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Metabolic Health Starts with This Often-Ignored Electrolyte

6/30/2025

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In conventional medicine, potassium is often treated as a number to worry about only when it's dangerously high or dangerously low. The standard lab reference range, typically 3.5 to 5.1 mmol/L, is used as a pass/fail system. As long as a child’s potassium is not flagged as critically abnormal, it’s rarely mentioned or addressed. But in functional and integrative medicine, we know that there’s a difference between “normal” and “optimal.” 
And that difference can significantly impact a child’s muscle tone, digestion, energy production, and neurological function.
This is especially true for children with complex needs, those with Down syndrome, autism, hypotonia, mitochondrial dysfunction, chronic constipation, or feeding challenges. For these children, even a mildly suboptimal potassium level (e.g., 3.6 or 3.8 mmol/L) can worsen symptoms that are already interfering with their daily life. It’s time to start recognizing potassium as a functional nutrient, not just an emergency electrolyte.
Potassium is the most abundant intracellular cation in the body. Approximately 98% of potassium is inside our cells, where it is responsible for a huge number of critical functions:
  • Generating electrical impulses in muscles and nerves
  • Maintaining smooth muscle tone, including in the intestines
  • Facilitating nutrient transport across cell membranes
  • Supporting glucose uptake into cells
  • Buffering pH and balancing acid-base status
  • Supporting enzyme function in energy metabolism pathways
  • Regulating heartbeat and cardiac rhythm
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When potassium is low, even within the low end of the reference range, these functions begin to degrade. Unfortunately, conventional lab interpretation doesn’t flag these early dysfunctions.

For example:
A potassium level of 3.5 to 3.9 mmol/L might not raise concern for a conventional provider. But in a child who has muscle weakness, poor stamina, constipation, or speech regression, these numbers are a red flag that cellular energy production and nerve transmission are not being properly supported.

Many children with neurodevelopmental disorders or genetic conditions have biochemical and physiological reasons that make them more susceptible to low or suboptimal potassium levels. For example, low muscle tone and reduced physical activity can impair potassium retention, as skeletal muscle serves as a major reservoir for this electrolyte. Chronic constipation often reflects smooth muscle fatigue or poor peristalsis, both of which rely on adequate intracellular potassium for proper function. Feeding challenges further limit intake of potassium-rich foods, particularly in children with restrictive diets or oral aversions.
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In addition, malabsorption and gut dysbiosis may reduce the body’s ability to absorb and utilize dietary potassium effectively. Mitochondrial dysfunction, which affects energy production in nearly every cell type, further impairs potassium uptake and utilization at the cellular level. Finally, thiamine deficiency, commonly seen in children with Down syndrome and metabolic vulnerability, can disrupt potassium transport into cells, while low potassium in turn can block thiamine uptake, creating a self-perpetuating cycle of fatigue, neurological dysfunction, and impaired motility.

In short, children with special needs are not only more vulnerable to potassium depletion, but often more affected by it, yet the problem is rarely investigated unless there's an acute crisis. 

Signs and Symptoms of Low Potassium


Even mild hypokalemia, when potassium levels are just slightly below optimal, can cause noticeable and impactful symptoms. These often present subtly at first but can significantly affect quality of life, especially in children with neurodevelopmental conditions. In those with Down syndrome, these symptoms are frequently overlooked or dismissed as just part of the diagnosis, when in fact they may reflect an underlying, correctable nutrient deficiency. This same pattern is seen with other nutrients as well, such as iron, zinc, thiamine, or magnesium, where functional symptoms are written off rather than addressed.

