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Nut 1 Semester 2 > Lipids > Flashcards

Lipids Flashcards

1
Q

What % of body comprised of fat?

A

16%.
NB Fats form part of every body cell.
Lipid content can = 70% in severe obesity.
Proteins = 17%

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2
Q

What did Ancel Keys proclaim?

A

Eating a high saturated fat diet would increase serum cholesterol and consequently lead to heart disease.

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3
Q

What did the Amerian Heart Association recommend post Ancel Keys research?

A
  1. Diet low in total fat, especially saturated fat and cholesterol,
  2. high in carbohydrates from grains
  3. substituting animal fats for seed oils.

This also resulted in the introduction of statins — one of the most profitable pharmaceutical industry drugs.

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4
Q

What is a cytokine?

A

Cell-signalling proteins

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5
Q

What lipid found in nerve cell membranes?

A

Sphingolipids. Found in nerve cell membranes eg myelin.

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6
Q

Functions of white adipose tissue (WAT)?

A

Complex, metabolically-active endocrine tissue.

  1. Secretion of hormones, growth factors, enzymes and cytokines and insulin.
  2. Protection of organ
  3. Insulation against temperature extremes
  4. Form of energy storage
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7
Q

EIGHT types of lipids in the body

A
  1. Individual fatty acids.
  2. Triglycerides.
  3. Phospholipids (in every cell membrane).
  4. Cholesterol and steroid-based compounds eg oestrogen.
  5. Sphingolipids.
  6. Glycolipids — involved in cell identity (like a cell ‘passport’).
  7. Cerebrosides - Glycosphingolipids found in brain
  8. Fat-soluble vits — A, D, E, K
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8
Q

Glycolipids?

A

Involved in cell identity (like a cell ‘passport’).

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9
Q

Cerebrosides?

A

Glycosphingolipids found in the brain.

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10
Q

FOUR functions of lipids?

A
  1. Energy (ATP) production .
  2. Energy storage — fats are a more efficient form of storing energy reserves than carbs or proteins.
  3. Cell membrane structure — phospholipids and cholesterol stabilise cell membranes, while allowing a degree of fluidity which is crucial to the function of every cell.
  4. Thermal insulation in subcutaneous tissue and protection around organs.
  5. Hormones — progestogens, androgens, glucocorticoids, mineralocorticoids and oestrogens are derived from cholesterol.
  6. Formation of eicosanoids — signalling molecules involved in a range of processes such as blood coagulation and inflammation.
  7. Growth and development — brain rich in AA and DHA arachidonic acid (AA) and docosahexaenoic acid (DHA).
  8. Constituents of nervous tissue structure (sphingomyelin).
  9. Aid to cell-signalling processes.
  10. Absorption of fat-soluble vitamins.
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11
Q

What are eicosanoids?

A

Signalling molecules involved in range of processes such as blood coagulation and inflammation (require lipids).

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12
Q

Too much omega 3?

A

Cells become too fluid

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13
Q

Chemical structure of fatty acids?

A

Fatty acids are hydrocarbon chains with:
1. an acid group (alpha or carboxylic (-COOH) at one end
2. methyl group (omega) at the other (-CH3)
end

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14
Q

Chemical structure of the FOUR fatty acid types?

A
  1. Short Chain Fatty Acids: up to 5 Cs
  2. MCFA: 6-12
  3. Long CFA: 13-22
  4. Very LCFA: >22
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15
Q

Function of medium-chain fatty acids (MCT)?

A

Travel directly to liver (as do SCFAs) where used to create:
- energy
- ketones.
Can be used as a source of energy before exercise (eg x1 tbsp).

6–12 Cs

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16
Q

What are long and very long chain fatty acids used for?

A

Build cell membranes.

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17
Q

How are SCFAs produced?

A

Dietary fibre is fermented in the colon

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18
Q

Name three SCFAs

A

Most common:
1. Acetate
2. Propionate
3. Butyrate

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19
Q

Importance of butryate?

A
  1. SCFA.
  2. Esp important for colon health because = primary energy source for colonocytes.
  3. Supports intestinal tight junctions.
  4. SCFAs are speculated to have a role in microbiota-gut-brain axis crosstalk.
  5. Butyrate thought to have anti-inflammatory effect on colon.
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20
Q

What one determining factor makes a fatty acid vulnerable?

A

Number of double carbon bonds.

More double bonds, less stable it is.
Increases susceptibility to oxidation.

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21
Q

What are the four types of fatty acid?

A
  1. Saturated
  2. Unsaturated
  3. Monounsaturated
  4. Polyunsaturated
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22
Q

Saturated fatty acid structure?

