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Physiology 2 > KIN 346 Module 2 > Flashcards

KIN 346 Module 2 Flashcards

1
Q

Why are lipids important?

A

cell membranes, bile acids, vitamin D, eicosanoids, hormones, source of energy, temperature regulation, transport of fat soluble vitamins, lipoproteins, protection of internal organs, taste (moist and crumbly), good smells, energy

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2
Q

What are lipids composed of?

A

C, H, and O. High proportion of C and H compated to O = more energy dense than CHOs

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3
Q

What are the types of lipids?

A

fatty acids (mono, polunsaturated, saturated), triglycerides, phospholipids, sterols

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4
Q

Fatty acid?

A

AN organic acis that is a chain of C atoms with H atoms attached with an acid group (COOH) at one end and a methyl group (CH3) at the other

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5
Q

FAs are differentiated by?

A

Length of the C chain, degree of saturation, location of the double bonds

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6
Q

Most naturally occurring FAs contain…

A

even numbers of Cs in their chains (up to 24 Cs)

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7
Q

Long chain FAs?

A

12-24 Cs…most abundant in the diet from meats, fish, and vegetable oils

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8
Q

Medium chain FAs?

A

6-10 Cs and short chains (<6Cs)…less abdunant in diet and from dairy products

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9
Q

What are the most common FAs in the diet?

A

18 C, with stearic acid being the most common from meat

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10
Q

A saturated FAs carries the maximum number of…

A

H atoms (no double bonds)

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11
Q

Formula for stearic acid and where it is mostly found?

A

18:0, mostly in animal fats

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12
Q

A unsaturated acid includes…

A

a point of unsaturation (double bond) between >2Cs and less Hs

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13
Q

Notation for oleic acid and where it is mostly found?

A

18:1 n-9. Olive and canola oils

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14
Q

Notation for linoleic acid, and where it is found?

A

18:2 n-6. Sunflower, safflower, corn and soybean oils

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15
Q

What is the omega number?

A

Describes the location of the doulbe bond(s) from the omega/methyl end

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16
Q

Notaiton for linolenic acid, and where it is found?

A

18:3 n-3. Soybean and canola oils, flaxseed, walnuts

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17
Q

Are FFAs usually found in the diet or the body?

A

no…majority are incorporated into triglycerides

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18
Q

What are triglycerides?

A

Lipids composed of 3 FAs attached to a molecule of glycerol

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19
Q

How does FA structure affect the foods we eat?

A

Chain length, degree of saturation, and location of double bond(s) can all impact the qualitites of the fats and oils found in the food supply

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20
Q

What qualities of food are affected based on FA structure?

A

Firmness at room temp (vegetable oils versus tropical oils vs animal fats). Susceptibility to oxidation/rancidity (natural nut butters versus butter)

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21
Q

What type of FAs are most likely to oxidize? Least?

A

Most = PUFAs (bonds are less stable) Least = saturated (bonds are more stable)

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22
Q

What is hydrogenation?

A

A process used by manufacturers to enhance the shelf life of fat containing products. Some or all the points of unsaturation are saturated by adding H molecules.

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23
Q

Adcantages to hydrogenation?

A

improves shelf life, protects against oxidation (natural vs hydrogenated nut butters), alters textures of foods (vegetable oils versus margarine)

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24
Q

Disadvantages to hydrogenation?

A

Creation of trains fatty acids

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25
Q

What are trans fatty acids?

A

A FA with its hydrogens on the opposite sides of the double bond, making them act more like saturated fats in the body

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26
Q

Trans Fat Task Force recommendations?

A
  1. Limit the trans fat content of vegetable oils and soft margarines to 2% total fat 2. Limit the trans fat content of all other foods to 5% total fat, including restaurant foods. 3. Encourage to replace trans fat with MUFAs and PUFAs (not saturated fats)
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27
Q

What sector presents the greatest challenge to reducing trans fat?

A

Cafeterias in schools and institutions because they don’t have the funding

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28
Q

For the most part, are most sectors under the limits under the trans fat amount?

A

Yes

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29
Q

What trans fat doesn’t need to appear on labels?

A

Conjugated linoleic acids (CLAs) and conjugated linolenic acids (CLNs) are found naturally in the meat and milk of ruminant animals (2-5% total fat) and do not fallt in CFIA’s trans definition…actually have health benefits

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30
Q

Total trans fat on the label can be rounded to zero when per serving…

A
  1. the food contains less than 0.2g trans fat 2. The food contains less than or equal to 2g saturated and trans fat combines 3. The food provides less than or equal to 15% energy from the sum of saturated and trans fats
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31
Q

Is the majority of trans fat labelling accurate?

A

Yes

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32
Q

Phospholipids?

A

Similar to TGs but have a phosphate group and choline in place of one of the FAs…used in the food industry as emulsifiers.

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33
Q

WHere are phospholipids naturally occurring?

A

Eggs, liver, soybeans, wheat germ, and peanuts

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34
Q

What is lecithin?

A

one of the phospholipids. Both nature and the food industry use lecithin as an emulsifer to conbine water-soluble and fat-soluble ingredients that do not ordinarily mix, such as water and oil

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35
Q

What makes phospholipids emulsifiers?

A

Contain a hydrophilic part (methioine part…the choline), and a hydrophpbic part (2 fatty acids)

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36
Q

Phospholipids in the body?

A

Major constituents of cell membranes. Help fat-soluble substances (vitamins and hormones) pass in out and cells, keeps fat suspended in the blood and body fluids, and major components of lipoproteins

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37
Q

Are lecithin supplements needed?

A

NO…your liver makes all the lecithin you need. It is not an essential nutrient. Too much can cause weight gain, GI distress, sweating, and loss of appetite

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38
Q

Percentage of Canadians that are regualr users of dietary supplements?

A

40-70%

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39
Q

What are sterols?

A

Lipids with multiple ring structures

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40
Q

Where are sterols found?

A

In both plants and animals, but only animal food contain cholesterol.

