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Nutrition 2 - Sem 2 Exam > 11. Cardiovascular Health > Flashcards

11. Cardiovascular Health Flashcards

1
Q

What is Cardiovascular disease?

A

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

How much of premature CVD is preventable?

A

75%

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3
Q

What can increase CVD risk?

A
  • Unhealthy dietary patterns (high intake of processed foods, sugar, salt, unhealthy fats, alcohol)
  • Lack of exercise
  • Excess body fat
  • Stress
  • Smoking
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4
Q

What is the Endothelium?

A

A monolayer of endothelial cells lining the blood interface throughout the CVS including cardiac chambers.

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5
Q

What is the Glycocalyx (GX)?

A

carbohydrate-rich protective layer covering the ED

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6
Q

What are the 3 functions of the glycocalyx?

A
  1. regulates permeability
  2. controls NO production
  3. acts as a mechanosensor of blood shear stress (Frictional force of blood on ED cells).
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7
Q

What can damage the Glycocalyx x5?

A

inflammation
hyperglycaemia
endotoxemia
oxidised low-density lipoproteins
abnormal blood shear stress.

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8
Q

What are the consequences of a damaged GX?

A

Commonly precedes further damage to the ED and promotes lipid deposition and atherosclerosis

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9
Q

What are the Vascular smooth muscle cells (VSMCs) (location and role?)

A

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

With the ED, VSMCs maintain the integrity and elasticity of blood vessels whilst limiting immune cell infiltration.

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10
Q

Key functions of the endothelium x6

A
  1. Semi-permeable barrier: Role in fluid balance, host defence and selective movement of substances e.g., glucose and oxygen.
  2. Regulates vascular tone: Secretes vasodilators (e.g., NO) and vasoconstrictors (e.g., endothelin).
  3. Enzymes: Contains angiotensin-converting enzyme (ACE) ― plays a key role in regulating blood pressure.
  4. Angiogenesis: ED cells are the origin of all new blood vessels.
  5. Haemostasis: The luminal surface of ED prevents platelet adherence and coagulation (non-thrombotic, anticoagulant).
  6. Immune defence: Healthy ED cells deflect leukocyte adhesion and oppose local inflammation.
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11
Q

What causes phenotypic modulation, altering cell structure and function to the VSMC ? and What diseases they cause?

A

inflammation, oxidative stress, telomere damage

changes are central to vascular disease, especially atherosclerosis and hypertension.

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12
Q

What is a phenotype modulation?

A

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

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13
Q

What is the role of NO in CV health?

A
  1. regulates vascular tone
  2. reduces platelet aggregation and VSMC proliferation
  3. inhibits leukocyte adhesion and inflammatory cytokines
  4. opposes oxidation of LDLs
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14
Q

From what amino acid is NO generated and by which enzyme?

A

generated from L-arginine by the ED enzyme eNOS

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15
Q

What molecule found in the diet can help us get NO via which mechanism? What is a good source?

A

Nitrates - in the oral microbiome helps to take the nitrates from food and convert that to nitrites in the body then into NO

Beetroots

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16
Q

what vitamin regulates NO synthesis by mediating eNOS?

A

Vitamin D

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17
Q

Reduction of NO contributes to what?

A

atheroma (atherosclerotic plaques) formation and drive the development of CVD.

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18
Q

What is the impact of oxidative stress and inflammation on the endothelial cells?

A
  • ↑ permeability, inflammatory cytokines and leukocyte adhesion.
  • Reduced vasodilator (NO, prostacyclin) molecules.
  • Increased risk of thrombosis.
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19
Q

What is the impact of oxidative stress and inflammation on VSMC?

A
  • Increased inflammatory cytokines and extracellular matrix synthesis.
  • Migration into the tunica intima and proliferation of VSMCs.
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20
Q

What is the Peroxisome proliferator-activated receptor (PPARs) ?

A

nuclear transcription factors that control gene expression involved in adipogenesis, lipid and glucose metabolism, cellular proliferation and apoptosis

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21
Q

What is the function of the PPARs

A

decrease inflammation and promote ED health

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22
Q

What PPARα activation does?

A

↑ HDL-C, ↓TGs (triglycerides) and inflammation and is anti-atherosclerotic

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23
Q

What are PPARα agonist foods?

A
  1. green tea
  2. resveratrol (up to 50 mg)
  3. dietary inclusion of oregano, thyme and rosemary
  4. naringenin (part of citrus bioflavonoid up to 100mg/day)
  5. omega-3 (up to 3 g).
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24
Q

What does PPAR-γ activation does?

A

PPAR-γ reduces blood glucose, fatty acids and insulin (enhance insulin sensitivity when activated).

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25
Q

What are PPAR-γ agonist foods?

