IS SALT REALLY BAD FOR YOU?

If you believe what governmental and nutritional agents are telling you then the answer is yes. But is it really true.

Sometimes these people don’t know what they are talking about. I have looked into the actual evidence that salt intake is bad for you and found that the question is not settled and the answer is probably, No. I also found that the whole subject has been overblown and misrepresented.

There are many clinical and epidemiological studies on the topic of the relationship of salt intake and increased heart and vascular disease (CVD), stroke and death rate and I have reviewed many of them. These studies fall into three categories:


1. Yes, salt intake may be associated with increase risks of cardiovascular disease (CVD), stroke and mortality (References 1-5).

2. No, salt intake does not increase risks of CVD, stroke and mortality (6,7).

3. Surprise, higher salt intake decreased the risks of CVD (1,8-10).

4. Another Surprise, lower salt intake increased risks of CVD and death (9,10).


WHAT A MESS

How could any government agency have the audacity to state that salt intake is dangerous for your health when the scientific literature is full of papers which display such divergent patterns. Obviously something is wrong. A large part of “Something is Wrong” is people in government agencies and nutritional advisors don’t read the scientific papers which are published on this topic. The scientists who write the papers are guided by a lack of objectivity which is present because of the “Band Wagon Effect”. If they get on the wagon they must remain because their funding, reputation and status depend on it.



READING BREAK



If you have had all you can take stop reading; however, if you want a more detailed and somewhat more technical explanation then read on.

Some of this bad information comes from scientists who do not take an honest and careful look at their own data. Their presumption that higher intake of salt will be associated with increased CVD, stroke and mortality over shadows their objective analysis of their own data. As an example of such a study I will use the following paper which incorrectly concluded that high salt intake increased risk of stroke and CVD (11).

In this paper by Strazzullo et al.(11) the results obtained from 19 cohort samples from13 studies have been combined and analyzed by a method called meta-analysis. This method brings together the good, the bad and the ugly and lumps them altogether with the hope that the result will fit the bias of the investigators. In this particular meta-analysis the risk of stroke and salt intake were reported for 14 studies, 10 of which showed no significant effect and 4 showed marginal significance, that is, just barely significant. The results are identical for effect of salt intake on cardiovascular disease: total, 14 studies, 10 showed no significant effect and 4 which showed marginal effects. Most scientists would not believe the conclusions of any study in which 71% of the observations showed no effect and 29% showed a marginal effect.

Yet, Strazzullo et al. conclude that high salt intake is associated with a statistically significant increased risk of stroke and cardiovascular disease. They based their conclusions on relative risks plus or minus confidence intervals (CI). In this kind of analysis if the CI does not include 1.0 then the data are considered to be statistically significant. As the number of subjects get higher the amount of error gets lower. Thus, the confidence interval (CI) gets smaller and is less likely to include the control group number of one.

As an example, a single study with a small number of subjects might have a relative risk (RR) of 1.2 with a CI of 0.6-2.4. Because the CI interval includes 1.0 this means the RR of 1.2 cannot be considered statistically significant. Now if you group together more studies as in a meta-analysis the number of subjects gets much larger and reduces the variability which reduces the interval of the CI. As a result one could obtain a RR of 1.2 with a CI of 1.01-2.0 and since this CI does not include 1.0 the RR is claimed to be statistically significant.



This is exactly what happen in the Strazzullo et al. combined studies which indicated a risk for stroke of RR 1.23 ( CI, 1.06-1.43) and for CVD of 1.17 (CI, 1.02-1.32). The RR of CVD became statistically significant when one of the studies (Alderman 1995) which did not agree with their bias was omitted.  Note that the lowest numbers for CI 1.06 for stroke and 1.02 for CVD are so close to 1.0 you have to hold your breath to claim these RRs are of any real significance.

It should also be noted that demonstrating statistical significance does not necessarily mean that the finding is of any biological significance.

NOTE: In another later blog I will discuss this method in more detail.


REFERECES


1. Tunstall-Pedoe H, Woodward M, Tavendale R, A’Brook R, McCluskey MK. Comparison of the prediction by 27 different factors of coronary heart disease and death in men and women of the Scottish heart health study: cohort study. BMJ. 1997;315:722–9.

2. He J, Ogden LG, Vupputuri S, Bassano LA, Loria C, Whelton PK. Dietary sodium intake and subsequent risk of cardiovascular disease in overweight adults. JAMA. 1999;282:2027–34.

3. Tuomilehto J, Jousilahti P, Rastenyte D, et al. Urinary sodium excretion and cardiovascular mortality in Finland: a prospective study. Lancet. 2001;347:848–51.

4. Nagata C, Takatsuka N, Shimizu N, Shimizu H. Sodium intake and risk of death from stroke in Japanese men and women. Stroke. 2004;15:1543–7.

5. Cook NR, Cutler JA, Obarzanek E, Buring JE, Rexrode KM, Kumanyika SK, Appel LJ, Whelton PK. Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of trials of hypertension prevention (TOHP). BMJ 2007 DOI 10.1136/bmj.39147.604896.55.

6. Kagen A, Popper JS, Rhoads GG, Yano K. Dietary and other risk factors for stroke in Hawaiian Japanese men. Stroke. 1985;16:390–6.

7. Cohen JD, Grandis G, Cutler JA, Neaton JD, Juller LH, Stamler J. Dietary sodium intake and mortality: MRFIT Follow-up Study Results (abstract). Circulation. 1999;100(suppl 1):1–524.

8. Alderman MH, Madhavan S, Cohen H, Sealey JE, Laragh JH. Low urinary sodium is associated with greater risk of myocardial infarction among treated hypertensive men. Hypertension. 1995;25:1144–52.

9. Alderman MH, Cohen H, Madhavan S. Dietary sodium intake and
mortality: the National Health and Nutrition Survey (NHANES I)>. Lancet. 1998;351:781–5.

10. Cohen HW, Hailpern SM, Fang J, Alderman MH. Sodium intake and mortality in the NHANES II Follow-up Study. Am J Med. 2006;119:274e7–5e14.

11. Strazzullo P. et al. Salt intake, stroke and cardiovascular disease: meta-analysis of prospective studies. BMJ 2009:339;b4567.