How Statins, Metformin, Diuretics, and Beta Blockers Deplete Nutrients: The Hidden Cardiometabolic Cost
How cardiometabolic medications alter mitochondrial function, mineral balance, and metabolic signaling—and what restores physiologic resilience
In the United States, prescription medication use has reached unprecedented levels. Nearly 50% of Americans take at least one prescription drug, and over 20% take five or more simultaneously (1). For many patients, the issue is not medication itself—but the absence of structured reassessment of how long-term drug use affects nutrient status, mitochondrial function, and metabolic physiology.
Many of these medications were originally developed for short-term or acute use, yet they are often continued indefinitely and layered without ongoing evaluation of downstream biochemical effects. Over time, this can alter nutrient reserves, mitochondrial efficiency, and electrolyte balance in ways that routine labs frequently miss.
This pattern does not simply carry a financial burden. It can gradually reduce cellular energy production, impair glucose handling, disrupt neuromuscular stability, and weaken cardiovascular resilience. Patients may develop fatigue, muscle pain, brain fog, cramping, blood sugar instability, or worsening lipid patterns—sometimes interpreted as disease progression rather than medication-related physiology.
Even when medications are clinically necessary, many come with a predictable physiological tradeoff: nutrient depletion. Statins, diuretics, and common diabetes drugs are well documented to reduce CoQ10, magnesium, potassium, and B-vitamins—nutrients foundational to mitochondrial ATP production, cardiac conduction, and metabolic stability. Identifying these patterns often requires more than routine labs. Standard panels frequently fail to detect intracellular nutrient depletion, early mitochondrial strain, or subtle shifts in metabolic signaling that precede overt dysfunction.
When cardiometabolic medications are part of a long-term plan, a more comprehensive assessment approach may be necessary.
→ Advanced Functional Lab Testing
When deficiencies present as new symptoms, they are frequently misclassified as new diagnoses—prompting additional prescriptions and perpetuating the cycle.
“You can trace every sickness, every disease, and every ailment to a mineral deficiency.”
— Linus Pauling, PhD (two-time Nobel Prize winner)
Breaking this cycle requires a different clinical lens—one that supports nutrient reserves, mitochondrial health, and metabolic flexibility rather than overriding physiology.
This article focuses specifically on cardiometabolic medications—including statins, metformin, diuretics, and beta blockers—and how they alter key nutrient pathways involved in mitochondrial energy production, electrolyte balance, glucose regulation, and cardiovascular resilience. We will examine the mechanisms behind CoQ10 depletion, vitamin B12 deficiency, magnesium and potassium loss, and impaired metabolic signaling, along with evidence-informed strategies to restore physiological stability while medications are in use.
Cardiometabolic Medications and Nutrient Depletion
Many commonly prescribed cardiometabolic medications interfere with the body’s ability to absorb, synthesize, transport, or utilize essential vitamins and minerals. Over time, this biochemical interference can lead to clinically meaningful deficiencies—even in individuals who consume a nutrient-dense, whole-food diet.
Unlike acute drug side effects, medication-induced nutrient depletion develops gradually. Symptoms such as fatigue, muscle weakness, exercise intolerance, brain fog, cramping, arrhythmia susceptibility, mood changes, or worsening metabolic markers are often attributed to aging or disease progression rather than recognized as downstream consequences of long-term medication use.
Statins, metformin, diuretics, and beta blockers are among the most widely prescribed cardiometabolic drugs in the United States. Each class is associated with predictable nutrient losses—including CoQ10 depletion, vitamin B12 deficiency, magnesium and potassium loss, and impaired mitochondrial signaling (2). Over time, these deficits can compromise ATP production, glucose regulation, cardiac conduction, and neuromuscular stability.
In the sections below, we examine how these medications alter nutrient pathways and mitochondrial function, along with evidence-informed strategies used to restore physiological balance while medications remain in place.
