degrees north latitude (a
line approximately between the northern border of California and Boston) is
insufficient for cutaneous vitamin D synthesis from November through
February [6]; in far northern latitudes, this reduced intensity lasts for up to 6
months. Latitudes below 34 degrees north (a line between Los Angeles and
Columbia, South Carolina) allow for cutaneous production of vitamin D
[throughout the year [14
The factors that affect UV radiation exposure and research to date on the
amount of sun exposure needed to maintain adequate vitamin D levels make
it difficult to provide general guidelines. It has been suggested by some
vitamin D researchers, for example, that approximately 5-30 minutes of sun
exposure between 10 AM and 3 PM at least twice a week to the face, arms,
legs, or back without sunscreen usually lead to sufficient vitamin D synthesis
and that the moderate use of commercial tanning beds that emit 2-6% UVB
radiation is also effective [11,28]. Individuals with limited sun exposure need
.to include good sources of vitamin D in their diet or take a supplement
Dietary supplements
In supplements and fortified foods, vitamin D is available in two forms, D2
(ergocalciferol) and D3 (cholecalciferol). Vitamin D2 is manufactured by the UV
irradiation of ergosterol in yeast, and vitamin D3 is manufactured by the
irradiation of 7-dehydrocholesterol from lanolin and the chemical conversion of
cholesterol [11]. The two forms have traditionally been regarded as equivalent
based on their ability to cure rickets, but evidence has been offered that they
are metabolized differently. Vitamin D3 could be more than three times as
effective as vitamin D2 in raising serum 25(OH)D concentrations and
maintaining those levels for a longer time, and its metabolites have superior
affinity for vitamin D-binding proteins in plasma [6,32,33]. Because metabolite
receptor affinity is not a functional assessment, as the earlier results for the
healing of rickets were, further research is needed on the comparative
physiological effects of both forms. Many supplements are being reformulated
to contain vitamin D3 instead of vitamin D2 [33]. Both forms (as well as vitamin
D in foods and from cutaneous synthesis) effectively raise serum 25(OH)D
.[levels [6
The 2000-2004 NHANES provided the most recent data on the vitamin D
nutritional status of the U.S. population [35]. Generally, younger people had
higher serum 25(OH)D levels than older people; males had higher levels than
females; and non-Hispanic whites had higher levels than Mexican Americans,
who in turn had higher levels than non-Hispanic blacks. Depending on the
population group, 1-9% had serum 25(OH)D levels <11 ng/mL (<27.5 nmol/L),
8-36% had levels <20 ng/mL (<50 nmol/L), and the majority (50-78%) had
levels <30 ng/mL (<75 nmol/L). Among adults in the United Kingdom,
nationally representative data collected between 1992 and 2001 show that 5-
20% in most age groups on average had serum 25(OH)D levels <10 ng/ml
(<25 nmol/L); the prevalence of deficiency was greater (range 20-40%) for
older people <65 years of age in residential care homes and among women
<85 years. Among all adults, 20-60% had levels ≥20 ng/ml (≥50 nmol/L) and
.[90% had levels ≥32 ng/ml (≥80 nmol/L) [36
Vitamin D Deficiency
Nutrient deficiencies are usually the result of dietary inadequacy, impaired
absorption and use, increased requirement, or increased excretion. A vitamin
D deficiency can occur when usual intake is lower than recommended levels
over time, exposure to sunlight is limited, the kidneys cannot convert vitamin
D to its active form, or absorption of vitamin D from the digestive tract is
inadequate. Vitamin D-deficient diets are associated with milk allergy, lactose
.[intolerance, and strict vegetarianism [37
Breastfed infants
Vitamin D requirements cannot be met by human milk alone [5,39], which
provides only about 25 IU/L [17]. A recent review of reports of nutritional
rickets found that a majority of cases occurred among young, breastfed
African Americans [40]. The sun is a potential source of vitamin D, but AAP
advises keeping infants out of direct sunlight and having them wear protective
clothing and sunscreen [41]. As noted earlier, AAP recommends that
exclusively and partially breastfed infants be supplemented with 400 IU of
.[vitamin D per day [18
Older adults
Americans aged 50 and older are at increased risk of developing vitamin D
insufficiency [28]. As people age, skin cannot synthesize vitamin D as
efficiently and the kidney is less able to convert vitamin D to its active
hormone form [5,42]. As many as half of older adults in the United States with
.[hip fractures could have serum 25(OH)D levels <12 ng/mL (<30 nmol/L) [6
Osteoporosis
More than 25 million adults in the United States have or are at risk of
developing osteoporosis, a disease characterized by fragile bones that
significantly increases the risk of bone fractures [50]. Osteoporosis is most
often associated with inadequate calcium intakes (generally <1,000-1,200
mg/day), but insufficient vitamin D contributes to osteoporosis by reducing
calcium absorption [51]. Although rickets and osteomalacia are extreme
examples of the effects of vitamin D deficiency, osteoporosis is an example of
a long-term effect of calcium and vitamin D insufficiency [52]. Adequate
storage levels of vitamin D maintain bone strength and might help prevent
osteoporosis in older adults, nonambulatory individuals who have difficulty
exercising, postmenopausal women, and individuals on chronic steroid therapy
.[[53
African Americans have lower levels of 25(OH)D than Caucasians, yet they
develop fewer osteoporotic fractures. This suggests that factors other than
vitamin D provide protection [57]. African Americans have an advantage in
bone density from early childhood, a function of their more efficient calcium
economy, and have a lower risk of fracture even when they have the same
bone density as Caucasians. They also have a higher prevalence of obesity,
and the resulting higher estrogen levels in obese women might protect them
from bone loss [57]. Further reducing the risk of osteoporosis in African
Americans are their lower levels of bone-turnover markers, shorter hip-axis
length, and superior renal calcium conservation. However, despite this
advantage in bone density, osteoporosis is a significant health problem among
.[African Americans as they age [57
Cancer
Laboratory and animal evidence as well as epidemiologic data suggest that
vitamin D status could affect cancer risk. Strong biological and mechanistic
bases indicate that vitamin D plays a role in the prevention of colon, prostate,
and breast cancers. Emerging epidemiologic data suggest that vitamin D has a
protective effect against colon cancer, but the data are not as strong for a
protective effect against prostate and breast cancer, and are variable for
cancers at other sites [58-59]. Studies do not consistently show a protective
effect or no effect, however. One study of Finnish smokers, for example, found
that subjects in the highest quintile of baseline vitamin D status have a three-
.[fold higher risk of developing pancreatic cancer [60
Other conditions
A growing body of research suggests that vitamin D might play some role in
the prevention and treatment of type 1 [65] and type 2 diabetes [66],
hypertension [67], glucose intolerance [68], multiple sclerosis [69], and other
medical conditions [70-71]. However, most evidence for these roles comes
from in vitro, animal, and epidemiological studies, not the randomized clinical
trials considered to be more definitive. Until such trials are conducted, the
implications of the available evidence for public health and patient care will be
.debated
Excessive sun exposure does not result in vitamin D toxicity because the
sustained heat on the skin is thought to photodegrade previtamin D3 and
vitamin D3 as it is formed [11,30]. High intakes of dietary vitamin D are very
unlikely to result in toxicity unless large amounts of cod liver oil are
.consumed; toxicity is more likely to occur from high intakes of supplements
Long-term intakes above the UL increase the risk of adverse health effects [5]
(Table 4). Substantially larger doses administered for a short time or
periodically (e.g., 50,000 IU/week for 8 weeks) do not cause toxicity. Rather,
the excess is stored and used as needed to maintain normal serum 25(OH)D
.[concentrations when vitamin D intakes or sun exposure are limited [15,76
Steroids
Corticosteroid medications such as prednisone, often prescribed to reduce
inflammation, can reduce calcium absorption [77-79] and impair vitamin D
metabolism. These effects can further contribute to the loss of bone and the
.[development of osteoporosis associated with their long-term use [78-79
Other medications
Both the weight-loss drug orlistat (brand names Xenical® and alli™) and the
cholesterol-lowering drug cholestyramine (brand names Questran®,
LoCholest®, and Prevalite®) can reduce the absorption of vitamin D and other
fat-soluble vitamins [80-81]. Both phenobarbital and phenytoin (brand name
Dilantin®), used to prevent and control epileptic seizures, increase the hepatic
metabolism of vitamin D to inactive compounds and reduce calcium
.[absorption [82
The Dietary Guidelines for Americans describes a healthy diet as one that
References
Office of Dietary
Supplements
National Institutes of Health
Bethesda, Maryland 20892
USA
Web: http://ods.od.nih.gov
E-mail: ods@nih.gov
Mechanism of action
Once vitamin D is produced in the skin or consumed in food, it is converted in the liver and kidney to form
1,25 dihydroxyvitamin D, (1,25(OH)2D) the physiologically active form of vitamin D .This metabolically
active form of vitamin D is known as calcitriol. Following this conversion, calcitriol is released into the
circulation, and by binding to a carrier protein in the plasma, vitamin D binding protein (VDBP(, it is
[
transported to various target organs.[7
Vitamin D also affects the immune system, and VDR are expressed in several white blood cells including
[
monocytes and activated T and B cells.[13
-----------------------------------------------------------------------------------------------------------------------------
Ultraviolet Radiation
All energies that move at the speed of light are collectivelly referred to as electromagnetic radiation or 'light'. Various
types of light differ in their wavelength, frequency and energy; higher energy waves have higher frequencies and
shorter wavelengths. Pigments inside the retina of our eyes absorb wavelengths of light between 400nm-700nm,
.collectively referred to as 'visible light'. A "nm'' is a nanometer which is one billionth, or 10e-9, meters
Stratospheric Oxygen and Ozone molecules absorb 97-99% of the sun's high freguency Ultraviolet light, light with
wavelengths between 150 and 300nm. Ultraviolet-B(UV-B) is a section of the UV spectrum, with wavelengths
.between 270 and 320nm
:The amount of UV-B light recieved by a location is strongly dependent on
latitude and elevation of the location. At the high-latitude polar regions the sun is always low in the sky;•
because the sunlight passes through more atmosphere so more of ithe UV-B is absorbed. For this reason
.average UV-B exposure at the poles is over a thousand times lower than at the equator
.cloud cover ; the reduction in UV-B exposure depends the cover's thickness•
proximity to an industrial area because of the protection offered by photochemical smog. Industrial•
processes produce ozone, one of the more irritaiting components of smog, which aborbs UV-B. This is
thought to be one of the main reasons that significant ozone losses in the southern hemisphere have not
.been mirrored in the northern hemisphere
The Cancer link The principle danger of skin cancer is to light-skinned peoples. A 1%decrease in the ozone layer will
cause a estimated 2%increase in UV-B irradiation; it is estimated that this will lead to a 4%increase in basal
carcinomas and 6%increase in squamous-cell carcinomas.[Graedel&Crutzen]. 90% of the skin carcinomas are
attributed to UV-B exposure [Wayne] and the chemical mechanism by which it causes skin cancer has been identified
[Tevini]. The above named carcinomas are relatively easy to treat, if detected in time, and are rarely fatal. But the
much more dangerous malignant melanoma is not as well understood. There appears to be a correlation between
brief, high intensity exposures to UV and eventual appearance (as long as 10-20yrs!) of melanoma. Twice as many
deaths due to melanomas are seen in the southern states of Texas and Florida, as in the northern states of Wisconsin
and Montana, but there could be many other factors involved. One undisputed effect of long-term sun exposure is the
premature aging of the skin due to both UV-A, UV-B and UV-C. Even careful tanning kills skin cells, damages DNA
and causes permanent changes in skin connective tissue which leads to wrinkle formation in later life. There is no
.such thing as a safe tan
Possible eye damage can result from high doses of UV light, particularly to the cornea which is a good absorber of
UV light. High doses of UV light can causes a temporary clouding of the cornea, called 'snow-blindness', and chronic
doses has been tenitively linked to the formation of cataracts. Higher incidences of cataracts are found at high
.(elevations,Tibet and Bolivia; and higher incidences are seen at lower latitudes(approaching the equator
Damage to marine life The penetration of increased amounts of UV-B light has caused great concern over the health
of marine plankton that densly populate the top 2 meters of ocean water. The natural protective-responce of most
chlorophyll containing cells to increased light-radiation is to produce more light-absorbing pigments but this protective
responce is not triggered by UV-B light. Another possible responce of plankton is to sink deeper into the water but this
reduces the amount of visible light they need for photosynthesis, and thereby reduces their growth and reproduction
rate. In other words, the amount of food and oxygen produced by plankton could be reduced by UV exposure without
:killing individual organisms. There are several other considerations
Ultraviolet levels are over 1,000 times higher at the equator than at the polar regions so it is presumed•
that marine life at the equator is much better adapted to the higher enviromental UV light than organisms
in the polar regions. The current concern of marine biologists is mostly over the more sensitive antarctic
phytoplankton which normally would recieve very low doses of UV. Only one large-scale field survey of
Anarctic phytoplankton has been carried out so far [Smith et.al _Science_1992] ; they found a 6-12%
drop in phytoplankton productivity once their ship entered the area of the spring-time ozone hole. Since
the hole only lasts from 10-12weeks this translates into a 2-4%loss overall, a measurable but not yet
.catastrophic loss
Both plants and phytoplankton vary widely in their sensitivity to UV-B. When over 200 agricultural plants•
were tested, more than half showed sensitivity to UV-B light. Other plants showed neglible effects or even
a small increase in vigor. Even within a species there were marked differences; for example one variety of
soybean showed a 16% decrease in growth while another variety of the same soybean showed no effect
[R.Parson]. An increase in UV-B could cause a shift in population rather than a large die-off of plants
