Into the Heart

Cocoa Powder Enhances Plasma HDL Cholesterol Concentrations

The oxidation of LDL cholesterol has a role in the development of coronary artery disease: atherosclerosis. Uptake of oxidized LDL by macrophages and smooth muscle cells leads to the formation of fatty streaks, a key stage in early atherosclerosis. These vascular lesions accumulate large amounts of lipids(fats) such as cholesterol ester.

In addition, oxidized LDL induces the expression of adhesion molecules in monocytes, such as vascular cell adhesion molecule-1 and intercellular adhesion molecule-1, and also increases production of growth factors by smooth muscle cells and fibroblasts.  These cellular components compile and create an inflammatory nest (cellular blockage) within the artery.  As such, inhibition of LDL oxidation is thought to suppress atherosclerotic lesions.

Cocoa powder is rich in polyphenols such as catechins and procyanidins and has been shown to inhibit LDL oxidation and atherogenesis. Studies indicate the intake of cocoa powder lessens the susceptibility of LDL to oxidation. This protective mechanism of cocoa consumption is brought about by an increase in HDL cholesterol concentrations. High HDL concentrations inhibit oxidation of LDL cholesterol.

The results of a current study indicate that consumption of cocoa powder containing 26 g/day of polyphenolic substances for twelve weeks increased the resistance of LDL to oxidation and increased HDL cholesterol concentrations in individuals with normal cholesterol and mildly high cholesterol.

In this study, a significantly greater increase in plasma HDL cholesterol (24%) was observed in the cocoa group than in the control group (5%).

The results of this study are consistent with other studies that show a positive correlation between inhibition of LDL oxidation and the phenolic compounds derived from (red) wine or the concentration of major polyphenols in cocoa powder such as catechin, epicatechin, and their oligomers.

The second study noted below reported that HDL-cholesterol concentrations increased by 11% and 14% after 3 week intake of dark chocolate or dark chocolate enriched with cocoa polyphenols. The daily consumption of catechin and procyanidins in this study was 270 mg with the dark chocolate and 420 mg with the polyphenol-enriched dark chocolate.

The results of this study indicate that the increase in plasma HDL-cholesterol concentrations caused by polyphenols may be dose-related. This study also hypothesize that chocolate fatty acids may modify the fatty acid composition of LDL and make it more resistant to oxidative damage.

According to Richard Karas, M.D., Ph.D., in a presentation at the American Heart Association Scientific Sessions 2004, changes in high density lipoprotein-cholesterol (HDL-C) and HDL-C-inclusive parameters are the strongest predictors of coronary heart disease risk reduction in lipid intervention trials.

Cacao beans are used as an ingredient in cocoa and chocolate. Cacao beans are rich in polyphenols, such as catechin, epicatechin, procyanidin B2 (dimer), procyanidin C1 (trimer), cinnamtannin A2 (tetramer), and other oligometric procyanidins.

Sources:
1) Cocoa powder reduces LDL oxidative susceptibility and has beneficial effects on plasma HDL-cholesterol concentrations in humans
Seigo Baba, Naomi Osakabe,
American Journal of Clinical Nutrition, Vol. 85, No. 3, 709-717, March 2007

2)Dark chocolate consumption increases HDL cholesterol concentration and chocolate fatty acids may inhibit lipid peroxidation in healthy humans.
Mursu J, Voutilainen S, Nurmi T, et al.
Free Radic Biol Med 2004;37:1351–9.

Estrogen Replacement . . . earlier

The vascular endothelium is a single layer of cells lining all the blood vessels in the body. The endothelium is essential for vasodilatation in response to increases in blood flow associated shear stress: termed endothelium dependent flow mediated vasodilatation (FMD).

Several vasodilators are released by the endothelium in response to shear stress including nitric oxide and prostacyclin. A small FMD response is interpreted as indicating a low nitric oxide bioavailability and is associated with an increased risk of vascular disease and cardiac events.

Vascular endothelial and smooth muscle cells express estrogen receptors A and B.

The study indicated below, evaluated flow mediated dilatation (FMD) of the brachial artery in 134 postmenopausal women before and after acute (1 hour) and chronic (3 months) of estrogen administration (replacement).

Estrogen administration improved FMD more in women within five years of menopause, (76% acute, 74% chronic administration) than in women more than five years since menopause (45% acute, 48% chronic).

Although acute and chronic estrogen administration improved endothelial function in all women, the improvement was dependent on time since menopause: the duration of hormone deprivation.

Women who had previously used estrogen replacement also had more improved FMD (59% acute, 63% chronic) upon administration than nonusers of estrogen replacement (31% acute, 38% chronic).

