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BPK 110 Lili > VITAMINS > Flashcards

VITAMINS Flashcards

1
Q

WHAT ARE VITAMINS

A

Vitamins are organic micronutrients. They do not provide energy, nor contribute to body structure, but are involved in numerous important biochemical processes

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2
Q

HOW MANY VITAMISN BDOY NEED TO SURVIVE

A

es 13 vitamins to survive and thrive

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3
Q

WHAT ARE VITAMINS CLASSIFIED INTO

A

water- or fat-soluble,according to their behaviour in water

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4
Q

WHAT ARE WATER SOULOUBLE VITAMINS

A

Water-soluble vitamins are hydrophilic dissolve readily in water.

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5
Q

WHAT ARE FAT SOLUBLE VITAMINS

A

fat-soluble vitamins are hydrophobic and require a lipoprotein transporter to move around the watery environments of the body

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6
Q

WHAT HAPPENS TO EXCESS WATER SOLUBLE VITAMINS AND FAT SOLBLE VITAMINS

A

Excess water-soluble vitamins are excreted in urine, while fat-soluble vitamins are
stored in adipose Ɵ ssue, where they can build-up and lead to toxicity. Luckily, this rarely occurs from vitamin consumpƟ on from food; it is more likely from over-supplementaƟ on

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7
Q

EXAMPLES OF VITAMIN WATER AND FAT SOLUBLE

A

WATER : B , C
FAT:A D E K

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8
Q

TRANSPORTAIN OF WATER AND FAT VITAMINS

A

WATER: NO TRANSPORT
FAT : LIPOPROTEIN TRANSPORTER

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9
Q

STORAGE OF VITAMIN WATEER AND FAT

A

WATER : NOT STORED EXCERTED IN URINE
FAT: STORED IN ADIPOSE TISSUE

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10
Q

CONSUMPTION OF WATER AND FAT VITAMINS

A

REQUIRED MORE EVERYDAY : FAT REQUIRED LESS EVERYFEW DAYS

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11
Q

TOXICITY OF WATER AND FAT VITAMINS

A

EXCERTED BY KIDNEY AND LESS LIKELY TO BE TOXIC: FAT : BUILDUP IN ADIPOSE TISSUE MORE LIKELY TO BE TOXIC

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12
Q

FUNCTIONS OF VITZMINS AS COENZYMES AND HOW THEY WORK

A

Many vitamins achieve their funcƟ on by acƟ ng as coenzymes. Coenzymes are non-protein factors required for
enzyme funcƟ on (Figure 8.1). When coenzymes bind to enzymes, they can acƟ vate the enzymes and allow them to funcƟ on. Vitamins are therefore important because they facilitate many enzyme-dependent body reacƟ ons

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13
Q

TRUE OR FALSE :: Many vitamins funcƟ on as coenzymes, which promote enzymaƟ c acƟ viƟ es

A

TRUE

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14
Q

WHAT DOES OUR DAILY VITAMIN NEEDS DEPEND ON

A

AGE AND LIFE STAGE

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15
Q

WHATS DRI FOR VITAMINS

A

younger individuals oŌ en have a lower
RDA/AI for the various vitamins, while pregnancy and lactaƟ on typically increase needs. I

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16
Q

WHAT ARE VITAMIN B GROUP

A

The B vitamins are a group of eight vitamins that facilitate energy metabolism through their coenzyme funcƟ ons.
To be clear, the B vitamins do not provide energy

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17
Q

WHAT DOES VITAMIN B DO

A

They support the enzymaƟ c acƟ vity that promotes energy metabolism.
We used to think that one vitamin facilitated energy metabolism. When it was discovered that it is actually several diff erent vitamins, they each received their own name and B vitamin number. There were originally 12 B vitamins, but some
were later ruled out as being essenƟ al , That is why there are only nine B vitamins even though vitamin B12 exists

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18
Q

IS VITAMIN B12 PRESENT IN PLANT FOODS

A

NO

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19
Q

WHATS THIAMINE AND ITS FUCNTION

A

REQUIRED BY ALL BODY TISSUES , MUSCULAR CONTRACTION , NERVE CONDUCTION , SYNTHESIS ATP , ALSO PART OF THIAMINE PRYOPHOSPHATE TPP IS ALSO REQUIRED FOR CITRIC ACID CYCLE , CELLULAR RESPIRATION , AND CARB METABLOISM

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20
Q

WHAT IS SOURCE OF THIAMINE

A

NUTS SEEDS EGG MILK POULTY , FORTIFIED CEREAL

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21
Q

THIAMINE DEFICIENCY

A

Thiamine defi ciency negaƟ vely eff ects the acƟ vity of thiamine-dependent enzymes. The brain is parƟ cularly
suscepƟ ble to thiamine defi ciency, where it can lead to neuronal death in areas with a higher thiamine requiremen

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22
Q

TRUE OR FALSE

A

Pregnant and breasƞ eeding women have a higher need for thiamine, TRUE

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23
Q

TRUE OR FALSE

A

TRUE : hiamine defi ciency is rare in Canada and the USA

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24
Q

WHAT IS THIAMINE DEFICIECNY ASSOCIATED WITH

A

ALCHOLOHILMS WHICH LEADS TO POOR DIET , DECREASED NUTRIENT , SO ALCOHO COMPROMISES THIAMINE SOTRAGE ,

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25
Q

WHAT DOES ALCOHOL RELATED CASE OF THIAMINE LEADS TO

A

WERNICKE SYNDROME : SHORT TERM MEMORY , CONFUSION , DISORIENTATION , EYE MOVEMNT CHANGE , THIAMLIL ADMINSTRATION TREATED IT CAN PROGRESS TO KOSAKOFF