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41
Q

What do sterols in plants do?

A

Interfere with choelsterol absorption, lowering blood cholesterol levels

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42
Q

Where sterols found in the body?

A

Bile acids, sex hormones, adrenal hormones, vitamin D, components of cell membranes

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43
Q

How much cholesterol does the liver manufacture per day?

A

800-1500 mg per day…>90% resides in the cells

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44
Q

Examples of sterols in the body?

A

Cholesterol and Vitamin D3

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45
Q

How many TGs do we consume per day?

A

50-100g

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46
Q

How man phospholipids do we consume per day?

A

4-8g

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47
Q

How much cholesterol do we consume per day?

A

200-350mg

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48
Q

What is the biggest problem when digesting fats?

A

They are hydrophobic and the enzymes that digest them are hydrophilic

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49
Q

What are lipids broken down into?

A

Monoglycerdies, fatty acids, glycerol

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50
Q

Can the body absorb triglycerides?

A

NO

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51
Q

How are triglycerides digested?

A

Hydrolysis

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52
Q

What happens with lipid digestion in the mouth?

A

Hard fats begin to melt as they reach body temperature, salivary glands at the base of the tongue release linguinal lipase (plays a minor role in fat digestion in adults but better at digesting short and medium chain FAs in milk for babies), end products of digestions are diglycerides and fatty acids

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53
Q

Lipid digestion in the stomach?

A

Strong muscle contraction of the stomach churn and propel its contents toward the pyloric sphincter. The churning action is important because it grinds solid pieces into finer particles, mixes the chyme, and disperses the fat into small droplets. Little digestion occurs, mostly juts exposes fat for attack by gastric lipase

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54
Q

What triggers the release of cholecystokinin (CCK)? from the gallbladder?

A

Fat in the SI

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55
Q

What do bile acids do in the SI?

A

Act as emulsifiers, drawing fat molecules into the surrounding watery fluid

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56
Q

What are the major fat digesting enzymes?

A

Pancreatic lipases…remove TGs’ outer FAs, leaving a monoglyceride (can be absorbed), occasionally, all FAs are removed, leaving glycerol

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57
Q

How are phospholipids digested?

A

In a similar way to TGs, with 2 FFAs and the choline part being the end products

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58
Q

How are sterols digested?

A

Most are absorbed as is

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59
Q

What are bile acids made of?

A

Cholesterol (hydrophobic) and amino acid (hydrophilic)

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60
Q

Where is bile made? Stored?

A

Liver, gall bladder

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61
Q

What is the goal of emulsification of fats?

A

Increase the surface area –> enhanced efficiency of digestion

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62
Q

Circulation of bile?

A

Made in liver –> stored in gall bladder –> enters SI through common bile duct in response to CCK –> recycled back to liver OR bound by soluble fibres and excreted in the feces

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63
Q

What are the problems caused by pancreatic insufficiency to make lipases, or decreased amount being released into the SI?

A

Fat malabsorption and fat-soluble vitamin malabsorbtion

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64
Q

What lipids diffuse easily into intestinal cells?

A

Small molecules of digested triglycerides (glycerol and short and medium chain FAs)

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65
Q

How are larger molecules (monoglycerides and long chain FAs) absorbed?

A

Merge into spherical complexes known as micells…emulsified fat droplets formed by molecules of bile surrounding monoglycerides and FAs –? soluble in intestinal fluids, transport to intestinal cells

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66
Q

Inside intestinal cells, what happend to monoglycerides and long-chain FAs?

A

Reassembled into new triglycerides

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67
Q

How are lipids transported from cells to the bloodstream?

A
  1. Newly made trigylcerides and other lipids (cholesterol, phospholipids, vitamisn) are packed with protein into lipoprotein transport vehicles called chylomicrons 2. Via pinocytosis, chylomicrons are released from intestinal cells to the lymphatic system –> entry into bloodstream via the thoracic duct –? blood carries the lipids to the rest of the body for immediate use or storage
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68
Q

4 lipoproteins from least dense to most dense?

A

Chylomicrons –> VLDL –> LDL –> HDL

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69
Q

What is the relationship between size, density, and lipid content?

A

Bigger the lipoprotein, the less dense it is and the the more TGs/lipids it contains

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70
Q

What are the largest and least dense lipoproteins?

A

Chylomicrons…lots of TGs

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71
Q

What do chylomicrons do?

A

Transport diet-derived lipids from small intestine to the rest of body

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72
Q

What happens to chylomicrons over time?

A

Body cells remove triglycerides, leaving chlyomicron remnants. Most TGs have been depleted 14 h after absorption leaving only a few remnants of protein, cholesterol, and phospholipid. Protein receptors on the liver recognize the remnants and remove them from the blood –? dismantling for use or recycling

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73
Q

What is VLDL?

A

Lipids made in the liver and those collected from chylomicrons remnants are packaged with proteins as VLDL and shipped to other parts of the body. VLDL travels through the body, TGs are removed and it shrinks/loses density –> shift in the proportion of lipids to become LDL

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74
Q

What does HDL do?

A

removes cholesterol from the cells and carry it back to the liver to be recycled or disposed

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75
Q

What is “bad” choelsterol?

A

Ldl…primarily choesterol…linked to heart disease…High LDL is not desirable

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76
Q

What is “good” cholesterol?

A

HDL…primary protein…carries cholesterol back from the rest of the body to the liver for breakdown.excretion…anti-inflammatory properties…high HDL is associated with a protective effect (desirable)

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77
Q

Factors that lower LDL and increase HDL?

A

weight control, MUFAs/PUFAs instead of saturated fat, soluble fibre, phytochemicals like sterols, moderate alcohol consumption, physical activity

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78
Q

Can HDL and LDL cholesterol be consumed?

A

NO, body makes it

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79
Q

Is the cholesterol from HDL different than that of LDL?

A

No, both same type of cholesterol, but it the proportion and composition of lipoprotein that make it different

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80
Q

Role of triglycerides?