An increase in UV-B will cause increased amounts of Ozone to be produced at lower levels in the•
atmosphere. While some have hailed the protection offered by this 'pollution-sheild' many plants have
.shown themselves to be very sensitive to photochemical smog
Ultraviolet Radiation
Gary Zeman, ScD, CHP
Ultraviolet (UV( radiation is defined as that portion of the electromagnetic spectrum between x rays and
visible light, i.e., between 40 and 400 nm (30–3 eV(. The UV spectrum is divided into Vacuum UV (40-190
nm(, Far UV (190-220 nm(, UVC (220-290 nm(, UVB (290-320(, and UVA (320-400 nm(. The sun is our
primary natural source of UV radiation. Artificial sources include tanning booths, black lights, curing
lamps, germicidal lamps, mercury vapor lamps, halogen lights, high-intensity discharge lamps, fluorescent
and incandescent sources, and some types of lasers (excimer lasers, nitrogen lasers, and third harmonic
Nd:YAG lasers(. Unique hazards apply to the different sources depending on the wavelength range of the
.emitted UV radiation
UVC is almost never observed in nature because it is absorbed completely in the atmosphere, as are Far UV
and Vacuum UV. Germicidal lamps are designed to emit UVC radiation because of its ability to kill
bacteria. In humans, UVC is absorbed in the outer dead layers of the epidermis. Accidental overexposure to
UVC can cause corneal burns, commonly termed welders' flash, and snow blindness, a severe sunburn to
.the face. While UVC injury usually clears up in a day or two, it can be extremely painful
UVB is typically the most destructive form of UV radiation because it has enough energy to cause
photochemical damage to cellular DNA, yet not enough to be completely absorbed by the atmosphere. UVB
is needed by humans for synthesis of vitamin D; however, harmful effects can include erythema (sunburn(,
cataracts, and development of skin cancer. Individuals working outdoors are at the greatest risk of UVB
effects. Most solar UVB is blocked by ozone in the atmosphere, and there is concern that reductions in
.atmospheric ozone could increase the prevalence of skin cancer
UVA is the most commonly encountered type of UV light. UVA exposure has an initial pigment-darkening
effect (tanning( followed by erythema if the exposure is excessive. Atmospheric ozone absorbs very little of
this part of the UV spectrum. UVA is needed by humans for synthesis of vitamin D; however, overexposure
to UVA has been associated with toughening of the skin, suppression of the immune system, and cataract
.formation. UVA light is often called black light. Most phototherapy and tanning booths use UVA lamps
The photochemical effects of UV radiation can be exacerbated by chemical agents including birth control
pills, tetracycline, sulphathizole, cyclamates, antidepressants, coal tar distillates found in antidandruff
shampoos, lime oil, and some cosmetics. Protection from UV is provided by clothing, polycarbonate, glass,
acrylics, and plastic diffusers used in office lighting. Sun-blocking lotions offer limited protection against
.UV exposure
Accidental UV overexposure can injure unaware victims due to the fact UV is invisible and does not
produce an immediate reaction. Labeling on UV sources usually consists of a caution or warning label on
the product or the bulb packaging cover or a warning sign on the entryway. Some type of emission indicator
as required with laser products is rarely found. Reported UV accident scenarios often involve work near UV
sources with protective coverings removed, cracked, or fallen off. Depending on the intensity of the UV
source and length of exposure, an accident victim may end up with a lost-time injury even though totally
unaware of the hazardous condition. Hazard communication training is especially important to help prevent
.accidental exposures in the workplace
Exposure guidelines for UV radiation have been established by the American Conference of Governmental
Industrial Hygienists and by the International Commission on Non-Ionizing Radiation Protection. Handheld
meters to measure UV radiation are commercially available, but expert advice is recommended to ensure
.selecting the correct detector and diffuser for the UV wavelengths emitted by the source
Some of the most frequently recognized types of energy are heat and light. These, along with others, can be
classified as a phenomenon known as electromagnetic radiation. Other types of electromagnetic radiation
are gamma rays, X-rays, visible light, infrared rays, and radio waves. The progression of electromagnetic
radiation through space can be visualized in different ways. Some experiments suggest that these rays travel
in the form of waves. A physicist can actually measure the length of those waves (simply called their
wavelength (. It turns out that a smaller wavelength means more energy. At other times, it is more plausible
.to describe electromagnetic radiation as being contained and traveling in little packets, called photons
The distinguishing factor among the different types of electromagnetic radiation is their energy content.
Ultraviolet radiation is more energetic than visible radiation and therefore has a shorter wavelength. To be
more specific: Ultraviolet rays have a wavelength between approximately 100 nanometers and 400
.nanometers whereas visible radiation includes wavelengths between 400 and 780 nanometers
?What does it do
Light enables us to see, and heat keeps us from being cold. However, ultraviolet rays often carry the
unfortunate circumstance of containing too much energy. For example, infrared rays create heat in much the
same way as rubbing your hands together does. The energy contained in the infrared rays causes the
molecules of the substance it hits to vibrate back and forth. However, the energy contained in ultraviolet
rays is higher, so instead of just causing the molecules to shake, it actually can knock electrons away from
the atoms, or causes molecules to split. This results in a change in the chemical structure of the molecule.
This change is especially detrimental to living organisms, as it can cause cell damage and deformities by
.actually mutating its genetic code
?What stops it
Ultraviolet rays can be subdivided into three different wavelength bands—UV-A, UV-B, and UV-C. This is
simply a convenient way of classifying the rays based on the amount of energy they contain and their effects
.on biological matter. UV-C is most energetic and most harmful; UV-A is least energetic and least harmful
Luckily,UV-C rays do not reach the earth’s surface because of the ozone layer. When UV-C rays meet the
ozone molecules at high layers of the atmosphere, the energy inherent in them is enough to break apart the
bond of the molecule and absorb the energy. Therefore, no UV-C rays from the sun ever come into contact
.with life on earth, though man-produced UV-C rays can be a hazard in certain professions, such as welders
UV-B rays have a lower energy level and a longer wavelength than UV-C. As their energy is often not
sufficient to split an ozone molecule, some of them extend down to the earth's surface. UV-A rays do not
have enough energy to break apart the bonds of the ozone, so UV-A radiation passes the earth's atmosphere
almost unfiltered. As both UV-B and UV-A rays can be detrimental to our health, it is important that we
protect ourselves. This can be done through a variety of ways. The most obvious is to reduce the amount of
time one spends in the sun, particularly between the hours of 11 am and 3 pm, when the sun is at its highest
in the sky. However, especially during the summer holidays, this does not always work out. More ways to
.protect ourselves can be found here
Variability of UV
UV levels are not constant over the course of a day, or even over the course of a year. An obvious factor is
the position of the sun in the sky. At noon, for example, the electromagnetic waves emitted from the sun
travel a much shorter path through the earth’s atmosphere then they would at, say, 5 pm, and thus noon-time
intensity is stronger. A second important parameter determining UV at the ground is the amount of ozone
present in the stratosphere. Low ozone correlates with much UV. However, there are many other features of
the environment that contribute to UV radiation variability. Most important are clouds. On cloudy days, UV
levels are usually lower than during clear skies as clouds can deflect rays up into space. Clouds can,
however, also lead to increased UV levels. This happens, for example, when the sun is not obscured by
clouds but clouds in the vicinity of the sun reflect additional radiation to the ground. So a general rule is not
!to feel save from UV radiation just because it's cloudy
The amounts of UV one is exposed to also varies with altitude. As a rule of thumb, UV levels increase about
4% for every 1,000 foot gain in altitude. This increase has nothing to do with being closer to the sun—any
elevation you might gain would be miniscule in comparison to the distance from the earth to the sun, and so
would have an insignificant outcome on UV levels. Instead, the increase is the result of a thinner
atmosphere with a smaller number of molecules being present to absorb or scatter UV. Examples of such
molecules are tropospheric ozone (commonly associated with smog( and aerosols, molecules that remain
suspended in the air. Aerosols can be a multitude of substances—dust, soot, sulfates, etc. These aerosols
.absorb and scatter UV rays, and so cut down on the ultimate UV irradiance
Other factors that have an influence on UV levels are the physical features of the land—sand, snow, and
water all tend to reflect UV rays. This phenomenon is called albedo. Some of the ultraviolet rays reflected
off the ground encounter scattering by air molecules, aerosols or clouds back down to the earth, thus
increasing the total irradiance. When there is snow on the ground the amount of time it takes for sunburn to
.occur is therefore significantly reduced
Also, the closer one is to the equator, the more ultraviolet rays one is exposed to. This can be explained by
the fact that the sun is usually higher at the sky at low latitudes. In addition, the ozone layer is thinner at the
.equator as it is over, for example the United States or Europe, and this also contributes to more UV
Since the 1980s, polar regions are affected by the ozone hole. Under the ozone hole, biologically relevant
UV levels are 2-3 times as high as they were before. Learn, based on real data, how UV levels are affected
by the ozone hole by going to the experiments page! Here you can compare UV radiation measured by the
.NSF network in Antarctica with satellite ozone data
Ultraviolet (UV( light is electromagnetic radiation with a wavelength shorter than that of visible light, but
longer than x-rays, in the range 400 nm to 10 nm, and energies from 3 eV to 124 eV. It is so named because
the spectrum consists of electromagnetic waves with frequencies higher than those that humans identify as
the color violet
Electromagnetic radiation—Any of a number of types of energy (i.e. radio waves, micro-
waves, ultraviolet rays, infrared or heat rays, light, X-rays, and gamma rays( that travel at
.the speed of light
Ultraviolet radiation (or UV radiation)— Electromagnetic radiation with wavelengths between 100 and .
400 nanometers. These rays are emitted from the sun and are not visible. They inflict increasingly more
damage upon a recipient as the wavelength decreases. Based on its effects, UV radiation is subdivided into
:three wavelength ranges named UV-A, UV-B and UV-C
UV-A covers the wavelength range 320-400 nm. UV-A is not absorbed by the ozone layer and is•
.the least harmful UV radiation
UV-B covers the wavelength range 280-320 nm. UV-B is more energetic than UV-A, and is•
partially absorbed by the ozone layer. UV-B rays that are not filtered out cause sunburn and other
.harmful effects to humans
UV-C covers the wavelength range 100-280 nm. UV-C is the most dangerous form of UV•
radiation, but is completely absorbed by the ozone layer. Artificial UV-C (for example emitted
.by electric discharges( is a threat for certain occupational group, like welders
UV Index—UV Index is a way of expressing the amount of sun-burning UV radiation. It was invented to
inform the public about the intensity of UV radiation, and is now published in newspapers and on TV. The
definition of the UV Index is the same throughout the world, so it's a great way to learn about the UV
hazards at your travel destinations. The Index is a simple number. 1-3 means low exposure; 4-6 means
.medium; 7-9 means high; and more than 10 means extreme exposure
Mostly wavelengths in the UV-B contribute to the UV Index. The contribution from the UV-A is only about
10%. Therefore, the UV Index is highly affected by the thickness of the ozone layer, in contrast to UV-A
.radiation
The time you can stay outside in the sun at a given UV Index depends also on on your skin type. For
example, if you have fair skin (skin type I( and the UV Index is seven, it takes less than 20 minutes until
your skin starts to redden. If you have a dark skin color the same UV level may need more than 40 minutes
to cause an effect. Check out the noontime UV Index at San Diego measured by the NSF network! During
.summer it is typically 10—this means extreme
Visible light—Electromagnetic radiation with wavelengths between 380 and 780 nanometers. It is the only
.type of radiation that the human eye can see
Wavelength—A concept used to describe the energy of electromagnetic radiation, in which the rays are
visualized as traveling in a wave-like pattern. The length of these peaks varies and is the identifying factor
.in the type of ray (e.g. x-ray, ultraviolet, visible(. A shorter wavelength means more energy
The sun radiates energy in a wide range of wavelengths, most of which are invisible to human eyes. The
shorter the wavelength, the more energetic the radiation, and the greater the potential for harm. Ultraviolet
(UV( radiation that reaches the Earth’s surface is in wavelengths between 290 and 400 nm (nanometers, or
.billionths of a meter(. This is shorter than wavelengths of visible light, which are 400 to 700 nm
UV radiation from the sun has always played important roles in our environment, and affects nearly all
living organisms. Biological actions of many kinds have evolved to deal with it. Yet UV radiation at
different wavelengths differs in its effects, and we have to live with the harmful effects as well as the
helpful ones. Radiation at the longer UV wavelengths of 320-400 nm, designated as UV-A, plays a helpful
and essential role in formation of Vitamin D by the skin, and plays a harmful role in that it causes sunburn
on human skin and cataracts in our eyes. Radiation at shorter wavelengths of 290-320 nm, designated as
UV-B, causes damage at the molecular level to the fundamental building block of life— deoxyribonucleic
.(acid (DNA
Electromagnetic radiation exists in a range of wavelengths, which are delineated into major divisions for
our convenience. Ultraviolet B radiation, harmful to living organisms, represents a small portion of the
(spectrum, from 290 to 320 nanometer wavelengths. (Illustration by Robert Simmon
DNA readily absorbs UV-B radiation, which commonly changes the shape of the molecule in one of several
ways. The illustration below illustrates one such change in shape due to exposure to UV-B radiation.
