How Professor Kausik Ray of Imperial College London Made the Evidence Sound Stronger Than It Was in His ESC Congress 2026 Interview Qaisar J. Qayyum, MDChief Editor, Noor Journal of Complementary and Contemporary Medicine, Oklahoma, USA Email: drqhealthyliving@gmail.com The Illusion of Success Abstract Expert commentary can clarify research, or it can make the evidence sound stronger by highlighting one result, leaving another out, or moving from what a study demonstrated to what it might mean in the future. This commentary examines Professor Kausik Ray’s ESC Congress 2026 interview on STAREE, AMUNDSEN and REACT [1]. It evaluates the presentation, not every aspect of the three studies. STAREE asked two equally important main questions. The interview presents the favorable answer and leaves out the other. Atorvastatin reduced a combined measure of cardiovascular events, but did not establish that participants lived longer without dementia or lasting physical disability. Ray highlights a “30% relative risk reduction” and calls the result “immediately translatable into clinical practice.” Notably, he gives neither the actual event rates, 8.3% with placebo and 6.0% with atorvastatin over a median of 5.9 years [2,3], nor the unsuccessful co-primary outcome. AMUNDSEN produced a large improvement in LDL cholesterol, a laboratory marker, but did not establish fewer deaths or unplanned cardiovascular hospitalizations at one year. The interview acknowledges this clinical result, then redirects attention toward benefits expected with longer treatment. Ray also claims that the result “categorically proves” that benefit from PCSK9 inhibition is “entirely driven by the LDL change and nothing else beyond that” [1]. An uncertain clinical result cannot prove that a treatment works through one biological mechanism alone. REACT documented the prevalence and extent of silent atherosclerosis in 16,808 adults, but it did not show that screening improves health. Plaque developing before symptoms was already known, and Ray acknowledges earlier autopsy evidence [1,7]. Yet the interview moves from detecting plaque toward the promise of better prevention. The baseline study did not compare imaging-guided prevention with usual care, and the planned randomized phase will mainly measure plaque progression, another surrogate outcome [8]. Finding plaque is not the same as proving that screening for it prevents heart attacks, strokes, disability or death. The concern is not that the data were fabricated. It is the selective emphasis, omission and extrapolation that must be exposed. The listener receives a persuasive account from a highly credentialed expert, but not all the information needed to judge it. That is how the illusion of stronger evidence is created. How Framing Makes Evidence Sound Stronger Than It Is The interview introduces Professor Ray as Professor of Public Health and Consultant Cardiologist at Imperial College London and Immediate Past President of the European Atherosclerosis Society [1]. These credentials are relevant, but professional authority can make an incomplete account appear complete. Scientific terms can also create impressions through their ordinary meanings. In everyday language, “significant” means important, substantial or meaningful. In medical research, “statistically significant” means only that a result crossed a chosen statistical threshold. It does not show how large the benefit was, whether it mattered clinically, or whether it outweighed side effects and treatment burden [4]. This difference matters. A reader may hear “statistically significant benefit” and naturally understand “important benefit.” But a small effect can cross the statistical threshold in a large study, while a potentially important effect may remain statistically uncertain in a smaller one. Statistical significance is not a certificate of clinical importance. Other forms of presentation work in a similar way. A “30% reduction” sounds large, although a relative percentage does not reveal how many people actually benefited. Finding disease early sounds useful, although detection alone does not prove that screening improves health. Studies show that patients and clinicians view the same treatment more favorably when its benefit is presented as a relative percentage rather than as the actual difference between groups [9–11]. “A 30% reduction” and “23 fewer events per 1,000 people” can describe the same result, but they do not create the same impression. The number may be correct while the message received by the listener is exaggerated. The medical literature uses the term spin for reporting or interpretation that makes research appear more favorable than its complete results justify [12]. Spin may involve highlighting a favorable result while pushing an unfavorable result into the background, omitting information that could change the reader’s judgment, or presenting a future possibility as though the study had already demonstrated it. Spin does not require fabricated data or proof of an intention to mislead. Every statement may be technically correct, while the selection, wording and arrangement of those statements create a conclusion that the complete evidence does not support. The criticism therefore follows three direct questions: What did the study actually establish? What impression did the interview create? What information capable of changing that impression was left out? STAREE: One Favorable Result Becomes the Whole Story STAREE compared atorvastatin 40 mg with placebo in 9,971 relatively healthy, community-dwelling adults aged 70 years or older. Median follow-up was 5.9 years [2]. The trial had two co-primary outcomes: a combined cardiovascular outcome and survival free of dementia or persistent physical disability. The interview reports a “30% relative risk reduction” in major cardiovascular events and calls it “immediately translatable into clinical practice” [1]. It gives neither the absolute event rates nor the other co-primary result. What the “30% Reduction” Means for Actual Patients The “30% reduction” sounds large, but it is a relative figure. Over nearly six years, cardiovascular events occurred in about 83 of every 1,000 people receiving placebo and 60 of every 1,000 taking atorvastatin [2,3]. That means about 23 fewer people per 1,000 experienced the combined cardiovascular outcome. Approximately 44 people would need to be treated over the study period to prevent one such event. The benefit was real but modest in absolute terms. The 30% headline makes it sound much larger than it was. The absolute difference was 2.3 percentage points, not 30 percentage points: about 23 fewer people per 1,000 experienced the combined outcome over nearly six years. It does not mean that 30 of every 100 patients benefited, nor does it mean that deaths fell by 30%. The relative figure attracts attention. The absolute figure reveals the scale. The interview supplies the first and leaves out the second. One Main Result Gets the Headline; the Other Disappears STAREE did not establish that atorvastatin helped participants live longer without dementia or persistent physical disability [2]. This was one of the trial’s two main measures of success and a major concern for older adults. Success on one main outcome cannot stand in for success on both. Notably, the favorable result came from a revised outcome. STAREE originally counted cardiovascular death, nonfatal heart attack and stroke. After a blinded review found fewer events than expected, coronary revascularization was added [13]. The original outcome showed no statistically significant benefit, while the broader outcome produced the reported 30% reduction [2]. The blinded review does not suggest manipulation, but the later protocol amendment changed what counted as a primary cardiovascular event. By adding a clinician-directed procedure, it turned an unsuccessful original outcome into the favorable result behind the “30% reduction” headline. It certainly does not mean that deaths, heart attacks and strokes each fell by 30%. The official report also noted more muscle-, liver- and diabetes-related adverse events with atorvastatin, although serious adverse events were equally frequent in both groups [3]. The interview nevertheless concludes that there is “no disincentive” to treatment [1]. Equal rates of serious events do not mean equal rates of all side effects. STAREE showed a modest cardiovascular benefit on the combined outcome. The spin lies in making it sound larger by leaving out its absolute size, its unsuccessful co-primary result and the burden of treatment. AMUNDSEN: The Blood Test Improved; Clinical Benefit Remained Unproved AMUNDSEN studied more than 2,100 heart attack patients undergoing coronary intervention [5,6]. Both groups received intensive cholesterol-lowering treatment, while the intervention group also received evolocumab immediately before the procedure. Evolocumab produced a large laboratory effect: 82% reached the LDL cholesterol target, compared with 40% receiving standard care [5]. But at one year, death or unplanned cardiovascular hospitalization occurred in 14.6% with evolocumab and 15.4% with standard care [5]. The blood test improved substantially. The hoped-for clinical benefit was not established. A favorable per-protocol analysis was described as hypothesis-generating and cannot replace the main randomized comparison [6]. The interview acknowledges that AMUNDSEN did not establish a clinical benefit at one year, then redirects attention toward what longer treatment might achieve [1]. Earlier trials make later benefit plausible [14], but they cannot turn a future expectation into an AMUNDSEN result. The trial’s unsuccessful clinical outcome is pushed aside, while hoped-for future success becomes the message. Ray then makes a claim that the trial cannot support, stating that the result “categorically proves” that benefit from PCSK9 lowering is “entirely driven by the LDL change and nothing else beyond that” [1]. The force of this statement comes from categorical wording and the authority of the speaker, not from evidence capable of proving it. AMUNDSEN was not designed to test every possible biological mechanism, and its uncertain clinical result cannot do so. Failure to demonstrate an additional early benefit may weaken the case for another mechanism. It cannot eliminate every other biological explanation. A result too uncertain to establish clinical benefit cannot be repurposed as categorical proof of its only possible cause. REACT: Finding Plaque Is Presented as Proof of Better Prevention REACT imaged 16,808 adults aged 18 to 70 years in Denmark and Spain who had no known atherosclerotic cardiovascular disease. Silent plaque was found in 57.1% [7]. The study provided detailed information about where plaque occurs, how extensive it is and how its prevalence changes across adult life. But REACT did not discover that atherosclerosis begins before symptoms. Ray himself acknowledges that autopsy studies had already established this [1]. REACT’s advance was the scale and detail of imaging in living people, not the discovery of silent disease Here, the interview delivers a subtle but powerful message through what it implies rather than what it says. Ray does not explicitly recommend universal screening or statins for everyone with visible plaque. He does not need to. By moving directly from finding plaque to changing behavior, preventing disease and preserving health, he leads listeners toward a conclusion the study never tested [1]. The implied chain is powerful: find plaque earlier, treat earlier, live healthier. REACT established only that plaque could be found. It did not establish that screening leads to better treatment decisions or better health. That is the art of spin: never state the unproved claim; shape the message so the listener reaches it alone. REACT established that plaque can be found. It did not establish that looking for it leaves patients better off. One statement in the interview requires direct correction. Ray says SCORE2 has “very low specificity” because a low score does not exclude plaque [1]. But REACT reported that a high SCORE2 category had 99.8% specificity and only 1.9% sensitivity [7]. A low score fails to rule out plaque because the test has very low sensitivity, not low specificity. The interview reverses the two statistical terms. The planned randomized phase will compare imaging-guided care with standard care, but its main outcome is plaque progression, another surrogate [8,15]. A positive result could therefore mean only that plaque progressed more slowly, not that patients lived longer or remained healthier. Before the strategy can claim clinical benefit, it must show fewer heart attacks, strokes, cases of disability or deaths, and prove that these gains outweigh unnecessary treatment and other harms. Even current European guidance draws a clear line: imaging may refine risk assessment in selected patients, but coronary imaging or calcium scoring is not recommended as a broad cardiovascular screening test [16]. A better scan does not prove that patients live longer, remain healthier or avoid major clinical events Extensive Industry Ties Require Close Scrutiny Professor Ray’s 2025 disclosure lists 23 companies under consulting or lecture honoraria, five under institutional research support, and three in which he held stock options [17]. These relationships are not identical, but together they reveal an extensive industry network. The interview prominently presents Ray’s Imperial College London position and former leadership of the European Atherosclerosis Society [1], yet leaves these financial ties undisclosed. His authority is placed before the listener; his financial context is left out. The overlap is clearest with AMUNDSEN. Ray discussed evolocumab, an Amgen drug, in a trial supported by Amgen and the ACTION Study Group [6]. His disclosures list honoraria and institutional research support from Amgen [17], and he wrote the accompanying editorial [1,18]. None of these connections was disclosed in the interview. These ties do not prove motive or invalidate the evidence. But when industry sponsorship, financial relationships, editorial involvement and favorable spin appear together, the independence of the interpretation demands close scrutiny. Even without those ties, the omissions, shifts in emphasis and unsupported mechanistic certainty remain. Consulting or lecture honoraria Institutional research support Stock options Abbott Laboratories Amgen New Amsterdam Pharma Amgen Daiichi Sankyo Scribe AstraZeneca Sanofi Pemi 31 Bayer Healthcare Pharmaceuticals Regeneron Boehringer Ingelheim Ultragenix* Cargene CRISPR Daiichi Sankyo Eli Lilly Company Emendobio Esperion Kowa New Amsterdam Pharma Novartis Corporation Nodthera GSK Novo Nordisk Pfizer Regeneron Sanofi Scribe Silence Therapeutics Vaxxinity Source: Professor Ray’s disclosure in the cited 2025 publication [17]. Each column is a separate list; alignment across rows does not imply a relationship between companies. “Ultragenix” appears to be a misspelling of Ultragenyx in the source. Conclusion The pattern is consistent across all three studies. STAREE’s modest absolute cardiovascular benefit becomes a “30% reduction” headline, while its unsuccessful co-primary outcome disappears. AMUNDSEN’s unproved early clinical benefit is replaced by the promise of later success, while an uncertain result is turned into categorical proof of an exclusive mechanism. REACT’s detection of silent plaque becomes an implied promise that screening will improve health before any clinical benefit has been demonstrated. These studies produced useful evidence. The spin lies in making each study appear to establish more than it did. The problem is not whether the quoted numbers are accurate. It is how selected results are used to create a clinical message that the complete evidence does not support. Disclosure. The author develops a herbal formula and owns Dr. Q Formula/Insulinn LLC. This commercial interest should be considered when assessing the author’s selection and interpretation of evidence, just as the financial relationships discussed above should be considered when assessing the expert commentary. Editorial assistance Artificial intelligence assisted with source retrieval, calculations and language editing. Sources include research papers, methodological publications, a statistical analysis plan, an interview transcript and official reports. In the event of any inadvertent errors, the responsibility lies with the AI/authors, and corrections will be made promptly upon identification. Acknowledgment I would like to express my sincere gratitude to [Reviewer name] for her thoughtful review and invaluable feedback, and [Reviewer name] for his valuable feedback. Their expertise and guidance have played a pivotal role in refining and enhancing this article. Scope This commentary evaluates the presentation of cardiovascular research. It does not advocate replacing evidence-based conventional care or evaluate complementary treatments. References 1. Ray KK. ESC 2026: Prof Kausik Ray on 3 Trials Shaping Cardiovascular Prevention. Radcliffe Cardiology. September 1, 2026. Interview and published transcript. https://www.radcliffecardiology.com/video-index/esc-2026-prof-kausik-ray-3-trials-shaping-cardiovascular-prevention 2. Zoungas S, Wolfe R, Moran C, et al. Atorvastatin, cardiovascular events, and disability-free survival in older adults. N Engl J Med. 2026. doi:10.1056/NEJMoa2607314. 3. European Society of Cardiology. Cholesterol-lowering medication reduces major cardiovascular events by 30 per cent in older people without known cardiovascular disease. August 29, 2026. https://www.escardio.org/news/press/press-releases/cholesterol-lowering-medication-reduces-major-cardiovascular-events-by-30-per-cent-in-older-people-without-known-cardiovascular-disease/ 4. American Statistical Association. ASA statement on statistical significance and P-values. March 7, 2016. https://www.amstat.org/asa/files/pdfs/p-valuestatement.pdf 5. Montalescot G, Ferrari E, Souteyrand G, et al. LDL cholesterol lowering with evolocumab before percutaneous coronary intervention for acute myocardial infarction: the AMUNDSEN randomized clinical trial. JAMA. Published online August 29, 2026. doi:10.1001/jama.2026.17302. 6. European Society of Cardiology. Immediate evolocumab after a heart attack improves LDL-cholesterol goals but not early cardiovascular outcomes. August 29, 2026. https://www.escardio.org/news/press/press-releases/immediate-evolocumab-after-a-heart-attack-improves-ldl-cholesterol-goals-but-not-early-cardiovascular-outcomes/ 7. Bundgaard H, García-Lunar I, Kofoed KF, et al. Prevalence of silent atherosclerosis across adult life. N Engl J Med. 2026. doi:10.1056/NEJMoa2609059. 8. Ibáñez B, Bundgaard H. REACT initiative: early cure of atherosclerosis through precision prevention. Eur Heart J. 2025;46(33):3244-3246. doi:10.1093/eurheartj/ehaf179. 9. Malenka DJ, Baron JA, Johansen S, Wahrenberger JW, Ross JM. The framing effect of relative and absolute risk. J Gen Intern Med. 1993;8(10):543-548. doi:10.1007/BF02599636. 10. Naylor CD, Chen E, Strauss B. Measured enthusiasm: does the method of reporting trial results alter perceptions of therapeutic effectiveness? Ann Intern Med. 1992;117(11):916-921. doi:10.7326/0003-4819-117-11-916. 11. Covey J. A meta-analysis of the effects of presenting treatment benefits in different formats. Med Decis Making. 2007;27(5):638-654. doi:10.1177/0272989X07306783. 12. Boutron I, Dutton S, Ravaud P, Altman DG. Reporting and interpretation of randomized controlled trials with statistically nonsignificant results for primary outcomes. JAMA. 2010;303(20):2058-2064. doi:10.1001/jama.2010.651. 13. Wolfe R, Heritier S, Zomer E, et al. A randomised clinical trial of STAtin therapy for Reducing Events in the Elderly (STAREE): statistical analysis plan. medRxiv. Preprint version 1, posted February 25, 2025. doi:10.1101/2025.02.24.25321974. 14. Sabatine MS, Giugliano RP, Keech AC, et al. Evolocumab and clinical outcomes in patients with cardiovascular disease. N Engl J Med. 2017;376(18):1713-1722. doi:10.1056/NEJMoa1615664. 15. Fleming TR, DeMets DL. Surrogate end points in clinical trials: are we being misled? Ann Intern Med. 1996;125(7):605-613. doi:10.7326/0003-4819-125-7-199610010-00011. 16. Mach F, Koskinas KC, Roeters van Lennep JE, et al. 2025 focused update of the 2019 ESC/EAS guidelines for the management of dyslipidaemias. Eur Heart J. 2025;46(42):4359-4378. doi:10.1093/eurheartj/ehaf190. 17. Parhofer KG, Aguiar C, Banach M, et al. Expert opinion on the integration of combination therapy into the treatment algorithm for the management of dyslipidaemia: the integration of ezetimibe and bempedoic acid may enhance goal attainment. Eur Heart J Cardiovasc Pharmacother. 2025;11(4):367-379. doi:10.1093/ehjcvp/pvaf007. 18. Ray KK, Stevens CAT. A marathon, not a sprint: AMUNDSEN and LDL-C lowering after myocardial infarction. JAMA. Published online August 29, 2026. doi:10.1001/jama.2026.16837.