A

Provide energy…>2x that of CHOs and proteins. Efficient storage form of energy. Body’s fat stores have virtually unlimited capacity; the fat cells of adipose tissue readily take up and store TGs

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81
Q

What are adipokines?

A

Adipose tissue secreted proteins that help regulate energy balance and influence several body dunctions

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82
Q

Examples of adipokines?

A

Leptin, adiponectin, resistin, visfatin

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83
Q

What are the 2 essential FAs?

A

Linoleic and linolenic acid

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84
Q

Why are linoleic and linolenic acid considered essentiaL?

A

Must be supplied by the diet because cells cannot convert omega-6 to omega-3 and vice versa

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85
Q

Why should EPA and DHA be taken in the diet, even thought the body can make them from linolenic acid?

A

Desaturation and elongation are possible to make longer FAs of the same family, but the process is very inefficient

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86
Q

What is linoleic acid?

A

18:2n-6. Important component of membrane phospholipids and primary member of the omega-6 family. Can be converted to arachidonic acid. In times of dietary inadequcy, arachadonic acid and all other omega-6s derived from linoleic acid become essential

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87
Q

WHat is linolenic acid?

A

18:3n-3. Primary member of omega-3 family. Important component of membrane phospholipids. Limited amounts of eicosapentaenoic acid (EPA, 20C) and docasahexaenoic acid (DHA, 22C) can be made.

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88
Q

What are EPA and DHA important for?

A

Found in eyes and brains. Essential for growth and cognitive development. Prevention and treatment of heart disease.

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89
Q

What are eicosanoids made from?

A

EPA and arachidonic acid

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90
Q

What type of eicosanoids have greater health benefits?

A

Those from EPA exude greater health effects –> lower BP, reduce blood clot formation, protect against irregular heart beats, reduce inflammation

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91
Q

Eicosanoids are described as “hormone like,” but how are they different from hormones?

A

Affect only cells in which they are made or nerby cells in the same localized environment and different effects on different cells and actions of various eicosanoids oppose each other

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92
Q

General recommendations for lipids and health?

A

Choose a diet that is low in saturated fat and trans fat and cholesterol and moderate in fate

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93
Q

Desirable level for total cholesterol?

A

Less the 5.2 mmol/L

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94
Q

Desirable level for LDL cholesteroL?

A

Less that 2.5 mmol/L

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95
Q

Desirable level for HDL cholesterol?

A

Greater than 1.5 mmol/L

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96
Q

Desirable level for TGs?

A

less than 1.7mmol/L

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97
Q

What type of fats raise LDL cholesterol?

A

Saturated fats…some raise it more than others

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98
Q

What type of saturated fats raise LDL the most?

A

tropical fats…lauric acid, myristic, and palmitic acids (12,14,16 C)

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99
Q

Does stearic acid raise LDL?

A

NOPE

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100
Q

How does sat. fat contribute to heart disease?

A

Promote blood clotting…atherosclerotic

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101
Q

Main sources of saturated fat?

A

Animal products (meat and milk), vegetable fats (coconut and palm), hydrogenated fats

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102
Q

Relationship between dietary trans fats and heart disease?

A

Trans fats raise LDL and lower HDL

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103
Q

Average daily intake of trans fat in Canada?

A

~3.4g/day (1.4% total energy) mostly from hydrogenated products

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104
Q

Why have trans fat intakes decreased over the past decades?

A

Trans Fat Task Force and people are more aware of it

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105
Q

What to look for on labels when wondering about trans fat?

A

Partially hydrogenated oil and shortening

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106
Q

What raises blood cholesterol more, dietary cholesterol or saturated and trans fat?

A

Saturated and trans fat do

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107
Q

How can cholesterol intake be lowered?

A

Consuming minimal animal products in moderation and avoiding especially high sources (also high in saturated fats)

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108
Q

Most effective dietary method for preventing heart disease?

A

Substituting MUFAs and PUFAs in the place of saturated and trans fat

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109
Q

Some major sources of MUFAs?

A

olive oil, canole oil, peanut oil, avocados, flax seed oil, walnuts

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110
Q

Major sources of PUFAs?

A

safflower oil, sesame oil, soy oil, corn oil, sunflowe oil, nuts, seeds

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111
Q

What is canola/rapeseed oil?

A

Low in saturated fats, higher in oleic acid(61%), linoelic acid(21%), and alpha-linoleic acid(11%), plant sterols, an tocopherols (vit. E/anti-oxidant) –> cardioprotecitve effects

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112
Q

What does regular cinsumption of omega-3s do?

A

Helps prevent blood clots, protects against irregualr heartbeats, lowers BP, especially in people with hypertension or atherosclerosis, anti-inflammatory properties, and improves immunity

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113
Q

Sources of linoleic acid?

A

vegetable oils (corn, sunflower, safflower, soybeanm cottonseed), poutry fat, nuts, seeds

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114
Q

What is arachidonic acid made from?

A

Linoleic acid

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115
Q

Sources of arachidonic acid?

A

Meats, poultry, egggs

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116
Q

Examples of linolenic acid?

A

oils (flaxseed, canola, walnut, wheat germ, soybean), nuts and seeds (butternut, flaxm walnuts, soybea kernels), soybeans

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117
Q

What are EPA and DHA made from?

A

linolenic acid

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118
Q

What are sources of EPA and DHA?

A

Human milk, Pacific oysters, and fatty fish

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119
Q

What are the best sources of EPA and DHA?

A

fatty fish…char, herring, mackerel, trout, sardines, and salmon

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120
Q

Fish high in mercury?

A

tilefish, swordfish, king mackerel, shark

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121
Q

Fish low in mercury>

A

cod, haddock, pollock, salmon, sole tilapia, most shellfish

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122
Q

What is more important to increase in your diet more…omega 3 or 6?

A

omega 3

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123
Q

AMDR for lipid intake?

A

20-35% for 19-30 years old

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124
Q

AI for omega-3 for males?

A

1.6 g

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125
Q

AI for omega-3 for females?