Changes in the DNA molecule often mean that protein-building enzymes cannot “read” the DNA code at
.that point on the molecule. As a result, distorted proteins can be made, or cells can die
.The darker the skin, the higher the risk of deficiency of vitamin d
Your location on earth and the altitude of where you live also makes a big difference. So does the season
.you are in and the UV index
For instance your skin gets to produce much higher vitamin d dosage at 10,000 feet elevation than at sea
.level
Also if you live near the equator, your skin will produce much higher amounts compared to other locations
.on earth
But no one of course should intentionally expose his or her skin to UV rays or ultraviolet radiation,
.especially if there is a family history of skin cancers
Otherwise, it is still considered very dangerous not to have any kind of sun protection or sun protective
.clothing while being out doors in the sun
.One could get it from a tanning bed too, but even that could be harmful to your skin
.The UV rays can lead to skin cancer, with melanoma being one of the deadliest
.Therefore, it might be more logical for certain individuals to obtain it thru foods rich in vitamin d
Milk, some cereals (1 cup, fortified with 10% daily value, 40 IU( and certain breads have been fortified for
.many years now
Also cooked fish like salmon (3.5oz, 360 IU( or canned tuna fish in oil (3oz, 200 IU( and sardines in oil
.(1.75oz, 250 IU( are considered natural vitamin d rich foods
Cod liver oil has the highest amount of vitamin D (1,360 IU per tablespoon( where as one cup of nonfat
.fortified milk contains 98 IU
s
Page 72 -- THE SUN
UV radiation is divided into UV-A, UV-B and UV-C. UV-C is absorbed by the ozone layer and does not
present any threat (man made sources of UV-C, like electric welding arcs, are very harmful to the eyes, if
you do not use the proper protection(. That's not true of UV-A and UV-B. More and more scientific
evidence is showing that exposure to both UV-A and UV-B can have damaging long and short term effects
.on your eyes and vision
If you are exposed, unprotected, to excessive amounts of UV radiation over a short period of time, you are
likely to experience an effect called photokeratitis. Like a "sunburn of the eye" it may be painful and you
may have symptoms including red eyes, a foreign body sensation or gritty feeling in the eyes, extreme
sensitivity to light and excessive tearing. Fortunately, this is usually temporary and rarely causes permanent
.damage to the eyes
Long term exposure to UV radiation can be more serious. A number of scientific studies and research have
shown that exposure to small amounts of UV-B radiation over a period of many years may increase your
chance of developing a cataract and can cause damage to the retina, the nerve-rich lining of your eye that is
.used for seeing. Damage to the retina is usually not reversible
edit[ Vitamin D [
The Earth's atmosphere blocks UV radiation from penetrating through the atmosphere by 98.7%. A positive
effect of UVB exposure is that it induces the production of vitamin D in the skin. It has been estimated that
tens of thousands of premature deaths occur in the United States annually from a range of cancers due to
vitamin D deficiency.[6] Another effect of vitamin D deficiency is bad absorption of calcium which can lead
.to bone diseases
[Some studies show most people get adequate Vitamin D through food and incidental exposure,[7
Many countries have fortified certain foods with Vitamin D to prevent deficiency. Eating fortified foods or
taking a dietary supplement pill is usually preferred to UVB exposure, due to the increased risk of skin
[
cancer from UV radiation.[7
edit[ Aesthetics [
Too little UVB radiation leads to a lack of Vitamin D. Too much UVB radiation leads to direct DNA
damages and sunburn. An appropriate amount of UVB (which varies according to skin color( leads to a
limited amount of direct DNA damage. This is recognized and repaired by the body. Then the melanin
production is increased which leads to a long lasting tan. This tan occurs with a 2 day lag phase after
irradiation, but it is much less harmful and long lasting than the one obtained from UVA. However some
.tanning lotions and sprays available in the market doesn't require UV exposition
edit[ Medical applications [
Ultraviolet radiation has other medical applications, in the treatment of skin conditions such as psoriasis and
vitiligo. UVA radiation can be used in conjunction with psoralens (PUVA treatment(. UVB radiation is
rarely used in conjunction with psoralens. In cases of psoriasis and vitiligo, UV light with wavelength of
[
311 nm is most effective.[citation needed
edit] Harmful effects]
An overexposure to UVB radiation can cause sunburn and some forms of skin cancer. In humans, prolonged
exposure to solar UV radiation may result in acute and chronic health effects on the skin, eye, and immune
system.[8] However the most deadly form - malignant melanoma - is mostly caused by the indirect DNA
damage (free radicals and oxidative stress(. This can be seen from the absence of a UV-signature mutation
[
in 92% of all melanoma.[9
UVC rays are the highest energy, most dangerous type of ultraviolet light. Little attention has been given to
UVC rays in the past since they are filtered out by the atmosphere. However, their use in equipment such as
pond sterilization units may pose an exposure risk, if the lamp is switched on outside of its enclosed pond
.sterilization unit
Ultraviolet photons harm the DNA molecules of living organisms in different ways. In one
common damage event, adjacent Thymine bases bond with each other, instead of across the
."ladder". This makes a bulge, and the distorted DNA molecule does not function properly
edit[ Skin [
“
Ultraviolet (UV) irradiation present in sunlight is an environmental human
carcinogen. The toxic effects of UV from natural sunlight and therapeutic artificial
lamps are a major concern for human health. The major acute effects of UV
irradiation on normal human skin comprise sunburn inflammation erythema,
.tanning, and local or systemic immunosuppression ”
Matsumura and Ananthaswamy —
UVA, UVB and UVC can all damage collagen fibers and thereby accelerate aging of the skin. Both UVA
and UVB destroy vitamin A in skin which may cause further damage.[11] In the past UVA was considered
less harmful, but today it is known that it can contribute to skin cancer via the indirect DNA damage (free
radicals and reactive oxygen species(. It penetrates deeply but it does not cause sunburn. UVA does not
damage DNA directly like UVB and UVC, but it can generate highly reactive chemical intermediates, such
as hydroxyl and oxygen radicals, which in turn can damage DNA. Because it does not cause reddening of
the skin (erythema( it cannot be measured in the SPF testing. There is no good clinical measurement of the
blocking of UVA radiation, but it is important that sunscreen block both UVA and UVB. Some scientists
blame the absence of UVA filters in sunscreens for the higher melanoma-risk that was found for sunscreen
[
users.[12
The reddening of the skin due to the action of sunlight depends both on the amount of
sunlight as well as the sensitivity of the skin ("erythemal action spectrum") over the UV
.spectrum
UVB light can cause direct DNA damage. The radiation excites DNA molecules in skin cells, causing
aberrant covalent bonds to form between adjacent cytosine bases, producing a dimer. When DNA
polymerase comes along to replicate this strand of DNA, it reads the dimer as "AA" and not the original
"CC". This causes the DNA replication mechanism to add a "TT" on the growing strand. This is a mutation,
which can result in cancerous growths and is known as a "classical C-T mutation". The mutations that are
caused by the direct DNA damage carry a UV signature mutation that is commonly seen in skin cancers.
The mutagenicity of UV radiation can be easily observed in bacteria cultures. This cancer connection is one
reason for concern about ozone depletion and the ozone hole. UVB causes some damage to collagen but at a
.very much slower rate than UVA
As a defense against UV radiation, the amount of the brown pigment melanin in the skin increases when
exposed to moderate (depending on skin type( levels of radiation; this is commonly known as a sun tan. The
purpose of melanin is to absorb UV radiation and dissipate the energy as harmless heat, blocking the UV
from damaging skin tissue. UVA gives a quick tan that lasts for days by oxidizing melanin that was already
present and triggers the release of the melanin from melanocytes. UVB yields a tan that takes roughly 2
days to develop because it stimulates the body to produce more melanin. The photochemical properties of
melanin make it an excellent photoprotectant. However, sunscreen chemicals can not dissipate the energy of
the excited state as efficiently as melanin and therefore the penetration of sunscreen ingredients into the
[
lower layers of the skin is increasing the amount of free radicals and ROS.[13
Sunscreen prevents the direct DNA damage which causes sunburn. Most of these products contain an SPF
rating to show how well they block UVB rays. The SPF rating, however, offers no data about UVA
protection. In the US, the FDA is considering adding a star rating system to show UVA protection. A similar
.system is already used in some European countries
Some sunscreen lotions now include compounds such as titanium dioxide which helps protect against UVA
rays. Other UVA blocking compounds found in sunscreen include zinc oxide and avobenzone. Cantaloupe
extract, rich in the compound superoxide dismutase (SOD(, can be bound with gliadin to form glisodin, an
orally-effective protectant against UVB radiation. There are also naturally occurring compounds found in
rainforest plants that have been known to protect the skin from UV radiation damage, such as the fern
.Phlebodium aureum
edit] Sunscreen safety debate]
Main article: Sunscreen controversy
Medical organizations recommend that patients protect themselves from UV radiation using sunscreen. Five
.(sunscreen ingredients have been shown to protect mice against skin tumors (see sunscreen
However, some sunscreen chemicals produce potentially harmful substances if they are illuminated while in
contact with living cells.[14][15][16] The amount of sunscreen which penetrates through the stratum corneum
[may or may not be large enough to cause damage. In one study of sunscreens, the authors write:[17
The question whether UV filters acts on or in the skin has so far not been fully answered. Despite the fact
that an answer would be a key to improve formulations of sun protection products, many publications
.carefully avoid addressing this question
In an experiment that was published in 2006 by Hanson et al, the amount of harmful reactive oxygen
species (ROS( had been measured in untreated and in sunscreen treated skin. In the first 20 minutes the film
of sunscreen had a protective effect and the number of ROS species was smaller. After 60 minutes however
the amount of absorbed sunscreen was so high, that the amount of ROS was higher in the sunscreen treated
[
skin than in the untreated skin.[13
edit[ Eye [
High intensities of UVB light are hazardous to the eyes, and exposure can cause welder's flash
.(photokeratitis or arc eye( and may lead to cataracts, pterygium,[18][19] and pinguecula formation
Protective eyewear is beneficial to those who are working with or those who might be exposed to ultraviolet
radiation, particularly short wave UV. Given that light may reach the eye from the sides, full coverage eye
protection is usually warranted if there is an increased risk of exposure, as in high altitude mountaineering.
Mountaineers are exposed to higher than ordinary levels of UV radiation, both because there is less
.atmospheric filtering and because of reflection from snow and ice
Ordinary, untreated eyeglasses give some protection. Most plastic lenses give more protection than glass
lenses, because, as noted above, glass is transparent to UVA and the common acrylic plastic used for lenses
is less so. Some plastic lens materials, such as polycarbonate, inherently block most UV. There are
protective treatments available for eyeglass lenses that need it which will give better protection. But even a
.treatment that completely blocks UV will not protect the eye from light that arrives around the lens
edit] Degradation of polymers, pigments and dyes]
Many polymers used in consumer products are degraded by UV light, and need addition of UV absorbers to
inhibit attack, especially if the products are used outdoors and so exposed to sunlight. The problem appears
as discoloration or fading, cracking and sometimes, total product disintegration if cracking has proceeded
.far enough. The rate of attack increases with exposure time and sunlight intensity
It is known as UV degradation, and is one form of polymer degradation. Sensitive polymers include
thermoplastics, such as polypropylene and polyethylene as well as speciality fibres like aramids. UV
absorption leads to chain degradation and loss of strength at sensitive points in the chain structure. They
.include tertiary carbon atoms, which in polypropylene occur in every repeat unit
In addition, many pigments and dyes absorb UV and change colour, so paintings and textiles may need extra
protection both from sunlight and fluorescent lamps, two common sources of UV radiation. Old and antique
paintings such as watercolour paintings for example, usually need to be placed away from direct sunlight.