Preface (ʿArz-e-Hal) Page 2 By Hazrat Hakeem Noor-ud-Deen, Khalifatul Masih I (ra) (1841–1914) English Translation: Nabila Amatul Naseer, M.Phil (Human Nutrition and Dietetics) Syeda Munazza Ahmad, M.Phil (Sociology) Medical Editor & Project Lead: Qaisar J. Qayyum, MD CAUTION Bayaz Noor-ud-Din is a historical medical work based on material dictated more than a century ago. Over the years, the text has passed through handwritten manuscripts, copies, transcription, typesetting, and subsequent publication. During this process, scribal, spelling, grammatical, punctuation, transcription, or printing errors may have entered the available text. In some places, missing or misplaced punctuation, variations in the spelling of medicines and herbs, or difficult Arabic, Persian, Urdu, and Unani/Hikmat terminology may significantly affect interpretation. Although considerable effort is being made to identify and correct such issues during translation and editorial review, complete accuracy of the historical source text, its interpretation, or the identification of every medicine, herb, preparation, dosage, and medical term cannot be guaranteed. This translation is published primarily for historical, educational, and scholarly purposes. It should not be used independently as a guide for diagnosis, treatment, preparation of medicines, or self-medication. Anyone considering the practical use of any remedy or treatment described in this work should first verify the original text, ingredients, identity, dosage, preparation, and suitability with an appropriately qualified Hakeem/Unani practitioner, Ayurvedic practitioner where applicable, physician, pharmacist, or other relevant healthcare professional. Readers are responsible for obtaining appropriate professional verification before acting upon any medical information contained in this historical work. The translators, editors, contributors, and publisher cannot accept responsibility for harm, loss, or adverse consequences resulting from the interpretation or practical use of the historical remedies or medical information presented in this publication. Note to the Reader This page is presented as a working translation of the original Byaz Noor-ud-Din. The aim is to preserve the original wording, terminology, remedies, doses, and arrangement as faithfully as possible while making the text understandable in modern English. Historical Unani/Hikmat terms are retained in parentheses, and verified English and botanical names are added where appropriate. Text shown in red indicates a word, reading, translation, botanical identification, dosage, or historical medical term that remains uncertain and requires further research or verification. In such cases, the original wording has intentionally been preserved rather than replaced by an unsupported assumption. Red text therefore does not necessarily indicate an error; it identifies an item still under editorial review. The medical concepts and treatments on this page reflect the historical text and medical understanding of its time and should not be interpreted as contemporary medical advice. بِسْمِ ٱللَّٰهِ ٱلرَّحْمَٰنِ ٱلرَّحِيمِ نَحْمَدُهُ وَنُصَلِّي عَلَى رَسُولِهِ الْكَرِيمِ Preface (ʿArz-e-Hal) Some time ago I published the proven remedies of my most gracious mentor and my greatest teacher, Maulana Hafiz Haji Nuruddin (may Allah be pleased with him), by means of the journal Tabib-e-Hazik. Then I published them in book form in three parts under the title Mujarrabat-e-Nuruddin (the proven remedies of Nuruddin), done during the life of His Holiness, under his own guidance and favor. I must openly acknowledge that a few errors remained in that edition. His Holiness instructed me to prepare a corrected edition of it, and he himself also completed this Bayaz. However, his illness and my own preoccupation did not allow me the opportunity to publish a second edition during his life. Now God Almighty has granted the opportunity to me, so that I am attaining the good fortune of accomplishing this magnificent service. Hazrat Maulana Nuruddin Sahib was, in reality, a King of Medicine. And one distinctive feature of his treatment was that he always prescribed remedies that were easy to obtain, quick in their effect, and inexpensive. His proven remedies (mujarrabat) were based on more than half a century of personal experience. In this Bayaz, he has prescribed only those remedies which he himself put to proof with thousands of patients and found beneficial. Compared with the first edition, this Bayaz has grown to more than twice its original size. Thus, this first part alone has grown larger than all three parts of Mujarrabat, while the second part is still remaining. I would also like to mention that this Bayaz has been registered, no person has any right to print it, in any form, even in part. This time, I have also included the medical biography of Hazrat Hakim-ul-Ummat. By the grace of Allah, I hope that I will soon be able to publish the second part of it as well. And Allah is the One Whose help is sought. Humbly, Fazl-ur-Rahman Qadian 24 December 1924 Index of Diseases, (Fihrist-e-Amraz), Bayaz-e-Nuruddin, Part One, Page 2 Format: modern correspondence, where one exists | English rendering | Roman Urdu | original Urdu 1.Chapter One: Diseases of the Head | Bab-e-Awwal dar Amraz-e-Sar | باب اوّل در امراضِ سر | Hot or Hot-Dry Headache | Suda, Garm ya Garm Khushk | صداع، گرم یا گرم خشک | Dry Headache | Suda-e-Yabis | صداعِ یابس Cold-stimulus headache, in part | Headache from Cold Alone | Sirf Sardi ka Sar Dard | صرف سردی کا سردرد | Hangover Headache | Suda-e-Khumari | صداعِ خماری | Sanguineous Headache | Suda-e-Damvi | صداعِ دموی | Bilious Headache | Suda-e-Safravi | صداعِ صفراوی | Phlegmatic Headache | Suda-e-Balghami | صداعِ بلغمی | Melancholic Headache | Suda-e-Saudavi | صداعِ سوداوی | Windy, or rather Nervous, Headache | Suda-e-Rihi, balkeh Asabi | صداعِ ریحی، بلکہ عصبی | Vaporous Headache | Suda-e-Bukhari | صداعِ بخاری | Headache of Debility | Suda-e-Zafi | صداعِ ضعفی | Crisis Headache | Suda-e-Buhrani | صداعِ بحرانی Headache attributed to rhinosinusitis | Catarrhal Headache | Suda-e-Nazli | صداعِ نزلی | Headache from Obstruction | Suda-e-Suddi | صداعِ سدی Odor-triggered headache | Olfactory Headache | Suda-e-Zakai | صداعِ ذکائی REFERENCE SOURCES FOR TERMINOLOGY Disease nomenclature WHO international standard terminologies on Unani medicine. World Health Organization, Geneva. https://iris.who.int/bitstream/handle/10665/365544/9789240064959-eng.pdf Standard Unani Medical Terminology. Central Council for Research in Unani Medicine (CCRUM), Ministry of Ayush, Government of India. Prepared under a collaborative programme of CCRUM and WHO for Traditional Medicine. https://ccrum.res.in/writereaddata/UploadFile/Standard%20Unani%20Medical%20Terminology_1430.pdf National Ayush Morbidity and Standardized Terminologies Electronic (NAMASTE) Portal, Ministry of Ayush, Government of India. Standardized terminologies and national morbidity codes for Ayurveda, Siddha and Unani, dual-coded with WHO ICD-10 and ICD-11. https://namaste.ayush.gov.in/about-namaste-portal Standard Unani Treatment Guidelines for Common Diseases, Volume II. CCRUM, Ministry of Ayush, Government of India. Contains the entry Sudā' Shirkī Mi'dī, referred headache of gastric origin. https://ccrum.res.in/writereaddata/UploadFile/Common%20Diseases,%20Vol%20II_1223.pdf International Classification of Diseases, 11th Revision, Chapter 26 Module 2 (TM2). World Health Organization. Ayush morbidity codes were mapped into TM2 and released on the ICD-11 Browser in February 2025. https://icd.who.int/browse11 Materia medica and pharmacopoeia Unani Pharmacopoeia of India. Pharmacopoeia Commission for Indian Medicine and Homoeopathy (PCIM&H), Ministry of Ayush, Government of India. https://www.portal.pcimh.gov.in Medicinal plants database. CCRUM, Ministry of Ayush, Government of India. https://ccrum.res.in/ViewData/Multiple?mid=1640 NOTE ON THE USE OF THESE SOURCES Terminology in the present translation has been checked against the sources above where a corresponding entry exists. Several categories in the Bayaz, among them Sudā'-i Khumārī, Sudā'-i Suddī and Sudā'-i Zakā'ī, do not appear in the standardized modern lists. These are recorded here as the compiler's own arrangement, and no modern equivalent has been supplied for them. Page 2 of original book TRANSLATION AND EDITORIAL CREDITS Original Work Hazrat Hakeem Noor-ud-Deen, Khalifatul Masih I (ra) (1841–1914)Bayaz Noor-ud-DinEminent Unani physician and former Personal Physician to His Highness the Maharaja of Kashmir English Translators Nabila Amatul Naseer, M.Phil Nutritionist and Dietitian Syeda Munazza Ahmad, M.Phil Sociologist, Researcher, and Academic Writer Project Lead, Scholarly and Medical Editor Qaisar J. Qayyum, MD Chief Editor, Noor Journal of Complementary and Contemporary Medicine (NJCCM) ACKNOWLEDGMENT The English translation of Bayaz Noor-ud-Din is a collaborative project undertaken to preserve and make accessible to English-language readers the historical Unani/Hikmat (Greco-Arab) medical writings of Hazrat Hakeem Noor-ud-Deen, Khalifatul Masih I (ra). The translated text undergoes scholarly and medical editorial review, including comparison with the original Urdu text; clarification of difficult or archaic Urdu, Persian, Arabic, and Unani/Hikmat terminology; review of historical medical concepts; research and verification of medicinal substances and botanical identities; and revision for accuracy, clarity, consistency, and readability while preserving the meaning and arrangement of the original work. Particular care is taken not to impose modern interpretations where the historical text does not support them. Where the meaning, reading, or botanical identity of a historical term cannot be established with reasonable confidence, the original terminology is retained or identified for further review rather than replaced by an unsupported interpretation. Bayaz Noor-ud-Din Project Team The Bayaz Noor-ud-Din Project Team serves in an advisory and collaborative capacity. Team members contribute through discussion of difficult passages, consideration of alternative interpretations, and input on linguistic, historical, medical, Unani/Hikmat, botanical, and editorial questions. Team members have contributed both through group discussions and by providing direct feedback, which, where appropriate, has been incorporated into the translation and editorial revisions. The Project Team's role is distinct from that of the two English translators, who are separately identified and credited above. USA Dr Abid and Dr Ayesha Haq, Snohomish, WA Dr Haroon Akhtar, Maryland Dr Shazli Naseer Dr Imtiaz Chaudary Malik Abdullah Munawar Ahmad Saqib, New Jersey, USA Sharif Ahmad, Atlanta, GA Dr Almas Nasar, Dallas, TX Bilal Ahmed Canada Mazhar Qasid Ahmad Bajwa Harisah Mehmood Pakistan Faizan Nabila Amatul Naseer, Chenab Nagar Syeda Munazza Ahmad, Multan United Kingdom Dr Ismaeel Mohammad Dr Qasid Ahmad Bajwa, Scunthorpe Australia Dr Mohammad Younus Dr Aamir Mahmood Ireland Dr Aida Nasar Khan — Dublin United Arab Emirates Dr Sulaiman Ahmad — Dubai Nepal Nasir Ahmad Bhatti FINANCIAL SUPPORT ACKNOWLEDGMENT This translation project has been made possible through the generous financial support of Ahmadi individuals from the NJCCM WhatsApp group who provided funding toward the cost of translating and preparing Bayaz Noor-ud-Din for English-language publication. We gratefully acknowledge their financial support in helping preserve this important historical work and make it accessible to a wider readership. Project Funding Financial supporters are listed in the order in which their contributions were received. Sharif Ahmad, USA Munawar Ahmad Saqib, New Jersey, USA Dr Qaisar J. Qayyum, Edmond, OK, USA Dr Amatulah, USA Dr Abid Haq & Ayesha Haq, Snohomish, WA, USA Professor Aftab Ahmad & Mrs Neena Ahmad, USA Dr Aamir Mahmood, Australia Mubashir Ahmed, Huntley, IL, USA Bushra Begum, RN, USA Dr Munawar Malik, USA Dr Amina Tariq, USA Dr Nasira Malik, USA Dr Aida Nasar Khan, Dublin Dr Almas Nasar, Dallas, TX Donors wishing to remain anonymous are gratefully acknowledged without being named. Published by Noor Journal of Complementary and Contemporary Medicine (NJCCM)

Fālij (Paralysis) and Istirkhā (Flaccidity)- Page 52/53 By Hazrat Hakeem Noor-ud-Deen, Khalifatul Masih I (ra) (1841–1914) English Translation: Nabila Amatul Naseer, M.Phil (Human Nutrition and Dietetics) Syeda Munazza Ahmad, M.Phil (Sociology) Medical Editor & Project Lead: Qaisar J. Qayyum, MD CAUTION Bayaz Noor-ud-Din is a historical medical work based on material dictated more than a century ago. Over the years, the text has passed through handwritten manuscripts, copies, transcription, typesetting, and subsequent publication. During this process, scribal, spelling, grammatical, punctuation, transcription, or printing errors may have entered the available text. In some places, missing or misplaced punctuation, variations in the spelling of medicines and herbs, or difficult Arabic, Persian, Urdu, and Unani/Hikmat terminology may significantly affect interpretation. Although considerable effort is being made to identify and correct such issues during translation and editorial review, complete accuracy of the historical source text, its interpretation, or the identification of every medicine, herb, preparation, dosage, and medical term cannot be guaranteed. This translation is published primarily for historical, educational, and scholarly purposes. It should not be used independently as a guide for diagnosis, treatment, preparation of medicines, or self-medication. Anyone considering the practical use of any remedy or treatment described in this work should first verify the original text, ingredients, identity, dosage, preparation, and suitability with an appropriately qualified Hakeem/Unani practitioner, Ayurvedic practitioner where applicable, physician, pharmacist, or other relevant healthcare professional. Readers are responsible for obtaining appropriate professional verification before acting upon any medical information contained in this historical work. The translators, editors, contributors, and publisher cannot accept responsibility for harm, loss, or adverse consequences resulting from the interpretation or practical use of the historical remedies or medical information presented in this publication. Note to the Reader This page is presented as a working translation of the original Byaz Noor-ud-Din. The aim is to preserve the original wording, terminology, remedies, doses, and arrangement as faithfully as possible while making the text understandable in modern English. Historical Unani/Hikmat terms are retained in parentheses, and verified English and botanical names are added where appropriate. Text shown in red indicates a word, reading, translation, botanical identification, dosage, or historical medical term that remains uncertain and requires further research or verification. In such cases, the original wording has intentionally been preserved rather than replaced by an unsupported assumption. Red text therefore does not necessarily indicate an error; it identifies an item still under editorial review. The medical concepts and treatments on this page reflect the historical text and medical understanding of its time and should not be interpreted as contemporary medical advice. Flaccidity/Weakness of an Organ (Istirkhā استرخاء) This is a condition in which an organ becomes partially or completely deficient in, or loses, its sensation (Hiss حس), movement (Harkat حرکت), or both. Paralysis (Fālij فالج) Numbness or loss of movement affecting one half of the body is called paralysis (Fālij فالج). This is the commonly used terminology of Unani physicians (Atibbā اطباء). When numbness or loss of movement is confined to a particular organ, they call it flaccidity/weakness (Istirkhā استرخاء). Causes of Flaccidity/Weakness (Asbāb-e-Istirkhā اسباب استرخاء) This condition may arise from coldness (Sardi سردی), heat (Garmi گرمی), moisture (Tari تری), or dryness (Khushki خشکی), or from pressure caused by a swelling (Waram ورم) or a bone. Causes of Paralysis (Asbāb-e-Fālij اسباب فالج) It may result from thickening of a muscle/fiber, or from its being severed due to an excess of one of the humors (Khilt خلط), or from a fall; epilepsy (Mirgi مرگی); stupor or profound unresponsiveness (Sakta سکتہ); colic pain (Qulanj قولنج); chronic or long-standing fever (Purāni Tap پرانی تپ); hysteria (Ikhtināq al-Raḥim- اختناق الرحم); inflammation/swelling of the brain (Dimāgh دماغ) or spinal cord (Harām Maghz حرام مغز); or inflammation of their membranes. Excessive sexual intercourse (Kasrat-e-Jimāʿ کثرت جماع), masturbation (Jalq جلق), alcohol consumption, intense anger, and carrying very heavy loads may also cause this condition. Context: In this Unani/Hikmat, coldness, heat, moisture, and dryness refer to the traditional qualitative states of the body or affected organ, rather than simply to environmental temperature or weather. Note (Fāʾidah فائدہ) If the tongue remains normal while sensation in the rest of the body is impaired, the disorder lies in the spinal cord (Nukhāʿ نخاع). If speech is impaired, the disorder lies in the brain (Dimāgh دماغ). If the lower part of the body becomes paralyzed while the upper part remains unaffected, the defect lies in a Kaad (Kaad کاڈ), which is part of the spinal cord (Harām Maghz حرام مغز). This lower-body paralysis (Isfali اسفلی) has two forms. One begins in the fingers and gradually progresses toward the navel. The second advances even further until the hands also become paralyzed. Paralysis occurring in young people, the elderly, or debilitated individuals, during the hot season, or affecting the left side of the body is considered dangerous. Note (Fāʾidah فائدہ) If a person develops an excessive desire to consume strengthening tonics (Muqawwiyāt مقویات), or greed for accumulating wealth, such thoughts may result in paralysis. Gradually, weakness develops in all the faculties of the body (Quwā قویٰ). If the condition is not recognized and treated in time, the patient may surely die. Fatal Cases (Muhlik مہلک) If this disease occurs in elderly people or affects the left side, it is considered fatal. The same applies when it results from an injury. Note (Fāʾidah فائدہ) It should be remembered that with Western treatment, some residual effect of this disease usually remains, whereas with Indian and Unani treatment it may be completely cured, that is because the Western physicians use laxatives/purgatives (Mushilāt مسہلات) and strengthening/tonic medicines (Muqawwiyāt مقویات) too sparingly. For four days, or sometimes even for a week, they may not actively treat such patients, perhaps out of concern for their professional reputation, even though this practice is incorrect Or they may wait until the course and severity of the illness become clearer. During this period, they rely only on honey water (Ma-ul-Asal ماء العسل). The formula for honey water is: mix one part honey with two, four, or eight parts water. Boil the mixture until one part has evaporated, leaving two parts remaining. Treatment (Ilāj علاج) Remove the underlying causes. For those with excessive heat, give the Sharbat of rock sugar (Misri مصری). Rose water (Arq-e-Gul عرقِ گل; rose distillate, generally corresponding to Arq-e-Gulab عرقِ گلاب) with Sikanjabeen (سکنجبین; traditional sweet-and-sour syrup) give London rocket/hedge mustard (Sisymbrium irio; Khub Kalan خوب کلاں) with Shisha (شیشہ) Arq-e-Gul (عرقِ گل) [botanical identification to be verified] If there is an excess of blood, perform venesection (Fasd فصد) of the Haft Andām vein (Rag-e-Haft Andām رگِ ہفت اندام). For those with excessive coldness or weakness, give honey water (Ma-ul-Asal ماء العسل) with fennel distillate (Arq-e-Badiyan عرق بادیان; Foeniculum vulgare) and cardamom distillate (Arq-e-Elāichi عرق الائچی; Elettaria cardamomum). And boil nutmeg (Myristica fragrans; Jaiphal جائفل), mace (Myristica fragrans; Javitri جاوتری), ginger (Zingiber officinale; Zanjabeel زنجبیل), cinnamon (Cinnamomum verum; Darchini دارچینی), and mastic (Pistacia lentiscus; Mastagi مصطگی) in fennel distillate (Arq-e-Badiyan عرق بادیان) and have the patient drink it. The earlier physicians used to give honey water (Ma-ul-Asal ماء العسل) after evacuation/purification (Tanqiyah تنقیہ). Its prescription/formula (Nuskha نسخہ) is as follows: Prescription/Formula (Nuskha نسخہ) - Decoction (Joshanda جوشاندہ) Take: Caper root (Capparis spinosa; Beekh Kabar بیخ کبر; Safed Jand سفید جند) — 1 Masha (≈ 1 g) Fennel root (Foeniculum vulgare; Beekh Badiyan بیخ بادیان) — 1 Masha (≈ 1 g) Licorice (Glycyrrhiza glabra; Mulathi ملٹھی) — 1 Masha (≈ 1 g) Azkhar root (Cymbopogon jwarancusa; Beekh Azkhar بیخ اذخر) — 1 Masha (≈ 1 g) Anise (Pimpinella anisum; Anesoon انیسون) — 1 Masha (≈ 1 g) Black seed (Nigella sativa; Kalonji کلونجی) — 1 Masha (≈ 1 g) French lavender (Lavandula stoechas; Ustukhuddus اسطوخودوس) — 2 Masha (≈ 2 g) Large, dried raisins (Vitis vinifera; Munaqqa منقہ) — 2 Masha (≈ 2 g) Prepare a decoction (Joshanda جوشاندہ), add rock sugar (Misri مصری) or white sugar (Shakar-e-Tari شکر تری) and administer it for seven to ten days. After this, give Habb-e-Ayārij (حبِ ایارج; a traditional Unani evacuative/purgative compound pill used for cleansing the stomach) at night with fennel distillate (Arq-e-Badiyan عرقِ بادیان). During the (daytime), give it with a decoction (Joshanda جوشاندہ) of French lavender (Lavandula stoechas; Ustukhuddus اسطوخودوس), Gawzaban (گاؤزبان), and large dried raisins (Vitis vinifera; Munaqqa منقہ). Gawzaban botanical note: The traditional name Gawzaban (گاؤزبان), also transliterated in modern sources as Gaozaban or Goazaban, is not botanically unambiguous across Unani literature. The Unani Pharmacopoeia of India identifies Goazaban as Onosma bracteatum Wall., while CCRUM sources also use Goazaban for Arnebia benthamii and elsewhere identify Gul-i-Gaozaban as Onosma bracteatum. Therefore, the original Bayaz term Gawzaban (گاؤزبان) is retained in this translation without imposing a single botanical identification.  