Salt & Human Health: Salt & Health Newsletter

The website of WASH (World Action on Salt and Health) states that a double-blind study of modest salt restriction caused a reduction in the severity of asthma attacks and a reduction in the use of medication and an improvement in the measurement of airways resistance. The article concludes with a statement:

"It seems therefore that, while salt is not a direct cause of asthma, a high salt intake can act as a major aggravating factor."

The CASH (Consensus Action on Salt and Health) website similarly states:

"There is evidence that bronchial reactivity in people with asthma is linked with salt intake. A recent review of epidemiological and intervention studies demonstrated that reducing salt intake may help to reduce the severity of an asthma attack and other breathing problems."

Going a step further, another CASH document confidently wrote with great anticipation of the upcoming University of Nottingham study which would once and for all establish the relationship between salt and asthma.

On page 15 of the CSPI (Center for Science in the Public Interest) book, Salt-The Forgotten Killer it states that:

"High-salt diets impair lung function and worsen asthma symptoms"

The NHLBI (National Heart, Lung, and Blood Institute) paper on salt and health, A Critical Review of Current Scientific Evidence indicates in their opening section on sodium intake and non-CVD conditions that:

"Several studies have shown direct associations between sodium intake and other conditions, including ....indicators of asthma."

All four websites claim to be portraying good science, responsible science, all in the public's interest, yet, all four made the relationship between salt and asthma as if there were a solid scientific relationship between the two. Grasping at whatever straws they could to forward their own parochial agendas, they misinformed the public in this matter of health. It will be interesting to see how long it takes for them to retract their statements on the relationship between salt and asthma. It will also be interesting to see if they apologize to their readership for misinforming them.

Today, June 16, 2008, reports started coming in from, among others, CBS, the CBC and The Press Association of the long-anticipated definitive University of Nottingham study to examine the relationship between salt intakes and asthma. The University of Nottingham press release was emblazoned with the title, "Low-sodium advice for asthmatics should be taken with a pinch of salt." The conclusion of their story stated that the new study by researchers at The University of Nottingham found no evidence that cutting back on salt helps patients with their asthma symptoms.

Once more, we see clear incontrovertible evidence of a patently obvious anti-salt movement that is only too willing to spread myth-information and pseudo-science about an issue, long before the actual science has been definitively established.

As I mentioned above, we will be revisiting the websites of these "scientists" in future to see how quickly they correct their misinformation and apologize for it. This may well show "the measure of the man."

Posted by Mort Satin at 01:38 PM | Permalink

Historically, aldosterone was considered a hormone released from the adrenal cortex in response to low salt intakes. It was thought to exert its effects solely through mineralocorticoid receptors, thereby causing sodium retention and potassium loss. More recently, however, a much wider role for aldosterone has been recognized.

Research efforts have revealed a host of new pathophysiologic mechanisms associated with elevated aldosterone that could be expected to contribute to the progression of congestive heart failure and sudden cardiovascular death.

More importantly, the recent evidence is based upon research into the actual metabolic mechanisms rather than epidemiological or observational studies, which are generally open to a range of mechanistic interpretations and confounding errors. A growing body of evidence suggests that aldosterone contributes to heart disease through endothelial dysfunction. The endothelium is the thin layer of cells that line the interior surface of all blood vessels. It serves as the interface between the circulating blood and the rest of the vessel wall. The condition of the endothelium plays a critical role in the regulation of vascular tone, platelet aggregation within the vessel, the adhesion of leukocytes and overall blood coagulation. When the endothelium is not right, as in endothelial dysfunction, it is predictive of future cardiovascular events.

Because low salt diets stimulate elevated aldosterone levels, this phenomenon may very well explain the repeated findings that more people on low salt diets succumb to cardiovascular disease than those on normal or high salt diets, which we reported on previously.

In the past, experimental studies have focused on the pathological effects of angiotensin II, rather than aldosterone, and demonstrated that angiotensin-converting enzyme inhibitors confer significant cardiovascular protection. However, more recently, research has revolutionized our view of aldosterone and its biological actions, and identified mineralocorticoids as important mediators of cardiovascular injury. Elevated aldosterone levels can cause cardiovascular injury without raising the blood pressure, and aldosterone blockers can exert significant protective effects without lowering the blood pressure.

Infants born with a low birth weights tend to have higher aldosterone levels when they are older. This corresponds to recent research, which we previously reported on demonstrating that low birth weight babies are also born with low sodium in their blood serum because their mothers were on low salt intakes.

The current evidence concludes that that a long-term increase in aldosterone production from early on in life is determined by an interaction of genetic and environmental factors, such as diets that are low in salt. This leads to cardiovascular damage in middle age and beyond. These results have been confirmed by at least two other studies, one from Israel and one from Japan, which further state that the current upper limit of 2300 mg sodium per day (6 g of salt), described in the Institute of Medicine Dietary Reference Intakes is insufficient to prevent the triggering of elevated aldosterone levels.

As more and more high quality evidence mounts on the malignant impact of elevated aldosterone levels upon cardiovascular function, it is hoped that the voice of the medical establishment and the new Dietary Guidelines on sodium will take this squarely into account.

Posted by Mort Satin at 11:14 AM | Permalink