Common window glass provides some protection by absorbing some of the harmful UV, but valuable
.artifacts need shielding
edit] Nutrition]
.Milk and cereal grains are often fortified with vitamin D
A blood calcidiol (25-hydroxy-vitamin D( level is the accepted way to determine vitamin D nutritional
status. The optimal level of serum 25-hydroxyvitamin D is 35–55 ng/mL; with some debate among medical
scientists for the slightly higher value. Supplementation of 100 IU (2.5 mcg( vitamin D3 raises circulating
[
25(OH(D by 2.5 nmol/l (1 ng/ml(.[16
Season, geographic latitude, time of day, cloud cover, smog, and sunscreen affect UV ray exposure and
vitamin D synthesis in the skin, and it is important for individuals with limited sun exposure to include good
sources of vitamin D in their diet. The 2005 Dietary Guidelines for Americans recommend that older adults,
people with dark skin, and those exposed to insufficient ultraviolet radiation (i.e., sunlight( consume extra
vitamin D from vitamin D-fortified foods and/or supplements. Individuals in these high-risk groups should
consume 25 μg (1000 IU( of vitamin D daily to maintain adequate blood concentrations of 25-
hydroxyvitamin D. The Canadian Pediatric Society recommends 2,000 IU daily for pregnant and
[
breastfeeding women.[17
In many countries, foods such as milk, yogurt, margarine, oil spreads, breakfast cereal, pastries, and bread
are fortified with vitamin D2 and/or vitamin D3, to minimize the risk of vitamin D deficiency.[18] In the
United States and Canada, for example, fortified milk typically provides 100 IU per glass, or one quarter of
[
the estimated adequate intake for adults over the age of 50.[1
Very few foods are naturally rich in vitamin D, so much vitamin D intake in the industrialized world is from
fortified products including milk, soy milk and breakfast cereals or supplements.[1] Natural sources of
[vitamin D include:[1
Fish liver oils, such as cod liver oil, 1 Tbs. (15 mL) provides 1,360 IU (one IU equals•
(25 ng
:Fatty fish species, such as•
Herring, 85g (3 oz) provides 1383 IU○
Catfish, 85g (3 oz) provides 425 IU○
Salmon, cooked, 3.5 oz provides 360 IU○
Mackerel, cooked, 3.5 oz, 345 IU○
Sardines, canned in oil, drained, 1.75 oz, 250 IU○
Tuna, canned in oil, 3 oz, 200 IU○
Eel, cooked, 3.5 oz, 200 IU○
One whole egg, provides 20 IU•
Beef liver, cooked, 3.5 ounces, provides 15 IU•
Deficiency of vitamin D can result from a number of factors including: inadequate intake coupled with
inadequate sunlight exposure, disorders that limit its absorption, conditions that impair conversion of
vitamin D into active metabolites, such as liver or kidney disorders and body characteristics such as skin
color and body fat. Rarely deficiency can result from a number of hereditary disorders.[2] Deficiency results
:in impaired bone mineralization, and leads to bone softening diseases[20] including
Rickets, a childhood disease characterized by impeded growth, and deformity, of•
the long bones. The role of diet in the development of rickets was determined by
Edward Mellanby between 1918–1920.[21] In 1921 Elmer McCollum identified a
substance found in certain fats that could prevent rickets. Prior to the fortification of
milk products with vitamin D, rickets was a major public health problem. In the
United States the fortification of milk with 10 micrograms (400 IU) of vitamin D per
[
quart in the 1930s led to a dramatic decline in the number of rickets cases.[15
Osteomalacia, a bone-thinning disorder that occurs exclusively in adults and is•
.characterized by proximal muscle weakness and bone fragility
Osteoporosis, a condition characterized by reduced bone mineral density and•
.increased bone fragility
Vitamin D malnutrition may also be linked to an increased susceptibility to several chronic diseases such as
high blood pressure, tuberculosis, cancer, periodontal disease, multiple sclerosis, chronic pain,
depression[22][not in citation given], schizophrenia[22], seasonal affective disorder[23][24], peripheral artery disease[25] and
several autoimmune diseases including type 1 diabetes (see role in immunomodulation(.[15][26] There is an
association between low vitamin D levels and Parkinson's disease, but whether Parkinson's causes low
vitamin D levels, or whether low vitamin D levels play a role in the pathogenesis of Parkinson's disease has
[
not been established.[27
edit] Overdose]
.For more details on this topic, see hypervitaminosis D
Vitamin D stored in the human body as calcidiol (25-hydroxy-vitamin D( has a large volume of distribution
and a half-life of about 20 to 29 days.[13] However, the synthesis of bioactive vitamin D hormone is tightly
regulated and vitamin D toxicity usually occurs only if excessive doses (prescription forms or rodenticide
analogs( are taken.[28] Although normal food and pill vitamin D concentration levels are far too low to be
toxic in adults, because of the high vitamin A content in codliver oil, it is possible to reach toxic levels of
vitamin A (but not vitamin D( via this route, [29] if taken in multiples of the normal dose in an attempt to
increase the intake of vitamin D. Most historical cases of vitamin D overdose have occurred due to
[
manufacturing and industrial accidents.[30
Exposure to sunlight for extended periods of time does not cause vitamin D toxicity.[30] This is because
within about 20 minutes of ultraviolet exposure in light skinned individuals (3–6 times longer for pigmented
skin( the concentration of vitamin D precursors produced in the skin reach an equilibrium, and any further
vitamin D that is produced is degraded.[31] Maximum endogenous production with full body exposure to
[
sunlight is 250 µg (10,000 IU( per day.[30
The exact long-term safe dose of vitamin D is not entirely known, but dosages up to 250 micrograms
(10,000 IU( /day in healthy adults are believed to be safe.[13], and all known cases of vitamin D toxicity with
hypercalcemia have involved intake of or over 1,000 micrograms (40,000 IU(/day[30]. The U.S. Dietary
Reference Intake Tolerable Upper Intake Level (UL( of vitamin D for children and adults is
50 micrograms/day (2,000 IU/day(, although this is widely presumed to be below actual physiological daily
requirements. In adults, sustained intake of 2500 micrograms/day (100,000 IU( can produce toxicity within
a few months.[2] For infants (birth to 12 months( the tolerable UL is set at 25 micrograms/day (1000 IU/day(,
and vitamin D concentrations of 1000 micrograms/day (40,000 IU( in infants has been shown to produce
toxicity within 1 to 4 months. In the United States, overdose exposure of vitamin D was reported by 284
individuals in 2004, leading to 1 death.[32] The Nutrition Desk Reference states "The threshold for toxicity is
500 to 600 micrograms [vitamin D] per kilogram body weight per day."[33] The United States Environmental
[
Protection Agency published an oral LD50 of 619 mg/kg for female rats.[34
Serum levels of calcidiol (25-hydroxy-vitamin D( are typically used to diagnose vitamin D overdose. In
healthy individuals, calcidiol levels are normally between 32 to 70 ng/mL (80 to 175 nmol/L(, but these
levels may be as much as 15-fold greater in cases of vitamin D toxicity. Serum levels of bioactive vitamin D
[
hormone (1,25(OH2(D( are usually normal in cases of vitamin D overdose.[2
Some symptoms of vitamin D toxicity are a result of hypercalcemia (an elevated level of calcium in the
blood( caused by increased intestinal calcium absorption. Vitamin D toxicity is known to be a cause of high
blood pressure.[35] Gastrointestinal symptoms of vitamin D toxicity can include anorexia, nausea, and
vomiting. These symptoms are often followed by polyuria (excessive production of urine(, polydipsia
(increased thirst(, weakness, nervousness, pruritus (itch(, and eventually renal failure. Other signals of
kidney disease including elevated protein levels in the urine, urinary casts, and a build up of wastes in the
blood stream can also develop.[2] In one study, hypercalciuria and bone loss occurred in four patients with
documented vitamin D toxicity.[36] Another study showed elevated risk of ischaemic heart disease when 25D
[was above 89 ng/mL.[37
Vitamin D toxicity is treated by discontinuing vitamin D supplementation, and restricting calcium intake. If
the toxicity is severe blood calcium levels can be further reduced with corticosteroids or bisphosphonates.
[
In some cases kidney damage may be irreversible.[2
edit] Role in immunomodulation]
The hormonally active form of vitamin D mediates immunological effects by binding to nuclear vitamin D
receptors (VDR( which are present in most immune cell types including both innate and adaptive immune
cells. The VDR is expressed constitutively in monocytes and in activated macrophages, dendritic cells, NK
cells, T and B cells. In line with this observation, activation of the VDR has potent anti-proliferative, pro-
differentiative, and immunomodulatory functions including both immune-enhancing and
[
immunosuppressive effects.[38
Effects of VDR-ligands, such as vitamin D hormone, on T-cells include suppression of T cell activation and
induction of regulatory T cells, as well as effects on cytokine secretion patterns.[39] VDR-ligands have also
been shown to affect maturation, differentiation, and migration of dendritic cells, and inhibits DC-dependent
[
T cell activation, resulting in an overall state of immunosuppression.[40
VDR ligands have also been shown to increase the activity of natural killer cells, and enhance the
phagocytic activity of macrophages.[13] Active vitamin D hormone also increases the production of
cathelicidin, an antimicrobial peptide that is produced in macrophages triggered by bacteria, viruses, and
fungi.[41] Vitamin D deficiency tends to increase the risk of infections, such as influenza[42] and
tuberculosis[43][44][45]. In a 1997 study, Ethiopian children with rickets were 13 times more likely to get
[
pneumonia than children without rickets.[46
These immunoregulatory properties indicate that ligands with the potential to activate the VDR, including
supplementation with calcitriol (as well as a number of synthetic modulators(, may have therapeutic clinical
applications in the treatment of; inflammatory diseases (rheumatoid arthritis, psoriatic arthritis(,
dermatological conditions (psoriasis, actinic keratosis(, osteoporosis, cancers (prostate, colon, breast,
myelodysplasia, leukemia, head and neck squamous cell carcinoma, and basal cell carcinoma(, and
autoimmune diseases (systemic lupus erythematosus, type I diabetes, multiple sclerosis( and in preventing
[
organ transplant rejection.[38
A 2006 study published in the Journal of the American Medical Association, reported evidence of a link
between Vitamin D deficiency and the onset of Multiple Sclerosis; the authors posit that this is due to the
[
immune-response suppression properties of Vitamin D.[47
edit] Role in cancer prevention and recovery]
The Canadian Cancer Society recommends that adults should consider supplementeing with 1,000 IU of
vitamin D per day during the fall and winter. They base this recommendation on the growing evidence for a
[
link between vitamin D and a reduced risk for colorectal, breast and prostate cancers.[48
The vitamin D hormone, calcitriol, has been found to induce death of cancer cells in vitro and in vivo.