PCIM&H, Ministry of AYUSH, Unani Pharmacopoeia of India, Goazaban:https://www.portal.pcimh.gov.in/product_details/99804698-e86a-4924-bbaa-9ae35be54bc9  CCRUM medicinal plants page:https://ccrum.res.in/ViewData/Multiple?mid=1640  CCRUM publication identifying Gul-i Gaozaban:https://ccrum.res.in/writereaddata/UploadFile/Palpitation0English0Folder_1923.pdf Bayaz Noor-ud-Din (1841–1914) Page 52/53 Other (Digar دیگر) Massage with castor oil (Ricinus communis; Roghan-e-Arand روغن ارنڈ) and fennel distillate (Arq-e-Badiyan عرق بادیان). If there is severe constipation, administer a soap-water enema (Huqnah حقنہ) containing traditional local soap, 2 Tola (≈ 24 g). After one or two administrations of a purgative/laxative (Mushil مُسہِل), administer asafoetida (Hing ہینگ), 2 Masha (≈ 2 g); Surkh Kuth (سرخ کٹھ) [botanical identification to be verified] — 1 Masha (≈ 1 g); and the inner honey material of marking nut (Semecarpus anacardium; Bhilawan بھلاواں / Baladur بلادر), 0.1 Masha (≈ 0.1 g), in divided doses. Also administer and massage with Malkangni oil (Celastrus paniculatus; Roghan-e-Malkangni روغن مال کنگنی). Other (Digar دیگر) Give two castor seeds (Ricinus communis; Arand ارنڈ) at night for some time. This is considered an elixir/highly effective remedy (Aksir اکسیر). Other (Digar دیگر) Take: Cloves (Syzygium aromaticum; Laung لونگ) — 6 Masha (≈ 6 g) Pellitory root (Anacyclus pyrethrum; Aqar Qarha عاقرقرحا, Hikmat/Unani) — 6 Masha (≈ 6 g) Sesame oil (Sesamum indicum; Roghan-e-Kunjad روغن کنجد) — 3 Tola (≈ 36 g) Use for massage. Other (Digar دیگر) Administer Majoon Kuchla (معجون کچلہ; a traditional Unani semisolid compound preparation containing processed/detoxified Kuchla [Nux vomica, Strychnos nux-vomica]) or Majoon Falasifa (معجون فلاسفہ). Other (Digar دیگر) Apply Syrian rue oil (Peganum harmala; Roghan-e-Asfand روغن اسفند). Other (Digar دیگر) Use costus root (Saussurea costus; Kuth Talkh کٹھ تلخ), bitter colchicum (Colchicum luteum; Suranjan Talkh سورنجان تلخ), ginger (Zingiber officinale; Zanjabeel زنجبیل), and sesame oil (Sesamum indicum; Roghan-e-Kunjad روغن کنجد) for massage. Prescription for Paralysis of the Hand (Nuskha Fālij-e-Hāth نسخہ فالج ہاتھ) Apply cinnamon (Cinnamomum verum; Darchini دارچینی) and Roghan-e-Siyah (روغن سیاہ) [botanical identification to be verified] by massage to the neck and head. Take: Senna leaves (Senna alexandrina, traditionally listed by the older botanical name Cassia angustifolia; Barg-e-Sana برگ سنا) — 2 Masha (≈ 2 g) Honey (Shehad شہد) — 6 Masha (≈ 6 g) Cow's ghee (Roghan-e-Gao روغن گاؤ) — 1 Masha (≈ 1 g) Habb-e-Siyah (حب سیاہ) [botanical identification to be verified] Preparation of Syrian Rue Oil (Roghan-e-Aspand ki Tarkīb روغن اسپند کی ترکیب) Place Syrian rue (Peganum harmala; Aspand اسپند) in an earthen pot (Ghara گھڑا). Make a hole in the bottom of the pot and insert small sticks (Tiliyan تیلیاں) through it. Heat the pot from above. The oil will collect and drip out from below. TRANSLATION AND EDITORIAL CREDITS Original Work Hazrat Hakeem Noor-ud-Deen, Khalifatul Masih I (ra) (1841–1914)Bayaz Noor-ud-DinEminent Unani physician and former Personal Physician to His Highness the Maharaja of Kashmir English Translators Nabila Amatul Naseer, M.Phil Nutritionist and Dietitian Syeda Munazza Ahmad, M.Phil Sociologist, Researcher, and Academic Writer Project Lead, Scholarly and Medical Editor Qaisar J. Qayyum, MD Chief Editor, Noor Journal of Complementary and Contemporary Medicine (NJCCM) ACKNOWLEDGMENT The English translation of Bayaz Noor-ud-Din is a collaborative project undertaken to preserve and make accessible to English-language readers the historical Unani/Hikmat (Greco-Arab) medical writings of Hazrat Hakeem Noor-ud-Deen, Khalifatul Masih I (ra). The translated text undergoes scholarly and medical editorial review, including comparison with the original Urdu text; clarification of difficult or archaic Urdu, Persian, Arabic, and Unani/Hikmat terminology; review of historical medical concepts; research and verification of medicinal substances and botanical identities; and revision for accuracy, clarity, consistency, and readability while preserving the meaning and arrangement of the original work. Particular care is taken not to impose modern interpretations where the historical text does not support them. Where the meaning, reading, or botanical identity of a historical term cannot be established with reasonable confidence, the original terminology is retained or identified for further review rather than replaced by an unsupported interpretation. Bayaz Noor-ud-Din Project Team The Bayaz Noor-ud-Din Project Team serves in an advisory and collaborative capacity. Team members contribute through discussion of difficult passages, consideration of alternative interpretations, and input on linguistic, historical, medical, Unani/Hikmat, botanical, and editorial questions. Team members have contributed both through group discussions and by providing direct feedback, which, where appropriate, has been incorporated into the translation and editorial revisions. The Project Team's role is distinct from that of the two English translators, who are separately identified and credited above. USA Dr Abid and Dr Ayesha Haq, Snohomish, WA Dr Haroon Akhtar, Maryland Dr Shazli Naseer Dr Imtiaz Chaudary Malik Abdullah Munawar Ahmad Saqib, New Jersey, USA Sharif Ahmad, Atlanta, GA Dr Almas Nasar, Dallas, TX TBA Canada Mazhar Qasid Ahmad Bajwa Harisah Mehmood Pakistan Faizan Nabila Amatul Naseer, Chenab Nagar Syeda Munazza Ahmad, Multan United Kingdom Dr Ismaeel Mohammad Dr Qasid Ahmad Bajwa, Scunthorpe Australia Dr Mohammad Younus Ireland Dr Aida Nasar Khan — Dublin United Arab Emirates Dr Sulaiman Ahmad — Dubai Nepal Nasir Ahmad Bhatti FINANCIAL SUPPORT ACKNOWLEDGMENT This translation project has been made possible through the generous financial support of Ahmadi individuals from the NJCCM WhatsApp group who provided funding toward the cost of translating and preparing Bayaz Noor-ud-Din for English-language publication. We gratefully acknowledge their financial support in helping preserve this important historical work and make it accessible to a wider readership. Project Funding Financial supporters are listed in the order in which their contributions were received. Sharif Ahmad, USA Munawar Ahmad Saqib, New Jersey, USA Dr Qaisar J. Qayyum, Edmond, OK, USA Dr Amatulah, USA Dr Abid Haq & Ayesha Haq, Snohomish, WA, USA Professor Aftab Ahmad & Mrs Neena Ahmad, USA Dr Aamir Mahmood, Australia Mubashir Ahmed, Huntley, IL, USA Bushra Begum, RN, USA Dr Munawar Malik, USA Dr Amina Tariq, USA Dr Nasira Malik, USA Dr Aida Nasar Khan, Dublin Dr Almas Nasar, Dallas, TX Donors wishing to remain anonymous are gratefully acknowledged without being named. Published by Noor Journal of Complementary and Contemporary Medicine (NJCCM)

Dr. Qaisar J. Qayyum Chief Editor, Noor Journal of Complementary and Contemporary Medicine, Clinical Assistant Professor, Oklahoma, USA Email: drqhealthyliving@gmail.com AL- BIRUNI - UNISCO Digital Library Abstract Complementary medicine represents a harmonious fusion of traditional healing practices and modern scientific inquiry. This article explores its philosophical foundations, examining historical contributions and modern breakthroughs that underscore the integration of diverse medical paradigms. Highlighting figures such as Al-Bīrūnī, Ibn Sina, and Al-Razi from the Islamic Golden Age, as well as innovators like Edward Jenner, Barry Marshall, and Tu Youyou, this article emphasizes the enduring relevance of curiosity, observation, and inclusivity in healthcare. By bridging ancient remedies and contemporary methodologies, our modern concept of complementary medicine offers a holistic approach to global healthcare challenges, and aims to provide affordable, inclusive, and effective solutions for today's healthcare challenges. Introduction Imagine a world where ancient wisdom meets modern science—a realm where simple observations revolutionize global healthcare. Modern complementary medicine thrives in this space, uniting centuries-old practices with cutting-edge innovations, which can be practiced by a wider range of practitioners. History shows that some of the greatest medical advancements arose not from elite institutions or advanced technologies but from simple curiosity and the courage to observe. Figures like Al-Bīrūnī, Ibn Sina, and Al-Razi demonstrated this during the Islamic Golden Age, achieving groundbreaking insights with limited resources (1, 2, 3). Similarly, pioneers like Edward Jenner, Barry Marshall, and Tu Youyou bridged the gap between traditional observations and modern scientific validation (4, 5, 6). The current complementary medicine field values the insights of the past while embracing the precision of modern science. It offers a platform to explore remedies that address physical, mental, and spiritual health comprehensively, and add value to existing scientific achievements. Complementary medicine offers an alternative, emphasizing: Championing Observational Knowledge: Encouraging real-world research inspired by traditional practices. Fostering Inclusivity: Inviting contributions from diverse voices, including those who are considered non-experts by some. Promoting Innovation: Highlighting remedies that are impactful and accessible, even if not commercially lucrative. Real-World Knowledge: Supporting research inspired by observations and traditional practices. Affordable Solutions: Highlighting remedies that may not generate excessive profits but help humanity. Bridging Traditions and Science: Validating traditional knowledge through modern methodologies. The Philosophy of Complementary Medicine: Innovation Open to All Complementary medicine challenges rigid scientific frameworks by fostering inclusivity and openness to diverse paradigms. As Alfred North Whitehead observed, "The Universe is vast. Nothing is more curious than the self-satisfied dogmatism with which mankind at each period of its history cherishes the delusion of the finality of existing modes of knowledge. Skeptics and believers are alike. At this moment scientists and skeptics are the leading dogmatists. Advance in detail is admitted; fundamental novelty is barred. This dogmatic common sense is the death of philosophic adventure..." (7). It embraces a broader understanding of evidence-based medicine, valuing centuries-old remedies validated through widespread and long-term use in different parts of the world. As one physician aptly noted, "Civilizations have done the studies for us." This inclusive perspective encourages bold exploration of untapped knowledge. This broader understanding allows for the integration of safe and effective traditional practices alongside cutting-edge modern therapies. Key principles of complementary medicine: Observation Matters: Many discoveries, like vaccines and antibiotics, started with simple observations. Respect for Traditions: Ancient remedies often hold valuable lessons for modern healthcare. Inclusivity Drives Innovation: Welcoming diverse ideas can lead to breakthroughs that benefit everyone. 2. Historical Inspirations 2.1 Al-Bīrūnī: Precision in Science Abu Rayhan Al-Bīrūnī (973–1048) calculated Earth's circumference with less than 1% error using basic tools (1). His interdisciplinary contributions inspire researchers to explore with creativity and determination, even when resources are limited. 2.2 Ibn Sina's Canon of Medicine Known as Avicenna, Ibn Sina's Canon of Medicine synthesized diverse traditions, emphasizing diet, exercise, and holistic care (2). His focus on individualized treatment mirrors modern complementary medicine's principles. 2.3 Al-Razi: Ethics and Experimentation Rhazes, a pioneer in clinical observation, wrote influential medical texts. He believed in ethical treatment and patient-centered care, values that align with complementary medicine today. Al-Razi's Kitab al-Hawi combined clinical observations with evidence-based experimentation, emphasizing ethical medical practices (3). Modern Pioneers and Breakthroughs 3.1 Edward Jenner and Immunology Edward Jenner's observation of milkmaids immune to smallpox paved the way for vaccinations, a cornerstone of preventive medicine (4). 3.2 Barry Marshall and Helicobacter pylori Marshall and Warren's discovery of bacterial causes for ulcers redefined treatment, earning the 2005 Nobel Prize in Physiology or Medicine (5). 3.3 Tu Youyou and Artemisinin Tu Youyou's work with Artemisia annua from Traditional Chinese Medicine revolutionized malaria treatment (6). 3.4 Lady Mary Wortley Montagu and Variolation Introduced by Lady Mary Wortley Montagu, this Ottoman practice was the precursor to vaccination (8). 3.5 Alexander Fleming and Penicillin An accidental discovery of mold that killed bacteria saved millions of lives (9). Bridging Tradition and Modern Science 4.1 Aspirin and Willow Bark Aspirin, derived from willow bark, exemplifies the transition of traditional remedies into modern pharmaceuticals (10). 4.2 Fagonia arabica (Suchi Booti) Traditional uses of Fagonia arabica are now validated through research, showcasing its anticancer and anti-inflammatory properties (11, 12). 4.3 Cinchona and Quinine Quinine's discovery from cinchona bark highlights the enduring value of ethnobotanical knowledge (13). A Vision for Complementary Medicine Complementary medicine promotes: Democratized Discovery Empowering individuals to contribute observations and personal experiences. Bridged Traditions and Science Creating platforms where diverse knowledge systems coexist. Holistic Approaches Addressing physical, mental, and spiritual well-being. A Philosophy of Certainty: From Knowing to Seeing to Experiencing Hadrat Mirza Ghulam Ahmad (as) elaborates on the three levels of knowledge in The Philosophy of the Teachings of Islam, emphasizing their relevance in understanding and validating truths (14): The knowledge of certainty (Ilm-ul-Yaqeen - علم اليقين): The foundational level of knowledge, akin to seeing smoke. This corresponds to understanding obtained through secondary sources like reading books or journals, providing theoretical awareness. The vision of certainty (Ain-ul-Yaqeen - عين اليقين): The intermediate level of knowledge, comparable to seeing fire. This is gained when your practical application of knowledge benefits others, such as when patients experience improvement through your treatments. The truth of certainty (Haqq-ul-Yaqeen - حق اليقين): The ultimate level of knowledge, akin to putting your hand in fire. This represents the certainty achieved through personal experience and direct observation of outcomes. These levels highlight the importance of practical and experiential knowledge in complementing theoretical understanding, underscoring the unique value of anecdotes and real-world application in enriching our comprehension of truth. Conclusion History of complementary medicine proves that innovation doesn't require billion-dollar labs or advanced degrees. From Al-Bīrūnī's calculations to modern breakthroughs like vaccines, history shows that simple observations can lead to extraordinary discoveries. Traditional medicine often employs complex herbal mixtures and multi-compound extracts (15), offering a polypharmacological approach better suited to addressing multifactorial conditions like chronic and degenerative diseases, unlike biomedicine's "one disease–one target–one drug" model (16). The future of Traditional Medicine relies on standardization (18, 19) and addressing challenges like non-standardized materials and the potential risks of contents like aristolochic acid, causing nephrotoxicity and carcinogenic effects (17), to enable its safe large-scale application. By embracing curiosity, tradition, and inclusiveness, complementary medicine seeks to build a healthier future for everyone. Message is clear: Anyone can make a breakthrough, and the past holds valuable lessons for the future. Acknowledgment This article was written with AI assistance. All claims are supported by credible, peer-reviewed references, which were validated for accuracy and authenticity. The AI synthesized information were reviewed by authors, ensuring scientific integrity throughout. In the event of any inadvertent errors, the responsibility lies with the AI/authors, and corrections will be made promptly upon identification. I would like to express my sincere gratitude to Dr. Tahira Khalid, for her thoughtful review and invaluable feedback. Her expertise and guidance have played a pivotal role in refining and enhancing this article. Conflict of Interest Statement The author is the developer of a herbal formula and the owner of Dr. Q Formula/Insulinn LLC. However, this affiliation has not influenced the content, analysis, or conclusions of this article. References Al-Bīrūnī: Persian scholar, astronomer, mathematician and geographer. Encyclopaedia Britannica. https://www.britannica.com/biography/al-Biruni Ibn Sīnā (Avicenna). The Canon of Medicine (al-Qānūn fī al-Ṭibb). Internet Archive. https://archive.org/details/AvicennasCanonOfMedicine Anjum S. Al-Razi: a distinguished physician of the medieval history. A review of his method and influence. Revelation and Science. 2015;5(2):59-66. doi:10.31436/revival.v5i2.161. https://journals.iium.edu.my/revival/index.php/revival/article/view/161 Jenner E. An Inquiry into the Causes and Effects of the Variolae Vaccinae. London: Sampson Low; 1798. Marshall BJ. Helicobacter connections. Nobel Lecture, 8 December 2005. NobelPrize.org. https://www.nobelprize.org/prizes/medicine/2005/marshall/lecture/ Tu Y. Artemisinin: a gift from traditional Chinese medicine to the world. Nobel Lecture, 7 December 2015. NobelPrize.org. https://www.nobelprize.org/prizes/medicine/2015/tu/lecture/ Price L, recorder. Dialogues of Alfred North Whitehead. Boston: David R. Godine; 2001 (first published 1954). p. 5. Smallpox: variolation. U.S. National Library of Medicine. https://www.nlm.nih.gov/exhibition/smallpox/sp_variolation.html The Nobel Prize in Physiology or Medicine 1945: Fleming, Chain and Florey. NobelPrize.org. https://www.nobelprize.org/prizes/medicine/1945/summary/ Aspirin: turn-of-the-century miracle drug. 