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Nutrition through life Part 1 > PART 5 - Fat, Carbohydrate, Fiber, Water and Micro-nutrient Requirements during Adulthood > Flashcards

PART 5 - Fat, Carbohydrate, Fiber, Water and Micro-nutrient Requirements during Adulthood Flashcards

1
Q

How was the AI for omega 3 and omega 6 fatty acids determined?

A

highest median intake by US adults without deficiency for different age groups and genders

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2
Q

Why is the ration of omega 3 and omega 6 fats important?

A

They are precursors for making the longer chain fatty acids. They compete for the same desaturase enzymes that are used to elongate and desaturate these fatty acids into longer ones. Too much omega 6 will increase the synthesis of arachidonic acid (inflammatory). Too much omega 3, not enough arachidonic.

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3
Q

Alpha-linolenic acid is turned into what fatty acid through desaturation and elongation?

A

EPA then docosahexaenoic acid (DHA)

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4
Q

Linoleic acid is turned into what fatty acid through desaturation and elongation?

A

Arachidonic acid

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5
Q

In what case is the ratio of omega 3 and omega 6 fatty acid less important?

A

When a diet involving high levels of the products of the desaturation and elongation reactions of those fatty acids

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6
Q

Why does the AI for omega 6 fatty acids decrease as you age?

A

With higher energy needs, there is a greater fatty oxidation rate. As you age your needs in energy go down

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7
Q

TRUE or FALSE. The consumption of EPA and DHA can contribute up to 10% of the omega 3 fatty acid needs.

A

TRUE

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8
Q

TRUE or FALSE. The consumption of EPA and DHA cannot contribute to reversing an omega 3 fatty acid deficiency.

A

FALSE. it can

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9
Q

How is the CHO requirement determined?

A

determined by the brain’s requirement (110-140g/d)

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10
Q

In a subject fully adapted to starvation, how much of the brain’s energy needs are filled by ketoacid oxidation?

A

80%

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11
Q

What is the EAR for CHO based on?

A

amount that would provide the brain with an adequate supply of glucose with using other sources of fuel

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12
Q

What assumption does the CHO EAR make?

A

The person is consuming an energy sufficient dies and glucose is not limited to the brain

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13
Q

How was the RDA calculated for CHO?

A

2 CV added to EAR. 1 CV is at 15%.

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14
Q

What is Total Fiber composed of?

A

Dietary Fiber + functional Fiber

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15
Q

What is dietary fiber?

A

CHO and lignins that are intrinsic and intact in plants that are not digested

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16
Q

What is functional fiber?

A

Isolated, extracted or synthetic nondigestible CHO with beneficial effects

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17
Q

TRUE or FALSE. There is a strong positive correlation between cereal fiber intake and risk of CHD.

A

FALSE. Negative correlation!!

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18
Q

what is the Fiber requirement based on?

A

Based on calories consumed

g of fiber per 1000kcal

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19
Q

What function does fiber have?

A

laxation, fuel for colonic cells, lower blood glucose and cholesterol (reduce heart disease), source of nutrient rich and low energy foods,

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20
Q

TRUE or FALSE. Fiber offers no calories.

A

FALSE. There’s a little bit but data goes around 2 cal/g

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21
Q

What is the AI for fiber based on?

A

Calculated with the amount of fiber per Cal, multiplied by the estimated energy requirement of the group

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22
Q

Why can’t we set an EAR for fiber?

A

There is benefit from increasing fiber intake without a cut off point… We don’t have enough information

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23
Q

Which are the best sources of fiber?

A

Pectin and cereal fiber

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24
Q

What composes Total Water Intake?

A

Total water intake= drinking water + water in beverages + water that is part of food

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25
Q

TRUE or FALSE. Most healthy adults consume enough water.

A

TRUE

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26
Q

TRUE or FALSE. Thirst dictates daily fluid intake, not behavior.

A

FALSE. Behavior dictates.

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27
Q

How is thirst sensed by the body?

A

Decrease in body water. Most often though, it is an increase in sodium concentration.

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28
Q

When is thirst detected?

A

When your body is already under stress. Thirst is not well correlated to fluid needs.

