Lipids Flashcards

1
Q

What are the functions of lipids?

A

They form part of every cell.

Far from being inert, white adipose tissue (WAT) is a complex, metabolically-active endocrine tissue.

Depending on where it is in the body it behaves in different ways. eg: inflmmatory cytokines in fat around the middle of the body.

1 Energy (ATP) production — each gram of fat supplies the body with about nine calories.
2 Storage of energy reserves — fats are a more efficient form of storage energy than carbohydrates or proteins, so the body stores any excess energy as fat.
3 Cell membrane structure — phospholipids and cholesterol stabilise cell membranes, whilst 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 Steroid 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 — the brain is rich in arachidonic acid (AA) and docosahexaenoic acid (DHA).
8. Constituents of nervous tissue structure (sphingomyelin).
9. Aid to cell-signalling processes.
10. Required for the absorption of fat-soluble vitamins.

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2
Q

Name the different types of lipids in the body

A
  • Individual fatty acids.
  • Triglycerides.
  • Phospholipids — in every cell membrane.
  • Cholesterol and steroid-based compounds (e.g. oestrogen).
  • Sphingolipids — found in nerve cell membranes, e.g. myelin.
  • Glycolipids — involved in cell identity (like a cell ‘passport’).
  • Cerebrosides — glycosphingolipids found in the brain.
  • Fat-soluble vitamins — A, D, E, K.
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3
Q

Name the four different fatty acid hydrocarbon chains and explain the difference

A

Fatty acids are hydrocarbon chains with an acid group at one end and a methyl group at the other. The number of carbons in the chain effect the way they behave.

Short-chain fatty acids (up to 5 Cs)
Medium-chain fatty acids (6–12 Cs) (coconut oil)
* Travel directly to the liver where they can be used to create energy or ketones.
* Much more readily converted to energy

Long-chain fatty acids (14–22 Cs)
Very long chain fatty acids (> 22 Cs)
* Used to build cell membranes.

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4
Q

When are SCFA’s produced?
What are the most common types?
What role do they play?

A

When are SCFA’s produced?
When dietary fibre is fermented in the colon.
Good fibre sources increase SCFA’s

What are the most common types?
Acetate, propionate and butyrate

What role do they play?

Speculated to have a role in the microbiota-gut-brain axis crosstalk.

Butyrate
- important for colon health because it is the primary energy source for colonocyte and supports the intestinal tight junctions.
- thought to have an
anti-inflammatory effect on the colon.

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5
Q

What is the omega system for naming fatty acids?

A

Uses
1. the number of carbon atoms
2. the number of double bonds
3. the number of carbons from the omega end to the first carbon in the double bond.

The omega-6 fatty acid, arachidonic acid, is referred to as 20:4 w6.

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6
Q

What is hydrogenation?

A

Fatty acids can be manipulated.

Unsaturated fats can be saturated by the addition of hydrogen

Hydrogenation = additiona of hydrogen

Makes oils into solid spreads.

Hydrogenation turns the natural fatty acid into unnatural forms (i.e. trans fats) which are damaging to health.

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7
Q

What is the difference between saturated and unsaturated fats.

A

The more double bonds in a fatty acid the less stable it is which means it is more prone to reactivity and thus oxidising

Saturated fatty acids
Contain no C-C double bonds. All the carbons are completely saturated with hydrogen bonds. Solid at room temperature.

Unsaturated fatty acids:
Contain one or more double bonds between carbons. Liquid at room temperature.

  • Monounsaturated fatty acids:
    Have one double bond in the chain.
  • Polyunsaturated fatty acids:
    Have several double bonds.
    Not saying that polyunsaturated fats are bad but they are less stable and more prone to oxidation
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8
Q

How are unnatural trans fats produced?
What foods do we find them in?
Why do they cause a problem in the body?
What problems do they cause?

A

**How are unnatural trans fats produced? **
High temperatures and hydrogenation.

What foods do we find them in?
margarine, processed foods and refined vegetable oils.

Why do they cause a problem in the body?
They stiffen cell membranes, making them prone to oxidation. This also alters their protective action and permeability, impeding normal cell function.