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A Believer's Perspective Supported With Psychiatric Research Sabr (patience), shukr (gratitude) and Tawakal (reliance upon God) : three classical Arabic terms this essay argues can fill a real gap in how anxiety and depression are treated today Author: Qaisar J. Qayyum, MD Clinical Assistant Professor, Internal Medicine and Geriatric Medicine, USA. Chief Editor, Noor Journal of Complementary and Contemporary Medicine A moment of quiet focus, an outward stillness, could well be istighraq (استغراق), immersion, deep spiritual absorption. Pictured: Hazrat Mirza Masroor Ahmad, Khalifatul Masih V, the fifth Caliph of the Ahmadiyya Muslim Community. Photo credit: Makhzan-e-Tasaweer, https://makhzan.org/en/search/?q=2645938F Abstract Anxiety and depression are among the most common problems encountered in clinical practice. Their causes are multifactorial and may include biological vulnerability, medical illness, medications, social circumstances, loss, trauma, uncertainty, sleep disturbance, substance use, and maladaptive patterns of thought. Pharmacotherapy and psychotherapy remain currently established treatment options when clinically indicated. For a person of faith, however, religious concepts can provide an additional framework through which ordinary distress, uncertainty, disappointment, and loss are not merely endured, but actively understood and managed. This article examines three classical Islamic disciplines: sabr (patience, steadfastness, and perseverance), shukr (gratitude), and tawakkul (reliance upon God after appropriate effort). These concepts are considered alongside modern research on "intolerance of uncertainty", "delay discounting", gratitude interventions, cognitive restructuring, neuroplasticity, mindfulness, and habit formation. The central claim is not that anxiety simply represents insufficient sabr or that depression simply represents insufficient shukr. Psychiatric conditions are heterogeneous and multifactorial, and this article does not argue otherwise. The proposition is more focused: modern psychiatric evidence is frequently presented in ways that shape how readers interpret the findings, sometimes beyond what the underlying data themselves justify, and low-risk, non-pharmacological disciplines deserve to be considered early, rather than only after medication, in appropriate cases. Background This perspective grows from decades of clinical experience caring for patients with psychiatric symptoms in inpatient psychiatric settings, nursing homes, and general medical practice in the United States and the United Kingdom. Anxiety and depression occur across the lifespan. The circumstances differ, but the underlying human experiences of uncertainty, perceived loss, frustration, and disappointment are often remarkably similar. This article also draws on Friday sermons and video question-and-answer sessions of Hazrat Mirza Masroor Ahmad (aba), Fifth Caliph of the Ahmadiyya Muslim Community, broadcast on Muslim Television Ahmadiyya (MTA). The purpose is not to replace psychiatry, nor to reduce psychiatric illness to a spiritual deficiency. It is to ask whether a believer's framework of patience, gratitude, and reliance upon God can perform meaningful clinical work alongside established treatment and, in appropriate cases, before pharmacological treatment is introduced. The Central Hypothesis, Stated Plainly In this author's clinical experience, a recurring pattern emerges: patients whose habitual response to uncertainty is impatience, and who find it especially difficult to tolerate not knowing, often develop a persistent cycle of worry. When this pattern is repeated over time, it may become less a response to one particular stressor and more a habitual way of responding to uncertainty itself. This is not a claim that patience protects every person from anxiety, nor that someone who develops anxiety must therefore have lacked sabr. Sufficiently severe circumstances can overwhelm even a naturally patient person. The claim is narrower: habitual impatience and intolerance of uncertainty may represent one important pathway through which ordinary uncertainty becomes chronic anxious vulnerability. Depression, Attention, and Shukr Gratitude and Mental Health A parallel clinical pattern appears in depression. Patients whose attention becomes persistently fixed on what is missing, lost, disappointing, or unfair may develop a low mood that continues well beyond the original event. This is again offered first as a clinical observation, with the research literature providing supporting evidence. A systematic review and meta-analysis of "gratitude interventions" found measurable benefit across several mental-health outcomes, including anxiety and depressive symptoms [5]. Other meta-analyses report similar findings, although the average effect is generally modest, and gratitude should not be presented as a stand-alone cure for major depressive disorder [6,7]. Interventions incorporating spirituality, connection with God, forgiveness, and gratitude have also shown improvement in psychological outcomes in selected populations [8]. These findings do not demonstrate that depression is caused by ingratitude. Major depressive disorder is biologically, psychologically, and socially complex. Severe depression itself can impair a person's ability to experience pleasure, hope, or gratitude, which is one reason gratitude practice should not be presented as a primary treatment for severe or psychotic depression. The clinically useful point is more specific: deliberately directing attention toward what remains present can counter, to a measurable degree, the distressed mind's tendency to remain fixed on loss, deficiency, and threat. For a believer, this deliberate redirection of attention is shukr. Tawakkul, and the Idea Underneath Tawakkul: What Cannot Be Controlled Sabr applies most directly to something that must be endured or awaited. But much everyday anxiety is not simply waiting for a known outcome. It is worry about something that has not yet been decided at all: an unpaid bill next month, a biopsy result not yet available, an uncertain job offer, or the safety of a loved one. For this kind of uncertainty, the Qur'an offers another concept: tawakkul 'ala Allah, trust and reliance upon God. The Holy Qur'an teaches that whoever places trust in Allah will find Him sufficient and that Allah may provide from directions a person could not have anticipated (65:3-4) [58]. Tawakkul does not mean passivity. The same teaching assumes appropriate effort and recognition that everything has its proper measure. Reasonable action still matters. What tawakkul seeks to remove is something different: the exhausting habit of mentally replaying the same unresolved worry after every useful action has already been taken. Plan reasonably for what lies within your control. Then recognize where your control ends. One idea sits underneath all three disciplines. Health, relationships, career, and family life all require genuine effort, yet none is completely under human control. We act, but outcomes depend on many factors beyond us. This is why sabr and tawakkul make sense. The timing and outcome were never fully ours to command. It is also why shukr makes sense. Much of what we possess cannot honestly be credited to personal effort alone. The Three Tools, Introduced Together The Qur'an repeatedly presents patience and gratitude as companion disciplines rather than isolated remedies. Sabr addresses what must be endured or awaited. Shukr addresses what is already present but has become less visible because familiarity or disappointment has shifted attention elsewhere. Tawakkul addresses a third category: genuine uncertainty in which there is no fixed outcome to wait for and no specific loss to reinterpret. Will the biopsy be malignant? Will the job offer come? Will the child remain safe? All three act, in different ways, upon attention and habitual response. They train the mind to respond differently from the pattern that otherwise sustains worry, frustration, and dissatisfaction. Putting It Into Practice The moments when attention becomes idle deserve particular attention because these are often the moments when negative thought moves fastest to fill the space. After finishing a task, at a red light, before reaching for the phone, while waiting for an appointment, or while lying down to sleep, the mind often begins searching automatically for unfinished problems. These small openings can instead become deliberate cues for shukr. Not merely the word Alhamdulillah spoken reflexively, but the specific recognition behind it: Alhamdulillah that I walked here without assistance. Alhamdulillah that this person is still in my life. Alhamdulillah that although this problem remains, this particular part of it has improved. The Arabic phrase is the cue. Conscious recognition is the exercise. A simple example comes from the life of the Prophet Muhammad, peace be upon him ("sa" is the abbreviation traditionally used for this phrase in Islamic writing). Once, he found a piece of bread that had been sitting out. Rather than throwing it away, he cleaned it and ate it, then told his wife Hazrat A'ishah that one should honor that which is honorable. And when he drank water, he never gulped it down, he took it in three separate breaths, pausing to give thanks after each one [27]. His daily practices likewise turned ordinary activities such as eating, drinking, sleeping, waking, and dressing into occasions for remembrance and gratitude. The lesson is not merely about bread. It is that repeated blessings become easy to overlook precisely because they are repeated. The same structure applies to sabr. Instead of the automatic thought, Why has this not happened yet?, the trained response becomes: I have done what I reasonably can. The outcome has its own timing. My responsibility now is sabr. For genuinely uncertain outcomes, the response becomes tawakkul: I will do what is within my control and leave what is beyond it to Allah. This is not a technique of suppression. Psychologist Daniel Wegner's classic "thought-suppression" research demonstrated this: he told people not to think about a "white bear" for five minutes. Almost everyone found the white bear popping into their mind anyway, more than if they'd never been told to avoid it. His conclusion: telling yourself "don't think about X" tends to backfire. The instruction itself keeps bringing the thought back [47,48]. Sabr, shukr, and tawakkul operate differently. They do not simply command the mind to stop thinking. They give attention a different direction. That is why they should be practiced proactively, before distress appears, rather than only used as emergency tools after the anxious or negative thought has already taken hold. Because negative thought can arise throughout the day without deliberate effort, the counter-practice must eventually compete on the same terms. It cannot remain confined to isolated moments such as prayer time or meals. Faith Across Traditions The pairing of patience and gratitude is not unique to Islam. The Psalms teach patient waiting upon God and thanksgiving [16]. Jewish teaching asks who is truly rich and answers: the person who is content with what he already has [20]. The New Testament instructs believers to bring their requests to God together with thanksgiving, before the answer is known [17]. The Bhagavad Gita describes steadiness during pleasure and pain, together with contentment, as signs of spiritual maturity [18]. Buddhist teaching also treats patience as active strength and gives gratitude a central place in moral and contemplative life [19]. These traditions are not theologically identical, and they should not be treated as though they are. What is noteworthy is that different religious traditions, arising in different cultures and centuries, repeatedly identified similar disciplines for dealing with uncertainty, adversity, desire, and dissatisfaction. That convergence deserves attention. Modern Variables: The Chemical Shortcut Human beings naturally seek rapid relief from distress. That tendency can lead toward alcohol, cannabis, sedatives, or inappropriate use of prescription medication, essentially a chemical shortcut to a state that sabr, shukr, and tawakkul attempt to reach through a very different route. Some psychiatric medications carry genuine risks of physiological dependence and withdrawal. Others do not produce addiction in the conventional medical sense. Medication can be appropriate and, at times, lifesaving in moderate-to-severe psychiatric illness. The concern here is narrower: medication should not automatically substitute for understanding the psychological, social, medical, and spiritual circumstances contributing to a patient's distress. Benzodiazepines Benzodiazepines such as alprazolam and diazepam warrant particular caution. Long-term use can produce "tolerance" and "physiological dependence," and abrupt or overly rapid discontinuation may trigger withdrawal, including rebound anxiety and insomnia [9,10]. This is especially important when benzodiazepines are used chronically for insomnia. Tolerance to the sedative effect may develop while dependence makes discontinuation progressively more difficult [36-38]. Older adults are particularly vulnerable to cognitive impairment, falls, fractures, and sedation. Benzodiazepines also alter normal sleep architecture, including slow-wave sleep. Deep non-rapid-eye-movement sleep is closely linked with restorative brain physiology, including the "glymphatic system" [59]. On this basis, it is biologically reasonable to ask whether chronic disruption of normal deep sleep could adversely affect these processes over time. Direct long-term impairment of human glymphatic clearance from benzodiazepine use has not yet been established, but the question deserves further study. Hours of pharmacologically induced sedation should not automatically be assumed to be physiologically identical to hours of natural restorative sleep. Cannabis is also not psychiatrically neutral. Evidence linking cannabis exposure, particularly heavier use, to serious psychiatric harm is strongest for psychotic outcomes in susceptible individuals [13]. Clinical experience points to cannabis causing harm across a broader range of domains than the published literature currently captures, worsened anxiety, reduced motivation, impaired cognition, and disrupted mood among them, though the strength of published evidence for each of these specific harms varies. On the depression side, polypharmacy, the use of multiple medications at once, is closely associated with depression in older adults and may function both as a contributor to and consequence of poor health and depressive illness [11,12]. Evidence and Its Presentation How Numbers Get Framed Skepticism toward psychiatric evidence is not the same as rejecting science. The issue is more specific: data can be technically accurate while their presentation and framing still creates a misleading clinical impression. A treatment may reduce an outcome from 3% to 2%. That can be reported as a 33% "relative risk reduction." The statement is mathematically correct. The same result can also be reported as a 1% "absolute risk reduction." That is equally correct. Yet the two statements do not create the same impression. This is why the phrase the evidence shows should not end the discussion. It should begin it. The physician should still ask: What were the actual event rates? What was the absolute benefit? How many patients needed treatment for one additional patient to benefit? How many were harmed? Was the endpoint clinically meaningful to patients, or mainly a surrogate measure? How long did the study last? Who was included and who was excluded? Who funded the study? Were unfavorable studies equally likely to be published? Does the conclusion accurately reflect the magnitude of the underlying result? These questions are not an attack on evidence-based medicine. They are evidence-based medicine. The Serotonin Story The serotonin story is one of the clearest examples of why this distinction matters. For decades, depression was frequently explained to patients as low serotonin corrected by medication. Moncrieff and colleagues' umbrella review concluded that the evidence did not support a simple "serotonin-deficiency" model of depression [56]. Others challenged aspects of that interpretation and emphasized that the biology of depression and the clinical effectiveness of antidepressants are separate questions [57]. The important conclusion is that their effects cannot be adequately explained by the simple model of a serotonin deficiency being corrected by medication. That distinction matters because the simplified explanation was often framed with much greater certainty than the evidence justified. A related observation further complicates the picture: psychiatric drugs with very different, and in some cases apparently opposite, effects on serotonin regulation have demonstrated antidepressant effects. If treatments acting in substantially different chemical directions can produce similar clinical outcomes, the simple chemical-imbalance explanation was never sufficient. How much of an antidepressant's measured benefit reflects pharmacology and how much may be influenced by trial design remains debated. Because antidepressants often produce noticeable effects, some researchers have questioned whether participants can sometimes guess which treatment arm they are in. If so, imperfect "blinding" could theoretically influence measured benefit over placebo [62,63]. A Critical Voice From Within Psychiatry Dr. James Davies, a psychotherapist and academic, has examined the expansion of psychiatric diagnoses and the historical development of the DSM [21-23]. He has also discussed concerns surrounding confidentiality agreements during DSM development and objections raised by prominent figures such as Robert Spitzer. Financial relationships between DSM panel members and pharmaceutical companies have been independently documented in peer-reviewed research [60]. These findings do not prove that all psychiatric diagnoses are invalid . They do, however, justify careful scrutiny of how diagnostic boundaries are established and how social and economic distress may become medicalized. Davies' broader argument is that modern economic and social pressures generate real suffering, while the system can sometimes relocate that suffering into an individual biological model without adequately addressing the circumstances that produced it. Psychiatric prescribing has increased dramatically over recent decades while reported mental-health problems have not disappeared. That observation alone does not establish causation. It does, however, justify asking whether symptom control, without attention to underlying social, psychological, spiritual, and behavioral causes, is sufficient. None of this means the evidence base is worthless. It means that readers and prescribers should ask not only: Is this statement technically true? but also: What did the way it was presented lead me to believe, and do the underlying numbers support that impression? Antidepressants and Suicidality Regulatory review of randomized trials led to FDA warnings concerning increased suicidal thoughts and behavior among children and adolescents receiving antidepressants, with later warnings extending concern to young adults [31]. At the same time, untreated major depression is itself an important risk factor for suicide [32]. The lesson is not that antidepressants should never be used. It is that initiation and dose changes require thoughtful assessment and appropriate monitoring, particularly in younger patients and in anyone with suicidal ideation. For less severe depression, NICE guidance specifically states that antidepressants should not routinely be offered as first-line treatment unless this represents the informed preference of the patient. Nutritional Approaches: Omega-3 and Dark Chocolate Meta-analytic evidence suggests that omega-3 preparations with relatively higher "EPA:DHA ratio," including EPA-predominant formulations, may have antidepressant effects in some populations [39,40]. Dark chocolate and cocoa show a real, consistently reported mood benefit, an effect widely noticed outside the lab as well and worth taking seriously in its own right even as the formal evidence base continues to build [41-43]. The