Using electrolytes to give your clients a clearer view of the impact of stress on their systems

If you’ve been thinking that you don’t quite have the full picture when it comes to your clients’ true stress load, it might be time to take a deeper look at their electrolyte balance. Using electrolytes as markers could identify many causes of stress in the body – from infection to exercise, and more. Read on to discover how electrolytes work in the body and how they can be used as an indicator of hidden health trends.

What is an electrolyte and how does it work in the body?

An electrolyte is a substance that breaks down into ions (positive and negative charged particles) when in a solution that is capable of electric signaling. They are involved in muscle contraction, heart function, endocrine secretion, regulating osmotic balance, buffering body fluids, controlling acid/base balance.

Electrolyte markers include Sodium, Potassium, Chloride, Co2, Magnesium, Calcium and Phosphate[i]. In this article we will be focusing on the first 4 of these.

SODIUM (Na⁺)

Sodium is the main extracellular cation (95% of total extracellular electrolytes)
It contributes to tonicity and induces the movement of water across cell membranes.
Serum Sodium reference range 136 – 145 mmol/L

POTASSIUM (K⁺)

Is the main intracellular ion.
In humans total body K is about 50 mmol/L/kg of body weight.
Complete and rapid absorption in the GIT
98% of total potassium in the body is stored intracellularly, with 80% of intracellular potassium found in skeletal muscle cells. The remaining 20% can be found in bones, liver and erythrocytes.
The remaining small percentage of total potassium in the body (2%) is found extracellularly, within the interstitial space and plasma[ii].
Serum potassium reference range 3.50 – 5.3 mmol/L.

BICARBONATE (CO₂)

The second most abundant anion in the blood.
Normally not excreted in urine, but conserved by the kidneys to be used in the body’s buffering system[iii].
Low levels of CO2 can lead to acidosis can be the result of acid build up in the blood or excessive loss of CO2 from the blood (metabolic acidosis). Acid can build up as a result of abnormal metabolism, like in poorly controlled T1DM or with impaired excretion associated with kidney dysfunction or failure.
Carbon dioxide build up in the blood due to poor lung function or depressed breathing (respiratory acidosis)[iv].
Serum bicarbonate reference range 22-29 mmol/L

CHLORIDE (Hcl)

Is the main extracellular anion[v].
It moves with sodium, in order to maintain electrical neutrality and proper hydration. Its main role is to regulate the body’s acid-base balance. Chloride channels also help regulate pancreatic juice secretion into the small intestine and flow of water into mucus.
Hydrochloric acid when combined with hydrogen.
Erythrocytes require Chloride to remove carbon dioxide from the body.
Like for the previous electrolytes, the kidneys are primarily responsible for keeping total body chloride concentration within range[vi].
Serum Chloride reference range 95-108 mmol/L – 98 to 106 mEq/L

How can electrolytes be used as an indicator of hidden health trends?

Potassium is generally considered to have protective effects, linked to its blood pressure lowering capacities and inhibitory effects on free radical genesis.

Increase of potassium intake has been inversely related to risk of kidney stones; potassium supplementation reduces excretion of calcium, which in turn reduces the risk of kidney stones formation[i].

Minimal decrease in serum K (0.3 mEq/L) following increase in blood glucose or insulin can decrease aldosterone by as much as 50%, independently of sodium intake[ii]. Aldosterone mediates the exchange of K and Na in the distal renal tubule cells. Aldosterone deficiency is known to result in hyperkalemia (>5.5 mmol/L), while aldosterone excess is associated with hypokalemia (<3.5 mmol/L)[iii].

↑serum K → ↑synthesis and release of aldosterone → ↑enhanced renal and extra renal potassium disposal

When aldosterone is mediated by rises in potassium, it is the first line of defense against hyperkalemia[iv].

What can affect aldosterone?

stress – psychological stress activates both HPA axis and SNS (sympathetic-adrenomedullary system). Activation of HPA axis directly elevates aldosterone, while the SNS increases aldosterone through activation of the renin-angiotensin system[v] and, as previously stated, elevated aldosterone results in lower potassium.
primary hyperaldosteronism (Conn’s syndrome).
Insulin, needed for potassium homeostasis (EC) K concentration. Glucose-induced insulin is responsible for increasing intracellular K uptake into muscle cells and liver through stimulation of the Na⁺K⁺-ATPase. But raised ECF K also stimulates insulin secretion[vi].
Catecholamines (dopamine, norepinephrine, epinephrine) bind to beta-2-receptors on muscle cells and increase activity of Na⁺/K⁺-ATPase pump stimulating intracellular K uptake in order to limit the increase of extracellular K[vii]. Linked with physical exercise – skeletal muscle is the major reservoir for K in the body, during physical activity interstitial K increases to promote vasodilation and blood flow[viii].

Severe loss of bodily fluids through diarrhoea and vomiting can affect all electrolytes.

Optimal Potassium range research suggests[ix] that even deviations within the normal K range were associated with an increased mortality risk. A serum K interval of 4.1 to 4.4 mmol/L was associated with the lowest risk of death.

Sodium:potassium ratio

Serum potassium and sodium represent the internal environment of the body, and the balance of the two plays a vital role in the regulation of blood pressure. Na:K ratio is obtained by dividing serum Na value by serum K value.

