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Evidence for salt reduction

We need less than 1g of salt per day, however around the world we are eating on average 10g salt per day.

We need less than 1g of salt per day for normal physiological function (1), however around the world we’re eating on average 10g salt per day, ranging from 4g in Kenya to 15g in Kazakhstan (2), and it’s putting our health at risk. As such, the World Health Organization recommends adults reduce their salt intake to less than 5g salt per day, and even less for children (3).

Salt reduction has been recognized as one of the most cost-effective interventions for reducing the burden of non-communicable diseases (NCDs), like cardiovascular disease, due its high impact on health, high feasibility, and low implementation costs (4). It has been considered on a global scale, as a priority intervention and a best buy in NCD disease prevention (5).

Salt and High Blood Pressure

The clearest adverse effect of sodium (mostly consumed in the form of salt) is on blood pressure; salt raises blood pressure (1,2). The more salt eaten, the higher the blood pressure and this is evident for females and males, all ethnic groups and for those with high and normal blood pressure levels (2, 3).

A systematic review of over 130 randomised trials comparing different levels of salt intake, measured using the gold standard method of 24-hour urinary sodium excretion, showed a greater reduction in salt intake produced a greater decrease in blood pressure (3). While all population subgroups benefitted from salt reduction, populations of older age, higher starting blood pressure levels, or non-white population achieved greater reductions in blood pressure from the same level of salt reduction.

High blood pressure is the leading risk factor for health loss worldwide, responsible for almost one of every five deaths (4). The number of people with high blood pressure is increasing, putting millions of people at increased risk of heart disease, stroke and chronic kidney disease (5).

References

  1. Aburto N J, Ziolkovska A, Hooper L, Elliott P, Cappuccio F P, Meerpohl J J et al. Effect of lower sodium intake on health: systematic review and meta-analyses. 2013; 346 :f1326.
  2. Filippini T, Malavolti M, Whelton PK, Naska A, Orsini N, Vinceti M. Blood Pressure Effects of Sodium Reduction: Dose-Response Meta-Analysis of Experimental Studies. Circulation. 2021 Apr 20;143(16):1542-1567.
  3. Huang L, Trieu K, Yoshimura S, Neal B, Woodward M, Campbell N R C et al. Effect of dose and duration of reduction in dietary sodium on blood pressure levels: systematic review and meta-analysis of randomised trials 2020; 368 :m315
  4. GBD 2019 Risk Factors Collaborators. Global burden of 87 risk factors in 204 countries and territories, 1990-2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet. 2020 Oct 17;396(10258):1223-1249.
  5. Forouzanfar MH, Liu P, Roth GA, et al. Global Burden of Hypertension and Systolic Blood Pressure of at Least 110 to 115 mm Hg, 1990-2015. JAMA. 2017;317(2):165–182.
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Salt and CVD (stroke, coronary heart disease and heart failure)

High salt intake is a well-established cause of high blood pressure (1,2), which is the major risk factor for cardiovascular disease (CVD) including stroke, heart disease and heart failure (3).

The 2019 Global Burden of Disease study reports that high systolic blood pressure is responsible for about 10 million deaths and 214 million Disability-adjusted life years (DALYs) due to CVD (3). In the same year, high salt intake is the leading cause of deaths and DALYs due to CVD among all dietary risk factors (3).

Reductions in salt intake have been shown to produce reductions in blood pressure (4). Moreover, in well-conducted prospective studies, lower levels of salt consumption, measured using multiple 24-hour urine collections, produced reduced cardiovascular events and mortality (5,6).

Meta-analyses of observational studies also showed that reductions in salt intake would lower CVD risk (1,7,8). It has been estimated that reducing salt intake from 10g to 5g per day would reduce stroke rate by 23% and overall CVD by 17% (7). A recent meta-analysis showed a linear 6% increase in CVD risk for every 2.5g increase in salt intake (8).