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26
Q

BERIBERI

A

THIAMINE DEFICIENCY
WET AND DRY : WET : IMPACTS CVD SYSTEM HEART FAILURE
DRY : NERVOUS AND MUSCUALR SYSTEM MSUCLE PARALYSIS
BERIBERI CAN LEAD TO KOSAKOFF SYNDROME

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27
Q

BROWN RICE HAS MROE THIAMINE THAN WHITE RICE

A

TRUE

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28
Q

VITAMIN B2 : RIBOFLAAVIN

A

HELPS TWO COENZYMES , s: fl avin mononucleoƟ de (FMN) and fl avin adenine dinucleoƟ de
(FAD). Recall from Chapter 3 that FAD picks up electrons during the citric acid cycle to become FADH2. It then transports
these electrons to the electron transport chain where they are necessary for ATP producƟ on

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29
Q

WHAT ARE THE OTHER FUNCTIONS OF B2

A

. These coenzymes are also involved in the conversion of the amino acid tryptophan to niacin. They are further involved in maintaining appropriate levels of homocysteine, a risk factor for cardiovascular disease (CVD) (NaƟ onal InsƟ tutes of Health,

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30
Q

WHAT ARE SOURCES OF RIBOFLAVIN

A

EGG YOLK , FORTIFIED CEREALS , OAT , ORGAN MEAT , TUNA , SALMON , MILK , ALMONDS , DAIRY

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31
Q

RIBFLAVIN SENSITIVITY

A

are typically packaged in opaque containers to preserve their
ribofl avin content, as ribofl avin is sensiƟ ve to light. Bacteria
in the large intesƟ ne further promote ribofl avin availability by
making it available from foods, especially plants

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32
Q

RIBOFLAVIN DEFICENCY

A

ARIBOFLAVINOSIS : SKIN DISORDER
SWELLING IN MOUTH
THROAT
DRY
CRACKED LIPS
IS RARE THROUGH HORMONAL THYROID BUT MAY
ANIMAL PRODUCT ARE BETTER SOURCE

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33
Q

RIBFLAVIN TOXICITY

A

IS RARE , BODY DOSENT ABSORB MORE THAN CERTAIN LEEVL . THE KIDNEY EXCERTS EXCESS , EXCESS INTAKE OF IT DOSENT LEAD TO TOXICITY , SO THERE IS NO UPPER LIMIT

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34
Q

VITAMIN B3 NIACIN

A

Niacin’s funcƟ ons are exerted by its main metabolically acƟ ve form: the coenzyme nicoƟ namide adenine dinucleoƟ de (NAD). Like FAD, NAD is a key electron transporter in cellular respiraƟ on, picking up electrons to become
NADH + H+
(Figure 8.7). It is accordingly criƟ cal to the metabolism of carbohydrates, lipids and proteins. This is just one
of the reducƟ on and oxidaƟ on reacƟ ons in which NAD is involved. NAD is criƟ cal to many metabolic reacƟ ons since
more than 400 enzymes require it to funcƟ on properly. In total, niacin is involved in more reacƟ ons than any other vitamin in the body

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35
Q

SPECIAL USE OF NIACIN

A

For years, niacin has been prescribed by doctors for improving the blood lipids associated with CVD. High doses
of niacin (>2000 mg) have been shown to reduce triglycerides and the lipid transporters VLDL and LDL, These niacin megadoses have also been shown to increase HDL, so-called good cholesterol.

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36
Q

niacin megadoses did not reduce overall mortality or heart aƩ ack and stroke incidence

A

TRUE

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37
Q

SOURDCE OF NIACIN

A

ANIMAL PRODYCT CHICKEN BEEF FISH NUTS LEGUMES GRAINS BUT THEY HAVE HALF THE NIACIN

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38
Q

Recall that FAD helps to convert the amino acid tryptophan to niacin, so geƫ ng adequate amounts of both
protein and ribofl avin can help promote niacin levels.

A

TRUE

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39
Q

NIACIN DEFICENCY

A

CAUSE PELLAGRA SUPMPTOMS : 3D : DERAMTISTIS , DIAREHA , DEMENTIA , CAN LEAD TO DEATH IN SOME CASES

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40
Q

NIACIN TOXICITY

A

RARE FROM FOOD ,, TAKIN GHIGH DOSE OF BLOOD LIPIDS AND CVC , DOSES OF 30MG OR MORE CAUSE NIACIN FLUSH , SKIN BURNING AND ITCHING , DOSE O 1000 MG CAN LEAD TO NAUSA OR VOMITING

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41
Q

VITAMN B 5 PANTOTHENIC ACID

A

PANTOTHENIC ACID HELPS FORM COENZYEM A , IS REQUIRE FOR LIPID CARB AND CERTAIN AMINOACIDS METABLOTICIS , TO ENTER CITRIC ACID CYCLE AS ACETYL COA

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42
Q

SOURCES OF PANTOTHENIC ACID

A

FORTIFIED CEREALS BEEF CHICKEN GRAINS VEGETABLES ARE RICH SOURCE

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43
Q

PANTOTNHIC ACID DEFICEINCY

A

ITS ABUNDANT IN MOST FOODS , SO ITS DEFICNECY IS RARE , SO MALNUTRITION OR MICRONUTRIEND , DEFICIENCY LEDAS TO NUMBNESS IN HADNS AND FEET M HEADACHE , TIREDNESS , DISTRUBED SLEEP , GASTRONCIALS ISSUES

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44
Q

PANTOTHENIC ACID TOXICITY

A

here has been no reported human toxicity from high amounts of pantothenic acid from foods. Accordingly,
there is no established upper limit. However, megadoses (10,000 mg) of pantothenic acid supplements have been associated with diarrhea and digesƟ ve tract distress

45
Q

VITAMIN B 6

A

Vitamin B6 is the generic name for six diff erent vitamers.