Statins and CoQ10 Depletion
Statins (such as Lipitor or Crestor) lower cholesterol by blocking an enzyme called HMG-CoA reductase. This enzyme is part of the mevalonate pathway, which your body uses to produce cholesterol.
Here’s the critical point:
That same pathway is also responsible for producing CoQ10, a compound your cells rely on to generate energy inside structures called mitochondria—the “power plants” of the cell.
When statins suppress this pathway, cholesterol production decreases—but so can CoQ10 production (3-5).
Because the heart and skeletal muscles require large amounts of energy, reduced CoQ10 can impair how efficiently these tissues function.
Common Nutrient and Metabolic Effects of Statins
CoQ10 depletion
Reduced mitochondrial ATP production
Possible changes in vitamin D and vitamin K2 levels
Potential effects on blood sugar regulation
CoQ10 plays a central role in the mitochondrial electron transport chain—the system your cells use to generate ATP, the body’s primary energy molecule. When CoQ10 levels fall, ATP production declines.
This helps explain why statin use is associated with:
Muscle pain
Weakness
Exercise intolerance
Persistent fatigue
Statins have also been associated with altered vitamin K2 status, which helps direct calcium into bones and away from arterial walls (6). When K2 is insufficient, calcium may accumulate in vascular tissue.
Emerging research suggests statins may influence GLP-1, a hormone involved in insulin sensitivity and blood sugar regulation (7). This may partially explain the increased risk of type 2 diabetes observed in certain populations taking statins (8).
Clinical Effects Associated with Statin-Related Nutrient Depletion
Reduced CoQ10, altered mitochondrial efficiency, and metabolic changes may contribute to:
Ongoing muscle soreness
Fatigue despite improved cholesterol numbers
Brain fog
Reduced stamina
Changes in glucose tolerance
These symptoms often develop gradually and may be mistaken for aging or disease progression rather than medication-related nutrient depletion.
Supporting Physiological Resilience During Statin Therapy
Statins are designed to reduce LDL cholesterol. Long-term cardiovascular health, however, depends on more than LDL reduction alone.
Supportive strategies that may help preserve mitochondrial and metabolic stability include:
CoQ10 (ubiquinol) to support ATP production
Magnesium to support muscle and vascular function
Omega-3 fatty acids to reduce inflammatory signaling
A nutrient-dense diet rich in fiber and phytonutrients
Regular resistance and aerobic training to improve insulin sensitivity and HDL function
These strategies support energy production and metabolic resilience while statin therapy is in place.
Can Statins Be Reduced?
Elevated cholesterol often reflects inflammation, insulin resistance, oxidative stress, and metabolic dysfunction—not simply excess cholesterol production.
When these upstream drivers are corrected, lipid patterns shift.
Plant-derived compounds have been shown to influence cholesterol synthesis, bile metabolism, LDL oxidation, and inflammatory signaling. Some interact with pathways similar to HMG-CoA reductase, while others improve triglyceride balance and endothelial function.
Dietary patterns rich in fiber, polyphenols, omega-3 fats, and phytonutrients can meaningfully improve lipid physiology. Strength training, reduction of visceral fat, and improved insulin sensitivity also reshape LDL particle quality and cardiovascular risk.
When inflammatory and metabolic markers normalize, medication requirements may change under structured supervision.
The goal is not simply lowering LDL.
The goal is restoring metabolic resilience.
Metformin and Vitamin B12 and Folate Depletion
Metformin is commonly prescribed for type 2 diabetes and insulin resistance. It lowers glucose production in the liver and improves insulin sensitivity through activation of an energy-regulating pathway called AMPK (AMP-activated protein kinase).
AMPK helps regulate how the body uses fuel. While this improves blood sugar control, metformin also affects absorption processes in the small intestine. Over time, this can reduce the body’s ability to absorb vitamin B12, and in some individuals may also influence folate status (9,10).