References

  1. Aburto NJ, Ziolkovska A, Hooper L, Elliott P, Cappuccio FP, Meerpohl JJ et al. Effect of lower sodium intake on health: systematic review and meta-analyses. BMJ. 2013;346:f1326
  2. Filippini T, Malavolti M, Whelton PK, Naska A, Orsini N, Vinceti M. Blood Pressure Effects of Sodium Reduction: Dose-Response Meta-Analysis of Experimental Studies. Circulation. Apr 2021;20;143(16):1542-1567.
  3. GBD 2019 Risk Factors Collaborators. Global burden of 87 risk factors in 204 countries and territories, 1990-2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet. Oct 2020;17;396(10258):1223-1249.
  4. Huang L, Trieu K, Yoshimura S, Neal B, Woodward M, Campbell N R C et al. Effect of dose and duration of reduction in dietary sodium on blood pressure levels: systematic review and meta-analysis of randomised trials. BMJ. 2020;368:m315.
  5. Cook NR, Appel LJ, Whelton PK. Lower levels of sodium intake and reduced cardiovascular risk. Circulation. 2014;129(9):981-9.
  6. Cook NR, Appel LJ, Whelton PK. Sodium intake and all-cause mortality over 20 years in the trials of hypertension prevention. Journal of the American College of Cardiology. 2016;68(15):1609-17.
  7. Strazzullo P, D’Elia L, Kandala N-B, Cappuccio FP. Salt intake, stroke, and cardiovascular disease: meta-analysis of prospective studies. BMJ. 2009-11-25 00:06:12 2009;339.
  8. Wang YJ, Yeh TL, Shih MC, Tu YK, Chien KL. Dietary Sodium Intake and Risk of Cardiovascular Disease: A Systematic Review and Dose-Response Meta-Analysis. Nutrients. Sep 2020;12(10):2934.
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Salt and Kidney Disease

Excessive salt intake is the most harmful of the dietary risk factors, associated with over 3 million deaths and the loss of 70 million DALYs in 2017 (1). Excess salt intake is a well-established cause of high blood pressure (BP) and increases the risk of cardiovascular disease and kidney disease (2).

Studies in humans have shown that high salt intake increases the amount of urinary albumin and the relationship is direct and dose-dependent (3, 4). Salt intake may affect the course of kidney disease directly, or through effects on BP (5) via hemodynamic (e.g. increased intraglomerular pressure) and non-hemodynamic mechanisms (e.g. increased oxidative stress), independent of blood pressure (6).

There is compelling evidence that reducing dietary sodium can reduce the risk for kidney function decline in individuals with chronic kidney disease (CKD) through significantly reducing 24-h urinary albumin and protein excretion (7),while being a cost-effective intervention with low risk of adverse effects (8).

There are also studies showing that a lower salt intake could slow down CKD progression (9). Although the relationship between dietary salt and kidney function or the development of CKD in individuals with normal kidney function requires further research, salt reduction efforts should be reinforced to save lives of people dying unnecessarily from CKD and other cardiovascular diseases each year.