A
  1. No double carbon bonds (C-C).
  2. All carbons are saturated with hydrogen bonds.
  3. Solid at room temp.
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23
Q

Unsaturated fatty acid structure?

A
  1. One or more double bonds betewwen carbons
  2. Liquid at room temperature.
  3. Slightly kinky - more kinky, easier it is for oxgyengation (bad) to happen.
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24
Q

Mono unsaturated fatty acid structure?

A

One double bond

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25
Q

Polyunsaturated fatty acid structure?

A

Several double bonds.

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26
Q

What is an unatural trans fatty acid?

A

Produced by:
1. high temperatures and
2. hydrogenation ie adding hydrogen atoms which solidifies unsaturated fat.

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27
Q

What is hydrogenaton?

A

Additon of hydrogen to solidfy an unsaturated fat

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28
Q

Where are unatural trans fats found?

A
  1. Margarine
  2. Processed foods
  3. Refined vegetable oils
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29
Q

THREE disbenefits of processed trans fats in the body ?

A
  1. Stiffens cell membranes, making them prone to oxidation.
  2. This also alters their protective action and permeability, impeding normal cell function.
  3. Alters blood triglyceride and cholesterol profile
  4. Linked to increased risk of CVD, insulin resistance and cancer.
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30
Q

THREE differences between CIS and TRANS fats

A

Both unsaturated fats.

  1. Cis fatty acid is bent, whereas trans fatty acid is more linear.
  2. Cis and trans fats have different properties:
    - CIS: H atoms on same side of double bond.
    - Trans: H atoms on separate sides of the double bond.
  3. Cis fats make cell membranes more flexibile while trans fats stiffen cell membranes and are prone to oxidative damage making them leaky.

NB Trans fats = unsaturated but behave like saturated fats because of unkinked shape.”

Chat:

Cis and trans fats are types of unsaturated fats that differ in the configuration of their hydrogen atoms around the double bonds in the fatty acid chain.

  1. Cis Fats:
    • Structure: In cis fats, the hydrogen atoms attached to the carbon atoms in the double bond are on the same side. This causes the fatty acid chain to bend or kink.
    • Properties: Because of the kink in their structure, cis fats are typically liquid at room temperature. They are found naturally in various foods, especially in plant oils and fatty fish.
    • Health Effects: Cis fats are generally considered healthier than trans fats. Omega-3 and omega-6 fatty acids, which are essential for human health, are examples of cis fats.
  2. Trans Fats:
    • Structure: In trans fats, the hydrogen atoms are on opposite sides of the double bond, making the fatty acid chain more linear.
    • Properties: This linear structure allows trans fats to pack more tightly and be solid at room temperature. Trans fats are rare in nature and are mainly found in partially hydrogenated oils used in processed foods to improve shelf life and stability.
    • Health Effects: Trans fats are associated with numerous health risks, including increased LDL cholesterol (bad cholesterol), decreased HDL cholesterol (good cholesterol), and a higher risk of heart disease, stroke, and type 2 diabetes.

The key difference lies in their molecular structure, which significantly impacts their physical properties and health effects. While cis fats are generally beneficial or neutral, trans fats are detrimental to health and are best minimized in the diet.

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31
Q

Conjugated means what?

A

Stabilised.

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32
Q

Benefits of conjugated linoleic acid (CLA)?

A

Natural trans fat found in grass-fed meat and dairy products. Helps increase lean muscle mass and decrease body fat.

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33
Q

Most common form of dietary fat?

A

Triglycerides

Also referred to as triacylglycerols (TAGs).
Major form of how the body stores fat.

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34
Q

Chemical structure of triglycerides?

A
  1. Lpid molecules made up of:
    - one unit of glycerol
    - three fatty acids.
  2. Three fatty acids can differ in length (number of carbon atoms) and degree of saturation (number of hydrogen molecules attached).
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35
Q

High triglycerides in blood lead to which pathologies?

A
  1. Atherosclerosis and then…
  2. Heart disease
  3. Stroke.
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36
Q

When does the body synthesise triglycerides?

A

Whenever caloric intake exceeds energy requirements.

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37
Q

Lipogenesis?

A

Excess dietary energy converted to triglycerides and taken up by adipose tissue.

Acetyl-CoA (via glycolysis) forms palmitic acid (C16).

Three fatty acids bound to glycerol and stored as triglycerides.

Adipocytes are supplied by an extensive network of blood vessels. Acquire triglycerides from circulating lipoproteins, chylomicrons and very low density lipoproteins.

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38
Q

Chylomicron?

