Keywords: Cortisol, HPA Axis, Insomnia, Magnesium Supplementation, Melatonin, Potassium Supplementation, Sleep Architecture, Type 2 Diabetes
Introduction
Chronic insomnia and dysregulated cortisol secretion have emerged as defining biomarkers of premature physiological ageing and metabolic dysfunction. Globally, insomnia disorder affects an estimated 10.5% of adults, approximately 554 million individuals, imposing enormous burdens on workforce productivity, quality of life, and long-term cardiometabolic health. Within this already substantial population, patients with type 2 diabetes mellitus (T2DM) and related metabolic conditions bear a disproportionately high burden: sleep disorders in this cohort are not merely comorbid, but mechanistically implicated in the perpetuation of insulin resistance, glycaemic dysregulation, and systemic inflammation [1,2,3].
Cortisol, the primary glucocorticoid secreted by the adrenal cortex in response to HPA axis activation, exerts potent catabolic and immunomodulatory effects when chronically elevated. Hypercortisolaemia disrupts slow-wave sleep architecture, suppresses nocturnal melatonin secretion, and perpetuates a vicious cycle in which poor sleep further stimulates adrenal cortisol release. From a longevity medicine perspective, this HPA-sleep feedback loop is a tractable therapeutic target: interventions that simultaneously lower cortisol and restore sleep architecture hold the potential to decelerate biological ageing and reduce the cumulative burden of metabolic disease [4].
Magnesium (Mg²⁺) and potassium (K⁺) are the most abundant divalent and monovalent intracellular cations, respectively, and are essential cofactors in over 300 enzymatic reactions. Both minerals play critical roles in neuronal excitability, smooth and skeletal muscle function, and the regulation of stress hormones. Despite this physiological centrality, dietary surveys consistently demonstrate that more than half of adults in Western populations fail to meet recommended daily allowances for magnesium, while potassium inadequacy is similarly prevalent in high-glycaemic diets. Importantly, diabetes itself, through glycosuria-associated urinary mineral losses and impaired intestinal absorption, dramatically amplifies micronutrient depletion [5,6].
This review synthesizes the emerging mechanistic and clinical evidence supporting combined Mg+K supplementation as a dual-target, non-pharmacological strategy for cortisol attenuation and insomnia resolution in patients with metabolic disease. The anchor of this synthesis is a landmark 2024 randomized controlled trial published in Frontiers in Endocrinology, which provides the most comprehensive head-to-head, placebo-controlled evidence to date on the independent and combined effects of these two minerals on sleep hormones and insomnia severity.
Epidemiology: The Intertwined Burden of Insomnia and Metabolic Disease
The global burden of insomnia disorder is staggering and has been systematically underestimated in epidemiological literature due to heterogeneity in diagnostic criteria. A 2025 systematic review-based analysis estimated a weighted global prevalence of 10.5%, with figures rising substantially in populations with chronic disease. In patients with T2DM specifically, prevalence of sleep disturbance has been reported as high as 50–70%, with insomnia serving both as a risk factor for and a consequence of poor glycaemic control [2,7,8].
The metabolic consequences of chronic insomnia extend well beyond fatigue. Epidemiological data demonstrate that individuals with insomnia disorder have a significantly elevated risk of developing T2DM, hypertension, cardiovascular disease, and all-cause mortality. The mechanistic bridge between disrupted sleep and metabolic deterioration is multi-layered but converges on the HPA axis: sleep fragmentation activates the HPA stress response, elevating morning cortisol, promoting hepatic gluconeogenesis, and inducing peripheral insulin resistance. This neuroendocrine cascade simultaneously increases visceral adiposity, reduces anabolic hormone secretion (including growth hormone and testosterone), and accelerates cellular senescence, a triad of pathological changes that define accelerated biological ageing [4,9].
From a longevity and preventive medicine standpoint, identifying modifiable upstream drivers of this insomnia-HPA axis cycle is a research and clinical priority. Micronutrient repletion, particularly of minerals depleted in metabolic disease, represents a compelling, low-risk, and widely accessible intervention strategy [5,10].
Magnesium and Potassium: Physiological Roles and Metabolic Vulnerability
Magnesium
Magnesium is the fourth most abundant mineral in the human body and the second most prevalent intracellular cation. It acts as a cofactor for ATP synthesis, DNA repair, protein biosynthesis, and the regulation of neuromuscular transmission. Of particular relevance to the sleep-stress axis, Mg²⁺ serves as a physiological antagonist of calcium at voltage-gated channels and as a blocking ion at N-methyl-D-aspartate (NMDA) glutamate receptors, two mechanisms that directly influence neuronal hyperexcitability, stress reactivity, and sleep initiation [6,11].