References

  1. Afshin A, Sur PJ, Fay KA, Cornaby L, Ferrara G, Salama JS, et al. Health effects of dietary risks in 195 countries, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2019;393(10184):1958-72.
  2. National Academies of Sciences, Engineering, and Medicine; Food and Nutrition Board; Committee to Review the Dietary Reference Intakes for Sodium and Potassium; Oria M, Harrison M, Stallings VA, editors. Dietary reference intakes for sodium and potassium. Washington (DC): National Academies Press (US); 2019 Mar 5.
  3. du Cailar G, Ribstein J, Mimran A. Dietary sodium and target organ damage in essential hypertension. American Journal of Hypertension. Mar 2002;15(3):222-9.
  4. Verhave JC, Hillege HL, Burgerhof JG, Janssen WM, Gansevoort RT, Navis G, et al. Sodium intake affects urinary albumin excretion especially in overweight subjects. Journal of Internal Medicine. 2004;256(4):324-30.
  5. Smyth A, Dunkler D, Gao P, Teo KK, Yusuf S, O’donnell MJ, et al. The relationship between estimated sodium and potassium excretion and subsequent renal outcomes. Kidney International. 2014;86(6):1205-12.
  6. Weir MR, Fink JC. Salt intake and progression of chronic kidney disease: an overlooked modifiable exposure? A commentary. American Journal of Kidney Diseases. 2005;45(1):176-88.
  7. McMahon EJ, Campbell KL, Bauer JD, Mudge DW. Altered dietary salt intake for people with chronic kidney disease. Cochrane Database of Systematic Reviews. 2015(2).
  8. Wang G, Labarthe D. The cost-effectiveness of interventions designed to reduce sodium intake. Journal of Hypertension. 2011;29(9):1693.
  9. Cianciaruso B, Bellizzi V, Minutolo R, Tavera A, Capuano A, Conte G, et al. Salt intake and renal outcome in patients with progressive renal disease. Mineral and Electrolyte Metabolism. 1998;24(4):296-301.
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Salt and Stomach Cancer

Excess salt intake is associated with an increase in stomach cancer (gastric cancer) morbidity and mortality (1, 2). A meta-analysis of prospective studies found high-salt food, salted fish, processed meats (e.g. ham, bacon and sausage) and excess salt intake were all significantly associated with increased risk for stomach cancer (1). Furthermore, there is a dose-response relationship whereby the risk of stomach cancer increased by 12% for every 5 g/day increase in dietary salt intake (1). This was supported by a previous meta-analysis of 10 cohorts, which pooled studies to show high and moderately high salt intake were associated with a 68% increased risk of stomach cancer, compared with low salt intake (3).

Salt may act as an irritant to the gastric mucosa (stomach lining) which causes chronic inflammation of the stomach lining (atrophic gastritis), increased DNA synthesis, tumorigenesis, and cell proliferation (1,2). Excess salt intake also worsens Helicobacter pylori, an infection which is the major risk factor for stomach cancer as it can lead to inflammation and gastric ulcers, providing an environment for carcinogenesis in which stomach cancer can develop (4).

A modelling study found that compared to no intervention, the low sodium-DASH diet could reduce stomach cancer risk by 24.8% for males and 21.2% for females and approximately 27 and 14 cases of gastric cancer per 10,000 individuals were prevented for males and females respectively (5).

Stomach cancer is the fifth most common cancer and the third biggest cancer killer globally (6). Therefore, stomach cancer prevention through lowering salt consumption and healthy dietary patterns is crucial. 

References

  1. Fang X, et al. Landscape of dietary factors associated with risk of gastric cancer: A systematic review and dose-response meta-analysis of prospective cohort studies.  European Journal of Cancer. 2015;51(18): 2820-2832.
  2. Yusefi AR et al. Risk Factors for Gastric Cancer: A Systematic Review. Asian Pacific Journal of Cancer Prevention. 2018; 19(3): 591-603.
  3. D’Elia L, Rossi G, Ippolito R, Cappuccio FP, Strazzullo P. Habitual salt intake and risk of gastric cancer: a meta-analysis of prospective studies. Clinical nutrition (Edinburgh, Scotland). Aug 2012;31(4): 489-498.
  4. Zhang X-Y, Zhang P-Y, Aboul-Soud MAM. From Inflammation to gastric cancer : Role of Helicobacter pylori (Review). Oncology Letters. 2016; 13(2): 543-548.
  5. Kim JK et al. Low sodium diet for gastric cancer prevention in the United States: Results of a Markov model. Cancer Medicine. 2020;10(2): 684-692.
  6. Fay S. Salt: shaking up the link with stomach cancer. World Cancer Research Fund International. 2016.
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Salt and Meniere’s Disease

Dietary salt restriction is widely used as the first-line treatment option of Ménière’s Disease (1). Ménière’s disease is an inner ear disorder characterised by spontaneous recurrence of vertigo, fluctuating hearing loss and tinnitus (ringing in the ear) (2). A high salt diet is believed to contribute to imbalances in the electrolyte composition in the inner ear fluid as well as fluid retention causing pressure in the inner ear, resulting in Ménière’s disease and the associated symptoms (2,3).