evidence is stronger and more mature for omega-3 fatty acids than for dark chocolate, but both are relevant to the broader discussion because they are food-based interventions with biological activity and relatively low treatment burden. The logical approach is to exhaust low-risk, side-effect-free options before reaching for medication carrying documented risks, including the antidepressant suicidality signal discussed above. This does not mean that every food is a treatment or that severe depression should be managed nutritionally. It means that the hierarchy of treatment should take into account not only efficacy, but also risk, tolerability, reversibility, nutritional value, patient preference, and the severity of illness. Clinical Safety Several safeguards remain non-negotiable and stand outside the rest of this discussion. Any patient expressing hopelessness must be assessed directly for suicidal or homicidal ideation. Asking clearly about abnormal thinking is not merely appropriate; it is essential in clinical practice. Immediate safety takes priority over every intervention discussed in this article. It is also important to state plainly that not every psychiatric presentation is anxiety or depression. People commonly group many forms of psychological distress under these labels, yet a range of other conditions, some far more serious and requiring urgent specialized care, fall outside this article's scope. Bipolar disorder is one example. It should be considered whenever depressive symptoms coexist with a history of "mania," an abnormally elevated, energized, impulsive, or reckless mood state, or "hypomania," a milder form of the same pattern. Antidepressant treatment can trigger mood switching in susceptible patients [44,45]. Schizophrenia, psychotic depression, and other major psychiatric illnesses fall outside the scope of this article in the same way and require specialized psychiatric evaluation. Medication review is particularly important in older adults, where polypharmacy and depression frequently coexist and interact [11,12]. Substance use should be actively screened. Medical causes of anxiety or depressive symptoms, including endocrine disease, neurologic disease, medication effects, sleep disorders, and pain, should be investigated where clinically appropriate. The practices described in this article, sabr, shukr, tawakkul, careful examination of evidence, and the preference for low-risk interventions where appropriate, all operate within this safety framework. None justifies delaying necessary assessment or treatment once serious illness is suspected. Take-Home Message When a patient presents with anxiety or low mood, the first task is to determine what is actually driving it: ordinary adjustment, a correctable medical or substance-related factor, a habitual way of responding to uncertainty, or a psychiatric disorder requiring specific treatment. Address what can be corrected. Where the wait itself is the problem, practice sabr. Where attention has become fixed on what is missing, practice shukr. Where the outcome is genuinely uncertain and reasonable effort has already been made, practice tawakkul. Where symptoms are severe, persistent, psychotic, manic, or suicidal, obtain psychiatric care without delay. Faith-based practice is not a substitute at that threshold. For everyday anxiety and low mood, this article draws on theological tradition together with a growing body of literature on "intolerance of uncertainty," gratitude, neuroplasticity, and habit formation to argue that these disciplines deserve to be considered early, before medication is automatically chosen. Faith and medicine are not competing here. They address different dimensions of the same suffering. For a believer, the practice carries an additional dimension: it may ease distress while simultaneously drawing the person closer to God. Scope of This Discussion This discussion concerns common symptoms of anxiety and low mood associated with everyday life stress, uncertainty, disappointment, and loss, particularly as encountered in primary care and general medical settings. Anxiety disorders are common in this setting. One large U.S. primary-care study found that approximately 19.5% of patients met criteria for at least one of four common anxiety disorders [33]. Depressive symptoms are similarly frequent [34]. An important distinction must be maintained throughout. Ordinary worry, adjustment-related distress, and everyday low mood are not simply milder forms of panic disorder, major depressive disorder with suicidal ideation, bipolar disorder, or schizophrenia. These conditions may share surface features, but they differ in diagnostic criteria, risk profile, biology, and treatment. This article adds one further specific point: under sufficient additional stress, sleep loss, bereavement, illness, the habitual impatience described earlier may contribute to an acute panic episode in some individuals. This is a claim about one possible contributing pathway, not a universal explanation for panic. Any patient with persistent, severe, recurrent, disabling, psychotic, manic, or suicidal symptoms requires formal psychiatric assessment, independent of the framework discussed here. This article does not attempt to treat bipolar disorder, schizophrenia-spectrum illness, severe or psychotic major depression, or any condition presenting with suicidal or homicidal ideation. Those conditions require professional psychiatric care without delay. A large genomic study found substantial shared genetic architecture between schizophrenia and bipolar disorder, while depression and anxiety show different patterns of genetic clustering [35], further supporting the distinction between major psychotic illness and the everyday distress addressed in this essay. Conclusion Habitual intolerance of uncertainty is probably not the sole cause of anxiety. Clinical observation, common sense, and a growing body of evidence nevertheless suggest that it can become an important root from which chronic anxious vulnerability develops, much as an occasional drink, repeated and unaddressed, can harden into alcoholism. Repeated patterns become easier to repeat. A mind that repeatedly responds to uncertainty with worry may gradually become more efficient at worrying. Sabr attempts to train that mechanism in the opposite direction. The same principle applies to shukr and tawakkul. Sabr addresses the wait for an outcome whose timing was never fully ours to control. Tawakkul addresses what remains outside our control after reasonable effort has been made. Shukr addresses what is already present in life but has become less visible because familiarity, disappointment, or loss has captured attention. These practices draw upon the same principle of neuroplasticity that underlies any form of habit development: repeated response strengthens future response. For a believer, however, they carry an additional meaning. They are not merely techniques of behavioral training. They are acts of worship. The Holy Qur'an describes sincere effort as capable of being multiplied far beyond its apparent scale, using the image of a grain producing seven ears, each carrying a hundred grains (2:262) [46]. For the believer, then, the practice is not only psychological. It is also spiritual. Robert Jastrow, an astrophysicist who directed NASA's Goddard Institute for Space Studies, wrote about this from an unusual position: he described himself as agnostic, not religious. Yet the physical evidence itself, not any theological argument, had led him to conclude the universe had a definite beginning rather than existing eternally, a conclusion he found personally unsettling. He described the scientist who spends a career climbing the mountain of ignorance through reason alone, only to reach the final peak and find theologians already there, waiting, as though they had known the answer for centuries [29]. For a scientist with no religious stake in the outcome, that was an uncomfortable place to land. For everyday anxiety and low mood, sabr, shukr, and tawakkul are offered here not as substitutes for necessary medical care, but as disciplines that deserve to be taken seriously and, in appropriate patients, tried early rather than relegated to the margins of treatment. Acknowledgment: This article was written with AI assistance. All claims are supported by credible, peer-reviewed references, which were validated for accuracy and authenticity. The AI synthesized information were reviewed by author, ensuring scientific integrity throughout. In the event of any inadvertent errors, the responsibility lies with the AI/authors, and corrections will be made promptly upon identification. I would like to express my sincere gratitude to Dr Tahira Khalid (USA) for her thoughtful review and invaluable feedback, Dr Ismaeel Mohammed (UK) for his valuable feedback. Their expertise and guidance have played a pivotal role in refining and enhancing this article. Conflict of Interest Statement: The author is the developer of a herbal formula and the owner of Dr. Q Formula/Insulinn LLC. However, this affiliation has not influenced the content, analysis, or conclusions of this article Author’s Note on Scope and Intent: This article does not advocate the replacement of evidence-based conventional care modalities. All complementary interventions are intended to supplement, not supplant, standard clinical practice, and are implemented within a physician-governed, ethically reviewed, and fully documented medical framework. References Probert-Lindström S, Perrin S. An examination of distress tolerance, anxiety sensitivity, and intolerance of uncertainty in adults in routine psychiatric care. Acta Psychologica. 2023;235:103902. https://doi.org/10.1016/j.actpsy.2023.103902 Laposa JM, Collimore KC, Hawley LL, Rector NA. Distress tolerance in OCD and anxiety disorders, and its relationship with anxiety sensitivity and intolerance of uncertainty. 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A response to Professor Tim Spector's Telegraph article A physician's response to a popular statin story Author: Qaisar J. Qayyum, MD Clinical Assistant Professor, Internal Medicine and Geriatric Medicine, USA. Chief Editor, Noor Journal of Complementary and Contemporary Medicine The illustration is a conceptual, non-literal representation intended to highlight the distinction between "not tested" and "tested and found absent," and does not depict any individual, institution, or organization. Popular science writing in the Telegraph wasn't written for a peer-review audience, and it doesn't need to be. This piece asks something different of you as a reader: every claim examined here, the study cited, the numbers quoted, the mechanism named, can be checked against its original source, and none of it requires taking anyone's word for it, including mine. What follows is that check, applied evenly, to a piece read by millions. I have a family history of coronary artery disease, and a personal one too. I still choose not to take statins. Every time I tried, my myalgias worsened, and some of that lingered at a moderate to severe level long after I stopped. Statins also carry a real risk of worsening insulin resistance, a serious concern for someone already managing diabetes.¹⁶ And the best-case return on that risk, even under ideal trial conditions, is small: out of 100 people followed for a year, about 1.36 would have a cardiovascular event without the drug, and 0.77, less than 1%, would have one if they take the drug.⁸ That's the real size of the benefit, half a percentage point a year, not the "1 in 30" figure Spector's article cites.¹ That's the actual trade I was weighing. When a Title Does the Talking The setting and presentation of his article caught our attention. I'm a physician myself, and being roughly his age, I've seen this pattern enough times over the years to recognize it immediately. None of what follows really surprised me. It's deceptive, and here's how. There's one trick worth naming first, because it shows up in every point below. A title works on a reader before a single fact does. Many readers already know Spector holds the title "Professor," from his TV appearances or the ZOE nutrition app he co-founded, before they even open this article. Then, inside the piece itself, he adds a second title: "NHS rheumatologist." That title is from more than thirty years ago. He hasn't practiced under it since 1992, when he moved into genetic epidemiology full time. Used here, decades later, it sounds like a clinician still seeing patients. Even if he were still active as a rheumatologist, that specialty was never expected to manage high cholesterol or statin therapy in the first place. It was never their territory, even back when he was active. By the time the real claim shows up, muscle pain, the nocebo effect, the "44 percent," most readers have already decided to believe it. Not because of the evidence. Because of who's talking. It's interesting how casually he leans on this, knowing full well it has nothing to do with the actual clinical question, while counting on readers walking away thinking they've heard from an experienced, practicing clinician. That's the trick worth spotting, not just here, but anywhere. Set the title aside first. Then look at what's actually being claimed. I did an HIV fellowship in 1994, and an infectious disease fellowship in 1998. I could flash my badge as an HIV expert and an infectious disease expert too. I won't. I haven't practiced either field in decades, and calling myself an expert now would mislead you. What I actually bring is decades of internal and geriatric medicine experience in UK and USA, and twenty years of my personal experience with statins. That's the disclaimer his sentence is missing. One: two symptoms, easily confused, rarely explained Professor Spector never uses the proper term myalgia anywhere in his article. He writes "muscle pains" and "muscle cramps" instead, using these terms to describe the same thing. But myalgia, not cramps, is what statins are generally known for and are the symptom patients are warned about. One major medical group that studies this even lists muscle cramps under myalgia, but only cramps tied to exercise. Nocturnal cramping, the kind that wakes someone up at night, exactly what Spector describes, is specifically carved out of that definition.²¹ This isn't a small mix-up. It's the same kind of mistake as confusing a sprained ankle with arthritis in that ankle because both are ankle pain, or chest wall pain with chest pain from the heart, because both come from the chest. Same general area, completely different condition. He's a trained physician. A doctor with that training knows, or should know, the difference. So the real question is simple: why blur it? Two: when the obvious explanation gets passed over In his own words: he already had occasional cramps before starting the statin. Two weeks in, they got worse. He stopped the drug. The cramps kept happening anyway. His own timeline answers the question by itself: the drug wasn't the cause. He didn't need any warning to explain what happened to him, he already had these cramps long before he ever touched a statin. There was nothing here to be alarmed about, just an old, pre-existing symptom, temporarily worse, then back to normal. That old symptom settled down on its own, and improved further once he started taking vitamin K2, the way ordinary cramps respond to a real, tested remedy.¹¹ Instead of accepting that simple explanation, he reaches for something else entirely. Three: misquoting a study to dismiss a symptom it never checked. Here's his exact claim: "62 side effects, including muscle pains, were reported by people taking the dummy pills," just as often as by people on the actual drug.¹ That's the claim this section checks. He cites a February 2026 Lancet paper as proof. That study tested 66 side effects. Only 4 were real. Got news for you: muscle pain wasn't one of the 66. The study's own chart proves it. Black circles mean tested and found real. Grey circles mean tested and found nothing. White circles mean excluded from testing entirely.² Muscle pain is marked with a white circle. Why did the study exclude it? Because the same team had already studied muscle pain on its own, back in 2022, and found something real: a small but genuine rise in muscle pain and weakness in the first year on the drug, roughly one extra case per hundred patients, with no added risk after that.³ Spector isn't the only one who ran with this without digging into what it actually excluded. A press release covering the same study, from the University of Oxford, went out under the headline "Massive study finds most statin side effects aren't caused by the drugs," published February 15, 2026.⁴ Read carefully, that headline is just as sweeping, and just as wrong about muscle pain specifically, as his own summary of it. This is disappointing to see from a professor at King's College London and a career researcher. A white circle instead of a grey one, with the study's own caption spelling out the difference, is about as clear a signal as a paper can give that something wasn't tested, not tested and cleared. Turning a clear non-finding into a stated finding, and telling millions of readers their muscle pain has been checked and cleared, isn't the kind of mistake a career built on reading data should make. Four: the nocebo effect misrepresented Mixing up two symptoms is not a mistake you'd expect from a clinician. And it's disappointing to watch how a researcher stretched a real scientific term until it fits whatever presentation he happens to have, instead of checking if it actually applies. He writes: "It's known as the 'nocebo effect'... I was so convinced that I would suffer from muscle cramps, that it happened."¹ That's the claim this section checks. Nocebo means a negative expectation can produce a real symptom, even though the drug itself isn't the cause. Myalgia, not cramps, is what statins are generally known for and what that kind of expectation would actually be built around. He already had those cramps before he ever touched the drug. That's an old symptom, flaring and fading the way it always had. Nothing needed to plant an expectation in his mind, because the symptom was already there, waiting to flare up again on its own. It's like someone with an old, occasional knee ache starting a new supplement, then feeling that same ache on a damp, rainy day, the way it always has, and blaming the supplement instead of the weather. They got worse, then settled down on their own. That's not nocebo. Suppose, for the sake of argument, we call it nocebo anyway. It still has nothing to do with the statin. He had these cramps before he ever started the drug, so whatever caused them the first time is still the most likely explanation for why they came back. And suppose we go further still, and grant that this really is what happened to him. Even then, one person's experience doesn't generalize. It doesn't tell us anything about what causes muscle symptoms in other patients on statins. Five: "Rubbish"? A rubbish claim Professor Spector writes: "Not only did the majority of the worries about statin side effects turn out to be rubbish, I saw first-hand how they can actually benefit your health."¹ A sweeping claim. No source attached. Just a statement expected to be believed because he holds a medical title. A few months of personal experience, dressed up as a life-changing verdict on a drug he's recommending people take for the rest of their lives. Here's the problem with "rubbish." The very same 2026 study he cites elsewhere in his article, the one he treats as clearing statins of most side effects, states plainly, in its own words: statins cause a real, dose-related rise in new diabetes, especially in people whose blood sugar is already borderline.² That's not a small footnote. For a diabetic patient, it's a real, documented cost. And it comes from the same paper he's using to call patient concerns "rubbish." Six: inventing a standard no major guideline recognizes. He writes: "My inflammation levels, measured by a high-sensitivity C-reactive protein (hs-CRP) test, have fallen by 40 per cent since I started the drug."