
AAS Email – July 2011
FEATURE ARTICLE
IAS
NEWS
CONFERENCES – ISA2012 close of
abstracts August 5, AAS 2011 close of abstracts August 14
SECRETARIAT
Welcome to our midyear 2011 eNewsletter. It is that time of year when the winter solstice has just passed and winter looks likely to be around for a few more months. It is also the time of year when major grant writing is behind us and NH&MRC rebuttals loom ahead. This is when we get an inkling of whether all our hard work and long hours in front of the computer may have paid dividends. For others, the fun is just beginning, with many hours of reading, ranking and panel discussions as grants get bumped up or down, as they jostle their way into their rightful (or sometimes questionable) order on the 1-7 ranking scale.
To lighten the mood somewhat, we asked Merlin Thomas, the Head of the Biochemistry of Diabetic Complications Laboratory at the BakerIDI Heart and Diabetes Institute to share with us a common misnomer that restricting salt intake is always a good thing. Merlin has written a delightful piece, and we hope you enjoy reading about the pros and cons of that irresistible salty snack! This edition also contains our other regular news and information segments highlighting “Whats-on” in 2011. Please enjoy reading our newsletter and we wish you good luck with those rebuttals!
Alison Heather and Judy de Haan
NEW FH AUSTRALASIA WEBSITE ….. Please have a look at the new website – it will change
and grow over the next few months, so why not bookmark it now? Any and all
suggestions are welcome!
FEATURE ARTICLE - SALT CUTS BOTH WAYS?
Professor Merlin Thomas, Baker IDI Heart and Diabetes Institute
Most nutritional guidelines advocate restricting our intake of salt to less than 100 mmol/day. This is about half of what most adults get each day from their diet. In those with high blood pressure, diabetes, kidney or heart disease lower targets are recommended (<65mmol/day).
The rationale for such recommendations is straightforward. Our daily intake of salt is correlated with our blood pressure levels. The more salt we eat, the higher our blood pressure. And high blood pressure damages blood vessels which leads to cardiovascular disease and strokes. In fact, along with smoking and diabetes, hypertension is one of the biggest killers of hearts and minds. Consequently, if we ate less salt in our diet, our blood pressure would be lower, and the risk of heart attacks and strokes would, in theory, be reduced, ad consequentiam.
While such logic is appealing, especially as a low-cost public health message, the actions of salt on human physiology are more complicated, and certainly extend beyond blood pressure regulation.
About a billion years ago, our ancestors emerged from the salty oceans. This exodus was achieved by taking part of it with us. Homeostasis of our inner sea is a fundamental part of our physiology. We can eat our salt and vinegar chips or drink gallons of fresh water, but our salt content hardly changes. We survive(d) by keeping things constant.
Our kidneys are the key regulators of this balance, filtering and reabsorbing over 25,000 mmol of salt every day, losing only 0.5% of the filtered load into the urine. In healthy individuals, this loss equates almost exactly with the amount of salt you eat (~100-200 mmol/day). Consequently, if we eat our salty chips (an extra 30 mmol of salt) it’s not a major effort to tune reabsorbtion down slightly and excrete sodium into our urine. Equally, if we didn’t get much salt today, it’s not hard to increase reabsorbtion very slightly to maintain the salt/water balance.
This balance is under tight neuro-hormonal control, involving a range of chemical signals between kidneys, the heart, the adrenal glands and of course the brain. The most well-known are the renin angiotensin system (RAS) and the sympathetic nervous system (SNS). If salt intake is reduced, these homeostatic pathways signal the kidney to hang onto more salt. If salt intake is increased, these pathways are suppressed as a means to increased salt excretion and offset increases in blood pressure that would otherwise occur.
And this is the rub. These same neuro-hormonal pathways are implicated in the development and progression of human disease, from cardiovascular disease and diabetes, to cancer and mental illness. For example, we know that RAS activation is directly pro-atherosclerotic. When you infuse angiotensin II into an apoE mouse it accumulates more plaque and this is not prevented by lowering the blood pressure with amlodipine. So when salt restriction increases angiotensin II it also increases atherosclerosis, even if it modestly lowers blood pressure. Indeed, the wide clinical utility and effects of drugs that block the RAS or SNS stand as testament to the importance of these pathways, beyond simple actions on blood pressure regulation. But again, if this is true, then by implication, salt intake must also have pleiotropic actions beyond simply those on blood pressure.
