Optimal sodium is 3-5g/day and potassium above 2g/day

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- in order to minimize the risk of cardio-vascular disease. This is based on thew recent study:
"Joint association of urinary sodium and potassium excretion with cardiovascular events and mortality: prospective cohort study", by Martin O’Donnell et al., BMJ 2019; 364

These guidelines are significantly higher than the existing WHO recommendations.

Fig 3

Heat map of risk for composite of cardiovascular events or death showing lowest risk in region of moderate sodium intake 3-5 g/day and higher potassium intake and highest risk in region of extremes of sodium excretion and low potassium excretion. The reference hazard for these hazard ratios was set at a value of sodium daily excretion/intake of 5.00 g and potassium daily excretion/intake of 2.25 g (median excretion of sodium and potassium), marked as X. The overlaid lines represent joint distribution quartiles; each region contains a quarter of the analysed participants. r=0.34

Non-compliant diabetics had lower CVD risk

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"Adherence to lipid-lowering medications and cardiovascular disease prevention in type 2 diabetes mellitus", by Karlsson, Sofia Axia, PhD thesis, University of Gothenburg, 7-Nov-2018


Quote:

Adjusted for potential confounders, risk of CV events was higher among patients with less than complete adherence to lipid lowering medications and that risk gradually increased as patient adherence declined, independent of prevention group.

Ketogenic diet protects against chemotherapy

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"β-Hydroxybutyrate, a ketone body, reduces the cytotoxic effect of cisplatin via activation of HDAC5 in human renal cortical epithelial cells", Daisuke Mikami et al., Life Sciences
Volume 222, 1 April 2019, Pages 125-132

Quote:

Main methods

In this study, we used human renal cortical epithelial (HRCE) cells. The anti-apoptotic effect of βOHB was evaluated using flow cytometry analysis. The expression of apoptosis-related proteins and HDACs was evaluated by western immunoblot.

Key findings

The results showed that βOHB significantly reduced cisplatin-induced apoptosis in HRCE cells. Furthermore, βOHB significantly reduced cisplatin-induced cleavage of caspase-3, acetylation of histone H3, and phosphorylation of AMP-activated kinase. This anti-apoptotic effect of βOHB was markedly attenuated by an inhibitor of HDAC4/5, and βOHB-mediated suppression of cleavage of caspase3 was significantly blocked by siRNA-induced gene silencing of HDAC5.

Significance

βOHB attenuates cisplatin-induced apoptosis by activation of HDAC5 in HRCE cells, suggesting that βOHB may be a new therapeutic agent for cisplatin nephropathy.