Vitamin B12 and folate are essential nutrients involved in nerve function, red blood cell production, DNA synthesis, and methylation—a biochemical process that supports detoxification, inflammation control, and cellular repair.
Common Nutrient Depletions Associated with Metformin
Vitamin B12
Folate
Long-term metformin use has been consistently linked to reduced B12 absorption. Because B12 stores can take years to deplete, symptoms often develop gradually rather than immediately.
Why Metformin-Induced B12 Depletion Matters
Vitamin B12 plays a central role in:
Maintaining nerve integrity
Supporting red blood cell formation
Regulating homocysteine
Assisting mitochondrial energy production
When B12 levels decline, individuals may experience:
Numbness or tingling in the hands and feet
Fatigue
Brain fog
Mood changes
Megaloblastic anemia
In people already living with insulin resistance—where mitochondrial stress is common—lower B12 availability can further reduce cellular energy efficiency.
Folate works alongside B12 in methylation pathways. If either nutrient becomes insufficient, homocysteine levels may rise, which is associated with increased cardiovascular risk.
Clinical Effects Associated with Metformin-Related Nutrient Depletion
Metformin-related B12 and folate depletion may contribute to:
Peripheral neuropathy
Persistent fatigue despite controlled glucose
Cognitive changes
Elevated homocysteine
Worsening mitochondrial inefficiency
Because neuropathy is also a complication of diabetes, medication-related B12 deficiency is sometimes misattributed to disease progression.
Supporting Physiological Resilience During Metformin Therapy
Metformin improves glucose regulation. Long-term metabolic stability, however, depends on improving insulin sensitivity and maintaining adequate nutrient status—not solely lowering glucose numbers.
Strategies that support metabolic resilience while on therapy include:
Monitoring and replenishing vitamin B12 when indicated
Ensuring adequate dietary folate from leafy greens, legumes, and whole foods
Strength training to improve skeletal muscle glucose uptake
Reducing refined carbohydrates to lower insulin demand
Supporting mitochondrial function with adequate protein and micronutrients
Natural folate from leafy greens differs from synthetic folic acid, which is commonly added to fortified cereals and processed grain products. Folic acid must be converted in the body before it becomes active. In the setting of low B12, high intake of synthetic folic acid can mask laboratory signs of deficiency while neurologic damage progresses.
For that reason, prioritizing naturally occurring folate—or using bioactive forms such as methylfolate under practitioner guidance—is often a more physiologically aligned strategy when addressing metformin-related nutrient depletion.
These measures strengthen metabolic physiology while medication remains in place.
Can Metformin Be Discontinued?
Type 2 diabetes and insulin resistance develop from sustained metabolic strain—not from a deficiency of metformin.
Improving insulin sensitivity changes the equation.
Plant-derived compounds have been shown to influence AMPK activation and glucose metabolism in measurable ways. Some act on pathways similar to metformin, while others improve insulin signaling and reduce oxidative stress.
When combined with strength training, improved body composition, dietary strategies, and sleep optimization, these interventions can meaningfully stabilize glucose regulation.
As fasting insulin, HbA1c, and glucose variability normalize, medication requirements may change under structured clinical supervision.
The objective is not indefinite glucose suppression.
The objective is restoring physiologic glucose regulation.
Diuretics and Electrolyte Depletion
Diuretics (such as hydrochlorothiazide or furosemide) lower blood pressure and reduce fluid retention by increasing urinary excretion of sodium and water. As urine output rises, the kidneys also excrete key electrolytes and water-soluble nutrients essential for cardiovascular stability, neuromuscular coordination, and mitochondrial energy production.
Because electrolyte balance is tightly regulated and critical for heart rhythm and nervous system signaling, even modest chronic losses can have significant physiological consequences.
Common Nutrient and Electrolyte Losses with Diuretics
Potassium
Magnesium
Sodium
Zinc
Thiamine (vitamin B1)
Diuretic therapy has been consistently associated with depletion of potassium and magnesium (11,12). These minerals regulate vascular tone, cardiac conduction, and muscle contraction. When levels decline, the risk of arrhythmias, muscle cramps, and fatigue increases (13).