Common symptoms of low or suboptimal potassium include:
  • Muscle weakness or low tone
  • Fatigue or low energy
  • Constipation or sluggish bowel movements
  • Irritability or mood lability
  • Tingling or numbness
  • Heart palpitations or irregular rhythm
  • Cramping or muscle twitching
  • Poor reflexes or difficulty initiating movement
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In functional medicine, we often see that these symptoms are disregarded when lab results are “within normal limits.” Yet correcting a potassium level from 3.5 up to 4.2 mmol/L can lead to remarkable improvements in energy, digestion, and physical coordination. Recognizing that these signs may point to a treatable deficiency, not simply a feature of a genetic condition, can dramatically shift the care approach and outcomes for these children.

​How to Test and What to Look For


​Potassium is most commonly measured in serum, and it’s included as part of a routine comprehensive metabolic panel (CMP), which many children receive during annual physicals or when evaluating fatigue, growth, or gastrointestinal symptoms. However, unless flagged as critically high or low, potassium levels are often overlooked or dismissed, especially if they fall within the lab’s reference range.

In functional and integrative care, we aim for an optimal potassium level between 4.0 and 5.0 mmol/L. Levels below 4.0, even if technically “normal,” can contribute to a wide range of symptoms, including fatigue, muscle weakness, constipation, and neurological slowing. For children with special needs, we pay close attention to any value below this threshold, particularly if clinical signs suggest impaired energy metabolism or poor neuromuscular tone.

If serum potassium is borderline low, and especially if magnesium is also deficient, it may be difficult to replete potassium effectively without correcting other imbalances.
The most accurate way to assess magnesium deficiency is by measuring a red blood cell (RBC) magnesium level. Reviewing potassium levels in the context of the broader metabolic picture, including magnesium, thiamine, and mitochondrial function, can offer deeper insight into what the body needs to return to balance.​

​Potassium and Thiamine

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​One of the least recognized but most critical biochemical relationships is between potassium and thiamine (vitamin B1). Thiamine is essential for glucose metabolism and mitochondrial energy production, acting as a cofactor in several key enzymatic pathways. However, thiamine cannot function where it’s needed unless it reaches the inside of the cell; and this transport process depends on adequate intracellular potassium levels.
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When potassium is low, thiamine uptake into cells becomes impaired, leading to a state of functional thiamine deficiency, even if blood levels of thiamine appear normal. At the same time, thiamine deficiency itself can disrupt the kidneys’ ability to retain potassium, resulting in increased urinary potassium loss. This reciprocal relationship sets up a vicious cycle: the lower the potassium, the less effective thiamine becomes, and the less thiamine available inside cells, the more potassium is lost.

This dynamic is particularly relevant in children with mitochondrial dysfunction, chronic feeding challenges, or a history of medications that deplete thiamine, such as diuretics, certain antibiotics, or high-sugar diets. In these cases, simply supplementing thiamine may not be enough to restore cellular function. Without simultaneously addressing potassium status, thiamine cannot be effectively absorbed and utilized where it matters most.

​Medications That Deplete Potassium


Low potassium isn’t always about diet. Several common medications can actively lower potassium levels, sometimes significantly. This is especially important to consider in children and adults with chronic health conditions, where medication use may be long-term and symptoms like fatigue or constipation are mistakenly attributed to the underlying condition rather than a correctable electrolyte imbalance.
​

Medications that commonly cause potassium loss include:
  • Diuretics (especially loop and thiazide diuretics)
    • Examples: furosemide (Lasix), hydrochlorothiazide (HCTZ)
    • These medications increase urinary excretion of potassium and are a leading cause of hypokalemia, especially in children with heart conditions, pulmonary hypertension, or kidney disease.
  • Certain antibiotics
    • Examples: penicillin (at high doses), amphotericin B
    • Can alter kidney function or affect potassium channels in the tubules.
  • Corticosteroids
    • Examples: prednisone, dexamethasone
    • These mimic aldosterone and promote potassium loss via the kidneys. Used frequently in asthma, autoimmune conditions, and neuroinflammation.
  • Beta-agonists and bronchodilators
    • Examples: albuterol, salbutamol (Ventolin)
    • These drive potassium into cells, lowering blood levels and sometimes triggering transient hypokalemia, especially during acute respiratory treatments.
  • Insulin (especially in IV or high doses)
    • Drives potassium into cells, which can cause a drop in serum potassium. This is more relevant in hospital or metabolic crisis settings but important to monitor in children with diabetes or insulin dysregulation.
  • High-dose bicarbonate or sodium bicarbonate therapy
    • Shifts potassium into cells by altering acid–base balance.

