Recently I watch a video where the doctor has mentioned that insulin is likely a higher driver of hypertension than sodium.
I’m not expecting anyone to watch it and he does go through all of the regular factors such as sleep, weight, exercise, sodium, potassium etc.
One thing he did not mention was whether this has an impact independent of insulin resistance. He suggested eating UPF frequently throughout the day will lead to frequent insulin release and water rention.
I know it plays some role as we see people losing water initially on low carb diets, but is this more about AUC insulin as opposed to spreading out your food is worse? And does this apply to healthy populations?
One other think he mentioned was the J-shaped curve, which I know largely disappears with appropriate urine collection. However something I haven’t heard is the mechanism by which he said low sodium can cause higher BP (renin–angiotensin–aldosterone system), leading to vasoconstriction. Is this overstated?
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This is a low carb trope that seemingly won’t die. Thanks, social media (I guess?)
The evidence for sodium’s independent effect on blood pressure is much stronger than insulin’s, and amongst the strongest in all of nutrition epidemiology. A brief review from some content I’ve been working on:
- DASH-Sodium showed dose-dependent BP reductions w/ sodium restriction in those w/ HTN
- INTERSALT showed a consistent linear relationship between sodium and blood pressure.
These are large, well-controlled trials showing the same thing, which have been repeated multiple times.
The insulin side is different. Yes, insulin resistance correlates with hypertension in the context of metabolic syndrome, but severe insulin resistance and hyperinsulinemia can occur without elevated blood pressure, and vice versa. The proposed mechanisms (renal sodium retention via ENaC stimulation, sympathetic nervous system activation, etc.) are real in isolation, but their magnitude as independent contributors to hypertension in humans appears modest.
Interestingly, most of the good evidence points to insulin resistance as a downstream marker of the same upstream problem (excess adiposity, particularly visceral fat) that also drives hypertension through separate pathways: physical kidney compression, leptin-mediated sympathetic activation, and RAAS dysregulation among them.
Saying insulin drives hypertension more than sodium requires ignoring the hierarchy of evidence. We have RCT data for sodium. We have cross-sectional associations and mechanistic speculation for insulin.
More silly things said irresponsibly by this individual:
- The claim that eating UPF frequently throughout the day produces meaningful water retention through repeated insulin secretion conflates a few things. Yes, insulin promotes renal sodium reabsorption. But the clinical significance of this in someone who is not insulin resistant is effectively zero.
- As for AUC insulin vs. meal frequency: total energy intake and body composition predict metabolic health outcomes far better than how many times per day someone eats. The meal-frequency-and-insulin framing is a downstream echo of the “insulin is the master hormone” narrative, which has not held up under scrutiny when tested against simpler explanations like energy balance and adiposity. Insulin is more of a response than a predictor.
- Yes, the J curve, the observation that cardiovascular disease (CVD) risk and mortality are low at moderate sodium intake but increase at both extremely high and low levels, disappears with proper measurement. Reverse causality is a major factor: people who are already sick eat less, including less sodium.
- Restricting sodium below a certain threshold activates the renin-angiotensin-aldosterone system (RAAS), increasing angiotensin II (a vasoconstrictor) and aldosterone. This is a well-characterized compensatory response to reduced extracellular volume. Whether this translates to a clinically relevant BP increase depends on how low “low” actually is. The DASH-Sodium tested intakes down to ~1,000 mg/day and still showed BP decreases. The activation of RAAS and/or sympathetic nervous system due to low sodium intake (that could be achieved while meeting energy needs) has to date not shown an increase in BP in those with normal or elevated BP.
It is frustrating that this message will likely reach 1/1000 of the individuals who watched his video, despite his video containing lots of misinformation.
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