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CNM NUTRITION 2 S2 > 11 CARDIOVASCULAR HEALTH > Flashcards

11 CARDIOVASCULAR HEALTH Flashcards

1
Q

What is CVD?

A

Cardiovascular Disease is a general term for conditions affecting the heart and blood vessels such as atherosclerosis, hypertension, angina, myocardial infarction and stroke.

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2
Q

What percentage of global deaths are attributed to CVD?

A

32%

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3
Q

TRUE or FALSE:
CVD is the most common non-communicable disease worldwide.

A

TRUE

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4
Q

What percentage of premature CVD is preventable?

A

75%

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5
Q

What are some lifestyle factors that increase CVD risk?

A

Unhealthy diet, lack of exercise, excess body fat, stress, smoking

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6
Q

What can damage the GX?

A

The GX is easily damaged by inflammation, hyperglycaemia, endotoxemia, oxidised low-density lipoproteins and abnormal blood shear stress.

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7
Q

What is the glycocalyx (GX)?

A

The glycocalyx (GX), a carbohydrate-rich protective layer covering the ED, regulates permeability, controls NO production and acts as a mechanosensor of blood shear stress.

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8
Q

What is shear stress in relation to Endothelium (ED) cells?

A

Frictional force of blood

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9
Q

What are the key functions of the ED?

A

• Semi-permeable barrier: Role in fluid balance, host defence and selective movement of substances e.g., glucose and oxygen.
• Regulates vascular tone: Secretes vasodilators (e.g., NO) and vasoconstrictors (e.g., endothelin).
• Enzymes: Contains angiotensin-converting enzyme (ACE) ― plays a key role in regulating blood pressure.
• Angiogenesis: ED cells are the origin of all new blood vessels.
• Haemostasis: The luminal surface of ED prevents platelet adherence and coagulation (non-thrombotic, anticoagulant).
• Immune defence: Healthy ED cells deflect leukocyte adhesion and oppose local inflammation.

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10
Q

Where are Vascular Smooth Muscle Cells (VSMCs) located and what is their role?

A

Located in the tunica media and play a key role in vessel contraction and dilation (regulate blood circulation and pressure).

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11
Q

What happens to VSMCs under pathological conditions (e.g., inflammation, oxidative stress, telomere damage?

A

VSMCs undergo phenotypic modulation, altering cell structure and function.

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12
Q

What is phenotype modulation?

A

Altering physical form/structure through the interaction of the genotype and environment

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13
Q

What is the result of reduced Nitric Oxide?

A

Reduced NO contributes to atheroma formation and CVD.

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14
Q

What are the physiological effects of NO?

A
  • Regulates vascular tone
  • reduces platelet aggregation and VSMC proliferation
  • inhibits leukocyte adhesion and inflammatory cytokines
  • opposes oxidation of LDLs.
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15
Q

How is NO generated?

A

It is continuously generated from L-arginine by endothelial nitric oxide synthase (eNOS).

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16
Q

What regulates NO synthesis?

A

Vitamin D regulates NO synthesis by mediating eNOS.

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17
Q

Characteristics and function of normal endothelial cells

A

• Impermeable to large molecules, anti-inflammatory, deflects leukocyte adhesion.
• Enhances vasodilation.
• Resists thrombosis.

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18
Q

Impact of oxidative stress and inflammation on endothelial cells (activated state)

A

• ↑ permeability, inflammatory cytokines and leukocyte adhesion.
• Reduced vasodilator (NO, prostacyclin) molecules.
• Increased risk of thrombosis.

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19
Q

Location of VSMCs in arteries

A

Tunica media

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20
Q

Characteristics and function of normal VSMCs

A

• Normal contractile function, maintains extracellular matrix.
• Contained within the tunica media.

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21
Q

Impact of activation on VSMCs

A

• Increased inflammatory cytokines and extracellular matrix synthesis.
• Migration into the tunica intima and proliferation of VSMCs.

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22
Q

What are PPARs?

A

Peroxisome proliferator-activated receptor (PPARs) are nuclear transcription factors that control gene expression involved in:
* adipogenesis
* lipid and glucose metabolism
* cellular proliferation and apoptosis.

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23
Q

What is the role of PPARα in cardiovascular health?

A

↑ HDL-C, ↓TGs and inflammation, anti-atherosclerotic

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24
Q

List natural PPAR-α agonists.

A

Green tea, resveratrol, oregano, thyme, rosemary, naringenin, omega-3

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25
Q

What effect does PPAR-γ have?
Name 3 natural PPAR-γ agonists.

A

Reduces blood glucose, fatty acids, insulin.
Apigenin, hesperidin, curcumin, resveratrol, EGCG

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26
Q

What overall benefits do PPARs provide?

A

Decrease inflammation, promote ED health

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27
Q

What is the risk increase for offspring of parents with premature CVD?

A

60–75%

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28
Q

Which genetic polymorphisms are associated with CVD risk?

A

MnSOD, NOS3, MTHFR, ACE

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29
Q

Which ethnicities have an enhanced risk of CVD?

A

South Asian, sub-Saharan African

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30
Q

Why is CVD risk in women often underestimated?

A

Vague symptoms, mistaken for menopause or heartburn

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31
Q

Dyslipidemia is a largely preventable risk factor for CVD. Which lifestyle and dietary factors can underlie this?

A

Associated with sedentary lifestyle, excess alcohol, smoking, obesity, high intake of saturated and trans fat, menopause. Risk increases in T2DM, hypothyroidism and chronic kidney disease.

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32
Q

Why is mitochondrial dysfunction a CVD risk factor?

A

ATP is required to pump Ca ions out of myocardial cells, allows relaxation and maintains electrochemical gradient across myocardial cell membrane. Consider statins/CoQ10.

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33
Q

Why is elevated homocysteine regarded as a CVD risk factor?

A

Associated with LDL oxidation, monocyte adhesion and ED dysfunction

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34
Q

Deficiency of which vitamins can lead to elevated homocysteine?

A

Folate, B12, B6

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35
Q

What genetic polymorphisms impact homocysteine levels?

A

MTHFR, FUT2, TCN, MTR, MTRR

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36
Q

Which two nutrients apart from B vitamins are needed for the methylation of homocysteine?

A

Choline, betaine

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37
Q

How could the thyroid be implicated in cardiovascular disease risk?