There are no safe levels of trans fats

What problems do they cause?
* Alter blood triglyceride and cholesterol profiles. Increase LDL and decrease HDL
* Linked to an increased risk of cardiovascular disease, insulin resistance and cancer.

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9
Q

What is a natural ‘TRANS’ fat

A

One on which the H atoms are on separate sides of the double bond. Conjugated linoleic acid is an example.

Most fatty acids are ‘CIS’ where the H atoms are on the same side as the double bond/

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10
Q

What are triglycerides?
What are they made up of?
What causes high serum tryglycerides?
What are high levels of triglycerides linked to?

A

What are triglycerides?
The major form of dietary fat, and the form in which fat is stored in the body.

What are they made up of?
One unit of glycerol (the backbone) and three fatty acids which can differ in length and degree of saturation with hydrogen molecules. .

What causes high serum tryglycerides?
1. Refined carbohysrates are the biggest cause
2. Alcohol
3. Obesity

What are high levels of triglycerides linked to?
Atherosclerosis, and hence heart disease and stroke.

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11
Q

Why does lipogenesis happen?

A

What is lipogenesis?
Whenever caloric intake exceeds energy requirements the excess dietary energy is converted to triglycerides via a process called lipogenesis.

Lipogenesis takes place in adipose tissue and the liver.

Excess ingested fat is taken up by adipose tissue.

Where does it happen?
Key sites are liver and adipocytes.
Also kidneys and lactating mammary glands.

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12
Q

What is lipogenesis?
Where does it happen?

A

It is the synthesis of fatty acids from non lipid sources, specifically carb rich food.

Excess glucose is converted to Acetyl-CoA which is converted to triglycerides (glycerol backbone + fatty acids) for storage in fat.

It happens when there is an excess of carbohydrates.

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13
Q

What is Lipolysis and when does it happen?

Why would insulin resistance reduce lipolysis?

A

When dietary energy is limited triglycerides from adipocytes are hydrolysed by lipase into fatty acids and glycerol are are mobilesed into circulation. This is called Lipolysis.

Lipolysis is switched on/stimulated by a number of hormones but insulin antagonises these lipolytic effects meaning it opposes the fat-burning (lipolytic) effects of certain hormones. The fat is not broken down and remains as central adiposity.

When insulin levels are high (e.g., after eating carbohydrates), it blocks fat burning by suppressing the actions of hormones that usually break down fat. This is why conditions like high insulin resistance can make fat loss more difficult.

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14
Q

What is the pathway for fatty acids to be turned into energy?

Which amino acid helps and how?

A

What is the pathway for fatty acids to be turned into energy?

Fatty acids cross the cell membrane, traverse the cytosol and reach the mitochondria.

Once they reach the mitichondria the fatty acids undergo beta-oxidation and are broken down into 2-carbon blocks as acetyl-CoA, which is oxidised via the Krebs cycle to CO2 and H2O.

Energy is then generated using the electron transport chain.

Which amino acid helps and how?
Carnitine facilitates the transport of fatty acids across the mitochondrial membrane.

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15
Q

What is ketone synthesis and why is it important for the brain?

A

When glucose are in short supply fat becomes the primary fuel for energy production but the brain cannot metabolise fatty acids so it can’t get its energy this way.

Luckily another fuel known as ketones are also made when glucose is in short supply. They are made overnight, when dieting or fasting.

Ketones can cross the blood-brain-barrier and supply fiel to the brain.

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16
Q

Name the ketones.

A

Aacetyl-CoA is converted to the ketones
* acetoacetate
* β-hydroxybutyrate (β-OHB).
* Acetoacetate can undergo decarboxylation to another ketone acetone.

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17
Q

How and when might we want to induce ketosis?

A

To shift the body’s primary fuel source from glucose to fat.

For most adults, this happens when carbohydrates are restricted to less than around 40 g a day.

Ketosis is linked with health benefits including
* Weight loss
* Management of epilepsy
* Parkinson’s and Alzheimer’s disease. (the theory is that a T3D in diseases such as these contribute to neurological degradation and a state of ketosis might help because it supplies energy to the brain)

NOTE: Nutritional ketosis is different from ketoacidosis — an unstable and dangerous condition

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18
Q

What aids the digestion of triglycerides?