A
  1. Apigenin (celery juice and parsley)
  2. Hesperidin
  3. curcumin (add pepper)
  4. resveratrol (red grapes, supplement)
  5. EGCG (polyphenol from green tea).
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26
Q

Non-modifiable CVD risk factors x7

A
  1. Family history: Siblings of CVD patients = 40% risk increase. Offspring of parents with premature CVD = 60–75% risk increase.
  2. Genetics: MnSOD, NOS3, MTHFR and ACE gene polymorphisms.
  3. Ethnicity: Individuals of South Asian or sub-Saharan African origin have an enhanced risk of CVD.
  4. Gender: Common view that CVD is predominantly a male pathology. CVD mortality in women (35–54) is increasing. Risk is underestimated as women tend to experience more vague physical signs e.g., lightheaded with exertion and symptoms can be mistaken for the menopause or heartburn.
  5. Dyslipidaemia: ↑ total cholesterol ― ↑ LDL, VLDL, IDL, Lp(a) (better measure than LDL of CVD risks), ↓ HDL (take cholesterol back from our body cells to the liver for breakdown); ↑ triglycerides.
  6. Hypertension: CVD pathologies tend to appear 5 years earlier in those with hypertension.
  7. Mitochondrial dysfunction: 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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27
Q

Why is dyslipidaemia largely preventable?

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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28
Q

Modifiable CVD risk factors x4

A
  1. Elevated Homocysteine: Associated with LDL oxidation, monocyte adhesion and ED dysfunction.
  2. Obesity: Excess adipose tissue perpetuates inflammation contributing to vascular breakdown and metabolic complications.
  3. Insuline resistance: Generates chronic hyperglycaemia leading to oxidative stress, inflammation and cellular damage.
  4. Advanced glycation end products (AGEs): Harmful compounds formed when protein or lipids becomes glycated after exposure to glucose.
    • Smoking: ↑ oxidative stress (ROS react with NO to form harmful peroxynitrite) and lowers antioxidants (1 cigarette = 25 mg loss of vitamin C). Nicotine over-stimulates SNS and increases BP.
  6. Sedentary lifestyle: Exercise has a positive effect on lipid profile and blood pressure and ↑ insulin sensitivity and NO production. Brisk walking 30 mins / day can protect against CVD mortality.
  7. Chronic stress: May cause ED dysfunction especially in the presence of 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.
  8. Periodontal disease — ↑ systemic inflammation (↑ TNF, IL-1, IL-6, CRP) which impair vasodilation. Promotes endothelial dysfunction, arterial stiffness and ↑ fibrinogen (plaque formation).
  9. Heavy metals — induce oxidative stress, lipid peroxidation and inflammatory cytokines. Cadmium and lead compete with zinc. A zinc deficiency increases atherosclerosis risk.
  10. Melatonin deficiency — melatonin is a potent antioxidant with anti- hypertensive properties. It protects against coronary artery disease.
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29
Q

What factors increase levels of homocysteine?

A
  1. Low folate and B12 — needed for the re-methylation of homocysteine to methionine; vitamin B6 — a co-factor in the conversion of homocysteine to cysteine in the methylation cycle.
  2. Genetic polymorphisms: MTHFR impacts supply of methyl groups needed to methylate B12 in the methionine cycle (in turn methylates homocysteine); FUT2, TCN impact B12 (all forms) absorption. MTR, MTRR impact B12 activation (application of a methyl group).
  3. The other route for methylating homocysteine is dependent on choline (PEMT and CHDH genes) and betaine (BHMT gene).
  4. Thyroid hormones (TH): TH 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.
  5. 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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30
Q

How obesity increase risk of CVD?

A
  1. Inflammation is linked with ↑ endothelin-1 (ET-1), a potent vasoconstrictor peptide. Elevated ET-1 leads to fibrosis of VSMCs and ↑ ROS.
  2. Adiponectin, a peptide that influences expression of ED cells, protecting against CVD, is decreased in obesity.
  3. Adiponectin also ↑ insulin sensitivity, thus low levels contribute to insulin resistance (IR).
  4. Obesity is associated with high levels of leptin, which activates the SNS causing sodium retention, vasoconstriction & ↑ blood pressure
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31
Q

How insulin resistance increase CVD risk?

A
  • IR contributes to the lipid triad (high plasma TGs, low HDL, small dense LDLs) and dyslipidaemia.
  • Dyslipidaemia along with ED damage (due to dysfunctional insulin signalling) leads to atherosclerotic plaque formation.
  • IR means that glucose is not cleared from the bloodstream as quickly as needed, increasing the risk of glycosylation reactions and the production of damaging compounds — advanced glycation end products (AGEs)..
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32
Q

How Advanced glycation end products (AGEs) increase risk of CVD? x2

A
  1. Receptor-mediated: Bind to the cell receptor RAGE (ED, VSMCs and immune cells) increasing inflammatory cytokines and ROS via activation of NADPH oxidase (an enzyme that increases ROS) which activates NF-kB.
  2. Non-receptor mediated: Increased EC matrix synthesis, trapping ED LDL and cross binding with collagen (vascular stiffening).
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33
Q

What triggers AGEs?

