Wednesday, October 20, 2010

Science trumps politics: urinary sodium data challenge US dietary sodium guideline -- McCarron et al. 92 (5): 1005 -- American Journal of Clinical Nutrition

Science trumps politics: urinary sodium data challenge US dietary sodium guideline -- McCarron et al. 92 (5): 1005 -- American Journal of Clinical Nutrition

Science trumps politics: urinary sodium data challenge US dietary sodium guideline1,2
David A McCarron, Tilman B Drüeke and Edward M Stricker

1 From the Department of Nutrition, University of California, Davis, CA (DAM); INSERM ERI-12, UFR de Médecine et de Pharmacie, Université de Picardie Jules Verne, Amiens, France (TBD); and the Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA (EMS).

2 Address correspondence and reprint requests to DA McCarron, The McCarron Group, 120 NW Ninth Avenue, Portland, OR 97209. E-mail: dmccarron@mccarrongroup.com.

See corresponding article on page 1172.

For the past 3 decades, the US government has promoted a policy of reduced dietary sodium intake as the principal nutritional means of reducing blood pressure and its attendant cardiovascular disorders in adults. Early on, this policy targeted at-risk individuals such as people with chronic arterial hypertension; however, in the past decade it has been applied to the population at large. Despite a litany of well-intended strategies from mandatory sodium labeling to extensive educational and social marketing efforts, there is little evidence that sodium intake has changed. In fact, some advocates of the policy have argued that sodium intake actually has increased, reaching extreme levels in some people (1). The failure of the government's efforts has been typically attributed to the food industry's excessive use of sodium in their products (1). Both the application of such a government policy to the entire population and the simplistic assessment that its failure to date can be attributed to the food industry's reluctance to provide lower sodium foods belie the scientific complexity of the issues, including sodium's role in health and disease.

In this issue of the Journal, Bernstein and Willett (2) provide a valuable analysis of 24-h urinary sodium (UNaV) data extracted from the medical literature published between 1957 and 2003. Their findings from the 38 US studies that met rigorous search criteria and involved 26,271 people confirm and extend the conclusions we published a year ago (3). Our analysis involved 19,151 people from 33 countries and 62 survey sites between 1984 and 2008. Like that of Bernstein and Willett, our analysis revealed a remarkably narrow range of UNaV across very diverse populations and eating habits, without the extreme levels often purported to exist by advocates of lower sodium intake (1) and no evidence of a change over time. The latter was best shown by the data of the UK Food Standards Agency between 1986 and 2008, which we noted (3) offered no evidence that an intense social marketing effort begun in 2005 had been successful.

One possible explanation, first raised by our report last year (3), is that human sodium intake is a parameter that even the most well intentioned public policy cannot modify in most people. An extensive body of basic science research, dating from Richter's seminal observations (4), has characterized an integrated network of peripheral hormonal signals interfaced with complex neural networks specific to regulating sodium intake of experimental animals (5). Although those basic research findings have not as yet been extrapolated to humans, they should not be completely ignored because they may yet provide a model of what is feasible in humans.

The current report extends our observations by documenting that, likewise, all the efforts in the United States over the past 3 decades have had no effect on the population's sodium intake. An alternative possibility for the stability of sodium intake is that sodium has been largely consumed in association with food intake, motivated by hunger and appetite. To the extent that caloric intake has been stable over populations and decades, so too has sodium. Thus, a potential benefit of reducing food sodium content would be a concurrent reduction of sodium. Working against that theoretical outcome, however, is the reality that over the millennia, before the introduction of processed foods, sodium was added to foods at the time of preservation, cooking, or consumption. An individual in our society has the identical options today as the food industry moves to offering more products whose ratio of calories to sodium is increased (ie, lower sodium content per serving). This individual choice could abrogate any effect on average sodium intake in society as these data indicate has happened.

Regardless of why sodium intake has been so stable, the data of Bernstein and Willett (2), as well those of McCarron et al (3), suggest that it is not a readily modifiable nutritional parameter for the population at large. Furthermore, a substantial body of research in humans provides evidence as to why this latest attempt to modify the general population's sodium intake is doomed to failure. Sodium has a critical role in extracellular fluid volume regulation as well as being of fundamental importance in cellular function across virtually all organ systems. Thus, it is unlikely that as an organism, humans would have evolved without the development of failsafe mechanisms to ensure sufficient sodium availability. Sodium is 1 of only 3 nutrients whose excretion in urine is recognized as regulated; water and glucose are the other 2. Consequently, deficits in these nutrients elicit immediate, potent, counterregulatory physiologic responses.

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