August 05, 2008

Aldosterone: Unlocking our understanding of cardiovascular risk

The general public understands that blood pressure is an important risk factor for cardiovascular health. Most people don’t realize that the hormone aldosterone is an even more powerful risk factor predicting cardiovascular
events and mortality. After reading the latest issue of the just-released Salt and Health newsletter, you will understand that aldosterone is the key to understanding why low-salt diets have not proved beneficial to human health.


July 16, 2008

Junk Science - It Can Take Your Breath Away!

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."

July 08, 2008

Aldosterone III

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.


June 12, 2008

Low-Salt Diets and Insulin Resistance

For years, medical experts have been trying to identify the various health outcomes that occur when humans restrict dietary salt. Blood pressure is well-known, of course. Increasing attention has been given to the fact that cutting salt stimulates production of hormones like renin and aldosterone, activates the sympathetic nervous system and induces insulin resistance. Healthy insulin sensitivity is important, so curtailing salt represents an obvious health risk.

Salt Institute technical director Mort Satin explores this issue in the just-released issue of Salt and Health newsletter.

April 11, 2008

Aldosterone II

Newspapers today reported on work being carried out at Glasgow University on the relationship of aldosterone to blood pressure. The research was presented at the annual Society for Endocrinology BES meeting in Harrogate, UK. The initial research indicates that in older people, higher levels of aldosterone in the bloodstream are associated with high blood pressure.

In a paper entitled, “Aldosterone and cardiovascular function: a lifetime of damage,” Dr. John Connell, who is Professor of Endocrinology at the University of Glasgow and Head of the of the Medical Research Council’s Blood Pressure Group, based in the British Heart Foundation’s Cardiovascular Research Centre in Glasgow described how an excess of aldosterone greatly increases the risk of stroke and heart failure, thus explaining the results of several previous research studies that revealed more cardiovascular patients dying on low salt diets than on regular diets.

Professor Connell said:

“Aldosterone is a key cardiovascular hormone. The higher the level of aldosterone in your blood, the more likely it is that you will suffer from high blood pressure, which will increase your risk of suffering a heart attack or a stroke.”
The research revealed that in older people, higher levels of aldosterone in the extracellular fluid are associated with high blood pressure. In young adults, high aldosterone levels predict that they will be more likely to develop hypertension later in their lives. There are a number of factors that determine elevated aldosterone levels in humans, including low birth weights, genetics and diet. More specifically, insufficient salt intakes will stimulate the renin-angiotensin-aldosterone system (RAAS) to produce more aldosterone in order to conserve the body's cache of sodium in order to retain osmotic balance.

Elevated aldosterone levels mean that throughout life, certain individuals will be more prone to developing high blood pressure, arterial stiffness and cardiovascular disease. Connell’s previous research indicated that aldosterone may be a causal factor in 10% of UK patients with high blood pressure*.

It is difficult to understand why the UK Food Standards Agency, the EU Commission and the Health Canada are all deliberately ignoring this research in their drive to reduce the levels of salt consumed. The mechanistic research work on the malignant role of elevated aldosterone levels upon the cardiovascular system brings far more weight to the salt and health outcomes question than the highly promoted, yet scientifically flawed epidemiological studies on salt and blood pressure.

The human body is an organism governed by biological mechanisms and no amount of bias, hype or imprudent policies will change this.
______
*Connell, J.M.C., Davies, E. 2005. Journal of Endocrinology, 186, 1-20.

April 10, 2008

Aldosterone I

Aldosterone is the primary mineralocorticoid hormone in humans. The mineralocorticoids are those steroid hormones, secreted by the adrenal cortex that regulate the balance of water and electrolytes in the body. Working at the distal tubule and collecting ducts of the kidney, aldosterone increases the permeability of their inner membranes to sodium and potassium and is responsible for reabsorbing sodium (Na+) ions and water from the urine back into the blood, while secreting potassium (K+) ions into the urine. Aldosterone is responsible for the reabsorption of virtually all the sodium content in human blood under normal kidney filtration function. Aldosterone also acts on specific receptors in the brain to conserve water and salt by controlling renal tubular resorption.

Unfortunately, chronic high levels of aldosterone in the blood can have major negative consequences for the cardiovascular system, including to induce myocardial fibrosis, renal damage and stiffening of the arteries.

After its discovery more than 50 years ago, the medical interest in aldosterone has been dramatically renewed because of it’s immense impact on the cardiovascular system. Aldosterone is now considered to be the most important cardiovascular hormone in the human body.

As an integral part of the renin-angiotensin-aldosterone system (RAAS), a key function of aldosterone is to conserve salt (sodium chloride), when an insufficient amount is consumed. The latest research published in Clinical Endocrinology indicates that for most healthy humans, anything less than 6 g/day of salt (2300 mg sodium) will be insufficient to prevent the RAAS system from kicking in. That’s right – anything less than 6 grams of salt a day!

But the Dietary Reference Intakes recommends that an adequate intake of salt is 3.8 g/day of salt – not 6 g/day. In fact, the dietary reference intakes state that 6 g/day of salt is the tolerable upper limit of salt intake. How can one recommendation state one figure for a maximum intake while the scientific research indicates that very same figure is a minimum intake?

Perhaps the answer lies in the paper given at the Institute of Medicine workshop “The Development of DRIs 1994-2004: Lessons Learned and New Challenges” held in Washington September 18-20, 2007 by Dr. Peter Greenwald, Director of Cancer Prevention at the National Cancer Institute of the National Institutes of Health. Dr Greenwald described how most of the figures behind the recommended dietary intakes were based upon expert opinion (the lowest quality evidence) rather than randomized controlled double blind clinical trials (the highest level of evidence).