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29
Q

How is hydration status assessed?

A

measure plasma or serum osmolality.

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30
Q

What is the difference between osmolality and osmolarity?

A

osmolality: measure of the osmose. osmose being 1 mole of any solute per Kg of solvent.
Osmolarity: measure of osmose but his time per liter of solvent.

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31
Q

Why do we use osmolality for hydration status, plasma,…?

A

The volume of the solution can change with temperature or other factors. Difficult to assess in osmolarity since the volume is changing as we add solute too.

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32
Q

When you are dehydrated your osmolality increases or decreases?

A

increase

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33
Q

When you are over-hydrated your osmolality will increase or decrease?

A

decrease

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34
Q

What hormone is secreted whe nyou are dehydrated?

A

ADH - anti diuretic hormone

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35
Q

What affects you water needs?

A

dietary conditions
physical activity
environment

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36
Q

Why is there no single total daily water requirement?

A

There are too many factors that are not based on metabolism that affect water needs of the individual to set an amount.

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37
Q

What are the effects of dehydration?

A

impaired heat dissipation, which leads to increase body temp and strain on CV system

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38
Q

TRUE or FALSE. Low intake of water has been associated with some chronic diseases like stroke.

A

TRUE

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39
Q

What is the objective of the water AI?

A

prevent the negative effects of dehydration. The effects of water on chronic disease is not included since lack of evidence.

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40
Q

How can dehydration increase the risk of having a stroke?

A

The viscosity of the blood will increase. This can increase the activity of platelets so there is a higher risk of forming blood clots and having a stroke.

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41
Q

How does hydration status affect the risk of type 2 diabetes?

A

It affects type 2 diabetes by the secretion of ADH. ADH increases water absorption and constricts the arterioles to raise blood pressure. ADH can also affect blood glucose homeostasis and insulin resistance. Elevated ADH leads to higher fasting glycemia in rats. In obese rats, it led to insulin intolerance and hyperglycemia. Hydration can also reduce the risk of type 2 diabetes by decreasing adiposity, a known risk factor. Possibly by increasing satiety and reducing energy intake.

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42
Q

What is the Water AI based on?

A

Median water intake of server data in the US

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43
Q

Why do we not have a UL for water?

A

there is a potential danger but it is very rare.

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44
Q

What is the result of excessive consumption of water?

A

Hyponatremia, very low sodium concentration

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45
Q

In what situation would someone consume so much water?

A

Usually due to mental illness like psychogenicpolydipsia.

polydipsia= drinking a lot

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46
Q

What does the RDA for calcium rely on?

A

Calcium balance studies. What calcium intake is necessary to gain small gains of bone mineral content

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47
Q

What risks are associated with low consumption of calcium?

A

osteoporosis, colon cancer and HTN (hypertension)

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48
Q

Which age group is most at risk of caclum deficiency?

A

The elderly

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49
Q

Phosphorus is primarily found in what form?

A

Phosphate (PO4)

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50
Q

What are the main function of phosphorus?

A

Major component of bones and teeth, maintain Ph by buffering excesses, temporarily store energy (ATP), helps activate catalytic proteins by phosphorylation

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51
Q

Phosphorus occurs in the body mostly in what form?

A

Phospholipids, nucleotides and nucleic acids

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52
Q

What is the EAR for phosphorus based on?

A

Based on studies of serum inorganic phosphate concentration in adults (Pi)
The EAR is based on the lower end of the range of normal serum Pi level (graph)

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53
Q

Where is most of the magnesium in the boy located?

A

In the bone

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54
Q

What is the function of magnesium?

A

cofactor for over 300 enzymes
reservoir in skeleton to maintain extracellular Mg levels
can also be used as buffer

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55
Q

What is the EAR for magnesium based on?

A

Uses balance studies based on maintenance of total body Mg

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56
Q

Why is the RDA for magnesium higher for and older population?

A

There have been more instances of negative balance in older people then for younger people consuming at the EAR. So the EAR (by extension the RDA too) was bumped up for older people
Renal function is also very important for magnesium status but older people tend to have diminished renal function

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57
Q

Most of the iron in the body is located where?