A

Carries tryglycerides from intestines to liver, skeletal muscle and adipose tissue

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39
Q

Where does lipogenesis take place?

A
  1. Adipose tissue
  2. Liver.
  3. Kidneys
  4. Lactating mammary glands
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40
Q

How do we get acetyl-CoA?

A

Glucose converts to 2 pyruvate then acetyl-CoA

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41
Q

What is lipolysis?

A

When dietary energy is limited fatty acids from triglycerides mobilised from adipocytes into circulation.

Triglycerides = hydrolysed by lipase into fatty acids and glycerol for use in the body.

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42
Q

Which hormones stimulate lipolysis?

A
  1. Adrenaline, noradrenaline (stress hormones)
  2. Adrenocorticotropic hormone (ACTH).
  3. Glucagon
  4. Growth hormone.
  5. Thyroid-stimulating hormone (TSH} and thyroxine (need T3 to activate the process).
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43
Q

Catabolism?

A

Breadown

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44
Q

What antagonises the lipolytic effects of hormones?

A

Insulin

Insulin hinders the lipolytic (lypolysis) effects of hormones such as TSH, ACHT, adrenaline and noradrenaline. Therefore insulin resistance leads to central adiposity.

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45
Q

Describe how fatty acids can be used for energy (catabolism) ie Krebs

A
  1. Fatty acids cross the cell membrane, traverse cytosol and reach mitochondria (aided by carnitine).
  2. Carnitine facilitates transport of fatty acids across mitochondrial membrane.
  3. Fatty acids undergo beta-oxidation (no pyruvation)
  4. Broken down into 2-carbon blocks as acetyl-CoA, which is oxidised via the Krebs cycle to waste materials CO2 and H2O.
  5. Energy then generated using the electron transport chain.
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46
Q

Decarboxy-lation?

A

Removal of a carboxyl group

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47
Q

What types of food can brain use?

A

Ketones and glucose

(Brain can’t metabolise fatty acids)

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48
Q

When ketones made?

A
  1. When glucose in short supply eg fasting, low carb intake.
  2. Made at night too.
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49
Q

Ketogenesis definition

A

Making of ketones

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50
Q

Describe the process of Ketogenesis

A

Acetyl-CoA converted to the ketone bodies:

  1. aceto-acetate or
  2. β-hydroxy-butyrate (β-OHB).

Acetoacetate can undergo decarboxylation to another ketone acetone (sweet-smelling).

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51
Q

Carb threshold for body to shift primary fuel source form glucose to fat?

A

Carbs restricted to < c. 40 g per day.

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52
Q

Can everyone switch from carb-burning to fat-burning?

A

Not everyone will be metabolically flexible enough to do ketosis.

Requires transition period. May feel rough. Stricter you are at begtinning the quicker the transition: nausea, blood glucose drops… need to de-mothball beta-oxidation proesses. MCT oil helps in the adaptation process. Drink lots of fluid.

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53
Q

Health benefits of ketosis?

A
  1. Weight loss
  2. Management of epilepsy
  3. Parkinson’s and Alzheimer’s disease (Type 3 diabetes - frontal lobe can’t use glucose anymore)
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54
Q

Ketoacidosis?

A

Unstable and dangerous condition that occurs when there is insufficient pancreatic insulin response to regulate serum β-OHB. Lowers blood pH.

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55
Q

Outline lipid digestion

A
  1. Gastric lipase in the stomach and pancreatic lipase in the duodenum, act to separate the glycerol and fatty acids/triglycerides to aid digestion.
  2. This process is facilitated greatly by the emulsifying action of bile, which increases surface area of fat droplets.
  3. Resulting two free fatty acids and monoglyceride (=glycerol + 1 fatty acid) transported into enterocytes, where they are rebuilt in the cell, packaged into chylomicrons and transported via the lymphatic system to the bloodstream.
  4. The fatty acids can be used or stored in adipose tissue.
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56
Q

Emulsification?

A

Breaks down fatty acids… so greater surface area for enzymes to work to break down.

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57
Q

How to optimise lipid digestion?

A
  1. Chew adequately
  2. Avoid drinking with meals.
  3. Increase bile production by optimising stomach acid levels via zinc and B6-rich foods, bitter foods (eg chicory, rocket)
  4. Stress management.
  5. Choleretics (increase bile production) and cholagogues
    (increase bile flow); e.g. dandelion, artichoke and turmeric.
  6. Ensure good hydration to support bile flow.
  7. Increase glycine and taurine, which are components of bile. Good sources = legumes, sea vegetables, spinach and eggs.
  8. Olive oil can also stimulate bile secretion.
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58
Q

Bile is made of?