Whilst there are no randomised controlled trials conducted to assess the effect of salt restriction on patients of Ménière’s disease,(3) there are some studies that suggest improvements in the symptoms of Ménière’s disease, including reduced number and severity of vertigo, with dietary modifications to lower salt intake (4, 5, 6).

Ménière’s disease is a progressive disease which damages the ear, resulting in frequent vertigo attacks, more prominent tinnitus and loss of hearing in the late stages (2). More high quality research is warranted to understand the effect of dietary modification on the management of Ménière’s disease (3).

References

  1. Acharya A, Singh M, Shrestha A. First Line Treatment of Meniere’s Disease. J Lumbini Med Coll. Dec 2016;4(2):68 -71.
  2. De Luca P, Cassandro C, Ralli M, Gioacchini FM, Turchetta R, Orlando MP, Iaccarino I, Cavaliere M, Cassandro E, Scarpa A. Dietary Restriction for The Treatment of Meniere’s Disease. Transl Med UniSa. May 2020;31;22:5-9.
  3. Hussain K, Murdin  L, Schilder  Restriction of salt, caffeine and alcohol intake for the treatment of Ménière’s disease or syndrome. Cochrane Database of Systematic Reviews. 2018;12. Art. No.: CD012173.
  4. Luxford E, Berliner KI, Lee J, Luxford WM. Dietary modification as adjunct treatment in Ménière’s disease: patient willingness and ability to comply. Otol Neurotol. Oct 2013;34(8):1438-43.
  5. Sheahan, S.L. and Fields, B. Sodium dietary restriction, knowledge, beliefs, and decision-making behavior of older females. Journal of the American Academy of Nurse Practitioners. 2008 Apr;20(4):217-224.
  6. Beard Trevor C. The Dietary Guideline with Great Therapeutic Potential. Australian Journal of Primary Health. 2008;14(3):120-131.
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Salt and Bone Density/Osteoporosis

High salt diets may increase calcium losses in the urine, and over time, could reduce bone density (1). Studies show there a significant correlation between urinary sodium and urinary calcium excretion (2, 3).

Urinary sodium excretion controls the urinary output of calcium. A high dietary salt intake may lead to increased calcium losses in the urine, which in long term may lead to calcium mobilization from the bones. 90% of calcium is stored in the bones. Calcium lost from the bones results in weakening of the bones, and ultimately osteoporosis.

A systematic review and meta-analysis of 13 cross-sectional and 2 cohort studies (n=39,065) found that higher salt consumption was associated with increased risk of osteoporosis, however there was high heterogeneity between studies (4). Together the students also showed there was no significant association between urinary or dietary sodium and bone mineral density and bone mineral content.

Findings from a randomized, repeat cross-over trial suggests that moderately high salt intake (11.2 g/day) significantly increased urinary calcium excretion (p=0.0008) in post-menopausal women (5). In another study of post-menopausal women, it was calculated that an increased sodium intake of 1150mg sodium/day for 10 years would deplete calcium stores by about 7.5% (6).

A cohort study found that high sodium intake measured by 24-hour urine was associated with increased loss of bone density at the hip sites in post-menopausal women (7). The study further suggests that if the daily excretion of sodium were halved, it would have an equivalent effect on bone density to that of increasing calcium intake by 891mg/day (7).