A

Thyroid Hormone receptors are present in the myocardium and vascular tissue and minor TH changes can alter CV homeostasis. Hypo and hyperthyroidism are linked with ED dysfunction, dyslipidaemia and BP changes.

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38
Q

Why is inflammation a CVD risk factor?

A

Inflammation has various origins including dyslipidaemia, dysbiosis and intestinal permeability, ROS, diabetes, excess adipose tissue and smoking. Inflammation contributes to ED dysfunction. In turn, ED dysfunction, subintimal cholesterol accumulation and recruitment of monocytes and T-cells drives the inflammatory response.

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39
Q

Why is obesity a CVD risk factor?

A

Excess adipose tissue perpetuates inflammation contributing to vascular breakdown and metabolic complications:
- Inflammation = Elevated ET-1 = fibrosis of VSMCs and ↑ ROS.
- ↓ Adiponectin = disrupted expression of ED cells = less protection against CVD
- ↑ Leptin = ↑ SNS = sodium retention, vasoconstriction & ↑ blood pressure.

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40
Q

Inflammation is linked with an increase in which vasoconstrictor peptide?

A

Endothelin-1 (ET-1)

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41
Q

Which gene polymorphisms may increase Endothelin-1 and CVD risk?

A

Polymorphisms of EDN1

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42
Q

Why is insulin resistance a CVD risk factor?

A

IR generates chronic hyperglycaemia leading to oxidative stress, inflammation and cellular damage:
- IR contributes to the lipid triad and dyslipidaemia.
- Dysfunctional insulin signalling → ED damage + Dyslipidaemia = leads to atherosclerotic plaque formation.
- IR → glucose is not cleared from the bloodstream as quickly as needed = ↑ risk of glycosylation reactions & AGEs.

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43
Q

What is the Lipid triad?

A
  • high plasma TGs
  • low HDL
  • small dense LDLs
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44
Q

What are advanced glycation end products (AGEs)?

A

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

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45
Q

Via which two main mechanisms do AGEs exert their effects?

A

Via receptor-mediated and non-receptor mediated mechanisms.

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46
Q

What is the receptor-mediated mechanism of AGEs?

A

AGEs bind to the cell receptor RAGE, increasing inflammatory cytokines and ROS via NADPH activation.

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47
Q

What is the non-receptor mediated mechanism of AGEs?

A

Increased EC matrix synthesis, trapping ED LDL and cross binding with collagen.

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48
Q

What does AGE/RAGE signaling lead to?

A

Induces fibroblast differentiation and downregulates intracellular detoxifying mechanisms.

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49
Q

What does glycation refer to?

A

The chemical addition of glucose molecule to lipids or proteins

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50
Q

What causes an increase in AGEs?

A

Advancing age, high refined carbohydrates, processed foods, meat, dairy, high heat cooking, smoking, sedentary lifestyle

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51
Q

What is the result of renal accumulation of AGEs?

A

Kidney dysfunction

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52
Q

What does the AGER gene encode?

A

RAGE

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53
Q

Which nutrient can ameliorate AGE-mediated complications?

A

Vitamin D

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54
Q

How does smoking impact cardiovascular health?

A
  • ↑ oxidative stress (ROS react with NO to form harmful peroxynitrite)
  • Lowers antioxidants (1 cigarette = 25 mg loss of vitamin C)
  • Nicotine over-stimulates SNS and increases BP.
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55
Q

How can exercise contribute to cardiovascular health?

A

Positive effect on lipid profile, blood pressure, insulin sensitivity, and NO production

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56
Q

How does chronic stress impact cardiovascular health?

A
  • May cause ED dysfunction (especially with other risks e.g., smoking).
  • Activates SNS and HPA-axis, ultimately ↑ inflammatory cytokines.
  • ↑ heart rate and blood pressure through the SNS.
  • Raised activity of the amygdala increases arterial inflammation.
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57
Q

How does stress increase heart rate and blood pressure?

A

Through SNS activation

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58
Q

What is the effect of periodontal disease on systemic inflammation?

A

↑ TNF, IL-1, IL-6, CRP

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59
Q

Why is periodontal disease a CVD risk factor?

A

Periodontal disease increase systemic inflammation (↑ TNF, IL-1, IL-6, CRP) which impair vasodilation. It promotes endothelial dysfunction, arterial stiffness, ↑ fibrinogen

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60
Q

How does heavy metals increase CVD risk?

A

Heavy metals induce oxidative stress, lipid peroxidation and inflammatory cytokines.
Cadmium and lead compete with zinc. A zinc deficiency increases atherosclerosis risk.

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61
Q

How does melatonin affect cardiovascular health?

A

Melatonin is a potent antioxidant with anti-hypertensive properties that protects against coronary artery disease.

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62
Q

Which harmful metabolite could result from alterations in gut microbiota and how does this relate to CVD risk?

A

Trimethylamine-N-oxide (TMAO), which is a proinflammatory metabolite that originates from the bacterial metabolism of choline-rich foods.
TMAO is associated with endothelial dysfunction and increased risk of CVD.

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63
Q

Which metabolites produced by gut microbiota reduces the risk of metabolic endotoxaemia and thus CVD and IR?

A

SCFAs.
They reduce serum lipids by inhibiting cholesterol synthesis or redirecting lipids to the liver.

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64
Q

Which foods have a high potential renal acid load (PRAL) and what is the impact of high PRAL foods on health?

A

Foods rich in protein such as meat and cheese. They may induce low-grade metabolic acidosis = risk for IR and CVD

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65
Q

How do trans fats affect health?

A

Promote dyslipidaemia, inflammation, ED dysfunction, visceral adiposity and IR risk

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66
Q

What is the consequence of high fructose intake on lipid metabolism?

A

Promotes de novo lipogenesis and ↑ fatty acids, especially palmitic acid which ↑ uptake of oxidised LDL (major driver of atherosclerosis and CAD).

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67
Q

Which nutrient deficiencies can be linked to cardiovascular health risks?

A

Vitamin C, D, E, CoQ10, Mg

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68
Q

What is a cardiac risk tool?

A

Calculates score based on CV risks such as age, BMI, smoking. (e.g. QRISK)

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69
Q

What is hs-cTnT and hs-cTnI?

A

Cardiac troponin proteins released when heart muscle is damaged (such as in Myocardial Infarction)

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70
Q

What is a normal TC level?

A

< 5 mmol / L

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71
Q

What is a normal HDL level for men?

A

> 1 mmol / L

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72
Q

What is a normal HDL level for women?

