The Fast Food Thread

https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD004022.pub5/full#CD004022-sec-0070

Authors' conclusions​

Implications for practice​

The present meta‐analysis shows that a low‐ versus high‐sodium diet in white people with normal blood pressure (BP) decreases BP less than 1%. A significant concomitant increase in plasma renin, plasma aldosterone, plasma noradrenalin, and to a lesser degree of plasma adrenaline may contribute to the small effect of sodium reduction on BP. Furthermore, sodium reduction resulted in a significant increase in plasma cholesterol and plasma triglyceride, which expressed in percentage, was numerically larger than the decrease in BP. Due to the relatively small effects and due to the antagonistic nature of the effects (decrease in BP, increase in hormones and lipids), these results do not support that sodium reduction may have net beneficial effects in a population of white people with normal BP.

In white people with elevated BP, sodium reduction decreases BP by about 3.5%, indicating that sodium reduction may be used as a supplementary treatment for hypertension. In Asian and black people the effect of sodium reduction was a little larger than in white people, but at present too few studies have been carried out to conclude differently from that above.

Implications for research​

The data suggesting that black and Asian populations are more sensitive to sodium reduction than white people requires further studies. In future studies of mixed populations, it is important that the effects on white, black and Asian populations are reported separately. Population studies have shown a U‐shaped association between sodium intake and mortality indicating that the beneficial effect of sodium reduction on BP outweigh the harmful effect on hormones and lipids at sodium intake above the usual sodium intake, but that the harms of sodium reduction outweigh the benefits at sodium intake below the usual sodium intake. Long‐term randomised controlled trials (RCTs) with mortality and morbidity outcomes would be desirable to confirm or reject these findings. However, such studies may not be practicable. After 195 RCTs and 27 population studies without an obvious signal in favour of sodium reduction below 100 mmol/day, another position could be to accept that the present usual sodium intake may be the optimal intake for the general population. As suggested by the National Academy of Medicine the primary need may be to revise the process of the establishment of the dietary guidelines.

https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD010070.pub3/full#CD010070-sec-0091

Authors' conclusions​

Implications for practice​

We found a strong case for the benefits of salt restriction in people with CKD. We found that reducing dietary salt considerably reduced BP in people with CKD. We found consistent evidence that dietary salt restriction reduced proteinuria in people with earlier stage (non‐dialysed, non‐transplanted) CKD by 34% to 36%. If such reductions were maintained long‐term, this may translate to clinically significant reductions in ESKD and cardiovascular events.

Reduced salt intake may increase symptomatic hypotension. Data were sparse for other types of adverse events.

Current evidence‐based clinical guidelines recommend a sodium intake target of less than 6 g of salt (100 mmol; 2300 mg sodium) per day for people with CKD, although achieving longer‐term adherence to this target can be challenging for patients without regular and ongoing support to improve their motivation, knowledge and prevent behaviour change decay. These findings were based on studies with intervention durations up to 6 months. There are ongoing studies with longer intervention durations which will strengthen the evidence for longer‐term effects.

Implications for research​

We found that salt reduction in people with CKD reduced BP considerably and consistently reduced proteinuria over a time‐frame of up to 6 months. We found a critical evidence gap in long‐term effects of salt restriction in people with CKD that meant we were unable to determine the direct effects of sodium restriction on critical outcomes such as death and progression to ESKD. If the reductions we found in short‐term studies could be maintained long‐term, these benefits may translate to clinically significant reductions in ESKD incidence and cardiovascular events. Research into longer‐term effects of dietary sodium restriction for people with CKD is warranted, along with investigation of adherence to a low salt diet.

Despite consistent data from observational and non‐randomised studies showing that salt restriction reduced fluid volume in people with CKD, high quality RCTs are lacking. Further research on the effect of salt restriction on other cardiac and vascular abnormalities such as arterial stiffness, left ventricular hypertrophy, inflammation and oxidative stress is warranted.

Future studies investigating salt restriction should employ methods that limit risk of bias due to dietary confounders where possible and should take care to adequately measure dietary intake of not only sodium, but other nutrients that may confound study results. Research into long‐term adherence to a sodium‐restricted diet may assist in translating these results into a practical setting.