Electrolytes and hormones are like vehicles sharing traffic on a two-way street. When one starts driving like they’re wearing a blindfold, everybody is late for work.
Take insulin and sodium for instance. Low-sodium diets may contribute to insulin resistance. And when insulin is low, you lose sodium more rapidly — that’s why people who eat a low-carb diet (like keto, paleo, or carnivore) need more salt.
That’s just one example. Did you know poor potassium status can suppress growth hormone? Or that low thyroid hormones can disrupt electrolyte excretion? Or that magnesium supplementation can lower cortisol?
I’ll cover all of these topics and more in this article, concluding with a few tips to keep your electrolytes and hormones operating in sweet synergy. I think you’ll learn something useful!
Electrolytes and Insulin
Let’s begin with the hormone insulin, which interacts with multiple electrolytes.
Sodium and Insulin
Many people understand insulin’s role in regulating blood sugar: When you eat carbs, your pancreas produces insulin, which helps move glucose (sugar) from your blood into your muscle, liver, or fat cells. Fewer people know that insulin also helps support sodium balance by signaling your kidneys to retain sodium.
This is why low-carb dieters often wind up sodium deficient; restricting carbs keeps blood sugar low, which means your pancreas produces less insulin, and minimizing insulin reduces sodium retention.
Conversely, electrolytes also support insulin function. Namely, sodium deficiency may contribute to insulin resistance, a condition in which insulin can’t effectively move blood sugar into cells. Consider the following studies:
- 2001 randomized controlled trial: People with primary hypertension experienced an 8% lower glycemic response at dietary sodium intakes of ~6,100 mg/day compared to ~2,700 mg/day, suggesting improved insulin function.
- 2003 randomized controlled trial: 15 healthy males experienced a median 15% decrease in insulin sensitivity at dietary sodium intakes of ~1,600 mg/day compared to ~4,000 mg/day.
- 2011 analysis of clinical data: 151 healthy men and women showed increased insulin resistance at dietary sodium intakes of less than 460 mg/day compared to intakes greater than 3,450 mg/day.
Supporting insulin function is a good move for longevity. Better insulin function is linked to a lower risk of heart disease, diabetes, cancer, Alzheimer’s, and all-cause mortality.
Magnesium and Insulin
Like sodium, magnesium supports insulin function. No surprise there. As a cofactor for over 300 enzymes, this mineral supports almost all of the human body’s physiological processes in one way or another.
A 2017 review of eight human trials found that magnesium supplementation reduced blood sugar levels, with seven suggesting magnesium lowers insulin resistance. Another 2024 randomized controlled trial found that 250 mg/day of magnesium oxide for two months enhanced insulin function in women with PCOS.
More research is needed on this front, but there’s no doubt that getting enough magnesium is a good thing for your hormones and health overall, especially considering that up to 30% of the population may be magnesium deficient.
Potassium and Insulin
The link between potassium and insulin is best explored through the lens of diabetes. When someone has type 1 diabetes, they can’t make insulin. This low insulin state predisposes them to hyperkalemia (high serum potassium) because — along with blood sugar — insulin also shuttles potassium from the blood into cells. No insulin, no shuttle.
Type 2 diabetics don’t typically have trouble making insulin. Their problem is insulin resistance. And insulin-resistant folks have trouble shuttling potassium too.
The complications of hyperkalemia can be life-threatening, so clinicians must pay special attention to serum electrolytes in anyone with diabetes. Let’s return to sodium now.
Sodium and the Renin-Angiotensin-Aldosterone System (RAAS)
Renin, angiotensin II, and aldosterone are the primary hormones that regulate blood pressure. When blood pressure falls, your kidneys secrete these three hormones to bring it up.
The RAAS also tells your kidneys to retain sodium, because retaining sodium can help boost blood volume and normalize blood pressure. As blood pressure and sodium status normalize, the RAAS shuts down like a gas pump clicking off when your tank is full.
Dietary habits affect the system too. While higher salt intakes fill your sodium tank and reduce unnecessary RAAS activity, sodium deficiency activates the RAAS. This helps the body hold onto sodium and stabilize sodium status, but the excess hormones can also unnecessarily raise blood pressure.
You might be thinking, aren’t low-sodium diets supposed to lower blood pressure?
