Lipids And EFAs Flashcards
(114 cards)
1
Q
What is the fat debate?
A
1950 : Keys declares high fat diet -> increase serum cholesterol -> CDV disease
American heart association recommended diet low in fat (esp. saturated and cholesterol), high in grains and seed oils instead of animal fat
Statins were also introduced
2
Q
What is white adipose tissue (WAT)?
A
Complex, METABOLICALLY ACTIVE ENDOCRINE TISSUE, its functions include : hormone secretion, growth factors, enzymes and cytokines, organs protection, energy storage, insulation
3
Q
What are the different lipids present in the body?
A
- Individual fatty acids
- Triglycerides
- Phospholipids
- Cholesterol and steroid-based compounds
- Sphinogolipids (e.g. myelin)
- Glycolipids
- Cerebrosides
- Fat soluble vitamins
4
Q
What are the functions of lipids? (10)
A
- Energy (ATP) production
- Storage for energy reserves
- Cell membrane structure
- Thermal insulation
- Steroid hormones
- Formation of eicosanoids (signalling molecules)
- Growth and development (AA and DHA)
- Constituents of nervous tissue structure
- Aid to cell-signalling processes
- Required for the absorption of fat-soluble vitamins
5
Q
What are fatty acids?
A
HYDROCARBON CHAIN with an ACID GROUP at one end and a METHYL GROUP on the other
6
Q
What are short medium and long chain fatty acids and what do they do?
A
SHORT (up to 5 Cs) and MEDIUM (6-12 Cs) chains travel directly to liver -> used to create ENERGY or ketones
LONG (14–22 Cs) and VERY long (22+ Cs) chains travel directly fatty acids are used to build CELL MEMBRANES
7
Q
What are short chain fatty acids?
A
Fatty acid chains with less than 6 carbon atoms
Speculated to have a role in gut-brain axis
8
Q
What are the most common SCFAs?
A
Acetate, proprionate and butyrate
Butyrate = primary energy source of colonocytes -> support intestinal tight junctions + thought to have anti-inflammatory effect
9
Q
How are fatty acids named?
A
Using their common names and the omega nomenclature system
10
Q
How does the omega nomenclature system work?
A
Uses number of carbon atoms, number of double bonds, and number of carbons from the omega end to the first carbon in the double bond
E.g. omega-6 -> 20:4 w6
20 = n of carbons
4 = n of double bonds
6 = n of carbons at first double bond
11
Q
What happens in hydrogenation?
A
Unsaturated fats become saturated with the addition of hydrogen (e.g. when oils are made into solid spreads) -> turns natural fatty acids into unnatural (trans) fats
12
Q
What is the structure of SATURATED FATTY ACIDS?
A
No C-C double bonds
All carbons are completely saturated with hydrogen bonds
Solid at room temperature
13
Q
What is the structure of UNSATURATED FATTY ACIDS?
A
Contain 1 or more double bonds between carbons
Liquid at room temperature
14
Q
What is the structure of MONOUNSATURATED FATTY ACIDS?
A
Have 1 double bond in the chain
15
Q
What is the structure of POLYUNSATURATED FATTY ACIDS?
A
Have several double bonds
The more double bonds in a fatty acid -> the less stable -> the more susceptible to oxidation
16
Q
What are unnatural trans fats?
A
Produced by high temperatures and hydrogenation
Found in margarine, refined vegetable oils
17
Q
What is the problem with trans fats?
A
- Stiffens cell membranes = prone to oxidation + alters their permeability
- Alter blood triglycerides and cholesterol profiles, link to increased risk of CDV disease, insulin resistance, cancer
18
Q
What is the difference between cis and trans fatty acids?
A
At each double bond, 2 possible isometric forms exist
- CIS : H atoms are on the same side of the double bond
- TRANS : H atoms are on separate sides of the double bond
19
Q
What are triglycerides?
A
Main dietary fat and also form in which fat is stored in the body -> they circulate in the blood when released for energy
But high levels in the blood have been linked to atherosclerosis
20
Q
How are triglycerides structured?
A
Lipid molecules made of 1 unit of glycerol and 3 fatty acids
The 3 fatty acids can differ in length (n of carbon atoms) and degree of saturation (n of hydrogen molecules)
21
Q
How are triglycerides synthesised by the body?