A

Water (97pc)
Bile salts (taurine and glycine)
Cholesterol

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59
Q

What are choleretics and cholagogues?

A

Choleretics (increase bile production) and cholagogues (increase bile flow); eg dandelion, artichoke and turmeric.

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60
Q

How can we make sure our fat consumption is healthy?

A
  1. Natural
  2. Mix of sat, mono and polyunsat fats. Not trans.
  3. Eat with antioxidant and vit E rich foods.
    ———////—/——————
  4. Eat fats from natural, unrefined foods.
  5. Should be a mix of saturated, monounsaturated and polyunsaturated fats, but absent of trans fats.
  6. Fat-soluble antioxidants eg vit E important when including fats in the diet. Vit E sources: sunflower seeds, almonds and wheat germ.
  7. Focus on quality of the fat and combine with foods naturally rich in antioxidants.
61
Q

FIVE benefits of eating healthy fats (inc cooking)

A
  1. Greater satiety
  2. Sources of essential fatty acids.
  3. Sources of choline (needed to synthesise phosphatidylcholine).
  4. Sources of essential fat-soluble vitamins and phytonutrients.
  5. Greater flavour enhancement in cooked food.
62
Q

FIVE Healthy dietary fats’ food sources?

A
  1. Fruit — avocado, olives.
  2. Seeds — chia, flax, pumpkin, hemp, seed butters.
  3. Seed oils — flax oil, chia oil, hemp oil, sunflower oil, olive oil. NB Ensure oils cold pressed.
  4. Nuts — almonds, cashews, walnuts, Brazil nuts, nut butters.
  5. Other — coconut oil, grass-fed meat.
  6. Oily fish — SMASH.
63
Q

Four healthy saturated fats

A
  1. Coconut
  2. Grass-fed meat (unprocessed)
  3. Eggs
  4. Dark chocolate
64
Q

Cite a medium-chain triglyceride (MCT)

A

Coconut oil contains MCTs which the body uses as a source of fuel or turns them into ketones.

65
Q

Benefits of MCTs

A
  1. Increase number of calories burned compared to longer-chain fatty acids.
  2. Coconut oil contains 50% lauric acid. Monolaurin formed from lauric acid. Both have antibacterial, antiviral and antifungal properties.
  3. ↑ HDL cholesterol, ↓ LDL cholesterol.
  4. Preliminary studies show positive outcomes
    in epilepsy and Alzheimer’s.
66
Q

Name FIVE saturated fatty acids

A
  1. Butyric acid: 4-C (butter, dairy, made in gut)
  2. Caprylic acid: 8-C (coconut, palm kernel, breast milk). Anti-fungal
  3. Lauric acid: 12-C (Coconut)
  4. Palmitic acid: 16-C (Coconut, palm and palm kernel)
  5. Stearic acid: 18-C (beef, pork, lamb, mutton, cocoa butter, shea butter, butter)
67
Q

TWO monounsaturated fatty acids

A
  1. Palmitoleic acid (Omega-7) eg seabuckthorn, macadamia, coconut.
  2. Oleic acid (Omega-9) - biggest source
68
Q

TWO sources of Oleic acid (Omega 9)

A
  1. Olives and olive oil
  2. Avocado
  3. Nuts: Almond, peanut, pistachio Brazil nuts, pecan, cashew Hazelnut, neem, macadamia
  4. Animal fat, butter
69
Q

Three types of polyunsaturated fats (Omega 3)

A
  1. ALA - (flax, hemp, chia, dark green leafies, pumpkin seeds, soybean, rapeseed, wheatgerm, walnuts.
  2. SDA - stearidonic acid (blackcurrant seeds only)
  3. EPA and DHA (SMASH, chlorella and spirulina)
70
Q

THREE sources of Alpha-linolenic acid
(ALA):

A
  1. Flaxseeds (richest source — 50% of its fatty acids are ALA)
  2. Chia seeds, hemp seeds, dark green leaves
  3. Pumpkin seeds, soybean, rapeseed (canola)
  4. Walnuts, wheat germ
71
Q

Name three omega 6 poly unsat fats

A
  1. Linoleic acid
  2. Gamma linolenic acid
  3. Arachidonic acid
72
Q

Sources of LA

A
  1. Safflower
  2. Sunflower
  3. Hemp
  4. Walnut
  5. Pumpkin seed
  6. Sesame
  7. Almond
  8. Chia
  9. Cashew
  10. Rapeseed
  11. Wheat germ
73
Q

Souces of GLA

A
  1. Borage oil
  2. Evening primrose oil
  3. Blackcurrant seed oil
  4. Hemp seed oil
74
Q

Sources of AA

A

Meat and dairy ie animal products

75
Q

Max level for cooking without smoke point

A

180 degrees c

76
Q

Why shouldn’t you use polyunsaturated fats for cooking?

