Cardiovascular Health

• The study notes are for Naturopathic Nutrition Year 2 and cover Cardiovascular Health

Learning Outcomes

• Knowledge of Cardiovascular Disease (CVD) is expected
• CVD Risk Factors
• Cardiovascular Markers
• Knowing how to approach CVD naturally regarding lifestyle and diet.
• Hypertension
• Atherosclerosis
• Ischaemic Heart Disease
• Peripheral Arterial Disease
• Heart Failure
• Varicose Veins and Haemorrhoids.

Cardiovascular Disease (CVD)

• CVD is a general term for conditions affecting the heart and blood vessels
• Examples include atherosclerosis, hypertension, angina, myocardial infarction, and stroke
• Globally, CVD accounts for 32% of all deaths
• CVD is the most common non-communicable disease worldwide.
• CVD costs the UK economy an estimated £19 billion / year
• Greater than 75% of premature CVD is thought to be preventable.
• Increased CVD risk has been linked to unhealthy dietary patterns, lack of exercise, excess body fat, stress, and smoking

Endothelium (ED)

• The Endothelium (ED) is a monolayer of endothelial cells lining the blood interface throughout the CVS
• The CVS includes cardiac chambers
• Normal functioning of the ED is critical to vascular health.
• The glycocalyx (GX) is a carbohydrate-rich protective layer covering the ED
• The GX regulates permeability, controls NO production.
• The GX acts as a mechanosensor of blood shear stress.
• Inflammation, hyperglycaemia, endotoxemia, oxidised low-density lipoproteins and abnormal blood shear stress can easily damage GX.
• Damage to GX can precede damage to the ED resulting in lipid deposition and atherosclerosis.
• Shear stress is the frictional force of blood on ED cells.

ED Functions

• Semi-permeable barrier with role in fluid balance, host defence and selective movement of substances e.g., glucose and oxygen
• Regulates vascular tone secreting vasodilators e.g., NO (nitric oxide) and vasoconstrictors (e.g., endothelin)
• Contains enzymes such as angiotensin-converting enzyme (ACE) playing a key role in regulating blood pressure
• Has an angiogenesis as ED cells are the origin of all new blood vessels
• Aids Haemostasis such that the luminal surface of ED prevents platelet adherence and coagulation (non-thrombotic, anticoagulant)
• Provides an Immune defence such that healthy ED cells deflect leukocyte adhesion and oppose local inflammation.

Vascular Smooth Muscle Cells (VSMCs)

• VSMCs are located in the tunica media.
• VSMCs play a key role in vessel contraction and dilation, regulating blood circulation and pressure.
• With the ED, VSMCs maintain the integrity and elasticity of blood vessels limiting immune cell infiltration.
• Inflammation, oxidative stress, and telomere damage to VSMCs promotes undergo phenotypic modulation, altering cell structure and function.
• Phenotype modulation alters the physical form and structure through the interaction of the genotype and environment
• Pathological conditions are central to vascular disease, especially atherosclerosis and hypertension.

Nitric Oxide

• NO (nitric oxide) plays a relevant role in CV health
• NO regulates vascular tone, reducing platelet aggregation and VSMC proliferation
• NO inhibits leukocyte adhesion and inflammatory cytokines and opposes oxidation of LDLs
• eNOS is endothelial nitric oxide synthase
• L-arginine is continuously generated by the ED enzyme eNOS which is a constant action, promoting cardiac health
• NO diffuses from ED into VSMCs and the bloodstream exerting physiological effects in large vessels
• Vitamin D regulates NO synthesis by mediating eNOS
• Reduced NO has been linked to atheroma formation and CVD.

Oxidative Stress and the ED and VSMCs

• Endothelial cells that are normal are impermeable, anti-inflammatory and deflect leukocyte adhesion, resulting in vasodilation and resists thrombosis
• Activated permeability increases cytokines and luekocyte adhesion, reducing vasodilation (NO, prostacyclin) molecules and increasing thrombosis
• Normal contractile function and maintains intracellular matrix, being contained within the tunica media is a key component of normal arteries and veins.
• When activated, arteries increase synthesis of cytokines and proliferation into the tunica intima

Peroxisome Proliferator-Activated Receptors (PPARs)

• PPARs are nuclear transcription factors that control gene expression in adipogenesis, and lipid/glucose metabolism, cellular proliferation and apoptosis
• PPARs decrease inflammation and promote ED health
• PPARα activation raises HDL-C, lowers TGs and inflammation and is anti-atherosclerotic
• PPAR- α agonists include green tea, resveratrol (up to 50 mg), dietary inclusion of oregano, thyme, rosemary, naringenin (citrus bioflavonoid up to 100mg/day) and omega-3 (up to 3 g)
• PPAR-y reduces blood glucose, fatty acids and insulin
• Natural PPAR-y agonists include apigenin, hesperidin, curcumin, resveratrol, EGCG (polyphenol from green tea).