A
  • Gastric lipase in the stomach and pancreatic lipase in the duodenum, which act to separate the glycerol and fatty acids.
  • This process is facilitated greatly by the emulsifying action of bile, which increases the surface area of fat droplets.

The resulting three fatty acids and monoglyceride are transported into enterocytes, where they are rebuilt in the cell, packaged into chylomicrons and
transported via the lymphatic system to the bloodstream.

The released fatty acids can be used or stored in adipose tissue.

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19
Q

How do we optimise lipid digestion?

A
  • Chew adequately and eat mindfully
  • Avoid drinking with meals
  • Stress management
  • Increase bile production by
    (a) optimising stomach acid levels via zinc and B6-rich foods, bitter foods (e.g. chicory, rocket)
    (b) Ensure good hydration to support bile flow.
    (c) Increase glycine and taurine, which are components of bile.
    (d) Olive oil can stimulate bile secretion.
    (e) Choleretics (increase bile production) and cholagogues (increase bile flow); e.g. dandelion, artichoke and turmeric.
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20
Q

What are the general recommendations for fat consumption?

A
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21
Q

What is wrong with government dietary guidlienes regarding fat consumption?

What should we be advising regarding fat?

A

What is wrong with government dietary guidlienes regarding fat consumption?

  • Low fat - often fat being replaced with refined carbohydrates and sugar.
  • Recommended unsaturated oils and spreads (may be highly refined and contain trans fats) and eat in small amounts
  • Without adequate energy from fat, people struggle to be sufficiently satiated. This has
    resulted in the consumption of ultra-processed foods.
  • No emphasis on healthy fats such as oily fish, avocado, nuts, seeds, extra virgin olive oil, egg yolk and grass-fed meat

What should we be advising regarding fat?

  • Love your fats
  • Eat fats from natural, unrefined foods
  • A mixture of saturated, monounsaturated and polyunsaturated fats, but absent of trans fats.
  • Fat-soluble antioxidants, e.g. vitamin E, are important when including fats in the diet.
  • Focus on the quality of the fat and combine with foods naturally rich in antioxidants.
  • Cold pressed oils as a lot of seed and vegetable oils are highly refined
  • Avoid farmed fish due to poor omega 6/3 ratio
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22
Q

Saturated fat:

What type of tryglyceride is Coconut oil?
What are its benefits?

A

What type of tryglyceride is Coconut oil?
Medium-chain triglycerides
Therefore used as a source of fuel or tunred into ketones

What are its benefits?
* as a MCT
- increases the number of calories burned compared to longer-chain fatty acids.
- Preliminary studies show positive outcomesin epilepsy and Alzheimer’s disease.

  • Antibacterial, antiviral and antifungal properties.
  • ↑ HDL cholesterol, ↓ LDL cholesterol.
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23
Q

Saturated fat:

Name a SCFA and where you find it

A

Butyric acid
* in butter and dairy
* Also produced in the gut which is why a good intake of fibre is needed

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24
Q

Saturated fat:

Name two MCFA and where you find them in order of abundance

A
  1. Carprylic acid

Coconut
Palm kernel
Breast milk

  1. Lauric acid

Coconut

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25
Q

Saturated fat:

Name two LCFA and where you find them.

A
  1. Palmitic acid

Coconut
Palm
Kernel

  1. Stearic acid
    Beef/Pork
    Lamb/mutton
    Cocoa/shea butter
    Butter
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26
Q

Monounsaturated fat:

What are the two types of monounsaturated fats and where do you find them (Listed in order of abundance)

A

Omega-7:

Sea buckthorn berries
Coconut
palm kernel
Madademia nuts

Omega-9
Olive oil, avocado
Almond, peanut, pistachio
Brazil nuts, pecan, cashew
Hazelnut, neem, macadamia
Animal fat, butter

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27
Q
A
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28
Q

Polyunsaturated fat:

A
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29
Q

Rules for cooking with fats

A
  1. Saturated fats such as coconut oil, ghee and butter have a high smoking point so are preferable for cooking
  2. Refined veg oils have a higher smoking point but are to be avoided because enzymes, flavour & pigments have been removed and you end up with damaged low quality oil.
  3. Monounsaturated fats such as extra virgin olive oil, avocado oil macadamia oil oxidise at high temperatures but can be used for low temperature cooking due to the naturally occurring antioxidants that help to stabilise the oil. These counteract the damage to the oil. Do not use at temperatures above 180°C
  4. Do not cook with polyunsaturated oil because they are unstable. Store in dark coloured bottles in the fridge or freezer (especially in summer) as they can go rancid quickly simply through direct light exposure and heat. Cold pressed ideally with a date they were pressed to ensure freshness.
  5. Ideally we want to keep frying to a minimum because it promotes free radicals production.