A
  • AGEs increase with advancing age. Renal accumulation of AGEs promotes kidney dysfunction.
  • Polymorphisms of the AGER gene (encodes RAGE) can ↑ disease risk.
  • Diet (exogenous AGEs) contribute to overall AGE pool: High refined carbohydrates (sucrose, HFD), processed foods, meat and dairy.
  • Cooking methods: High heat, grilling, roasting, searing / frying promote AGE formation.
  • Smoking and sedentary lifestyles enhance AGE accumulation.
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34
Q

Explain the gut microbiome and CVD risk

A
  • SCFAs produced by the microbiota, ↓ risk of metabolic endotoxaemia (a key risk factor for CVD and IR) by maintaining intestinal barrier integrity. SCFAs reduce serum lipids by inhibiting cholesterol synthesis or redirecting lipids to the liver.
  • The gut microbiota play a role in cholesterol regulation by altering bile acids that influence systemic cholesterol levels.
  • Alterations in the gut microbiota can lead to an increase in harmful metabolites such as trimethylamine-N-oxide (TMAO). TMAO is associated with endothelial dysfunction and increased risk of CVD.
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35
Q

What are TMAO?

A

TMAO = a proinflammatory metabolite that originates from the bacterial metabolism of choline-rich foods

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36
Q

What are dietary considerations that increase risk of CVD?

A
  • High PRAL — foods rich in protein (e.g., meat, cheese) may induce low-grade metabolic acidosis, a risk factor for IR and CVD.
  • Trans fats — promote dyslipidaemia (↑ LDL-C, TGLs, ↓ HDL-C), increase inflammation, contribute to ED dysfunction,
    encourage visceral adiposity and increase risk of IR.
  • Fructose — high fructose intake promotes de novo lipogenesis, ↑ fatty acids, in particular palmitic acid.
    Palmitic acid ↑ expression of the receptor involved in the uptake of oxidised LDLs and is a major driver of atherosclerosis and CAD.
  • Nutrient deficiencies (e.g., vitamin C, D, E, CoQ10, Mg). See therapeutics.
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37
Q

What is PRAL?

A

Potential Renal Acid Load = measure potential acidity of a diet

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38
Q

What are the main CV markers ?

A
  • Cardiac risk tools (e.g., QRISK ®): calculate score based on CV risks e.g., age, BMI, smoking. QRISK score 10% = 1 in 10 chance of developing CVD in next ten years.
  • Cardiac troponin: Cardiac troponin proteins hs-cTnT and hs-cTnI are released into the blood when heart muscle is damaged
    e.g., MI. Often measured alongside an ECG (electrocardiogram).
  • Lipid profile: TC (total cholesterol), non-HDL, TG and LDL-C, TC:HDL ratio.
  • Lp-PLA 2: Enzyme produced by monocytes, macrophages, T-cells. Upregulated in atherosclerotic plaques and vascular inflammation.
  • hsCRP: Inhibits NO and e-NOS and is involved in plaque deposition. Low risk: < 1.0 mg / L. High risk: > 3.0 mg / L.
  • MPO: 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. Exacerbated by high BP, obesity and smoking. Low=<470 pmol/L, high ≥ 540 pmol/L.
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39
Q

What are the 3 recommended diet for CVD?

A
  • Adopt the principles of the CNM Naturopathic Diet.
  • Plant-based and Mediterranean-style diets are associated with significantly reduced CVD risk showing: ↓ inflammatory mediators, ROS and RNS; reduced adiposity (especially visceral) and risk of thrombosis; ↑ SCFA production, improved insulin sensitivity, ↑ adiponectin and improved ED function.
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40
Q

Key nutrient for CVD - Vitamin D - functions x3 and dose?

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

500–1000 mg 3 x daily

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41
Q

Key nutrient for CVD - Vitamin E - functions x3 and dose?

A
  1. Mixed tocotrienols and tocopherols — along with vitamin C protects the endothelium from ROS and supports NO synthesis.
  2. ↓ oxidation of LDL-C and deposition in arterial walls.
  3. Inhibits platelet aggregation and ↓ clotting factors to support healthy blood viscosity.

Vitamin E 400–800 iu / day

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42
Q

Key nutrient for CVD - Vitamin D - functions x2 and dose?

A
  1. Modulates NO synthesis and influences cells involved in atherogenesis e.g., ED, VSMCs, monocytes and cardiac myocytes.
  2. Modulates RAAS and lowers BP.

Vitamin D - 600–1000 iu / day

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43
Q

Key nutrient for CVD - Omega 3 - functions x4 and dose?

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

3–6 g / day

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44
Q

Key nutrient for CVD - Magnesium Glycinate / taurate - functions x2 and dose?

A
  1. Through regulation of ion transporters e.g., potassium and calcium channels, plays a central role in modulating neuronal excitation, intracardiac conduction and myocardial contraction.
  2. Helps regulate vascular tone and stabilise heart rhythm.

500–800 mg / day

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45
Q

Key nutrient for CVD - CoQ10 - functions x3 and dose?