Magnesium deficiency, defined clinically as serum Mg below 0.74 mmol/L, though tissue depletion may precede serum abnormalities, is highly prevalent in metabolic disease. Patients with T2DM exhibit significantly higher rates of hypomagnesaemia compared to normoglycaemic individuals, driven by osmotic urinary losses, reduced intestinal absorption secondary to hyperglycaemia, and impaired tubular reabsorption. Analysis of NHANES data spanning 2003–2018 confirmed that higher magnesium depletion scores are independently associated with greater odds of metabolic syndrome [5,6].
Potassium
Potassium is the most abundant intracellular cation in the human body, essential for maintaining resting membrane potential, regulating cardiac rhythm, and supporting smooth muscle function. At the neurobiological level, potassium channels modulate action potential repolarization and are involved in the regulation of circadian oscillator gene expression in peripheral tissues. Studies in circadian biology demonstrate that ambient potassium levels influence the period length of circadian oscillations, and dietary potassium intake timing has been inversely associated with insomnia severity scores [12].
Clinically, potassium depletion (hypokalaemia) is associated with fatigue, muscle cramps, cardiac arrhythmias, and poor sleep quality. In patients with diabetes, osmotic diuresis-mediated urinary potassium losses are compounded by inadequate dietary potassium intake, a pattern common to high-glycaemic, processed-food diets that paradoxically predominate in metabolic disease populations [13].
Mechanism of Action: HPA Axis Modulation and Sleep Regulation
Magnesium and the HPA Axis
The regulatory relationship between magnesium and the HPA axis is bidirectional and self-reinforcing, a “vicious cycle” wherein Mg deficiency amplifies stress reactivity, and chronic stress further depletes Mg through stress-induced urinary magnesium excretion. Mechanistically, Mg²⁺ exerts inhibitory effects at multiple levels of the stress hormone cascade: (1) it attenuates corticotropin-releasing hormone (CRH) release from hypothalamic paraventricular neurons; (2) it reduces the pituitary’s adrenocorticotropic hormone (ACTH) secretory response; and (3) it modulates adrenocortical sensitivity to circulating ACTH, directly limiting cortisol synthesis and release [10,14].
At the receptor level, Mg²⁺ functions as an endogenous NMDA receptor antagonist, blocking the calcium-permeable ion channel pore in a voltage-dependent manner. This action reduces glutamatergic excitatory neurotransmission, which is a critical driver of hyperarousal states associated with insomnia and anxiety. Simultaneously, magnesium exerts GABA-agonistic properties, enhancing inhibitory neurotransmission through GABA-A receptor modulation, a mechanism shared by several first-line pharmacological sleep aids, but achieved here through a nutritional substrate [11,15].
Magnesium, Melatonin, and Circadian Biology
Magnesium is a required cofactor for the enzyme arylalkylamine N-acetyltransferase (AANAT), which catalyzes the rate-limiting step in melatonin biosynthesis from serotonin. Accordingly, Mg deficiency is associated with reduced nocturnal melatonin production, contributing to delayed sleep onset and reduced sleep efficiency. Mg supplementation in elderly insomniacs has been shown to significantly elevate serum melatonin levels, improve subjective sleep quality, and increase total sleep time in double-blind, placebo-controlled conditions. Furthermore, Mg²⁺ assists in the regulation of clock gene expression (CLOCK, BMAL1, PER2), helping entrain circadian rhythms to the 24-hour light-dark cycle and normalizing the diurnal cortisol pattern [15,16].
Potassium’s Neuroendocrine Contributions
While the mechanistic evidence for potassium in the HPA axis is less extensively characterized than for magnesium, emerging data suggest important contributions. Potassium channels in adrenocortical cells modulate cortisol secretion by regulating membrane polarization: hypokalaemia is associated with relative adrenal hyperstimulation, partially explaining why low dietary potassium correlates with elevated basal cortisol in observational data. At the sleep level, short-term potassium infusion studies in the 1990s demonstrated objectively measurable improvements in sleep continuity measured by actigraphy, suggesting a direct electrophysiological role for K⁺ in sustaining sleep architecture [12].