Thiamine plays a central role in mitochondrial ATP production. Chronic diuretic use has been linked to thiamine depletion, particularly in heart failure populations, where deficiency can impair cardiac function (14).
Clinical Effects Associated with Diuretic-Related Depletion
Electrolyte and micronutrient loss may contribute to:
Irregular heartbeat or palpitations
Muscle cramps or weakness
Low energy and dizziness
Increased thirst and salt cravings
Reduced exercise tolerance
Worsening heart failure in the setting of thiamine deficiency
These symptoms are often attributed solely to cardiovascular disease progression rather than ongoing electrolyte depletion.
Supporting Physiological Resilience During Diuretic Therapy
Maintaining electrolyte balance is foundational for cardiovascular resilience.
Supportive strategies include:
Replenishing magnesium and potassium when clinically indicated
Emphasizing mineral-rich foods such as leafy greens, avocados, nuts, and seeds
Supporting thiamine status when depletion risk is present
Ensuring consistent hydration
Avoiding unnecessary extreme sodium restriction that destabilizes mineral balance
Electrolyte sufficiency improves vascular tone, neuromuscular coordination, and mitochondrial efficiency.
Can Diuretics Be Reduced?
High blood pressure and fluid retention often reflect deeper drivers such as insulin resistance, chronic sympathetic activation, poor sleep, excess visceral fat, and inflammatory load.
Improving vascular function changes the equation.
Plant-derived compounds have been shown to influence endothelial function, nitric oxide signaling, and vascular relaxation in measurable ways. Certain botanical extracts support healthy blood pressure through mechanisms distinct from simple fluid removal.
Strength training, weight reduction, improved sleep, mineral repletion, and reduction of refined carbohydrates can significantly influence blood pressure physiology.
As vascular tone stabilizes and inflammatory markers decline, medication requirements may change under structured clinical supervision.
The goal is not indefinite fluid suppression.
The goal is restoring vascular and metabolic strength.
Beta Blockers and Mitochondrial Energy Depletion
Beta blockers (such as atenolol, metoprolol, or propranolol) lower blood pressure and heart rate by blocking the effects of adrenaline on beta-adrenergic receptors. This reduces cardiac workload and sympathetic nervous system activity.
While this can be protective in certain settings, beta blockade also influences mitochondrial energy production, circadian signaling, and micronutrient balance—particularly with long-term use.
Tissues such as the heart, brain, and skeletal muscle rely heavily on efficient mitochondrial function. When energy production declines, symptoms often follow.
Common Nutrient and Hormonal Effects of Beta Blockers
CoQ10 depletion
Reduced mitochondrial ATP production
Lower melatonin levels
Altered zinc status
Beta blockers have been associated with reduced CoQ10 availability (15,16). CoQ10 is a critical component of the mitochondrial electron transport chain, which produces ATP—the body’s primary energy molecule. Lower CoQ10 can reduce energy output in high-demand tissues such as the heart and skeletal muscle.
Beta blockers are also linked to decreased melatonin production (17). Melatonin regulates circadian rhythm, sleep quality, and nighttime cardiovascular recovery. Suppression may contribute to insomnia and non-restorative sleep.
Some evidence suggests beta blockade may influence zinc metabolism (18). Zinc supports immune regulation, hormone signaling, antioxidant defense, and cellular repair.
Clinical Effects Associated with Beta Blocker–Related Depletion
Reduced mitochondrial efficiency and altered circadian signaling may contribute to:
Persistent fatigue
Reduced exercise tolerance
Cold hands and feet
Sleep disruption
Mood changes or cognitive dulling
Sexual dysfunction
When combined with existing metabolic strain, these effects may compound cardiovascular and neurologic symptoms.
