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Many have asked me this, and I point out that "salt" is not to blame, but rather a diet rich in chloride (contained in salt), and low in potsassium (in many cases). My guess is that having arachidonic acid in one's cells makes the situation much worse, leading to many cases of hypertension that would not occur if the Mead acid was in one's cells, even if the diet was chloride rich and potassium poor. For example: QUOTE: Nitric oxide (NO), a multifunctional effector molecule that plays a central role in the maintenance of vascular homeostasis, regulates vascular tone and inhibits platelet and leukocyte adhesion to endothelial cells. NO status is related to the endothelial function. Patients with hypertension have lower levels of NO, increased free radical production, higher oxidative stress, augmented platelet aggregation, and a change in the arachidonic acid cascade metabolism, all leading to the acceleration of the atherosclerotic process. The study subjects included a group of 21 normotensive healthy subjects (8 males and 13 females) with a mean age of 39.2 +/- 1.8 years and a body mass index of 27.9 kg/m, and another group of 42 patients (19 males and 23 females) with untreated essential hypertension with a mean age of 47.6 +/- 1.7 years and a body mass index of 28.3 kg/m. Serum levels and urinary excretion of NO determined as combined nitrate/nitrite (NOx) and serum malondialdehyde (MDA) concentrations were measured in the 2 groups of subjects. The serum levels and 24-hour urinary excretion of NOx were significantly higher and the renal clearance of NO was lower in the normotensive group than in the hypertensive patients, indicating decreased NO status in hypertension. There was a negative correlation between serum NO levels and mean arterial pressure, suggesting that a decrease in NO availability is related to increase in blood pressure. Serum concentrations of MDA were higher in the hypertensive patients as compared with the normotensive individuals, suggesting increased oxidative stress in hypertensive patients. These results are in agreement with previous studies showing decreased NO and increased oxidative stress in hypertension. In conclusion, patients with essential hypertension as compared with normotensive individuals have lower NO status, which may contribute to the endothelial dysfunction in hypertension. Increased serum malondialdehyde in hypertensives suggests an association between increased oxidative stress with higher blood pressure. UNQUOTE. |
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A new report is consistent with the oxidative stress/inflammation explanation, though, as usual, the researchers are more interested in the idea of inhibiting a protetin that is expressed in larger than normal amounts when the cell is under certain kinds of stress, rather than preventing the stress in the first place:
QUOTE: Dr. Hidefumi Waki, working in a research group led by Professor Julian Paton, has found a novel role for the protein, JAM-1 (junctional adhesion molecule-1), which is located in the walls of blood vessels in the brain.
JAM-1 traps white blood cells called leukocytes which, once trapped, can cause inflammation and may obstruct blood flow, resulting in poor oxygen supply to the brain. This has led to the idea that high blood pressure -- hypertension -- is an inflammatory vascular disease of the brain.
One in three people in the UK are likely to develop hypertension, and with 600 million people affected world wide, it is of pandemic proportions. UNQUOTE.
SOURCE: http://www.sciencedaily.com/releases/2007/04/070415110120.htm |
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QUOTE: ...In 1981, the FDA launched a series of "sodium initiatives" aimed at reducing the nation's salt intake.
Not until after these campaigns were well under way, however, did researchers set out to do studies that might be powerful enough to resolve the underlying controversy. The first was the Scottish Heart Health Study, launched in 1984 by epidemiologist Hugh Tunstall-Pedoe and colleagues at the Ninewells Hospital and Medical School in Dundee, Scotland. The researchers used questionnaires, physical exams, and 24-hour urine samples to establish the risk factors for cardiovascular disease in 7300 Scottish men. This was an order of magnitude larger than any intrapopulation study ever done with 24-hour urine samples. The BMJ published the results in 1988: Potassium, which is in fruits and vegetables, seemed to have a beneficial effect on blood pressure. Sodium had no effect.
With this result, the Scottish study vanished from the debate. Advocates of salt reduction argued that the negative result was no surprise because the study, despite its size, was still not large enough to overcome the measurement problems that beset all other intrapopulation studies. When the NHBPEP recommended universal salt reduction in its landmark 1993 report, it cited 327 different journal articles in support of its recommendations. The Scottish study was not among them. (In 1998, Tunstall-Pedoe and his collaborators published a 10-year follow-up: Sodium intake now showed no relationship to either coronary heart disease or death.)
The second collaboration was Intersalt, led by Stamler and Rose. Unlike the relentlessly negative Scottish Heart Health Study, Intersalt would become the most influential and controversial study in the salt debate. Intersalt was designed specifically to resolve the contradiction between ecologic and intrapopulation studies. It would compare blood pressure and salt consumption, as measured by 24-hour urine samples, from 52 communities around the globe, from the highest to the lowest extremes of salt intake. Two hundred individuals--half males, half females, 50 from each decade of life between 20 and 60--were chosen at random from each population. In effect, Intersalt would be 52 small but identical intrapopulation studies combined into a single huge ecologic study.
After years of work by nearly 150 researchers, the results appeared in the same 1988 BMJ issue that included the Scottish Heart Health Study. Intersalt had failed to confirm its primary hypothesis, which was the existence of a linear relationship between salt intake and blood pressure... UNQUOTE.
Source: "The (Political) Science of Salt."
By Gary Taubes, Copyright 1998 American Association for the Advancement of Science Science (August 14, 1998).
On the internet: http://www.junkscience.com/news3/taubes.htm |
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Recent Patents Cardiovasc Drug Discov. 2006 Jan;1(1):67-72.
"Soluble epoxide hydrolase: a novel target for the treatment of hypertension."
Abstract: Epoxide hydrolases are a group of enzymes that convert the epoxide group of chemical compounds to corresponding diols by the addition of water. Soluble epoxide hydrolase (sEH, formerly referred to as cytosolic epoxide hydrolase), which is widely distributed in mammalian tissues, is the primary enzyme responsible for the conversion of epoxyeicosatrienoic acids (EETs), the bioactive lipid mediators formed from arachidonic acid by cytochrome P450 epoxygenase, to their corresponding diols. EETs, but not their diols, are endogenous anti-hypertensive eicosanoids. Disruption of the sEH gene in male mice decreases blood pressure, and inhibition of sEH decreases blood pressure in several experimental hypertensive models. Potent selective sEH inhibitors have been developed, and these sEH inhibitors have potential to become a novel class of anti-hypertensive drug. |
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