A
  1. Protects against endothelial dysfunction and reduces LDL oxidation (↓ atherosclerosis risk).
  2. Increases superoxide dismutase activity, which preserves the activity of NO (↓ risk of high BP).
  3. Supports mitochondrial health and production of ATP.

60–300 mg / day

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46
Q

Key herb for CVD - Hawthorn - functions x3 and dose?

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

1,000–1,500 mg

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47
Q

Key herb for CVD - Garlic - functions x5 and dose?

A
  1. Antihypertensive effects by stimulating NO production in ED cells. Lowers homocysteine↓ CVD risk.
  2. Decreases arterial calcification (stiffness).
  3. Reduces LDL cholesterol and LDL oxidation.
  4. Enhances glutathione and SOD.
  5. Protects against abnormal platelet aggregation.

2–5 g fresh bulb /day

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48
Q

How exercise help with CVD?

A

Exercise: regular physical activity and exercise significantly reduces CVD risk and is associated with a reduction in all-cause mortality.
– Leads to a more favourable lipoprotein profile; ↓ 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).

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49
Q

How to help with stress management for CVD?

A

Stress management: Encourage diaphragmatic breathing exercises, humming, singing to promote parasympathetic activity. Include herbal teas to relieve stress e.g., chamomile, passionflower, lemon balm, lime flower tea.

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50
Q

What CVD drugs can add to nutrient depletion in CVD? x5

A
  1. Statins: Block HMG CoA-reductase ↓ coenzyme Q10 synthesis.
  2. Cholestyramine (↓ cholesterol): A bile acid sequestrant. ↓ absorption of fat-soluble vitamins and beta-carotene.
  3. Loop and thiazide diuretics: ↑ potassium, calcium, thiamine and zinc (thiazide) excretion.
  4. ACE inhibitors: Bind with zinc preventing utilisation by the body.
  5. Beta-blockers: ↓ melatonin production by inhibiting adrenergic beta1 receptors; block the biological pathway of CoQ10-dependent enzymes.
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51
Q

What is hypertension, how is BP expressed?

A

Hypertension (HTN) = a leading contributor to CVD.
* Blood pressure (BP) reflects the force of circulating blood against the walls of the arteries (CO + total PR).
* It is expressed as a ratio of systolic BP (the pressure blood exerts on arterial walls when the heart contracts) and diastolic BP (pressure when the heart relaxes).
* In the UK, HTN is currently defined as 140/90 mmHg or higher.

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52
Q

What are the signs and symptoms of HBP?

A

Fatigue, headache, dizziness, visual disturbance. However, is often asymptomatic, hence BP testing is standard practice. HTN can ↓ life expectancy by 5 years.

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53
Q

What is essential vs secondary hypertension? What is malignant hypertension?

A
  • Essential [or primary] (95%) ― no specific underlying medical cause. Drivers include vascular resistance (due to vasoconstriction, atherosclerosis, loss of blood vessel elasticity, increased blood viscosity), obesity, stress and anxiety, smoking, high salt intake.
  • Secondary hypertension (5%) ― due to diseases of the kidneys, adrenals, thyroid, diabetes.
  • Malignant hypertension is pressure above 180/120, which risks damaging organs, e.g., kidneys (medical emergency).
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54
Q

Causes and risk factors for HBP/Hypertension? x10

A
  1. Genetic — normotensive offspring of HTN parents often have ED impairment suggesting a genetic link.
  2. Obesity (especially ↑ abdominal adiposity) — activates the RAAS causing vasoconstriction and water retention.
  3. 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.
  4. Stress — ↑ SNS activity causing vasoconstriction. High cortisol ↑ the potent vasoconstrictor ET-1; activates the RAAS (RAAS = renin angiotensin aldosterone system).
  5. Nutritional deficiencies — especially magnesium (vasodilates), potassium (↑ urinary excretion of sodium, ↓ blood volume).
  6. 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.
  7. Inactivity — associated with higher HR, increased cardiac contractility and greater force on the arteries.
  8. Smoking — damages endothelium; nicotine constricts blood vessels and increases heart rate.
  9. Drugs — NSAIDs, corticosteroids, decongestants can ↑ BP.
    *10. Raised uric acid — 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).
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55
Q

What are the natural approach to hypertension ? x5

A
  1. Increase potassium / sodium ratio >3:1
  2. DASH Diet (dietary approach to stop hypertension)
  3. ACE inhibitory peptides
  4. Optimise sleep (see previous lectures) — melatonin is associated with anti-hypertensive effects through GABA stimulation, angiotensin-II inhibition and increases in NO.
  5. Optimise weight; include aerobic and resistance exercise; stress management; support PSNS (Vagal) activity — see earlier lectures.
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56
Q

How to increase potassium / sodium ratio >3:1 for hypertension?

A
  1. Include fresh fruit and vegetables (high potassium / sodium ratio).
  2. Potassium increases natriuresis, encourages vasodilation reduces sensitivity to angiotensin II and lowers SNS activity.
  3. Lowers NADPH oxidase, decreasing ROS in the vascular wall.
  4. Avoid potassium supplements and take care with potassium intake in renal disease and with ACE inhibitors and K-sparing diuretics.
  5. Restrict sodium intake to 1.5g / day.
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57
Q

What are ACE inhibitory peptides for hypertension and in which food to find them?