¹ He treats that as personal proof the statin is working. Maybe. But if it really worked that way, why haven't guidelines caught up to this? The link between CRP and cardiovascular outcomes is real and well-studied.¹²,¹³ No major guideline, American or European, recommends routine CRP retesting to judge whether a statin is working. The concept has been floated as a hypothesis in cardiology literature, based on post-hoc trial data, but even guideline authors have called the evidence too thin to turn it into an actual recommendation.⁵ The most current joint guideline from the American College of Cardiology and American Heart Association calls for a lipid panel 4 to 12 weeks after starting or adjusting therapy, then every 6 to 12 months after that.⁵ CRP doesn't appear anywhere in that follow-up schedule. Seven: the illusion in the numbers He says statins prevent "one major cardiovascular event in every 30 people." He doesn't name a trial. The number most closely matches JUPITER, the landmark trial for rosuvastatin 20mg, the exact drug and dose he says he takes.⁸ It's likely where the figure comes from, though he never says so directly. There are many kinds of numbers used in medicine, but the two that matter most here are relative and absolute. A relative number tells you how two groups compare to each other. An absolute number tells you what actually happens to you. Behind his "1 in 30" claim sits a 44 percent relative risk reduction, the actual figure from JUPITER. On its own, that number means nothing to you personally. Now the absolute number, the one that actually matters. JUPITER found: 1.36% of people on placebo had an event in a single year. 0.77% of people on the drug did, that same year. That's the real difference, per year: about half a percent. That is the actual arithmetic behind the trial he's likely drawing from. Let's look at the bigger picture, over a longer stretch of time. For people without existing heart disease, the typical benefit added up over five full years of taking the drug is closer to just 1-2%, sometimes less.¹⁷,¹⁸,¹⁹ Spread evenly across five years, that works out to somewhere around 0.2 to 0.4 percent per year, even smaller than the JUPITER figure above. For people at the lowest risk, one summary of the research found no statistically significant reduction in death at all, based on a meta-analysis of 22 trials and over 130,000 patients.²⁰ One must remember this difference. Relative number: sounds big, tells you nothing about your own odds. Absolute number: sounds small, tells you the truth. Every time a headline quotes a percentage, ask which one you're looking at. Eight: the evidence that got left out Professor Spector writes: "there are signs that, by lowering inflammation in our gut, statins are changing the composition of the microbes that live in our intestines."¹ No study named, no citation. The most likely research behind that claim is a study comparing statin users to non-users, and that study's own lead researcher said on the record: "this study design does not allow inferring causality."¹⁰ Meanwhile, actual lab studies looking for cause and effect point the other way. One found statins harm gut bacteria health through a specific biological pathway in murine model.¹⁴ Another found statins can cause "leaky gut" and disrupt blood sugar control.¹⁵ A third found statins can worsen insulin resistance through changes in gut bacteria.¹⁶ For someone with diabetes, that's the opposite of good news. His dementia and antidepressant claims get an honest caveat in his own words: "while not concrete yet, are very promising."¹ The gut microbiome claim gets no such caution, even though it deserves the same one. Nine: "Trust me, I'm a doctor." By this point, he's already misapplied a study, redefined a scientific term to fit his own symptom, and called patient concerns "rubbish" with nothing to back it up. His closing line is where all of that gets cashed in. It doesn't sound like evidence, because it isn't. His closing line: "It's all so encouraging that I've decided to stay on statins, I've been taking them since last February, with just a few months' break when I thought they were behind my muscle cramps, and monitor my progress as time goes on."¹ Strip away the impressive titles, and here's what that sentence really says: "I've been on this pill a few months, minus a break, and I feel good about it." One person's experience, presented as a success story for readers to follow. Not a study. Not even a group. That's not a conclusion. That's a guess wearing a lab coat. Ten: right study, wrong symptom He never names a trial for his vitamin K2 claim. Here's his full quote: "While there's really no magic treatment for them, I've found that vitamin K2 helps... it is the best studied in a clinical trial for easing muscle pain."¹ Searching for the actual research behind that claim turns up one clear match: a study specifically about nighttime leg cramps in older adults, not muscle pain.¹¹ The trial tested cramps. His own words say muscle pain. That's not what it tested. Two Truths Left Out Two real, physical explanations for statin muscle pain exist, and neither one made it into his article. The first is a mechanism, not just a statistic. In January 2026, Columbia scientists watched it happen at the molecular level: a statin physically forcing open a channel in muscle cells, causing damage over time.⁹ Not a survey response. An actual photograph of the process happening. The second is a diagnosis. There's a rare disease where the body's immune system attacks its own muscle after a statin, confirmed by blood test, sometimes biopsy.⁶,⁷ Unlike ordinary muscle aches, it often doesn't go away when the drug stops. Both are rare. Both are real. And both are exactly what "it's probably just in your head" misses. None of this is an argument against the drug. It's an argument for reading the actual research yourself, before trusting a headline. A Responsible Telegraph We're not asking the Telegraph to retract this piece in its entirety. Much of it is personal experience and framing, not something a correction process exists for. But one specific claim in it is factually false in a way that's easy to check and hard to defend: the article states that a large 2026 study found muscle pain occurred no more often on statins than on placebo. The study's own chart says otherwise, muscle pain wasn't tested in that comparison at all, marked with a different symbol than every outcome the study actually assessed, with the paper's own caption explaining why. That's not a matter of interpretation. It's a factual misstatement of what a cited study found, the kind of error most reputable outlets correct once it's brought to their attention. We'd encourage the Telegraph to issue a correction making this plain to the readers who saw the original claim: the study did not clear statin-associated muscle pain. It excluded it from testing entirely, because the same research group had already found a real, if small, effect in earlier work. Readers deserve to know that distinction as clearly as they were told the opposite. Acknowledgment: This article was written with AI assistance. All claims are supported by credible, peer-reviewed references, which were validated for accuracy and authenticity. The AI synthesized information were reviewed by author, ensuring scientific integrity throughout. In the event of any inadvertent errors, the responsibility lies with the AI/authors, and corrections will be made promptly upon identification. I would like to express my sincere gratitude to Dr Tahira Khalid (USA) for her thoughtful review and invaluable feedback, Dr Amir Malik MD. FACS (USA) for his valuable feedback and Dr Ghafoor Manan (UK). Their expertise and guidance have played a pivotal role in refining and enhancing this article. Conflict of Interest Statement: The author is the developer of a herbal formula and the owner of Dr. Q Formula/Insulinn LLC. However, this affiliation has not influenced the content, analysis, or conclusions of this article Author’s Note on Scope and Intent: This article does not advocate the replacement of evidence-based conventional care modalities. All complementary interventions are intended to supplement, not supplant, standard clinical practice, and are implemented within a physician-governed, ethically reviewed, and fully documented medical framework. References Spector T. Why I'm taking statins after avoiding them for nearly a decade. The Telegraph. July 7, 2026. https://www.telegraph.co.uk/health-fitness/diet/nutrition/tim-spector-statins-sceptic-now-convert/ Cholesterol Treatment Trialists' (CTT) Collaboration (Reith C, et al.). Assessment of adverse effects attributed to statin therapy in product labels. Lancet. 2026;407(10529):689-703. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(25)01578-8/fulltext Reith C, Baigent C, Blackwell L, et al. Effect of statin therapy on muscle symptoms. Lancet. 2022;400(10355):832-845. https://pmc.ncbi.nlm.nih.gov/articles/PMC7613583/ University of Oxford. Massive study finds most statin side effects aren't caused by the drugs. ScienceDaily. 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Lancet. 2010;376(9753):1670-1681. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)61350-5/fulltext Extent of Low-density Lipoprotein Cholesterol Reduction and All-cause and Cardiovascular Mortality Benefit: A Systematic Review and Meta-analysis. PMC. https://pmc.ncbi.nlm.nih.gov/articles/PMC9812424/ Personalized absolute benefit of statin treatment for primary or secondary prevention of vascular disease in individual elderly patients. PMC. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5226996/ Statins in Persons at Low Risk of Cardiovascular Disease. TheNNT. https://thennt.com/nnt/statins-persons-low-risk-cardiovascular-disease/ Rosenson RS, Baker SK, Jacobson TA, Kopecky SL, Parker BA; The National Lipid Association's Muscle Safety Expert Panel. An assessment by the Statin Muscle Safety Task Force: 2014 update. J Clin Lipidol. 2014;8(3 Suppl):S58-S71. https://pubmed.ncbi.nlm.nih.gov/24793443/

Subtitle: When the Machine Tells Half the Truth: How Clinical AI Inherited Pharma's Statistical Deception and Why It Matters at the Bedside Author: Qaisar J. Qayyum, MD Clinical Assistant Professor, Internal Medicine and Geriatric Medicine. Chief Editor, Noor Journal of Complementary and Contemporary Medicine The same data. Relative risk reduction shows 50%. Absolute risk reduction shows reduction from 2% to 1%. One in 100 patients benefits. Which number should patients see first? Abstract Clinical artificial intelligence tools are increasingly embedded in physician workflows as point-of-care decision support resources. A critical and underexamined problem has emerged: these tools routinely present efficacy data using relative risk reduction (RRR) as the primary, and often sole, metric, without accompanying absolute risk reduction (ARR) or natural frequency equivalents. This framing convention, long documented in pharmaceutical marketing literature as a systematic driver of prescribing inflation, now risks institutionalization within AI-generated clinical guidance. Using long-term antiplatelet therapy in chronic atherosclerotic cardiovascular disease (ASCVD) as an anchor case study, and a comparative analysis of UpToDate Expert AI and Open Evidence platforms, this article documents the pattern, quantifies its distorting effect, and offers both a conceptual critique and a practical bedside framework for clinicians navigating AI-assisted decision-making. The patient, not an abstraction, is the one who pays the price. Keywords: relative risk reduction, absolute risk reduction, natural frequency, clinical AI, antiplatelet therapy, ASCVD, evidence-based medicine, statistical framing, physician decision support, guideline reflexivity 1. Introduction The promise of clinical artificial intelligence is significant: rapid synthesis of complex evidence, reduction of cognitive load at the point of care, and democratization of specialist-level knowledge across clinical settings. Tools such as UpToDate Expert AI and emerging large language model-based clinical assistants are now routinely consulted by physicians during active patient encounters, often functioning as the final, and unquestioned, reference before a prescribing decision is made. Yet the quality of a clinical AI response is not determined solely by the accuracy of its source data. It is equally determined by how that data is framed. A response that is mathematically and technically correct but clinically misleading is not a neutral tool, it is a vector for systematic bias in clinical decision-making, operating at the scale of every physician who queries it. The problem this article addresses is not new to medicine. For decades, pharmaceutical industry communications have preferentially reported efficacy in terms of relative risk reduction, a metric that consistently inflates the perceived benefit of an intervention without technically misrepresenting the data. What is new, and deeply concerning, is that this same framing convention now appears to have been adopted, whether by design or by default, by clinical AI platforms that physicians increasingly trust as objective arbiters of evidence. Unlike a pharmaceutical sales representative or a journal advertisement, a clinical AI tool carries no visible commercial affiliation. It occupies the epistemic space of a trusted, disinterested consultant. This makes its framing choices more consequential than those of industry, and raises the standard of transparency to which such tools must be held. 2. Background: The Framing Problem in Evidence-Based Medicine 2.1 Relative Versus Absolute Risk — Not the Same Claim When a therapy reduces a clinical outcome from 10% to 8%, three mathematically valid statements can be made simultaneously: The therapy produces a 20% relative risk reduction (2 ÷ 10 = 20%) The therapy produces a 2% absolute risk reduction (10% − 8% = 2%) Out of every 1,000 patients treated, 20 fewer will experience the outcome — meaning 980 patients take the medication daily, bear its risks and costs, and derive no event-level benefit Each statement describes identical data. Only the third makes the clinical reality immediately and intuitively visible, to the physician, and to the patient sitting across the desk. The relative risk figure invites the inference that nearly 1 in 5 patients is meaningfully protected. The absolute and natural frequency figures force the clinician to ask: is treating 1,000 patients to protect 20 worth the cumulative cost, side effect burden, and risk of harm to the remaining 980? This is the essence of individualized, patient-centered evidence-based medicine. Relative risk framing skips this question entirely. 2.2 A Well-Documented Problem — Now Migrating Into AI The preferential use of RRR in clinical communications has been extensively documented and criticized. Bucher, Weinbacher, and Gyr demonstrated in a seminal 1994 BMJ study that physicians shown RRR alone rated treatments as significantly more effective and expressed higher prescribing intent than those shown absolute numbers for identical underlying data.¹ Nuovo, Melnikow, and Chang, reviewing major journals over a decade, found that absolute risk figures were explicitly reported in only a minority of randomized controlled trial publications despite repeated formal calls for improvement.² Gerd Gigerenzer, German psychologist, director of the Harding Center for Risk Literacy, and named by Switzerland's Duttweiler Institute as one of the hundred most influential thinkers in the world, spent decades demonstrating that collective statistical illiteracy is widespread not only among patients but among physicians, judges, and policymakers, and that the remedy is not better math education but better data presentation.³ His term for the solution was simple: natural frequencies, telling people that 20 out of 1,000 patients benefit, not that there is a "20% reduction." What has not been adequately examined is the migration of this framing problem into clinical AI platforms, tools that occupy a position of perceived objectivity and are consulted precisely because clinicians trust them to present evidence free of commercial bias. 3. Case Study: Antiplatelet Therapy in Chronic ASCVD 3.1 The Query A direct clinical query was submitted to UpToDate Expert AI regarding the rationale for long-term antiplatelet therapy in chronic atherosclerotic cardiovascular disease, in the context of secondary prevention. 3.2 The Initial AI Responses UpToDate Expert AI responded with this headline claim: "Antiplatelet therapy reduces subsequent vascular events by about 22% across high-risk patients with established cardiovascular disease." This figure, drawn from the landmark Antithrombotic Trialists' Collaboration (ATC) meta-analysis⁴, is the relative odds reduction. It was presented without qualification, without the corresponding absolute risk reduction, and without natural frequency equivalents. The control-group event rate, the denominator that gives the 22% figure its entire clinical meaning, was absent. Open Evidence responded differently but with the same fundamental problem. It opened with guideline recommendations rather than primary evidence, led with the same relative risk figure ("~20% reduction in nonfatal MI and cardiovascular mortality"), and required escalation to produce absolute numbers. 3.3 Escalating the Challenge: How Many Questions to Get Complete Data? Only after additional direct challenges, first requesting absolute numbers, then explicitly demanding control-group event rates, did either tool produce the underlying data. This is a critical finding in itself: a busy clinician who accepts a first-response AI summary walks away with a relative risk figure and no basis for patient-level benefit-risk calculation. The complete picture, drawn from the ATC source data both tools cited, is presented in Table 1. Table 1. Effect of Antiplatelet Therapy on Vascular Events (Antithrombotic Trialists' Collaboration; reproduced in UpToDate, 2026) Patient Category Control Event Rate Antiplatelet Event Rate Absolute Difference Patients Helped per 1,000 Treated Odds Reduction All trials (high/low risk) 13.2% 10.7% 2.5% 25 per 1,000 22±2% Prior MI 17.0% 13.5% 3.5% 35 per 1,000 25±4% Prior stroke / TIA 21.4% 17.8% 3.6% 36 per 1,000 22±4% Stable angina / CAD 14.1% 9.9% 4.2% 42 per 1,000 33±9% Unstable angina 13.3% 8.0% 5.3% 53 per 1,000 46±7% Peripheral arterial disease 7.1% 5.8% 1.3% 13 per 1,000 23±8% Primary prevention (low risk) 4.9% 4.5% 0.4% 4 per 1,000 10% Treatment duration 2 years for most subgroups. "Patients helped per 1,000 treated" calculated by the AI from ATC source data. 3.4 What the Full Data Reveals — In Human Terms Across all trials, the "22% odds reduction" resolves to an absolute benefit of 25 per 1,000 treated over 2 years. In stable angina/CAD, the most common chronic ASCVD phenotype encountered in outpatient practice, the absolute benefit is 42 patients protected per 1,000 treated over two years, which is clinically meaningful but requires careful contextualization against individual bleeding risk. In peripheral arterial disease, the odds reduction of 23% sounds comparable to other subgroups, but the absolute benefit of 13 per 1,000 tells a very different story about the magnitude of benefit. Most strikingly, in primary prevention, a population in which aspirin prescribing was common for decades, the 10% odds reduction resolves to an absolute benefit of just 4 per 1,000 treated over two years. This is the same dataset that has appropriately driven major guideline revisions away from routine aspirin in primary prevention. The absolute benefit of 4 per 1,000 is not visible in the relative risk figure. It is only visible when the full data is presented. 