Search
Newsletter Signup
join our mailing list

Ads by Google

Are you a ticking timebomb for a heart attack?

As a specialist physician in private practice I have done many insurance medicals to declare people “medically fit and healthy. ” It is quite alarming that the cardiac assessmant required for these insurance medicals is a fasting lipogram, glucose and a stress ecg. First of all it is inflamed, oxidized cholesterol that is linked to coronary artery disease and not just cholesterol per se. Secondly a stress ecg is not the best test to assess the state of coronary artery disease since the test is frequently negative whilst coronary artery disease is clearly apparent on say ct scanning of the coronaries. Often (in women in particular) the stress ecg can be falsely positive as well. Thirdly there is a much bigger picture to the prevention of coronary artery disease than merely lowering cholesterol.

Opposite to common thought that cholesterol is “bad”, people do need cholesterol for normal bodily functioning. Cholesterol is the precursor to vitamin D, steroid hormones (such as estrogen, progesterone, testosterone, dhea, pregnenolone and cortisol), and the bile acids required for digestion. Cholesterol is also required to form the membrane around cells and for regeneration of damaged endothelial cells.

The main sources of cholesterol are liver production (about 800mg a day). Main dietary sources include meat, cheese, milk and eggs. Cholesterol is transported in the blood by lipoproteins. A healthy cell cannot be overfilled with cholesterol unless the cholesterol is oxidized and enters an already inflamed arterial tissue. Cholesterol is in itself not the culprit here. Nature wouldn’t give you a system designed to kill you. The issue is inability to process cholesterol, inflammation and oxidative stress.

The body’s antioxidant system as well as antioxidant supplements and natural anti-inflammatories safeguard against cholesterol deposition in the blood vessel walls resulting in atherosclerosis (blood vessel disease resulting in heart disease, stroke and peripheral vascular disease). The reverse cholesterol transport system that removes cholesterol from one’s arteries requires phosphatidylcholine (PC) and LCAT (lecithin cholesterol acyl transferase). LCAT, an enzyme removes a fatty acid particle from PC and binds it to cholesterol producing an ester. HDL, a circulating “good” cholesterol transports this ester back to the liver.

So Good cholesterol includes:

a) HDL

b) Non-oxidized LDL (essential for normal bodily function)

Bad cholesterol:

a) Oxidized LDL…. This is the cholesterol that leads to blood vessel disease. Deposition in blood vessel walls lead to foam cell formation, plaque formation, blood clotting.

b) lipoprotein (a)…. This is a cholesterol molecule attached to a protein apolipoprotein (a). This molecule has repair function to the arterial wall, however too much of it (usually genetic) promotes formation of blood clots and build up of plaque. This narrows the blood vessel and worsens symptoms.

It is also important to remember that one can check the degree of inflammation in the body by doing a test called hscrp (highly sensitive crp). A value of less than 1 is normal. Increasing values lead to increases in heart and blood vessel diseases.

If you have a high hscrp natural anti-iflammatories like omega 3 fishoil and curcumin are ideal supplements to lower your risk of cholesterol being oxidized and inflamed in blood vessel walls.

High blood pressure, elevated LDL and triglycerides, low hdl, cigarette smoking, elevated LDL and triglycerides, low HDL, diabetes, obesity, and lack of exercise contribute to endothelial dysfunction and the subsequent development of atherosclerosis. 15-25.

Additional endothelial-damaging factors include excess levels of glucose, insulin, iron, homocysteine, fibrinogen, and C-reactive protein, as well as low HDL and free testosterone (in men). 3, 9, 10, 24, 26-28.

Homocysteine is particularly dangerous because it can induce the initial injury to the endothelium. Homocysteine then facilitates oxidation of the fat/LDL that accumulates beneath the damaged endothelium, and finally contributes to the abnormal accumulation of blood components around the atherosclerotic lesion. 29

Fibrinogen is a clotting factor that accumulates at the site of the endothelial lesion. Fibrinogen may contribute to plaque buildup or participate in blood clot-induced blockage of an artery after an unstable atherosclerotic plaque ruptures. 30

Glucose at even high-normal levels may accelerate the glycation process that causes arterial stiffening, while high-normal fasting insulin inflicts direct damage to the endothelium. 31-36

High levels of iron promote LDL oxidation in the damaged endothelium, while low levels of testosterone appear to interfere with normal endothelial function. 9, 11, 14

C-reactive protein is not only an inflammatory marker, but also directly damages the endothelium. Chronic inflammation, as evidenced by persistent high levels of C-reactive protein, creates initial injuries to the endothelium and also accelerates the progression of existing atherosclerotic lesions. 3, 27

In response to numerous published studies, health-conscious people are altering their diets, taking drugs, hormones, and dietary supplements, and trying to exercise regularly in order to reduce these atherosclerosis risk factors. However, these efforts alone cannot be completely successful because age itself is a major risk factor for atherosclerosis.