A

Oxidise easy when heated and produce free radicals that damage cells.

77
Q

Advice for storing polyunsaturated fats

A

Only be used in their raw, cold-pressed form for pouring over cooked or raw foods or using in dressings.

Store in dark-coloured bottles in fridge/freezer as can go rancid (unpleasant smell/taste) quickly and be oxidised through direct light exposure.

Pressing date as well as a use-by date

78
Q

Fats are more prone to oxidation because:

A
  1. High in polyunsaturated fat.
  2. Exposed to prolonged heat, light or oxygen.
  3. Naturally low in antioxidants.
  4. Refined or heavily processed.
79
Q

Chemical process by which fatty acids go rancid?

A

By releasing the fatty acids from the glycerol.

Unsat fatty acids within triglycerides also go rancid when the double bonds are oxidised.

80
Q

What types of nasty compounds result when fats go rancid?

A
  1. Aldehydes
  2. Ketones
  3. Hydrocarbons.
  4. Oxidation of double bonds leads to production of malondialdehyde = potential mutagen. Found
    in some hydrogenated or overheated fats.
81
Q

Two fatty acids that can’t be made in the body

A

Hence essential ie from the diet.
1. Linoleic acid (an omega-6 fatty acid).
2. Alpha-linolenic acid (an omega-3 fatty acid).

82
Q

Which enzyme is needed to produce GLA and EPA?

A

Delta-6-desaturase.

Also Delta-5 and Delta-4

83
Q

Omega 6:3 ratios?

A

Historically 1:1. Now 16:1.

84
Q

What kind of nutrients are EPA and DHA?

A

Conditionally essential nutrients
Due to relatively low rate of conversion of ALA to EPA / DHA.

85
Q

FIVE functions of EFAs

A
  1. Vital components of cell membranes and help to maintain cell membrane fluidity. Must be
    maintained within certain range for cell to function properly.
  2. Act with cell membrane proteins thereby affecting cell transport ie of substances in and out of the cell.
  3. Key components of organelle membranes eg mitochondria.
  4. Cell-to-cell communication.
  5. Essential for foetal and child brain development.
  6. Precursors of eicosanoids, which are ‘local’ hormones.
86
Q

Three clinical indicators of EFA deficiency on skin?

A
  1. Dry, flaky, scaly, chapped lips (also dry eyes) - could be zinc and B vits too.
  2. Hyperkeratosis pilaris - if white grains in them could be low in A and C.
  3. Delayed wound healing - could also be low E, C, zinc.
  4. Nails: Dry / brittle, red / swollen cuticles - mostly EFA but could be low zinc.
  5. Hair: Dry / oily, split ends, alopecia - could be heat damage or hypothyroidism.
  6. Acne / eczema / psoriasis / dermatitis -
87
Q

Three clinical indicators of EFA deficiency on endocrine?

A
  1. Weight imbalances (obesity / weight loss).
  2. PMS / painful menstrual cramps / sore breasts.
  3. Hyperinsulinaemia.
88
Q

Three clinical indicators of EFA deficiency on reproductive?

A
  1. Infertility / impotence / history of repeated miscarriages.
  2. Ovarian cysts / fibrocystic breast disease.
89
Q

Three clinical indicators of EFA deficiency on circulatory?

A
  1. Frequent nosebleeds, bleeding gums (vit C and coQ10),
  2. Easy bruising
  3. delayed reovery from exercise
90
Q

Three clinical indicators of EFA deficiency on MSK?

A
  1. Arthritis
  2. Chronic joint pain
  3. Delayed recovery.
91
Q

ONE clinical indicator of EFA deficiency on immune?

A

Susceptibility to infections (A, D, E, zinc)

92
Q

Three clinical indicators of EFA deficiency on nervous system?

A
  1. Dementia / Alzheimers
  2. Parkinson’s
  3. Irritability / nervousness
  4. Tingling ams and legs (B12 poss).
  5. CFS / ME
93
Q

THREE key ALA therapeutic areas?

A
  1. CVD
  2. Neurological - strokes and depression
  3. Anti-inflammatory esp AI eg asthma, IBD.
  4. EPA/DHA also supports foetal brain development. Possible allergy protection if mothers supplement during pregnancy.
94
Q

Therapeutic uses of ALA, EPA and DHA for CVD?

NB Most research on fish oils.