3.5 A Note on Methodology: This Was a Clinic Query, Not a Literature Search This interaction with the AI tool was conducted the way a practicing physician asks a clinical question: directly, under time pressure, expecting a complete and clinically actionable answer on the first response. A busy clinician between patients does not submit a multi-part methodologically refined query. They ask a straightforward clinical question and act on what comes back from a trusted source which is specifically developed for physicians. What came back was a relative risk figure, presented confidently without qualification. It took more than one rounds of escalating follow-up questions, each requiring additional time and statistical sophistication that most clinicians will not invest during an active clinic session, before the complete picture emerged. The methodology was limited by design, because the patient's physician will be too. 3.6 A Second Data Point: Open Evidence The identical query was submitted to Open Evidence, a separate AI-powered clinical decision support tool drawing on peer-reviewed literature and major society guidelines. Open Evidence performed one round better than UpToDate, producing absolute numbers on the second ask rather than the third, and explicitly included harm data that UpToDate required escalation to produce: "aspirin prevents approximately 15 serious vascular events per 1,000 patient-years at the cost of approximately 0.3 additional major bleeds per 1,000 patient-years." On these measures, Open Evidence demonstrated better statistical transparency. However, both tools failed the test that matters most: the first response test. Both led with relative risk figures without qualification, requiring escalation to produce complete data. Neither tool offered natural frequencies unprompted. The second failure was unique to Open Evidence: rather than leading with quantitative evidence, the platform led with guideline architecture — Class I recommendations, Level A designations, DAPT duration algorithms, and consensus statements — while absolute risk figures were absent from the opening response entirely. Guidelines have a legitimate role, but the physician did not ask what guidelines recommend. The physician asked what the evidence shows. These are not the same question. 4. Why This Pattern Exists and Why It Matters 4.1 The Illusion of Objectivity — AI's Most Dangerous Quality There is a reason pharmaceutical sales representatives no longer have unfettered access to physician offices. Decades of research confirmed what clinicians already suspected: industry-sponsored communications, however accurate in their data, are shaped by commercial intent. Physicians know this. They expect it. They have learned to read a drug company's numbers with appropriate skepticism. Clinical AI arrives differently. It carries no brand logo, no sales quota, no free lunch. It speaks in the language of citations, meta-analyses, and evidence hierarchies. To the physician consulting it between patients, it feels less like a resource and more like a revelation, the most advanced, most current, most comprehensive way to access scientific truth available at the point of care. That is its appeal. That is also its danger, because that trust is not fully earned. AI does not write its own rules. It does not choose its own framing. Every default, every presentation hierarchy, every decision about which number appears first and which gets buried in follow-up questions deep, these are human choices, embedded in the system's design and training data. When an AI tool consistently leads with relative risk reduction and omits absolute numbers, that is not a neutral algorithmic output. That is a design choice. Someone decided, or failed to decide otherwise, and the system executes that choice millions of times a day, in clinics around the world, with the full authority of something physicians have been told represents the future of evidence-based medicine. This is not conspiracy. But it is not innocent either. Bias embedded in training data and default outputs is still bias, it simply operates at a scale and with a credibility that no pharmaceutical sales representative could ever achieve. A drug company advertisement that cherry-picks statistics is immediately recognizable for what it is. Clinical AI presenting the same cherry-picked statistic is received as scientific truth. The number is identical. The trust is not. Physicians are not consulting a salesperson. They believe they are consulting science itself. That belief is exactly what is being exploited, whether anyone intended it or not is open for debate. 4.2 Statistical Framing Is Not a Style Choice — It Is a Decision Architecture Framing is not a presentation preference. It is a decision architecture with predictable, directional consequences. Decades of behavioral economics and medical decision-making research confirm that the same underlying data presented as relative versus absolute figures produces measurably different prescribing intentions in physicians, even experienced ones. The framing effect is not a product of physician naivety, it is a robust cognitive phenomenon that operates independently of clinical expertise or statistical training. When a clinical AI tool defaults to relative risk reduction, it is not being neutral. It is making a framing choice with a predictable directional effect: toward prescribing, toward intervention, toward the treatment arm. The patient who experiences a preventable drug-related harm because their physician's risk perception was shaped by an incomplete number is the one who ultimately absorbs the cost of that framing choice. 4.3 Institutional Inertia and the Training Data Problem It is worth acknowledging that relative risk-first framing in clinical summaries predates AI. It appears throughout human-authored clinical reference content, in FDA drug labeling summaries, in cardiology society guideline summaries, and in the abstracts of landmark clinical trials themselves. Clinical AI tools trained on or summarizing this literature will naturally inherit its framing conventions. This does not excuse the practice. It explains its persistence, and it underscores why explicit corrective standards must be externally imposed rather than assumed to emerge organically from the technology. A system trained on biased inputs does not self-correct. It scales the bias. 4.4 Why Guidelines Are Not the Answer: Conflicts, Commerce, and the Illusion of Universal Truth When clinical AI defaults to guideline recommendations instead of primary evidence, it is not retreating to safer ground. It is retreating to ground that is compromised in ways most physicians have never been required to examine closely. Guidelines Are Not Universal — They Were Never Designed to Be A guideline written in the United States reflects the disease burden, health system economics, payer structures, and patient demographics of the United States. Applied globally without adaptation, it can actively harm patients whose baseline risk profile is fundamentally different. The aspirin primary prevention story is again instructive. A direct comparison of US guidelines applied to the Japanese population found that the incidence of coronary heart disease in middle-aged Japanese men is nearly four times lower than in American men, while the rate of hemorrhagic stroke is three times higher, meaning the recommended risk threshold for Japanese patients would need to be two to five times higher than the American threshold to achieve the same benefit-to-harm ratio.⁹ The same guideline that protects an American patient could harm a Japanese one. A global modeling study examining statin prescribing thresholds across 186 countries found that a single CVD risk threshold, the kind embedded in international guidelines, is not appropriate across different populations, with optimal thresholds varying substantially by country, age, sex, and local disease burden.¹⁰ Multiple Guidelines, Same Disease, Different Answers For virtually every major clinical question in cardiovascular medicine, multiple organizations produce competing recommendations that differ in their thresholds, their drug preferences, and their risk calculations. A direct comparison of statin eligibility for primary prevention under 2021 European Society of Cardiology guidelines versus ACC/AHA and NICE guidelines found substantial differences in which patients qualified for treatment, meaning the same patient might or might not receive a statin depending solely on which guideline their physician consulted.¹¹ The Money Behind the Guidelines The conflict of interest problem in guideline development is extensively documented and inadequately resolved. A systematic analysis of European Society of Cardiology guidelines across five major cardiovascular conditions found that up to 64% of studies used to support guideline recommendations were either fully or partially funded by the pharmaceutical industry.¹² The ACC/AHA guidelines have faced similar scrutiny, the 2013 cholesterol guidelines, which dramatically expanded the target population for statin therapy, were criticized at publication for the prevalence of financial relationships between committee members and pharmaceutical companies with direct commercial interests in the recommendations.¹³ A prominent panel of physicians and researchers concluded that medical societies' reliance on industry funds "inevitably creates the perception of and reality of conflicts of interest and jeopardizes public trust", recommending that professional associations aim for zero industry funding for guideline-writing activities and appoint only conflict-free physicians to guideline committees.¹⁴ The Regulator Is Not Independent Either The deepest layer of this problem reaches the regulatory agency that approves the drugs that guidelines recommend. The US Food and Drug Administration, the world's most influential drug regulatory body, had pharmaceutical industry user fees account for 66% of the human drugs program budget in fiscal year 2022, meaning two thirds of the budget of the agency responsible for determining which drugs are safe and effective came directly from the companies seeking that determination.¹⁵ By fiscal year 2026, industry user fees account for nearly 51% of the FDA's total program budget.¹⁶ A systematic review found that public speakers at FDA advisory committee hearings with disclosed conflicts of interest were between three and six times more likely to deliver testimony favorable to industry products compared to speakers without conflicts.¹⁷ What This Means for Clinical AI A clinical AI tool that responds to evidence questions with guideline recommendations is not giving the physician a shortcut to truth. It is presenting the output of a system shaped, at multiple levels, by documented financial relationships, as if it were neutral scientific consensus. The primary evidence, the actual trial numbers, the absolute event rates, the natural frequencies that show how many patients benefit and how many are harmed — exists independently of these influences. It is available. It is citable. It is what physicians need at the bedside. Primary evidence is not without its own limitations: publication bias exists, industry-sponsored trials carry their own conflicts, and absolute risk figures are reported in fewer than one in ten published studies. But imperfect primary evidence, read critically, remains a more reliable compass than guidelines shaped by the consensus of committees whose independence is structurally compromised. This is not an argument against guidelines. In areas where robust trial data is absent, guidelines represent the best available synthesis of expert consensus, and in medico-legal contexts, they remain the defensible standard of care. The argument is narrower: when primary evidence exists and is accessible, it should be what clinical AI offers first. We have learned to be cautious of processed food, stripped of nutrients, optimized for palatability, and shaped by commercial interests rather than health. Processed evidence is no different. 5. How to Combat the AI Algorithm: A Practical Framework for Clinicians The solution is not to stop using clinical AI. The solution is to use it the way a skilled clinician uses any imperfect tool: with informed skepticism. By the time a physician consults a clinical AI, they have already survived medical school, residency, and years of practice navigating pharmaceutical representatives, sponsored continuing medical education, and guideline committees whose independence is, as documented above, structurally compromised. This is the same skepticism, applied to a new kind of representative. Because that is what an AI tool becomes when it reports benefit without harm, leads with relative risk, and answers evidence questions with guideline recommendations: a pharmaceutical representative with no badge, no disclosed conflicts, and the credibility of science itself. The physician who recognizes this is already most of the way there. The three questions below complete the journey. Question 1: Freedom From Spoon Feeding — Is This a Relative or Absolute Number? Any percentage reduction stated without a baseline event rate is mathematically valid but clinically incomplete. The single diagnostic question is: "Reduced from what to what, and for how many patients in how much time?" Demand actual numbers from the actual data. In the ATC meta-analysis documented in this article, the headline "33% odds reduction" in stable CAD resolves to 42 patients protected out of every 1,000 treated over two years.⁴ The headline "10% odds reduction" in primary prevention resolves to just 4 patients protected out of every 1,000 treated over two years.⁴ Same confident language. Tenfold difference in absolute benefit. Only the actual numbers reveal the distinction. If the AI cannot provide this in its first response, the response is incomplete. We must keep in the back of our minds that under the trusting name of AI, there could be a hidden pharma rep. If a pharmaceutical sales representative had just told you the same thing your AI told you, in the same language, with the same numbers, would you prescribe on that basis alone? If the answer is no, do not prescribe on the AI's basis alone either. Question 2: Keep It Simple — Who Benefits and Who Is Harmed, Out of How Many? An honest broker presents both sides of every transaction. Benefit without harm is not evidence-based medicine. It is a sales pitch. Translate every efficacy claim into two natural frequencies, benefit and harm, in the same currency, for the same 1,000 patients, over the same time horizon: In secondary prevention, aspirin prevents approximately 15 serious vascular events per 1,000 patient-years at the cost of approximately 3 additional major extracranial bleeds per 1,000 patient-years, a favorable ratio for most patients.⁴,¹⁸ In primary prevention, aspirin prevents approximately 4 events per 1,000 patient-years while bleeding risk remains unchanged, a ratio that drove guideline reversal after decades of routine prescribing.¹⁹ These two numbers, side by side, are the entire benefit-risk conversation. A clinical AI that gives you only the first number is not giving you half the answer. It is giving you the half that most reliably produces a prescription. A clinical AI that provides complete data only when interrogated is not a functional decision support tool. Question 3: Is This Evidence or Is This a Guideline — And Does It Matter Here? When an AI responds with Class I recommendations before a single absolute number, ask: "What do the actual trial numbers show, not what the guidelines recommend?" Guidelines have a legitimate role: where robust trial data is absent, they represent the best available expert consensus, and in medico-legal contexts, they remain the defensible standard of care. The question is not whether guidelines are useful. The question is whether they are being substituted for evidence that already exists and is accessible. We have learned to be cautious of processed food, stripped of nutrients, optimized for palatability, and shaped by commercial interests rather than health. Processed evidence is no different. The more steps between raw trial data and the AI's response, journal publication, guideline committee, specialty society endorsement, payer modification, the more cautiously that response deserves to be received. Ask for the compass. Not the map someone else drew from it. Ask More Questions — It Will Not Cost You As Much Time As You Think These three questions are not academic extras. They are the minimum your patient's safety requires. Ask them every time. Push back until you get complete answers: Is this a relative or absolute number? I want absolute numbers, real patients, real events, real frequencies. Who benefits and who is harmed — out of how many? I want all of it, the good, the bad, and the ugly. Benefit and harm, side by side, for the same 1,000 patients. Is this evidence or is this a guideline? I want the real evidence, the actual trial numbers I can review myself. Not pre-digested consensus. Not spoon feeding. If the AI cannot answer all three completely on the first response, it has not finished its job. Keep asking. And for the physician who says they do not have time, these three questions take sixty seconds. The harm from skipping them can last a lifetime. Combat the algorithm. Your patient cannot do it for themselves. 6. A Technical Action Plan for Clinical AI Developers Treat Others As You Like To Be Treated Yourself — Patient Safety Must Take Precedence You have read the evidence. You understand the problem. Before you read the action plan below, consider one thing: you are also a patient. One day you will sit in an examination room while a physician consults a clinical AI tool, possibly one you helped build. The information that tool surfaces in that moment will shape the decision that follows. Build the tool you would want your physician to use. Here is how. Action 1: Change the Default Output Format What: Replace relative risk as the default headline metric with natural frequencies. How: Identify every output template that generates an efficacy statement Insert a mandatory natural frequency conversion after every relative risk figure "22% reduction in vascular events" becomes: "25 fewer patients experience a vascular event out of every 1,000 treated over 2 years" Relative figures may remain, labeled explicitly as relative, positioned after the natural frequency Acceptance criterion: Zero first responses that lead with a relative risk figure without an accompanying natural frequency. Action 2: Make Harm Mandatory — Not Optional What: Every benefit statement must be paired with a harm statement in identical format. Where validated risk calculators exist, link to them. How: Build a harm-retrieval trigger into every efficacy output template Benefit and harm must appear in the same response, same format, same patient population, same time horizon For aspirin in secondary prevention, the output must pair both statements: "Aspirin prevents approximately 15 serious vascular events per 1,000 patient-years at the cost of approximately 3 additional major extracranial bleeds per 1,000 patient-years" [ATT Collaboration, Lancet 2009]⁴ Where validated risk calculators exist for the specific clinical question, embed or link to them: For antiplatelet-related bleeding risk: HAS-BLED calculator (bleeding risk in anticoagulated patients) For DAPT duration decisions: DAPT Score calculator or PRECISE-DAPT (individualized bleeding risk during dual antiplatelet therapy) For ACS bleeding risk: CRUSADE score (bleeding risk stratification) If harm data is unavailable for the specific query, the response must explicitly state this, not silently omit it A clinical AI that reports only benefit is functioning as a pharmaceutical representative. That is not the product you are building. Acceptance criterion: No first response reports efficacy without a corresponding harm statement. Validated risk calculators are linked where they exist for the specific clinical scenario. Action 3: Tag Every Response — Evidence or Guideline What: Every clinical response must carry a visible source classification at the point of output. How: Implement mandatory source tagging in the response header or inline: [Primary trial evidence — specify source and year] [Guideline recommendation, specify organization, year, and evidence class] [Expert consensus — no randomized trial data available] Where guideline-producing organizations have documented industry relationships relevant to the recommendation, add: [Note: relevant financial conflicts of interest exist among guideline authors, see source disclosure] This is a metadata problem. Your pipeline already knows the source. Surface it. Acceptance criterion: Every response is tagged. No unattributed clinical recommendations. Action 4: Surface Guideline Contradictions — Do Not Hide Them What: Where multiple guidelines exist for the same clinical question and differ in their recommendations, present all of them, with their contradictions explicitly disclosed. How: When a query returns recommendations from more than one guideline-producing organization, present each separately with its source, year, and evidence classification Flag contradictions explicitly at the point of output with their direct clinical implications Real example 1 — Aspirin in primary prevention: same patient, three different answers [ACC/AHA 2019: Aspirin may be considered for primary prevention in adults aged 40–70 at higher ASCVD risk and low bleeding risk, Class IIb. Recommended against routinely in adults over 70, Class III.]