46
Q

WHAT ARE VITAMERS

A

Vitamers are diff erent forms of the same vitamin that
have a common funcƟ on. These vitamers act as coenzymes in the catalyzaƟ on of more than 100 enzymaƟ c reacƟ ons,
including the metabolism of carbohydrates, lipids and amino acids. They also help form certain neurotransmiƩ ers, such
as serotonin and norepinephrine, which support cogniƟ ve funcƟ on. Furthermore, vitamin B6 helps lower homocysteine
levels by converƟ ng it to cysteine (Figure 8.12). Elevated levels of homocysteine are a risk factor for CVD.

47
Q

SPECIAL USE OF VITAMIN B6

A

improving cogniƟ ve funcƟ on and reducing cancer risk ,Since vitamin B6 is associated with lower levels
of homocysteine – a marker for CVD – it has also been suggested that supplementaƟ on may decrease risk. However,
vitamin B6 supplementaƟ on has not been shown to decrease CVD incidence, o decrease symptoms of premenstrual
syndrome, with confl icƟ ng result, reducing vomiƟ ng and nausea in pregnancy. However, no fi rm link has been established for
any of these special uses.

48
Q

SOURCE OF VITAMIN B 6

A

FOUND IN MANY ANIMAL AND PLANT PRODUCTS , CHKPEAS , WHILE BEEF LOVER , TUNA , SALMON , CHICKEN , CEREALS , GRAIN S, POTAOTES , ABNANAS , SQUASH RICE ,

49
Q

WHATS PYRIODIXINE

A

e. Pyridoxine is
the form of vitamin B6 that is typically found in supplements.

50
Q

VITAMIN B DEFICIENCY

A

Vitamin B6 defi ciency is rare in isolaƟ on and is oŌ en found in combinaƟ on with other B vitamin defi ciencies. In
more pronounced cases, vitamin B6 defi ciency can lead to microcyƟ c anemia, a condiƟ on in which red blood cells are
small and do not properly transport oxygen. Symptoms include faƟ gue, lethargy, dry and cracked lips, and a swollen
tongue. Individuals with kidney issues, alcohol dependency and certain autoimmune disorders tend to have lower vitamin B6 levels and have an increased risk for defi ciency

51
Q

VITAMIN B 6 TOXICITY

A

High vitamin B6 intake from food has not been shown to have adverse eff ects. However, prolonged supplementaƟ on of more than 1000 mg per day of pyridoxine, the supplement form of vitamin B6, can lead to a loss of control
over body movements (Bendich & Cohen, 1990). High supplement doses should be taken only under the advice of a
medical doctor and closely monitored.

52
Q

VITAMIN B 7 BIOTIN

A

BioƟ n is the generic name for fi ve vitamers that funcƟ on as coenzymes. These coenzymes are involved in
the metabolism of carbohydrates, lipids and proteins. They are also involved in cell signalling and DNA structure and
funcƟ on

53
Q

SPECIAL USE OF BIOTIN

A

Because defi ciency is associated with compromised hair, nail and skin health, supplements of B7 are someƟ mes
sold to improve these condiƟ ons. However, the results of studies into the ability of bioƟ n to improve these Ɵ ssues are
mixed.

54
Q

SURCES OF BIOTIN

A

BioƟ n is abundant in many foods (Figure 8.14). One
serving of beef liver aff ords 100% of the RDA. Other animal
products such as chicken, tuna and pork are also excellent
sources. Plant products such as sunfl ower seeds, sweet potatoes, almonds, spinach and broccoli are also high in bioƟ n.

55
Q

BIOTIN DEFICIENCY

A

IS RARE , BioƟ n defi ciency is rare but may occur with certain condiƟ ons (NaƟ onal InsƟ tutes of Health, n.d.-a). A rare genetic condiƟ on called bioƟ nidase defi ciency negaƟ vely aff ects bioƟ n availability and can lead to defi ciency. Chronic alcohol
abuse can also lead to defi ciency since it negaƟ vely aff ects bioƟ n absorpƟ on. Signs and symptoms of defi ciency include
hair loss, red eyes and rashes around the eyes, nose and mouth. More serious cases may progress to seizures, depression
and decreased muscle tone and strength.

56
Q

BIOTIN TOXICITY

A

High intakes of bioƟ n from food do not lead to symptoms of toxicity and there is no set upper limit. However,
higher than normal intakes may aff ect laboratory test results and mimic the signs of a thyroid condiƟ on known as Graves’
disease (Kummer et al., 2016; Sharma et al., 2017). Those who supplement with bioƟ n should inform their doctor before
laboratory tests are administered.

57
Q

VITAMIN B 9 FOLATE

A

Vitamin B9 can exist in a basic form as folate or in an acidic form as folic acid. Folate is predominant in food sources,
while vitamin supplements and forƟ fi ed foods typically have folic acid, which is more stable. Since they have similar physiological eff ects, the terms are typically used interchangeably

58
Q

FOALTE FUCNTION S

A

Folate and folic acid funcƟ on as coenzymes in the synthesis of DNA and RNA. They are also involved in the metabolism of amino acids. Further, they are involved in the conversion of homocysteine to methionine (

59
Q

SOURCE OF FOLATE

A

Beef liver is in the most concentrated source of
folate, with one serving providing more than half of the
RDA. Spinach, legumes, asparagus, Brussels sprouts and
avocados are also high in folate (Figure 8.15). In 1998,
both the Canadian and American governments began a
mandatory forƟ fi caƟ on program requiring the addiƟ on
of folic acid to cereal grains. Accordingly, these are also
good sources of folic acid.