A
Body synthesises triglycerides when caloric intake exceeds energy requirements
Excess energy is converted in triglycerides via LIPOGENESIS, happening in the liver and adipose tissue
22
Q
What is lipogenesis?
A
Process through which acetyl-CoA is converted to triglycerides for storage in fat
23
Q
How does lipogenesis take place?
A
Excess carbohydrate (-> acetyl-CoA) = synthesis of fatty acids -> 3 fatty acids are bound to glycerol and stored as triglycerides
Fatty acids are synthesised in liver, adipocytes, kidneys, and lactating mammary glands
24
Q
What is Lipolysis?
A
When dietary energy is limited, fatty acids from triglycerides are mobilised from adipocytes into the circulation
25
How does Lipolysis work?
Triglycerides are hydrolysed by lipase into fatty acids and glycerol for use in the body
Stimulated by : adrenaline, noradrenaline, ACTH, glucagon and growth hormone, thyroid stimulating hormone, and thyroxine
26
What is the effect of insulin on Lipolysis?
Insulin antagonises Lipolysis -> insulin resistance = central adiposity
27
How can we get energy from fatty acids?
Fatty acids can cross the cell membrane, traverse the cytosol and reach the mitochondria -> CARNITINE facilitates the passage through the mitochondrial membrane
Fatty acid undergoes beta-oxidation = broken into 2 carbon blocks as Acetyl-CoA (-> Kerbs cycle)
Energy is finally generated via electron transport chain
28
When is ketone synthesis necessary?
When carb intake is low and fat becomes primary source of energy, ketone synthesis becomes necessary to fuel the brain (that cannot metabolise fatty acids)
29
How does ketogenesis take place?
Acetyl-CoA is converted into ketones :
1. Acetoacetate and 2. Beta-hydroxybutyrate
(Acetoacetate can undergo further decarboxylation and become acetone -> acetone build up gives the characteristic sweet breath)
30
What happens during Ketosis?
The low carb intake (<40 g x day) initiates a fundamental shift in the body’s primary fuel source from glucose to fat
31
What are the possible benefits of Ketosis?
Weight loss, epilepsy management, management of Parkinson’s and Alzheimer’s
32
What is the difference between nutritional Ketosis and ketoacidosis?
Ketoacidosis is an unstable and dangerous condition where there is insufficient pancreatic insulin response to regulate serum beta-hydroxybutyrate (beta-OHB)
33
How can you optimise lipid digestion?
1. Chew and avoid drinking at meals
2. Optimise stomach acid levels (B6 and zinc, bitters, ..) to increase bile production
3. Choleretics (increase bile prediction) and cholagogues (increase bile flow), e.g. dandelion, artichoke, turmeric
4. Good hydration to support bile flow
5. Increase glycine and taurine -> components of bile
34
What are generic fat intake recommendations?
Tot = 20-35% of total energy
Saturated = 10%
Polyunsaturated = 6-11%
Omega-3 = 0.5-2 %
35
What impact have dietary guidelines had on fat consumption?
The advice to reduce dietary fats led to :
- Fat foods being replaced with refined carbs and sugar
- Lack of dietary fats = decreased satiety = ultra-processed foods consumption
36
What should our fat intake look like?
Prioritise fats form natural, unrefined foods -> mixture of saturated, monounsaturated and polyunsaturated fats (no trans fats)
+ fat-soluble antioxidants, e.g. vit. E
37
What are the benefits of including healthy fats in the diet?
- Satiety
- Sources of EFAs
- Sources of choline
- Sources of essential fat-soluble vitamins and phytonutrients
- Flavour enhancement
38
Are saturated fats bad?
Not inherently, for example
Coconut oil (medium chain triglycerides)
- Source of fuel/ketones
- Contains lauric acid = antibacterial/viral/fungal
- Raise HDL lower LDL
39
What foods are rich in omega-9 oleic acid?
Olives, avocado, almonds, peanuts, pistachios, Brazil and pecan nuts, cashew, hazelnuts, macadamia, animal fat, butter
40
What foods are rich in omega-3 alpha linolenic acid?