A

1.1 g

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126
Q

AI for omega-6 for males?

A

17 g

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127
Q

AI for omega-6 for females?

A

12 g

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128
Q

Suggested DV of fat based on a 2000 kcall diet?

A

65 g

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129
Q

DV for saturated fat?

A

20 g or 10%

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130
Q

DV for cholesterol?

A

300 mg…200 for people with dyslipidemia

131
Q

When does atherosclerosis begin?

A

Early in life, most people have well-developed plaques by age 30

132
Q

What is a main contributor to atherosclerosis?

A

Diet high in saturated fat

133
Q

Diet related modifiable risk factors for CHD?

A

High LDL and low HDL cholesterol. Hypertension. Diabetes. Obesity (especially abdominal). Atherogenic diet (high in saturated fats, low in vegetables, fruits and whole grains)

134
Q

What is a atherogenic diet?

A

High in saturated fats, trans fats, and cholesterol and low vegetables, fruits and whole grains –> elevates LDL cholesterol

135
Q

What type of diet lowers LDL?

A

Diets rich in fruits, vegetables and whole grains lower the risk of CHD

136
Q

Primary and secondary prevention for energy balance?

A
  1. Balance energy in with energy out to maintain a healthy weight 2. Obesity (esp. abdominal) and physical inactivity increase the risk for CHD by contributing to high LDL, low HDL, hypertension, and diabetes.
137
Q

Primary and secondary prevention for saturated and trans fats and cholesterol?

A

1) Chooose lean meats, vegetables, and lower fat milk products 2) Limit saturated fats to <10% 3) Trans fats to 1% of total intake 4) Saturated fats raise LDL; trans fats raise LDL and decrease HDL

138
Q

What should you replace saturated and trans fats with to lower risk of CAD?

A

Replace saturated and trans fats with MUFAs and PUFAs, with an emphasis on MUFAs

139
Q

What do PUFAs do to cholesterol levels?

A

Decrease total cholesterol

140
Q

What do MUFAs do to cholesterol?

A

MUFAs decreases LDL without decreasing HDL

141
Q

What types of foods should you choose to increase soluble fibers?

A

A diet rich in vegetables, fruits, whole grains and other foods high in soluble fibers like oats and barley

142
Q

Primary and secondary prevention for potassium an sodium?

A

1) Choose a diet high in potassium-rich fruits and vegetables, low fat milk products, nuts and whole grains 2) Use little to no added salt (<2300 mg/d total)

143
Q

What is the recommendation for added sugars for females? Males?

A

Females is <150kcal/d

144
Q

What are high sugar intakes associated with?

A

An increase in TGs

145
Q

Primary and secondary prevention for fish and omega-3 and CHD?

A

Consume fatty fish rich in omega-3s at least 2x/week.

146
Q

How do omega-3s help with CAD?

A

Prevents blood clots, protects against irregular heartbeats, lowers blood pressures

147
Q

What do plant sterols do in regards to CAD?

A

Reduces total cholesterol and LDL by interfering with absoprtion

148
Q

Primary and secondary prevention for soy consumption and CAD?

A

Consume soy foods more often to replace animal and dairy products that contain saturated fats and cholesterol.

149
Q

What does soy do in regards to CAD?

A

Promotes reduction in total and LDL cholesterol, reduces BP and inflammation

150
Q

Alcohol recommendations for CAD?

A

Limit to one drink daily for women and two for men. Excessive intakes raise TGs, BP, and may promote weight gain

151
Q

Physical activity recommendation for CAD prevention?

A

Minimum of 30 minutes of moderate-to-vigorous PA most days of week

152
Q

How does physical activity decrease CAD risk?

A

Lowers LDL, raises HDL, improves insulin sensitivity, lowers blood pressure, increases energy expenditure, improves body composition

153
Q

What is the French Paradox?

A

Low coronary heart disease rates despite high intakes of cholesterol and saturated fat

154
Q

Why do French people have lower coronary disease rates even though they eat so much saturated fats?

A

Consume more red wine than many other populations. There is an inverse relationship between moderate alcohol consumption and CHD risk. Red wine, in particular, contains resveratrol and other polyphenols that reduce inflammation, prevents damage to blood vessels, reduces LDL and prevents blood clots, and raises HDL

155
Q

What is reseveratrol, what does it do, and what foods contain it?

A

It is a polyphenol that reduces inflammation, prevents damage to blood vessels, reduces LDL and prevents blood clots, and raises HDL. RED wine, grapes, grape juice, peanuts, cranberries, and blueberries contain it.

156
Q

What is the Mediterranean Diet?

A

Main focus on plant-based foods. olive oil, herbs and spices, red wine in moderation. Little red meat.

157
Q

When assessing a diet for CVD risk, what are the main nutrients you should be looking at?

A

Sodium, saturated fat, trans fat, added sugar, cholesterol, and alcohol

158
Q

Basic structure of all amino acids?

A

Central C, with an H atom, amino group (NH2), acid group (COOH), unique side group/chain

159
Q

What is an essential amino acid?

A

Human body cannot make at all or cannot make in sufficient quantity…must be supplied by the diet/indispensible

160
Q

How many essential amino acids are there?

A

9

161
Q

How many dispensable/nonessential AAs are there?

A

11

162
Q

What must be available for the body to synthesize AAs?

A

requires nitrogen to form the amino group and fragments from CHO to form the rest of the structure, plus adequate energy

163
Q

What conditionally essential amino acids?

A

some nonessential AAs become essential under special circumstances. Phenylalanine is ussed to make tyrosine (nonessential). If diet fails to provide phenylalanine OR the conversion of phenyalanine to tyrosine cannot occur, tyrosine becomes conditionally essential.

164
Q

How many nonessential AAs are there for infants?