Supporting Physiological Resilience During Beta Blocker Therapy
Protecting mitochondrial and autonomic function is central when beta blockers are used long term.
Supportive strategies may include:
CoQ10 (ubiquinol) to support ATP production
Magnesium to support heart rhythm and vascular tone
Zinc when deficiency risk is present
Short-term melatonin support when sleep disruption develops
Nutrient-dense dietary patterns that support mitochondrial health
Consistent sleep timing, breath-focused practices, and regular movement support autonomic balance and circulation.
Can Beta Blockers Be Reduced?
Persistent sympathetic activation—often driven by chronic stress, poor sleep, insulin resistance, and inflammatory load—contributes to elevated heart rate and blood pressure.
Addressing these upstream drivers changes autonomic tone.
Plant-derived compounds and lifestyle interventions have been shown to influence vascular relaxation, endothelial function, nitric oxide signaling, and stress adaptation in measurable ways. These mechanisms affect heart rate and blood pressure regulation beyond receptor blockade alone.
Improving sleep quality, restoring mineral balance, reducing visceral fat, strengthening skeletal muscle, and stabilizing metabolic health can meaningfully shift cardiovascular physiology.
As autonomic balance improves and inflammatory markers decline, medication requirements may change under structured clinical supervision.
The goal is not indefinite sympathetic suppression.
The goal is restoring autonomic and metabolic resilience.
How to Restore Heart and Metabolic Health While Taking Cardiometabolic Medications
Statins, metformin, diuretics, and beta blockers are designed to control cholesterol levels, blood pressure, glucose, and heart rate. They are not designed to restore mitochondrial energy production, correct nutrient depletion, or resolve the underlying drivers of cardiometabolic dysfunction.
When medication-induced nutrient depletion accumulates, symptoms such as fatigue, muscle weakness, brain fog, exercise intolerance, blood sugar instability, and arrhythmia susceptibility often persist despite “normal” laboratory markers.
Restoring cardiometabolic resilience requires addressing what has been depleted and correcting the upstream physiology driving metabolic strain.
How Cardiometabolic Medications Affect Nutrient Status and Mitochondrial Function
Cardiometabolic medications commonly affect:
CoQ10 production and mitochondrial ATP generation
Vitamin B12 and folate absorption
Magnesium and potassium balance
Thiamine status
Circadian signaling and melatonin regulation
Mitochondria require adequate micronutrients to generate ATP efficiently. When key cofactors decline, cellular energy production becomes less efficient, even if blood pressure, LDL, or glucose appear controlled.
Understanding whether persistent symptoms reflect disease progression or medication-related metabolic strain changes the clinical strategy entirely.
How to Correct Medication-Induced Nutrient Depletion
Precision matters.
Restoring nutrient balance may include:
Replenishing CoQ10 in the setting of statin use
Correcting vitamin B12 and folate depletion with metformin
Rebalancing magnesium, potassium, and thiamine during diuretic therapy
Supporting mitochondrial and circadian stability during beta blocker use
Correction is not based on guesswork. It is based on identifying what has been depleted and restoring physiologic balance with appropriate forms and dosing.
Lifestyle Strategies That Improve Insulin Sensitivity and Cardiovascular Resilience
Medication controls numbers. Lifestyle reshapes physiology.
Foundational strategies that improve cardiometabolic health include:
Strength training to enhance skeletal muscle glucose uptake
Reduction of refined carbohydrates and excess inflammatory oils
Nutrient-dense whole foods rich in minerals and phytonutrients
Adequate protein to support mitochondrial repair
Sleep optimization to restore autonomic balance
Reduction of chronic inflammatory load
These interventions improve insulin sensitivity, vascular tone, lipid physiology, and metabolic flexibility at the root level.
When Cardiometabolic Medication Requirements May Change
Elevated cholesterol, high blood pressure, and insulin resistance often reflect inflammation, excess visceral fat, disrupted circadian rhythm, chronic stress activation, and impaired mitochondrial efficiency.