​Foods High in Potassium

Unlike sodium, which is abundant in processed foods, potassium is mostly found in fresh, whole foods, particularly fruits and vegetables. Unfortunately, many children with feeding issues often avoid exactly these foods.
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Top potassium-rich foods include:
  • Sweet potatoes
  • White potatoes with skin
  • Avocados
  • Bananas
  • Coconut water
  • Winter squash (butternut, acorn)
  • Spinach and beet greens
  • Lentils, kidney beans, black beans
  • Oranges and orange juice
  • Dried fruits like apricots, prunes, dates
  • Yogurt (if tolerated)
  • Beets, parsnips, and Brussels sprouts​
Even adding one potassium-rich food per day can help gently raise potassium stores.

​Treatment

Treating suboptimal potassium levels, especially in children with neurodevelopmental challenges, is rarely as simple as adding more potassium. Like most things in functional medicine, it requires a multifactorial approach that addresses not only intake, but also absorption, retention, and the broader metabolic environment. Restoring potassium to optimal levels often involves supporting magnesium status, improving thiamine availability, correcting gut dysbiosis or malabsorption, evaluating for medication-induced losses, and increasing whole-food sources of potassium. In some cases, supplementation with potassium citrate or bicarbonate may be necessary, but only after considering the full context. Without addressing these interconnected factors, efforts to replete potassium may fall short or fail to produce the clinical improvements you're hoping for.

When potassium levels remain suboptimal despite good dietary intake, and especially when symptoms like fatigue, muscle weakness, or constipation persist, oral supplementation may be needed under medical supervision. In children, potassium dosing is typically based on weight, with a general therapeutic range of 1 to 2 mEq per kilogram of body weight per day, divided into two or three doses. Since 1 mEq of potassium equals 39 mg of elemental potassium, this translates to 39 to 78 mg per kg per day.

For example, a 50-pound child (approximately 23 kg) may require 23 to 46 mEq of potassium daily, which equals 900 to 1,800 mg of elemental potassium per day. This total amount is usually divided into two or three doses. A common starting dose might be 5 to 10 mEq (195 to 390 mg) once or twice daily, with careful monitoring and gradual increases based on lab values and clinical response.
​
Potassium is typically supplemented in the form of potassium citrate, gluconate, or bicarbonate, which are more gentle on the stomach and have alkalizing effects, unlike potassium chloride. Because high doses of potassium can be dangerous if not properly monitored, it is essential that supplementation be guided by a healthcare provider.

Final Thoughts


Potassium is far more than just an electrolyte monitored in emergency rooms or during hospital admissions. It is a foundational mineral involved in nearly every aspect of cellular function, from nerve conduction and muscle contraction to energy production and nutrient transport. In children and adults with special needs, especially those with Down syndrome, autism, or mitochondrial dysfunction, even mildly suboptimal potassium levels can quietly undermine progress in motor development, mood regulation, digestion, and stamina.

Too often, low potassium is overlooked when lab values fall within the conventional reference range, or symptoms like fatigue, constipation, or irritability are attributed solely to a child’s diagnosis rather than considered as signs of a correctable deficiency. This tendency to normalize dysfunction within a diagnosis can delay or prevent meaningful interventions. Functional and integrative approaches encourage us to look deeper, to consider not just whether a level is "normal," but whether it is optimal for that individual’s function and quality of life.

