Tuesday, August 5, 2025

Beyond the Pill: A Critical Review of Pharmacology, Chronic Disease, and the Path to Root-Cause Healing



A Critical Review of Pharmacology:

by Lin Ru Wu alias Lim Ju Boo

 

This paper is written initially for medical doctors, but it is reachable to ordinary lay readers. The purpose of this paper is for us - doctors and non-doctors  to understand drugs do not cure any disease unless that root causes of the disease are removed. The explanation is below this paper under: 

4.1 The River Analogy and,  

4.2 Masking vs Healing.

Despite their limitations, certain drugs are life-saving as described under:  

5. Role of Pharmacology in Emergencies:  pharmacological agents are indispensable in acute care.

Pharmacological Agents in Modern Medicine: Mechanisms, Applications, and Limitations in Chronic Disease Management to me as I begin to write my thoughts, is like “Chemical Interventions and Biological Rivers: A Systems Perspective on Drug Therapy and Chronic Disease” 


I shall follow this paper up with another paper on how some of these emergency drugs are used under: 


"Emergency Protocol for the Management of the Unconscious or Critically Ill Patient" 


Abstract:


This paper provides a comprehensive overview of pharmacological agents widely used in contemporary medicine, including their pharmacodynamics, pharmacokinetics, therapeutic applications, side effects, drug interactions, and contraindications. It further critiques the limitations of these drugs in addressing chronic diseases due to the failure to treat root causes. The discussion is enriched with analogies illustrating systemic effects of masking symptoms without curing underlying pathology. Despite their shortcomings in chronic care, emergency and critical care pharmacotherapeutics are acknowledged for their indispensable life-saving roles.


1. Introduction: 


Pharmacology is the science of drug action on biological systems and comprises two major branches: pharmacodynamics (what the drug does to the body) and pharmacokinetics (what the body does to the drug) [1]. A rational approach to pharmacotherapy requires a thorough understanding of both aspects, as well as disease pathophysiology, to select the right drug for the right patient under the right conditions.


2. Pharmacological Classes and Mechanisms


2.1 Antibiotics: 


Antibiotics target bacterial structures or functions, including cell wall synthesis (e.g., beta-lactams), protein synthesis (e.g., macrolides), and DNA replication (e.g., fluoroquinolones) [2]. While generally well-tolerated, side effects include gastrointestinal upset, antibiotic-associated colitis, and the development of resistance. Co-administration with antacids or iron may interfere with absorption.


2.2 Antivirals: 


Antivirals inhibit viral replication through mechanisms such as neuraminidase inhibition (e.g., oseltamivir) or nucleotide analog incorporation (e.g., acyclovir) [3]. Drug resistance and toxicity (renal, hepatic) are notable issues.


2.3 Anti-inflammatory Agents:


NSAIDs (e.g., ibuprofen, diclofenac) inhibit cyclooxygenase enzymes (COX-1 and COX-2), reducing prostaglandin synthesis [4]. While effective in inflammation and pain, they pose risks for gastric ulceration, renal impairment, and cardiovascular events, especially when combined with ACE inhibitors or diuretics ("triple whammy effect") [5].


2.4 Analgesics:


Paracetamol acts centrally to inhibit prostaglandin synthesis. Opioids (e.g., morphine, fentanyl) act on mu-opioid receptors, providing potent pain relief but are associated with respiratory depression, tolerance, and dependence [6].


2.5 Corticosteroids:


Steroids such as prednisone suppress inflammation and immune response via genomic and non-genomic pathways [7]. Chronic use can cause adrenal suppression, osteoporosis, hyperglycemia, and increased infection risk.


2.6 Antitussives and Expectorants:


Dextromethorphan (antitussive) acts on the cough center in the medulla. Guaifenesin (expectorant) increases mucus clearance. While useful in symptomatic relief, they do not address the cause of cough [8].


2.7 Proton Pump Inhibitors (PPIs):


PPIs like omeprazole inhibit the H+/K+ ATPase pump in gastric parietal cells. Long-term use has been linked to B12 deficiency, hypomagnesemia, and increased risk of enteric infections [9].


2.8 Antihypertensive:


These include ACE inhibitors (e.g., enalapril), beta-blockers (e.g., propranolol), calcium channel blockers (e.g., amlodipine), and diuretics. Each class acts via distinct pathways, such as RAAS blockade or vasodilation. Side effects and interactions vary: e.g., ACE inhibitors may cause hyperkalemia or cough [10].


2.9 Antidiabetic Agents:


Insulin and oral agents like metformin (inhibits hepatic gluconeogenesis), sulfonylureas (stimulate insulin release), and SGLT2 inhibitors (promote renal glucose excretion) are used in diabetes management [11]. Hypoglycemia, lactic acidosis, and urinary tract infections are common concerns.