When those upstream drivers are corrected, measurable changes occur:
Improved fasting insulin
Stabilized HbA1c
Healthier triglyceride-to-HDL ratios
Improved endothelial function
Restored mineral balance
As objective markers normalize, medication requirements may shift under structured clinical supervision.
The goal is not indefinite biochemical suppression.
The goal is restoring metabolic strength and physiologic resilience.
Restore Cardiometabolic Resilience at the Root
At Denver Sports & Holistic Medicine, cardiometabolic recovery begins with identifying what has been depleted and correcting what has been disrupted.
Statins, metformin, diuretics, and beta blockers influence nutrient reserves, mitochondrial energy production, mineral balance, and metabolic signaling. When fatigue, muscle weakness, neuropathy, blood sugar instability, or reduced exercise tolerance persist, the question is not simply whether numbers are controlled—it is whether physiology is supported.
A root-cause approach clarifies:
Which nutrients have been depleted
Whether mitochondrial function is compromised
How insulin signaling and vascular tone are functioning
Whether symptoms reflect disease progression or medication-related metabolic strain
Restoring metabolic resilience requires rebuilding cellular energy production, correcting mineral imbalances, and stabilizing glucose and cardiovascular physiology—not layering additional medications onto unresolved dysfunction.
→ Functional & Integrative Medicine
This article focused specifically on cardiometabolic medications. Additional articles in this series examine how other common drug classes affect gut health, hormone balance, and detoxification pathways.
Restoring Heart and Metabolic Function
If you are taking statins, metformin, diuretics, beta blockers, or other cardiometabolic medications and continue to experience fatigue, muscle pain, brain fog, blood sugar instability, or reduced exercise tolerance, these symptoms often reflect nutrient depletion, mitochondrial strain, or impaired metabolic flexibility rather than simple disease progression.
Cardiometabolic medications alter micronutrient reserves, mitochondrial energy production, mineral balance, and metabolic signaling. Identifying what has been depleted requires objective laboratory evaluation and structured clinical analysis.
→ Advanced Functional Lab Testing
Precise testing clarifies whether symptoms reflect medication-related nutrient loss, mitochondrial dysfunction, or deeper metabolic imbalance. This allows for targeted correction rather than additional symptom suppression.
You may request a free 15-minute consultation with Dr. Martina Sturm to review your health concerns and outline appropriate next steps within a root-cause, systems-based framework.
Frequently Asked Questions About Heart, Metabolic Medications, and Nutrient Depletion
Do statins deplete CoQ10?
Yes. Statins block the HMG-CoA reductase pathway, which is required to produce both cholesterol and CoQ10. When CoQ10 levels decline, mitochondrial ATP production may decrease, particularly in heart and skeletal muscle tissue. This is one reason statin use is associated with muscle pain, fatigue, and reduced exercise tolerance.
Why do statins cause muscle pain and fatigue?
Statin-related muscle symptoms are strongly associated with reduced CoQ10 production and impaired mitochondrial energy generation. When ATP production declines, muscle tissue becomes more susceptible to weakness, soreness, and exercise intolerance. These symptoms may occur even when cholesterol levels appear improved.
Can statins increase blood sugar or diabetes risk?
Research has shown that statins may slightly increase the risk of developing type 2 diabetes in certain populations. Proposed mechanisms include impaired insulin sensitivity and altered GLP-1 signaling. This does not occur in every case, but blood sugar trends should be monitored during long-term therapy.
Does metformin cause vitamin B12 deficiency?
Yes. Long-term metformin use is associated with reduced absorption of vitamin B12 in the small intestine. B12 deficiency may develop gradually and can contribute to neuropathy, fatigue, brain fog, and anemia if not identified and corrected.
How does metformin affect folate levels?
Metformin may influence folate metabolism, particularly when vitamin B12 levels are low. Because B12 and folate work together in methylation pathways, depletion of one can disrupt the function of the other. Elevated homocysteine may signal imbalance in this system.