Many observational studies have looked at the association between salt intake with heart disease and the risk of premature mortality. Some have shown that high salt intake is associated with poor health, some have found no effect at all, while others have found that individuals with a low salt intake have worse clinical outcomes. This is despite trials clearly showing that salt restriction lowers blood pressure.
This inconsistency forms the basis of the so-called “salt wars”, an unscientific and often vitriolic war of words between (blood-pressure centric) salt reformers and (pleiotropic) salt sceptics. Each has some scientific data to support their stance, and sound scientific reasons for doubting the opposing viewpoint.
For example, in response to an article published recently in JAMA that showed a modestly reduced survival in individuals on a low salt diet, one well known advocate of salt restriction was quoted as saying “it doesn’t make (any) sense... it’s like saying we don’t think cigarettes are harmful! ... I don’t think this is worth paying attention to.. he is just trying to make a name for himself”.
His rationale is clearly stated. “Everything else that has been shown to lower blood pressure is beneficial in terms of heart attacks and strokes.” So why should salt intake be any different?
The salt sceptics argue that this is not always true. For
example, a recent clinical trial of blood pressure lowering in diabetic
patients (ACCORD) failed to show effects on cardiovascular events or mortality,
despite achieving very significant falls in blood pressure. Moreover, many
drugs are readily ascribed blood pressure-independent effects on health
outcomes. Why not salt?
A parable once told by Michael Alderman (a notable sceptic) goes something like this. Weight loss is safe and effective for lowering blood pressure in obese and overweight individuals. So once upon a time, pregnant women were advised to limit their weight gain in order to reduce their risks from hypertension during pregnancy (known as eclampsia). From a blood pressure centric point of view, this worked very well. But while eclampsia was prevented and blood pressure lowered, fetal mortality was dramatically increased. So no one now recommends weight restriction during pregnancy. It might be lowering the blood pressure, but what else is salt restriction doing?
The likely truth is that some individuals will benefit from salt restriction, while others may not. Blood pressure control is important, but it is not a panacea. For some, salt-sensitive hypertension is more important than neurohormonal activation. One example is in the elderly, in whom low-renin hypertension and renal impairment predominates. Here, salt restriction is a logical and important health message. In other contexts, neuro-hormonal activation may have primacy over blood pressure, and salt restriction may lead to less favourable or even adverse outcomes.
It is unlikely that anyone will accept this middle ground in an inconclusive and ongoing war.
Editors note: To hear more from Merlin, please join us in Adelaide where he is one of our invited speakers!
AAS ANNUAL SCIENTIFIC
MEETING 2011 – Abstracts due August 14
October 19-21, National Wine Centre, Adelaide

The Organising Committee of Terri Allen, Peter Clifton, Judy de Haan, Karin Jandeleit-Dahm, Heather Medbury and Peter Meikle have been working with the Australian and New Zealand Society of Obesity to put together an inspiring scientific program. Details are available via the Meetings First website.
o Dr Ira Tabas, Columbia University
o Professor Caroline McMillen, UniSA
o Dr Alex Brown, Baker IDI Heart and Diabetes Institute
o Professor Jacob George, Westmead Millennium Institute for Medical Research
o Professor Mark Daniel, UniSA
o Professor Mark Febbraio, Baker IDI Heart and Diabetes Institute
o Professor Wendy Jessup, University of NSW
o A/Professor Karlheinz Peter, Baker IDI Heart and Diabetes Institute
o Professor Kerry Rye, Heart Research Institute
o Professor Andrew Tonkin, Monash University
o A/Professor Jennifer Keogh, University of South Australia
o A/Professor Chris Sobey, Monash University
o Professor Merlin Thomas, Baker IDI Heart and Diabetes Institute
INTERNATIONAL SOCIETY OF ATHEROSCLEROSIS (IAS) NEWS
October 19-21, 2011
AAS Annual Scientific Meeting
Adelaide
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