A

Naturally-occurring ACE inhibitory peptides can be found in certain plants and foods and act like a decoy encouraging ACE to react with peptides, reducing vasoconstriction via angiotensin II.

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

57
Q

What is the DASH diet for hypertension?

A

DASH consists of fresh vegetables and fruits, legumes, nuts, seeds, whole grains, fish, lean meat and low-fat dairy and limits saturated fats and salt. PUFA / MUFA are preferred. Sodium is restricted.

58
Q

Key nutrient for HTN - Vitamin D - functions x3 and dose?

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.

Dose as needed to reach optimal levels

59
Q

Key nutrient for HTN - Magnesium glycerinate/taurate - functions x1 and dose?

A

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

500–800 mg / day

60
Q

Key nutrient for HTN - L-arginine - functions x1 and dose? x3

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 to 2000 mg x 3 daily

61
Q

Key nutrient for HTN - Vitamin B6 - functions x1 and dose? x2

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!

100 mg 1–2 x daily

62
Q

Herb for hypertension x4

A

Thetraditional ‘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).

To support blood pressure lowering, dandelion leaf is a diuretic and naturally rich in potassium. 1–2 teaspoons infused, 2–3 cups daily, or 3–4 fresh leaves in salads / smoothies.

63
Q

Why is stress management essential for HTN? + 2 strategies

A

Stress management: Essential because of the physiological effects of the stress response on CV health.
1. 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.
2. Earthing: (Walking barefoot on grass or sand) improves heart rate variability, lowers night-time cortisol and promotes a parasympathetic state.

64
Q

What is Atherosclerosis ?

A

Atherosclerosis = narrowing and hardening of large and medium arteries, which reduces blood flow.

65
Q

What is the pathophysiology of Atherosclerosis ?

A
  • ED dysfunction plays a central role in the formation of fatty streaks, a primary event in atherosclerosis.
  • Increased permeability facilitates entry of LDL into the intima. LDL becomes ‘trapped’ within the vessel wall and is oxidised to mLDL.
  • mLDL (modifiedLDL) recruit leukocytes expressing high levels of pro-inflammatory cytokines. Also trigger cytokine release from ED and VSMC cells.
  • Macrophages imbibe lipoproteins to form foam cells. Cellular debris is incorporated and inflammation drives plaque formation.
  • A cap is formed over the plaque to wall off the plaque from blood.
66
Q

What is the aetiology of atherosclerosis? x3

A
  1. endothelial dysfunction
  2. inflammation
  3. dyslipidaemia
67
Q

Explain endothelial dysfunction in the aetiology of atherosclerosis ?

A
  1. Disturbance to the protective glycocalyx layer and damage to ED cells. Factors include inflammation, ↑ oxidative stress, oxidised LDLs, hyperglycaemia, endotoxaemia, abnormal shear stress.
  2. Leads to altered regulation of inflammatory cytokines, eicosanoids and compounds that promote clotting risk.
  3. Upregulation of chemo-attractant molecules promotes migration of phagocytic and inflammatory immune cells into blood vessels.
  4. Disturbs NO metabolism ↑ hypertension risk  increases shear stress worsening endothelial dysfunction => plaque development.
68
Q

Explain inflammation in the aetiology of atherosclerosis ?

A
  1. ED dysfunction, subintimal cholesterol accumulation and monocyte / T-cell recruitment drives the inflammatory response.
  2. 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.
  3. Inflammation thins the fibrous plaque cap => instability / rupture.
  4. Pro-inflammatory cytokines differentiate VSMC into osteoblast-like cells increasing plaque calcification.
69
Q

Explain dyslipidaemia in the aetiology of atherosclerosis ?

A
  1. Lipids are a fundamental component of atherosclerotic plaques. Thus, dyslipidaemia is a significant risk factor and is marked by:
    – ↑ total cholesterol — ↑ LDL, VLDL, IDL, Lp(a), ↓ HDL; ↑ TGs.
  2. 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.
  3. High TGs are also linked with low HDLs
70
Q

What are the pillars of natural approach to Atherosclerosis ? x3

A
  1. Promote a healthy lipid profile
  2. Support endothelial health and vasodilation
  3. Promote and support liver detoxification
71
Q

How to Promote a healthy lipid profile for atherosclerosis - natural approach

A
  1. Avoid high saturated fat to reduce risk of CV events.
  2. Increase omega-3 FAs (see later) and MUFAs: E.g., avocado, unrefined olive oil. Regular EVOO consumption reduces LDL-C and oxidised LDLs, and improves post-prandial glycaemic profiles.
  3. EVOO polyphenols oleocanthal and oleacein have antioxidant and anti-inflammatory effects (↓ markers including CRP and IL-6).
  4. Red yeast rice (2400–4800 mg / day) ― contains monacolin K, an inhibitor of cholesterol synthesis via HMG CoA reductase.
  5. Soluble fibre (vegetables, fruits, psyllium husk, pectin, gums) are associated with a decrease in TC and LDL-C.
  6. Include dietary sources of beta-glucans (soluble + insoluble fibre) e.g., oats, mushrooms, seaweed, barley. Interactwith lipids and biliary salts in the bowel and lower LDL-C, non-HDL-cholesterol and ApoB.
  7. Are also a source of SCFAs — decrease liver cholesterol synthesis and increase bile excretion, and interact with innate immunity receptors to modulate immune function
72
Q