A

In erythrocytes

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58
Q

What is the main function of Iron?

A

It is a component in a number of proteins with critical functions. Also oxygen transport

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59
Q

How was the Iron EAR determined?

A 
Used factorial modeling. The components of Fe requirement used as factors that are put together:
Basal Iron losses
Menstrual losses
Fetal requirements
Growth
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60
Q

What is the EAR for Iron based on?

A

Bioavailability (heme and nonheme iron)
need to maintain a normal functional Fe
Iron Stores / or maintenance of minimal stores (people with more serum ferritin and good iron stores will absorb a lot less iron because they don’t need it)

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61
Q

How is the RDA for Iron determined?

A

adding to SD to the EAR

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62
Q

Which factors are taken into account for men when calculating the EAR of iron?

A

Basal Iron losses

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63
Q

Which factors are taken into account for women when calculating the EAR of iron?

A

Basal Iron losses and Menstrual losses

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64
Q

Why does the RDA for women fall after 50 years of age?

A

Women stop menstruating after menopause

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65
Q

What are the beneficial effects of adequate intake of potassium?

A

Lowering blood pressure
blunting adverse BP effects of salt intake
reducing the risk of kidney stones
potentially reducing bone loss

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66
Q

What criteria is the AI for potassium based on?

A

Lowering blood pressure
blunting adverse BP effects of salt intake
reducing the risk of kidney stones
potentially reducing bone loss

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67
Q

What is hypokalemia and what are its effects?

A

Low potassium in the blood, can lead to cardiac arrhythmia, muscle weakness or even glucose intolerance

68
Q

What effects does a potassium deficiency have (not reaching hypokalemia)?

A

high blood pressure
increased salt sensitivity
increase risk of kidney stones
increase bone turnover

69
Q

How can potassium affect sodium status?

A

Hypokalemia can decrease sodium excretion

70
Q

When is Magnesium used as a buffer?

A

When not enough potassium is naturally present in the diet. The anions conjugated are used to make bicarbonate to buffer acids.

71
Q

In what form does potassium come in the diet?

A

Potassium usually comes conjugated to an anion such as citrate

72
Q

Why is the natural form of potassium found in fruits and vegetables important?

A

The anions conjugated to potassium can be converted to bicarbonate that acts as a buffer and neutralize acids from the diet such as sulfuric acid or sulfur containing AA. When you don’t have enough bicarbonate precursors, the body needs to use another type of buffer by drawing from the bone matrix. Can result in bone demineralization. and increased bone turn over.

73
Q

Why is it suggested to get our potassium from natural fruits and vegetables and not low sodium salts or other replacements?

A

The potassium is not conjugated to anions that can be turned into bicarbonate and can lead to bone demineralization.

74
Q

Why are athletes encouraged to eat fruits and vegetables that are high in potassium?

A

They sweat more so they lose more potassium.

75
Q

Why is there no UL for potassium?

A

No adverse effects known for healthy people.

76
Q

If there is no UL for potassium, how can hyperkalemia occur?

A

Happens in people who have difficulty excreting potassium.

77
Q

Why is potassium AI the same for sedentary adults and physically active adults?

A

There is too little potassium in sweat compared to the AI.

78
Q

what is the primary route for sodium loss?

A

Urine

79
Q

Which organ can control sodium levels?

A

The kidney can control excretion rates

80
Q

Why is the suggested daily sodium intake not apply to most athletes?

A

Usually we suggest to cut back. Athletes are suggested to salt liberally to replenish their sodium stores especially while training in hot climates.

81
Q

Why is the AI for sodium variable?

A

Sweat loss can exceed 10 g/day (extreme though). depends on the person and physical activity

82
Q

How do we get our sulfur?

A

From sulfur containing proteins (methionine, Cysteine, Cystine)

83
Q

What are the functions of sulfur?

A

Essential component of essential compounds (like glutathione)

84
Q

What is glutathione (GSH)?

A

Powerful antioxidant present in all mammalian tissues involved in the detoxification reactions of drugs and toxins and is heavily involved in redox reactions (reduction and oxidation)

85
Q

Why is there no intake requirement established?