For example in a stir fry you can use water and then stir in a little bit of oil at the end to add flavour.

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30
Q

Rancidity in oils

What is it?

What makes fats vulnerable to rancidity

Why is it a problem?

A

What is it?
Fatty acids within triglycerides go rancid by releasing the fatty acids from glycerol.

What makes fats vulnerable to rancidity?
Fats are more prone to oxidation if they:
1. Are high in polyunsaturated fat.
2. Are exposed to prolonged heat, light or oxygen.
3. Are naturally low in antioxidants
4. Are refined or heavily processed

Why is it a problem?
Oxidation of the double bonds generally leads to the production of malondialdehyde, a potential mutagen
It interacts with DNA and proteins in the body

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31
Q

Name the two EFA’s

A

Alpha-linolenic acid - an omega-3 fatty acid

(ALA)Linoleic acid - an omega-6 fatty acid (LA)

32
Q

Explain the Omega 3 and omega 6 chain

A

From ALA (omega-3) and LA (omega-6) there follows a manufactured sequence in the body from the preceding fatty acid in the chain to further transform into other fatty acids.

so…with each step that moves ahead it utlises the fatty acid before it.

It does this with the help of special enzymes.

The most important enzyme that catalyses the chemical reaction to produce GLA and EPA is Delta-6-desaturase. It is a limiting enzyme meaning without it the process will stop at ALA and LA rather tahn work its way down the sequence.

33
Q

Why is EPA and DHA considered to be confitionally essential nutrients

A

Because of the low rate of conversion of ALA to EPA/DHA.

To achieve the EFSA recommended intake of 250 mg EPA / DHA, consume 2–3 portions of oily fish per week or from an algal source

34
Q

What are the six fatty acids in the Omega 3 chain?

A

ALA (Alpha-Linoleic Acid)
SDA (Stearidonic acid)

Eicosatetraenoic
**EPA **
DPA
DHA

35
Q

What are the six fatty acids in the Omega 6 chain?

A

LA - Linoleic Acid
GLA - Gamma Linoleic Acid

DGLA
AA- Arachidonic Acid
Adrenic Acid
DPA - Socosapentaenoic

36
Q

Name 6 functions of EFA’s

A
  1. EFAs are vital components of all cell membranes and help to maintain membrane fluidity.
  2. They act with cell membrane proteins thereby affecting the transport of substances into and out of the cell.
  3. EFAs are key components of organelle membranes such as those of the mitochondria.
  4. EFAs are necessary for cell-to-cell communication.
  5. They are essential for foetal and child brain development.
  6. EFAs are precursors of eicosanoids, which are ‘local’ hormones
37
Q

What are the clinical indicators that EFA is required. Think about this by system

A
  1. Skin/hair/nails
    skin: dry, flaky, scaley, hyperkeratosis pilaris, acne, psoriasis, dermatitis, delayed wound healing
    nails: dry, brittle, Paronychia
    hair: dry, oily, split ends, alopecia
  2. Endocrine system
    * Weight imbalances (obesity / weight loss).
    * PMS / painful menstrual cramps / sore breasts.
    * Hyperinsulinaemia.
  3. Reproductive system
    * Infertility / impotence / history of repeated miscarriages.
    * Ovarian cysts / fibrocystic breast disease
  4. Circulatory
    * Frequent nosebleeds / bleeding gums.
    * Easy bruising.
    * Delayed recovery from exercise
  5. Musculoskeletal
    * Chronic joint pain / arthritis.
    * Delayed recovery from injuries
  6. Immune
    Susceptibility to infections
  7. Neurological
    * Dementia / Alzheimer’s.
    * Parkinson’s disease.
    * Irritability / nervousness.
    * Tingling arms and legs.
    * CFS / ME.
38
Q