Synergism: Why Combination Outperforms Monotherapy
The biological rationale for combining Mg and K is rooted in their complementary and mutually potentiating mechanisms. Mg directly suppresses HPA axis activation and enhances GABAergic and melatonergic neurotransmission, while K supports membrane polarization stability, circadian gene expression, and adrenocortical tone regulation. At the intracellular level, both ions cooperate in maintaining the electrochemical gradient required for neuronal function; their co-depletion, common in metabolic disease, produces compounded dysregulation of sleep-wake architecture and stress hormone profiles. Clinically, this synergy predicts superior outcomes from combination therapy compared to either mineral administered alone, a hypothesis confirmed by the 2024 Khalid et al. trial.
Clinical Evidence: The 2024 frontiers in Endocrinology Randomized Controlled Trial
Study Design and Population
Khalid et al. (2024) conducted a single-blind, four-arm randomized controlled trial at the Akhuwat Health Services Diabetes Centre in Lahore, Pakistan. A total of 320 patients with diabetes mellitus and insomnia (confirmed by the Insomnia Severity Index, ISI) were enrolled, with 290 completing the 8-week follow-up (9.4% dropout). Participants were stratified into four treatment groups: T1 (placebo, starch 250 mg twice daily), T2 (magnesium gluconate, 250 mg twice daily), T3 (potassium chloride, 250 mg twice daily), and T4 (combined Mg + K, 250 mg each twice daily) [17].
The study population had a mean age of 48–51 years across groups, with a 2:1 female-to-male ratio (67.9% women). This gender distribution is clinically meaningful: women with diabetes exhibit greater HPA axis reactivity and higher insomnia prevalence compared to male counterparts, making female-predominant findings particularly relevant to real-world metabolic populations. Exclusion criteria were appropriately rigorous, eliminating confounding conditions including psychological insomnia, cardiovascular disease, severe hepatic or renal impairment, hormonal therapy, and drug-induced sleep disorders. Blood samples were collected under fasting conditions before and after the trial, with sleep hormones (cortisol AM and melatonin) quantified by ELISA [17].
Key Outcome Measures
Primary outcome measures included the Insomnia Severity Index (ISI), a validated 7-item self-report instrument classifying insomnia as: no clinically significant insomnia (ISI 0–7), sub-threshold (8–14), moderate clinical insomnia (15–21), and severe clinical insomnia (22–28). Secondary measures were morning serum cortisol (μg/dL) and nocturnal melatonin (pg/mL), both measured by enzyme-linked immunosorbent assay (ELISA). Statistical analyses employed the Kruskal–Wallis H-test and chi-square tests, with significance set at p ≤ 0.05 [17].
Results: Cortisol Reduction, Melatonin Restoration, and Insomnia Resolution
Cortisol: ~45% Reduction with Combined Supplementation
The most striking finding of the trial was the magnitude of cortisol suppression achieved by combined Mg+K supplementation. The T4 group demonstrated a reduction in morning serum cortisol from a pre-trial mean of 41.57 ± 10.01 μg/dL to 22.70 ± 4.07 μg/dL post-trial, representing a net decline of 18.87 μg/dL or approximately 45.4%, that was highly statistically significant (p=0.001). By comparison, magnesium alone (T2) reduced cortisol by 39.2% (40.71 to 24.75 μg/dL), potassium alone (T3) by 23.5% (41.44 to 31.69 μg/dL), and placebo (T1) by a non-significant 4.2% (p=0.247). The T4 combination arm achieved cortisol levels substantially lower than either monotherapy, consistent with the predicted synergistic suppression of HPA axis activity [17].
These cortisol reductions are clinically significant in absolute terms. Normal morning serum cortisol falls within 6–23 μg/dL in most laboratory references. Pre-trial values in all groups (mean ~41 μg/dL) indicated functional hypercortisolaemia, consistent with chronic HPA hyperactivation in this metabolically stressed diabetic-insomnia population. Post-intervention T4 values (22.70 μg/dL) normalised effectively to within or near the upper bound of physiological range, a clinically meaningful endpoint for practitioners managing cortisol-associated metabolic complications.
Melatonin: Supracompensatory Restoration in the Combination Group
Serum melatonin demonstrated equally impressive and differential responses. The T4 (Mg+K) group exhibited a mean melatonin increase from 6.12 ± 2.25 pg/mL to 15.37 ± 17.37 pg/mL (p=0.001), a rise of approximately 151%, suggesting melatonin biosynthetic capacity was substantially restored by combined mineral repletion. The large post-trial standard deviation in the T4 melatonin group (17.37 pg/mL) warrants acknowledgement: this likely reflects inter-individual variability in baseline melatonin depletion severity and biosynthetic capacity, rather than instability of the treatment effect. Placebo group melatonin remained essentially unchanged (7.03 to 6.84 pg/mL; p=0.502), confirming that observed changes were attributable to active intervention rather than temporal or placebo effects [17].