A

> 1.2 mmol / L

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73
Q

What TG and TC:HDL ratio indicates higher risk for CVD?

A

TC:HDL > 6

74
Q

What is TC?

A

Total cholesterol

75
Q

What is Lp-PLA2 and what is it upregulated in?

A

Enzyme produced by monocytes, macrophages and T-cells that is upregulated in atherosclerotic plaques and vascular inflammation.

76
Q

What are the low and high risk levels for hsCRP?

A

< 1.0 mg/L (low risk), > 3.0 mg/L (high risk)

77
Q

What dietary and lifestyle factors elevate both Lp-PLA2 and hsCRP?

A
  • Smoking
  • westernised diet
  • sedentary lifestyle
  • periodontal disease
78
Q

What is MPO and what does it measure?

A

Myeloperoxidase. It is released by macrophages and measures the body’s response to damaged arterial walls.
High MPO is associated with inflammation / oxidative stress and a poor prognosis.

79
Q

What are the reference ranges for MPO levels?

A

Low=<470 pmol/L, high ≥ 540 pmol/L

80
Q

What is LDL-P and why does it reveal more about CV health than LDL-C?

A

The number of LDL particles (LDL-P) plays a much stronger role in the development of CVD than the mass of cholesterol within these particles (LDL-C). LDL-P correlates with carotid atherosclerosis and is more closely associated with obesity, diabetes, and insulin resistance than LDL-C.

81
Q

Which types of diets are associated with significantly reduced CVD risk?

A

Plant-based and mediterranean-style diets

82
Q

List four benefits of plant-based and Mediterranean-style diets

A
  • ↓ inflammatory mediators, ROS and RNS
  • reduced adiposity and risk of thrombosis
  • ↑ SCFA production
  • improved insulin sensitivity
  • ↑ adiponectin
  • improved ED function
83
Q

How does vitamin C promote cardiovascular health?

A

• Downregulates NADPH oxidase, a key source of ROS in the vascular wall.
• Upregulates endothelial NO synthase (catalyses synthesis of NO from arginine).
• Lowers tendency for platelet aggregation.

84
Q

How does vitamin E promote cardiovascular health?

A

• Protecting the endothelium from ROS and supporting NO synthesis.
• ↓ oxidation of LDL-C and deposition in arterial walls.
• Inhibits platelet aggregation and ↓ clotting factors to support healthy blood viscosity.

85
Q

How does Vitamin D promote CV health?

A
  • Modulates NO synthesis (influences cells involved in atherogenesis e.g., ED, VSMCs, monocytes and cardiac myocytes).
  • Modulates RAAS and lowers BP
86
Q

How do Omega-3 fatty acids support cardiovascular health?

A

• Improve lipid and lipoprotein profiles.
• Involved in the synthesis of key regulators of inflammation, vasodilation and platelet aggregation.
• EPA stabilises cellular membranes allowing neutralisation of extracellular ROS.
• DHA supports membrane fluidity.

87
Q

How is Co-enzyme Q10 beneficial for cardiovascular health?

A

• CoQ10 protects against endothelial dysfunction and reduces LDL oxidation (↓ atherosclerosis risk).
• Increases superoxide dismutase activity, which preserves the activity of NO (↓ risk of high BP).
• Supports mitochondrial health and production of ATP.

88
Q

Why would you consider Magnesium supplementation to support a client’s cardiovascular health? Which type of magnesium and at which dosage?

A

• Magnesium regulates ion transporters e.g., potassium and calcium channels, plays a central role in modulating neuronal excitation, intracardiac conduction and myocardial contraction.
• Helps regulate vascular tone and stabilise heart rhythm.
* Magnesium glycinate / taurate at 500–800 mg / day

89
Q

How does hawthorn promote CV health?

A

• Cardiac tonic, strengthens and improves vascular elasticity, ACE-inhibiting actions (↓ BP)
• Hawthorn reduces ET-1 and increases NO levels, hence having vasodilatory effects.
• Antioxidant (e.g., ↑ SOD), anti-inflammatory (inhibits NF-κB).

90
Q

Which of the following properties of garlic are useful in CV health?
a) Antihypertensive
b) Reduces HDL
c) Lowers homocysteine
d) Stimulates platelet aggregation

A

a) Antihypertensive
c) Lowers homocysteine

91
Q

Discuss the mechanisms by which regular exercise can reduce CVD risk.

A

– Leads to a more favourable lipoprotein profile and ↓ TGs.
– Improves insulin sensitivity, and insulin signaling in the vascular endothelium, activating eNOS, which ↑ NO synthesis.
– Regular exercise promotes a net reduction in blood pressure at rest (cardiac output and BP transiently ↑ during exercise).

92
Q

Which stress management activities could you recommend to promote parasympathetic activity?

A

Diaphragmatic breathing, humming, singing

93
Q

Recommend four herbal teas for stress relief.

A

Chamomile, passionflower, lemon balm, lime flower

94
Q

What enzyme and resulting nutrient do statins block?

A

HMG CoA-reductase = ↓ coenzyme Q10 synthesis.

95
Q

What is cholestyramine and how does it affect fat-soluble vitamins?

A

A bile acid sequestrant that ↓ absorption of fat-soluble vitamins and beta-carotene.

96
Q

What minerals do loop and thiazide diuretics increase excretion of?

A

Potassium, calcium, thiamine, and zinc (thiazide only)

97
Q

Which mineral does ACE inhibitors bind with?

A

Zinc

98
Q

What is the effect of beta-blockers on melatonin production?

A

Beta-blockers decrease melatonin production by inhibiting adrenergic beta1 receptors; block the biological pathway of CoQ10-dependent enzymes.

99
Q

What is hypertension (HTN)?

A

Leading contributor to CVD

100
Q

How is blood pressure (BP) defined?

A

Ratio of systolic and diastolic BP

101
Q

What are the signs and symptoms of hypertension?

A

Fatigue, headache, dizziness, visual disturbance

102
Q

Define essential hypertension

A

No specific underlying medical cause.

103
Q

What drives essential hypertension?

A
  • Vascular resistance
  • Obesity
  • Stress and anxiety
  • Smoking
  • High salt intake
104
Q

What is secondary hypertension due to?

A

Disease of the kidneys, adrenals, thyroid, diabetes

105
Q

What is malignant hypertension?