Estrogen tends to exert a favorable effect on endothelial function and arterial health when estrogen replacement therapy (ERT) or HRT is initiated soon after menopause.

Keep in mind, the type/dose, time of initiation of ERT or HRT should be customized to a woman’s age, cardiovascular risk factors and pre-existing cardiovascular conditions.

Source:

Time Since Menopause Influences the Acute and Chronic Effect of Estrogens on Endothelial Function. Cristiana Vitale, Giuseppe Mercuro MD’s

Arteriosclerosis, Thrombosis and Vascular Biology. 2008;28:348

Six Breaths . . . lower blood pressure

Baroreceptors help maintain short term control of blood pressure. Pressure receptors called arterial baroreceptors (sensory nerve endings in the vessel walls) are located in the carotid arteries and the arch of the aorta.  They monitor the pressure of the blood coming from the aorta and carotid arteries. An increase in arterial pressure triggers these receptors to send impulses to the cardiovascular control center. 

A rise in blood pressure sends a message (increased discharge) from the baroreceptors to the cardiovascular control center in the brain. This leads to an increased discharge of parasympathetic nerves to the heart and a decreased discharge of the sympathetic nerves to the heart, which decreases the heart rate and stroke volume (amount of blood ejected from the heart with one contraction).

There is also a decreased discharge down the sympathetic nerves to the arterioles, producing vasodilation (widening) and thus a decrease in peripheral resistance which in turn returns blood pressure to normal.

The baroreflex is one of the most important cardiovascular control mechanisms adjusting heart rate and sympathetic output to the blood vessels on a beat-by-beat basis. Sympathetic nerves are extremely important in regulating blood pressure and blood flow.

Sympathetic hyperactivity and parasympathetic withdrawal may cause and sustain hypertension. An imbalance in this system is related to a reduced or reset arterial baroreflex sensitivity. However there is good news . . . slow breathing at six breaths per minute increases baroreflex sensitivity and reduces sympathetic activity suggesting a potentially beneficial effect in hypertension.

The study noted below indicates slow breathing is capable of modifying blood pressure and improving baroreflex sensitivity in individuals with hypertension. Twenty individuals, average age 56 with essential hypertension and twenty six individual (controls), average age 52 without hypertension were studied.

Baroreflex sensitivity was measured by autoregressive spectral analysis and "alpha angle" method. Slow breathing at six breaths per minute decreased systolic pressure in hypertensive subjects from 149.7±3.7 to 141.1±4 mm Hg and diastolic pressure from 82.7±3 to 77.8±3.7 mm Hg.

Controlled breathing at 15 breaths per minute decreased systolic to 142.8±3.9 mm Hg but not diastolic pressure and decreased RR interval without altering the baroreflex.

Slow breathing increased baroreflex sensitivity in hypertensives from 5.8±0.7 to 10.3±2.0 ms/mm Hg and controls from 10.9±1.0 to 16.0±1.5 ms/mm Hg without inducing hyperventilation.

Six breaths per minute . . .  lower blood pressure, enhanced baroreflex sensitivity: something to keep in mind.

Source:
Slow Breathing Improves Arterial Baroreflex Sensitivity and Decreases Blood Pressure in Essential Hypertension
Luciano Bernardi, MD
Hypertension. 2005;46:714.

Blood Volume/Pressure . . . Salt

Blood pressure is the force exerted by blood against the arterial walls. It is determined by how much blood is pumped and the resistance to blood flow.

Acute (short term) regulation of blood pressure is achieved by the sympathetic nervous system. Long term regulation of blood pressure is primarily a function of the kidneys. The kidneys regulate blood pressure by helping control blood volume. The amount of fluid in the blood (blood volume) is determined by the amount of water and sodium taken in, and the amount of water and sodium excreted by the kidneys into urine (and lost through the gastrointestinal tract, lungs and skin).

If too much sodium or water is retained blood volume increases. An increase in blood volume causes the heart to pump harder to circulate more fluid . . . causing blood pressure to increase (hypertension).

The hormones renin, angiotensin II, aldosterone and vasopressin (ADH) increase blood volume, which results in increased  blood pressure.

The incremental rise in blood pressure with age, and the prevalence of hypertension are directly related to sodium intake. A 1.3-g/day lower lifetime sodium intake translates into an approximately 5-mm smaller rise in systolic blood pressure as individuals advance from 25 to 55 years of age. Such sodium reduction is estimated to save 150,000 (U.S) lives annually.

Keep in mind: the majority of sodium consumption in the United States is derived from amounts added during food processing and preparation.

Source:
Reducing the Population Burden of Cardiovascular Disease by Reducing Sodium Intake.
Barry D Dickinson, PhD; Stephen Havas, MD, MPH, MS
Arch Intern Med 2007;167:1460-1468