Omega 3:

What foods are high in ALA?
List in order of abundance

A

It is relatively easy to get into the diet

  1. Flaxseeds (richest source —
  2. 50% of its fatty acids are ALA)
  3. Chia seeds, hemp seeds, dark green leaves
  4. Pumpkin seeds, soybean, rapeseed (canola)
  5. Walnuts, wheat germ
40
Q

Omega 3:

List the theraputic uses for ALA

A

1. CARDIOVASCULAR DISEASE
Decreases the risk of myocardial infarctions, atherosclerosis development and strokes.
- Reduces C-reactive protein levels(an inflammatory marker used to evaluate CVD risk).
- Anti-arrhythmic effect stabilises electrical activity.
- Anti-hypertensive — ALA lowers the activity of angiotensin-converting enzyme (ACE).
- Shown to lower LDL cholesterol (whole flaxseed).

  1. NEUROLOGICAL
    - Strokes– promotes vasodilation in the brain and increases brain-derived neurotropic factor (BDNF), exerting a neuroprotective effect.
    - Depression
    - BDNF plays a critical role in neuronal maintenance, learning and memory and mood-boosting effects.
  2. Anti-inflammatory
    Used in cases such as inflammatory bowel disease, asthma and other autoimmune conditions.
41
Q

Omega 3:

Which medications have interactions with ALA and why?

A
  1. Blood-thinning medications: eg;warfarin and aspirin. May increase the anti-coagulant effects of blood-thinning medications
  2. Cholesterol-lowering medications (i.e. statins): May have an agonist effect when combined with statins.
42
Q

Omega 3:

What are EPA and DHA formed from.

What are the main food sources in order of abundance?

A

Formed from alpha-linolenic acid (ALA).

Sources:
* Cold-water fish oil
* Salmon, trout, tuna, anchovies, mackerel
* Sardines, herring
* Spirulina, chlorella

43
Q

Omega 3:

List the therapuetics uses of EPA and DHA

A
  1. CARDIOVASCULAR DISEASE
    * Supplementation can significantly reduce blood triglyceride levels.
  2. Can lower blood pressure
  3. Preventative against the formation of atherosclerosis.
  4. Research showed a reduction in myocardial reinfarction after a daily intake of 900 mg EPA / DHA.
    Supplemental fish oil dosage: EPA + DHA 0.8 – 3g/day
  5. ANTI-INFLAMMATORY
    * Profound anti-inflammatory effects — inhibiting NFκB, TNF-α and Interleukin-6.
    * Useful in inflammatory conditions, especially various forms of arthritis (e.g. osteo and rheumatoid), inflammatory bowel diseases, eczema and SLE.
  6. NEUROLOGCAL HEALTH
    * Neuroprotective properties and increase BDNF.
    * Lower levels of EPA and DHA are associated with more learning and behavioural problems.
    * Depression & ADHD
    * Alzheimer’s disease
  7. FOETAL HEALTH
    * Support foetal brain developmen (language, visual, motor functions) and used for pregnancy support.
    * There is evidence that mothers who supplement EPA and DHA during pregnancy and breastfeeding may protect their children against allergies.
44
Q

Omega 3:

How can a vegetarian or vegan diet can meet EPA / DHA needs:

A
  • Include good sources of alpha-linolenic acid in the daily diet, such as flaxseed and hempseed.
  • Support EFA conversion through increasing dietary intake of enzyme co-factors (zinc, magnesium and B6).
  • Moderate the use of oils rich in omega-6 fatty acids, and avoid processed foods rich in these oils.
  • Consider algal EPA / DHA supplements.
45
Q

Omega 3:

What are the factors that determine Omega Fish oil quality?

A
  1. **Sustainability practices **- check if it is made from sustainably caught fish approved by the Marine Stewardship Council, where bycatch of non-targeted species is minimised.
  2. Check that the oil is independently tested for purity and toxins, This will ensure minimal levels of toxic chemicals such
    as dioxins, PCB’s and heavy metals.
  3. When selecting a fish oil, make sure that the EPA and DHA content is listed on the label.
46
Q

Omega 3:

What are the factors that determine vegan Omega quality?

