Into the Heart

Barley lowers LDL cholesterol & triglycerides

Elevated LDL cholesterol has a role in the development of coronary plaque instability. Lowering LDL cholesterol stabilizes plaques and reduces the likelihood of acute coronary syndromes. Lowering total cholesterol also reduces the risk of coronary heart disease.

In an analysis of eight randomized controlled trials participants consuming barley had statistically significant reductions in total cholesterol –13 mg/dL, LDL cholesterol –10 mg/dL, and triglycerides –12 mg/dL compared with study participants who did not consume barley.

The study trials were 4 -12 weeks in duration. Study participants consumed 3 to 10 g of β-glucan from various forms of barley.

Furthermore, a significant reduction in total cholesterol and LDL cholesterol was found regardless of whether participants followed a low-fat diet or a regular (bacon & eggs) type diet. It is still more healthful to avoid bacon and such.

Barley (and oats) have a similar concentration of soluble fibers called β-glucan. Wheat and rice do not have this type of fiber. A diet high in β-glucan has been shown to slow gastric emptying, digestion, and absorption. These effects are associated with increased excretion of bile acids and neutral sterols, increased breakdown of cholesterol, and reduced absorption of cholesterol and fat.

Fillet of sole with barley and asparagus makes a heartwarming dinner. For more barley recipes visit www.Barleyfoods.org  click on the Let’s Eat tab.

Source:
Annals of Family Medicine 7:157-163 (2009)
Craig I. Coleman, PharmD, University of Connecticut School of Pharmacy

 

Hot Flashes a Matter of Her Heart

Emerging research suggests underlying vascular changes among women with hot flashes.

The study noted below examined associations between hot flashes and indices of subclinical cardiovascular disease including flow mediated dilation , coronary artery calcification , and aortic calcification.

Impaired flow mediated dilation is an indicator of endothelial dysfunction. The endothelium is the protective inner lining of the artery. Upon calcification arteries become easily damaged and stiff. The heart then has to pump harder and will wear out faster.

In the study noted hot flashes were associated with significantly lower flow mediated dilation and greater coronary artery and aortic calcification in age and race adjusted models.

Keep in mind pectin , the soluble fiber in prunes helps inhibit aortic calcification. Additionally, Vitamin K-2 is required for the activation of the vascular protein MGP (Matrix Gla Protein) , which is the primary inhibitor of arterial calcification. Butter and cheese produced from grass feed cows, and fermented foods contain vitamin K-2.

For postmenopausal women diminishing hot flashes is a serious matter of the heart.

From the Study of Women’s Health Across the Nation Heart Study. Participants were 492 women (35% black, 65% white) 45 to 58 years of age who were free of clinical cardiovascular disease and had a uterus and at least one ovary.

Source:
Hot Flashes and Subclinical Cardiovascular Disease
Circulation. 2008;118:1234-1240.
American Heart Association, Inc. 2008

A Hot Flash … A Burst of Oxidative Stress

During a hot flash the blood vessels close to the skin open wider than usual. This allows for more blood flow which generates a sense of warmth. Perspiration then occurs on the skin to cool down the body.

A burst of oxidative stress also accompanies a hot flash. The oxidative stress causes LDL cholesterol in the arteries to essentially brew contributing to inflamed, stiffened coronary arteries. Oxidative stress also wears down the protective inner lining of the artery: the endothelium. This leads to torn and tightened arteries.

For post menopausal women who experience ongoing hot flashes it is cardio protective to diminish the occurrence of hot flashes and counteract the bursts of oxidative stress. Berries, red peppers and prunes are high in water soluble inner cell antioxidants.

However, the oxidative stress that accompanies a hot flash effects the fat soluble membrane of the cell. Enhancing vitamin E intake will be beneficial because vitamin E is the prime cell membrane stabilizer and antioxidant. Vitamin E does not necessarily reduce hot flashes but is able to provide cellular protection from oxidative stress.