Although the anti-cancer activity of vitamin D is not fully understood, it is thought that these effects are
mediated through vitamin D receptors expressed in cancer cells, and may be related to its
immunomodulatory abilities. The anti-cancer activity of vitamin D observed in the laboratory has prompted
some to propose that vitamin D supplementation might be beneficial in the treatment or prevention of some
[
types of cancer.[13
A search of primary and review medical literature published between 1970 and 2007 found an increasing
body of research supporting the hypothesis that the active form of vitamin D has significant, protective
effects against the development of cancer. Epidemiological studies show an inverse association between sun
exposure, serum levels of 25(OH(D, and intakes of vitamin D and risk of developing and/or surviving
cancer. The protective effects of vitamin D result from its role as a nuclear transcription factor that regulates
cell growth, differentiation, apoptosis and a wide range of cellular mechanisms central to the development
of cancer.[49] In 2005, scientists released a metastudy which demonstrated a beneficial correlation between
vitamin D intake and prevention of cancer. Drawing from a meta-analysis of 63 published reports, the
authors showed that intake of an additional 1,000 international units (IU( (or 25 micrograms( of vitamin D
daily reduced an individual's colon cancer risk by 50%, and breast and ovarian cancer risks by 30%.[50]
Research has also shown a beneficial effect of high levels of calcitriol on patients with advanced prostate
cancer.[51] A randomized intervention study involving 1,200 women, published in June 2007, reports that
vitamin D supplementation (1,100 international units (IU(/day( resulted in a 60% reduction in cancer
incidence, during a four-year clinical trial, rising to a 77% reduction for cancers diagnosed after the first
year (and therefore excluding those cancers more likely to have originated prior to the vitamin D
intervention(.[52][53] In 2006, a study at Northwestern University found that taking the U.S. RDA of vitamin
D (400 IU per day( cut the risk of pancreatic cancer by 43% in a sample of more than 120,000 people from
[
two long-term health surveys.[54][55
A 2006 study using data on over 4 million cancer patients from 13 different countries showed a marked
difference in cancer risk between countries classified as sunny and countries classified as less–sunny for a
number of different cancers.[56] Research has also suggested that cancer patients who have surgery or
treatment in the summer — and therefore make more endogenous vitamin D — have a better chance of
surviving their cancer than those who undergo treatment in the winter when they are exposed to less
[
sunlight.[57
A scientific review undertaken by the National Cancer Institute found no link between baseline vitamin D
status and overall cancer mortality. They did find that vitamin D was beneficial in preventing colorectal
cancer, which showed an inverse relationship with blood levels "80 nmol/L or higher associated with a 72%
[
risk reduction".[58
Vitamin D regulates the expression of genes associated with cancers and autoimmune disease by controlling
the activation of the vitamin D receptor (VDR(, a type 1 nuclear receptor and DNA transcription factor.[59]
Research has indicated that vitamin D deficiency is linked to colon cancer and more recently, to breast
[
cancer.[60
edit] Role in cardiovascular disease prevention]
Research indicates that vitamin D may play a role in preventing or reversing coronary disease.[61][62] Vitamin
D deficiency is associated with an increase in high blood pressure and cardiovascular risk. When
researchers monitored the vitamin D levels, blood pressure and other cardiovascular risk factors of 1739
people, of an average age of 59 years for 5 years, they found that those people with low levels of vitamin D
[
had a 62% higher risk of a cardiovascular event than those with normal vitamin D levels.[63
A report from the National Health and Nutrition Examination Survey (NHANES( found that low levels of
vitamin D were associated with an increased risk of peripheral artery disease (PAD(. Researchers divided
4,839 participantes in NHANES into quartiles (four groups( based on their blood levels of vitamin D, and
found that increasing levels of vitamin D were associated with a lower prevalence of PAD. The authors
adjusted for other factors which could influence the development of PAD (such as smoking and high
cholesterol( and found that among participants with the lowest vitamin D levels (<17.8 ng/mL( PAD was
[
80% more common than in individuals with the highest levels (>29.2 ng/mL( of vitamin D. [25
Researchers publishing in the Journal of Circulation studied the blood levels of vitamin D in 1739 middle-
aged children of partipants in the Framingham Heart Study in Framinhgam, Massachussetts (their mean age
was 59 years; 55% were women; all were white( who did not have any prior history of cardiovascular
disease. These subjects were followed for a mean of 5.4 years. The authors adjusted for other conventional
risk factors for cardiovascular disease which could have confounded the results and still found that among
the 120 individuals in this group who suffered a first cardiovascular event, those who had the lowest levels
of vitamin D were most likely to have had an event. Individuals with lowest levels of vitamin D (<15
ng/mL( had a 62% increased risk (95% confidence interval 1.11 to 2.36, P=0.01( for having a first
cardiovascular event compared with those with vitamin D levels of 15 ng/mL. This effect was evident in
[
participants with hypertension, but not in those without hypertension. [64
In a study of 34 middle-aged men, researchers found that low levels of vitamin D were associated with
[
hypertension, elevated VLDL triglycerides, and impaired insulin metabolism.[65
As with cancer incidence, a qualitative inverse correlations was found between coronary disease incidence
and serum vitamin D levels of 32.0 versus 35.5 ng/mL.[66] Cholesterol levels were found to be reduced in
gardeners in the UK during the summer months.[67] Heart attacks peak in winter and decline in summer in
[
temperate[68] but not tropical latitudes.[69
The issue of vitamin D in heart health has not yet been settled. Exercise may account for some of the benefit
attributed to vitamin D, since vitamin D levels are higher in physically active persons.[70] Moreover, there
may be an upper limit after which cardiac benefits decline. One study found an elevated risk of ischaemic
heart disease in Southern India in individuals whose vitamin D levels were above 89 ng/mL.[71] These sun-
living groups results do not generalize to sun-deprived urban dwellers. Among a group with heavy sun
exposure, taking supplemental vitamin D are unlikely to result in blood levels over the ideal range, while
urban dwellers not taking supplemental vitamin D may fall under the levels recognized as ideal, and being
.below the preferable levels may cause adverse affects on the health of each group
edit] Role in all-cause mortality]
Low vitamin D levels are associated with cancer, diabetes, and hypertension, and in increased mortality
among patients undergoing dialysis. Using the National Health and Nutrition Examination Survey Melamed
and coworkers at the Albert Einstein College of Medicine evaluated whether low serum vitamin D levels
were associated with mortality in the general population. The researchers studied the association of low
vitamin D levels with all-cause mortality, cancer, and cardiovascular disease (CVD( mortality among
13,331 diverse American adults who were 20 years or older. Vitamin D levels of these participants were
collected over a 6-year period (from 1988 through 1994(, and individuals were passively followed for
mortality through the year 2000. The researchers found that being older, female, nonwhite, having diabetes,
a current smoker, and having a higher body mass index were all independently associated with a greater risk
of being vitamin D deficient, while greater physical activity, vitamin D supplementation, and evaluating
subjects in a non-winter season (greater exposure to sunshine( were all associated with higher levels. During
a median of 8.7 years of follow-up, there were 1806 deaths, including 777 (43%( from CVD. The authors
divided the participants into 4 groups (quartiles( based on their serum vitamin D levels, and adjusted for
baseline demographics, season, and CVD risk factors. Being in the lowest quartile (vitamin D levels <17.8
ng/mL( was associated with a 26% increased rate of all-cause mortality (mortality rate ratio, 1.26; 95% CI,
1.08-1.46(. The adjusted models of CVD and cancer mortality revealed a higher risk, but it was not
statistically significant. The authors concluded that having low levels of vitamin D (<17.8 ng/mL( was
[
independently associated with an increase in all-cause mortality in the general population. [72
Among many factors that may be responsible for vitamin D's apparent beneficial effect on all-cause
mortality is its effect on telomeres and its potential effect on slowing aging. Richards and coworkers
examined whether vitamin D concentrations would slow the rate of shortening of leukocyte telomeres (a
marker of aging(. The authors stated that vitamin D is a potent inhibitor of the proinflammatory response
and slows the turnover of leukocytes. Leukocyte telomere length (LTL( predicts the development of aging-
related disease, and length of these telomeres decreases with each cell division and with increased
inflammation (more common in the elderly(. Researchers measured serum vitamin D concentrations in 2160
women aged 18-79 years (mean age: 49.4( from a large population-based cohort of twins. This study
divided the group into thirds [tertiles http://en.wiktionary.org/wiki/tertile] based on vitamin D levels, and
found that increased age was significantly associated with shorter LTL (r = -0.40, P < 0.0001(. Higher serum
vitamin D concentrations were significantly associated with longer LTL (r = 0.07, P = 0.0010(, and this
finding persisted even after adjustment for age (r = 0.09, P < 0.0001( and other variables that independently
could affect LTL (age, season of vitamin D measurement, menopausal status, use of hormone replacement
therapy, and physical activity(. The difference in LTL between the highest and lowest tertiles of vitamin D
was highly significant (P = 0.0009(, and the authors stated that this was equivalent to 5.0 years of aging.
The authors concluded that higher vitamin D levels, (easily modifiable through nutritional
supplementation(, were associated with longer LTL, which underscores the potentially beneficial effects of
[
vitamin D on aging and age-related diseases. [73
ietary Supplement Fact Sheet: Vitamin D
Introduction
Reference Intakes
Sources of Vitamin D
Vitamin D Intakes and Status
Vitamin D Deficiency
Groups at Risk of Vitamin D Inadequacy
Vitamin D and Health
Health Risks from Excessive Vitamin D
Interactions with Medications
Vitamin D and Healthful Diets
References
Introduction
Vitamin D is a fat-soluble vitamin that is naturally present in very few foods, added to others,
and available as a dietary supplement. It is also produced endogenously when ultraviolet rays
from sunlight strike the skin and trigger vitamin D synthesis [1-3]. Vitamin D obtained from sun
exposure, food, and supplements is biologically inert and must undergo two hydroxylations in
the body for activation. The first occurs in the liver and converts vitamin D to 25-
hydroxyvitamin D [25(OH)D], also known as calcidiol. The second occurs primarily in the kidney
and forms the physiologically active 1,25-dihydroxyvitamin D [1,25(OH)2D], also known as
.[calcitriol [4
Vitamin D is essential for promoting calcium absorption in the gut and maintaining adequate
serum calcium and phosphate concentrations to enable normal mineralization of bone and
prevent hypocalcemic tetany. It is also needed for bone growth and bone remodeling by
osteoblasts and osteoclasts [4-6]. Without sufficient vitamin D, bones can become thin, brittle,
or misshapen. Vitamin D sufficiency prevents rickets in children and osteomalacia in adults
.[3,7,8]. Together with calcium, vitamin D also helps protect older adults from osteoporosis
Vitamin D has other roles in human health, including modulation of neuromuscular and
immune function and reduction of inflammation. Many genes encoding proteins that regulate
cell proliferation, differentiation, and apoptosis are modulated in part by vitamin D [4,6,9,10].
Many laboratory-cultured human cells have vitamin D receptors and some convert 25(OH)D to
1,25(OH)2D [11]. It remains to be determined whether cells with vitamin D receptors in the
.intact human carry out this conversion
Serum concentration of 25(OH)D is the best indicator of vitamin D status. It reflects vitamin D
produced cutaneously and that obtained from food and supplements [5] and has a fairly long
circulating half-life of 15 days [15]. However, serum 25(OH)D levels do not indicate the amount
of vitamin D stored in other body tissues. Circulating 1,25(OH)2D is generally not a good
indicator of vitamin D status because it has a short half-life of 15 hours and serum
concentrations are closely regulated by parathyroid hormone, calcium, and phosphate [15].
.[Levels of 1,25(OH)2D do not typically decrease until vitamin D deficiency is severe [6,11
Serum concentrations of 25(OH)D are reported in both nanograms per milliliter (ng/mL) and *
.(nanomoles per liter (nmol/L
.ng/mL = 2.5 nmol/L 1 **
Vitamin D
Buy the Book
Pronunciations
cholecalciferol
corticosteroid
ergocalciferol
hypercalcemia
hyperparathyroidism
osteoma
osteomalacia
osteoporosis
rifampin
Causes
The most common cause is inadequate exposure to sunlight. Thus, vitamin D
deficiency occurs mainly among people who do not spend much time outdoors:
older people and people who live in an institution such as a nursing home. The
deficiency can also occur in the winter at northern and southern latitudes or in
people who keep their bodies covered, such as Muslim women. Because breast
milk contains only small amounts of vitamin D, breastfed infants who are not
.exposed to enough sunlight are at risk of the deficiency and rickets
When the skin is exposed to enough sunlight, the body usually forms enough
vitamin D. However, certain circumstances increase the risk of vitamin D
:deficiency even when there is exposure to sunlight
The skin forms less vitamin D in response to sunlight in certain•
groups of people. They include people with darker skin (particularly
.blacks(, older people, and people who use sunscreen
The body may not be able to absorb enough vitamin D from foods. In•
malabsorption disorders, people cannot absorb fats normally (see
Malabsorption(. They also cannot absorb vitamin D because it is a
fat-soluble vitamin, which is normally absorbed with fats in the small
.intestine
The body may not be able to convert vitamin D to an active form.•
Certain kidney and liver disorders and several rare hereditary
disorders interfere with this conversion, as do certain drugs, such as
some anticonvulsants and rifampin Some Trade Names
RIFADIN
RIMACTANE
.
Spotlight on Aging
Older people are likely to develop
vitamin D deficiency for several
:reasons
Their requirements are•
.higher than younger persons
They tend to spend less time•
outdoors, or stay indoors
more in the winter, and thus
are not exposed to enough
.sunlight
They may not be exposed to•
enough sunlight because they
are housebound, live in long-
term care facilities, or need
to stay in the hospital for a
.long time
When exposed to sunlight,•
their skin does not form as
.much vitamin D
They consume so little•
vitamin D in their diet that
even taking vitamin D
supplements in low doses
(such as 400 units per day(
does not prevent the
.deficiency
They may have disorders or•
take drugs that interfere with
.the processing of vitamin D
New studies suggest that older adults
may need more vitamin D than the
current recommended dietary allowance
or even the recommended upper limits.
In fact, they may need 1000 to 2000 IU
(or more( daily, but taking such high
amounts should be done only after
consulting a doctor. Older people who
take high amounts of vitamin D
supplements need to have periodic
blood tests to check their levels of
calcium, vitamin D, and parathyroid
.hormone
Symptoms
Vitamin D deficiency can cause muscle aches, weakness, and bone pain in
people of all ages. Muscle spasms, which are caused by a low calcium level, may
.be the first sign of rickets in infants
In young infants who have rickets, the entire skull may be soft. Older infants
may be slow to sit and crawl, and the spaces between the skull bones
(fontanelles( may be slow to close. In children aged 1 to 4 years, bone growth
may be abnormal, causing an abnormal curve in the spine and bowlegs or knock-
knees. These children may be slow to walk. For older children and adolescents,
walking is painful. The pelvic bones may flatten, narrowing the birth canal in
adolescent girls. In adults, the bones, particularly the spine, pelvis, and leg bones,
.weaken. Affected areas may be painful to touch, and fractures may occur
.In older people, bone fractures may result from only slight jarring or a minor fall
Diagnosis
Doctors suspect vitamin D deficiency when people report an inadequate diet or
exposure to sunlight. Doctors also suspect the deficiency in older adults,
especially in those with decreased bone density (for example, with osteoporosis(
or broken bones. Blood tests to measure vitamin D can confirm the deficiency.