It’s complicated. Low sodium diets can lower blood pressure meaningfully in hypertensives, but not quite as much as expected. The RAAS could explain why, since too little sodium can trigger the release of those hormones and inadvertently blunt the blood pressure improvements.
For example, in a 2020 Cochrane review of 195 randomized controlled trials (RCTs) studying 12,296 normotensives and hypertensives, researchers found that reducing sodium intake from ~4,700 to 1,500 mg/day had the following effects:
- White normotensives’ mean arterial pressure decreased by less than 1% (0.4 mmHg).
- White hypertensives’ mean arterial pressure decreased by about 3.5% (4 mmHg).
- Lower-quality evidence showed slightly greater reductions in blood pressure for black and Asian participants.
- Renin increased 55% for more than 2,900 participants.
- Aldosterone increased 127% for more than 2,500 participants.
On sodium-restricted diets, blood pressure falls, but RAAS hormones rise. But there’s more to this story — let’s talk about two important adrenal hormones next.
Sodium, Epinephrine, and Norepinephrine
The same 2020 Cochrane review that discovered an increase in renin and aldosterone on low-sodium diets also found significant increases in epinephrine (27%) and norepinephrine (14%). Like the RAAS, these fight-or-flight hormones trigger sodium retention and raise blood pressure. This elevated activity of the sympathetic nervous system caused by a low-sodium diet may lead to worse sleep.
Sodium restriction may also raise baseline heart rate, which has been linked to increased cardiovascular and all-cause mortality. A 2016 meta-analysis of normotensive and hypertensive populations within 63 RCTs found that sodium reduction decreased systolic blood pressure by 2.5%, but also increased baseline heart rate by 2.4%
These sodium restriction side effects (and effects on insulin and the RAAS) may explain, at least in part, why sodium reduction studies fail to show a heart disease or all-cause mortality benefit despite reducing blood pressure in hypertensives.
Sodium and Antidiuretic Hormone (ADH)
When you’re dehydrated, your brain secretes antidiuretic hormone (ADH) to retain fluids and electrolytes. Consequently, you pee less. Ever wondered why alcohol makes you pee like a racehorse? It’s because alcohol blocks ADH secretion.
Similarly, being low on sodium may impair ADH secretion. In one study, ADH levels fell by 60% in 12 young men after a week of sodium restriction. Getting enough sodium, on the other hand, likely supports ADH. More salt, fewer midnight bathroom breaks interrupting your sleep!
Conversely, some people may make too much ADH. Common drivers of excessive ADH production include central nervous system issues, cancer, drugs, and HIV. This syndrome of inappropriate ADH secretion (SIADH) causes excessive fluid retention and dilutes blood sodium levels, resulting in hyponatremia (low serum sodium). Clinicians often treat the resulting hyponatremia with intravenous saline.
Potassium and Growth Hormone
The research on electrolytes for growth hormone is sparse, but worth investigating.
When young rats are fed potassium-deficient chow, their growth is severely compromised. In one study, potassium-deficient rats gained 97% less weight than controls over 10 days. Don’t worry, the rodents recovered rapidly when they started eating potassium again.
Other rat research suggests potassium deficiency may cause growth hormone resistance. In other words, cells stop listening to growth hormone — preventing the growth of muscle, bone, and other tissue — in the context of poor potassium status.
We definitely need more research, but I have a feeling these findings may translate to humans. In children with Bartter syndrome, you find both potassium depletion and stunted growth. In older adults, potassium depletion is linked to muscle wasting and higher mortality risk.
Electrolytes and Thyroid Hormones
The thyroid hormones T3 and T4 serve to increase metabolic rate, muscle protein synthesis, bone development, and — you guessed it — maintain fluid and electrolyte balance.
People with hypothyroidism (low thyroid hormone) have reduced plasma renin activity and plasma aldosterone levels. These two hormones are on the frontlines of fluid and electrolyte balance, stimulating a vital enzyme called the sodium-potassium pump. This pump facilitates the flow of fluid and electrolytes in and out of almost every human cell. If renin and aldosterone are the wardens calling the shots, our sodium-potassium pumps are the guards bringing electrolytes in and out of our cells.