A

Pressure above 180/20, which risks damaging organs e.g kidneys (medical emergency)

106
Q

Hypertension causes and risk factors

A
  • Genetic — normotensive offspring of HTN parents often have ED impairment suggesting genetic link.
  • Obesity (especially ↑ abdominal adiposity) — activates the RAAS causing vasoconstriction and water retention.
  • Excess alcohol — ↓ the baroreceptor reflex (ability to respond to BP changes) by interacting with receptors in the brain stem; ↑ sympathetic outflow ↑ heart rate and BP; stimulates the ED to release vasoconstrictors, activates the RAAS.
  • Stress — ↑ SNS activity causing vasoconstriction. High cortisol ↑ the potent vasoconstrictor ET-1; activates the RAAS.
107
Q

Hypertension causes and risk factors (part 2)

A
  • Nutritional deficiencies — especially magnesium (vasodilates), potassium (↑ urinary excretion of sodium, ↓ blood volume).
  • High table salt intake and / or low potassium. Salt-sensitive HTN occurs in 50% of HTN individuals. Unrefined salts e.g., Celtic are preferable (contain trace minerals), however, moderate intake.
    • Inactivity— associated with higher HR, increased cardiac contractility and greater force on the arteries.
    • Smoking— damages endothelium; nicotine constricts blood vessels and increases heart rate.
    • Drugs — NSAIDs, corticosteroids, decongestants can ↑ BP.
108
Q

Why is raised uric acid a cause/risk factor of hypertension?

A

Stimulates the RAGE pathway, which increases NF-KB and disrupts eNOS
activity. It exacerbates endothelial
insulin resistance and lowers NO, whilst also upregulating genes that code for components of the RAAS (increasing BP).
Note: Hyperinsulinaemia also ↓urinary excretion of uric acid.

109
Q

Natural Approach to hypertension

A
  • Adapt the Natural Approach to CVD.
  • Increase potassium / sodium ratio >3:1:
  • Include fresh fruit and vegetables
  • Potassium increases natriuresis, encourages vasodilation, reduces sensitivity to angiotensin II and lowers SNS activity. Lowers NADPH oxidase, decreasing ROS in the vascular wall.
    • Avoid potassium supplements and take care with potassium intake in renal disease and with ACE inhibitors and K-sparing diuretics.
    • Restrict sodium intake to 1.5g / day.
110
Q

Why is the DASH diet good for hypertension?

A
  • Studies reveal significant systolic
    and diastolic BP reduction in hypertensive individuals following the DASH diet.
  • DASH consists of fresh vegetables
    and fruits, legumes, nuts, seeds, whole grains, fish, lean meat and low-fat dairy. - Limits saturated fats and salt. PUFA / MUFA are preferred. Sodium is restricted.

DASH = dietary approaches to stop hypertension

111
Q

ACE inhibitory peptides as a natural approach to hypertension

A

Naturally-occurring ACE inhibitory peptides can be found in certain plants and foods.

They act like a decoy, encouraging ACE to react with peptides, reducing vasoconstriction via angiotensin II.

Sources include spirulina, mushrooms, spinach, hemp seeds, walnuts and bitter melon seeds.

112
Q

Why is melatonin associated with anti-hypertensive effects?

A

through GABA stimulation, angiotensin-II inhibition and it increases NO.

113
Q

Nutrients for hypertension: Vitamin D function

A

• Deficiency of vitamin D leads to overexpression of renin, activating RAS— ↑ vasoconstriction and retention of sodium and water.
• ↓ proinflammatory cytokines, ↑ NO, ED function and arterial elasticity and ↓ hs-CRP.
• The lower the levels of vitamin D the greater the risk of hypertension.

114
Q

Nutrients for hypertension: Magnesium function

A

Deficiency is associated with hypertension (HTN). Alterations in intracellular and extracellular magnesium affects cardiac and vascular tone and reactivity.

Glycinate/taurate
500-800mg per day

115
Q

Nutrients for hypertension: L-arginine function

A

Arginine is the principle substrate for vascular NO synthesis.

• Modulates the RAS, inhibiting ACE activity, thereby decreasing angiotensin II and its downstream effects.
• Hypertensive patients display high hs-CRP, low apelin (stimulates NO in ED) and increased arginase (breaks down arginine).

1000-2000mg 3x daily

116
Q

Nutrients for hypertension: B6 function

A
  • B6 deficiency is associated with hypertension. It is an important co-factor (e.g. NA, adrenaline, serotonin). Increases cysteine synthesis, glutathione, blocks Ca
    channels and reduces SNS tone. Reduced with diuretics!
117
Q

Tissue salts for hypertension

A

6 x one pillule 4 times per day.
* Mag. phos. and / or Kali. phos. (may reduce systolic
and diastolic pressure) and Nat. sulph. (improves
urine output and thus helps reduce blood volume).
* Calc. fluor. ― to strengthen arterial walls, improve
elasticity and reduce arteriosclerosis.

118
Q

Herbal support for hypertension

A
  • The traditional ‘C.A.T.’ formula: Equal parts dried herbs infused, 1 cup 2–3 x daily.

– Crataegus spp. [hawthorn] (cardiotonic, hypotensive).
– Achillea millefolium [yarrow] (diuretic, hypotensive).
– Tilia europea [lime flower] (nervine relaxant, diuretic, anti-hyperlipidaemic).

119
Q

Stress management for hypertension

A

Essential because of the physiological
effects of the stress response on CV health.

– Diaphragmatic breathing: Shown to decrease systolic and diastolic BP, heart rate and anxiety, and promote a sense of relaxation in pre-hypertensive and hypertensive individuals.
– Earthing/grounding: (Walking barefoot on grass or sand) improves heart rate variability, lowers night-time cortisol and promotes a parasympathetic state.

120
Q

Define Atherosclerosis

A

Narrowing and hardening of large
and medium arteries, which reduces blood flow.

120
Q

Exercise for hypertension

A

Start gently and gradually ↑ CV fitness.

Aerobic exercise e.g., walking, swimming, cycling and jogging is recommended. Avoid exercise
that is very intense in short bursts e.g., sprinting, weightlifting.