The daily reference intakes for vitamin E is 15 mg. One quarter cup a sunflower seeds has 17 mg of vitamin E. Olive oil and wheat germ oil are also good sources of vitamin E. Vitamin E also helps reduce production of thromboxane A2 which causes platelet clumping.

Source:
Influence of the presence of hot flashes during menopause on the metabolism of nitric oxide.
Med Clin (Barc). 2000 Jan 22;114(2):41-5
Leal Hernandez M, Abellan Alernan J

Hot Flashes and Systolic Blood Pressure

The hormone estrogen has a regulatory role in arterial structure and function. During the menopausal transition estrogen fluctuations, primarily diminished estrogen contributes to vasomotor symptoms: hot flashes.

While hot flashes are disruptive there is more serious reason to be concerned. According to a study noted in Menopause 2007, menopausal women with hot flashes tend to have elevated systolic blood pressure when compared to menopausal women who do not experience hot flashes. Elevated systolic blood pressure contributes to damaged, stiff arteries which increases cardiovascular risk. Torn damaged arteries stimulate a cascade of inflammatory cellular mediators which leads to arterial build-up an plaque.

The association between hot flashes and systolic blood pressure is independent of age, race/ethnicity, body mass index, and menopausal status. Hot flashes were not associated with changes in diastolic blood pressure.

Milled flaxseed, (calcium enriched & organic soy milk nice/nurturing) soy nuts, the supplement pycnogenol and soy based estrogen replacement (cream, gel or patch) are all options to help diminish hot flashes in menopausal and post menopausal women.

Source:
Hot flashes are associated with increased ambulatory systolic blood pressure.
Menopause. 2007; 14:308-315.
Gerber LM, et al.

More Kale . . . Less LDL Cholesterol

People who consume more fruits and vegetables have lower risk factors for cardiovascular disease such as hypertension, obesity, and type 2 diabetes. Cruciferous vegetables which includes broccoli, cabbage, cauliflower, kale, brussel sprouts, turnips, and radishes generate the greatest protection.The enhanced cardioprotection of cruciferous vegetables are thought to result from indolic compounds.

Plant indoles appear to have beneficial effects on cholesterol synthesis by lessing the activity of Apolipoprotein B-100.

Apolipoprotein B-100 is a key protein involved in the synthesis and transport of LDL "bad" cholesterol. Reducing apoB-100 results in substantial reductions in atherosclerosis (fatty deposits in the arteries).

Researchers from the University of Hawaii found that the phytonutrient (indole 3 carbinol) found in cruciferous vegetable lowered liver cell secretion of apolipoprotein B-100 by more than half.  Significant decreases in cellular lipid synthesis, including triglycerides and cholesterol esters were also observed in cells treated with indole 3 carbinol.

Kale is a nutritional dense food source of indole 3 carbinol. Kale can be served cold as the base of a salad or lightly heated in olive oil and garlic. Adding in a few diced prunes will also enhance cholesterol absorption. Prunes are high in pectin & antioxidants. Pectin acts as a cholesterol sponge in the intestine.  Kale & prunes added to meal planning can significantly reduce the production & transport of LDL artery clogging cholesterol.

In addition to helping reducing Apo B-100, kale is high in the eye protecting nutrients lutein & zeaxanthin (3276 mcg per one cup).

Source:
Cruciferous Indole-3-Carbinol Inhibits Apolipoprotein B Secretion in HepG2 Cells
Geoffrey K. Maiyoh4,5, Joan E. Kuh
J. Nutr. 137:2185-2189, October 2007

Modular Structure of Solubilized Human Apolipoprotein B-100
Alexander Johs, Michal Hammel
J. Biol. Chem., Vol. 281, Issue 28, 19732-19739, July 14, 2006

A Little Dark Chocolate . . . Less C-Reactive Protein

C-reactive protein reflects the presence and intensity of inflammation in the body. Inflammation (swelling) of the arteries is a risk factor for cardiovascular disease. Inflammation draws in other cellular components that build up in the artery wall. This build-up eventually contributes to narrow rigid arteries.