3. Interactions and Contraindications:


Polypharmacy often leads to drug-drug interactions. For instance, NSAIDs with ACE inhibitors and diuretics increase the risk of renal failure. SSRIs with NSAIDs increase bleeding risk. Contraindications may include pregnancy (e.g., tetracyclines), renal failure (e.g., metformin), or heart block (e.g., beta-blockers in severe bradycardia) [12].


4. Limitations in Chronic Disease:

 Management While these drugs provide symptom relief, they often fail in chronic diseases such as hypertension, metabolic syndrome, or cardiovascular disease, because they do not address the root causes, often poor diet, sedentary lifestyle, and environmental exposures.


4.1 The River Analogy: 


Imagine the body as a river with clean water flowing from a healthy source. Disease arises when pollutants (e.g., poor diet, stress, toxins) enter the source. Medications act like barriers downstream, trying to prevent polluted water from reaching villages (organs). But unless the source is cleaned, the pollution continues. Blocking it may cause overflow, damaging surrounding systems, analogous to drug side effects or new disease manifestations (e.g., polypharmacy leading to organ dysfunction).


4.2 Masking vs Healing: 


In chronic conditions, suppressing blood pressure or blood glucose without lifestyle intervention is akin to painting over rust without removing it, it temporarily masks the problem but does not halt progression. Studies have shown that lifestyle interventions such as plant-based diets, exercise, and stress reduction can reverse or mitigate diseases like type 2 diabetes and atherosclerosis [13][14].


5. Role of Pharmacology in Emergencies Despite limitations, pharmacological agents are indispensable in acute care. For instance:

  • Adrenaline in anaphylaxis restores airway and circulation.

  • Nitroglycerin in acute coronary syndrome rapidly relieves ischemic pain.

  • Intravenous fluids and vasopressors restore hemodynamic stability in shock.

  • Benzodiazepines control status epilepticus.

  • Tranexamic acid limits bleeding in trauma [15][16].


Such drugs stabilize patients, buying time for the body’s healing systems to activate or for surgical interventions to take place. Their short-acting but rapid mechanisms are tailored for life-saving actions. I shall address this in my next article I have written for doctors (but reachable for lay readers)  under "Emergency Protocol for the Management of the Unconscious or Critically Ill Patient" 


Pharmacological agents play essential roles in symptom control, acute management, and life-saving interventions. However, chronic disease treatment demands a paradigm shift from symptomatic suppression to addressing root causes. Integrative strategies combining pharmacology with lifestyle and preventive medicine offer the most promising path toward long-term health.


References

  1. Rang HP, Dale MM, Ritter JM, Flower RJ. Rang & Dale's Pharmacology. 9th ed. Elsevier; 2019.

  2. Katzung BG, Trevor AJ. Basic and Clinical Pharmacology. 15th ed. McGraw-Hill; 2021.

  3. De Clercq E. Antiviral drug discovery and development: where chemistry meets with biomedicine. Antiviral Res. 2005;67(2):56–75.

  4. Vane JR, Botting RM. Mechanism of action of NSAIDs. Am J Med. 1998;104(3A):2S–8S.

  5. Whelton A. Nephrotoxicity of nonsteroidal anti-inflammatory drugs: physiologic foundations and clinical implications. Am J Med. 1999;106(5B):13S–24S.

  6. Trescot AM et al. Opioid pharmacology. Pain Physician. 2008;11(2 Suppl):S133–S153.

  7. Barnes PJ. Anti-inflammatory actions of glucocorticoids. Eur J Clin Pharmacol. 1998;53(6):455–461.

  8. Dicpinigaitis PV. Antitussive effects of theobromine. Faseb J. 2004;18(7):A991.

  9. Lam JR et al. Proton pump inhibitor and vitamin B12 deficiency. JAMA. 2013;310(22):2435–2442.

  10. Williams B et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension. Eur Heart J. 2018;39(33):3021–3104.

  11. American Diabetes Association. Standards of Medical Care in Diabetes—2022. Diabetes Care. 2022;45(Suppl 1):S1–S108.

  12. FDA Drug Safety Communications. www.fda.gov (Accessed 2025).

  13. Ornish D et al. Intensive lifestyle changes for reversal of coronary heart disease. JAMA. 1998;280(23):2001–2007.

  14. Barnard ND et al. A low-fat vegan diet improves glycemic control. Diabetes Care. 2006;29(8):1777–1783.

  15. NICE Guidelines: Anaphylaxis: Assessment and Referral. 2011.

  16. CRASH-2 trial collaborators. Effects of tranexamic acid on death and vascular occlusive events in bleeding trauma patients. Lancet. 2010;376(9734):23–32.

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Beyond the Pill: A Critical Review of Pharmacology, Chronic Disease, and the Path to Root-Cause Healing

A Critical Review of Pharmacology: by Lin Ru Wu alias Lim Ju Boo   This paper is written initially for medical doctors, but it is reachable ...