A

5 AAs; the other nonessential AAs are conditionally essential until the metabolic pathways are developed enough to make those AAs from a polypeptide

165
Q

Conditionally indispensable/essential AAs

A

arginine, cysteine, glitamine, glycine, proline, tyrosine

166
Q

Indispensable/essential AAs

A

phenylalanine, valine, thronine, trytophan, isoleucine, methionine, histadine, leucine, lysine

167
Q

Indispensable/nonessential AAs

A

alanine, asparagine, aspartic acid, glutamin acid, serine

168
Q

How are AAs bound together to form proteins?

A

condensation reactions

169
Q

2 AAs bonded together?

A

dipeptide

170
Q

3 AAs bonded together?

A

tripeptide

171
Q

Protein digestion in the mouth?

A

no enzymatic digestion, proteins are crushed and moistened

172
Q

Protein digestion in the stomach?

A

Partial breakdown (hydrolysis) of proteins –> HCl uncoils/denatures each protein’s tangled strands –> facilitates attack of peptide bonds via digestive enzymes. HCl converts the inactive form of the enzyme pepsinogen to its active form, pepsin –> cleaves proteins into smaller polypeptides and some AAs

173
Q

Protein digestion in SI?

A

pancreatic and intestinal proteases hydrolyze polypeptides into short peptide chains and AAs. Peptidase enzymes split most dipeptides and tripeptides into single AAs

174
Q

Absoprtion of proteins in SI?

A

Specific carriers transport AAs (along with some di and tripeptides) into the intestinal cells.

175
Q

Once AAs are absorbed into the intestinal cells, what are their fates?

A

Inside the intestinal cells, AAs may be used for energy or to synthesize needed compounds. Unused AAs are transported across the cell membrane into the surrounding fluid where they enter the capillaries on their way to the liver.

176
Q

Some roles on protein in the body?

A

Building materials for growth and maintenance, act as enzymes, act of hormones, regulate fluid balance, mainteance of acid-base balance, act as transporters, act as antibodies, a source of energy an glucose, blood clotting, tissue repair, and vision

177
Q

Examples of protein hormones?

A

INsulin, glucagon, thyroxin, calcitonin, parathyroid hormone

178
Q

How do proteins contribute to edema?

A

Proteins don’t normally cross the walls of the blood vessels; in times of critical ilness or malnutrition, plasma proteins leak out of blood vessels into tissues –> accumulation of fluid –> edema

179
Q

How do proteins contribute to acid-base balance?

A

Accept and release H+ ions to maintain a constant pH. Acidosis and alkalosis lead to come and death, as they denature proteins.

180
Q

How do proteins act as transporters?

A

Na-K pump, lipoproteins, hemoglobin

181
Q

how to proteins act as antibodies?

A

defend against invading antigens

182
Q

How do proteins contribute as a source of energy and glucose?

A

proteins will be sacrificed to provideenergy and glucose duing times of starvation or insufficient CHO or total energy intake at the expense of lean tissue

183
Q

What is the amino acid pool?

A

AA cannot be stored, so they form a pool in the blood through a continuous porcess of breakdown.

184
Q

What can AAs in the AA pool be used for?

A

body proteins or other N-containing compounds (NTs, thyroxine), also be stripped of N, leaving a C backbone, which can be used be energy or stored as fat

185
Q

What is nitrogen balance?

A

the amount of N consumed as compared with the amount of N excreted in a give time period

186
Q

What is a positive nitrogen balance, and when does it occur?

A

N in > N out. Growing children, a person building muscle, a pregnant women

187
Q

What is a nitrogen equilibrium, and when does it occur?

A

N in = N out. Occurs in a healthy college student or retiree

188
Q

What is a negative nitrogen balance, and when does it occur?

A

N in < N out. An astronaut, surgery patient, burn victim, anorexic person

189
Q

RDA for protein?

A

0.8g/kg/day. Covers the needs for replacing worn out tissue. Increases for larger body sizes. Assumes that dietary protein is of mixed quality and the CHO, fat, micronutrient and energy intakes are sufficient

190
Q

RDA for protein for active athletes?

A

1.2-1.7g/kg/day

191
Q

Problems associated with too much protein?

A

heart diease, cancer, osteoporosis, obesity, kidney stones

192
Q

AMDR for protein?

A

10-35% total energy

193
Q

average intake of proteins for Canadians?

A

16.5% total energy

194
Q

Acute protein energy malnutrition?

A

recent severe food deprivation, underweight for height, kwashiorkor

195
Q

Chronic protein energy malnutrition?

A

long-term food deprivation, short for age, marasmus

196
Q

Features of marasmus?

A

Chronic PEM, mostly children 6-18 months of age. Muscle wasting and weakening, impaired brain development and learning ability, reduced synthesis or key hormones –> slowed metabolism and lowered body temp, cessation of growth, deterioration of GI tract lining –> food cannot be properly absorbed or digested

197
Q

Features of kwashiorkor?

A

Acute PEM. Mostly in children 18 months-2years of age. Often precipitated by illness or infection, Less severe loss of bodyweight, but muscle wasting may occur, swelling of the abdomen and limbs (edema), fatty liver, loss of hair colour, patchy, scaly skin, sores that fail to heal. Unbound iron –> promotes bacterial growth and free radical damage.

198
Q

What is a vegetarian?

A

Person who excludes meat, fish or fofwl and products containing these foods

199
Q

Most strict vegetarian?

A

vegan/total vegetarian

200
Q

Percentage of Canadians that are vegetarians?

A

4% (900,00) in 2002

201
Q

Position statement of the ADA and DC on vegetarian diets?

A

appropriately planned vegetarian diets are healthful, nutritionally adequate and provide health benefits in the prevention and ttreatment of certain diseases, appropriate for all stages of life, including pregnancy and lactation.

202
Q

Benefits of a vegetarian diet?

A

Lower in sat. fats, cholesterol, and animal protein. Higher in CHO, fibre, magnesium, folate, antioxidants, vitamin C, vitamin E, carotenoids, and phytochemicals. Lower BMI, decreased risk of CVD, diabetes, and cancer

203
Q

What micronutrients pose a threat for inadequacy in vegetarians?