Restoring potassium to optimal levels requires more than just a supplement. It involves recognizing and treating related deficiencies such as magnesium and thiamine, improving dietary intake, assessing absorption and renal losses, and supporting mitochondrial health. When these pieces come together, the difference in daily functioning, more stable energy, fewer meltdowns, better bowel movements, and improved physical strength, can be striking.
​
Supporting a child’s biochemistry is one of the most empowering tools we have. Potassium may seem simple, but when it's optimized, it has the power to shift the entire system toward healing, growth, and resilience.
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Why Diuretics Like Lasix Can Be Harmful for Children with Down Syndrome

6/4/2025

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​Children with Down syndrome face unique biochemical and metabolic challenges that demand special consideration when prescribing medications. One critical concern is the use of diuretics, such as furosemide (Lasix), which are commonly given to manage fluid overload in cases of congenital heart defects or pulmonary hypertension. While these drugs may be necessary in acute care, they are not without significant long-term risks, especially for children with Down syndrome.
Children with Down syndrome are already predisposed to thiamine (vitamin B1) deficiency due to a combination of factors, including:
  • Malabsorption and gut dysbiosis
  • Increased oxidative stress and mitochondrial dysfunction
  • Higher metabolic needs for methylation and energy production
Thiamine is a critical cofactor for enzymes involved in mitochondrial energy production, including pyruvate dehydrogenase (PDH), alpha-ketoglutarate dehydrogenase, and transketolase. Without adequate thiamine, glucose metabolism is impaired, leading to lactic acidosis, fatigue, and neurodevelopmental delay.
Loop diuretics like furosemide cause urinary loss of thiamine, magnesium, potassium, and other electrolytes. This has been documented in both adult and pediatric populations. Studies show that furosemide therapy significantly reduces plasma and whole-blood thiamine levels, often to deficient levels, even after short-term use. (1, 2, 3, 4)

Children with Down syndrome are particularly vulnerable. When you add Lasix to an already thiamine-depleted child, you risk triggering a biochemical cascade that can manifest in serious and even life-threatening symptoms.
Thiamine deficiency in pediatrics can present subtly or with acute symptoms. These include:
  • Fatigue, lethargy
  • Poor feeding, vomiting
  • Constipation, gastroparesis, and reflux
  • Muscle weakness, hypotonia
  • Developmental delays and irritability
  • Tachypnea or labored breathing
  • Cardiomegaly, heart failure symptoms
In its more advanced form, infantile beriberi (5), often under-recognized in modern pediatric medicine, can involve:
  • Recurrent vomiting
  • Aphonia (loss of voice)
  • Edema and heart failure
  • Lactic acidosis
  • Esotropia (crossed eyes)
  • Gastrointestinal dysmotility
  • Sudden cardiovascular collapse
Several studies have linked thiamine deficiency with pulmonary hypertension, a common and life-threatening issue in children with Down syndrome, especially those with congenital heart defects or lung disease. (6, 7, 8)
​
Thiamine deficiency can lead to vasoconstriction and increased vascular resistance, possibly through disruption of mitochondrial energy metabolism in the pulmonary vasculature.