X-rays may also be taken. The diagnosis of rickets or osteomalacia is based on
symptoms, the characteristic appearance of bones on x-rays, and a low level of
.vitamin D in the blood
Prevention and Treatment
Many people need to take vitamin D supplements. Getting enough exposure to
sunlight may be difficult, especially because the skin also needs to be protected
from sun damage. The diet rarely contains enough vitamin D to compensate for
lack of sunlight. Many multiple vitamins contain little or no vitamin D, so most
people need to take vitamin D supplements. These supplements are particularly
important for people who are at risk (such as people who are older, housebound,
or living in long-term care facilities(. Commercially available liquid milk (but
not cheese or yogurt( is fortified in the United States and Canada. Many other
countries do not fortify milk with vitamin D. Breakfast cereals may also be
.fortified
In breastfed infants, starting vitamin D supplements at birth is particularly
important because breast milk contains little vitamin D. Commercial infant
.formulas contain enough vitamin D
Treatment involves taking high doses of vitamin D by mouth or by injection
daily or weekly for 1 to 2 months or longer. If muscle spasms are present or
calcium is thought to be deficient, calcium supplements are also given. If
phosphate is deficient, phosphate supplements are given. Usually, this treatment
leads to a complete recovery. People with a chronic liver or kidney disorder may
.require special formulations of vitamin D supplements
Vitamin D Excess
Taking very high daily doses of vitamin D—for example, 50 or more times the
recommended daily allowance (RDA(—over several months can cause toxicity
and a high calcium level in the blood (hypercalcemia—see Minerals and
.(Electrolytes: Hypercalcemia
Early symptoms are loss of appetite, nausea, and vomiting, followed by
excessive thirst, weakness, nervousness, and high blood pressure. Because the
calcium level is high, calcium may be deposited throughout the body, particularly
in the kidneys, blood vessels, lungs, and heart. The kidneys may be permanently
.damaged and malfunction, resulting in kidney failure
Vitamin D excess is usually diagnosed when blood tests detect a high calcium
level in a person who takes high doses of vitamin D. The diagnosis is confirmed
.by measuring the level of vitamin D in the blood
:Treatment consists of the following
Stopping vitamin D supplements•
Following a low-calcium diet for a while to offset the effects of a high•
calcium level in the body
Taking drugs (such as corticosteroids or bisphosphonates( to suppress•
the release of calcium from the bones
Last full review/revision August 2007 by Larry E. Johnson, MD, PhD
Vitamin D Deficiency
Vitamin D deficiency is common, particularly in children, pregnant women, breastfed
babies, and anyone who stays indoors or covers their skin. It is important to treat and
prevent deficiency to ensure good health, growth and strong bones. See your doctor if
you think you are at risk of vitamin D deficiency, or if you have symptoms such as
muscle or bone pains. Vitamin D deficiency is easily treated and prevented with vitamin
supplements. Pregnant and breastfeeding women, breastfed babies, and other people
.at risk of vitamin D deficiency should take vitamin D supplements
Growing children, pregnant women, and breastfeeding women need extra vitamin D because it is required
:for growth. So, vitamin D deficiency is more likely to develop in the following groups of people
.Pregnant or breastfeeding women•
Breastfed babies whose mothers are lacking in vitamin D, or with prolonged•
breastfeeding. (These babies do not need to stop breastfeeding, they can have
.(“breast milk plus vitamin drops – “breast is still best
People who get very little sunlight on their skin such as those who are stay indoors•
.a lot, or cover up when outside, for example, if wearing a veil
People with conditions that affect the way the body handles vitamin D such as those•
.with coeliac disease, Crohn’s disease, and some types of liver and kidney disease
People taking certain medicines: carbamezepine, phenytoin, primidone or•
.barbiturates
People with dark skins or of South Asian origin, elderly people, and those with a•
.family history of vitamin D deficiency
Sometimes, a wrist x-ray is done for a child. This can assess how severe the problem is by looking for
.changes in the wrist bones
Extra tests may be needed if the cause of the deficiency is in doubt, or if there are other vitamin or mineral
deficiencies. For example, if anaemia is found as well, you should have a blood test to look for coeliac
.disease
?What is the treatment for vitamin D deficiency
.Note: if you are pregnant or breastfeeding, see the next section after this
The treatment is to take vitamin D supplements. This is a form of vitamin D called ergocalciferol or
calciferol. (The dose of ergocalciferol is written in units known as international units or IU. Some people
use microgrammes or μg instead, which are not the same as units.( There are various different ways of
:taking vitamin D, which are
Injection
A single small injection of vitamin D will last for about six months. This is a very effective and convenient
treatment. It is useful for people who do not like taking medicines by mouth, or who are likely to forget to
.take their tablets
High dose tablets or liquids
There are different strengths available and a dose may be taken either daily, weekly or monthly. This will
depend on your situation and on which particular treatment guideline your doctor is using. Always check
with your doctor that you understand the instructions - with high doses of vitamin D it is important to take
the medicine correctly. The advantage of the higher dose treatment is that the deficiency improves quickly -
.important in growing children
Standard dose tablets, powders or liquids
These need to be taken every day for about 12 months in order that the body can "catch up" on the missing
vitamin D. This is a rather slow method of replacing vitamin D, but is suitable if the deficiency is mild, or
for prevention. A disadvantage is that all these preparations contain either calcium or other vitamins, giving
.them a strong taste which some people dislike. Cod liver oil is an alternative
Important note: if you are pregnant or breastfeeding you should not use high doses of vitamin D (the
injections and high dose tablets/liquids described above(. This is because of uncertainty about whether these
doses are too high for the baby. Doctors tend to be cautious about the dose of vitamin D given to pregnant
or breastfeeding women, and will often limit the dose to 1,000 units daily. This is a safe dose. It is likely
.that higher doses are safe for pregnant women, but we are waiting for more guidance on this subject
Important note: if you are pregnant, do not take supplements containing large amounts of vitamin A.
Supplements labelled as suitable for pregnancy are safe to use. Also, do not eat liver which contains large
.amounts of vitamin A, as too much can harm the baby. Vitamin A is safe if you are breastfeeding
?Are there any side-effects from vitamin D supplements
It is very unusual to get side effects from vitamin D if taken in the prescribed dose. However, very high
doses can raise calcium levels in the blood. This would cause symptoms such as thirst, passing a lot of
urine, nausea or vomiting, dizziness and headaches. If you have these symptoms, see a doctor immediately
.so that your calcium level can be checked with a blood test
Some guidelines advise that people taking high vitamin D doses should have their calcium levels checked
during the first few weeks. In practice, this is not usually done unless you have symptoms of high calcium
.as described above
?What is the outcome with vitamin D deficiency
The outcome is generally very good. Both the vitamin levels and the symptoms usually respond well to
treatment. However, it can take time (months( for bones to recover. So, if you have symptoms such as bone
.pain, this will also take time to improve
There are some possible complications of severe deficiency (see below(. Most of these will improve or
.recover with treatment
Very severe, prolonged deficiency may cause bone problems (rickets or osteomalacia( which could lead to a
.deformity if treated very late
?Are there any complications from vitamin D deficiency
Mild or short-lived vitamin D deficiency usually causes no symptoms. With prolonged deficiency, the risk
of getting osteoporosis (bone thinning and fractures in old age( is probably increased. The risk of getting
other diseases might also be increased. This is uncertain, but it is possible that vitamin D helps to prevent
.some conditions such as diabetes, heart disease and cancer
Follow up
Most people who are treated for vitamin D deficiency will need to be reviewed a few weeks or months after
.starting treatment - depending how severe their symptoms are. A further review after one year is advised
Prevention
Once you have been treated for vitamin D deficiency, prevention is needed to stop the deficiency from
recurring again in the future. Diet change and sunshine can help (see below(. Many people find it hard to
change their diets or to get more sunshine, and so will need to take long-term vitamin D supplements.
:Supplements to prevent deficiency are
Babies under one year: should have 200 units (5 micrograms) daily of vitamin D.•
Breastfed babies should be given vitamin drops (see breastfeeding section above).
Babies fed by formula milk do not need vitamin drops, as this milk already contains
.vitamin D
Children aged over one year: should have 280-400 units (7-10 micrograms) daily•
of vitamin D. This is usually given as vitamin drops or tablets. Babies fed by formula
milk do not need vitamin drops, as this milk already contains vitamin D. But when
weaned on to ordinary milk they should have supplements, as ordinary milk in the
UK contains little vitamin D. (Note: some countries outside of the UK do add
(.vitamins to ordinary milk
Adults: supplements of 400 units (10 micrograms) daily. However, people who get•
no sunshine, and the elderly, probably need more - approximately 800 units (20
.micrograms) daily
Higher preventative doses may be needed in certain situations. For•
example, for people on certain medicines (carbamezepine, phenytoin, primidone
.and barbiturates) and with other conditions such as liver or kidney disease
Cod liver oil can be taken instead of the usual vitamin D supplements (to give the same dose of vitamin D(.
However, be careful about using cod liver oil if you are pregnant, as it also contains vitamin A, which may
be harmful in large amounts (see pregnancy section(. Another option, instead of daily supplements, is to use
the higher dose tablets, liquids or injections, taken at longer intervals. For example, this could be a weekly
or monthly high dose tablet, or an injection every six to twelve months. You can discuss these options with
.your doctor
Diet and sunshine for vitamin D
Foods containing good amounts of vitamin D are: liver, some fish (mainly oily fish such as herring,
sardines, pilchards, trout, salmon, tuna and mackerel(, egg yolk, and 'fortified' foods (which have vitamin D
.added( such as some margarines and breakfast cereals
Sunshine: 15 minutes three times weekly from April to September, with hands, arms and face uncovered, is
said to be enough for fair-skinned people. Darker-skinned people will need more sunshine (we don't know
how much more(. However, in winter in cold climates, there is not enough sunshine to maintain vitamin D
.levels
A useful source of information
Healthy Start Scheme
Web: www.healthystart.nhs.uk
A government run scheme. With Healthy Start, you can get free vouchers every week which you swap for
milk, fresh fruit, fresh vegetables and infant formula milk. You can also get free vitamins. You could qualify
.if you're on benefits or you're pregnant and under 18
:See also
Vitamin•
Dietary Supplement•
Cholesterol•
Chronic Illness•
Nutrition•
Leukemia•
Reference
B vitamins•
Essential nutrient•
Vitamin D•
Vitamin K•
In a new report Trevor Marshall, Ph.D., professor at Australia’s Murdoch University School of Biological
Medicine and Biotechnology, explains how increased vitamin D intake affects much more than just nutrition
or bone health. The paper explains how the Vitamin D Nuclear Receptor (VDR( acts in the repression or
transcription of hundreds of genes, including genes associated with diseases ranging from cancers to
.multiple sclerosis
The VDR is at the heart of innate immunity, being responsible for expression of most of the antimicrobial"
.peptides, which are the body’s ultimate response to infection," Marshall said
Molecular biology is now forcing us to re-think the idea that a low measured value of vitamin D means we"
simply must add more to our diet. Supplemental vitamin D has been used for decades, and yet the epidemics
".of chronic disease, such as heart disease and obesity, are just getting worse
Our disease model has shown us why low levels of vitamin D are observed in association with major and"
chronic illness," Marshall added. "Vitamin D is a secosteroid hormone, and the body regulates the
production of all it needs. In fact, the use of supplements can be harmful, because they suppress the immune
".system so that the body cannot fight disease and infection effectively
Marshall's research has demonstrated how ingested vitamin D can actually block VDR activation, the
opposite effect to that of Sunshine. Instead of a positive effect on gene expression, Marshall reported that
his own work, as well as the work of others, shows that quite nominal doses of ingested vitamin D can
suppress the proper operation of the immune system. It is a different metabolite, a secosteroid hormone
called 1,25-dihydroxyvitamin D, which activates the VDR to regulate the expression of the genes. Under
conditions that exist in infection or inflammation, the body automatically regulates its production of all the
vitamin D metabolites, including 25-hydroxyvitamin D, the metabolite which is usually measured to
.indicate vitamin D status
Vitamin D deficiency, long interpreted as a cause of disease, is more likely the result of the disease process,
and increasing intake of vitamin D often makes the disease worse. "Dysregulation of vitamin D has been
observed in many chronic diseases, including many thought to be autoimmune," said J.C. Waterhouse,
.Ph.D., lead author of a book chapter on vitamin D and chronic disease
We have found that vitamin D supplementation, even at levels many consider desirable, interferes with"
".recovery in these patients
We need to discard the notion that vitamin D affects a disease state in a simple way," Marshall said."