A
  1. Extracted microalgae using water extraction methods (instead of hexane, alcohol and other solvents), to provide DHA.
  2. Extracted from echium seed oil which contains** stearidonic acid** (SDA) which is easily converted to EPA and DHA.
  3. Free from carrageenan which may induce inflammation in colonic cells.
  4. Cold-pressed, organic.
47
Q

Omega 3:

Which medications have interactions with EPA and DHA and why?

A
  • Anticoagulants — EPA may increase bleeding time so fish oil could make the effects of these drugs stronger.
  • Aspirin — in combination with aspirin, fish oil could be helpful in the treatment of some forms of coronary artery disease BUT this combination may also increase the risk of bleeding.
  • Diabetes medications — fish oil supplements may lower blood glucose levels and could make effects of diabetes drugs stronger.
  • Blood pressure medication — DHA may lower blood pressure (so monitor).
48
Q

How does Linoleic acid (LA) get its name?

What type of fat is it?

What are the food sources listed in order of abundance?

A

The lino refers to flax (seeds)
The leic to olive oil

This is because both of these foods are very high in omega six.

LA It is an omega 6 fatty acid.

Safflower
Sunflower, hemp, soybean, walnut
Nuts, seeds amd some vegetables

49
Q

What co-factors are required to convert LA to GLA? Gamma linoleic acid

Why is this important?

A

Conversion of LA to GLA requires vitamins B3, B6 and C, Mg and Zn.

GLA - has more biological/therapeutic effects in the human body but we don’t get it from a lot of foods

50
Q

What are the main food sources of Gamma-linoleic acid (GLA)?

A

Blackcurrant seed oil

Borage oil

Evening Primrose oil

Hemp oil

There are not many food sources so often we are relying on LA to be converted to GLA (which requires vitamins B3, B6 and C, Mg and Zn.

or it is supplemented in which case we dont have to worry about the conversion of LA.

51
Q

What are the therapeutic uses of GLA?

A

An omega 6 fatty acid

  1. Rheumatoid arthritis reducing inflammation and therefore reduced joint pain, swelling and morning stiffness. Dosage of 1.4 g per day of borage seed oil.
  2. ADHD - combined with EPA it shows improvements in attention and impulsivity
  3. Eczema - reduced inflammation; improves skin symptoms
    Dosage of 320 mg of GLA a day (be careful not to raise arachadinic acid levels
52
Q

What are the therapeutic uses of Primrose oil and why could we apply this research to LA and GLA in combination!

A

Primrose oil is a a rich source of L and also contains GLA.

  1. PMS: Inhibits prolactin
    A lot of women have elevated levels of prolactin or increased sensitivity to prolactin. This hormone can generate imbalance between oestrogen and progesterone which leads to the symptoms of PMS. Elevated prolactin can also cause symptoms like depression and anxiety.

1500 mg a day for three months with the aim to bring the hormones back into balance.

  1. Cyclical mastalgia (breast pain)
    Anti inflammatory and Inhibits prolactin
    1000 mg three times daily for 4 to 6 months
  2. Female fertility
    It optimises cervical mucus to ensure the sperm can make their way through the female reproductive tract.
    1500 to 2000 mg daily from day one of the menstrual cycle
53
Q

Borage seed oil

When should you not use it?

Drug interactions?

A

recommended not to use it during pregnancy - or other gLA sources

Less than 3000 mg per day.

May increase treatment effects of:
* Ceftazidime (antibiotic)
* Chemotherapy
* Cyclosporine (immunosuppressant)

NSAIDS - may counteract the effects of GLA

Phenothiazines (anti psychotics) - may increase seizures

54
Q

What is Arachidonic acid and in what foods is it found?

A

It is an omega six fatty acid.

Is primarily found an animal product such as meat and eggs and dairy and especially when those animals are intensively farmed.

55
Q

Arachidonic acid gets a bad rap and is seen as inflammatory but why are we being a little too hard on AA?

What are some examples
of inflammatory effects?

A

Inflammation is the key part of the immune systems response to infection.

Inflammatory effects include Fever, vascular permeability and vasodilation, pain and oedema

AA unlikley to be in excess if good balance with omega 3

56
Q

What are eicosanoids?

