12 January - 20 June 2016

Can low sodium intake lead to the development of atherosclerosis?

9 Jan 13

Dietary salt is essential for the body to maintain homeostasis of water and sodium and plays an important role in the regulation of blood pressure.  High sodium intake has lead to increases of blood pressure and risk factor for atherosclerosis; however there have been conflicting results in atherosclerosis studies using mouse models.  A study published in the Journal of Nutritional Biochemistry has hypothesised that low dietary sodium intake would contribute to development of atherosclerosis via activation of the renin angiotensin system (RAS).  Previous animal and human studies have found that restricted sodium intake activates RAS which increases blood pressure and contributes to the development of atherosclerosis.    Daugherty et al. split 8 week old male LDL receptor mice into three groups and fed them a diet containing the same amount of saturated fat but each group received varying amounts of sodium (Na 0.01%, 0.1% or 2% w/w) for 12 weeks.    At baseline and weeks 4, 8 and 12 blood pressure was measured and after 10 weeks 24hr urine was collected. The scientists also measured plasma concentration and lipoprotein distributions from samples taken from 5-6 animals from each groups. Daugherty et al. measured renin in the kidneys using real time polymerase chain reaction and also measured plasma renin concentrations using radioimmunoassay.   They report that urine sodium excretion was as expected and related to dietary sodium concentrations.    Mice fed Na 2% had greater water consumption and urine volume at 24 hr period than those fed the Na at 0.01% or Na 0.1%, however although food consumption was similar in all groups the NA 2% gained less body weight compared to the other two groups.  Plasma cholesterol concentration was more than 1000 mg/dl in all mice three groups.    Those fed Na 0.01% or Na 0.1% had moderately higher plasma cholesterol than those fed Na 2%, with HDL cholesterol being the same amongst all three groups and LDL cholesterol concentration being higher in mice fed Na 0.01% or Na 0.1%.   Only mice fed Na at 2% had significant increased systolic blood pressure during the 12 week feed.  Renal renin mRNA was more abundant in mice fed Na 0.01% than those fed Na 2% or Na 0.1%.  High dietary sodium was found to decrease both plasma renin concentration and atherlosclerotic lesion areas.  In conclusion Daugherty reports high dietary sodium intake led to higher systolic blood pressure while low dietary sodium intake augmented atherosclerosis in hypercholesterolemic mice.

RSSL can determine the composition of food and drink products, including the sodium content (UKAS accredited). For more information please contact Customer Services on Freephone 0800 243482 or email enquiries@rssl.com

RSSL's Product and Ingredient Innovation Team, has considerable experience in re-formulating products to provide more healthy options including low salt, low sugar versions and using pre- and probiotics.  Using RSSL can help speed up your development cycle considerably.  For more information please contact Customer Services on Freephone 0800 243482 or email enquiries@rssl.com

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