A

vitamin B12, vitamin D, calcium, zinc, riboflavin, also concerns for protein intake

204
Q

Protein needs of vegan vegetarians compared to non-vegetarians? Why?

A

may be increased by 15-20% because plant proteins have lower digestibility

205
Q

What is PDCAAS?

A

protein digestibility corrected amino acid score…used to assess protein quality

206
Q

Protein digestibility depends on?

A

protein source and other foods consumed with protein

207
Q

Digestibility of animal proteins?

A

90-99%

208
Q

Digestibility of plant proteins?

A

7-90% (>90% for soy and legumes)

209
Q

AA content/composition of a protein in regards to its quality?

A

Dietary protein must be supply at least the 9 essential AAs and enough N-containing amino groups to manufacture the non-essential ones.

210
Q

What is a limiting AA?

A

essential AA supplied in less than the amount needed to support protein synthesis

211
Q

How is the quality of food protein determined?

A

Comparing its AA composition with the essential Aa requirements of preschool children

212
Q

Is gelatin a high quality protein?

A

NO…but most animal proteins are

213
Q

Are plant proteins high quality proteins?

A

Most tend to be limiting in one or more of the essential AAs

214
Q

What are complementary proteins?

A

Proteins that when consumed together, contain all the essential AAs in quantities sufficient to support health. Consumed over the day, not necessarily at the same eating occasion. Whole grains, legumes, seeds, nuts, vegetables.

215
Q

Why is iron a concern in vegetarian diets?

A

absorbability from plant sources < animal sources. More susceptible to inhibitors and enhancers

216
Q

Iron recommendation for vegetarians compared to omnivores?

A

1.8x omnivores because of lower bioavailability in plant based diets

217
Q

Iron consumption in different types of vegetarians from least to most?

A

non-vegetarians < lacto-ova vegetarians < vegans

218
Q

Why is zinc a concern in vegetarian diets?

A

phyate (from plant foods) binds zinc, soy interfers with zinc absoprtion, animal protein enhances zinc absoprtion. Some vegetarians zinc intakes are significantly below RDA

219
Q

Recommendations for vegetarians and zinc?

A

eat a variety of nutrient-dense foods. Include whole-grains, nuts and legumes and sufficient energy. Oystersm crabmeat, ans shrimp for pescatarians/

220
Q

Some good courses of calcium for vegetarians?

A

low0oxalate greens (kale, okra, collards, broccoli), figs, some legumes, almonds, sesame seeds, calcium-set tofu, fortified foods (OJ, cereals, soy milk)

221
Q

Recommendations for calcium consumption for vegetarians?

A

greater than 8 servings per day of foods that provide 10-15% of the RDA for calcium (1000 mg), fortified foods or supplements may be helpful

222
Q

Why is vitamin B12 a concern for vegetarians?

A

Beyond animal foods, vitamin B12 is found only in fortified products or supplements. Unless fortified, no plant foods contain significant vitamin B12.

223
Q

One plant food that contains Vitamin B12?

A

Marmite

224
Q

Why are omega-3 FAs a concern for vegetarians?

A

mostly found in fatty fish and some meats

225
Q

Recommendations for vegetarians and omega-3s?

A

include good courses of ALA in the diet (ground flax seed) and DHA-rich microalge capsules may be helpful for some individuals, especially those with higher requirements.

226
Q

What are anabolic reactions?

A

Energy requiring reactions that form glycogen, TGs, and proteins

227
Q

What are catabolic reactions?

A

Reactions that break down fat, carbs, and proteins to release energy

228
Q

What happens if there is excess energy intake?

A

fat formation

229
Q

Excess energy can come from?

A

protein, CHO, or fat

230
Q

What pathways for fat storage is most direct?

A

pathways from dietary fat to body fat is most direct and efficient

231
Q

What is fasting?

A

Body is not supplied food as fuel

232
Q

What is the difference between fasting and starvation>

A

Fasting is by choice, starvation is forced…body cannot discern them, though

233
Q

Order of fuel sources used during starvation/fasting?

A

glycogen (liver) and fatty acidsd (from adipose tissue) first, when glycogen stores depleted low blood glucose promotes further fat breakdown and release of amino acids from muscle

234
Q

What is the primary energy source for the CNS, RBC, WBC?

A

Glucose

235
Q

Amount of total glucose the brain and nerve cells consumer each day?

A

about 1/2 total glucose

236
Q

During the first several days of fasting who much of the glucose is provided by protein? By glycerol?

A

90% protein, 10% glycerol

237
Q

How does the body adapt to fasting to spare use of proteins?

A

Produces ketone bodies

238
Q

What are ketone bodies?

A

Combining Acetyl-CoA fragments from fatty acids, production rises over about 10 days

239
Q

Effects of ketosis?

A

Blood pH drops due to presence of keto acids, elevated blood ketones excreted in urine, acetone breath, suppression of appetite, slows metabolism…all are starvation adaptations

240
Q

How long can you survive just relying on ketosis?

A

2 months

241
Q

Weight maintenance?

A

energy in = energy out

242
Q

Energy IN is from what?

A

kcal from food and beverage

243
Q

Energy OUT is from?

A

basal metabolism, physical activity, thermic effect of food, adaptive thermogenesis

244
Q

1 lb = how many kcals and grams?

A

3500 kcals, 454 g

245
Q

Composition of the “fuel mix” used by cells depends on?

A

availability of different energy-yielding nutrients in the diet, physical activity

246
Q

2 ways energy in food is measured (direct and indirect)?

A

Amount of heat gives a direct measure of food’s energy value. Amount of oxygen consumed gives an indirect measure of the amount of energy released.

247
Q

Why does a bomb calorimeter overestimate the amount off energy in a food?

A

Body is less efficient than calorimeter

248
Q

What is appetite?

A

Prompts a person to eat or not to eat. Response to sight, smell, thought, or taste of food

249
Q

What is hunger?

A

Physiological response to need for food…painful sensation caused by lack of food…determines what, when, and how much we eat

250
Q

What trigggers hunger?