“Little research of the most useful type (randomized clinical trials) is available, whereas there is an enormous amount of information that is not very meaningful. This needs to be reversed.”

Later Dr. Greenwald goes on to say:
“To underscore the importance of “getting the science right,” we need only turn to a recent article in the New York Times Magazine written by a respected science reporter. It was entitled “Why can’t we trust much of what we hear about diet, health and behavior-related diseases?” (Taubes, 2007). The reporter includes several examples, many in nutrition epidemiology, where there is so much conflicting evidence that people do not believe it. Clearly, we have a serious problem, and we must push for the conduct of definitive studies before we make pronouncements on public health.”

As noted in an earlier article, the latest evidence reported by Shapiro, Boaz et al from the Tel Aviv University Medical School reveals that healthy young adults who have been asked to limit their salt intake to 6 g/day (2300 mg sodium) were found to have elevated aldosterone levels indicating that their bodies were in a salt conservation mode. Unfortunately, these elevated levels of aldosterone quickly led to stiffening of the arteries. The conclusion was that for healthy young adults, the Dietary Guideline tolerable upper limit for salt was insufficient to prevent stimulation of aldosterone production. What would happen if the population actually consumed the level of salt recommended by the Guidelines? Would we be condemning an entire population to premature arterial stiffening? Would the government take responsibility for this or would it somehow contrive to blame the food industry for this problem?

In Europe, the EU Commission, led in large part by the UK and its Food Standards Agency has decided that public policy to reduce salt intake will trump basic human physiology. Charging forward pell-mell, the EU Commission, deliberately ignoring the latest scientific evidence, believes that they could not possibly go wrong on this issue because of the support of medical advocates, who have long ago given up any pretence of scientific objectivity.

The world has seen, time and again, that we ignore the science at our peril and as usual, consumers will end up being the victims.

The EU Commission has set the stage for the largest nutrition experiment ever carried out in history with the half billion citizens of the European Union expected to serve as the guinea pigs. When the compulsion to be seen as a driving force for change grabs policy makers by the throat, there is little left to do but allow that change to take place, regardless of the potentially disastrous consequences.

Not wanting to be perceived as being left out of this salt-reduction policy wave, Canada is set to follow suit – again totally ignoring the science and putting Canadian citizens at an elevated risk. One would think that some caution would be in order, but once again, backed by medical advisors and institutions that have done far more advocacy than homework, the government believes it cannot lose on this issue. Since when does ignoring the science and putting a population at an elevated risk give the Government a free pass?

So here we are, in the early part of 2008, with the drumbeat of scientific evidence piling up that the dietary guideline recommendations for sodium are largely irrelevant for the general population and insufficient to prevent production of elevated levels of aldosterone. For the majority of the people, salt, like water is a self-limiting nutrient. We know that aldosterone, chronically maintained at elevated levels as a result of reduced salt intake, will have major negative consequences on the integrity of our cardiovascular system. Like the mythical lemmings that march inexorably over the cliffs to their watery demise, it appears that the EU and Canada are on a track guided by what they don’t know, rather than by what they know – by urban myth and prejudice rather than science.

It is hoped that the new Committee selected to establish the Dietary Guidelines for 2010 will not feel obliged to make poor quality, knee-jerk decisions based upon subjective opinion and search out the most current scientific data upon which to establish their recommendations. Our health is at stake here.

April 02, 2008

No justification for dietary recommendations

Today's news services ran an interesting story regarding the recommended dietary intakes for water of 9 - 13 cups as highlighted in the Institute of Medicine's Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate (2004). CBS, NBC, ABC, the BBC, the Guardian, the Telegraph and Daily Mail, among others have all featured articles saying that there is not a single drop of evidence behind the myth of drinking eight glasses or more of water a day.

It turns out that the dietary recommendations from noted medical authorities as well as self-appointed health gurus to drink two or more liters of water per day are totally unsupported by any scientific evidence. Doctors Dan Negoianu and Stanley Goldfarb from the University of Pennsylvania in Philadelphia reviewed all the published clinical studies on the subject and concluded that no data exists for average healthy individuals regarding the amount of water they should consume on a daily basis.

Indeed, it is unclear where this recommendation came from," the University spokesman added.

Their research also debunked the myth that drinking water makes the skin more supple and made it easier to lose weight. "There is simply a lack of evidence in general," they reported in the Journal of the American Society of Nephrology .

Reuters reports that this was not the first time such a conclusion was made since Dr. Heinz Valtin of Dartmouth Medical School found the recommendations to drink that amount of water to be totally lacking in scientific merit.

Because we all have specific individual needs for water, Goldfarb recommended, "If you're thirsty, drink. If you're not thirsty, you needn't drink."

This most recent article highlights the specificity of an individual's metabolic need, a situation paralleled by salt intake. The human body has an ability to excrete 250 times the maximum recommended intake of salt - an amount of salt that is virtually impossible for anyone to consume. In other words, our salt consumption is not limited by our ability to excrete it, but rather by our innate senses - sensory perception and biological feedback mechanisms. Both of these mechanisms are specific for every individual, just as water is.

For this reason, it is the very same folly to apply a "one size fits all" set of policy recommendations to salt consumption as it is for water consumption. Salt consumption is self-limiting and regulated by nature's biology, not by shortsighted dietary recommendations.