This melatonin rebound has direct clinical implications beyond sleep. Melatonin is a potent mitochondrial antioxidant with anti-inflammatory and immunomodulatory properties, properties particularly relevant to slowing the accelerated cellular ageing characteristic of chronic metabolic disease. From a longevity medicine perspective, the capacity of a simple dual-mineral supplementation protocol to restore nocturnal melatonin levels to or above those of younger, healthier individuals represents a meaningful physiological rejuvenation.
Insomnia Severity Index: Complete Elimination of Severe Insomnia
The ISI data yielded what is arguably the most clinically impactful finding of the trial. At baseline, severe clinical insomnia was present in 33.8% of placebo participants, 20.0% of T2 (Mg), 10.8% of T3 (K), and 27.4% of T4 (Mg+K) participants. After 8 weeks, the distribution changed dramatically: in all three active treatment groups, the proportion of participants with severe clinical insomnia fell to 0.0%, while 39.7% of placebo participants had deteriorated to or remained in the severe insomnia category (p=0.0001) [17].
In the T4 group, 41.1% of participants achieved the highest category of improvement, no clinically significant insomnia, post-trial, compared to 0.0% in the placebo group. This represents a complete categorical shift across the ISI distribution in the active arms, a magnitude of improvement rarely observed in non-pharmacological insomnia trials. The overall between-group ISI comparison was significant at p=0.0001, with the highest mean rank improvements in the Mg+K combination arm [17].
Contextualizing The Evidence: Prior Clinical Literature
The 2024 Khalid et al. findings build on a growing body of clinical evidence supporting magnesium’s role in sleep and stress biology. Abbasi et al. (2012) demonstrated in a double-blind, placebo-controlled RCT in elderly patients (n=46) that 500 mg/day magnesium supplementation for 8 weeks significantly reduced ISI scores (p=0.006), increased serum melatonin (p=0.007), and improved objective sleep parameters including sleep efficiency and early morning awakening [16].
A 2023 systematic review by Arab et al. in Biological Trace Element Research confirmed that observational data robustly link higher magnesium status with better sleep quality, including reduced daytime sleepiness, improved sleep duration, and lower insomnia severity scores. The same review noted that while mechanistic evidence is strong, the heterogeneity of RCT designs, varying magnesium formulations, doses, and outcome instruments, precludes firm meta-analytic conclusions from intervention studies alone, underscoring the importance of the 2024 Khalid et al. trial as the largest and most design-rigorous contribution to date [15].
Djokic et al. (2019) provided complementary evidence that multi-target mineral and hormone supplementation (magnesium combined with melatonin and vitamin B complex) significantly improved insomnia outcomes across all etiological subtypes over 3 months, supporting a multifactorial approach to sleep restoration. Held et al. (2002) demonstrated in a randomized crossover study that oral magnesium supplementation in older adults reversed age-related reductions in slow-wave (Stage N3) sleep, the sleep phase most critical for cortisol downregulation, growth hormone release, and cellular repair [18,19].
Systematic reviews of micronutrient-sleep relationships (Ji et al., 2017) have consistently found that potassium deficiency, alongside copper and zinc, correlates negatively with sleep duration, while magnesium and iron correlate positively. The convergence of observational and interventional data across independent research groups lends substantial credibility to the 2024 trial’s findings and underscores the biological plausibility of Mg+K combination therapy as a first-line micronutrient intervention for insomnia in metabolic disease [20].
Clinical Implications for Longevity, Wellness, and Preventive Metabolic Medicine
The therapeutic implications of the Khalid et al. trial extend significantly beyond the primary diabetic population studied. The HPA axis dysregulation and insomnia phenotype observed in this cohort are not unique to diabetes, they are a broader signature of metabolic disease, chronic psychological stress, and modern lifestyle patterns characterized by poor diet, physical inactivity, and circadian disruption. Several groups for whom these findings may be most actionable in a longevity and preventive medicine context include:
Metabolic syndrome and pre-diabetes populations. Given that magnesium depletion is strongly inversely associated with metabolic syndrome across large cross-sectional studies, individuals with insulin resistance and abdominal adiposity represent a high-priority group for preventive Mg+K repletion, potentially interrupting the insomnia-cortisol cascade before overt diabetes develops [5].