A

triggered by nerve signals and chemical messengers originating and acting in the brain, primarily by the hypothalamus.

251
Q

What influences hunger?

A

presence or absence of nutrients in the bloodstream, size and composition of the preceding meal, customary eating patterns, climate, exercise, hormones, illness (physical an mental)

252
Q

Does appetite = hunger?

A

NO

253
Q

What is satiation?

A

feeling of fullness an satisfaction that occurs during a meal and halts eating. Determines how much food is eaten during a meal. Develops as hunger diminishes. Receptors in stomach stretch and hormones such as CCK become active

254
Q

What is satiety?

A

feeling of fullness and satisfaction that occurs after a meal, inhibits eating until next meal, determines how much time passes between each meal

255
Q

Does satiation = satiety/

A

NO!…satiation determines how much we eat, satiety determines how much time passes until we eat again

256
Q

Signals other than hunger that can trigger or suppress hunger?

A

boredom, anxiety, positive stress, negative stress

257
Q

External cues that influence eating?

A

availability, sight, taste, time of day, large portion sizes, abundance, variety

258
Q

The extent to which foods produce satiation and sustain satiety depends in part on?

A

The nutrient composition of the meal

259
Q

What foods are the most satiating?

A

Protein is the most satiating. Foods low in energy density are more satiating. High fibre foods fill the stomach and delay the absoprtion of nutrients

260
Q

Fat’s effect on satiation?

A

Relatively weak…passive overconsumption

261
Q

Fat’s effect on satiety?

A

High effect

262
Q

Recommendations for portion size and recommended foods for controlling energy in?

A

large portions of low fat, high fibre food and lower energy density

263
Q

Components of energy expenditure?

A

Basal metabolism (50-65%), physical activity (30-50%), thermic effects of food (10%), adaptive thermogenesis (TRAUMA)

264
Q

BMR needs for men? Women?

A

> 1kcal.min or 24kcal/day for men. (1kcal/min or 23kcal/day.

265
Q

Factors that increaseBMR?

A

height, growth, fever, stress, environmental temp., hormones, gender, smoking, caffeine

266
Q

Factors that decrease BMR?

A

fasting/starvation, malnutrition, sleep

267
Q

EER depends on?

A

gender, age, growth, physical activity, body composition, body size

268
Q

Direct calorimetry for assessing estimated energy expenditure?

A

measures the amount of heat released

269
Q

Indirect calorimetry for estimating energy expenditure?

A

measures amount of O2 consumed and CO2 expelled via a metabolic cart or whole body calorimetry unit

270
Q

How is energy out estimated using doubly labeled water?

A

subject drinks known amount of two different stable isotopic forms of water. Urine samples used to measure rate of which the 2 isotopes disappear from the body. Accurate over a period of 1-3 weeks. Best available method for providing average estimates of the 24-h energy expenditure of free-living subjects over an extended time

271
Q

How is body com indirectly measured in humans since it cannot be directly measured?

A

body weight = fat + lean tissues (including water)

272
Q

Problems typically develop when body fat exceeds what in young men? Men >40? Young women? Women >40?

A

22%, 25%, 32%, 35%

273
Q

What is visceral fat, and why is it bad?

A

Stored around the organs of the abdomen, referred to as central obesity. Associated with increase risk of heart disease, stroke, diabetes, insulin resistance, hypertenion, gallstones and some types of cancer (independent of total fat or BMI)

274
Q

What gender has more visceral fat?

A

Men

275
Q

Is subcutaneous fat (mostly in womeN) dangerous?

A

Seems relatively harmless

276
Q

Thresholds of risk of obesoty-related health problems for waist circumference?

A

greater than 88cm in women and 102cm for men

277
Q

waist-to-hip ratio recommended for women and men?

A

<1.0 for men

278
Q

Measures of body comp?

A

skinfolds, hydrodensitometry, air displacement plethysmography, bioelectrical impedence, total body water, dual energy x-ray absorptiometry (DEXA), near-infared spectroptometry, ultrasound, computed tomography, MRI

279
Q

Is high body fat always unhealthy?

A

No…overweight fit individuals have a lower risk of mortality than normal weight unfit individuals

280
Q

Percentage of Canadian adults that are overweight?

A

60%

281
Q

Percentage of Canadian youths that are overweight?

A

32%

282
Q

When did the greatest increase in obesity happen in Canada?

A

between 2000-2008

283
Q

At the most simple level what is the determinant of overweight and obesity?

A

energy in vs. energy out.

284
Q

Factors aside from energy in versus energy out that affect obesity?

A

individual choices < interpersonal choices < school and work environment < neighbourhood/community physical and social environments < policy input

285
Q

When does the number of fat cell increase most rapidly?

A

during the growing years

286
Q

After growth, when does the number of fat cells increase?

A

In time of positive energy balance

287
Q

The fats cells of obese people in comparison to lean people?

A

More fat cells and larger fat cells

288
Q

Prevention of obesity is most critical when?

A

During the growing years, when fat cells increase in number

289
Q

What does lipoprotein lipase do?

A

Removed triglycerides from the blood for storage in adipose tissue and muscle cells

290
Q

Do obese or lean people have more LPL?

A

Ibese people have much more LPL activity in adipose cells than lean people do –> makes fat storage highly efficient

291
Q

LPL activity is greatest where in women?

A

breasts, hips, thighs

292
Q

LPL activity is greatest where in men?

A

abdomen

293
Q

Release of lower body fat is _____ in women

A

less active

294
Q

After weight loss, LPL activity ________

A

increases –> people easily regain weight after loss

295
Q

Dietary fat oxidation correlates ______ with body fatness?

A

negatively…obese people have less of it

296
Q

What is the set point theory?

A

Many internal physiological variables remain fairly stable under a variety of conditions thanks to the hypothalamus and other regulatory centres. After weight gains or losses, the body adjusts its metabolism to restore the original weight. Energy expenditure increases after wight gain and decreases after weight loss. Changes in energy expediture differ from what would be expected based on body composition alone. Possible explanation for why it is difficult to maintain weight losses and gains.