A
  1. Lowered risk of myocardial infarctions, atherosclerosis development and strokes.
  2. Reduces C-reactive protein levels (inflammatory marker used to evaluate CVD risk).
  3. Anti-arrhythmic effect – incorporation of ALA into
    cell membranes of cardiomyocytes modifies ionic channel currents, stabilising electrical activity. Add in Mg too.
  4. Anti-hypertensive — ALA lowers the activity of
    angiotensin-converting enzyme (ACE) while EPA/DHA via the effects of series 3 prostaglandins.
  5. Lowers LDL cholesterol.
  6. EPA/DHA: reduces blood triglycerides.
95
Q

How does ALA, EPA/DHA reduce stroke risk?

A
  1. ALA promotes vasodilation in the brain
  2. All three increase brain-derived neurotropic factor (BDNF), exerting a neuroprotective effect.
  3. Lower levels of EPA and DHA associated with more learning and behavioural problems

Also why good for depression – BDNF plays a critical role in neuronal maintenance, learning and memory. It has also been specifically implicated in mood-boosting effects.

96
Q

Drug interactions with ALA, EPA, DHA.

A
  1. Blood-thinners may increase anti-coagulant (and vasodilator) effects ie bleeding. While combo of aspirin and n-3 fatty acids may be helpful, under certain circumstances (such as CVD), these should only be taken under GP supervision.
  2. Statins ALA may have an agonist effect when combined with statins.
  3. Diabetes medications — fish oil supplements (not ALA) may lower blood glucose levels and could potentiate effects of diabetes drugs.
  4. Blood pressure medication — DHA may lower blood pressure (so monitor)
97
Q

Co-factors needed to convert ALA to EPA/DHA and LA to GLA

A

ALA to EPA/DHA:
1. Zn
2. Mg
3. B6

LA to GLA:
1. Zn, Mg, B6 as above +
2. Vit C, B3

98
Q

How do vegans get EPA/DHA?

A
  1. Algal supplements (make sure water extraction process)
  2. Flaxseeds, hemp seeds.
  3. Echium seed oil which contains stearidonic acid (SDA) which easily converted to EPA and DHA.

Make sure all oils are cold-pressed and organic.

99
Q

Food sources of linoleic acid (LA) n-6.

A
  1. Flax and hemp seed oils = best
  2. Vegetable oils
  3. Safflower,
  4. Sunflower, soybean, and corn oils.
  5. Nuts, seeds and some vegetables.

LA is an omega-6 fatty acid, 18:2 n-6

100
Q

Main food sources of GLA?

A
  1. Evening primrose oil
  2. Blackcurrant seed oil
  3. Hemp and borage oils
101
Q

GLA therapeutic uses

A
  1. Rheumatoid arthritis
  2. ADHD
  3. Eczema
  4. PMS
  5. Cyclical breast pain
  6. Female fertility
102
Q

Why is GLA good for RI?

A

↓ joint pain, swelling and morning stiffness in RA.
GLA is converted to PG1, which has immuneregulatory and anti-inflammatory effects. Includes a reduction in NF-kB activity.

103
Q

|Why GLA good for eczema?

A

Reduces inflammation.

Take with EPA.

104
Q

Why GLA good for ADHD

A

A combination of GLA and EPA shows improvements in attention and impulsivity.

105
Q

Which two fatty acids does evening primrose oil (EPO) contain?

A
  1. LA
  2. GLA.
106
Q

THREE things Evening Primrose Oil good for?

A

GLA = precursor to PG1 (anti-inflammatory).

  1. PMS: PG1 inhibits prolactin (prolactin increased in women with PMS).
  2. Cyclical mastalgia (breast pain): PG1 inhibits synthesis of arachidonic acid metabolites
  3. ** Fertility**: increases and optimises cervical mucus to sustain sperm during conception.

1500 mg daily (ave)

107
Q

GLA contraindications?

A
  1. Not during pregnancy
  2. Doses of 3000 mg / day may increase AA production.
  3. Drug interactions: NSAIDs, chemotherapy.
108
Q

AA food sources

A

Animal products such as meat, eggs and dairy esp. when animals intensively raised on grain.

109
Q

n-6 precursors pathway

A
  1. Linoleic acid
  2. Gamma linoleic acid
  3. Dihomo-gamma-linoleic acid
  4. Arachidonic acid
  5. Adrenic acid
  6. Doco~sapent~aenoic acid (DPA)
110
Q

Link between AA and COX?

A

COX-1 and COX-2 responsible for catalyzing conversion of AA into prostaglandins, specifically inflammatory prostaglandin 2 series.

111
Q

What does PG2 do?

A

Prostaglandin 2 (converted from AA).