A

A type of prostaglandin - locally acting hormone like signalling molecules

Involved in
* Inflammation
* **Blood vessel **permeability and constriction
* Blood coagulation
* Immune cell behaviour
* Lipid accumulation
* Central nervous system signalling

57
Q

How are eicosanoids produced?

A
  • Made by the oxidation of omega 3 and 6 fats

Step 1: **Phospholipase A2 (enzyme) **releases fatty acids from phospholipids on cell membranes.

Step 2: These are converted to eicosanoids
by **cyclooxygenase (COX) and lipoxygenase (LOX) **—

Eicosanoids can be made from arachidonic acid (AA), eicosapentaenoic acid (EPA)
and dihomo-y-linolenic acid (DGLA).

What they convert to and whether they have pro or anti-inflammatory effects depends on the fatty acid they are made from.

58
Q

Explain the 3 families that prostoglandins fall into.

Name the series
What is made from
What it does
Pro or anti inflammatory?

A

Series 1 Prostaglandins (PG1)
- made from DGLA
- Keep blood platelets from sticking together, remove excess sodium and water from the body and relax blood vessels promoting circulation.
- ANTI-INFLAMMATORY

**Series 2 Prostaglandins (PG2) **
- made from AA
- Oppose functions of series-1 prostaglandins by promoting platelet aggregation and sodium and water retention (↑ BP)
- INFLAMMATORY

**Series 3 Prostaglandins (PG3) **
- Made from EPA
- Some have weak platelet aggregating properties, Prevent the release of AA from cell membranes
- ANTI INFLAMMATORY

59
Q

Why is the balance between omega 3 and 6 consumption important when it comes to inflammation?

A

Eicosanoids made from the omega 6 arachidonic acid (Series 2 Prostaglandin) produce initial inflammation.

This is ‘shut off’ by the introduction of eicosanoids made from omega 6 DGLA (series 1) and omega 3 EPA (series 3).

If not AA rules and we get a chronic inflammatory state.

60
Q

What might an imbalance of too much omega-3 to omega-6 do to the body?

A

Omega three and six compete for enzyme active sites and the more abundant fatty acids will occupy more of these.

A high consumption of EPA and DHA from omega-3 means that a higher proportion of fatty acids resides in the cell membrane as the expense of AA. This can result in immune suppression preventing AA from launching an inflammatory response when needed.

In practical terms therefore if you are seeing somebody in clinic with signs of immune suppression such as wounds that aren’t healing or constant colds it is worth looking at their omega 3 to 6 balance .

61
Q

When a diet is rich in Arachadonic acid (AA) which prostaglandin does this lead to the formation of?

A

Pg2

And if the diet were more abundant in EPA and DHA, it would be more abundant in PG1 and PG3 consecutively

62
Q

Name four things that influence EFA metabolism

A
  1. Genetic variability: polymorphisms are common in the gene coding for delta 6 and Delta 5 desaturase which can alter how effectively an individual can convert down the omega fatty acid chain
  2. Competition for enzymes which is affected by the balance of omega-3 and omega six competing for the desaturates and elongase enzymes.
  3. Having the right nutrients to support those enzymes.
  4. Life stage. For example women of reproductive age convert ALA 2.5 times better than men.
63
Q

Name up to 8 factors that inhibit Delta-6-Desturase

A
  1. Missing cofactors: Magnesium, B3, B6, Vit C, zinc deficiency
  2. Insulin resistance switches off enzyme activity
  3. Alcohol
  4. Excess trans fats and cholesterol
  5. Stress hormones, e.g. cortisol switches off enzyme activity
  6. High intake of EPA / DHA
  7. Viruses
  8. Refined sugars
64
Q

Name up to 6 factors that inhibit Delta-5-Desturase

A
  1. Missing cofactors: Vit B3, Vit C, Zinc deficiency
  2. Insulin resistance switches off enzyme activity
  3. Alcohol
  4. Excess trans fats and cholesterol
  5. Stress hormones, e.g. cortisol switches off enzyme activity
  6. High intake of EPA / DHA
65
Q

What are the 3 markers you would look at in EFA testing?

