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Nutrition 2 (Semester II) > 11b. CV Health - Risk Factors > Flashcards

11b. CV Health - Risk Factors Flashcards

1
Q

What are the risk factors for CVD?

A

Family history
Genetics
Ethnicity
Gender
Smoking
Sedentary lifestyle
Chronic stress
Periodontal disease
Heavy metals
Dysbiosis
Poor diet
Dyslipidaemia
Hypertension
Inflammation
Obesity
Insulin resistance
Mitochondrial dysfunction
Elevated homocysteine
Thyroid hormones
Advanced glycation end products
Melatonin deficiency

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2
Q

How does family history pose a risk factor for CVD?

A

Offspring of parents = 60-75% risk increase
Siblings = 40% risk increase

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3
Q

SNPs on which genes pose a risk for CVD?

A

MTHFR
ACE
NOS3
MnSOD

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4
Q

Which ethnicities face an increased risk of CVD?

A

South Asian
Sub-Saharan African

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5
Q

Why does gender pose a risk to CVD?

A

Common view that CVD is male pathology
Mortality in women (35-54) increasing
Women experience more vague signs - lightheaded with exertion
Symptoms can be mistaken for menopause or heartburn

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6
Q

Why is dyslipidaemia a risk factor for CVD?

A

Increased total cholesterol
Increased LDL, VLDL, Lp(a)
Increased triglycerides
Reduced HDL

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7
Q

What diet and lifestyle factors are associated with dyslipidaemia?

A

Sedentary lifestyle
Excess alcohol
Smoking
Obesity
High intake of saturated/trans fats
Menopause

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8
Q

Which conditions increase the risk of dyslipidaemia?

A

T2D
Hypothyroidism
CKD

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9
Q

Why is mitochondrial dysfunction a risk factor for CVD?

A

ATP is required to pump Ca ions out of the myocardial cells
Aids relaxation

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10
Q

Why is elevated homocysteine a risk factor for CVD?

A

Associated with LDL oxidation
Monocyte adhesion
Endothelium dysfunction

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11
Q

What can contribute to elevated homocysteine?

A

Low folate
Low B12
SNPs

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12
Q

Why can low folate and B12 lead to elevated homocysteine?

A

Needed for re-methylation of homocysteine to methionine

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13
Q

Which SNPs can lead to elevated homocysteine?

A

MTHFR
MTR/MTRR
FUT2
TCN

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14
Q

How can a SNP on MTHFR lead to elevated homocysteine?

A

Impacts supply of methyl groups needed to methylate B12 in methionine cycle

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15
Q

How can a SNP on MTR/MTRR lead to elevated homocysteine?

A

Impacts B12 activation

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16
Q

How can a SNP on FUT2/TCN lead to elevated homocysteine?

A

Impacts B12 absorption

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17
Q

Which other genes are needed for methylating homocysteine?

A

PEMT/COMT (choline)
BHMT (betaine)

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18
Q

How can thyroid hormones be a risk factor for CVD?

A

TH receptors are present in the myocardium and vascular tissue
Minor TH changes can alter CV homostasis
Hypo and hyperthyroidism are linked with endothelium dysfunction, dyslipidaemia and BP changes

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19
Q

How does inflammation pose a risk to CVD?

A

Inflammation contributes to endothelium dysfunction
In turn, endothelium dysfunction, subintimal cholesterol accumulation and recruitment of monocytes and T-cells drives the inflammatory response

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20
Q

How does obesity pose a risk to CVD?

A

Excess adipose tissue perpetuates inflammation, contributing to vascular breakdown and metabolic complications

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21
Q

What is the vasoconstrictor peptide that inflammation is linked with?

A

Endothelin-1 (ET-1)

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22
Q

What can elevated ET-1 lead to?

A

Fibrosis of VSMCs
Increased ROS

23
Q

What role does adiponectin have in CVD?

A

Protective against CVD
Decreased levels in obesity
Decreased levels also contribute to IR

24
Q

What role does leptin play in CVD?

A

Activates the SNS causing sodium retention, vasoconstriction and increased blood pressure

25
Q

What roles does IR play in CVD?

A

IR contributes to lipid triad - high plasma triglycerides, low HDL, small dense LDLs
Also contributes to dyslipidaemia
Dyslipidaemia + endothelial cell damage = atherosclerotic plaque formation

26
Q

What does hyperglycaemia increase the risk of in the bloodstream?