A

Since we get our sulfur from AA turnover, the average american is actually in excess. If a person gets enough protein they are definitely getting enough sulfur. Evidence of this is shown by measuring sulfure excretion in relation to protein consumption.

86
Q

What is the function of Thiamine?

A

Coenzyme in the metabolism of CHO (as thiamin pyrophosphate) and branched chain AA

87
Q

What is the requirement of thiamine based on?

A

Based on thiamine needed to achieve and maintain RBC transketolase activity without excessive thiamin excretion

88
Q

What is transketolase?

A

Important enzyme for 2 reactions in the penthose phosphate pathway to make NADPH

89
Q

What is the penthose phosphate pathway?

A

Works in parallel to glycolysis. Unlike glycolysis, it is anabolic. Oxidates glucose but to make NADPH. particularly important for RBC

90
Q

What is NADPH?

A

A co-factor used in many anabolic reactions as a reducing agent. used to make lipids, nucleic acids…

91
Q

How are thiamine and NADPH related?

A

thiamine is essential for the functioning of transketolase. Transketolase is needed for the PPP. The PPP produces NADPH by the oxidation of glucose.

92
Q

What products does the Penthose Phosphate Pathway make?

A

NADPH, Pentoses and ribose-5-phosphate (precursor to nucleotide and DNA)

93
Q

What are the symptoms of Thiamine deficiency and what is it called?

A

Beri Beri, affects heart and circulatory system mainly

94
Q

Beri Beri is very rare in industrialized countries, in what situation could it be seen?

A

Heavy alcohol consumption

95
Q

A slight deficiency in Thiamine (sub-clinical) is characterized by what and how would you measure it?

A

measuring erythrocyte transketolase activity
concentration of thiamine or its derivatives in the blood (esters and phosphorylated)
urinary excretion of thiamine pre and post loading of thiamine

96
Q

What form of thiamin does transketolase need?

A

Thiamine pyrophosphate (CHO metabolism)

97
Q

Why do women need less thiamine?

A

involved in energy production and women need less energy and are of smaller size

98
Q

What are the functions of riboflavin?

A

Coenzyme in numerous oxidation-reduction reactions

99
Q

What is the requirement of riboflavin based on?

A

Based on erythrocyte glutathione reductase activity
riboflavin concentration in RBS
urinary excretion of riboflavin

100
Q

What is the function of glutathione reductase?

A

GSH is oxidized to make H and GS. 2 GS fuse together to make oxidized form. glutathione reductase turns it back

101
Q

How do you calculate the EAR of riboflavin?

A 
studies of the occurrence of clinical deficiency
biochemical values (changes can be seen before clinical deficiency)
urinary excretion in relation to dietary intake
102
Q

What is the relationship between iron and riboflavin?

A

If you have low iron intake coupled with low riboflavin levels, it affects the way you handle iron (and other nutrients). mechanism not known

103
Q

In what case could there be a riboflavin deficiency?

A

Heavy alcohol consumption because people usually eat a lot more than the RDA

104
Q

What are the functions of Niacin?

A

cosubstrate or coenzyme for H- transfer (dehydrogenases)

so its a donor or accepter of H-

105
Q

What type of reaction do dehydrogenases accomplish?

A

oxidation reduction reaction

106
Q

In what mechanisms does the oxidation reduction reaction take place (Niacin)?

A

intracellular respiration, fuel oxidation, fatty acid and steroid synthesis

107
Q

What is the primary criterion for the RDA of Niacin?

A

urinary excretion of niacin metabolites

108
Q

What is the Niacin requirement expressed as and why?

A

expressed as niacin equivalents since we don’t get all our niacin as whole niacin, we transform some tryptophan into niacin too

109
Q

The conversion of tryptophan into Niacin depends on what?

A

genetics
dietary factors (deficiencies can decrease conversion)
metabolic factors

110
Q

Why is the variability (CV) of niacin higher than for other nutrients?

A

to account for the individual aspect of tryptophan to niacin conversion

111
Q

What are the functions of B6 (pyridoxine)?

A

coenzyme in metabolism of AA, glycogen and sphingoid bases

112
Q

What are sphingoid bases?