This means that giving Lasix to a child with Down syndrome and pulmonary hypertension, without concurrent thiamine repletion, can worsen the condition it was intended to treat.
Magnesium is another critical nutrient lost through diuretic therapy. It serves as a cofactor for hundreds of enzymes, including those involved in ATP production, nerve conduction, and muscle relaxation. Magnesium deficiency exacerbates thiamine deficiency, as these two nutrients work synergistically in the mitochondria.
For children with Down syndrome, any use of diuretics should be accompanied by proactive nutrient monitoring and supplementation of thiamine and magnesium. In many cases, high-dose thiamine in the form of benfotiamine or thiamine tetrahydrofurfuryl disulfide (TTFD) is well-tolerated and crosses cell membranes more effectively than standard thiamine HCl.
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When supplementing a child on Lasix to prevent or correct thiamine and magnesium deficiency, age-appropriate dosing is key. Benfotiamine, a fat-soluble derivative of thiamine with superior cellular absorption, is generally well tolerated and effective. For children ages 1 to 3 years, a typical starting dose is 25-50 mg once daily. For ages 4 to 8, consider 50-100 mg daily, and for older children 9 and up, 100-150 mg per day is often appropriate. Some clinicians may use higher doses in acute deficiency or if symptoms of beriberi or pulmonary hypertension are present. 
Magnesium glycinate is commonly used to replenish magnesium lost through diuretics. A general guideline is 5-10 mg of elemental magnesium per kg of body weight per day, divided into 1-2 doses. For example, a 20 kg child might receive 100-200 mg of elemental magnesium daily. Always adjust dosing based on individual needs, lab markers, and clinical symptoms, and consult with a pediatric provider knowledgeable in nutritional medicine.
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Recommended considerations:
  • Supplement thiamine daily in children on Lasix or other diuretics
  • Ensure adequate magnesium status via bloodwork (preferably RBC magnesium)
  • Monitor for signs of fatigue, vomiting/reflux, constipation, or neurodevelopmental delay
  • Re-evaluate the need for continued diuretic therapy as the child's condition stabilizes
Children with Down syndrome deserve care tailored to their unique metabolic needs. Diuretics like Lasix may offer short-term relief but come at the cost of worsening thiamine and magnesium deficiencies, nutrients essential for brain, heart, and mitochondrial function. By supplementing proactively and recognizing the symptoms of deficiency, we can prevent complications like pulmonary hypertension and support healthier development in these vulnerable children.
References:
1. Rieck J, Halkin H, Almog S, Seligman H, Lubetsky A, Olchovsky D, Ezra D. Urinary loss of thiamine is increased by low doses of furosemide in healthy volunteers. J Lab Clin Med. 1999 Sep;134(3):238-43. doi: 10.1016/s0022-2143(99)90203-2. 
2. Sica DA. Loop diuretic therapy, thiamine balance, and heart failure. Congest Heart Fail. 2007 Jul-Aug;13(4):244-7. doi: 10.1111/j.1527-5299.2007.06260.x.
3. Ritorto G, Ussia S, Mollace R, Serra M, Tavernese A, Palma E, Muscoli C, Mollace V, Macrì R. The Pivotal Role of Thiamine Supplementation in Counteracting Cardiometabolic Dysfunctions Associated with Thiamine Deficiency. Int J Mol Sci. 2025 Mar 27;26(7):3090. doi: 10.3390/ijms26073090.
4. Ryan MP. Diuretics and potassium/magnesium depletion. Directions for treatment. Am J Med. 1987 Mar 20;82(3A):38-47. doi: 10.1016/0002-9343(87)90131-8. 
5. Rabinowitz, SS. Pediatric Beriberi Clinical Presentation. Medscape, Mar 17, 2014​
6. Panigrahy N, Chirla DK, Shetty R, Shaikh FAR, Kumar PP, Madappa R, Lingan A, Lakshminrusimha S. Thiamine-Responsive Acute Pulmonary Hypertension of Early Infancy (TRAPHEI)-A Case Series and Clinical Review. Children (Basel). 2020 Oct 28;7(11):199. doi: 10.3390/children7110199.
7. Pache-Wannaz L, Voicu C, Boillat L, Sekarski N. Case Report: severe pulmonary hypertension in a child with micronutrient deficiency. Front Pediatr. 2025 Jan 31;13:1478889. doi: 10.3389/fped.2025.1478889.
8. C S, Kundana PK, Reddy N, Reddy B S, Poddutoor P, Rizwan A, Konanki R. Thiamine-responsive, life-threatening, pulmonary hypertensive crisis with encephalopathy in young infants: A case series. Eur J Paediatr Neurol. 2022 Jan;36:93-98. doi: 10.1016/j.ejpn.2021.12.010.
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    Dr. Erica Peirson

    Dr. Peirson is dedicated to helping children with developmental and learning challenges reach their fullest potential.

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