Studies have suggested that the Na:K ratio could serve as a prognostic marker of cardiovascular disease (CVD), however these looked at dietary intake rather than serum levels. A systematic review and meta-analysis investigated the association[i] between serum Na:K ratio and blood pressure and confirmed that a lower sodium to potassium ratio was associated with a remarkable reduction in systolic and diastolic blood pressure in adults and suggests a lower sodium:potassium diet to be beneficial for blood pressure control.

One study suggested that elevated plasma Na:K ratio could be used as a better indicator for hypertension than either Na or K alone[ii].

A low Na:K ratio can indicate a loss of K into the interstitial space, as tissue is broken down and cells are destroyed. A low ratio is associated with adrenal insufficiency, impaired glucose tolerance, infections, impaired digestion (resulting in breakdown of protein for conversion into sugar to maintain adequate energy production levels)[iii]

Elevated Na:K ratio could indicate acute stress as increased adrenal activity and aldosterone production cause Na to be retained in the body, causing serum levels to increase while more K is excreted.

Low Na:K ratio can be a better indicator of chronic stress and possible adrenal fatigue/insufficiency resulting in decreased aldosterone production = higher volume of Na is excreted, K is retained. Decreased Na:K ratio is also an indicator of higher cortisol output, associated with tissue breakdown.

Identifying your clients’ health status using electrolyte markers

Electrolytes enter into circulation through the digestive tract; in healthy conditions excretion is mainly handled by the kidneys, with lower amounts lost in feces and sweat. In unhealthy conditions or after prolonged stress, you may observe:

Hypernatremia (>145 mmol/L) or excess sodium intake

Caused by:

Primary aldosteronism (Conn’s syndrome) or Cushing syndrome. Aldosterone, an adrenal corticosteroid that acts on the kidneys, stimulates reabsorption of sodium and secretion of K; excess production of aldosterone results in elevated sodium through increase in sodium retention, while aldosterone deficiency increases sodium excretion[i]. Primary aldosteronism is the most common cause of secondary hypertension[ii].

Inadequate water intake.

Hypotonic fluid due to GI losses (osmotic diarrhoea, vomiting) or Renal losses (kidney dysfunction, diabetes insipidus).

Medications (diuretics).

Hyponatremia (<136 mmol/L) is one of the most common electrolytes imbalances in humans.

It is an acknowledged mortality predictor, and a recent meta-analysis has confirmed that its improvement is independently associated with the reduction of all-cause mortality risk.

Caused by:

Cardiovascular, endocrine, hepatic, metabolic or renal dysfunction[iii]. Additionally…

Infection induced hyponatremia (<135 mmol/L)

Hyponatremia reported in existing, active infections. The most common infections associated with hyponatremia were bacterial and viral (influenza and respiratory viruses, including the most recent COVID-19; HIV disease or AIDS). Low serum sodium was a common finding in bacterial infections and both DNA and RNA viruses are known to affect the Na⁺K⁺-ATPase, however the aetiology remains unclear. It could be associated with the infection itself but other factors such as medications, malnutrition, renal or intracranial pathologies often coexist[iv];[v].

A recent study on non-ICU COVID19 patients found Na to be inversely related to IL-6 (released by monocytes and macrophages), possibly through IL-6 inducing non-osmotic release of vasopressin but further studies are required to confirm this[vi].

Exercise associated hyponatremia (EAH)

Often seen in long and high intensity physical activity, copious loss of hypotonic fluid would be expected to concentrate and raise serum Na but the opposite is often observed.

Loss of sodium through sweat or overconsumption of hypotonic fluids can impact serum Na.

Disturbances in the suppression of hormone AVP (arginine vasopressin, regulator of water excretion) can lead to inappropriate water retention. If paired with excessive water intake it might lead to hyponatremia. Stimulation of AVP can also occur as the result of increased inflammatory cytokine IL-6, which also tends to elevated during exercise[vii].

Hypothyroidism which is associated with low serum Na.

A study aimed at identifying the effects of hypothyroidism on lipid, electrolyte and mineral status found blood sodium levels to be significantly lower in hypothyroid cases compared to controls.

The study also found a negative correlation between serum TSH and serum sodium and potassium, the higher the TSH levels, the lower serum Na and K. This could be the result of suppressed Plasma Renin Activity and Plasma Aldosterone and subsequent exaggerated Na excretion. Reduced serum K, although not statistically significant, was also observed in hypothyroid patients[viii].

Other markers to consider in relation to electrolytes

Metabolic markers: Anion gap [(Na⁺ + K⁺) – (Cl^–+ CO₂)] if elevated it is associated with metabolic acidosis[i], uric acid (tissue breakdown?).
Sugars: C-Peptide (link with Na K-ATPase), glucose, HbA1C, fasting insulin.
Kidney markers: creatinine, urea (in relation to hyperkalemia and hyperchloremia) (BUN in relation to low chloride).
Calcium and Phosphate.
Hormones – DHEA-S (check to establish health of adrenal glands and address possible adrenal dysfunction, as DHEA-S is produced exclusively in the adrenals).