297
Q

What is the Thrifty Gene Theory?

A

Suggests that people who use energy sparingly will store more fat more readily, putting them at a greater risk for weight gain. Was advantageous on the past when food supplies were unpredictable and scarce. In today’s world of food abundance it may be a contributing factor to weight gain. Recent advances in identifying interaction between obesity-related genes, behaviours and environmental factors have broadened our understanding of the factors affecting weight gain

298
Q

What is leptin?

A

an adipokine coded by the ob gene that signals sufficient energy stores and promotes negative energy balance by suppressing appetite and increasing energy expenditure

299
Q

Assumptions that overweight people are…

A

lazy, lack self control

300
Q

Clinical practice guidelines for obesity management?

A

“We recommend an energy-reduced diet and regualr physical activity as the first treatment option for overweight and obese adults and children to achieve clinically important weight loss and reduce obesity-related symtoms”

301
Q

Recommended deficit for weight loss?

A

500-1000 kcal/day = 1-2 lbs per week (10% body weight in 6 months)

302
Q

Diets less than _______ cannot provide adequate micronutrients

A

1200 kcal/day

303
Q

Why is skipping breakfast counterproductive?

A

Breakfast frequency is inversely associated with obesity. Breakfast is associated with better overall diet quality.

304
Q

When trying to loss weight in a healthy manner, what type of foods should be consumed?

A

nutrient dense foods and foods with lower energy density

305
Q

When choosing a weight loss goal, what is the number one rule?

A

must be realistic and suustainable

306
Q

Benefits of incorporating physical activity into weight loss strategies?

A

1) Lose more fat, retain more lean body mass 2) regain less weight, maintain losses 3) follow diet plans more closely, improved appetite control 4) reduced abdominal adiposity, improved body composition 5) improved blood pressure, insulin resistance and cardiorespiratory fitness, regardless of weight loss 6) short term increase in EE 7) increased BMR (over time) 8) increased self-esteem

307
Q

Some examples of popular fad diets?

A

low CHO and high fat, low fat and high CHO, liquid diets, food delivery, shakes/meal replacement/bars, blood type, single food diets, colon cleansers, Weight Watchers

308
Q

What is the basic premise of popular fad diets?

A

Restriction of CHO to <20g/day (5-10% of total energy intake)…want to achieve ketotic acidosis –? forcing the body to use fat as its main energy source

309
Q

Claims of low CHO diets?

A

rapid weight loss, improvements in risk factors for heart disease, hypertension, and diabetes, inflammation, benefits in treating epilepsy and decreasing obesity in children and adolescents

310
Q

Facts against low CHO diets?

A

initial rapid weight loss if the result of glycogen depletion (primarily fluid rather than fat), no evidence thata high-fat, high protein diet is particularly thermogenic, longer weight lossses may be the result of restriction of food choices, research indiciates that low CHO diets may produce increased weight loss over 3-6 months, but over 12 months shows no advantage compared to low fat, calorie-reduced diets. Low adherence and high drop out rates. Unpleasant side effects, poor maintenance

311
Q

Health effects of low CHO diets?

A

initial weight loss refelcts loss of glycogen, body protein, water and important minerals. Stage of ketsosis can cause nausea, hadeache, fatigue, and bad breath. Can lead to elevates uric acid levels, hypokalemia, and exacerbates kidney disease and gout in susceptible individuals. Eliminates most sources of dietary fibre as well as many nutrient dense foods (fruits and veggies). High intakes of animal foods which maycontribute to CVD and some cancers

312
Q

What can you eat on the paleo diet?

A

fish, meats, eggs, veggies, fruits, roots, and nuts

313
Q

What can’t you eat on the paleo diet?

A

grains, legumes, dairy, potatoes, processed foods high in salt and sugar, oils

314
Q

Claims of the paleo diet?

A

eradication of the chronic diseases of modern Western lifestyles such as obesity, CVD, type 2 diabetes, cancer, autoimmune disorders, osteoporsis, acne, myopia, varicose veins…

315
Q

Health effects of paleo diet?

A

complete exclusion of milk products can lead to deficiencies in calcium and vitamin S, especially with less sun exposure. Very high fibre content can cause loss of nutrients. High protein content can contribute to development of osteoporosis, renal stones, and loss of muscle mass. Exclusion of entire food groups has the potential to lead to numerous micronutrient deficiencies

316
Q

Potential for what nutrient deficiencies on the gluten free diet?

A

folate, iron, fibre and B vitamins

317
Q

What is intermittent fasting>

A

encourages fasting for 24 hours, 1-2x/week. Small meals on fasting days, “regular eating” while not fasting

318
Q

Claimed benefits of IF?

A

reduced blood glucose and insulin, increased fatty acid oxidation, preserves lean body mass, lower inflammation, lower blood pressure, reduced oxidative stress, increaed protection against neuordegenerative disease, healthy metabolism, increased longevity. “not being a slave to eating all day,” “learning how to enjoy eating again,” improved athletic performance, end to yo-yo weight loss and gain, steady energy, increased alertness and focus.

319
Q

Problems with intermittent fasting?

A

Will not lead to weight loss if kcal consumed on non-fasting days are in excess of requirements. Considerable evidence for the consumption of breakfast. Fasting likely to lead to bingeing, unhealthing relationship with food, and disordered eating patterns. Overall diet is important, not the time of intake. Research is inconclusive on the benfits of fasting–much more research is necessary.

320
Q

Does the different compositions of fat, proteins, and carbs matter when on a calories restricted diet?

A

No, restricted calories will cause weight loss

321
Q

Healthy weight gain requires?

A

a high energy diet, physical conditioning

322
Q

Weight gain strategies?

A

energy dense foods, regular meals, large portions, extra snacks, juice milk, protein powder, exercise

323
Q

Underweight affects what percentage of Canadians?

A

<2%

Physiology 2 (16 decks)

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