"Vitamin D affects the expression of over 1,000 genes, so we should not expect a simplistic cause and effect
between vitamin D supplementation and disease. The comprehensive studies are just not showing that
".supplementary vitamin D makes people healthier
Journal reference: Marshall TG. Vitamin D discovery outpaces FDA decision making. Bioessays. 2008 Jan
15;30(2(:173-182 [Epub ahead of print] Online ISSN: 1521-1878 Print ISSN: 0265-9247 PMID: 18200565
:Need to cite this story in your essay, paper, or report? Use one of the following formats
APA
MLA
Autoimmunity Research Foundation (2008, January 27). Vitamin D Deficiency Study Raises
New Questions About Disease And Supplements. ScienceDaily. Retrieved January 8, 2009,
from http://www.sciencedaily.com/releases/2008/01/080125223302.htm
Vitamin D deficiency
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Definition
Vitamin D deficiency exists when the concentration of 25-hydroxy-vitamin D (25-OH-D( in the blood
serum occurs at 12 nanograms/milliliter (ng/ml( or less. This is one-half to one-fourth the amount normally
present. When vitamin D deficiency continues for many months in growing children, the disease commonly
.referred to as rickets occurs
Description
Vitamin D is a fat-soluble vitamin, meaning it can be dissolved in fat. While some vitamin D is supplied by
the diet, most of it is made in the body. To make vitamin D, cholesterol, a substance widely distributed in
animal tissues, the yolk of eggs, and various oils and fats, is necessary. Once cholesterol enters the body, a
slight alteration in the cholesterol molecule occurs, with one change taking place in the skin. This alteration
requires ultraviolet light, a component of sunlight. Vitamin D deficiency and rickets tend to occur in
.children who do not get enough sunlight and who do not eat foods that are rich in vitamin D
Once consumed or made in the body, vitamin D is further altered to produce a substance called 1,25-
dihydroxy-vitamin D (1,25-diOH-D(. The conversion of vitamin D to 1,25-diOH-D occurs in the liver and
kidney. The role of 1,25-diOH-D in the body is to keep the concentration of calcium at a constant level in
the bloodstream. Maintaining calcium at a constant level is absolutely required for human life, since
dissolved calcium is required for nerves and muscles to work. One of the ways in which 1,25-diOH-D
.accomplishes this is by stimulating the absorption of dietary calcium by the intestines
The sequence of events that can lead to vitamin D deficiency and later to bone disease, is as follows: a lack
of vitamin D in the body creates an inability to manufacture 1,25-diOH-D. This results in decreased
absorption of dietary calcium and an increased loss of calcium in the feces. When this happens, the bones
are affected. Vitamin D deficiency results in a lack of bone mineralization (calcification( in growing
.children
Demographics
Vitamin D deficiency is not common in the United States and other industrialized countries because of the
wide availability of vitamin D fortified infant formulas and milks. It is somewhat more common in northern
areas where there is not as much sunlight present during many parts of the year. Vitamin D deficiency is
also slightly more common in inner city areas, because environmental factors, such as smog, can block the
necessary ultraviolet (UV( component of sunlight. Children with darkly pigmented skin are more likely to
be vitamin D deficient than light skinned children. Children who are exclusively breast-fed without vitamin
D supplementation, particularly if they are not exposed to sunlight, are at higher risk of vitamin D
.deficiency
Causes and symptoms
Vitamin D deficiency can be caused by conditions that result in little exposure to sunlight. These conditions
include: living in northern regions, having dark skin, and having little chance to go outside. Children whose
faces and bodies remain covered when outside can develop vitamin D deficiency even while living in a
sunny climate. In-born errors of vitamin D metabolism can also cause vitamin D deficiency and rickets;
these children cannot convert inactive vitamin D to active vitamin D and suffer the same symptoms as
.children with a nutritional deficiency
Most foods contain little or no vitamin D. As a result, sunshine is often a deciding factor in whether vitamin
D deficiency occurs. Although fortified milk and fortified infant formula contain high levels of vitamin D,
human breast milk is rather low in the vitamin. (The term fortified means that vitamins are added to the
(.food by the manufacturer
The Recommended Dietary Allowance (RDA( of vitamin D for both children and adults is 200 International
Units (IU( per day. Saltwater fish such as salmon, herring, and sardines are naturally rich in vitamin D.
Vitamin D fortified milk contains 400 IU per quart (liter(, so half a quart (liter( of milk provides the RDA.
.For comparison, human breast milk contains only 4 to 60 IU per quart
No harm is likely to result from vitamin D deficiency that occurs only a few days a year. If the deficiency
occurs for a period of many months or years, however, rickets may develop. The symptoms of rickets
include bowed legs and bowed arms. The bowed appearance is due to the softening of bones, and their
bending if the bones are weight-bearing. Bone growth occurs through the creation of new cartilage, a soft
substance at the ends of bones. When the mineral calcium phosphate is deposited onto the cartilage, a hard
structure is created. In vitamin D deficiency, though, calcium is not available to create hardened bone, and
the result is soft bone. Other symptoms of rickets include bony bumps on the ribs called rachitic rosary
(beadlike prominences at the junction of the ribs with their cartilages( and knock-knees. Seizures may also
occasionally occur in a child with rickets, because of reduced levels of dissolved calcium in the
.bloodstream
When to call the doctor
The doctor should be called if the parent notices that the child has any signs of vitamin D deficiency or
rickets. Such signs include skeletal pain, bowed limbs, and impaired growth. If there are lifestyle factors
that make the child at risk for vitamin D deficiency, such as low milk or formula intake, a doctor should be
.consulted about the possibility of using vitamin D supplements
Diagnosis
Vitamin D deficiency is diagnosed by measuring the level of 25-hydroxy-vitamin D in the blood serum. The
normal concentration of this form of vitamin D ranges from 25 to 50 ng/ml. Deficiency occurs
.when this level decreases to about 12 ng/ml or less
Rickets is diagnosed by x-ray examination of the leg bones. A distinct pattern of irregularities,
abnormalities, and a coarse appearance can be clearly seen if a child has rickets. Measurements of blood
plasma 25-OH-D, blood plasma calcium, and blood plasma parathyroid hormone must also be obtained for
the diagnosis of this disease. Parathyroid hormone and 1,25-diOH-D work together in the body to regulate
.the levels of calcium in the blood
Treatment
Rickets heals promptly with large doses vitamin D administered orally each day for approximately one
month. During this treatment, the doctor should monitor the levels of 25-OH-D in the plasma to make sure
that they are raised to a normal level. The bone abnormalities (visible by x ray( generally disappear
gradually over a period of three to nine months. Parents are instructed to take their infants outdoors for
approximately 20 minutes per day with their faces exposed. Children should be encouraged to play outside
and to eat foods that are good sources of vitamin D. These foods include cod liver oil, egg yolks, butter, oily
.fish and also foods, including milk and breakfast cereals, that are fortified with synthetic vitamin D
Care must be taken in treating vitamin D deficiency, since high doses of vitamin D are toxic (poisonous(
and can result in the permanent deposit of minerals in the heart, lungs, and kidneys. Symptoms of toxicity
are nausea, vomiting, pain in the joints, and lack of interest in eating food. In adults, vitamin D toxicity
occurs with eating 50,000 IU or more per day. In infants, toxicity occurs with 1,000 IU per day. The
.continued intake of toxic doses results in death
Rickets are usually treated with oral supplements of vitamin D, with the recommendation to acquire daily
exposure to direct sunlight. An alternative to sunlight is the use of an ultraviolet lamp. When people use UV
lamps, they need to cover their eyes to protect them against damage. Many types of sunglasses allow UV
light to pass through, so only those that are opaque to UV light should be used. Attempts to acquire sunlight
through glass windows fail to help the body make vitamin D because UV light does not pass through
.window glass
Rickets may also occur with calcium deficiency, even when a child is regularly exposed to sunshine. This
type of rickets has been found in various parts of Africa. The bone deformities are similar to, or are the
same as, those that occur in typical rickets; however, calcium deficiency rickets is treated by increasing the
amount of calcium in the diet. No amount of vitamin D can cure the rickets of a child with a diet that is
extremely low in calcium. For this reason, it is recommended that calcium be given in conjunction with
.vitamin D supplementation
Prognosis
The prognosis for correcting vitamin D deficiency and rickets is excellent. Vitamin D treatment results in
the return of bone mineralization to a normal rate, the correction of low plasma calcium levels, the
prevention of seizures, and a recovery from bone pain. On the other hand, already established deformities
.such as bowed legs and the rachitic rosary persist throughout adult life
Prevention
Vitamin D deficiency is a very preventable. Eating foods that are high in vitamin D or foods that have been
fortified with additional vitamins in combination with getting moderate amounts of exposure to direct
.sunlight, are usually enough to prevent vitamin D deficiency
KEY TERMS
.hydroxy-vitamin D—The form of vitamin D that is measured in order to assess vitamin D deficiency-25
Cholesterol—A steroid fat found in animal foods that is also produced in the human body from saturated
fat. Cholesterol is used to form cell membranes and process hormones and vitamin D. High cholesterol
.levels contribute to the development of atherosclerosis
Fat-soluble vitamin—A vitamin that dissolves easily in fat or oil, but not in water. The fat-soluble vitamins
.are vitamins D, E, A, and K
International unit (IU)—A measurement of biological activity in which one IU is equal to one mg
.((milligram
Rachitic rosary—Beadlike bumps present at the junction of the ribs with their cartilages. It is often seen in
.children with rickets
Recommended Dietary Allowance (RDA)—The Recommended Dietary Allowances (RDAs( are
quantities of nutrients in the diet that are required to maintain good health in people. RDAs are established
by the Food and Nutrition Board of the National Academy of Sciences, and may be revised every few years.