60
Q

FOLATE DEFICIENCY

A

Folate defi ciency in non-pregnant individuals is rare. If it does occur, it is typically associated with other micronutrient defi ciencies that might occur due to poor diet, alcohol dependency or absorpƟ on issues.

61
Q

NEURAL TUBE DEFECTS

A

Pregnant women with inadequate folate levels are more likely to have off spring that develop neural tube defects

62
Q

SPINA BIFIDA

A

eads to physical problems, such as leg weakness, scoliosis and bladder and bowel issues, as well as neurological problems in which planning, organizing and aƩ enƟ on are compromised. More seriously, neural tube defects can also lead to
anencephaly, which is when a child is born missing major parts of their brain. This defect typically results in infant death
within a few hours of birth. Thankfully, the mandatory forƟ fi caƟ on of folic acid into grains has contributed to a 45% decrease in neural tube defects in Canada (

63
Q

MEGALOBASTIC ANEMIA

A

Folate defi ciency can also lead
to megaloblasƟ c anemia – a disorder
in which red blood cells are immature,
large, misshapen and unable to properly
carry oxygen (

64
Q

HATS THE REAON OF MEGALOBLASTIC ANEMIA

A

This is due to
their inability to properly synthesize DNA
during red blood cell producƟ on. Both folate and vitamin B12 defi ciency can cause
this type of anemia, which leads to Ɵ redness, weakness and heart irregulariƟ es

65
Q

ATUISM SPECTRUM DISORDER

A

AuƟ sm is a complex disorder whose causes are not fully understood. An interesƟ ng newer area of research
explores whether folic acid supplementaƟ on before and during pregnancy lowers the risk of auƟ sm in children. Some
epidemiological evidence supports this link (Levine et al., 2018; Schmidt et al., 2012), however, other studies show confl icƟ ng results (Virk et al., 2016). More research is needed before a link can confi dently be established. Folic acid supplementaƟ on is nonetheless recommended before and during pregnancy to reduce the risk of neural tube defects.

66
Q

FOALTE TOXICITY

A

Folate is generally well tolerated. Symptoms of toxicity are uncommon, but may include nausea, bloaƟ ng, decreased appeƟ te and diffi culty sleeping. Both folate and vitamin B12 are involved in the conversion of homocysteine to
methionine as well as in the prevenƟ on of megaloblasƟ c anemia. If folate intake is high, it can accordingly mask a vitamin
B12 defi ciency. While folate supplementaƟ on can correct the neurological damage of megaloblasƟ c anemia, it cannot
correct the neurological damage from a vitamin B12 defi ciency. Folic acid may also interact with certain medicaƟ ons, so
doctors and pharmacists should be made aware of supplementaƟ on before prescripƟ ons are wriƩ en and fi lled.

67
Q

VITAMIN B 12 COBLALAMIN FUCNTIONS

A

Vitamin B12 has various vitamers that are collecƟ vely known as cobalamins. These are required for DNA synthesis, the formaƟ on of mature red blood cells and brain funcƟ on. Vitamin B12 also acts as a coenzyme in the conversion of
homocysteine to methionine (Figure 8.12). It is furthermore involved in fat and protein metabolism.

68
Q

VITAMIN B12 SPECIAL USE

A

Vitamin B12 has been proposed as way to decrease the risk of demenƟ a. While research is ongoing, the evidence is currently insuffi cient to recommend supplementaƟ on

69
Q

ABSPORBTION OF VITAMIN B12

A

The digesƟ on and absorpƟ on of vitamin B12 relies on stomach secreƟ ons. The process begins with the acƟ vity
of hydrochloric acid in the stomach, which helps release vitamin B12 from food (Figure 8.18). The stomach also releases intrinsic factor (IF), which is needed later in the small intesƟ ne for vitamin B12 absorpƟ on. Vitamin B12 cannot be
absorbed in free form, and thus binds to IF, which allows it to enter the villi of the ileum. Factors that negaƟ vely aff ect
the stomach or intrinsic factor secreƟ on can thus negaƟ vely aff ect vitamin B12 bioavailability. Indeed, atrophic gastriƟ s,
an autoimmune disorder that results in the breakdown of the stomach’s lining, restricts intrinsic factor secreƟ on and
signifi cantly increases the risk for vitamin B12 defi ciency (InsƟ tute of Medicine, 1998). This is especially common in older
adults.

70
Q

SOURCES OF VITAMIN B12

A

Vitamin B12 is found in a wide variety of animal
products (Figure 8.19). Shellfi sh, fi sh and beef liver are
parƟ cularly high in vitamin B12. Plant foods do not typically
contain vitamin B12 unless they are forƟ fi ed. NutriƟ onal yeast is another potenƟ al source that can supplement
vitamin B12 into the vegetarian or vegan diet. Vitamin B12
supplementaƟ on is one of the most common recommendaƟ ons for those who follow a parƟ al or fully plant-based diet.