CVD Risk Factors

• Family history: Siblings of CVD patients have a 40% increased risk; Offspring of parents with premature CVD: 60–75% increased risk.
• MnSOD, NOS3, MTHFR and ACE gene polymorphisms are key genetic contributors
• South Asian or sub-Saharan African individuals demonstrate an enhanced risk of CVD.
• The common belief is that CVD is predominantly a male pathology: CVD mortality in women (35–54) is increasing, and the risk factors are underestimated.

More CVD Risk Factors

• Dyslipidaemia:
• ↑ total cholesterol — ↑ LDL, VLDL, IDL, Lp(a), ↓ HDL; ↑ triglycerides.
• Lp(a) = lipoprotein A, a form of LDL. Also acts as a clotting factor further ↑ CVD risk
• Sedentary lifestyle, excess alcohol, smoking, obesity, high intake of saturated and trans fat, menopause. increases risk
• Risk increases are more common in T2DM, hypothyroidism and chronic kidney disease
• Dyslipidaemia is largely preventable!
• CVD pathologies tend to appear 5 years earlier in those with hypertension.
• ATP is required to pump Ca ions out of myocardial cells, allowing relaxation and maintains electrochemical gradient across myocardial cell membrane; consider statins/CoQ10

Elevated Homocysteine

• Elevated homocysteine is associated with LDL oxidation, monocyte adhesion and ED dysfunction and is linked to the genetic pathways
• Increases in homocysteine levels relate to low folate and B12 which is needed for re-methylation of homocysteine to methionine
• Genetic polymorphisms are key, such as the MTHFR, FUT2, TCN and MTR/MRR genetic alleles that promote disease incidence.
• Vitamin B6 is a cofactor, a co-factor in the conversion of homocysteine to cysteine in the methylation cycle.
• The other route for methylating homocysteine is dependent on choline (PEMT and CHDH genes) and betaine (BHMT gene).

Thyroid Hormones, Inflammation, and Cardiovascular Health

• 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 Dyslipidaemia, dysbiosis and intestinal permeability, ROS, diabetes, excess adipose tissue and smoking cause inflammation Inflammation contributes to ED dysfunction, which further promotes subintimal cholesterol accumulation and inflammatory response.

Obesity

• Obesity: Excess adipose tissue perpetuates inflammation contributing to vascular breakdown and metabolic complications.
• Inflammation is linked with ↑ endothelin-1 (ET-1), a potent vasoconstrictor peptide; elevated ET-1 leads to fibrosis of VSMCs and ↑ ROS.
• Adiponectin, a peptide that influences the expression of ED cells, is decreased in obesity protecting against CVD.
• Adiponectin also ↑ insulin sensitivity, low levels contribute to insulin resistance (IR).
• Obesity is associated with high levels of leptin, which activates the SNS causing sodium retention, vasoconstriction & ↑ blood pressure

Insulin Resistance

• Insulin resistance (IR) generates chronic hyperglycaemia
• IR ->Oxidative stress, inflammation and cellular damage IR contributes to the lipid triad (high plasma TGs, low HDL, small dense LDLs) promoting dyslipidaemia, along with ED damage and plaque foramtion
• Glucose is not cleared from the bloodstream quick enough when glucose levels are high, increasing the risk of glycosylation reactions and production of damaging compounds
• This is known as advanced glycation end products (AGEs).