  1. Causes inflammatory effects including fever, vascular permeability and vasodilation, pain and oedema.
  2. To prevent excessive inflammation PG2 induces 15-LOX activity, leading to lipoxin formation (anti-inflammatory)
112
Q

What are Eicosanoids?

A

20 carbon atoms (eicosa)

Locally-acting hormone-like signalling molecule

Signalling molecule that acts like a hormone (TS)

113
Q

How are eicosanoids made?

A
  1. Oxidation of omega-3 and omega-6 fats ie DGLA, AA and EPA.
  2. Fatty acids released from membrane phospholipids by phospholipase A2 enzyme.
  3. Converted to eicosanoids by COX and LOX — dependent on starting fatty acid (AA, EPA, DGLA) and an outside stimulus.
  4. Pro- and anti-inflammatory effects.
114
Q

Which immune system molecules classed as eicosanoids x4?

A
  1. Prostaglandins
  2. Leukotrienes
  3. Thromboxanes
  4. Resolvins
  5. Protectins.
115
Q

THREE functions of eicosanoids?

A
  1. Inflammation
  2. Blood vessel permeability and constriction
  3. Blood coagulation
  4. Immune cell behaviour
  5. Lipid accumulation
  6. CNS signallng
116
Q

Where are most AAs found?

A

Cell membrane phospholipids

117
Q

What do cox and lox stand for?

A

Cyclooxygenase (COX)
Lipoxygenase (LOX)

118
Q

How are fatty acids released from the membrane phosholipids?

A

Enxyme phospholipase A2

119
Q

Is AA good or bad?

A

Good. AA needed as part of immune inflammatory response but only in small amounts. All about the n-3 to n-6 ratio.

120
Q

NB Exam tips

A

Needs to know slide 69 - eicosanoids.

121
Q

How many prostaglandin families?

A

3

122
Q

*What is each prostaglandin made from?

A

PG1: Made from DGLA.
PG2: AA
PG3: EPA

123
Q

Which three areas do PGs modulate?

A
  1. Blood platelets
  2. Sodium and water balance
  3. Blood vessel contraction / relaxation
124
Q

*PG1 function?

A
  1. Keeps blood platelets from sticking together
  2. Removes excess sodium and water from body
  3. Relaxes blood vessels promoting circulation
125
Q

*PG2 function?

A
  1. Mostly platelet aggregation (PG1 prevents from sticking together)
  2. Promotes sodium and water retention (raised BP)
  3. Opposes functions of PG1 on blood vessels ie vasoconstricts.
126
Q

*PG3 function?

A
  1. Weak platelet aggregating properties (PG1 looks after this)
  2. Prevents the release of AA from cell membranes.
  3. EPA is most important factor limiting PG2.
127
Q

What determines which prostaglandins will dominate?

A

Cell membrane fatty acid composition

Diet rich in AA leads to formation of more pro-inflammatory PG2.

NB importance of omega-3 and 6 balance.

High EPA and DHA from omega-3 = higher proportion of fatty acids resides in cell membrane at expense of AA poss resulting in immune-suppression. All about balance.

128
Q

Polymorphism?

A

Genetic variation

129
Q

What factors inhibit the synthesis of EPA and DHA?

A
  1. Genetic variability: polymorphisms common in genes coding for delta-6 and delta-5 desaturase.
  2. Desaturation: addition of double bond between two carbon atoms and / or elongation — addition of two carbon atoms.
  3. Both LA and ALA compete for the same desaturase and elongase enzymes.
130
Q

How much ALA converted to EPA?

A
  1. Only 1–20%

Women of reproductive age convert ALA 2.5 times better than men.

131
Q

*Co-factors for delta-6 and delta-5 desaturase ?

A

Delta-6
Vit C
B3
Zn
B6
Mg

Delta-5
Vit C
B3
Zn

132
Q

Co-factors for elongase?

A

B6

133
Q

What are inhibitors of Delta-6 and Delta5 desaturase?

A

Delta-6-inhibited and Delta-5 by:
1. Alcohol
2. Cholesterol (excess)
3. EPA/DHA high dose
4. Insulin resistance
5. Stress hormones, eg cortisol
6. IR
7. Trans fats
8. Zn deficiency

Delta-6 only
1. Deficiencies in Mg, B6
2. Viruses
3. Refined sugars
Delta-5 only:
1. Alcohol

Trans fats

134
Q

What three tests does EFA testing include?

A
  1. Omega-3 index — CV risk marker.
  2. Omega-6:3 ratio — chronic illness marker.
  3. AA:EPA ratio — marker of silent inflammation.
135
Q

Main pupose of cholesterol

A

Cell structure and function

136
Q

Cholesterol is essential for the synthesis or action of?