High-stress and occupational burnout populations. The vicious cycle of Mg depletion and cortisol hypersecretion described by Pickering et al. is highly relevant to individuals with chronic psychosocial stress. Stress-induced urinary magnesium losses exacerbate HPA axis hyperreactivity, and co-administration of both Mg and K may constitute a safe, accessible adjunct to psychological and lifestyle interventions [10].
Older adults and longevity medicine patients. The age-related decline in magnesium absorption, coupled with reduced dietary intake and polypharmacy-associated mineral depletion, makes magnesium-potassium supplementation particularly relevant in healthy ageing programs focused on preserving sleep architecture, HPA resilience, and cognitive function.
From a prescribing perspective, the formulations used in the trial (magnesium gluconate and potassium chloride, 250 mg twice daily) are widely available, generally well-tolerated, and low-cost. Magnesium gluconate is among the better-absorbed oral magnesium salts compared to oxide forms, and potassium chloride at these doses falls well within safe supplementation ranges. Practitioners should screen for contraindications in patients with impaired renal function, where potassium accumulation poses arrhythmia risk.
Limitations and Future Research Directions
Despite the clinical significance of the findings, several limitations of the 2024 Khalid et al. trial must be acknowledged. First, the single-blind rather than double-blind design introduces the possibility of outcome reporting bias, as participants were not fully blinded to treatment assignment. Second, the study was conducted at a single centre in Lahore, Pakistan, limiting generalizability to other ethnic, dietary, and socioeconomic contexts. Third, all patients were recruited irrespective of diabetes duration, creating potential confounding from varying degrees of neuropathic and metabolic deterioration [17].
Fourth, the ISI is a validated but subjective patient-reported instrument. The absence of polysomnographic (PSG) or actigraphy-based objective sleep outcomes limits interpretation of which specific sleep stages were most affected, a critical distinction for understanding whether Mg+K acts primarily on sleep initiation, maintenance, or deep sleep architecture. Fifth, the trial did not screen for anxiety or depression, which are major independent confounders of both sleep quality and HPA axis activity.
Future research should prioritize: (1) large-scale, multi-centre, double-blind RCTs with polysomnographic endpoints; (2) dose-response studies evaluating whether higher Mg or K doses confer additional benefit; (3) investigations in non-diabetic metabolic syndrome, burnout, and ageing populations; (4) mechanistic sub studies measuring CRH, ACTH, and adrenal sensitivity markers to map the HPA axis intervention point; and (5) longer-term follow-up (≥12 months) to assess durability of response and impacts on glycaemic control, cardiovascular biomarkers, and cognitive function as secondary endpoints.
Conclusion
The combined supplementation of magnesium and potassium represents a physiologically coherent, evidence-supported, and clinically practical intervention for two of the most clinically burdensome manifestations of metabolic disease: chronic hypercortisolaemia and insomnia. The 2024 Khalid et al. randomized controlled trial provides compelling proof-of-concept data: an 8-week Mg+K protocol in diabetic insomniacs achieved approximately 45% cortisol reduction, 151% melatonin restoration, and complete elimination of severe insomnia in all active treatment arms, outcomes unmatched by either mineral administered alone and dramatically exceeding the placebo arm [17].
These findings are grounded in a well-characterized mechanistic framework: Mg²⁺ suppresses HPA axis activation at multiple neuroendocrine checkpoints, enhances GABAergic inhibitory neurotransmission, blocks NMDA receptor-mediated neuronal hyperexcitability, and is required for melatonin biosynthesis. Potassium complements these actions through membrane polarization stability, circadian oscillator modulation, and adrenocortical tone regulation. Together, they address the upstream neuroendocrine drivers of insomnia with a precision that neither mineral achieves independently.
For practitioners in longevity medicine, integrative health, and preventive metabolic care, these data provide a strong rationale for routinely assessing magnesium and potassium status in patients presenting with insomnia, elevated morning cortisol, and metabolic disease. Repletion strategies should be part of a comprehensive approach that includes circadian hygiene, dietary optimizations, and stress management, but the evidence now clearly supports combined Mg+K supplementation as a core, non-pharmacological component of that approach.
As the global burden of metabolic disease and sleep disorders continues to rise in parallel, identifying cost-effective, low-risk micronutrient interventions that target shared pathophysiological mechanisms is both scientifically justified and urgently needed. The findings reviewed here position combined magnesium-potassium therapy as a promising, evidence-based tool in the preventive medicine and longevity practitioner’s arsenal.
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