How to support endothelial health and vasodilation for atherosclerosis - natural approach

A
  1. Hawthorn berries, bilberry, blueberries and blackcurrants are antioxidant and support blood vessel integrity and tone.
  2. Lower ET-1 levels: Enhance citrus flavonoids, quercetin, epicatechins, garlic, olive oil, ginkgo, folate, blackcurrant.
  3. 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.
  4. L-theanine ↑ NO production in ED cells through eNOS phosphorylation (green tea is a key source).
  5. Reduce homocysteine: B6, folate and B12 (supplement methylfolate and methylcobalamin supplementation), TMG (3 g twice daily).
  6. 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.
73
Q

How to promote and support liver detoxification - natural approach

A
  1. Ensure availability of all substrates required for detoxification pathways (review Metabolic Detoxification lecture).
  2. Poor liver function can increase circulation of inflammatory mediators, impede cholesterol metabolism and comprise essential fatty acid status.
  3. 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’.
74
Q

Nutrients for Atherosclerosis x9

A
  1. L-citrulline
  2. Pantothenic acid / pantetheine
  3. Niacin (B3)
  4. Omega 3
  5. Pomegranate
  6. Pycogenol
  7. Lycopene
  8. Citrus Bergamia
  9. Globe artichoke
75
Q

Nutrient for atherosclerosis - functions and dose - L-citrulline

A
  1. NO is synthesised from L-arginine by eNOS.
  2. 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.
  3. Renal arginine regulates BP, blocks formation of endothelin, ↓ renal sodium reabsorption and is a potent antioxidant.

500-3000mg/day

76
Q

Nutrient for atherosclerosis - functions and dose - pantothenic acid / pantetheine (active form of Viyt B5)

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

300mg 3x/day

77
Q

Nutrient for atherosclerosis - functions and dose - niacin B3

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

500-3000mg/day

78
Q

Nutrient for atherosclerosis - functions and dose - Omega-3

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

3000-5000 mg/day

79
Q

Nutrient for atherosclerosis - functions and dose - Pomegranate

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

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

80
Q

Nutrient for atherosclerosis - functions and dose - Pycogenol (pine bark extract)

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

100-200mg/day

81
Q

Nutrient for atherosclerosis - functions and dose - Lycopene

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

25mg/day

82
Q

Nutrient for atherosclerosis - functions and dose - Citrus Bergamia

A
  1. Bergamot (citrus fruit): Natural source of flavonoids, e.g., naringin, hesperidin, neohesperidin and neoeriocitrin.
  2. Lowers LDL and TGs. Increases PPAR activation.
  3. Reduces ROS, oxidised LDL, balances blood glucose and reduces weight.
  4. Improves serum glucose via AMPK (AMPK (AMP-activated protein kinase) = a central regulator of energy homeostasis) and GLUT 4 receptor.

500-1000mg/day

83
Q

Nutrient for atherosclerosis - functions and dose - Globe artichoke

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

Dietary + 1–2 g / day powdered

84
Q

Other stress management and exercise strategies for atherosclerosis?

A
  1. Sauna: ↑ circulation and arterial vasodilation. Avoid in unstable angina / recent MI and hypertension.
  2. Dry skin brushing: Supports circulation and lymphatic function, increases toxin elimination.
  3. Contrast hydrotherapy (alternating warm / cold water): improves circulation and supports removal of toxins. If circulation is compromised end on warm.
  4. Tai Chi Chuan, yoga and acupuncture have shown to reduce ET-1 levels.
85
Q

What is Ischaemic Heart Disease? IHD

A

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

Atheroma and inappropriate vasoconstriction reduce blood vessel lumen size and coronary blood flow. When oxygen demand > oxygen supply, myocardial hypoxia, accumulation of waste metabolites and ischaemia ensues.

86
Q

What commonly causes Ischaemic Heart Disease?

A

atherosclerosis

87
Q

What are the two Ischaemic Heart Disease syndromes?

A

angina (stable and unstable)
myocardial infarction.

88
Q

IHD - what is Angina ?

A

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

89
Q

IHD - What are the two types of Angina?

A
  1. Stable angina: Predictable transient chest pain during exertion or emotional stress. Ischaemia with symptoms resolve once oxygen balance is restored.
  2. Unstable angina: Unpredictable / occurs at rest. Plaque disruption initiates platelet aggregation, thrombus formation and vasoconstriction. May be a precursor to acute MI.
90
Q

IHD - What are stable angina signs and symptoms?