Flaxseeds, chia and hemp seeds, dark green leaves, pumpkin seeds, soybean, rapeseed, walnuts, wheat germs
41
What foods are rich of omega-3 EPA and DHA?
Cold-water fish oil, salmon, trout, tuna, anchovies, mackerel, sardine, herring, spirulina, chlorella
42
What foods are rich in omega-6 linoleic acid?
Sunflower, hemp, soybean, walnuts, pumpkin seeds, sesame, almond, chia, cashew, rapeseed, wheat germ, avocado, Brazil nut
43
What foods are rich in omega-6 gamma linoleic acid?
Borage oil, evening primrose and hemp oil, blackcurrant seed oil
44
What foods are rich in omega-6 arachidonic acid?
Meat and animal products
45
What fats are preferable for cooking?
Saturated fats can tolerate being heated : coconut oil, butter, ghee
Monounsaturated fats (EVO, avocado oil) oxidise at high temperatures (above 180 c) but can be used at lower temperatures due to their antioxidant content
46
Why are polyunsaturated fats not ideal for cooking?
Oxidise when heated and produce free radicals that damage cells -> should only be used when cold-pressed, poured over cooked or raw food
47
What happens when lipids go rancid?
Fats break down into compounds which are transformed into products e.g. aldehydes, ketones and hydrocarbons
When double bonds are oxidised = malondialdehyde = very reactive compound inducing oxidative stress, ALSO a potential mutagen
48
When are fats more prone to oxidation?
- When high in polyunsaturated fatty acids
- When exposed to prolonged heat / light / oxygen
- When naturally low in antioxidants
- When refined or heavily processed
49
Why are saturated fats safe for cooking?
Lack of double bonds = more stable, less prone to oxidation
50
What are essential fatty acids?
Fatty acids that cannot be made by the body and need to be taken from diet :
1. Linoleic acid (omega-6)
2. Alpha-linoleic acid (omega-3)
51
What is the most important enzyme involved in the omega 3 and 6 fatty acids transformation from food sources into GLA and EPA?
Delta-6 desaturase
52
What is the ideal omega 3:6 ratio?
Human beings evolved with a 1:1 ratio
Today’s western diet is around 16:1
53
What is the problem with the modern omega 6:3 ratio?
Relatively low conversion rate of ALA to EPA/DHA -> EPA/DHA become conditionally essential
54
What are the 6 functions of EFAs (LA and ALA)
1. Vital components of cell membrane x fluidity
2. They act with cell membranes proteins -> affect substances transport in/out of cell
3. Key components of organelle membranes (e.g. mitochondria)
4. Necessary for cell-to-cell communication
5. Precursors of eicosanoids (= local hormones)
55
What are clinical indicators of EFA requirement on the SKIN?
- Dry, flaky, scaly, chapped lips and dry eyes
- Hyperkeratosis pilaris
- Acne, eczema, psoriasis, dermatitis
- Delayed wound healing
- Nails : dry/brittle, red/swollen cuticles
56
What are the clinical indicators of EFA requirement on the ENDOCRINE SYSTEM?
- Weight imbalances
- PMS/painful menstrual cramps/sore breasts
- Hyperinsulinaemia
57
What are the clinical indicators of EFA requirement on the REPRODUCTIVE SYSTEM?
- Infertility/ impotence/ repeated miscarriages
- Ovarian cysts/ fibrocystic breast disease
58
What are clinical indicators of EFA requirement on CIRCULATORY SYSTEM?
- Frequent nosebleeds / bleeding gums
- Easy bruising
- Delayed recovery from exercise
59
What are clinical indicators of EFA requirement on the MUSCOSKELETAL system?
- Chronic joint pain/ arthritis
- Delayed recovery from injuries
60
What are clinical indicators of EFA requirement on the IMMUNE SYSTEM?
Susceptibility to infections
61
What are NEUROLOGICAL clinical indicators of EFA requirement?
- Dementia/ Alzheimer’s
- Parkinson’s
- Irritability/ nervousness
- Tingling arms/ legs
- CSF/ME
62
What is the technical name of alpha-linoleic acid?
18:3 n-3
= 18 carbon polyunsaturated fatty acid
63
What are the neurological therapeutic uses of ALA?