71
Q

VITAMI B12 DEFICINECY

A

MegaloblasƟ c anemia (Figure 8.17) is the main outcome of vitamin B12 defi ciency. Accordingly, individuals with
vitamin B12 defi ciency may experience faƟ gue, weakness and lethargy, consƟ paƟ on and loss of appeƟ te (Bernard et al.,
1998). Due to its impacts on the nervous system, defi ciency can also lead to balance issues, depression, poor memory
and confusion (Boƫ glieri, 1996). Excess folate can mask a vitamin B12 defi ciency because it is enough to correct megaloblasƟ c anemia. However, supplemenƟ ng with folate when B12 defi ciency exists cannot fi x the neurological impact of
a B12 defi ciency.

72
Q

VITAMIN B12 TOXICITY

A

There are no reported adverse aff ects of excess vitamin B12 intake, either from supplements or food. There is
therefore no upper limit for vitamin B12. However, B12 can interact with certain medicaƟ ons and higher intake levels
from supplements should be menƟ oned to doctors and pharmacists.

73
Q

VITAMIN C FUNCTIONS ASCORBIC ACID

A

Ascorbic acid, L-ascorbic acid or simply vitamin C is involved in a wide range of body processes. It is criƟ cal in the
formaƟ on of the protein collagen, which forms the main structure of bones, ligaments, skin and a variety of other body
structures. Without adequate vitamin C, collagen fi bres do not properly cross-link and organize themselves (Figure 8.20).
This can negaƟ vely aff ect collagen-dependent structures as well as wound healing (Li & Schellhorn, 2007). Vitamin C is
also involved in the metabolism of protein. In addiƟ on, it is well known for its anƟ oxidant funcƟ on. Another well-known
benefi t of vitamin C is its ability to increase the absorpƟ on of iron, reducing the risk for iron-defi ciency anemia. It is also
one of the body’s key anƟ oxidants

74
Q

SPECIAL USE OF VITAMIN C

A

IMMUNE YSTEM: Vitamin C has long-been suggested as a treatment for the common cold and other infecƟ ons. While vitamin C
does support the proper funcƟ on of the immune system, it does not cure the common cold, which has no cure. A large
systemaƟ c review of randomized control trials that used vitamin C doses of 200 mg/day or more did not fi nd a reducƟ on in the risk of developing a cold in the general populaƟ on (Douglas et al., 2007). However, they found that in studies
involving athletes, such as marathon runners and skiers, a 50% decrease in cold incidence was observed, but only if the
supplement was taken before the cold began. , CHRONIC DISEASE , While vitamin C has been studied for its potenƟ al eff ects on reducing cancer and CVD risk, the results are oŌ en
confl icƟ ng and do not off er enough evidence to show that vitamin C supplementaƟ on alone decreases risk (NaƟ onal InsƟ tutes of Health, n.d.-g). However, increased consumpƟ on of foods that contain vitamin C – like many fruits and vegetables – is associated with a lower risk of both diseases.

75
Q

SOURCES OF VITAMIN C

A

Vitamin C is synthesized by most animals except for
humans. We therefore must consume this vitamin from food
or supplements to meet our needs. Vitamin C is abundant in
fruits and vegetables (Figure 8.22). Just half a cup of raw red
peppers or ¾ of a cup of orange juice provides more than
100% of the RDA. It is parƟ cularly abundant in citrus fruits,
such as oranges, grapefruits, kiwis and lemons, as well as tomatoes and strawberries. The vegetables broccoli, Brussels
sprouts and caulifl ower are also quality sources. In addiƟ on,
it is forƟ fi ed into certain grains and breakfast cereals

76
Q

VITAMIN C DEFICINCY

A

Although rare in developed countries, extreme or total absence of vitamin C can lead to scurvy in as liƩ le as one
month (Weinstein et al., 2001). Scurvy (Box 8.2) is evidenced by faƟ gue and gum infl ammaƟ on. If defi ciency is prolonged, it can negaƟ vely aff ect collagen formaƟ on, wound healing and joint integrity leading to bleeding gums and loss
of hair and teeth. Nowadays, scurvy is rare in populaƟ ons that consume a variety of fruits and vegetables.

77
Q

VITAMIN C TOXICITY

A

Though an upper limit of 2000 mg is set, toxicity from vitamin C is relaƟ vely mild. GastrointesƟ nal eff ects such
as diarrhea, nausea and abdominal cramps may occur in those who consume too much (Jacob & Sotoudeh, 2002). Like
other supplements, vitamin C may interact with medicaƟ ons.

78
Q

what are fat soluble vitamins

A

There are four fat-soluble vitamins – vitamins A, D, E and K. Like the water-soluble vitamins, these vitamins each
have various roles in the body. But unlike the water-soluble vitamins, these vitamins are stored in fat Ɵ ssue, so we need
them less oŌ en

79
Q

WHY CAN FAT SOLUBEL VTIAMINS BE TOXIC

A

Since they are stored, they are also more likely to lead to symptoms of toxicity. Toxic levels of fat-soluble vitamins are rarely aƩ ained from dietary consumpƟ on and are most oŌ en due to over-supplementaƟ on. S

80
Q

TRANSPORTATION OF FAT SOLUBLE VITAMINS

A

Since these
vitamins are fat-soluble, their absorpƟ on and transport are dependent on lipid carriers such as micelles and lipoproteins.
When the body is defi cient in lipids, or if there are issues with lipid absorpƟ on, the bioavailability of fat-soluble vitamins
suff ers, and defi ciency can occur

81
Q

VITAMIN A

A

Vitamin A has several vitamers that include reƟ nol, reƟ nal and reƟ nyl esters. As a group, they are referred to as
reƟ noids. We consume vitamin A in one of two forms: provitamin A and preformed vitamin A