Advanced Glycation End Products (AGEs)

• Advanced glycation end products (AGEs) are harmful.
• AGE’s from proteins or lipids becomes glycated after exposure to glucose Two main pathways:
• Receptor-mediated- Bind to the cell receptor
• Non- receptor mediated- Increased EC matrix synthesis
• Lead to oxidative stress, vascular ED and immune cell dysfunction, AGE signalling induces fibroblast differentiation and downregulates detox mechanisms, contributing to disease

AGEs and CVDs

• AGEs increase with advancing age; Renal accumulation of AGEs promotes kidney dysfunction
• Polymorphisms of the AGER gene (encodes RAGE) can ↑ disease risk
• Consumption of exogenous AGEs contributes to overall AGEs pool; includes refined carbohydrates (sucrose, HFD), processed foods, meat and dairy
• Cooking methods such as High heat, grilling, roasting, searing/frying promote AGE formation.
• Smoking and sedentary enhances AGE accumulation Vitamin D appears to ameliorate AGE-mediated complications.

Additional CVD Risk Factors

• Smoking: ↑ oxidative stress and lowers antioxidants. (1 cigarette = 25 mg loss of vitamin C).,
• Sedentary lifestyle: Exercise has a positive effect on lipid profile and blood pressure, as little as 30 mins/day can protect
• Chronic Stress: Causes endothelial dysfunction especially in the presence of other risks e.g smoking.
• The following also contribute:
• Activates SNS and HPA-axis increases inflammatory cytokines.
• Increases hear rate.
• blood pressure through the SNS.
• Raises activity of the amygdala increases arterialinflammation

Periodontal Disease, Heavy Metals, and Melatonin

• Periodontal disease causes systemic inflammation, promoting endothelial dysfunction, arterial stiffness and plaque formation
• Heavy metals induce oxidative stress, leading to risk of zinc deficieny which decreases atherosclerosis risk.
• Melatonin deficiency relates to potential anti-hypertensive issues protecting against CVD

CVD Risk Factors Related to Digestion

• Increased TMAO leads to vascular diseases
• SCFAs produced by the microbiota: Risk metabolic endotoxaemia
• Gut microbiota play a large hand in chlostero regulation
• Gut microbiota promote metabolitis that lead to harmfull effects

Dietary Consideration Risk Factors

• High PRAL protein, (meat, cheese) - > metabolic acidosis
• Trans fats - > dyslipidemia, viscosisty

Fructose -> High fructose intake -> lipogenesis

• Lacking nutritional value is another issue that promote these risk Factors

Cardiovascular Markers

• Testing is necessary to assess cardiovascular functional marker
• Cardiac risk tools provide a risk score. QRISK score over 10% = 1 of 10 chance.
• Cardiac tool protein are in the blood when your heart muscle is damage
• Lipid profile: TCs, non-HDL, TG & LDL C, TC: HDL

Cardiovascular Functional Testing

Lp-PLA 2 : Enzyme in mono, macro and T

• Low risk: < 1. mg
• High risk: > 3.0 mg Smoking can cause both

Natural Approach to CVD

• Plant-based and Meditteranean provide anti inflimmatorial results, and reduces the risk of thrombosis, improved SCFA production, reduced adpisocity, and insulin, and endothelial health

Natural Diet

• Vitamin C
• Reductants
• Vitamin E
• Antioxidents for endothelium
• Vitamin D
• Modulates NO production Omega 3 Fatty Acids

• Improives cells and inflammation

• Co enzymie Q10
• Stabilizes cells
• Magmesium
• Improves vascular tone

Hawthorn and herbs promote cardiovascular heath, with the natural approach

• Thiamine
• Promotes enzyme production
• Ginko
• Enhances blood circulation

Notes About HTN

• Symptoms reflect the force and circulation
• It has an exression from systolic and diastolic pressure
• It is 140/90 mmHG or higher(UK) on a regular basic
• Asymptomatic

More About Hypertension

• Essential or secondary
• Essential (90%) -> Primary cause
• Secondary has problems with organs Pressure over 180/120 is malignant, which is dangerous

CAUSES OF HTN

• Offspring
• Obesity
• Genetic
• Alcohol and low recetpor activation to changes affect the brain
• RAAs with Et- 1 to activate.

Hypertension Risk factors

• High table salt increase the likeliness of a stroke
• Higher HR and increased activity can damage your rate
• Damages the endothelitum and damages the Blood Vessel
• NASID, COrticosteroids damgae the BP system

RAaD and Endotherlium

• Acid stimulates the rage pathway which increases NOs disruptos
• Hyperinsuliaemia also has lower
• Diet includes the endotheilum and has muscles with increased arterial stiffness

Natural Approaches to HyperTension

• Reduce pressure
• Reduce potassium intake
• Reduce potassium and ACE

Dash Diet

• Reveals more significant systolic and diasolic BP reduction

Natural Supplementa Approach to hypertension

• Melation is essential for anti hypertentive.
• Peptides are important due to vessel tone and vascular system from the blood
• See previous lecture about Melatonin production

Natural Herbal Approach to Hypertension

• Vitamin D promotes hypertension
• magnesium in cells promote vascular activity

L Arginine, Vitamin B to provide good structure to the cardio vacsular system

• For further results, use Vitamin C, CO10 And Hawthorne, which improve function,
• Mag PHOS promotes better circulation.

