Browse evidence-based analysis of health-related claims and assertions
Mice missing the KDM6A gene in their kidneys show more water-absorbing proteins, which might make them hold onto more water.
When mice lose the KDM6A gene in their kidneys, certain salt-handling proteins increase, which makes it harder for their kidneys to get rid of salt.
When mice lose the KDM6A gene in their kidney cells, their kidneys hold onto more salt and their blood pressure goes up, which might be linked to changes in a specific protein mark.
In mice, AMPK is linked to how the kidneys function.
When mice lose both AMPKα1 and AMPKα2 in their kidneys, they lose too much water and salt in their urine.
Even though these mice have less red blood cells, their blood plasma volume is higher than normal mice.
Mice missing the AMPKα1 gene produce more aldosterone in their urine and have lower blood pressure than normal mice.
When mice lack the AMPKα1 gene, their kidneys handle salt normally and produce less urine than usual.
Processed food consumption disrupts multiple regulatory mechanisms in the blood pressure system, leading to hypertension.
Patients with insulin resistance or metabolic syndrome experience minimal blood pressure reduction from salt restriction alone due to hormonal drivers of hypertension.
Antihypertensive medications lower blood pressure but do not address the underlying physiological causes of hypertension.
Poor sleep increases sympathetic nervous system activity, raising heart rate and vascular resistance, while restorative sleep enhances parasympathetic activity, lowering cardiac output and vascular resistance.
Dietary fiber slows glucose absorption, reducing postprandial insulin spikes and enabling normal sodium regulation by the kidneys.
Physical activity increases endothelial nitric oxide production, resulting in sustained vascular relaxation and reduced blood pressure.
Processed foods are typically low in potassium, which is necessary for sodium excretion and vascular relaxation.
Processed foods contain high levels of sodium and refined carbohydrates, which together cause acute plasma volume expansion and chronic hormonal dysregulation of blood pressure.
Insulin resistance causes chronically elevated insulin, leading to sodium retention by kidneys and reduced nitric oxide production, resulting in increased vascular resistance and blood pressure.
Fructose metabolism produces uric acid, which impairs endothelial function and directly increases renal sodium reabsorption.
Chronic insulin elevation activates the sympathetic nervous system, increasing heart rate, cardiac output, and peripheral vascular resistance.
Insulin acts as a sodium-retaining hormone, causing the kidneys to retain sodium independent of dietary sodium intake.
Individual salt sensitivity varies based on kidney function, nitric oxide production, and genetic factors.
The kidneys regulate blood pressure through the renin-angiotensin-aldosterone system (RAAS), excreting sodium and water when pressure is high and retaining sodium when pressure is low.
Sodium intake increases blood pressure through osmotic water retention, expanding plasma volume.
Endothelial nitric oxide production regulates vascular resistance; reduced nitric oxide causes arterial stiffening and increased resistance.