82
Q

WHATS PROTAMIN A

A

Provitamin A is found in plants and its vitamers are collecƟ vely known as carotenoids. Carotenoids are not in
their acƟ ve form of vitamin A and must be converted into reƟ nols before they can be further modifi ed into their acƟ ve
form. The most well-known carotenoid is beta-carotene, which helps give certain plants their orange colour

83
Q

WHATS PREFORMED VITQMIN A

A

Preformed vitamin A is found in its almost-acƟ ve forms: reƟ nol and reƟ nal ester. These reƟ nols are found in
animal products including dairy. Animal products also contain provitamin A, but to a lesser degree.
For reƟ noids to become fully acƟ ve, the body must metabolize them into reƟ nal and reƟ noic acid – the acƟ ve
forms of vitamin A

84
Q

VTIAMIN A FUNCTIONS

A

role in the visual pathway (Figure
8.23). Vitamin A-derived reƟ nal binds to the protein opsin to form the visual pigment rhodopsin, found in the rods of
the eye’s reƟ na. W

85
Q

WHAT DOES RHODOPSIN DO

A

When rhodopsin absorbs light, a message is sent along the visual pathway to help us interpret what was
seen. This helps improve our vision at night or in low light. The body requires a conƟ nual stream of reƟ nal, and thus vitamin A, to replenish rhodopsin and contribute to proper visual interpretaƟ on. However, the claim that vitamin A improves
our ability to see at night is not true (

86
Q

OTHER CUNTION OF VITAMIN A

A

Vitamin A is also involved in gene expression, helping to turn certain genes on or off . This aff ects whether DNA
is transcribed into proteins. Vitamin A is also involved in immune funcƟ on, specifi cally by contribuƟ ng to the formaƟ on
of infecƟ on-fi ghƟ ng T-cells. The carotenoid form of vitamin A found in plants further acts as an anƟ oxidant (Figure 8.21),
helping to reduce the acƟ vity of potenƟ ally harmful free radicals.

87
Q

SPECIAL USES OF VITAMIN A

A

amin A promotes skin health by switching on the genes that
cause immature skin cells to become mature and health

88
Q

RETIONOID

A

ReƟ noids are accordingly found in many topical skin care
products (Figure 8.24). There is evidence to support a reducƟ on in the
signs of skin aging with the use of these products (Hubbard et al., 2014;
Mukherjee et al., 2006). However, individuals who overuse reƟ noids
may experience skin irritaƟ on, burning, scaling and dermaƟƟ s. Products
with higher reƟ noid doses, such as the reƟ noic acid product Accutane,
are also someƟ mes prescribed for the treatment of severe acne. While
eff ecƟ ve, this product can have severe skin, gastrointesƟ nal, nervous
system and cardiovascular side eff ects (McLane, 2001). Pregnant women are recommended against Accutane use because it increases the
amount of reƟ noic acid delivered to the developing off spring, which can
lead to birth defects. Accutane is accordingly only available by prescripƟ on in Canada and the USA

89
Q

SOURCES OF VITAMIN A

A

Preformed vitamin A is available in many animal products, while provitamin A is found in many orange and leafy green
plants (Figure 8.25). Beef liver is especially high in vitamin A,
aff ording more than seven Ɵ mes the RDA in a single serving. This
is because in both humans and other animals, most vitamin A is
stored in the liver. Other animal products that are good sources
include fi sh oils, milk and eggs. Recall that these provide vitamin
A in its preformed version. The provitamin form of vitamin A is
found in many plant products. A single serving of sweet potatoes
has more than the RDA. Spinach, carrots, pumpkin, cantaloupes,
red peppers and other orange and leafy green vegetables are also
excellent sources of provitamin A.

90
Q

VITAMIN A DEFICIENCY

A

While rare in Canada and the USA, vitamin A defi ciency is common in developing countries. It is typically due to
poverty leading to a less varied diet that is low in both preformed and provitamin A (Ross, 2010). In these cases, defi -
ciency oŌ en begins in infancy due to low levels of vitamin A in breastmilk (World Health OrganizaƟ on, 2009). Vitamin
A defi ciency in children and pregnant women is typically evidenced by xerophthalmia – abnormal dryness of the eye
that aff ects the body’s ability to form tears. If untreated it can lead to breaks in the cornea of the eye, leading to further
damage and potenƟ ally blindness. Night blindness is an early sign of xeropthalmia (Figure 8.26). Defi ciency of vitamin A
is also a common cause of preventable blindness is children (World Health OrganizaƟ on, 2009). Pregnant women have a
higher RDA for vitamin A, while infants and children in developing countries oŌ en have low intakes – all three are parƟ cularly suscepƟ ble to defi ciency

91
Q

VITAMIN A TOXICITY

A

There are no reported negaƟ ve health eff ects of consuming carotenoids from plant products. In some cases, the
skin may turn slightly orange due to the extra pigments consumed, but symptoms are not otherwise evidenced. Conversely, high intakes of preformed vitamin A from animal products can lead to serious side eff ects. Prolonged excessive
preformed vitamin A intake increases the risk of elevated pressure around the brain, dizziness, nausea, headaches and
can be fatal (InsƟ tute of Medicine, 2001). This is almost always due to overconsuming supplements. However, cases of
acute vitamin A toxicity have also been observed in arcƟ c explorers who consume polar bear liver, which is excessively
high in preformed A

92
Q

VITAMIN D FUNCTIONS

A

Vitamin D is the generic name for a group of compounds, the most important ones being vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol). These compounds are criƟ cal to maintaining calcium homeostasis. Specifi cally, they
increase calcium absorpƟ on in the digesƟ ve tract, while also contribuƟ ng to the absorpƟ on of other bone-mineralizing
minerals like magnesium and phosphate. Adequate vitamin D levels are thus criƟ cal for bone health (Holick, 2004). Vitamin D also plays roles in cellular growth, immune funcƟ on and the reducƟ on of infl ammaƟ on