A

class of lipids found in the brain

113
Q

What primary criterion is used for the RDA of vitamin B6

A

Maintenance of adequate blood 5’-pyridoxal phosphate levels

114
Q

What is the active form of vitamin B6?

A

5’-pyridoxal phosphate

115
Q

What is the function of foalte?

A

coenzyme in single carbon transfers in metabolism of nucleic and AA acids

116
Q

What is the primary indicator for RDA of folate?

A

erythrocyte folate, blood homocysteine and blood folate

117
Q

What is the dietary folate based on and why?

A

dietary folate equivalents (DFEs) to account for the lower bioavailability of food folate VS the supplement of folic acid

118
Q

1 ug of DFE is equal to how much food folate and folic acid?

A

1 ug DFE=
1 ug food folate
0.6 ug folic acid
0.5 ug folic acid on empty stomach

119
Q

What does vitamin B12 do?

A

coenzyme for methyl transfer rx homocysteine –> methionine

also: coenzyme A –> succinyl-CoA

120
Q

What is the RDA of vitamin B12 based on?

A

Maintenance of hematological status (everything that has to do with blood) and normal blood B12 values

121
Q

What does Biotin do?

A

Coenzyme in bicarbonate-dependent carboxylation reactions

122
Q

Why do we have an AI for Biotin?

A

Not enough info

123
Q

What did we use to set the AI for Biotin?

A

Estimates of intake

124
Q

What does Choline do?

A

precursor for acetylcholine, phospholipids and the methyl donor betaine

125
Q

What is the primary criterion used to estimate the AI of choline?

A

prevention of liver damage as assessed by serum alanine aminotransferase levels (ALT)

126
Q

Why do we test for ALT as a sign of liver damage?

A

If you have liver damage, the liver will start releasing ALT in the bloodstream

127
Q

What are the consequences of choline deficiency?

A

cause muscle damage and abnormal fat deposition in the liver (non-alcoholic fatty liver disease)

128
Q

How does choline deficiency lead to non-alcoholic fatty liver disease?

A

We know that fat and cholesterol that we consume are transported into the liver in chylomicrons. When the chylomicrons reach the liver the fat and cholesterol are packaged into lipoproteins. The lipoproteins are transported into tissues. In order to make lipoproteins and secrete them from the liver, we need phosphatidylcholine (so we need choline).

129
Q

Phosphatidylcholine is also known as?

A

lecithin

130
Q

TRUE or FALSE. lecithin (Phosphatidylcholine) has been used as a treatment for high cholesterol?

A

TRUE. lecithin cholesterol acyltransferase has important role in the removal of cholesterol from tissues by adding ester to cholesterol to promote HDL formation

131
Q

TRUE or FALSE. Choline is not essential.

A

TRUE

132
Q

Why was choline not essential initially? Why is it essential now?

A

we can make choline endogenously (de novo) from metabolism of phosphatidylcholine. Now we know that the De Novo synthesis is not enough since there are clear signs of deficiency on the liver with a low choline diet

133
Q

How is choline needs affected by the nutrient status of other nutrients?

A

Since the de novo synthesis is dependent on methylation starting from SAM (from folate and B12 pathway)

134
Q

What is choline requirement influenced by?

A

methionine and folate availability

gender, pregnancy, lactation, stage of development

135
Q

Why do we have an AI and not an EAR? Where does the AI come from?

A

Not enough studies done with diverse groups for an EAR. AI came from a dose that prevented alanine aminotransferase abnormalities

136
Q

What is the function of Pantothenic Acid?

A

Component of coenzyme A and phosphopantetheine (fatty acid metabolism)

137
Q

Since it is difficult to get a deficiency, how would it happen?

A

elemental diet or semisynthetic diet or if you take an antagonist

138
Q

What is the primary criterion for setting the AI of pantothenic acid?

A

intake adequate to replace urinary excretion of pantothenic acid

139
Q

What are the functions of vitamin C?

A

water soluble antioxidant

cofactor for enzymes involved in biosynthesis of collagen, carnitine (fatty acid oxidation) and neurotransmitters

140
Q

What is the RDA of vitamin C based on?