A
  1. Vit D & Ca metabolism.
  2. Cortisol and related hormones.
  3. Aldosterone for mineral and fluid balance.
  4. Sex hormones — oestrogen, progesterone and testosterone.
  5. Bile salts and acids needed for digestion.
  6. Membrane integrity, especially in the brain.
  7. Lipoproteins, needed for triglyceride transport.
137
Q

What helps cholesterol excretion?

A

Fibre
Gut bacteria metabolise cholesterol and stop it being reabsorped. Healthy microbiome vital.

138
Q

Primary function of LDL and HDL?

A

Lipoprotein carriers of cholesterol. Also carry:

  1. CoQ10
  2. Betacarotenes
  3. Vit E.
139
Q

LDL, VDL and HDL roles in cholesterol transport?

A
  1. LDL takes cholesterol from liver to cells.
  2. VLDL: new triglycerides from liver to cells.
  3. HDL: collects cholesterol from cells to transport back to liver.
140
Q

LDL and atherosclerosis?

A

Atherosclerosis requires LDL cholesterol to deposit in the arterial wall and become oxidised.

In absence of inflammation or injury to the endothelium, cholesterol does not deposit. Atherosclerosis = inflammatory disease

141
Q

Why is LDL/HDL particle size more useful marker?

A

If LDL particles predominantly small and dense have a threefold greater risk of coronary artery disease

Large and fluffy particles may be protective.

Larger HDL particles:
1. more effective at removing cholesterol from blood.
2. Better exert anti-inflammatory effect
3. Better exert anti-thrombotic effect
4. Promoting nitric oxide production in endothelial cells.

142
Q

FIVE cardiovascular generic markers

A
  1. Lipoprotein (a): blood clotting agent. Genetic risk factor in coronary artery disease. Higher levels = greater risk. Mine is 126! Shld be 75.
  2. Fibrinogen: raised levels = clot formation risk factor.
  3. C-reactive protein: inflammatory marker associated with CVD.
  4. Lp-PLA2: enzyme. Role in endothelial inflammation and atherosclerosis.
  5. Lipid peroxides: raised levels reflect oxidative damage to membranes.
143
Q

Types of phospholipids

A
  1. Phosphatides: contain:
    a) glycerol
    b) two long chain fatty acids
    c) phosphate group and
    d) either inositol, choline or serine.
  2. Phosphatidylcholine — predominant phospholipid in body.
  3. Lecithin: synthesised by liver and plays role in
    - emulsification (fat digestion).
    ~ Increases solubility of cholesterol
    ~ helps improve cognitive function.
  4. Inositol:
    insulin-signalling
144
Q

Inositol therapeutic use?

A

Improves insulin sensitivity. Good for insulin resistance eg T2DM, PCOS.

145
Q

Phosphatidylserine therapeutic uses?

A

Improves neuronal membrane functioning and
cognitive function.
1. Depression
2. Insomnia
3. Stress.

146
Q

Phosphatidylcholine therapeutic uses?

A
  1. Neuro- and hepato-protective.
  2. Supplies choline for synthesis of acetylcholine (neurotransmitter).
  3. Important for cognition, memory, immunity and hormone function.
147
Q

Which table should I learn?

A

The one on p.73

148
Q

Choloretics x3

A

Choleretics
Increase Bile Production)
1. Milk Thistle (Silybum marianum)
2. Artichoke (Cynara scolymus)
3. Turmeric (Curcuma longa)
4. Peppermint (Mentha piperita)
5. Ginger (Zingiber officinale)
6. Boldo (Peumus boldus)
7. Globe Artichoke (Cynara scolymus)
8. Barberry (Berberis vulgaris)
9. Greater Celandine (Chelidonium majus)

  1. Dandelion (Taraxacum officinale)
  2. Radish (Raphanus sativus)
  3. Yellow Dock (Rumex crispus)
  4. Chicory (Cichorium intybus)
  5. Peppermint (Mentha piperita)
  6. Ginger (Zingiber officinale)
  7. Boldo (Peumus boldus)

Some herbs, like peppermint, ginger, and boldo, have properties that allow them to act as both choleretics and cholagogues.

149
Q

ONE example of low EFAs on each body system

A

Skin: Hyperkeratosis pilaris - if white grains in them could be low in A and C.
Endocrine: Hyperinsulinaemia.
Repro: ovarian cysts
Circulatory: nose and gum bleeds
MSK: arthritis
Immune: frequent infections
Nervous: Alzheimer’s and Parkinson’s

Nut 1 Semester 2 (9 decks)

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