Atherosclerotic risk conferred by age is attributable in large measure to pathological endothelial dysfunction. 37, 38 As noted earlier, endothelial dysfunction is not synonymous with atherosclerosis, but the two processes are increasingly intertwined with advancing age.

ENDOTHELIAL DYSFUNCTION MARKERS:

1. VEGF (Vascular endothelial growth factor)

2. ADMA (Asymmetric dimethylarginine)

3. VCAM-1 (vascular cell adhesion molecule-s)

4. NOS (Nitric oxide synthase)

ADMA is involved in the pathogenesis of hypertension and atherosclerosis through its inhibition of the formation of the endogenous vasculoprotective molecule, nitric oxide (NO). Determination of ADMA can thus help to predict both the likelihood of developing cardiovascular diseaseand its prognosis. A new competitive ELISA test for ADMA is a useful and fully validated tool suitable for routine laboratory use.
Availalble tests to detect endothelial dysfunction in south Africa include:

a) hsCRP

b) Von Willebrand Factor (WF)

c) PAI-1 (Plasminogen activator inhibitor-1)

d) FDP (Fibrinogen degradation products) – as D-dimer

e) NT-proBNP

f) Homocysteine

g) Active renin

h) Lipids (lipogram) and lipoproteins

i) ACE (angiotensin converting enzyme)

An article published online on October 21, 2008 in the journal Nutrition & Metabolism reported the discovery of Italian researchers of an association between decreased plasma levels of several antioxidants and early carotid atherosclerotic lesions in asymptomatic middle-aged individuals.

“Atherosclerosis remains clinically mute for a long time and frequently manifests itself with an acute cardiovascular event; therefore, the possibility of detecting the disease in a subclinical phase and reducing or reversing its progression is an issue of relevance, ” the authors write. “Antioxidants, which may inhibit lipid peroxidation, could play an important protective role against the formation of simple and complex atherosclerotic lesions, which progressively protrude into the arterial lumen, causing stenosis or occlusion. In particular, increased carotid intima-media thickness represents an early phase of the atherosclerotic process and is widely used as a marker of subclinical atherosclerosis which correlates with established coronary heart disease. ”

Two hundred twenty men and women between the ages of 45 and 65 without history of transient ischemic attack, stroke, or other conditions related to carotid artery disease were enrolled at the San Camillo de Lellis Hospital, in Manfredonia, Italy. Participants underwent ultrasonographic evaluation of the extracranial carotid arteries, and blood samples were analyzed for lipids, C-reactive protein and other factors, in addition to plasma levels of vitamin A, vitamin E, beta-carotene and lycopene.

One hundred twenty-five participants were found to have carotid atherosclerosis as determined by carotid intima-media thickness of 0. 8 millimeters or more. Body mass index, plasma hemoglobin, and high-density lipoprotein cholesterol were marginally higher among those diagnosed with atherosclerosis, and all of the nutrients measured were significantly reduced. Vitamin A, vitamin E, and lycopene levels were decreased by 50 percent or more among those with atherosclerosis compared with participants who were not diagnosed with the condition, and beta-carotene levels were less than a third of those without atherosclerosis.

Oxidative stress resulting from the oxidation of low-density lipoprotein (LDL) cholesterol in the wall of the artery results in inflammation which stimulates the differentiation of immune system cells called monocytes into macrophages. Macrophages accumulate lipids to form foam cells which thicken the walls of the artery. Antioxidants such as those evaluated in the current study could help protect against this process by preventing LDL oxidation.

“Regular intake of foods rich in lycopene and other antioxidant vitamins may slow the progression of atherosclerotic processes and modify the early stages of atherosclerosis, with a consequent reduction in cardiovascular events, ” the authors conclude.

OXIDATIVE STRESS PROFILE (blood)

1. Malondialdehyde

2. Glutathione

3. CoEnzyme Q10

4. Vitamin C

5. b-Carotene (including cryptoxanthin and lycopene)

Supplements to consider taking to lower “bad” cholesterol and heart disease

Remember as a rule of thumb that most nutritional supplements work best together rather than as individuals, and you should use natural forms and not synthetic.