Herbal Support for Hypertension

• C.A.T. has great benefits for equal herbs infused for the cardoivasular system
• To support blood presure to lower and promote a rich potassium for the diet

Manage Strese for Hypertension

• Diaphragmatic deep breathing for best results
• Exercise with walking to regulate health
• Aerobic activity is reccomended

Atherclosis

• Modified by LDL
• Narrowy artery
• Ed dysfunctional promotes plaque build up with fat
• increased level facilitates LDL
• Macros imbole proteins
• Caps form as plauqe
• Dystermia. endothelia dysfunction has shear stress

What Are Atherosclerosis Risk Factors?

• Disturbance to a protecive glycococylx

Aetiology -Inflmmation & Athersclorosis

• Drives inflammatory response
• Intervations of Ill-6 promote CRP production
• inflammation can thin fiverous plaque for insitiability and ruptrue
• Pro inflammation increase calification, and cause cells to multiplys

Dyslipidaemis & Atherslcorosis

• lipidis and plauqe is a fundament component
• dyslpemia = risic factor, HDL
• Increase TG prevent proteins to truvel in plasma

Natural Approach to CVD

• Avvid saturated dat
• Increased Omega 3 Fatty Acids. =MUF
• Regular consumption reduce LOdl cholestrol
• Red yesat ricewith cholerstrol produce through reductase

Approaches for a healthy heart

• Dietary fiber 45g a day
• Soublr vvegetabelse to decrese lDlc
• • Beeta lucan is important
• • SCFAs lower liver production and increase innated immunity.

Support Endothelial health and vasoldilation

• Harvthorn is a great option
• Lower Esit -1 levels. Enhance Quercetin olive oil foliate, and black
• Beet root promotes homocysiene
• • Green Tea* Theanine increases ED cell production

Arterosclorosis

• B6, Folate and B12 for homeostcines and low levels • High fibers

Heart Disease

MI -> Blockage of coronary system • Proolonged Eschemics promote necrosis and can be bad in health • Damamge can cause a stroke

• S-T elevation = full bloackage
• N-ST elevation = partial bl

Other Risk factos

• Drug induced from cocai e that promote blood flow.

Sign and Symptoms of Strokes and M1s

• Severe pain of retrosternal with pain in jaw,neck • Swearting • Allipathci- Oxygenm beta blovckers

Ischemic Heart Disease"

• Causes by Asvatherosclorosis

Signs and Symptons

• Angina -> Stable or unstable by stress
• Myocardial Ischemia

Agina

• It is not enough blood through Coronary Artery
• Charecterized: Stable/ unstable, that can lead to acute MI
• Cosnttricting chets pain. And Sob breathing and fatigue

Agina RISK factors

• See earlier section on CVD.
• Cigareette Smoking
• Vitman D effenicy

Heart Failure

-Signs is Breathless ess

• Complication if fibrillations -> Ventricular fibrialltion

Natrual Approach to Heatr Failure

• Digoxin
• Diueretics" Calcium Inhibitors Ace Inhibitor
• Low CVD Risk Factors
• Correvt Nutrionaly Ecnoure smoking cessation

Heart Failure, continued

• 2x daily
• *VaIcOse,

" - Dilated viens in lower linbs

• Comopliications -> Venus Preus
• Haermoids

Key notes to take/

• Inherited VaIle defeCTS” > ABSENCE OF VALVES "”>CIGARETTE SMOKNG , HYPOXIA
• DIETAY CONNECVTE TISSIE SUPPORT “” low Vit C

A Natural Approach to Veins

•Vamin C rich Foods •Bioflavanol such as “Rutim - and Food sources

Reduce Weight to Avoid Venous Issues

• Enhance fibers with galirc, Onion and Ginger
• Improve Livers Functon For a Healthy Balance
• Raise feet above heart
• Lymphatic Draininge for blood poling.
• Use herbal suppoet to help.