This came up on one of my feeds, but is actually a 1983 paper. It is, however, interesting in conclusion because of the idea that a limit on sodium activates the ANS.
In the UK we call Norepinephrine noradrenaline
https://academic.oup.com/jcem/article-abstract/56/3/553/2675275
Abstract
Plasma norepinephrine levels in 10 healthy young males were significantly elevated after 3 days of a low sodium (<500 mg/day) diet. The low sodium diet was also associated with disturbed sleep patterns: decreased rapid eye movement and slow wave sleep and increased wakefulness. These sleep changes are similar to those seen in normal aged adults, who also undergo elevations of daytime and nighttime plasma norepinephrine. These results suggest the possibility that increased sympathetic nervous system activity may affect sleep patterns, and that therapies altering sympathetic activity may affect sleep. (J Clin Endocrinol Metab 56 : 553, 1983)
I have set O3 on trying to get a summary/critique. I donât think it found the paper, but it did find a little more
Article at a glance
| Citation | Vitiello MV, Prinz PN, Halter JB. Sodiumârestricted diet increases nighttime plasma norepinephrine and impairs sleep patterns in man. J Clin Endocrinol Metab. 1983;56(3):553â556. |
| Design | Repeatedâmeasures laboratory study in which each participant served as his own control. Ten healthy young men were studied during a normalâsodium diet and, ~2 months later, after three days on a veryâlowâsodium diet (< 500 mg Naâș dayâ»Âč). (Oxford Academic) |
| Key measures | Nightâtime plasma norepinephrine (NE) concentrations (multiple venous samples) and full polysomnographyâderived sleep architecture. |
| Principal findings | Low sodium intake raised nightâtime plasma NE and was accompanied by less rapidâeyeâmovement (REM) and slowâwave sleep and more wakefulness. (PubMed) |
| Authorsâ interpretation | The sympathetic activation provoked by acute sodium restriction may be sufficient to disturb sleep; similar mechanisms might underlie ageârelated sleep fragmentation. (PubMed) |
Strengths
- Withinâsubject control: Each volunteer underwent both diet conditions, reducing interâindividual variability.
- Objective sleep assessment: Polysomnography was stateâofâtheâart for 1983 and remains the gold standard.
- Physiological linkage: Simultaneous quantification of catecholamines and sleep stages offered a mechanistic bridge between diet, autonomic activity and sleep.
Limitations
| Domain | Concern | Why it matters |
|---|---|---|
| Sample | n = 10, all healthy young men | Underâpowered for subtle effects; not generalisable to women, older adults or people with hypertension/sleep disorders. |
| Intervention intensity & duration | < 500 mg Naâș dayâ»Âč for only 3 days | Far below current publicâhealth targets (~2 g dayâ»Âč). Acute responses may differ from chronic adaptation. |
| Blinding & expectancy | Diet was obvious; nightâtime blood draws disturb sleep | Placebo/nocebo or procedural arousal could exaggerate effects attributed to sodium. |
| Outcome scope | Catecholamines only; no reninâangiotensin, heartârate variability or cortisol | Limits mechanistic insight and the ability to disentangle volumeâdepletion from sympathetic drive. |
| Statistical detail | The brief report (4 pages) provides minimal information on variance, effect sizes or correction for multiple sleep variables | Makes it hard to judge robustness or clinical relevance. |
Context with later literature
- Subsequent kinetic studies confirm that severe sodium restriction elevates sympathetic tone, but most show modest or null effects on sleep at intakes recommended today.
- Large epidemiological cohorts relate highânot lowâsodium diets to poor sleep, possibly via hypertension and nocturia.
- Thus, the 1983 findings are best viewed as an upperâbound demonstration of what extreme sodium depletion can do, rather than evidence against current saltâreduction guidelines.
Overall appraisal
This classic short communication was innovative for its time, prompting researchers to think of dietâautonomicâsleep interactions. However, its tiny, homogeneous sample and extreme intervention limit external validity, and the sparse statistical reporting does not meet modern standards. Contemporary investigators should:
- Replicate with larger, sexâbalanced samples across the adult lifespan.
- Use rangeâfinding sodium intakes (e.g., 0.5 g â 2 g â 4 g dayâ»Âč) to map doseâresponse curves.
- Incorporate comprehensive autonomic and hormonal profiling plus subjective sleep quality.
Until such data exist, clinicians should not infer that modest salt reduction will fragment sleepâespecially in populations who stand to gain cardiovascular benefit from lowering sodium.