93
Q

SPECIAL USE OF VITAMIN D

A

Vitamin D has been studied for its potenƟ al role in cancer protecƟ on. Indeed, a prospecƟ ve cross-secƟ onal study
of more that 3,000 men over 50 years old found that those with the highest levels of vitamin D in their blood had the
lowest risk of cancerous formaƟ ons (Lieberman et al., 2003). However, an intervenƟ on study of 35,000 postmenopausal
women found that those who were given vitamin D plus calcium had no diff erence in cancer incidence aŌ er seven years
compared to controls (Wactawski-Wende et al., 2006). Furthermore, a systemaƟ c review and meta-analysis of 30 randomized control trials found that vitamin D supplementaƟ on did not reduce cancer incidence or mortality (Goulão et al.,
2018). Taken together, establishing adequate vitamin D from food may have a role in cancer prevenƟ on, but supplementaƟ on has not been established to lower risk.

94
Q

SOURCE OF VTIAMIN D

A

Vitamin D is not widely available in foods. FaƩ y fi sh
such as salmon, tuna and mackerel as well as fi sh oils are
naturally high in vitamin D (Figure 8.27). Certain foods like orange juice and milk products are also someƟ mes forƟ fi ed with
vitamin D, but do not contain signifi cant amounts naturally. In
Canada, food and drug regulaƟ ons mandate the forƟ fi caƟ on of
vitamin D into fl uid milk
Since vitamin D is not found in many foods, sun exposure is our main source. To be clear, vitamin D is not absorbed through the skin from the sun. Instead, ultraviolet B (UVB) light penetrates the skin and promotes the conversion
of vitamin D precursors to its fully acƟ ve form (Figure 8.28). This does not occur in a single step and requires the proper
funcƟ oning of the kidney and liver (InsƟ tute of Medicine, 2011). Time of year, Ɵ me of day and potenƟ al factors that block
UVB rays, such as cloud and smog, can aff ect vitamin D formaƟ on. There is a balance between geƫ ng enough UVB exposure to promote vitamin D synthesis and not geƫ ng so much that leads to skin damage or even skin cancer. It is generally
advised to limit sun exposure during peak UVB Ɵ mes of the day to between 10 and 30 minutes

95
Q

VITAMIN D DEFICIENCY

A

Vitamin D defi ciency is common and can be due to
both inadequate vitamin D from the diet or limited sun exposure. In children, vitamin D defi ciency can lead to rickets.
Rickets is associated with a lack of bone mineral density that
leads to soŌ bones. Accordingly, legs that curve outwards
(Figure 8.29) is a characterisƟ c sign of rickets. This occurs because vitamin D defi ciency impairs bone mineral availability,
and the weight of the growing body causes weakened bones
to bow outwards. Rickets was a common problem all over
the world unƟ l it was found that cod liver oil could reverse it.
It was later discovered that it was t

96
Q

WHAT DOES VITAMIN D DEFICENCY LEAD TO

A

In adults, vitamin D defi ciency can lead to osteomalacia – a soŌ ening of the bones due to decreases in bone
mineralizaƟ on. While calcium defi ciency can also lead to osteomalacia, its most common cause is vitamin D defi ciency. In
addiƟ on to weaker and soŌ er bones, people with osteomalacia may experience muscle weakness, diffi culty walking and
pain in the bones and joints. Prolonged vitamin D and calcium defi ciency may progress to osteoporosis, a condiƟ on in
which bones are not only weakened but have less hardened bone Ɵ ssue, making them more likely to break.

97
Q

WHAT FACTORS INCREASE VITAMIN D DEFICIENCY

A

Many factors increase the risk for vitamin D defi ciency. For example, those who have darker skin are more likely
to be defi cient since dark skin limits the ability to produce vitamin D precursors. Those that limit milk intake due to allergy, intolerances or vegetarianism also tend to have higher risk. Since breastmilk does not have enough vitamin D to meet
needs, breasƞ ed infants are also at risk for defi ciency (Picciano, 2001). Older adults have a more diffi cult Ɵ me synthesizing vitamin D precursors from sun exposure and are less likely to spend Ɵ me outdoors, making them another high-risk
group (InsƟ tute of Medicine, 2011). Accordingly, the RDA for vitamin D increases by more than 30% aŌ er the age of 80.
Obesity can increase vitamin D needs as there is more potenƟ al for its storage in fat Ɵ ssue leading to lower availability.
Moreover, if individuals with obesity undergo gastric surgeries, their fat intake and absorpƟ on tend to decrease, thus
decreasing vitamin D bioavailability. Indeed, some forms of gastric surgery involve bypassing the duodenum, where the
majority of vitamin D absorpƟ on occurs.

98
Q

VITAMIN D TOXICITY

A

Excessive vitamin D intake from food is rare and toxicity is typically due to over-supplementaƟ on. Anorexia,
weight loss, increased urinaƟ on and irregular heart rhythms are potenƟ al symptoms of toxicity. However, the main toxicity risk is that excessive vitamin D intake can increase calcium levels to a harmful level. Excessively high blood calcium
can harden blood vessels and eyes and can negaƟ vely aff ect the kidneys and heart (InsƟ tute of Medicine, 2011). Vitamin
D toxicity may also increase the risk of kidney stones due to the high mineral concentraƟ on of the blood

99
Q

VITAMIN E

A

Vitamin E is the generic term for a group of eight vitamers. These are further divided into tocotrienols and tocopherols,
the most notable and nutriƟ onally relevant of which is alpha tocopherol.