An Italian based study reported in the October 2008 issue of the Journal of Nutrition noted that consuming moderate amounts of dark chocolate can significantly reduce levels of C-reactive protein (CRP).

The lowering of CRP in study participants corresponded to a shift from medium risk of cardiovascular disease to low risk. On average there was a 17% risk reduction observed. 

Participants who consumed 1 serving (20g) of dark chocolate every three days had CRP concentrations significantly lower than those who did not consume any or . . . had larger amounts of chocolate. If you eat to much . . . the protection effect tends to disappear.

Extra Dark Chocolate with 70% and 85% cocoa has higher cardioprotective & antioxidant benefits.
So Indulge. . . a little.

Source:
Regular Consumption of Dark Chocolate Is Associated with Low Serum Concentrations of C-Reactive Protein in a Healthy Italian Population
Romina di Giuseppe3, Augusto Di Castelnuovo
J. Nutr. 2008 Oct; 138:1939-1945

Cocoa Antioxidants and Cardiovascular Health.
Keen CL
Am J Clin Nutr. 2005 Jan; 81:2985-303S

Berries, Reduce Blood Pressure and Inhibit Platelet Function

Previous scientific studies indicate that the consumption of polyphenol-rich foods (cocoa, tea, and red wine) are beneficial to cardiovascular health. In addition to vitamin C, folate, potassium, and soluble fiber, various types of berries are also a rich source of polyphenols.

A recent study conducted in Helsinki, Finland aimed to investigate the effects of berry consumption on hemostatic function, serum lipids, and blood pressure. In this study, seventy-two male and female middle-aged volunteers with cardiovascular risk factors consumed moderate amounts of berry or placebo control products for 8 weeks. (100 g berries + 1 small glass of berry drink per day).

The results were impressive: berry consumption inhibited platelet function by 11% in the berry group and 1.4% control group. Plasma biomarkers of platelet activation, coagulation, and fibrinolysis did not change during the intervention. Serum HDL-cholesterol concentrations (good cholesterol) increased significantly more in the berry group 5.2% than in the control group 0.6%. However total cholesterol and triacylglycerol remained unchanged.

Systolic blood pressure decreased significantly. This decrease mostly occurred in subjects with high baseline blood pressure (7.3 mm Hg in the highest tertile). Polyphenol and vitamin C concentrations in plasma increased. However, other nutritional biomarkers (ie, folate, tocopherols, sodium, and potassium) were unaffected.

The plasma concentrations of polyphenols, such as quercetin, caffeic acid, protocatechuic acid, p-coumaric acid, and vanillic acid, were significantly greater in the berry group. The berry products were prepared from black currants, lingonberries (similar to small cranberries), bilberries (sometimes called European blueberries), and chokeberries, as well as from small amounts of strawberries, red raspberries, and sucrose.

The consumption of moderate amounts of berries resulted in favorable changes in platelet function, HDL cholesterol, and blood pressure. The results of this study indicate that regular consumption of berries may play a role in the prevention of cardiovascular disease.

A visit to the strawberry field nurtures the soul, the berries nurture the heart.

Source:
Favorable effects of berry consumption on platelet function, blood pressure, and HDL cholesterol
Iris Erlund, Raika Koli, Georg Alfthan, Jukka Marniemi
American Journal of Clinical Nutrition, Vol. 87, No. 2, 323-331, February 2008

Aerobic Interval Exercise: an effective treatment for metabolic syndrome

When clustered together high blood sugar (hyperglycemia), high cholesterol/triglycerides (hyperlipidemia),  high blood pressure (hypertension) and excess belly fat are referred to as metabolic syndrome. Individuals with metabolic syndrome die prematurely and are three times more likely to die of heart disease than those without this cluster of disorders. Medical studies indicate that exercise can prevent and/or reverse metabolic syndrome; with high intensity exercise resulting in a greater therapeutic benefit than moderate exercise.

According to a study noted in the July 2008 edition of Circulation, researchers at the Norwegian University of Science and Technology evaluated two exercise programs to identify which is most effective at reversing metabolic syndrome; participants diagnosed with metabolic syndrome were divided into three groups: aerobic interval training, continuous moderate exercise or a non specific exercise group.