Why do diuretics cause muscle cramps and palpitations?
Diuretics increase urinary excretion of potassium and magnesium—minerals essential for muscle contraction and cardiac conduction. When these electrolytes decline, muscle cramps, weakness, irregular heartbeat, and dizziness may develop.
Can diuretics cause vitamin deficiencies?
Yes. In addition to electrolyte loss, chronic diuretic use has been associated with thiamine (vitamin B1) depletion. Thiamine plays a central role in mitochondrial energy production and cardiac function. Deficiency may contribute to fatigue and reduced cardiovascular efficiency.
Do beta blockers reduce energy levels?
Beta blockers can reduce heart rate and sympathetic activation, which lowers cardiac workload. However, they are also associated with reduced CoQ10 availability and mitochondrial efficiency in some cases. This may contribute to fatigue and decreased exercise tolerance.
Why do beta blockers affect sleep?
Beta blockers may suppress melatonin production by altering sympathetic nervous system signaling. Because melatonin regulates circadian rhythm and sleep quality, suppression may lead to insomnia or non-restorative sleep in certain patients.
How do I know if my medication is causing nutrient depletion?
Persistent fatigue, muscle weakness, neuropathy, sleep disruption, blood sugar instability, or exercise intolerance while taking cardiometabolic medications may signal underlying nutrient depletion or mitochondrial strain. Standard lab panels often do not assess intracellular micronutrient status, so more comprehensive evaluation may be required.
Can cardiometabolic medications be reduced naturally?
Medication requirements sometimes change when insulin sensitivity improves, inflammation decreases, mineral balance stabilizes, and mitochondrial function strengthens. Any reduction must be guided by objective data and structured clinical supervision. The goal is restoring metabolic resilience—not abruptly discontinuing therapy.
What is the root-cause approach to medication-related fatigue?
A root-cause approach evaluates how medications affect nutrient status, mitochondrial energy production, mineral balance, and metabolic signaling. Correction focuses on targeted nutrient repletion, dietary improvement, strength training, sleep optimization, and reducing inflammatory load to restore physiologic regulation.
Still Have Questions?
If the topics above reflect ongoing symptoms or unanswered concerns, a brief conversation can help clarify whether a root-cause approach is appropriate.
Resources
Centers for Disease Control and Prevention (CDC) – Prescription Drug Use in the United States
Pharmacology & Therapeutics – Drug-Induced Nutrient Depletion and Clinical Implications
Journal of Clinical Lipidology – Statin-Associated Muscle Symptoms and Coenzyme Q10
Mitochondrion – The Mevalonate Pathway and CoQ10 Suppression
American Journal of Cardiology – Effects of Statins on Coenzyme Q10 Levels
Nutrients – Vitamin K2 and Vascular Calcification Mechanisms
Frontiers in Endocrinology – Statins, GLP-1 Signaling, and Metabolic Regulation
BMJ – Statin Therapy and Risk of Type 2 Diabetes: Meta-Analysis
Diabetes Care – Long-Term Metformin Use and Vitamin B12 Deficiency
Journal of Clinical Endocrinology & Metabolism – Folate, B12, and Methylation Pathways in Metabolic Disease
Journal of Hypertension – Thiazide Diuretics and Potassium Depletion
American Journal of Medicine – Magnesium Loss Associated with Diuretic Therapy
Heart Rhythm – Electrolyte Imbalance and Arrhythmia Risk
Journal of Cardiac Failure – Thiamine Deficiency in Patients with Chronic Diuretic Use
Journal of Cardiovascular Pharmacology – Beta Blockade and Coenzyme Q10 Reduction
Molecular Aspects of Medicine – Mitochondrial Bioenergetics and Beta-Adrenergic Inhibition
Sleep Medicine Reviews – Beta Blockers and Melatonin Suppression
Biological Trace Element Research – Zinc Metabolism and Cardiovascular Function