Preserving/Restoring Vascular Health

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“Metabolic syndrome” – typically associated with increased abdominal fat, elevated levels of triglycerides and insulin, low HDL cholesterol, and raised blood pressure – is a key cause of vascular disease, diabetes, and cancer. This syndrome is usually associated with increased activity of the sympathetic nervous system – often manifesting as high resting heart rate and blood pressure – and such an increase appears to increase risk for vascular disorders, cancer, and total mortality. The drug carvedilol, often used to treat hypertension and heart failure, may provide notable protection to people with metabolic syndrome by blocking the effects of excessive sympathetic activity.

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A concise summary of lifestyle strategies for reducing your risk for stroke.

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Although moderate elevations of the metabolite homocysteine (hcy) correlate with increased risk for heart attack and stroke, the failure of vitamin therapies which lower hcy to reduce vascular risk reveals that moderately elevated hcy per se does not cause heart disease. Why then do hcy levels correlate with risk? It is proposed that hcy levels are often elevated because of the actions of the hormone-like compounds interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) on the liver – and that these hormones do indeed promote vascular disease, in part by inducing the liver to make the pro-inflammatory factor serum amyloid A. Hence, lowering the level or the activity of IL-6 and TNF-alpha may be expected to alleviate the excess cardiovascular risk associated with elevated hcy.

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There is reason to suspect that both dietary nitrate – found in green leafy vegetables and beets – and the key phytochemical in spirulina, phycocyanobilin (PhyCB), can act on the kidneys to promote more efficient excretion of sodium, owing to their ability to boost the bioactivity of the protective hormone nitric oxide while controlling oxidative stress. This in turn would be expected to lessen adrenal production of marinobufagenin, a hormone suspected to mediate both the increase in blood pressure, and the increased risk or vascular diseases, associated with salt-sensitive hypertension. Nitrate and PhyCB might also act directly on MBG’s target tissues to lessen its pathogenic impact.

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In people said to be “salt-sensitive”, a salty diet provokes a temporary fluid overload that is compensated by adrenal secretion of the hormone marinobufagenin (MBG). Although MBG acts on the kidneys to promote sodium and fluid excretion, it also acts on vascular smooth muscle to increase the peripheral resistance to blood flow, raising blood pressure. But the pathogenic impact of salt-sensitive hypertension is greater than can be explained by an increase in hydrostatic pressure alone, and so MBG is suspected to exert additional deleterious effects. MBG is capable of exerting hormone-like effects on certain cells by interaction with the “sodium pump”. It is proposed that one of these hormonal effects is to increase activity of the enzyme NADPH oxidase in the endothelial lining of blood vessels; this might account for the oxidative stress and pro-inflammatory behavior noted in the endothelium of people with salt-sensitive hypertension, and could help to explain the excess vascular risk associated with this disorder.

Published in Medical Hypotheses 2012;78(2):191-6.

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Metabolic syndrome, an important cause of vascular disease and type 2 diabetes, and a risk factor for cancer, is driven by an inflammatory state that arises in overstuffed fat cells (adipocytes). The diabetes drug pioglitazone (Actos) is useful for dampening this adipocyte inflammation and ameliorating metabolic syndrome, but has side effects which limit its broad use. This essay proposes that spirulina and salsalate also have the potential to act directly on adipocytes to quell inflammation, and may complement the utility of pioglitazone in this regard, or be employed as an alternative approach to improving adipocyte function.

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Although a systemic inflammatory state associated with elevated C-reactive protein (CRP) is clearly associated with increased cardiovascular risk, CRP per se does not appear to mediate this association. There is better reason to suspect that elevated serum amyloid A – like CRP, an “acute phase reactant” produced by the liver – is a true cause of cardiovascular disease. This essay suggests that the liver’s production of serum amyloid A could be suppressed by various agents, including spirulina, salsalate, metformin or berberine, and tocotrienols.

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