1. Strokes -> promotes vasodilation and BDNF (= neuroprotective effect)
2. Depression -> BDNF has a critical role in neuronal maintenance, learning, memory + mood-boosting effect
64
What are the therapeutic uses of ALA as an anti-inflammatory?
Inflammatory bowel disease, asthma, autoimmune conditions
(Dependent on ALA transformation into EPA and DHA)
65
What are the therapeutic uses of ALA for cardiovascular disease?
- Decrease risk of atherosclerosis (-> myocardial infractions and strokes)
- Reduces C-reactive protein levels (inflammatory marker)
- Anti-arrhythmic effect
- Anti-hypertensive -> lowers activity of angiotensin-converting enzyme
- Lowers LDL cholesterol
66
What drug interacts with ALA?
1. Blood thinning medications : increase anti-coagulant effect
2. Cholesterol-lowering medications : agonist effect when combined with statins
67
What are EPA and DHA formed from?
ALA
68
What is EPA?
Eicosapentaenoic acid = omega 3 = 20:5 n-3
69
What is DHA?
Docosahexaenoic acid = omega 3 = 22:6 n-3
70
Therapeutic uses of EPA and DHA (i.e. fish oils) for CDV disease
1. Reduce blood triglycerides
2. Lowers blood pressure
3. Preventative for atherosclerosis
71
Therapeutic uses of EPA and DHA (i.e. fish oils) for neurological health
- Neuroprotective properties, increase BDNF
- Low DHA/EPA associated with learning and behavioral problems
-> support depression, ADHD, Alzheimer’s
72
Therapeutic uses of EPA and DHA in pregnancy support
Support foetal brain development
73
Therapeutic uses of EPA and DHA as anti-inflammatory
- Inhibit NFkB, TNF-alpha and interleukin-6
- Useful in inflammatory conditions e.g. arthritis, IBD, eczema, SLE
74
How can a veggie or vegan diet meet EPA/DHA needs?
- Include sources of ALA, e.g. flax and hempseeds
- Support EFA conversion -> increase dietary zinc, magnesium, B6
- Moderate intake of omega-6
- Consider supplementation
75
What are factors that determine quality of fish oil?
- Sustainability of the company (sustainably caught fish)
- Oils independently tested for purity and toxins
- Make sure EPA and DHA content is listed on the table
76
What are factors determining omega oil quality?
- Water extraction from micro algae schizocytrium -> DHA
- Extraction from echium seed oil containing SDA -> easily converted in DHA/EPA
- Free from carrageenan which may induce colonic inflammation
- Cold pressed and organic
77
Are there any drug interactions with EPA and DHA?
- Anticoagulants : EPA may increase bleeding time -> make drug stronger
- Aspirin : may benefit treatment of coronary artery disease but also increase risk of bleeding
- Diabetes medications : may lower blood glucose -> increase effect of diabetic medications
- Blood pressure medications : DHA may lower blood pressure
78
What is linoleic acid (LA)?
An omega 6 fatty acid, 18:2 n-6
79
What are food sources of LA?
Vegetable oils, sunflower, soybean, corn oils
Nuts and seeds
80
What is LA converted into?
It is converted into GLA, the conversion requires vit. C, B3, B6, zinc, magnesium
81
What is GLA?
Gamma linoleic acid = omega 6 fatty acid = 18:3 n-6
82
What are the main food sources of GLA?
Evening primrose oil, blackcurrant seed oil, borage and hemp oils
83
Therapeutic uses of GLA?
- Rheumatoid arthritis
- ADHD
- Eczema
84
What are therapeutic uses of evening primrose oil?
- PMS
- Cyclical mastalgia (breast pain)
- Female fertility
85
Are there drug interactions for GLA?
- Ceftazidime (antibiotic)
- Chemotherapy
- NSAIDs
86
What is AA?
Arachidonic acid = omega 6 = 20:4, n-6
87
What are main sources of AA?
Animal products, especially when intensively raised on grains
88
Is AA inflammatory?
Yes : it’s metabolised by COX1 and COX2 enzymes in the inflammatory prostaglandins series 2 = fever, vascular permeability, vasodilation
89
What are eicosanoids?