References

  1. Bedford JL, and Barr SI. Higher Urinary Sodium, a Proxy for Intake, Is Associated with Increased Calcium Excretion and Lower Hip Bone Density in Healthy Young Women with Lower Calcium Intakes. Nutrients. 2011;3:951-961.
  2. Itoh R, Suyama Y. Sodium excretion in relation to calcium and hydroxyproline excretion in a healthy Japanese population. The American journal of clinical nutrition. May 1996;63(5):735-740.
  3. Heaney RP. Role of dietary sodium in osteoporosis. Journal of the American College of Nutrition. Jun 2006;25(3 Suppl):271S-276S.
  4. Fatahi S, et al. The Association of Dietary and Urinary Sodium With Bone Mineral Density and Risk of Osteoporosis: A Systematic Review and Meta-Analysis. Journal of the American College of Nutrition. 2018;37(6):522–532.
  5. Teucher B, et al. Sodium and Bone Health: Impact of Moderately High and Low Salt Intakes on Calcium Metabolism in Postmenopausal Women. Journal of Bone and Mineral Research. 2008;23(9):1477-1485.
  6. Zarkadas M, Gougeon-Reyburn R, Marliss EB, Block E, Alton-Mackey M. Sodium chloride supplementation and urinary calcium excretion in postmenopausal women. The American journal of clinical nutrition. Nov 1989;50(5):1088-1094.
  7. Devine A, Criddle RA, Dick IM, Kerr DA, Prince RL. A longitudinal study of the effect of sodium and calcium intakes on regional bone density in postmenopausal women. The American journal of clinical nutrition. Oct 1995;62(4):740-745.
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Salt and Overweight/Obesity

The prevalence of overweight and obesity among adults and children has become a leading global health concern over the past three decades (1).  Excess body weight is associated with a range of health outcomes (2) and unhealthy diets are a major contributing factor (3,4).

There is some indication that diets high in salt contribute to overweight and obesity in children and adults (5,6,7,8,9,10,11,12). This is most clearly evidenced through the link between high salt intake and the consumption of sugar-sweetened beverages – a known risk factor for obesity (13).

A recent systematic review and meta-analysis which examined the relationship between dietary salt intake and measures of adiposity in cross sectional, longitudinal and randomized controlled trials provides some indication of an association, however, there remains a lack of high quality studies to provide robust evidence (14).

Although the evidence of high salt intake and overweight and obesity is unclear, it is important to consider additional health concerns of a high salt diet beyond the known risks, including high blood pressure (15) and cardiovascular health (16), which are important when informing obesity prevention strategies.

High quality longitudinal studies which include robust measure of sodium intake such as repeated 24hr urinary sodium excretion, and energy intake combined with objective anthropometry measures are required to clearly confirm the relationship between overweight and obesity and diets high in salt.

References

  1. Ng M, Fleming T, Robinson M, et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. Aug 2014;384(9945):766-781.
  2. Wang YC, McPherson K, Marsh T, et al. Health and economic burden of the projected obesity trends in the USA and the UK. Lancet. Aug 2011;378(9793):815-825.
  3. Bleich SN, Cutler D, Murray C, Adams A. Why is the developed world obese? Annual Review of Public Health. Apr 2008;29:273-295.
  4. Swinburn B, Sacks G, Ravussin E. Increased food energy supply is more than sufficient to explain the US epidemic of obesity. Am J Clin Nutr. Dec 2009;90(6):1453-1456.
  5. Grimes CA, Riddell LJ, Campbell KJ, He FJ, Nowson CA. (2016) 24-h urinary sodium excretion is associated with obesity in a cross-sectional sample of Australian schoolchildren. Br J Nutr 115, 1071-1079.
  6. Libuda L, Kersting M, Alexy U. Consumption of dietary salt measured by urinary sodium excretion and its association with body weight status in healthy children and adolescents. Public Health Nutr. Mar 2012;15(3):433-441.
  7. Zhu H, et al. Dietary sodium, adiposity, and inflammation in healthy adolescents. Pediatrics. Mar 2014;133(3):635-e642.
  8. Larsen SC, Ängquist L, Sørensen TIA, Heitmann BL. 24h Urinary Sodium Excretion and Subsequent Change in Weight, Waist Circumference and Body Composition. PLoS ONE. Jul 2013;8(7):e69689.
  9. Ma Y, He FJ, MacGregor GA. High salt intake: Independent risk factor for obesity? Hypertension. Oct 2015;66(4):843-849.
  10. Yi SS, Firestone MJ, Beasley JM. Independent associations of sodium intake with measures of body size and predictive body fatness. Obesity. Jan 2015;23(1):20-23.
  11. Yi SS & Kansagra SM. Associations of sodium intake with obesity, body mass index, waist circumference, and weight. Am J Prev Med. Jun 2014;46(6):e53-e55.
  12. Yoon YS & Oh SW. Sodium density and obesity; the Korea National Health and Nutrition Examination Survey 2007-2010. Eur J Clin Nutr. Feb 2013;67(2):141-146.
  13. He FJ, Marrero NM, MacGregor GA. Salt intake is related to soft drink consumption in children and adolescents: A link to obesity? Hypertension. 2008;51(3):629-634.
  14. Grimes CA, Bolton KA, Booth AB, Khokhar D, He FH, Nowson CA. The association between dietary sodium intake, adiposity and sugar-sweetened beverages in children and adults: a systematic review and meta-analysis. British Journal of Nutrition, 1-53.
  15. Brown IJ, Tzoulaki I, Candeias V, Elliot P. Salt intakes around the world: implications for public health. Int J Epidemiol. Jun 2009;38(3):791-813.
  16. He FJ, Li J, MacGregor GA. Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomised trials. BMJ. Apr 2013;346:f1325.
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Salt and Asthma