Low renin and aldosterone leads to underactive sodium-potassium pumps, disrupting guard duty and ultimately leading to greater electrolyte losses. So, in short, people with low thyroid hormones might lose too much sodium and potassium. This may lead to low levels of both electrolytes in the blood, as well as an accumulation of water inside cells (which can contribute to the weight gain characteristic of hypothyroidism.
A 2022 study found lower potassium levels correlated with lower thyroid hormones in 150 women with hypothyroidism. Another study on 9,012 emergency room patients found links between hypothyroidism, hypokalemia (low serum potassium), and hyponatremia (low serum sodium).
As is common in science, other studies find the contrary — that neither sodium or potassium imbalance are associated with hypothyroidism. The practical thing to do? If you have thyroid issues, watch your blood electrolyte levels carefully. There’s no harm in keeping an eye on them.
Magnesium, Sodium, and Cortisol
Cortisol is a glucocorticoid — a type of steroid hormone that binds to nearly every human cell. Colloquially, you may know it as the “stress hormone.” When you’re stressed, the adrenal glands release a surge of cortisol, which raises blood sugar and breaks down muscle for quick energy.
These are positive adaptations if you’re playing hide-and-seek with a polar bear in the Arctic — you need as much energy to outrun that bear as you can get. But if you’re merely battling Amazon for a $14 refund, excess cortisol is not your friend.
Enter magnesium. Magnesium lowers cortisol by stimulating 11β‐HSD type 2. No, that’s not your router’s model number — it’s an enzyme that metabolizes glucocorticoids. This enzyme reduces cortisol levels by turning cortisol into cortisone, a biologically inactive compound. On the clinical side, a 2021 study found that supplementing 350 mg of magnesium daily for 24 weeks lowered urinary cortisol levels in 49 overweight people.
Sodium also plays a role here. A 2017 study of over 3,200 patients found that people with blood sodium levels within the normal range of 136–150 mEq/L had lower cortisol levels compared to those with abnormally high or low blood sodium levels. Researchers consider this cortisol surge an “appropriate stress response” to the harms of a sodium imbalance — after all, maintaining a normal blood sodium level is extremely important for the body to function properly.
Magnesium and Hormones for Bone Health
Magnesium, your do-it-all mineral, is essential for the function of three bone health hormones:
- Parathyroid hormone (PTH) regulates bone mineralization, the process of building bone. While small, intermittent spurts of PTH help build bone, too much PTH can lead to bone breakdown. Higher magnesium levels support bone strengthening by suppressing PTH.
- Vitamin D is considered a vitamin and a hormone. Vitamin D regulates bone health, immunity, mood, intestinal magnesium absorption, and much more. Magnesium helps out by supporting vitamin D transport and activation.
- Estrogen promotes bone growth in males and females. It also stimulates magnesium absorption. Low magnesium intakes are linked to bone disorders and higher rates of blood clotting in women.
Bone health is an immense topic, and I can’t do it justice in this article. Check out this article on improving bone density for a deeper dive.
How to Keep Electrolytes and Hormones in Harmony
To keep your electrolytes and hormones operating in parallel requires a bit of vigilance. You have to be proactive. The most straightforward approach is to get enough electrolytes.
Research-backed targets are 4–6 grams of sodium, 3.5–5 grams of potassium, and 400–600 mg of magnesium daily. Figure out your baseline intake by tracking what you eat; any diet tracking app will do. Optimize your diet first, and then supplement as needed to hit your targets.
We didn’t cover the electrolytes calcium or phosphorus today. These minerals interrelate with hormones too, but if I covered every connection, I’d be publishing a book. Shoot for about 1 gram of calcium through diet (one clean egg shell contains over 2 grams calcium). Don’t worry about phosphorus; it’s abundant in food.
For a look under the hood at how your electrolyte levels and hormones are behaving in practice, you can also track your bloodwork. You won’t check everything — like RAAS or epinephrine, for instance — and that’s okay! Work with a clinician that understands your unique situation to check your serum electrolytes, insulin, thyroid hormones, and other biomarkers. Don’t skip this bloodwork step if you have diabetes, hypothyroidism, or another chronic health issue.
Most importantly, remember that electrolytes are just one piece of the puzzle when it comes to hormone health. The fundamentals are key: Get enough sleep. Exercise. Eat a nutrient-dense diet. Favor whole foods, not processed foods. Your body will thank you later.