Locally-acting hormone-like signalling molecules
-> prostaglandins, leukotrienes, thromboxanes, resolvins and protectins
Made by the oxidation od omega 3 and 6
90
What are eicosanoids involved in?
- Inflammatino
- Blood vessels permeability and constriction
- Blood coagulation
- Immune cell behaviour
- CNS signalling
91
How are eicosanoids formed?
Fatty acids (AA, EP or DGLA) are released from membrane phospholipids by PHOSPHOLIPASE A2
Fatty acids are then converted into eicosanoids by COX and LOX
Can have both pro and anti inflammatory effect depending on starting fatty acid and outside stimulus
92
What are the 3 families of prostaglandins?
PG1 (from DGLA) -> anti-inflammatory
PG2 (from AA) -> pro-inflammatory
PG3 (from EPA) -> anti-inflammatory
PG2 produce the initial inflammation that is later shut off by PG1 and PG3
93
What determines which prostaglandins predominate?
Cell membrane fatty acids composition -> the more abundant fatty acid will occupy the enzyme active sites
94
Can you have too much omega-3?
High consumption of Omega 3 means that there will be limited space for AA on cell membranes —> this may result in immune suppression (its all about balance!)
95
How can omega 3 and 6 be synthesised from ALA and LA?
By DESATURATION (addition 1 double bond between 2 carbon atoms) —> desaturase
And/or ELONGATION (addition of 2 carbon atoms) —> elongase
Both LA and ALA compete for these enzymes -> only 1-20% of ALA is converted in EPA (women of reproductive age are more efficient in conversion)
96
What inhibits delta-6-desaturase?
Magnesium, B6, zinc deficiencies
Insulin resistance
Viruses
Refined sugars/alcohol
Stress hormones
Excess EPA/DHA
Excess trans fats/cholesterol
97
What inhibits delta-5-desaturase?
Insulin resistance
Zinc deficiency
Alcohol
Stress hormones
Excess trans fats/ cholesterol/ EPA/ DHA
98
What can you see by testing EFAs?
- Omega 3 index = marker for CDV risk
- Omega 3:6 ratio = marker for chronic illness
- AA:EPA ratio = marker for silent inflammation
99
How can one support the balance of omega-3 and 6?
Supplementing EPA/DHA
Addressing any conversion co-factor deficiency
100
What is cholesterol?
An important compound for cell structure and function
101
What is cholesterol involved with?
Synthesis/action of :
- Vitamin D and calcium metabolism
- Cortisol and related hormones
- Aldosterone for mineral and fluid balance
- Sex hormones
- Bile salts and acids
- Membrane integrity (esp. brain)
- Lipoproteins (to transport triglycerides)
102
What stimulates cholesterol synthesis?
A diet rich in triglycerides
Dietary cholesterol does not significantly affect plasma cholesterol
103
How does the body get rid of cholesterol?
Excreted in stool mostly as bile products
Excretion is increased by insoluble fibre
Absorption is limited by healthy gut bacteria
104
What are LDL and HDL?
Lipoproteins : they transport cholesterol, CoQ10, beta-carotene, vit. E,…
105
What do LDL do?
Take cholesterol from liver to cells
106
What do VLDL do?
Take triglycerides to cells
107
What does HDL do?
Collects cholesterol from cells and transport it back to the liver
108
What is the truth about high cholesterol?
A study in 2009 found lower “bad” cholesterol in people with heart disease
Increased cholesterol may indicate an increased demand for its anti-inflammatory function or need to repair membranes, make hormones,…
109
What is a better health risk indicator than total cholesterol particles?
The size of the particles
- LDL : large and fluffy = protective / small and dense = CVD risk
- HDL : larger are most effective at removing cholesterol from blood
110
What are phosphatides?
Phospholipids made of glycerol, 2 long chain fatty acids, a phosphate group + either inositol / choline / serine
111
What is phosphatidylcholine?
Predominant phospholipid in the body
Neuro and hepato-protective (-> cognition, memory, immunity, hormone function)
112
What is lecithin?
A phospholipid synthesised by liver -> emulsifies fat and increase cholesterol solubility
113
What is inositol?
A phospholipid that increases insulin sensitivity
114
What is phosphatdylserine?
A phospholipid that support neuronal membrane functioning and cognitive function