100
Q

VITAMIN E FUNCTIONS

A

Vitamin E exerts its main eff ects through its anƟ oxidant role (Figure 8.21). It can help protect cells from the
harmful eff ects of free radicals by donaƟ ng electrons and neutralizing them. Vitamin E is further involved in immune
funcƟ on, cell signaling and gene expression.

101
Q

SPECIAL USE OF VITAMN E

A

Vitamin E has been studied for its potenƟ al to decrease the risk of cancer and CVD. However, a 10-year randomized control trial involving more than 14,000 male physicians found that neither vitamin E nor vitamin C decreased the
risk of CVD (Sesso et al., 2008). Similarly, a randomized control trial involving about 40,000 women over 12 years old
found no cardiovascular benefi ts from vitamin E supplementaƟ on (Lee et al., 2005). Taken together, vitamin E supplements do not reduce cardiovascular deaths or disease. Vitamin E supplementaƟ on has also been studied for its eff ects on
cancer risk, Alzheimer’s disease, age-related macular degeneraƟ on and cataract. To date, there is not

102
Q

SOURCES OF VITAMIN E

A

Vitamin E is found primarily in the oily germ of cereal
grains. Accordingly, the richest sources of vitamin E are vegetable
oils. FaƩ y shellfi sh and faƩ y plants such as nuts, seeds, forƟ fi ed
cereals and nut buƩ er are also good

103
Q

VITAMIN E DEFICIENCY

A

Vitamin E defi ciency is rare in Canada and the USA. If found, it is oŌ en associated with compromised fat absorpƟ on, such as in individuals who have had gastric surgery or in individuals with Chron’s disease or cysƟ c fi brosis. Symptoms
may include peripheral neuropathy, movement diffi culƟ es, muscle disorders and an impaired immune response.

104
Q

VITAMIN E TOXICITY

A

Vitamin E toxicity has not been established from food consumpƟ on. However, supplements of vitamin E may
lead to a higher mortality risk (Bjelakovic et al., 2007). Indeed, two clinical trials both found that prolonged intake of high
levels of vitamin E increased the risk of stroke (Alpha-Tocopherol, Beta Carotene Cancer PrevenƟ on Study Group, 1994;
Sesso et al., 2008). Vitamin E has also been linked with lung issues in those who vape (Box 8.4). Accordingly, cauƟ on
should be taken with supplementaƟ on

105
Q

VITAMIN K

A

Vitamin K was named based on the Danish word koagulaƟ on, whose English translaƟ on coagulaƟ on refers to
blood cloƫ ng. Indeed, the vitamin K family of vitamers funcƟ on as coenzymes in the pathway that leads to blood coagulaƟ on. Specifi cally, synthesis of the protein prothrombin is dependent on a vitamin K coenzyme (Figure 8.31). Prothrombin is a proenzyme that is acƟ vated into thrombin. Thrombin, in turn, helps convert the proenzyme fi brinogen into fi brin.
Fibrin fi bres are sƟ cky and link together to help the blood clump together, causing it to coagula

106
Q

SOURCES OF VITAMIN K

A

Vitamin K is found in leafy-green vegetables, such as
spinach and broccoli, as well as oils and nuts (Figure 8.32).
It can also be aƩ ained from animal products such as liver,
ham, cheese and milk. A healthy gut microbiota contributes
to vitamin K bioavailability, as certain organisms can synthesize diff erent forms of vitamin K. Accordingly the use of
anƟ bioƟ cs can negaƟ vely aff ect vitamin K status.

107
Q

VITAMIN K DEFICIENCY

A

Vitamin K defi ciency is rare in healthy adults unless they have an issue with vitamin K absorpƟ on. IniƟ al symptoms of vitamin K defi ciency may not be evidenced unƟ l it progresses to more severe clinical symptoms such as increased bleeding and hemorrhaging. InteresƟ ngly, drugs that impair vitamin K’s acƟ on are someƟ mes prescribed to
decrease blood cloƫ ng in those at risk of CVD (Box 8.5).
Newborns are at high risk for vitamin K defi ciency since it is poorly delivered via the placenta (InsƟ tute of Medicine, 2001). Accordingly, the Canadian Pediatric Society and the American Academy of Pediatrics recommend a single
dose of 0.5 to 1.0 mg of vitamin K to all newborns (Canadian Pediatric Society, n.d.). Vitamin K is also involved in bone
mineralizaƟ on, so defi ciency may lead to decreased bone density and even osteoporosis. Vitamin K defi ciency can someƟ mes be discovered through a prothrombin Ɵ me test – an exam that evaluates how well the blood coagulates.

108
Q

VITAMIN K TOXICITY

A

Vitamin K does not have an upper limit – no adverse eff ects from foods or supplements have been observed.

109
Q

VITAMIN INFUSED BEVRAGES

A

There are currently several vitamin-infused beverages on the market. These products make vague promises
based on providing a parƟ cular blend of vitamins. In Canada, vitamin-infused beverages are considered natural health
products, not foods. Accordingly, their labels do not have to list their caloric or nutrient breakdown and may therefore
mask a high added sugar content. In addiƟ on, since these beverages have a water base, they can only contain water-soluble vitamins – those that are less likely to be defi cient in the North American diet. Furthermore, drinking these beverages
may provide a false sense of healthfulness to someone with a less healthy diet. Indeed, scienƟ sts at Ryerson University
and the University of Toronto found minimal or no benefi t from the addiƟ on of vitamins to water and energy drinks

BPK 110 Lili (7 decks)

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