A

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

91
Q

IHD - What are angina causes and risk factors?

A
  1. See earlier section on CVD risk factors. Also consider:
  2. Cigarette smoking ― linked to endothelial dysfunction, CAS (coronary artery spasm), vessel wall injury, oxidative stress, elevates fibrinogen, platelet activation and inflammation. Smoking cessation in angina can prevent recurrent angina events.
  3. 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.
  4. Family history of premature IHD is a strong risk factor for angina.
92
Q

Orthodox diagnosis of angina ?

A

ECG, cardiac stress testing, angiography

93
Q

Allopathic treatment of angina>

A

Nitrates (e.g., GTN)
calcium channel blockers (e.g., amlodipine)
beta-blocker (e.g., atenolol)
revascularisation (angioplasty, stents and coronary artery bypass graft surgery).

94
Q

IHD - What is Myocardial Infarction (MI)?

A

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

95
Q

IHD - what is the pathophysiology of MI?

A
  • 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.
96
Q

IHD - what are the two types of MI?

A

– ST-Segment Elevation MI (STEMI) = full occlusion (severe).
– Non-ST-Elevation MI (NSTEMI) = partial occlusion.

97
Q

IHD - causes and risk factors for MI?

A
  • See earlier section on CVD risk factors. Also consider:
  • Sex: Males ~ 3 times more likely to experience MI. High androgen levels contribute to 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).
98
Q

Signs and symptoms of MI?

A
  1. Severe prolonged crushing retrosternal chest pain. Pain radiates to the left shoulder, jaw / neck or arms. Sweating, cool / clammy skin. Feeling of ‘impending doom’.
  2. Dyspnoea and syncope.
  3. Nausea, vomiting, weakness.
99
Q

Complications, diagnosis and allopathic approach of MI?

A

Complications: Arrhythmias, heart failure, cardiogenic shock, death.

Diagnosis: ECG findings.

Allopathic approach: Fibrinolysis, O2 therapy, morphine, nitrates, beta blockers, aspirin for acute management.

100
Q

Natural approach to IHD?

A

Apply the Natural Approach to CVD, with a focus on supporting myocardial blood flow. Key considerations:
1. Optimise vitamin D status – supports endothelial health and promotes vasodilation (↑ NO).
2. Warming herbs / spices to support blood flow, e.g., ginger, cayenne.
3. Increasing movement — care is needed to avoid triggering angina attacks — focus on gentle exercise i.e., Tai Chi, Qi Gong, walking. Gradually increase as capacity improves.
4. Address stress. Breathing exercises. Nervine herbs (e.g., passionflower 1–2 tsps dried herb 2–3 x per day (infusion).

101
Q

Nutrients for IHD x4

A
  1. L-Carnitine
  2. Magnesium
  3. CoQ10
  4. L-Arginine
102
Q

Nutrient for IHD - functions and dose - L-Carnitine

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.

1000mg 2x/day

103
Q

Nutrient for IHD - functions and dose - magnesium

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.

200-400mg 3xdaily

104
Q

Nutrient for IHD - functions and dose - CoQ10

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 statin) mg / day

105
Q

Nutrient for IHD - functions and dose - L-Arginine

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

1000-2000mg 3x/day

106
Q

Herb for IHD - functions and dose - hawthorn

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.

1000-1500mg

107
Q

Herb for IHD - functions and dose - ginkgo balboa

A

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

60-120mg/day

108
Q

What is heart failure ?

A

Heart failure (HF) = a syndrome in which the heart is impaired as a pump ― failing to supply sufficient blood flow.

109
Q

Signs and 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

110
Q

Complication of HF

A

Atrial fibrillation, ventricular arrhythmias, CKD (Chronic kidney disease), sudden cardiac death.

111
Q

Allopathic approach to HF?

A

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.

112
Q

Causes and risk factors of HF?

A

Results from various CV conditions ― e.g., IHD (most common cause ― review previous risks), hypertension, AF, cardiomyopathy, LVF (left ventricle failure), pulmonary hypertension, heart valve abnormalities.
– See earlier risk factors, e.g., smoking (leads to LV hypertrophy and systolic dysfunction); raised homocysteine; sedentary etc.

  1. 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.
  2. Obesity ― alters cardiac structure, promotes endothelial dysfunction, contributes to IR and ↑ inflammatory cytokines.
  3. 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
113
Q

HF co-morbidities

A

Co-morbidities (so causes of each apply) ― e.g., CKD (Chronic kidney disease), 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.

114
Q

HF nutrient deficiencies ?

A
  1. CoQ10 (normally ↓ ROS and ↑ NO)
  2. Vitamin D (normally ↓ inflammatory cytokines and ↑ calcium absorption etc.)
  3. 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

115
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 (see previous slides) — 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

116
Q

Nutrient for HF x5 + 1 herb

A
  1. CoQ10
  2. D-ribose
  3. Magnesium
  4. Thiamine
  5. L-Carnitine
  6. Hawthorn
117
Q

Nutrient for HF - functions and dose - CoQ10

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.