A

You are measuring the amount of diffrent fatty acids in the blood cell membrane

Omega-3 index — Very low is a marker for cardiovascular risk.
Omega-6:3 ratio — a marker for chronic illness.
AA:EPA ratio — a marker of ‘silent’ inflammation.

66
Q

Beneficial properties of cholesterol are often overlooked because of negative perceptions around cardiovascular disease risk.

List 5 areas that cholesterol is essential for the sysnthesis or action of

A
  • Vitamin D and calcium metabolism.
  • All steroid Hormones including:
    1. Cortisol and related hormones.
    2. Aldosterone for mineral and fluid balance.
    3. Sex hormones — oestrogen, progesterone and testosterone.
  • Bile salts and acids needed for digestion.
  • Membrane integrity, especially in the brain. Maintains fluidity
  • Lipoproteins, needed for triglyceride transport
67
Q

Is cholesterol in the diet responsible for high plasma cholesterol levels?

How is it removed from the body and what helps with this?

A

Is cholesterol in the diet responsible for high plasma cholesterol levels?
No it does not significantly affect plasma cholesterol levels in most people as they are primarily influenced by genetic and nutritional factors such as fibre intake and gut bacterial health.

How is it removed from the body and what helps with this?
It is excreted in the stool intact, mostly as bile products.
The excretion is increased by absorption onto non-digestible carbohydrates (fibre).
Gut bacteria from healthy microbiomes metabolise cholesterol = less reabsorption.

68
Q

What is LDL, VLDL and HDL

A

They are carriers of fat soluble proteins which includes cholesterol but also othe fat soluble compunds such as CoQ10, beta-carotene and vitamin E

LDL (low density) — takes cholesterol from the liver to cells.
VLDL (very low density) — takes triglycerides to cells.
HDL (high density) — collects cholesterol from cells to transport back to the liver.

70
Q

What % of ALA is converted to EPA in the fatty acid chain?

A

Only 1 to 20%

71
Q

LDL cholesterol levles on their own are not the problem. Discuss

A
  • LDL is not problematic in its own right.
  • In fact an increase in LDL could be a sign of a need for increased demand for its anti inflammatory function or its membrane repair function or its hornone production function.
  • In the absence of inflammation or injury cholesterol does not deposit. Where LDL is a problem is when there is exisiting damage to the arterial wall which roughen it and causes LDL to stick to it where it is prone to oxidation.
72
Q

Measuring particle size rather than total cholesterol is a better health indicator. Discuss

A

There are varying sizes of LDL cholesterol.for both LDL and HLDL larger particle size is better.

LDL particle size — people whose LDL particles are predominantly small and dense have a threefold greater risk of coronary artery disease, whereas the large and fluffy type may be protective.

HDL particle size — larger HDL particles are more effective at
- removing cholesterol from the blood.
- exerting anti-inflammatory and anti-thrombotic effects
- promoting nitric oxide production in endothelial cells.

73
Q

What are the most useful cardiovascular markers you would wany to check before putting someone on statins for example.

A
  • Not necessarily serum cholesterol
  • Not tryglycerides unless they are fasting tryglycerides because otherwise it is influenced by what you ate prior to the test.
  1. Lipoprotein (a) — lipoprotein (a) is a blood clotting agent. It appears to be a key genetic risk factor in coronary artery disease. Higher levels are associated with greater risk.
  2. Lp-PLA2 — an enzyme that plays a role in endothelial inflammation and atherosclerosis.
  3. Fibrinogen — raised levels are a risk factor for clot formation.
  4. C-reactive protein — inflammatory marker associated with CVD and other places in the body
  5. Lipid peroxides — raised levels reflect oxidative damage to fatty acids and phospolipids in cell membranes under stress.
  6. Size of LDL and HDL particles
74
Q

What are the therapeutic uses of the three key phospholipids?

A

Inositol: Improves insulin sensitivity and can subsequently be used in cases of insulin resistance
(e.g. Type 2 diabetes, PCOS).

Phosphatidylserine: Improves neuronal membrane functioning and cognitive function. It can be used in cases of depression, insomnia and stress. Dampens down what can become damaging effects of cortisol

Phosphatidylcholine:
* Neuro- and hepato-protective. It supplies choline for the synthesis of the neurotransmitter acetylcholine.
* Important for cognition, memory, immunity and hormone function