Whilst previous studies suggested that a high salt diet could aggravate symptoms of asthma (1,2,3,4) more recent reviews have indicated an absence of evidence to support this (5, 6).

A 1993 observational study on 138 men with initial to moderate asthma showed that bronchial reactivity was strongly related to 24-hour urinary sodium excretion (1). Two trials conducted in men (27 patients in the first trial and 36 in the second) in 1989 showed that an increase in dietary sodium, 80mmol/day in one and 204mmol/day in the other, increased both the severity of asthma and bronchial reactivity (2, 3). A 2008 study showed that, for children aged 6-7 years, adding salt to foods was strongly associated with an increased risk of respiratory symptoms such as wheezing and asthma (4). However, subsequent reviews have highlighted the limitations in these studies and demonstrate that the evidence is less clear.

A 2010 review of studies examining whether reducing dietary salt intake potentially improves pulmonary function and airway hyper-responsiveness in asthmatics, as well as studies evaluating dietary salt intake on the severity of exercise-induced bronchoconstriction said the data on the former was encouraging but not clinically convincing. In contrast a low-sodium diet maintained for 1 to 2 weeks did decrease bronchoconstriction in response to exercise in individuals with asthma but there were no data on the longer-term effects (5).

A subsequent 2011 Cochrane systematic review and meta-analysis similarly did not find any evidence that dietary sodium reduction significantly improves asthma control. It also concluded that, although dietary sodium reduction may result in improvements in lung function in exercise-induced asthma, the clinical significance of this effect was unclear as the studies were small and the reductions in salt large (6).  

As a low-sodium diet has other beneficial health effects, it could be recommended for adults with asthma, but as an additional complementary intervention to supplement, rather than as alternative to regular treatment (5).

References

    1. Carey OJ, Locke C, Cookson JB. Effect of alterations of dietary sodium on the severity of asthma in men. Jul 1993;48(7):714-718.
    2. Burney PG, Neild JE, Twort CH, et al. Effect of changing dietary sodium on the airway response to histamine. Jan 1989;44(1):36-41.
    3. Burney PG, Britton JR, Chinn S, et al. Response to inhaled histamine and 24 hour sodium excretion. British Medical Journal (Clinical research ed.). 1986;292(6534):1483-1486.
    4. Corbo GM, Forastiere F, De Sario M, et al. Wheeze and asthma in children: associations with body mass index, sports, television viewing, and diet. Epidemiology (Cambridge, Mass.). Sep 2008;19(5):747-755.
    5. Mickleborough TD. Salt intake, asthma, and exercise-induced bronchoconstriction: a review. Phys Sportsmed. Apr 2010;38(1):118-31.
    6. Cochrane. Does reducing the amount of salt in a diet improve asthma symptoms? Mar 2011.
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Salt and Cognitive Decline