The aerobic interval training program instructed participants to warm up at 70% of their maximum heart rate for ten minutes. The warm up was followed by four four-minute intervals of intense exercise (90% of their maximum heart rate) with three minute recovery periods at 70% of their maximum heart rate between intense intervals. These sessions ended with a five minute cool-down period.

Excess belly fat, metabolic syndrome and high blood pressure

Belly fat (visceral obesity) is considered to have a fundamental role in the simultaneous development of high blood sugar (hyperglycemia), high cholesterol/triglycerides (hyperlipidemia), and high blood pressure (hypertension). When clustered together these disorders are referred to as the metabolic syndrome. This syndrome results in a significant increase in cardiovascular morbidity and mortality. Studies indicate visceral obesity, the accumulation of belly fat (adipose tissue) is the main cause of metabolic syndrome.

Adipose (fat) tissue is a major endocrine organ that secrets a variety of bioactive substances termed adipocytokines. Accumulated visceral adipose (fat) tissue produce and secrete a number of adipocytokines, such as the hormone leptin, tumor necrosis factor-α, interleukin-6, angiotensinogen, and free fatty acids which contribute to the development of hypertension. The connection between visceral obesity, metabolic syndrome, and the development of hypertension is related in the next three overviews.

Keep in mind for individuals with excess belly fat and those who are overweight, weight loss will lessen the activity of the bioactive substances that contribute to the development of hypertension.

Sources:
A high-fat, refined-carbohydrate diet induces endothelial dysfunction and oxidant/antioxidant imbalance and depresses NOS protein expression.
Roberts CK, Barnard RJ, Sindhu RK
J Appl Physiol 2005, 98:203-210.

The underlying mechanisms for the development of hypertension in the metabolic syndrome.
Hidekatsu Yana, Yoshiharu Tomona
Nutrition Journal 2008

Insulin Resistance, metabolic syndrome and high blood pressure

One role of the hormone insulin is to transport glucose to cells to be used as energy. Insulin resistance occurs when the cells do not take in/accept glucose. The glucose then remains in the blood stream and cells have inadequate energy which generates fatigue. Obesity, and excess belly fat are the primary causes of insulin resistance. Obesity, is associated with decreased activity of insulin receptors, a decreased number of insulin receptors and with post-receptor failure to activate tyrosine kinase.

Insulin resistance is the primary disease driver of metabolic syndrome. Several mechanisms connect insulin resistance and metabolic syndrome with hypertension. Data indicates that insulin stimulates renal (kidney) sodium re-absorption. Insulin resistance is also associated with the development of salt-sensitive hypertension through the anti-natriuretic effect of insulin. An anti-natriuretic agent causes the body to retain sodium. Essentially, high insulin levels cause the body to hold salt, which increases blood volume. High blood volume causes the heart and arteries to work harder to push blood through circulatory system. As such, the increase in blood volume contributes to high blood pressure.

High serum insulin levels are also associated with an increase in circulating endothelin-1 in healthy and insulin-resistant individuals. Endothelin-1 is a blood vessel tightening (vasocontrictor) peptide. Elevated levels of endothelin-1 have been demonstrated in various disease conditions that are characterized by sodium retention and/or renal vasoconstriction.

Obesity and excess belly fat stimulate high insulin levels. The high insulin levels then contribute to vasoconstriction, increased intravascular fluid, and decreased vasodilatation, which contribute to the development of hypertension. The good news is that for those with excess weight and/or excess belly fat, weight loss can substantially lessen the bioactive mechanisms that lead to the development of insulin resistance and hypertension.

Sources:

Abnormalities of renal sodium handling in the metabolic syndrome. Results of the Olivetti Heart Study. Strazzullo P, Barbato A, Galletti F
J Hypertens 2006, 24:1633-1639

The underlying mechanisms for the development of hypertension in the metabolic syndrome.
Hidekatsu Yana, Yoshiharu Tomona
Nutrition Journal 2008