300–400 mg daily.

118
Q

Nutrient for HF - functions and dose - D-Ribose

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.

D-ribose
5–15 g daily

119
Q

Nutrient for HF - functions and dose - Magnesium citrate

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 magnesium citrate

120
Q

Nutrient for HF - functions and dose - Thiamine

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/day

121
Q

Nutrient for HF - functions and dose - L-Carnitine

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/day

122
Q

Herb for HF - functions and dose - Hawthorn

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

123
Q

What are varicose veins?

A

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

124
Q

Varicose veins signs and symptoms?

A

Visible vein dilation; aching, burning, throbbing, heaviness.
Worse for prolonged standing and at the end of the day.

125
Q

Varicose veins - complication

A

↑ venous pressure = fluid leakage into surrounding tissues (‘varicose eczema’). Slow healing varicose ulcers.

126
Q

What are Haemorrhoids

A

dilated veins in the anal canal. Internal or external.

127
Q

Haemorrhoids signs and symptoms

A

Bright red blood with blood movements, protruding haemorrhoids, anal itching.

128
Q

Varicose veins / Haemorrhoids causes/risk factors? x9

A
  1. Increased abdominal pressure ― constipation, obesity, pregnancy, childbirth and post-labour, ascites.
  2. Inherited valve defects ― an absence of some valves or faulty valves.
  3. Cigarette smoking (= hypoxia, which results in endothelial damage, vessel wall inflammation and a loss of elasticity).
  4. Being sedentary (increasing venous pressure).
  5. Lack of dietary connective tissue support, e.g., low vitamin C (increases type I collagen synthesis), low bioflavonoids (support connective tissue integrity).
  6. Portal hypertension ― increased portal vein pressure e.g., due to liver cirrhosis and heart failure.
  7. Increased blood viscosity and stagnation ― dehydration, liver congestion, sedentary lifestyle. Also haemorrhoids, post-food fatigue, purple tongue, thick white / yellow tongue coating.
  8. Abdominal bloating (not obesity) ― distended and uncomfortable. E.g., associated with SIBO.
  9. Structural ― e.g., poor diaphragm motion (consider causes such as stress, asthma etc.), weak pelvic floor (consider pregnancy).
129
Q

Natural approach to varicose veins / Haemorrhoids x3 diet

A
  1. CNM Naturopathic Diet. Reduce inflammation, increase blood flow and speed up repair of damaged veins / valves. Correct root causes!
  2. Vitamin C-rich foods (to support collagen synthesis).
  3. 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
130
Q

Natural approach to varicose veins / Haemorrhoids lifestyle x5

A
  1. Enhance fibrinolytic activity — garlic, onions, ginger, cayenne. Include bromelain sources to increase plasminogen activator status.
  2. Optimise liver function — alleviate downward pressure. Fibre-rich plant foods: Reduce venous pressure with defecation. Ground flaxseed, or psyllium husk (15–30 g / day). See detox lecture.
  3. Raise feet above heart (20 mins / day) — reduces blood pooling and improves venous return.
  4. Lymphatic drainage / massage — for mild cases only — aids circulation and avoids blood pooling. Consider dry brushing.
  5. Reduce weight: Address cause and exercise!
131
Q

Nutrient for varicose veins / Haemorrhoids x1

A

Vitamin C with bioflavonoids
1.5–2 g through the day

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

132
Q

Herbs for varicose veins / Haemorrhoids x4

A
  1. Horse chestnut
  2. Gotu Kola
  3. Butcher’s broom
  4. Pycnogenol
133
Q

Herbs for varicose veins / Haemorrhoids - Horse chestnut

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.

134
Q

Herbs for varicose veins / Haemorrhoids - Gotu Kola

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.

500 mg x 2 daily
Note: Avoid in liver disease

135
Q

Herbs for varicose veins / Haemorrhoids - Butcher’s broom

A

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

300–500 mg x 2 daily

136
Q

Herbs for varicose veins / Haemorrhoids - Pycnogenol

A

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

150–300 mg / day

137
Q

Natural approach to varicose veins / Haemorrhoids (lifestyle x2, tissue salts, topical application)

A
  1. Regular exercise (e.g., aim for a target of steps walking; jogging etc.). Exercise sitting (rotate ankles). Avoid prolonged standing.
  2. Weight loss where applicable. Support stockings esp. if standing for prolonged periods is unavoidable. Elevate the legs periodically.
  3. Tissue salts — calc. fluor. (tissue strengthening). If bleeding add ferrum. phos. 4 pills x 3 daily.
  4. Topical application of astringent herbs: Horse chestnut (Aesculus hippocastanum),witch hazel (Hamamelis virginiana), yarrow (Achillea millefolium).
138
Q

Homeopathy for varicose veins / Haemorrhoids

A

Homeopathy: 3 pills twice daily until symptoms subside.
* 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.

139
Q

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

Blood stagnation is associated with a purple tongue

Nutrition 2 - Sem 2 Exam (7 decks)

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