1. Anti-oxidants to help prevent the oxidation of cholesterol include:

a) vitamin e

b) vitamin c

c) co q10

d) bioflavanoids

e) alphalipoic acid

f) lycopene

g) selenium

h) beta carotene

2. Fish oil

There is overwhelming evidence for the reduced risk of cardiac disease and the use of omega 3 fishoil. Fishoil has enormous health benefits, even over and above cardiovascular disease reduction.

The heart and blood vessel benefits include:

a) decreased liporotein (a), triglycerides and blood pressure

b) elevation of hdl

c) reduction of inflammation in the blood vessel walls

d) endothelial function improvement (inner lining of blood vessel walls)

e) makes blood less likely to form clots

f) reverses and stabilizes plaques

g) contributes to the energy of the heart

h) counteracts dysrhythmias (irregular heart beats)

3. Magnesium

A lot of heart disease sufferers, especially diabetics and postmenopausal women, and acute disease are magnesium deficient. Magnesium helps so many heart conditions including arterial disease, stroke, ischaemic heart disease, heart failure, high blood pressure.

4. L-arginine

An aminoacid that improves nitric oxide, which relaxes arteries, promotes blood flow and keeps them flexible.

5. Some supplements to lower bad cholesterol:

a) RED YEAST RICE, for example Solal’s Cholestaway
A red powder powder produced by the fermentation of a strain of monascus purpureus
It is an antioxidant, may lower LDL cholesterol, increase HDL cholesterol and decrease triglyceride levels
It may inhibit HMG coA reductase as do statin drugs, and Coenzyme q10 supplementation is recommended as with statin drugs
Redyeast rice may also lower LDL cholesterol Contraindications include:

  • the use of grapefruit juice increases levels 15 fold when used in conjuction
  • not to be used in pregnancy or lactation

  • With high doses of nicotinic acid (>1g/d)

  • increased risk of muscular breakdown (rhabdomyolysis)

The usual dosage is 600-2400 mg/d taken as 1 to 4 divided doses.

b) Policosanol

A group of related lipid alcohols (long chain fatty alcohols)
Policosanol may inhibit synthesis of endogenous cholesterol, may inhibit oxidation of cholesterol and may elevate hdl
Usual dosages are 5-20mg /day

c) Beta-Sitosterol

300mg / day may compete with cholesterol absorption in the small intestine, thereby reducing absorption of cholesterol
Beta sitosterol is an ingredient in mixed phytosterol products
Beta sitosterol is part of some formulas designed to lower blood cholesterol, treat enlarged prostate (due to 5alpha reductase inhibition)
Or treat endogenous testosterone levels
General therapeutic doses are 60-130mg /day

d) Niacin / nicotinic acid

A special form of vitamin B3
Benefits include :
a) life extension properties due to surtuin gene activation
b) cardiovascular benefits include :
reversal of atherosclerosis, improvement of blood circulation, helps prevent abnormal blood clotting, may lower heart attack risk, may alleviate raynaud’s disease, lowers LDL, increases HDL, decreases VLDL, may inhibit crosslinking, may lower lipoprotein (a), lowers triglycerides.

side effects include: diarrhoea, nausea, muscle cramps, headaches, dry skin, erythema, flushing.

Niacin is an overlooked, wonderful supplement, that has lost favour to statin drugs. Niacin should be revisited and considered by more people wanting natural ways to manage their cholesterol and health.

6. Vitamin k2

Mk7 is a form of vitamin k2.
The most familiar vitamin k is vitamin k1 found in green leafy vegetables or supplements.
Vitamin k2 is less easy to find. It is found in fermented Japanese soy dish natto as well as in fermented and curderd cheese.
Both vitamin k1 and k2 are important for the health of the skeletal system as well as the heath of the blood vessel system, but vitamin k2 is the more beneficial. Vitamin k2 supplementation equates to better bone health and heart and blood vessel health.

7. ATP/ energy enhancers

A) Coenyzme q10 and solal’s superior form idebenone does so many good things and should be seriously considered for those seeking good health as they get older.

Coq10 does the following :

a) slows the aging process and helps prevent disease

b) helps heart disease sufferers

c) reduces hypertension

d) generates energy and strength

e) enhances the immune system and helps reduce cancer risk

f) counteracts depletions caused by statin drug therapy

g) improves neurological disorders

h) protects against gum disease

B) L-carnitine

L-carnitine helps transport fatty acids into the mitochondria to produce ATP (the molecule of energy). It also transports waste, aterial out of the mitochondria

C) D-ribose

“A new kid on the block” it rapidly restores depleted energy in sick hearts since it is a building block of ATP.