121
Q

______ plays a central role in the formation of _____, a primary event in atherosclerosis.

  • Increased permeability facilitates entry of ___ into the ___. ___
    becomes ‘trapped’ within the vessel wall and is oxidised to ____
  • ___ recruit ___ expressing high levels of pro-inflammatory ___. Also trigger cytokine release from ED and ___ cells.
  • Macrophages imbibe lipoproteins to form ____. Cellular debris is incorporated and inflammation drives plaque formation.
  • A cap is formed over the plaque to wall off the plaque from blood.
A

Endothelial dysfunction
fatty streaks
LDL
intima
LDL
mLDL
mLDL
leukocytes
cytokines
VSMC
foam cells

122
Q

Aetiology of endothelial dysfunction (ED precedes atherosclerosis)

A

Disturbance to the protective glycocalyx layer and damage to ED cells. Factors include inflammation,
↑ oxidative stress, oxidised LDLs, hyperglycaemia, endotoxaemia, abnormal shear stress.

This leads to altered regulation of inflammatory cytokines, eicosanoids, and compounds that promote clotting risk.

Upregulation of chemo-attractant molecules promotes migration of phagocytic and inflammatory immune cells into blood vessels.

Disturbs NO metabolism ↑ hypertension risk > increases shear
stress worsening endothelial dysfunction > plaque development.

123
Q

Aetiology of inflammation (plays a critical role in the genesis, progression, and manifestation of atherosclerotic disease).

A
  • ED dysfunction, subintimal cholesterol accumulation and monocyte/ T-cell recruitment drive the inflammatory response.
  • Monocytes become resident macrophages in the sub-endothelial
    space and form ‘inflammasomes’ releasing inflammatory cytokines which activate IL-6 and stimulate CRP production, enhancing the inflammatory cascade in the vessel walls.
  • Inflammation thins the fibrous plaque cap > instability / rupture.
  • Pro-inflammatory cytokines differentiate VSMC into osteoblast-like cells increasing plaque calcification.
124
Q

Aetiology of dyslipidaemia (lipids are a fundamental component of atherosclerotic plaques).

A

Thus, dyslipidaemia is a significant risk factor and is marked by:
– ↑ total cholesterol — ↑ LDL, VLDL, IDL, Lp(a), ↓ HDL; ↑ TGs.

  • TGs are hydrophobic and must combine with lipoproteins to travel in
    plasma. In a similar manner to oxidised LDLs, TG-rich lipoproteins
    (e.g., VLDLs and VLDL remnants) are
    prone to endothelial accumulation and uptake by foam cells and are strongly linked with endothelial dysfunction.
  • High TGs are also linked with low HDLs.
125
Q

Promoting a healthy lipid profile in Atherosclerosis

A
  • Avoid high saturated fat to reduce risk of CV events.
  • Increase omega-3 FAs and MUFAs: E.g., avocado, unrefined olive oil. Regular EVOO consumption reduces LDL-C and oxidised LDLs, and improves post-prandial glycaemic profiles.
  • EVOO polyphenols oleocanthal and oleacein have antioxidant and anti-inflammatory effects (↓ markers including CRP and IL-6).
  • Red yeast rice (2400–4800 mg / day) ― contains monacolin K, an inhibitor of cholesterol synthesis via HMG CoA reductase.
  • Increase dietary fibre (30–35 g / day). Soluble fibre (vegetables, fruits, psyllium husk, pectin, gums) are associated with a decrease in TC and LDL-C.
  • Include dietary sources of beta-glucans (soluble + insoluble fibre)
    e.g., oats, mushrooms, seaweed, barley.
126
Q

Supporting endothelial health and vasodilation in Atherosclerosis

A
  • Hawthorn berries, bilberry, blueberries and blackcurrants are
    antioxidant and support blood vessel integrity and tone.
  • Lower ET-1 levels: Enhance citrus flavonoids, quercetin, epicatechins, garlic, olive oil, ginkgo, folate, and blackcurrant.
  • Beetroot contains inorganic nitrates that convert to NO in the body. Also ↓ homocysteine ― contains betaine
    which is utilised by the enzyme BHMT that re-methylates homocysteine to methionine.
  • L-theanine ↑ NO production in ED cells through eNOS phosphorylation (green tea is a key source).
  • Reduce homocysteine: B6, folate and B12 (supplement methylfolate and methylcobalamin supplementation), TMG (3 g twice daily).
  • Lower fibrinogen levels: High fibrinogen promotes atherosclerosis by increasing blood viscosity, stimulating fibrin formation and increasing platelet aggregation.
  • Mediterranean-style diets promote healthy levels. Garlic reduces fibrinogen, ↑ fibrinolytic activity (also ↓ atherogenicity of LDLs).
  • Mild to moderate exercise reduces fibrinogen levels.
127
Q

Promoting and supporting liver detoxification in Atherosclerosis

A
  • Ensure availability of all substrates required for detoxification pathways.
  • Poor liver function can increase circulation of inflammatory mediators, impede cholesterol
    metabolism and comprise essential fatty acid status.
  • Schisandra fruit supports liver function and is a powerful activator of phase I detoxification without increasing harmful bioactivation (antioxidant and hepatoprotective effects). Enhances phase II detoxification. Dose: 2–3 dried fruit
    infused twice daily. Dried berries can be eaten as a ‘superfood’.
128
Q

L-citrulline function Atherosclerosis

A
  • NO is synthesised from L-arginine by eNOS.
  • Arginase in intestinal enterocytes and first-pass metabolism (FPM) in the liver ↓ the availability of oral L-arginine supplementation. L-citrulline is not affected by arginase and skips FPM before conversion to arginine by
    argininosuccinate lyase in the kidneys, so is preferrable to enhance both arginine and NO bioavailability.
  • Renal arginine regulates BP, blocks the formation of endothelin, ↓ renal sodium reabsorption, and is a potent antioxidant.

500–3000 mg / day

129
Q

Pantothenic acid / pantetheine (B5) function Atherosclerosis

A
  • Metabolised to cystamine-SH. Reduces TC, LDL, Apo-B, TG and increases HDL over 4 months with a peak effect at 6 months.
  • Reduces lipid deposition, oxidation and fatty streak formation. Appears to be especially useful in lowering lipids in diabetic patients.

300 mg x 3 daily

130
Q

Niacin (B3) function Atherosclerosis

A
  • Niacin reduces TC, LDL, Apo-B,
    LDL-P, TGs and VLDL.
  • Also shown to decrease fibrinogen.
  • Note: Can cause niacin flush, and GI disturbance.

500–3000 mg daily

131
Q

Omega-3 function Atherosclerosis

A
  • Reduces TG, VLDL, LDL-P, and chylomicron remnants. Uniquely reduces Lp-PLA 2.
  • Anti-inflammatory, anti-thrombotic, lowers BP, heart rate and IR. PPAR-α agonist.
  • Reduces CVD progression and stabilises plaques.