A

intake needed to maintain near-maximal neutrophil concentration of vitamin C with minimal urinary excretion

141
Q

Why do women need less vitamin C?

A

Smaller and less total body water. women keep higher vitamin C levels in blood at given vitamin C intake

142
Q

What are the functions of Vitamin A?

A 
Normal vision
gene expression
reproduction
embryonic development
growth
immune function
143
Q

What is the EAR of vitamin A based on?

A

Based on assurance of adequate stores

amount of dietary vitamin A required to maintain given body-pool size in well-nourished subjects

144
Q

What are the sources of vitamin A?

A

animal derived foods –> preformed vitamin A

plants –> provitamin A carotenoids

145
Q

What is the unit used for vitamin a requirements and why do we use it?

A

RAE - Retinol activity equivalents

use it because they’re are many forms of vitamin A

146
Q

What are the vitamin A equivalents?

A 
to get 1 RAE you need this much of each:
Beta-carotene RAE = 12ug
Alpha-carotene RAE = 24 ug
Beta-cryptoxanthin RAE = 24 ug
1 ug RAE= 1 ug retinol (pre-formed) =12 =24= 24
147
Q

What are the functions of vitamin D?

A

increases efficiency of absorption of Ca and P and maintains blood Ca and P
potent antiproliferatve and prodifferentiation effects in a variety of tissues

148
Q

what are the 2 major physiologically relevant forms?

A

Vitamin D2 - ergocalciferol

Vitamin D3 - cholecalciferol

149
Q

What is particular about the functions of vitamin E?

A

Doesn’t have a Major specific role.

150
Q

What are the functions of vitamin E?

A

protect against reactive oxygen species and lipid peroxidation

151
Q

How is the RDA for vitamin E calculated?

A

based on vitamin deficiency induced in humans (in vitro on withdrawn blood)
correlation between H2O2 induced erythrocyte lysis and blood alpha tocopherol

152
Q

What 2 groups of vitamin E are there?

A

Tocopherols and tocotrienols (alpha, beta, gamma, delta)

153
Q

Describe the structure of Vitamin E

A

Ring (with substituted groups) and tail (phytyl tail)

154
Q

What is the difference between the 4 tocopherols and 4 tocotrienols?

A

Number of methyl groups on the ring

155
Q

What form is found in nature?

A

RRR (the methyl groups on the chain are all on the right) the others are stereoisomers

156
Q

What is the All racemic mixture of vitamin E?

A

Group of 8 stereoisomers made synthetically since we can’t make only the natural RRR form
all-rac has 1/2 the activity of RRR or other 2R forms

157
Q

The definition of vitamin E according to the DRI is limited to which of the stereoisomeric forms?

A

When carbon 2 is R

2R- stereoisomers

158
Q

TRUE or FALSE. The vitamin E forms are interconvertible in humans

A

FALSE, they are NOT interconvertible

159
Q

What is the plasma vitamin E concentration dependent on?

A

depends on the affinity of the stereoisomer with hepatic alpha-tocopherol transfer protein (alpha-TTP)
RRR are maintained in the human plasma
the different alpha tocopherol molecules molecules have different affinity

160
Q

What does alpha-TTP do? (hepatic alpha-tocopherol transfer protein)

A

Packages the vitamin E forms into lipoproteins for delivery to peripheral tissues

161
Q

What is used to estimate vitamin E requirement?

A

the 2R-stereoisomers forms are used

the other forms aren’t used

162
Q

Vitamin E has EARs, RDAs and AIs, why?

A

Because infants all have an AI

163
Q

What are the functions of vitamin K?

A

Coenzyme during synthesis of the biologically active form of a number of proteins involved in blood coagulation and bone metabolism

164
Q

What is the AI for vitamin K based on?

A

dietary intake data for healthy individuals

165
Q

What 2 forms does vitamin K come in and where do they come from?

A

Phylloquinone: diet
Menaquinones: bacteria in bowel

166
Q

Why is it hard to get a vitamin K deficiency?

A

Some production of vitamin K in the microbiota (menaquinones)

Nutrition through life Part 1 (6 decks)

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