8. Others, and so many more!!

a) Pomegranate juice : lowers blood pressure, reduces oxidized cholesterol, decreases carotid artery wall thickness

b) Garlic contains powerful sulphur and selenium compounds used for the prevention and treatment of diseases for many years

c) B vitamins like B6, B12, folic acid help lower homocysteine and cardiovascular disease

References:
1. Selnes OA, Grega MA, Borowicz LM, Jr. , et al. Self-reported memory symptoms with coronary artery disease: a prospective study of CABG patients and nonsurgical controls. Cogn Behav Neurol. 2004 Sep;17(3):148-56.
2. Toner I, Peden CJ, Hamid SK, et al. Magnetic resonance imaging and neuropsychological changes after coronary artery bypass graft surgery: preliminary findings. J Neurosurg Anesthesiol. 1994 Jul;6(3):163-9.
3. Rasouli ML, Nasir K, Blumenthal RS, et al. Plasma homocysteine predicts progression of atherosclerosis. Atherosclerosis. 2005 Jul;181(1):159-65.
4. Xie LQ, Wang X. C-reactive protein and atherosclerosis. Sheng Li Ke Xue Jin Zhan. 2004 Apr;35(2):113-8.
5. Verma S. C-reactive protein incites atherosclerosis. Can J Cardiol. 2004 Aug;20 Suppl B29B-31B.
6. Stochmal E, Szurkowska M, Czarnecka D, et al. Association of coronary atherosclerosis with insulin resistance in patients with impaired glucose tolerance. Acta Cardiol. 2005 Jun;60(3):325-31.
7. Sharrett AR, Patsch W, Sorlie PD, et al. Associations of lipoprotein cholesterols, apolipoproteins A-I and B, and triglycerides with carotid atherosclerosis and coronary heart disease. The Atherosclerosis Risk in Communities (ARIC) Study. Arterioscler Thromb. 1994 Jul;14(7):1098-104.
8. Muis MJ, Bots ML, Bilo HJ, et al. High cumulative insulin exposure: a risk factor of atherosclerosis in type 1 diabetes? Atherosclerosis. 2005 Jul;181(1):185-92.
9. Malkin CJ, Pugh PJ, Jones RD, Jones TH, Channer KS. Testosterone as a protective factor against atherosclerosis—immunomodulation and influence upon plaque development and stability. J Endocrinol. 2003 Sep;178(3):373-80.
10. Howes PS, Zacharski LR, Sullivan J, Chow B. Role of stored iron in atherosclerosis. J Vasc Nurs. 2000 Dec;18(4):109-14.
11. Jones RD, Nettleship JE, Kapoor D, Jones HT, Channer KS. Testosterone and atherosclerosis in aging men: purported association and clinical implications. Am J Cardiovasc Drugs. 2005;5(3):141-54.
12. de Valk B, Marx JJ. Iron, atherosclerosis, and ischemic heart disease. Arch Intern Med. 1999 Jul 26;159(14):1542-8.
13. Drexel H, Amann FW, Beran J, et al. Plasma triglycerides and three lipoprotein cholesterol fractions are independent predictors of the extent of coronary atherosclerosis. Circulation. 1994 Nov;90(5):2230-5.
14. Chau LY. Iron and atherosclerosis. Proc Natl Sci Counc Repub China B. 2000 Oct;24(4):151-5.
15. Bolad I, Delafontaine P. Endothelial dysfunction: its role in hypertensive coronary disease. Curr Opin Cardiol. 2005 Jul;20(4):270-4.
16. Chakraphan D, Sridulyakul P, Thipakorn B, et al. Attenuation of endothelial dysfunction by exercise training in STZ-induced diabetic rats. Clin Hemorheol Microcirc. 2005;32(3):217-26.
17. Harvey PJ, Picton PE, Su WS, et al. Exercise as an alternative to oral estrogen for amelioration of endothelial dysfunction in postmenopausal women. Am Heart J. 2005 Feb;149(2):291-7.
18. Hink U, Tsilimingas N, Wendt M, Munzel T. Mechanisms underlying endothelial dysfunction in diabetes mellitus: therapeutic implications. Treat Endocrinol. 2003;2(5):293-304.
19. Lteif AA, Han K, Mather KJ. Obesity, insulin resistance, and the metabolic syndrome: determinants of endothelial dysfunction in whites and blacks. Circulation. 2005 Jul 5;112(1):32-8.