3000–5000 mg / day.

132
Q

Pomegranate function Atherosclerosis

A
  • Improves HDL function, ↑ reverse cholesterol transport.
  • Potent antioxidant, ↓ oxLDL, and macrophage LDL uptake.
  • Decreases progression of carotid
    artery IMT (marker of atherosclerosis).
  • Reduces BP mostly in those with high oxidative stress.

250 ml of juice (pure) per day or 1–2 cups of seeds per day

133
Q

Pycogenol (pine bark extract) function Atherosclerosis

A
  • Flavonoid, antioxidant, anti-inflammatory, anti-thrombotic.
  • Enhances NO and ED function, and reduces BP and Hs-CRP.
  • ↓ myeloperoxidase ― an enzyme secreted from macrophages that ↑ oxidation of lipoproteins in atheroma.
  • Appears to reduce foam cell formation in atherosclerosis.

100–200 mg / day

134
Q

Lycopene function Atherosclerosis

A
  • Anti-oxidant. Suppresses intestinal
    cholesterol absorption. Lowers TC, LDL-C, inflammation and increases HDL-C.
  • Activates PPAR-γ.
  • Studies show a reduction in carotid atherosclerosis.

25 mg / day

135
Q

Citrus Bergamia function Atherosclerosis

A
  • Bergamot (citrus fruit): Natural source of flavonoids, e.g., naringin, hesperidin, neohesperidin and neoeriocitrin.
  • Lowers LDL and TGs. Increases PPAR activation.
  • Reduces ROS, oxidised LDL, balances blood glucose and reduces weight.
  • Improves serum glucose via AMPK and GLUT 4 receptor.

500-1000 mg/ day.

136
Q

Globe artichoke function Atherosclerosis

A
  • Reduces serum LDL, TC and TGs.
  • Regulates lipid metabolism, increases bile production, is antioxidant and hepatoprotective.

Dietary + 1–2 g / day powdered

137
Q

Other therapies for Atherosclerosis

A
  • Sauna: ↑ circulation and arterial vasodilation. Avoid in unstable angina / recent MI and hypertension.
  • Dry skin brushing: Supports circulation and lymphatic function, increases toxin elimination.
  • Contrast hydrotherapy (alternating warm / cold water): improves circulation and supports removal
    of toxins. If circulation is compromised end on warm.
  • Tai Chi Chuan, yoga and acupuncture have shown to reduce ET-1 (endothelin) levels.
138
Q

Ischaemic Heart Disease (IHD)

A

An imbalance between myocardial oxygen supply and demand, is associated with inadequate arterial supply via the coronary arteries.

IHD is commonly caused by atherosclerosis.

IHD syndromes include angina (stable and unstable) and myocardial infarction.

139
Q

Ischaemic Heart Disease (IHD)
___ and inappropriate ___ reduce blood vessel lumen size and coronary blood flow. When oxygen demand __ oxygen
supply, ______, ______, and ____ ensues.

A

Atheroma
vasoconstriction
exceeds
myocardial hypoxia
accumulation of waste metabolites
ischaemia

140
Q

Angina

A

chest pain caused by an insufficient supply of oxygenated blood supply to the myocardium by the coronary arteries.

141
Q

Define stable angina & the signs and symptoms

A

Predictable transient chest pain
during exertion or emotional stress. Ischaemia with symptoms resolves once oxygen balance is restored.

Constricting chest pain (can radiate to the neck, L shoulder / arm and jaw), worsened by exertion, relieved by rest. SOB, sweating, nausea.

142
Q

Unstable angina

A

Unpredictable / occurs at rest.
Plaque disruption initiates platelet aggregation, thrombus formation, and vasoconstriction. May be a precursor to acute MI.

143
Q

Causes / risk factors of Angina

A
  • Cigarette smoking ― linked to endothelial dysfunction, CAS, vessel wall injury, oxidative stress, elevates fibrinogen, platelet activation, and inflammation. Smoking cessation
    in angina can prevent recurrent angina events.
  • Vitamin D deficiency ― significant correlation between vitamin D deficiency and chronic angina. Improves endothelial function by signalling for the transcription of eNOS; modulates the RAAS to lower BP.
  • Family history of premature IHD is a strong risk factor for angina.
144
Q

Orthodox diagnosis and allopathic approach to Angina

A
  • Orthodox diagnosis: ECG, cardiac
    stress testing, angiography (see image).
  • Allopathic approach: Nitrates
    (e.g., GTN), calcium channel blockers
    (e.g., amlodipine), beta-blockers
    (e.g., atenolol), revascularisation
    (angioplasty, stents and coronary
    artery bypass graft surgery).
145
Q

Myocardial Infarction (MI)

A

An acute blockage of a coronary artery usually due to a thrombus, resulting in the death of myocardial tissue.

  • Prolonged ischaemia leads to myocardial necrosis. Ischaemic myocardial cells release adenosine and lactate onto nerve endings causing pain.
  • Infarcted areas produce scar tissue. The remaining tissue hypertrophies and can result in cardiac dysfunction and heart failure.
  • Divided into:
    – ST-Segment Elevation MI (STEMI) = full occlusion (severe).
    – Non-ST-Elevation MI (NSTEMI) = partial occlusion.
146
Q

Myocardial Infarction (MI) causes and risk factors

A
  • Sex: Males ~ 3 times more likely to experience MI. High androgen levels contribute to the development of atherosclerosis.
  • Psychosocial factors: Stress (e.g., financial). Loss of locus of control, sudden life events (e.g., job loss, marital separation) increase MI risk.
  • Others: Drug-induced (cocaine), significant myocardial O2 demand (e.g., severe hypertension) or reduced O2 supply (e.g., severe anaemia), vasculitis syndromes (e.g., temporal arteritis).
147
Q

Myocardial Infarction (MI) signs and symptoms

A

Severe prolonged crushing retrosternal chest pain. Pain radiates to the left shoulder, jaw / neck or arms. Sweating, cool / clammy skin. Feeling of ‘impending doom’. Dyspnoea and syncope. Nausea, vomiting, weakness.

148
Q

Myocardial Infarction (MI):

Complications
Diagnosis
Allopathic approach

A

Complications: Arrhythmias, heart failure, cardiogenic shock, death.
* Diagnosis: ECG findings.
* Allopathic approach: Fibrinolysis, O2 therapy, morphine, nitrates, beta blockers, aspirin for acute management.

