Browse evidence-based analysis of health-related claims and assertions
Antihypertensive medications reduce blood pressure through specific mechanisms but do not address the underlying metabolic causes of hypertension.
Sleep deprivation increases sympathetic nervous system activity, elevating heart rate and vascular resistance, while restorative sleep enhances parasympathetic activity, reducing cardiac output and vascular resistance.
Dietary fiber reduces postprandial blood glucose spikes by slowing absorption, thereby decreasing insulin secretion and enabling normal renal sodium excretion.
Aerobic exercise induces shear stress on blood vessel walls, stimulating endothelial nitric oxide production, which results in sustained reduction in vascular resistance.
Processed foods are typically low in potassium, which normally aids sodium excretion and vascular relaxation, exacerbating hypertension when combined with high sodium and refined carbs.
Processed foods contain engineered combinations of high sodium and refined carbohydrates, which together cause acute plasma volume expansion and chronic hormonal sodium retention, leading to sustained hypertension.
Chronic insulin resistance impairs endothelial function by reducing nitric oxide production, leading to arterial stiffness and increased vascular resistance.
Insulin resistance results in chronically elevated insulin levels, causing the kidneys to continuously retain sodium due to persistent hormonal signaling.
Elevated uric acid levels directly increase renal sodium reabsorption without insulin involvement.
Fructose metabolism in the liver produces uric acid, which impairs endothelial function by reducing nitric oxide availability and arterial relaxation.
Chronic elevation of insulin activates the sympathetic nervous system, leading to increased heart rate, cardiac output, and peripheral vasoconstriction, thereby raising blood pressure.
Insulin signaling causes the kidneys to retain sodium, independent of dietary sodium intake.
Sodium intake increases plasma volume through osmotic water retention, leading to higher blood pressure due to increased fluid in a closed circulatory system.
People with a condition called primary aldosteronism have 6% more fluid outside their cells than others, but their sodium excretion doesn't affect this fluid level.
People with high blood pressure who aren't taking medication have similar sodium excretion and body fluid levels outside their cells as people with normal blood pressure.
The levels of various blood chemicals like electrolytes, hormones, and kidney markers don't change based on how much sodium someone excretes in their urine.
Sodium excretion levels don't affect blood pressure, heart rate, or how much blood the heart pumps when lying down.
People who excrete more sodium in their urine tend to have more fluid outside their cells.
After starting dapagliflozin, the kidneys produced more aldosterone hormone for a few days, which might help the body retain salt, but this effect didn't last after two weeks.
People with type 2 diabetes and healthy kidneys lost about 0.8 kg after a few days and 1.8 kg after two weeks of taking dapagliflozin, likely due to water loss.
Dapagliflozin made the kidneys less able to reabsorb sodium in the first part of the nephron, which is why more lithium was excreted, showing the drug's effect on kidney function.
As expected, dapagliflozin caused people with type 2 diabetes to excrete much more sugar in their urine, which is how the drug works to lower blood sugar.
Dapagliflozin didn't significantly change the amount of fluid in the bloodstream of people with type 2 diabetes and healthy kidneys, even after two weeks of treatment.
Dapagliflozin caused a temporary decrease in body fluid volume outside cells after 4 days, but this effect went away after two weeks in people with type 2 diabetes and healthy kidneys.