The burden of cognitive decline, Alzheimer’s disease and dementia is increasing globally. Every year, there are about 10 million new dementia cases (1). Cognitive decline can be defined as the worsening or the increase in frequency of confusion or memory loss. It is also one of the earliest noticeable symptoms of Alzheimer’s disease and related dementias (2).

In terms of diet related risk for cognitive decline, Alzheimer’s disease and dementia, the Mediterranean diet has been extensively studied. Two systematic reviews of observational studies found that high levels of adherence to a Mediterranean diet was associated with decreased risk of mild cognitive impairment and Alzheimer’s disease (3,4). There is also evidence that adherence to a healthy, balance diet is beneficial in reducing the risk of cognitive impairment (1).

While there is a growing body of evidence on diet patterns and risk factors for cognitive decline (1), the number of studies that have focused on salt intake and that measured salt intake using the gold standard method of 24-hour urinary sodium excretion are limited. Given high blood pressure is an important risk factor for cognitive decline, it is likely that efforts to reduce salt, would also have benefits in reducing the burden of cognitive decline, Alzheimer’s disease, and related dementias (5).

In a recent systematic review investigating the link between salt intake, cognitive function and dementia risk, study authors stated that there was “some” evidence that high salt intake is associated with poor cognition (6). However, only two studies (out of 15), measured salt intake by 24-hour urinary sodium (7,8). One of these studies was conducted in women only, with 24-hour urines used on a subsample to correct for the dietary self-report (7). In the other study, 24-h urines were collected for all participants, and it was found that higher sodium intake was associated with cognitive impairment, yet this study was small (119 people) (8).

There is no cure for dementia so modifiable lifestyle interventions are key to slow or prevent cognitive impairment and the progression of disease (1). Salt reduction are likely to be important, but more research, using higher quality methods to measure salt intake, is required to substantiate this.  

References

  1. World Health Organization: Risk reduction of cognitive decline and dementia: WHO guidelines. 2019.
  2. Alzheimer’s Association. Mild Cognitive Impairment (MCI). 2021.
  3. Singh B, Parsaik AK, Mielke MM, Erwin PJ, Knopman DS, Petersen RC, Roberts RO. Association of mediterranean diet with mild cognitive impairment and Alzheimer’s disease: a systematic review and meta-analysis. Journal of Alzheimer’s disease. 2014;39(2):271-282.
  4. Wu L, Sun D. Adherence to Mediterranean diet and risk of developing cognitive disorders: An updated systematic review and meta-analysis of prospective cohort studies. Scientific Reports. 2017;7(1):1-9.
  5. Livingston G, Huntley J, Sommerlad A, Ames D, Ballard C, Banerjee S, et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. The Lancet. 2020;396(10248):413-446.
  6. Mohan D, Yap KH, Reidpath D, Soh YC, McGrattan A, Stephan BCM, Robinson L, Chaiyakunapruk N, Siervo M; DePEC team. Link between dietary sodium intake, cognitive function, and dementia risk in middle-aged and older adults: A systematic review. Journal of Alzheimer’s Disease. 2020(Preprint):1-27.
  7. Haring B, Wu C, Coker LH, Seth A, Snetselaar L, Manson JE, Rossouw JE, Wassertheil-Smoller S. Hypertension, dietary sodium, and cognitive decline: results from the women’s health initiative memory study. American journal of hypertension. 2016;29(2):202-216.
  8. Afsar B. The relationship between cognitive function, depressive behaviour and sleep quality with 24-h urinary sodium excretion in patients with essential hypertension. High Blood Pressure Cardiovascular Prevention. 2013;20(1):19-24.
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