149
Q

Natural approach to Ischaemic Heart Disease

A
  • Apply the natural approach to CVD, with a focus on supporting myocardial blood flow.
  • Optimise vitamin D status - supports endothelial health and promotes vasodilation (increased nitric oxide).
  • Warming herbs/spices to support blood flow (ginger, cayenne).
  • Increasing movement - care is needed to avoid triggering angina attacks. Gentle exercise (Tai Chi, walking).
  • Address stress - breathing, nervine herbs (passionflower).
150
Q

L-carnitine function for IHD

A

Improves FA utilisation and myocardial ATP production,
which may also prevent the production of toxic FA
metabolites. These would normally impact cardiac
cell membranes = impaired myocardial contractility.

1000 mg 2x daily

151
Q

Magnesium function for IHD

A

Magnesium deficiency has been shown to produce
coronary artery spasms. Magnesium controls the
movement of calcium into smooth muscle cells, leading
to smooth muscle contraction. Deficiency also ↑ ROS.

200-400 mg 3x daily

152
Q

Hawthorn function for IHD

A

Its flavonoids have been shown to inhibit the enzyme 3’,5’-cyclic-AMP, which is thought to be
responsible for dilating the coronary arteries.

1000-1500 mg

153
Q

CoQ10 function for IHD

A
  • Increases eNOS and NO, improves ED function and
    vascular elasticity.
  • Exerts anti-inflammatory effects – lowers TNF-α and IL-6.
    NF-κB can be inhibited by CoQ10’s anti-oxidant activity.

100-300 (if on statins) mg daily

154
Q

L-arginine function for IHD

A
  • Promotes vasodilation by increasing NO.
  • Increases SOD levels, reduces lipid peroxidation and xanthine oxidase activity (reducing uric
    acid formation); uric acid stimulates RAGE.

1000-2000 mg 3x daily

155
Q

Ginkgo biloba function for IHD

A
  • Enhances microcirculation and tissue perfusion (antagonises ‘platelet activating
    factor’ by blocking receptors). Scavenges ROS.

60-120mg daily

156
Q

Heat failure definition

A

A syndrome in which the heart is impaired as a pump ― failing to supply sufficient blood flow.

157
Q

Signs & symptoms of heart failure

A
  • Breathlessness (on exertion, at rest, orthopnoea),
  • Nocturnal dyspnoea
  • Fluid retention (e.g., ankle
    oedema, abdominal swelling). - Fatigue
  • Exercise intolerance
  • Lightheadedness
  • Syncope
  • Tachycardia.
158
Q

Heart failure complications & allopathic approach

A
  • Complications: Atrial fibrillation, ventricular arrhythmias, CKD, sudden cardiac death.
  • Allopathic approach: Digoxin (a synthetic form of digitoxin, from
    Digitalis purpurea (foxglove) that increases the force of myocardial contraction), diuretics, calcium channel blockers, ACE-inhibitors.
159
Q

Heart failure causes/risk factors

A
  • Results from various CV conditions ― e.g., IHD (most common cause), hypertension, AF, cardiomyopathy, LVF, pulmonary hypertension, heart valve abnormalities.
    – See earlier risk factors, e.g., smoking (leads to LV hypertrophy and systolic dysfunction); raised homocysteine; sedentary etc.
  • Co-morbidities ― e.g., CKD,
    anaemia, T2DM, thyrotoxicosis, hypothyroidism, COPD
    all impair functional status and prognosis of HF.
    – CKD causes a chronic proinflammatory state that can
    result in atherosclerotic lesions and myocardial fibrosis.
  • IR ― IR ↓ myocardial glucose utilisation and ↑ FFA oxidation,
    ↑ myocardial oxygen consumption and the generation of ROS. This impairs cardiac contractibility by changing sarcoplasmic reticular calcium stores and ↑ mitochondrial dysfunction.
  • Obesity ― alters cardiac structure, promotes endothelial
    dysfunction, contributes to IR and ↑ inflammatory cytokines.
  • Nutrient deficiencies ― CoQ10 (normally ↓ ROS and ↑ NO), vitamin D (normally ↓ inflammatory cytokines and ↑ calcium absorption etc.),
    B1 (common in HF due to chronic alcohol ingestion; normally acts as a coenzyme for glucose metabolism). Also vitamin B2, folate, B12,
    Ca, Cu, Mg, Mn, K, Se, Fe — needed for normal cardiac metabolism.
160
Q

Natural Approach to HF

A

Apply the Natural Approach to CVD, with a focus on supporting myocardial energy production. Key considerations:
* Lower CVD risk factors — follow previous naturopathic approaches e.g., hypertension.
Consider approaches for obesity, IR and T2DM.

  • Correct nutrient deficiencies
    — correct identified anaemias. Consider a high-quality multivitamin / mineral formula. Correct

K:Na ratio. Work to achieve ideal body weight.

  • Encourage smoking cessation where applicable.
161
Q

CoQ10 function for heart failure

A

Cardiac myocytes contain >3500 mitochondria / cell and require the highest levels of ATP activity. CoQ10 is essential in the ETC and is a powerful antioxidant.
CoQ10 depletion is associated with worse HF outcomes.

300-400mg daily

162
Q

D-ribose function for heart failure

A

Has been shown to regenerate low myocardial ATP with an accompanying improvement in ventricular function following ischaemia. Symptom improvements (e.g., fatigue) in chronic HF have been observed.

5-15g daily

163
Q

Magnesium function for heart failure

A

Critical for ATP. When deficient increases RAAS (increasing
BP), predisposes to low K and may worsen cardiac contractility, increase vasoconstriction and deplete cardiac energy stores.

400-800mg daily (citrate)

164
Q

Thiamine for heart failure

A

Thiamine is a required coenzyme in energy-producing
reactions — fuelling myocardial contraction. Note: CVD drugs e.g., diuretics cause a B1 deficiency.

100-200mg daily

165
Q

L-carnitine for heart failure

A

Facilitates the transfer of fatty acids across mitochondrial membranes to initiate beta-oxidation. The heart uses free fatty acids as its main energy source!

2000-3000mg daily

166
Q

Hawthorn for heart failure

A

Benefits have been observed in cases of chronic heart failure. This is attributed to hawthorn’s vasodilatory effects on the coronary arteries and potent
antioxidant properties. Increases NO.