A

Glycosylation reactions
Production of advanced glycation end products (AGEs)

27
Q

What are AGEs?

A

Harmful compounds formed when protein or lipids become glycated after exposure to glucose

28
Q

How do AGEs exert their effects?

A

Receptor mediated
Non-receptor mediated

29
Q

How do receptor mediated AGEs work?

A

Binding to the cell receptor RAGE, increasing inflammatory cytokines and ROS via activation of NADPH oxidase, which activates NF-kB

30
Q

How do non-receptor mediated AGEs work?

A

Increased extracellular matrix synthesis, trapping endothelium LDL and cross binding with collagen
This leads to OS, vascular endothelium dysfunction and immune cell dysfunction

31
Q

Do AGEs increase with age?

A

Yes

32
Q

A SNP on which gene can increase risk from AGEs?

A

AGER
(encodes for RAGE)

33
Q

Examples of exogenous AGEs in the diet

A

High refined carbs - sucrose, HFD
Processed foods
Meat
Dairy

34
Q

Examples of exogenous AGEs in cooking methods

A

High heat
Grilling
Roasting
Searing
Frying

35
Q

Examples of lifestyle that enhance AGE accumulation

A

Smoking
Sedentary

36
Q

Which vitamin improves AGE-mediated complications?

A

D

37
Q

How is smoking a risk factor for CVD?

A

Increases OS
Lowers AOs
Nicotine overstimulates SNS and increases BP

38
Q

How can a sedentary lifestyle be a risk factor for CVD?

A

Exercise has a positive effect on lipid profile and BP, insulin sensitivity and NO production
Brisk walking 30 mins/day can protect against CVD mortality

39
Q

How can chronic stress be a risk factor for CVD?

A

May cause endothelium dysfunction especially in the presence of other risks e.g. smoking
Stress activates SNS and HPA-axis, ultimately increasing inflammatory cytokines
Increased HR and BP through the SNS
Raised activity of the amygdala increased arterial inflammation

40
Q

Why is periodontal disease a risk factor for CVD?

A

Increased systemic inflammation which impairs vasodilation
Promotes endothelial dysfunction, arterial stiffness and increased fibrinogen

41
Q

How can heavy metals be a risk factor for CVD?

A

Induce OS, lipid peroxidation and inflammatory cytokines
Cadmium and lead compete with Zn
Zn deficiency increases atherosclerosis risk

42
Q

Why is melatonin deficiency a risk factor for CVD?

A

Melatonin is a potent AO with anti-hypertensive properties
Protects against coronary heart disease

43
Q

How can dysbiosis be a risk factor for CVD?

A

SCFAs reduce risk of metabolic endotoxaemia by maintaining intestinal barrier integrity
SCFAs reduce serum lipids by inhibiting cholesterol synthesis or redirecting lipids to the liver

44
Q

How does the gut microbiota play a role in cholesterol regulation?

A

By altering bile acids that influence systemic cholesterol levels

45
Q

What is TMAO?

A

A pro-inflammatory metabolite that originates from the bacterial metabolism of choline rich foods

46
Q

How does TMAO increase CVD risk?

A

Associated with endothelium dysfunction

47
Q

What dietary considerations increase the risk of CVD?

A

High PRAL foods
Trans fats
Fructose
Nutrient deficiencies

48
Q

What is PRAL?

A

Potential renal acid load

49
Q

What are high PRAL foods?

A

Foods rich in protein (meat, cheese)

50
Q

How do high PRAL foods increase the risk of CVD?

A

May induce low grade metabolic acidosis

51
Q

How do trans fats increase the risk of CVD?

A

Promote dyslipidaemia
Increase inflammation
Contribute to endothelium dysfunction
Encourage visceral adiposity
Increase risk of IR

52
Q

How does fructose intake increase the risk of CVD?

A

Promotes de novo lipogenesis
Increases fatty acids - particularly palmitic acid

53
Q

Food sources of palmitic acid

A

Dairy
Cheese
Meat
Coconut oil
Egg yolk
Peanut butter

54
Q

Deficiencies in which nutrients can lead to CVD?

A

C, D, E
CoQ10
Mg

Nutrition 2 (Semester II) (55 decks)

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