TABLE 4.
Examples of expert committee evaluations of the sodium, blood pressure, and CVD relation1
| Expert committee, year (ref) | Sodium and BP | BP and CVD | Sodium and CVD | Recommendation/conclusion |
| Diet and Health, 1989 (23) | Strong epidemiologic evidence | High BP is a major CVD risk factor | — | BP levels are strongly and positively correlated with habitual intake of salt. |
| Supportive animal data | Limit total daily intake of salt (sodium chloride) to ≤6 g. | |||
| Dietary Reference Intakes, 2005 (24) | Rigorous dose-response trials | Persuasive results: observational studies and drug trials | Animal models: strong association | There is a progressive, direct effect of dietary sodium intake on BP in nonhypertensive and hypertensive individuals and a direct relation between BP and risk of CVD and end-stage renal disease. |
| Well-accepted public health tenet | Observational studies: association | |||
| Sodium Intake in Populations, 2013 (25) | Intervention studies: dose-response between sodium intake and BP in normotensive and hypertensive individuals | Strong support for high BP and higher risk of CVD | Consistent evidence for association between excessive sodium intakes and increased risk of CVD | Evidence of direct health outcomes: a positive relation between higher sodium intakes and risk of CVD, which are consistent with the known effects of sodium intake on BP. |
| BP as a surrogate endpoint for risk of CVD and stroke is widely recognized and accepted | Inconsistent evidence for beneficial or adverse effects of intakes <2300 mg/d | There is inconsistent and insufficient evidence to conclude that decreasing sodium intakes to <2300 mg/d either increases or decreases risk of CVD outcomes or all-cause mortality. | ||
| AHA/ACC: Lifestyle Management to Reduce CVD Risk, 2013 (21) | Strong and consistent clinical trial data of relation (high)2 | Considered BP a modifiable risk factor for CVD prevention and treatment4 | Observational data: higher sodium intake is associated with greater risk for fatal and nonfatal stroke and CVD (low)5 | Advise adults who would benefit from BP lowering to decrease sodium intake. |
| Reduce sodium to ∼2400 mg/d (moderate)3 | ||||
| Reduce sodium intake by ∼1000 mg/d (high) | ||||
| Dietary Guidelines Advisory Committee, 2015 (8) | Strong evidence linking sodium and BP | — | Moderate evidence linking sodium to CVD (on the basis of an updated review of the 2013 IOM and AHA/ACC evidence reviews) | Consume <2300 mg Na/d; recommendation included considerations of evidence on BP as a surrogate indicator of CVD risk. |
| Moderate evidence on amounts of sodium intakes | Grade not assignable that intakes <2300 mg/d increase or decrease CVD risk; limited evidence that lowering sodium intake by 1000 mg/d might lower CVD risk by 30% |
AHA/ACC, American Heart Association/American College of Cardiology; BP, blood pressure; CVD, cardiovascular disease; IOM, Institute of Medicine; ref, reference.
High strength-of-evidence grade is based on results from well-designed and well-executed randomized clinical trials. There is high certainty about the estimate of the effect. Further research is unlikely to change confidence in the estimate of the effect (8, 21).
Moderate strength-of-evidence grade reflects evidence from randomized clinical trials with minor limitations, well-designed and well-executed nonrandomized controlled studies, and well-designed and well-executed observational studies (8, 21). There is moderate certainty about the estimate of the effect. Further research may have an impact on confidence in the estimate of the effect and may change the estimate.
Modifiable risk factors and markers are also sometimes called surrogate endpoints and may serve as surrogates for the incidence of chronic diseases (31). Modifiable risk factors are modified by the intervention of interest and can be used to estimate population-attributable risk that can be attributed to a particular risk factor for a particular chronic disease (32).
Low strength-of-evidence grade reflects evidence from randomized clinical trials with major limitations, nonrandomized controlled studies and observational studies with major limitations, and uncontrolled clinical observations without an appropriate comparison group. There is low certainty about the estimate of the effect. Further research is likely to have an impact on confidence in the estimate of the effect and is likely to change the estimate (8, 21).