1000-1500mg daily

167
Q

Varicose veins

A

Dilated / distorted superficial veins in the lower limbs where the pressure is higher due to gravity.

  • Signs and symptoms: Visible vein dilation; aching, burning, throbbing, heaviness. Worse
    for prolonged standing and at the end of the day.
  • Complications: ↑ venous pressure = fluid leakage into surrounding tissues (‘varicose
    eczema’). Slow healing varicose ulcers.
168
Q

Haemorrhoids

A

Dilated veins in the anal canal. Internal or external.

  • Signs and symptoms: Bright red blood with blood movements, protruding haemorrhoids, anal itching.
169
Q

Varicose Veins / Haemorrhoids causes/risk factors (part 1)

A
  • Increased abdominal pressure ― constipation, obesity,
    pregnancy, childbirth and post-labour, ascites.
  • Inherited valve defects ― an absence of some valves or faulty valves.
  • Cigarette smoking (= hypoxia, which results in endothelial
    damage, vessel wall inflammation and a loss of elasticity).
  • Being sedentary (increasing venous pressure).
  • Lack of dietary connective tissue support, e.g., low vitamin C (increases type I collagen synthesis), low bioflavonoids (support connective tissue integrity).
170
Q

Varicose Veins / Haemorrhoids causes/risk factors (part 2)

A
  • Portal hypertension ― increased portal vein pressure e.g., due to liver cirrhosis and heart failure.
  • Increased blood viscosity and stagnation ― dehydration,
    liver congestion, sedentary lifestyle. Additional signs /
    symptoms: haemorrhoids, post-food fatigue, purple tongue, thick white / yellow tongue coating.
  • Abdominal bloating (not obesity) ― distended
    and uncomfortable. E.g., associated with SIBO.
  • Structural ― e.g., poor diaphragm motion (consider causes such as stress, asthma etc.), weak pelvic floor (consider pregnancy).
171
Q

Varicose Veins / Haemorrhoids natural approach (part 1)

A

CNM Naturopathic Diet. Reduce inflammation, increase blood flow and speed up repair of damaged veins / valves. Correct root causes!

  • Vitamin C-rich foods (to support collagen synthesis).
  • Bioflavonoids such as rutin, proanthocyanidins and
    anthocyanins which improve the integrity of ground substance and the vascular system, whilst also acting as antioxidants. Food source examples: buckwheat (highest source of rutin) grapes,
    apples, cranberry, blueberry, figs, blackcurrants, capers, asparagus, green tea.
172
Q

Varicose Veins / Haemorrhoids natural approach (part 2)

A
  • Enhance fibrinolytic activity — garlic, onions, ginger, cayenne.
    Include bromelain sources to increase plasminogen activator status.
  • Optimise liver function — alleviate downward pressure. Fibre-rich plant foods: Reduce venous pressure with defecation. Ground
    flaxseed, or psyllium husk (15–30 g / day).
  • Raise feet above heart (20 mins / day) — reduces blood pooling and improves venous return.
  • Lymphatic drainage / massage — for mild cases only — aids
    circulation and avoids blood pooling. Consider dry brushing.
  • Reduce weight: Address cause and exercise!
  • Tissue salts — calc. fluor. (tissue strengthening).
    If bleeding add ferrum. phos. 4 pills x 3 daily.
  • Topical application of astringent herbs: Horse
    chestnut, witch hazel,
    yarrow.
  • For haemorrhoids: Sitz
    Bath (a shallow hip bath) with a small amount of Mg salts or a strong cup of cooled chamomile tea. Soak for 10‒15 minutes
173
Q

Vitamin C with bioflavonoids for VV/Haemorrhoids

A

Support connective tissue integrity ― increases collagen synthesis and ground substance integrity.

1.5-2g through the day

174
Q

Horse chestnut for VV/Haemorrhoids

A
  • An astringent herb that ↑ venous tone by ↑ the production of prostaglandin F2, which regulates the contractile action of veins, and inhibits the
    catabolism of venous tissue mucopolysaccharides. Also likely through its effects on 5-HT2A receptors.
  • Inhibits enzymes that destroy
    venous structures, e.g., collagenase, hyaluronidase, and elastase.

400 mg (seed) daily or 15 drops of tincture 3 x daily between meals, for 3 months. Topically as a balm. Avoid raw seed, bark, flower or leaf.

175
Q

Gotu kola for VV/Haemorrhoids

A
  • Contains triterpenic acids that are thought to be responsible for its supportive effects on connective tissue.
  • Stimulates glycosaminoglycan and collagen synthesis, which supports vein structure and improves blood flow.

500mg 2x daily. Avoid in liver disease.

176
Q

Butcher’s broom for VV/Haemorrhoids

A

Vasoconstrictive and astringent (its ruscogenin content has anti-elastase activity, which ↓ the diameter of veins).

300-500mg 2x daily

177
Q

Pycnogenol for VV/Haemorrhoids

A

Contains proanthocyanidins and has collagen stabilising properties. Decreases passive dilation and stretching and gives vein walls a greater tonic recovery and elasticity.

150-300mg daily

178
Q

Homeopathy for VV/Haemorrhoids

A
  • Hamemelis 3 x ― varicose veins are large, sore and easily irritated and stinging. Bleed very easily.
  • Aesculus 3 x ― haemorrhoids are congested and purple. Pain in the rectum feels “as if the
    rectum were full of sticks”. Pain radiates to the small of the back and hips. Sharp, shooting pain upwards from the rectum.
  • Nux. vomica 6C ― haemorrhoids that are better for warmth and better for passing stool. History of
    overindulgence in alcohol, coffee, other stimulants, etc.
179
Q

TCM and VV/Haemorrhoids

A

In TCM, it is associated with Blood stagnation (consistent with the Western understanding of poor blood circulation), but also a weak digestive system (Spleen Qi deficiency). The Spleen is said to produce Blood, govern smooth muscle and hold Blood in the vessels.

  • Support Spleen Qi (Nutrition year 1).
  • A tea with equal parts cinnamon, ginger, and tangerine peel stimulates Qi and blood circulation.
  • Resolve Blood stasis by reducing stress and exercising frequently.
  • Include foods that disperse stagnant blood, e.g., chives, leeks.
  • Include blood-nourishing dark leafy greens, beetroot.

CNM NUTRITION 2 S2 (10 decks)

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