A separate RDA value exists for each nutrient. The RDA values refer to the amount of nutrient expected to
maintain good health in people. The actual amounts of each nutrient required to maintain good health in
.specific individuals differ from person to person
Rickets—A condition caused by the dietary deficiency of vitamin D, calcium, and usually phosphorus, seen
.primarily in infancy and childhood, and characterized by abnormal bone formation
Some authorities still recommend exposure to sunshine as a way to prevent vitamin D deficiency, but early
exposure to direct sunlight may be linked to a higher incidence of skin cancer later in life, so other experts
recommend that infants not be taken into direct sunlight without protective coverings or sunscreen until at
least six months of age. These experts recommend that supplemental drops or fortified formulas instead of
direct sunlight provide infants' daily requirements of Vitamin D. Children playing in the sunlight with
sunscreen on is not an effective way for them to get vitamin D because the sunscreen inhibits its production
.in the skin
Nutritional concerns
Vitamin D deficiency is caused by the child not getting enough vitamin D through nutrition and exposure
to sunshine. Even after a case of vitamin D deficiency has successfully been resolved special care should be
.taken with the child's diet, as vitamin D deficiency can reoccur
Parental concerns
Vitamin D deficiency can cause rickets, which can lead to permanently stunted or irregular growth. Vitamin
D deficiency can usually be easily corrected if it is noticed early, and if so the symptoms often resolve
.themselves. However, negative effects such as short stature and pelvic deformations can be permanent
Vitamin D
Vitamin D has two main forms: D2 (ergocalciferol( and D3 (cholecalciferol(. Vitamin D3 is synthesized in
skin by exposure to sunlight (ultraviolet radiation( and obtained in the diet chiefly in fish liver oils and egg
yolks. In some developed countries, milk and other foods are fortified with vitamin D. Human breast milk is
low in vitamin D, containing an average of only 10% of the amount in fortified cow's milk. Requirements
for vitamin D increase with aging. Vitamin D is a prohormone with several active metabolites that act as
hormones. Vitamin D3 is metabolized by the liver to 25(OH(D, which is then converted by the kidneys to
1,25(OH(2D (1,25-dihydroxycholecalciferol, calcitriol, or active vitamin D hormone(. 25(OH(D, the major
circulating form, has some metabolic activity, but 1,25(OH(2D is the most metabolically active. Inadequate
exposure to sunlight may cause vitamin D deficiency. Deficiency impairs bone mineralization, causing
.rickets in children and osteomalacia in adults and may contribute to osteoporosis
Cholecalciferol
(Vitamin D3(
Vitamin D metabolism
The current recommendations from the Institute of Medicine are 200 IU/day from birth through age 50, 400
IU for those aged 51 to 70, and 600 IU for those over 70 years. These recommendations were established by
determining the level of Vitamin D that was enough to prevent bone demineralization or rickets. The safe
.tolerable upper intake level for Vitamin D is 10,000 IU/day
Randomized trials using the currently recommended intakes of 400 IU of Vitamin D/day have shown no
appreciable reduction in fracture risk. In contrast, trials using 700–800 IU Vitamin D/day found less fracture
incidence[8]. Adults should be consuming at least 1000 IU per day of Vitamin D to maintain blood serum
.levels that are effective for strengthening the bones
Rickets
Causes Of Rickets•
Abnormality In Vitamin D Metabolism○
Associated with hyperparathyroidism
Vitamin D deficiency
Dietary lack of vitamin D•
Famine osteomalacia•
Lack of sunshine exposure
Malabsorption of vitamin D
Pancreatitis and biliary tract disease•
Steatorrhea, celiac disease, postgastrectomy•
Inflammatory bowel disease•
Defective conversion of vitamin D to 25-OH-cholecalciferol in liver○
Liver disease
Anticonvulsant drug therapy (= induction of hepatic enzymes that
accelerate degradation of biologically active vitamin D
(metabolites
Defective conversion of 25-OH-D3 to 1,25-OH-D3 in kidney○
Chronic renal failure = renal osteodystrophy
Vitamin D-dependent rickets = autosomal recessive enzyme defect
of 1-OHase
Abnormality In Phosphate Metabolism•
Not associated with hyperparathyroidism secondary to normal serum calcium○
Phosphate deficiency○
Intestinal malabsorption of phosphates
Ingestion of aluminum salts [Al(OH(2] forming insoluble
complexes with phosphate
Low phosphate feeding in prematurely born infants
Severe malabsorption state
Parenteral hyperalimentation
Disorders of renal tubular reabsorption of phosphate
(Renal tubular acidosis (renal loss of alkali•
deToni-Debré-Fanconi syndrome =•
hypophosphatemia, glucosuria, aminoaciduria
Vitamin D-resistant rickets•
Cystinosis•
Tyrosinosis•
Lowe syndrome•
Hypophosphatemia with nonendocrine tumors○
Oncogenic rickets - elaboration of humeral substance which
inhibits tubular reabsorption of phosphates
Sclerosing hemangioma•
Hemangiopericytoma•
Ossifying mesenchymal tumor•
Nonossifying fibroma•
Hypophosphatasia○
Calcium Deficiency•
(Dietary rickets = milk-free diet (extremely rare○
Malabsorption○
Consumption of substances forming chelates with calcium○
Classification Of Rickets•
Primary vitamin D-deficiency rickets○
Gastrointestinal malabsorption○
Partial gastrectomy
Small intestinal disease: gluten-sensitive enteropathy / regional
enteritis
Hepatobiliary disease: chronic biliary obstruction / biliary
cirrhosis
Pancreatic disease: chronic pancreatitis
Primary hypophosphatemia; vitamin D-deficiency rickets○
Renal disease○
Chronic renal failure
Renal tubular disorders: renal tubular acidosis
Multiple renal defects
Hypophosphatasia and pseudohypophosphatasia•
Fibrogenesis imperfecta osseum○
Axial osteomalacia○
Miscellaneous•
Hypoparathyroidism, hyperparathyroidism, thyrotoxicosis, osteoporosis, Paget○
,disease, fluoride ingestion
ureterosigmoidostomy, neurofibromatosis, osteopetrosis, macroglobulinemia,○
malignancy
Abstract
Aim This aim of this study was to identify the prevalence of vitamin D deficiency in
pregnant women of a Wellington general practice where 10 cases of childhood rickets had
.been diagnosed over the past 3 years
Methods Ninety pregnant women were screened for vitamin D deficiency by measuring
25-hydroxy vitamin D by DiaSorin radioimmunoassay. Recruitment into the study was over
a 12-month period. A second appointment was arranged for clinical review and drawing of
.blood for parathyroid hormone, adjusted calcium, and alkaline phosphatase
Results 100% of women presenting to the general practice for antenatal care consented
to the study. 87% of women had 25-hydroxy vitamin D levels below 50 nmol/L. 61.2% of
women had a vitamin D level below 25 nmol/L consistent with severe vitamin D deficiency.
10 women had an elevated parathyroid hormone consistent with secondary
hyperparathyroidism. Only 22% of our patients were veiled, and included a diverse ethnic
.population, including African, Maori, European, Middle Eastern, and Polynesian women
Nozza and Rodda from their review of children with rickets in Melbourne, Australia have
recommended pregnant women with dark skin pigment or “veiling” should have their vitamin
D level checked. If vitamin D levels are low (<50 nmol/L) then supplementation should be
given to the mother as well as supplements to the breast feed infants of deficient mothers.3
During pregnancy and lactation, the current consensus is that the vitamin D status of the
infant is strongly influenced by the vitamin D status of the mother during pregnancy. During
pregnancy, 80% of the fetal skeleton is mineralised in the third trimester, so maternal
adaptations to fetal calcium demands are most important in the third trimester. The major
adaptive process in humans is a two-fold increase in maternal intestinal calcium absorption,
mediated by increases in 1-25 dihydroxy vitamin D. Therefore the level of 25-hydroxy vitamin
D and the parathyroid hormone levels are felt to give the best indication of the body’s
.balance of vitamin D during pregnancy
A review of their database for children under the age of 5 years identified 10 cases with a
diagnosis of rickets over the last 3 years (Figure 1 and 2). Because of the re-emergence of
childhood rickets in this practice, and in many countries around the world, a prospective
clinical study was undertaken. We offered vitamin D screening for all pregnant women
.presenting for antenatal care to this general practice
Figure 1. Six-month-old child with rachitic changes showing expansion of the costochondral
(junction (arrowed
Figure 2. Classic rachitic metaphyseal changes: cupping, fraying, widening, and fuzziness of
(the zone of provisional calcification immediately under the growth plate (arrowed
The study aim was to identify the prevalence of vitamin D deficiency in pregnant women of
this small, busy primary health organisation (PHO). With an intention to treat vitamin D
deficiency in order to prevent neonatal or childhood rickets in this population. We aimed to
recruit 120 women to the study and replace vitamin D with ergocalciferol (vitamin D2) in
those who were deficient from as early as 13 weeks gestation and continue this treatment
.throughout pregnancy and up to 6 months postpartum
Methods
In addition to the first antenatal bloods done routinely at commencement of maternity
services, a 25-hydroxy vitamin D level was performed after consent was obtained. Each
woman was asked to complete a simple dietary and sun exposure questionnaire. At the same
time, an information sheet about vitamin D was provided and was available in several
.languages
At the second appointment, additional blood tests for parathyroid hormone (PTH), adjusted
calcium, alkaline phosphatase, and phosphate were taken. Parathyroid hormone was
measured by a Roche immunoassay (Basel, Switzerland). In pregnant women of 13 weeks
gestation and over, with a vitamin D level of less than 50 nmol/L, ergocalciferol (vitamin D2)
was prescribed as one 1,000 IU tablet per day. Follow up of the women later in pregnancy and
in the postpartum period is the focus of the continuing prospective study. Daily
supplementation of 400–1000 IU/day in pregnancy is felt to be safe.1,12–16
The study received ethics approval from the Wellington Ethics Committee. Vitamin D in the
form of ergocalciferol (vitamin D2) was purchased from New Hope Nutrition Ltd (Browns Bay,
Auckland, New Zealand). The only active ingredient was vitamin D as ergocalciferol (vitamin
.(D2) 1,000 IU (release limits 900–1650 IU
Results
To date, of the 90 pregnant women that have been seen at Newtown Union Health, 100%
consented to be study participants. The community of this general practice is multicultural
and was reflected in the diverse ethnic groups included in the study. Of the 90 pregnant
women, 78 (87%) were vitamin D deficient—with 25-hydroxy vitamin D levels below 50
(.nmol/L. (See Table 1 below
Table 1. Pregnant women (n=90) screened at Newtown Union Health (Wellington) for vitamin
D deficiency
Conclusions
Deficiency of vitamin D is common in this general practice’s (Newtown Union Health’s)
population of pregnant women. This practice does serve a diverse population and will not be
the same for all other New Zealand general practices. However some of the significant
findings include the high incidence of vitamin D deficiency (in our study group) in New
.Zealand Maori, Samoans, and other Pacific Islanders
The African, Middle Eastern, and Asian groups showed a very high incidence of vitamin D
deficiency, which was perhaps not unexpected. Secondary hyperparathyroidism and
hypocalcaemia due to the vitamin D deficiency were also common, reflecting the severity of
.the deficiency
Previously described risk factors for vitamin D deficiency include veiling with traditional dress.
This only contributed to a minority of cases in our series with only 22% wearing veils. Sunlight
exposure may also be related to the ability to sit outside for periods of time but only 33 of the
.90 women were living in apartments
In a general practice with a re-emergence of rickets in children, this study highlights the
potential magnitude of this preventable disease. All these women have gone onto receive
treatment where they have elected to continue with the pregnancy. Further follow up on the
.efficacy of treatment is planned
Because of the high incidence of vitamin D deficiency in this group of pregnant women we
seriously believe that further population studies are needed. It is also important to make
midwives, general practitioners, endocrinologists, and obstetric medicine physicians aware
.that vitamin D deficiency is common in the pregnant patient
Indeed, in our study population, vitamin D deficiency was not only common in the veiled and
.dark-skinned patients but among all ethnicities in our pregnant general practice population
Author information: Annie Judkins, General Practitioner, Newtown Union Health Services;
Carl Eagleton, Endocrinologist, Department of Endocrinology, Wellington Hospital; Newtown,
Wellington
Definition
Rickets (in children( and osteomalacia (in adults( are two forms of a metabolic bone disease resulting from
vitamin D deficiency. Both cause softening and weakening of bones because of defective or inadequate
.bone mineralization
Rickets
Causes
:Rickets and osteomalacia result when there is a vitamin D deficiency in the body. This may occur when
.The supply of vitamin D from the diet or sun exposure is inadequate•
.The metabolism of vitamin D is abnormal•
.Tissue is resistant to the action of vitamin D•
Vitamin D regulates calcium absorption in the body. It also controls levels of calcium and phosphate in
bone. Vitamin D is absorbed in the intestines from food. Vitamin D is also produced by the skin during
.exposure to sunlight
:Most often, rickets and osteomalacia are caused by a deficiency of vitamin D. This can result from
:Insufficient vitamin D in the diet. In children, this may be related to•
Insufficient consumption of vitamin D-fortified milk○
Insufficient intake of vitamin D supplements to children being○
breastfed or to children who are lactose intolerant
.Lack of exposure to sunlight•
Less often, rickets and osteomalacia can be caused by other disorders that affect vitamin D absorption,
:metabolism, or action in the body such as
:Kidney problems•
A hereditary disorder of the kidney called vitamin D-resistant rickets○
Renal tubular acidosis—a nonhereditary kidney disorder which causes○
bone calcium to dissolve
Chronic kidney failure○
Long-term kidney dialysis○
Diseases of the small intestines with malabsorption•
Disorders of the liver or pancreas disease•
Cancer•
:Certain drugs, such as•
Certain seizure medications, such as phenytoin or phenobarbital○
Acetazolamide○
Ammonium chloride○
Disodium etidronate○
Fluoride treatment○
:Toxicity or poisoning from•
Cadmium○
Lead○
Aluminum○
Outdated tetracycline○
Risk Factors
A risk factor is something that increases your chance of getting a disease or condition. Risk factors for
:rickets/osteomalacia include
Age in children: 6 to 24 months old•
Either the child is consuming breast milk (from a mother who is○
.deficient in vitamin D) or milk not fortified with vitamin D
Age in adults: 50-80 years•
Lactose intolerance with inadequate intake of vitamin D-fortified milk•
Family history of rickets•
Race: Black, especially in association with breastfeeding•
Symptoms
:Symptoms may include
Bone pain and tenderness•
Skeletal and/or skull deformities•
Bow legs or knock knees•
Deformity or curvature of the spine•
(Pigeon chest (forward protrusion of the chest bone•
Impaired growth, resulting in short stature•
Susceptibility to bone fractures•
Dental deformities•
Delayed tooth formation•
Defects in teeth•
Increased cavities•
Loss of appetite or weight loss•
Difficulty sleeping•
Poor muscle development and tone•
Muscle weakness•
Delay of learning to walk in children•
Diagnosis
The doctor will ask about your symptoms and medical history, and perform a physical exam. Tests to
:confirm the diagnosis may include
Blood and urine tests•
Bone x-rays•
Bone biopsy, when other tests are not conclusive•
Treatment
:Treatment attempts to
Correct the underlying cause•
Relieve or reverse symptoms•
Treating Symptoms
:Treatment to relieve or correct symptoms may include
Wearing braces to reduce or prevent bony deformities•
In severe cases, surgery to correct bony deformities•
Prevention
:To help prevent rickets or osteomalacia
.Drink vitamin D-fortified milk•
Consume sufficient vitamin D, calcium, and other minerals. If you think your diet•
may be deficient, talk with your doctor about alternate sources of vitamins and
.minerals
Get sufficient, but not excessive, exposure to sunlight. Fifteen minutes a day is•
usually considered sufficient. Any longer than that requires sun protection with
clothing or sunscreens, especially in fair-skinned infants or children. Children with
dark skin and their mothers are at increased risk for rickets and may need more sun
.exposure and dietary supplementation with vitamin D
Breastfed, dark-skinned babies should receive 400 International Units per day (IU/d)•
.of supplementation with vitamin D starting at no later than two months of age
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