20. Newby DE, McLeod AL, Uren NG, et al. Impaired coronary tissue plasminogen activator release is associated with coronary atherosclerosis and cigarette smoking: direct link between endothelial dysfunction and atherothrombosis. Circulation. 2001 Apr 17;103(15):1936-41.
21. Panus C, Mota M, Vladu D, Vanghelie L, Raducanu CL. The endothelial dysfunction in diabetes mellitus. Rom J Intern Med. 2003;41(1):27-33.
22. Papamichael CM, Aznaouridis KA, Stamatelopoulos KS, et al. Endothelial dysfunction and type of cigarette smoked: the impact of ‘light’ versus regular cigarette smoking. Vasc Med. 2004 May;9(2):103-5.
23. Suvorava T, Lauer N, Kojda G. Physical inactivity causes endothelial dysfunction in healthy young mice. J Am Coll Cardiol. 2004 Sep 15;44(6):1320-7.
24. Toikka JO, Ahotupa M, Viikari JS, et al. Constantly low HDL-cholesterol concentration relates to endothelial dysfunction and increased in vivo LDL-oxidation in healthy young men. Atherosclerosis. 1999 Nov 1;147(1):133-8.
25. Vakkilainen J, Makimattila S, Seppala-Lindroos A, et al. Endothelial dysfunction in men with small LDL particles. Circulation. 2000 Aug 15;102(7):716-21.
26. Apetrei E, Ciobanu-Jurcut R, Rugina M, Gavrila A, Uscatescu V. C-reactive protein, prothrombotic imbalance and endothelial dysfunction in acute coronary syndromes without ST elevation. Rom J Intern Med. 2004;42(1):95-102.
27. Kunes P. C-reactive protein in the pathogenesis of atherosclerosis: advantage and pitfalls of the “Mainz hypothesis. ” Cas Lek Cesk. 2005;144(1):25-31.
28. Targher G, Bertolini L, Zoppini G, Zenari L, Falezza G. Increased plasma markers of inflammation and endothelial dysfunction and their association with microvascular complications in Type 1 diabetic patients without clinically manifest macroangiopathy. Diabet Med. 2005 Aug;22(8):999-1004.
29. Sainani GS, Sainani R. Homocysteine and its role in the pathogenesis of atherosclerotic vascular disease. J Assoc Physicians India. 2002 May;50 Suppl16-23.
30. Drouet L, Bal dit SC. Is fibrinogen a predictor or a marker of the risk of cardiovascular events? Therapie. 2005 Mar;60(2):125-36.
31. Caballero AE, Arora S, Saouaf R, et al. Microvascular and macrovascular reactivity is reduced in subjects at risk for type 2 diabetes. Diabetes. 1999 Sep;48(9):1856-62.
32. Ceriello A. Hyperglycaemia: the bridge between non-enzymatic glycation and oxidative stress in the pathogenesis of diabetic complications. Diabetes Nutr Metab. 1999 Feb;12(1):42-6.
33. Cubeddu LX, Hoffmann IS. Insulin resistance and upper-normal glucose levels in hypertension: a review. J Hum Hypertens. 2002 Mar;16 Suppl 1S52-5.
34. Nowak A, Stankiewicz W, Szczesniak L, Korman E. Glucosamine in the blood serum of young people with diabetes mellitus type 1. Endokrynol Diabetol Chor Przemiany Materii Wieku Rozw. 1999;5(2):97-101.
35. Steinbaum SR. The metabolic syndrome: an emerging health epidemic in women. Prog Cardiovasc Dis. 2004 Jan;46(4):321-36.
36. Woodman RJ, Chew GT, Watts GF. Mechanisms, significance and treatment of vascular dysfunction in type 2 diabetes mellitus: focus on lipid-regulating therapy. Drugs. 2005;65(1):31-74.
37. Brandes RP, Fleming I, Busse R. Endothelial aging. Cardiovasc Res. 2005 May 1;66(2):286-94.
38. Kravchenko J, Goldschmidt-Clermont PJ, Powell T, et al. Endothelial progenitor cell therapy for atherosclerosis: the philosopher’s stone for an aging population? Sci Aging Knowledge Environ. 2005 Jun 22;2005(25):e18.
39. Rubanyi GM. The role of endothelium in cardiovascular homeostasis and diseases. J Cardiovasc Pharmacol. 1993;22 Suppl 4:S1-14.
40. Available at: http://www. medreviews. com/ pdfs/articles/RIU_5Suppl7_S21. pdf. Accessed April 20, 2005.

 
Share this page on facebook