² [ESC 2021: Aspirin not recommended for primary prevention due to unfavorable bleeding risk — Class III. Consistent with ACC/AHA on high-risk exception — Class IIb.]³ [USPSTF 2022: Aspirin not recommended for initiation in adults aged 60 and older. Individualized decision for adults aged 40–59 at 10% or greater 10-year CVD risk.]⁴ [Guideline contradiction: ACC/AHA permits aspirin consideration in adults aged 40–70 at high ASCVD risk; USPSTF restricts initiation to adults under 60. A patient aged 62 at high ASCVD risk meets ACC/AHA criteria but not USPSTF criteria for aspirin initiation. The treating physician must be aware of this discrepancy and exercise independent clinical judgment.] Real example 2 — DAPT duration after PCI: same procedure, different standards [ACC/AHA 2023: DAPT for 6 months post-PCI for chronic coronary disease, followed by single antiplatelet therapy — Class I, Level A.]⁵ [ESC 2023: In selected low-bleeding-risk patients post-PCI, P2Y12 inhibitor monotherapy after 1–3 months of DAPT may be considered to reduce bleeding — Class IIa, Level A.]⁶ [Guideline contradiction: ACC/AHA recommends 6 months of DAPT as standard; ESC permits discontinuation of aspirin after as little as 1 month in selected patients. The same post-PCI patient may receive meaningfully different therapy depending solely on which guideline their physician consulted.] On the objection that surfacing multiple guidelines makes responses exhaustively long: Guideline contradictions are not created by surfacing them, they already exist. A physician unaware of the contradiction between ACC/AHA and USPSTF aspirin recommendations for a 62-year-old patient is not protected by their ignorance, they are exposed by it. Conflict of interest disclosures are already published in guideline documents, surfacing them is a metadata tagging problem, not an original research requirement. The engineering effort is finite. The patient safety consequence of concealment is not. When response length is cited as a reason to withhold clinically meaningful information, patient safety must take precedence. Always. Acceptance criterion: No query returns a single guideline recommendation where multiple contradictory guidelines exist, without disclosure of the contradiction and its clinical implications. Action 5: Audit Training Data for Framing Bias What: Quantify and correct the framing imbalance inherited from the source literature. How: Run a systematic audit of training data: what percentage of source documents report ARR and natural frequencies alongside RRR? Build a framing completeness score for each source Up-weight sources that consistently report absolute figures and natural frequencies Down-weight sources that report relative risk only Re-audit after every major training data update Acceptance criterion: Framing completeness is a documented, tracked metric in the training data quality dashboard, weighted equally alongside impact factor and recency. Action 6: Implement a Standard QA Stress Test What: Before any clinical AI output is approved for deployment, stress-test it against a standardized set of clinical efficacy queries. How: Develop a library of benchmark queries covering major therapeutic areas Submit each query and evaluate the first response against the following pass criteria: Criterion Pass Fail Natural frequency for benefit stated First response Requires follow-up Natural frequency for harm stated First response Absent or requires follow-up Source tagged as evidence or guideline First response Absent Guideline contradictions disclosed First response Single guideline presented without disclosure Conflicts of interest tagged First response Absent Relative risk labeled as relative First response Presented as primary metric Any fail on any criterion = output not cleared for clinical deployment Re-test after every model update Acceptance criterion: 100% pass rate on benchmark query library before deployment. No exceptions. Action 7: Adopt One Governing Principle What: A single ethical standard that supersedes all technical specifications. The principle: If a physician acting on your first response alone could make a prescribing decision that harms a patient, a decision they would not have made had they seen the complete data, your first response is inadequate. Apply this question to every output template, every training data curation decision, and every default setting. When the answer is yes, fix it before deployment, not after. This is not a technical standard. It is the same standard of honesty that physicians owe their patients, extended, by the people who build these tools, to every physician who trusts them. The Minimum Acceptable Standard — At a Glance A clinical AI response is not ready for clinical deployment until it delivers, on the first response, without escalation: ✅ Efficacy in natural frequencies ✅ Harm in natural frequencies, same population, same time horizon ✅ All relevant guidelines surfaced with contradictions disclosed ✅ Conflicts of interest tagged at source level ✅ Source clearly tagged as primary evidence or guideline consensus ✅ Relative risk figures labeled as relative ✅ Treatment duration specified ✅ Validated risk calculators linked where they exist Every day these defaults remain unchanged, a physician somewhere acts on an incomplete answer. You know what needs to be done. A patient's life could be at risk. 7. Conclusion This article began with a simple observation: a major clinical AI tool, when asked about the rationale for antiplatelet therapy in chronic ASCVD, led with a relative risk figure and required rounds of escalating questions before producing the absolute numbers that allow individualized clinical decision-making. That observation expanded into three nested problems: First: Clinical AI tools systematically present efficacy data using relative risk reduction as the default metric, a statistical framing convention inherited directly from pharmaceutical marketing, a practice long documented to inflate perceived benefit and drive prescribing behavior. Second: These tools substitute guideline recommendations for primary evidence, presenting the output of committees whose independence is structurally compromised by industry relationships as if it were neutral scientific consensus. Third: The regulatory agencies, guideline-producing organizations, and AI companies involved in this chain have the power and the resources to fix these problems today. What This Means for Medicine A clinical AI tool that presents incomplete, misleading or misrepresenting data is not a neutral tool. It is a vector for systematic bias, operating at the scale of every physician who consults it, in the language of evidence, with the credibility of science itself. The physician who recognizes this and asks the three questions is practicing medicine. The responsibility for change, however, does not end with the clinician. It lies with the people who built the tool. What This Means for Patients A third of adults aged 70 and older, approximately 9 million individuals, continued taking aspirin for primary prevention despite guideline reversal, with a net potential for harm.²⁰ How many patients are currently prescribed medications based on AI-generated responses that lead with relative risk? How many will experience preventable harm because a clinical AI tool presented the half of the truth that most reliably produces a prescription? We do not yet know. But the mechanism is established, the problem is documented, and the solution is available. Patients deserve access to the complete statistical picture which assist in accurate clinical decision making, not the processed, filtered, commercially optimized derivative that currently passes for evidence-based medicine. The Path Forward This article has documented a specific failure in specific tools. But it has identified a systemic problem: the framing conventions of pharmaceutical marketing have been inherited, through training data, through default settings, through institutional inertia, by the AI systems now reshaping clinical decision-making. The path forward requires simultaneous action at three levels: Clinicians must demand more. Ask the three questions. Push back on relative risk figures. Refuse to prescribe on the basis of incomplete data. AI developers must build differently. The seven actions outlined in Section 6 are the minimum acceptable standard. Implement them. Test against them. Deploy only when the standard is met. Regulators and professional bodies must enforce accountability. Clinical AI tools that present efficacy data without absolute risk figures should not be permitted in clinical settings, not as a best practice, but as a regulatory requirement. A Final Word The patient sitting across the desk from a physician consulting a clinical AI tool has no idea what defaults are built into that system. They do not know whether the recommendation they are about to receive is based on primary evidence or guideline consensus. They do not know whether the benefit number they are hearing is the complete picture or the carefully selected half of one. Gerd Gigerenzer spent decades teaching the world that humans are not bad at thinking. We are simply given information in the wrong format. When presented with natural frequencies, "25 out of 1,000 patients benefit", people understand risk intuitively.³ The choice of format is not a technical detail. It is a choice about whose interests the information serves. For too long, that choice has served the interests of people selling medications. It is time for clinical AI to serve the interests of people taking them. The patient is waiting. You know what needs to be done. A patient's life could be at risk. Acknowledgment: This article was written with AI assistance. All claims are supported by credible, peer-reviewed references, which were validated for accuracy and authenticity. The AI synthesized information were reviewed by author, ensuring scientific integrity throughout. In the event of any inadvertent errors, the responsibility lies with the AI/authors, and corrections will be made promptly upon identification. I would like to express my sincere gratitude to Dr Tahira Khalid for her thoughtful review and invaluable feedback, and Professor Aftab Ahmad (I.T) for his valuable feedback. Their expertise and guidance have played a pivotal role in refining and enhancing this article. Conflict of Interest Statement: The author is the developer of a herbal formula and the owner of Dr. Q Formula/Insulinn LLC. However, this affiliation has not influenced the content, analysis, or conclusions of this article Author’s Note on Scope and Intent: This article does not advocate the replacement of evidence-based conventional care modalities. All complementary interventions are intended to supplement, not supplant, standard clinical practice, and are implemented within a physician-governed, ethically reviewed, and fully documented medical framework. References Bucher HC, Weinbacher M, Gyr K. Influence of method of reporting study results on decision of physicians to prescribe drugs to lower cholesterol concentration. BMJ. 1994;309(6957):761–764. Link: https://www.bmj.com/content/309/6957/761 Nuovo J, Melnikow J, Chang D. Reporting number needed to treat and absolute risk reduction in randomized controlled trials. JAMA. 2002;287(21):2813–2814. Link: https://pubmed.ncbi.nlm.nih.gov/12038920/ Gigerenzer G, Gaissmaier W, Kurz-Milcke E, Schwartz LM, Woloshin S. Helping doctors and patients make sense of health statistics. Psychol Sci Public Interest. 2007;8(2):53–96. Link: https://pubmed.ncbi.nlm.nih.gov/26161749/ Antithrombotic Trialists' Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ. 2002;324(7329):71–86. Link: https://www.bmj.com/content/324/7329/71 Office of the Assistant Secretary for Planning and Evaluation. 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Application of U.S. guidelines in other countries: Aspirin for the primary prevention of cardiovascular events in Japan. Am J Med. 2004;117(7):459–468. Link: https://www.amjmed.com/article/S0002-9343(04)00426-7/fulltext Yebyo HG, Zappacosta S, Aschmann HE, Haile SR, Puhan MA. Global variation of risk thresholds for initiating statins for primary prevention of cardiovascular disease: a benefit-harm balance modelling study. BMC Cardiovasc Disord. 2020;20(1):418. Link: https://bmccardiovascdisord.biomedcentral.com/articles/10.1186/s12872-020-01697-6 Mortensen MB, Nordestgaard BG, Tybjærg-Hansen A, Afzal S, Saeed S. Statin eligibility for primary prevention of cardiovascular disease according to 2021 European prevention guidelines compared with other international guidelines. JAMA Cardiol. 2022;7(10):1078–1086. Link: https://jamanetwork.com/journals/jamacardiology/fullarticle/2793729 Camm AJ, Califf RM, Dittrich HC, et al. Analysis of conflicts of interest among authors and researchers of European clinical guidelines in cardiovascular medicine. Eur Heart J Open. 2021;1(1):oeab011. Link: https://pmc.ncbi.nlm.nih.gov/articles/PMC8002771/ Ioannidis JPA. Professional societies should abstain from authorship of guidelines and disease definition statements. Circ Cardiovasc Qual Outcomes. 2018;11(1):e004889. Link: https://www.ahajournals.org/doi/10.1161/CIRCOUTCOMES.118.004889 Coyle SL; Ethics and Human Rights Committee, American College of Physicians-American Society of Internal Medicine. Physician-industry relations. Ann Intern Med. 2002;136(5):396–402. Link: https://pubmed.ncbi.nlm.nih.gov/11874314/ [Same as Reference 5 — FDA User Fees document] Link: https://aspe.hhs.gov/sites/default/files/documents/eafc804ad2c90d9b2a8dd1e04059b378/FDA-User-Fee-Issue-Brief.pdf [Same as Reference 6 — Congressional Research Service] Link: https://congress.gov/crs-product/R44750 Gentilini A, Raymakers AJN, Rand L. Conflicts of interest for FDA advisory committee members and public speakers: systematic review. Value Health. 2026. Primary source Link: https://www.madinamerica.com/2026/05/pharma-cash-creates-conflicts-of-interest-in-fda-testimony-and-clinical-practice-guidelines/ [Same as Reference 7 — ATT Collaboration Lancet 2009] Link: https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(09)60503-1/fulltext Vandvik PO, Lincoff AM, Gore JM, et al. Primary and secondary prevention of cardiovascular disease: Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2012;141(2 Suppl):e637S–e668S. Link: https://journal.chestnet.org/article/S0012-3692(12)60134-2/fulltext Yadav K, Medsker B, Vu A, Aroda VR. Recent trends in aspirin use for cardiovascular disease prevention in the United States, 2015 to 2023. JACC Adv. 2025. Link: https://www.jacc.org/doi/10.1016/j.jacadv.2025.101699

Author:  Dr Qaisar J. Qayyum, MD — Chief Editor, Noor Journal of Complementary and Contemporary Medicine (NJCCM) ; Clinical Assistant Professor of Medicine, Oklahoma, USA. Figure 1.   Classical Mizaj Categories Mapped to Modern Neurocognitive Correlates Abstract Alzheimer’s disease now affects one in nine adults over 65 years in the United States [4]. Long before modern disease labels, classical Unani (Yoonani یونانی) physicians articulated universal therapeutic principles for all illnesses. Central among these is that treatment must fit the individual’s temperament, not merely the diagnosis. Ibn Sina taught, “Treatment must follow the temperament” [1], and Hakim Nuruddin ؓ stated, “True treatment consists of removing the causes in accordance with the temperament” [3]. These maxims capture a timeless truth: two people may share the same disease, yet each requires management tailored to his or her unique mizaj (temperament). This paper (Part 1) aligns Unani (Greco–Arabic) theory with modern neurocognitive and biochemical evidence. It explains the four temperaments, their physiological parallels, and how personalized medicine today echoes what Unani Hikmat established a millennium ago. Introduction “It’s far more important to know what person has the disease than what disease the person has.” — Hippocrates (حکیم بقراط, PMC3296331) Unani medicine (al-tibb al-yoonani) evolved from Greek, Arabic, and Persian scholarship, an integrated system where healing is guided by mizaj (temperament). The concept was introduced by Galen (Jalinoos جالینوس), refined by Ibn Sina (Avicenna), and later reinterpreted by Indian–Persian sages including Hakim Nuruddin ؓ, whose Bayaz-e-Nuruddin serves as a bridge between classical theory and modern practice. In this approach, treatment must correspond to the individual’s internal balance of hot–cold and moist–dry qualities through carefully selected remedies, diet, and lifestyle suited to their unique mizaj (temperament). By aligning therapy with the patient’s inherent state, the physician minimizes adverse effects and identifies the most effective medicinal agents for restoring balance and function. Modern neuroscience is rediscovering this truth through the lens of genetics, biochemistry, and stress physiology: mizaj is the phenotype of the genotype — a dynamic expression of constitutional and environmental interaction. The Golden Rule of Hikmat Ibn Sina (Avicenna), al-Qanun fi’l-Tibb (The Canon of Medicine): “Treatment must follow the temperament.” [1] Hakim Nuruddin ؓ , Bayaz-e-Nuruddin: “اصل علاج تو ہے کہ ازالہ اسباب حسب مزاج کیا جاوے” “True treatment consists of removing the causes in accordance with the temperament.” [3] This principle underscores a fundamental reality: disease may be universal, but healing must be individualized. Personalization, not uniformity, is the essence of medicine, classical or modern. Philosophy of Integration: Hikmat and Modern Science Classical physicians of Hikmat (Unani medicine) such as Ibn Sina and Hakim Nuruddin ؓ taught through observation and reasoning, not blind imitation. Their concept of mizaj (temperament) explained individual differences in health and healing. Today, modern neuroscience and biochemistry describe similar ideas through genetics, inflammation, and neurohormonal balance. Our purpose is not revival for its own sake, but selective adoption of principles that remain physiologically sound and clinically verifiable. When interpreted through evidence-based understanding, Hikmat offers a framework for truly personalized medicine, one that treats causes, respects individuality, and unites body, mind, and spirit. Author’s Clinical Observation and Experiment As part of an exploratory n-of-1 observation on cognitive performance, I conducted a self-experiment using a natural formulation derived from culinary and traditional principles. The intervention consisted of a mixture of approximately ½ tablespoon Kashmiri chili powder (≈2 g) , ½ tablespoon organic apple cider vinegar (≈5 g) , and ½ tablespoon local raw honey (≈12 g) , administered once daily. This initial dose produced noticeable mental clarity and improved alertness without any discomfort. To explore potential dose–response effects, the amount was tripled to roughly 1½ tablespoons of each component (≈6 g chili, 15 g vinegar, and 36 g honey) . Within 24 hours, this higher dose produced transient retrosternal spasmodic discomfort, prompting emergency evaluation. Cardiac workup—including ECG, cardiac biomarkers, and echocardiogram—was normal. A consulting cardiologist (with background in South Asian therapeutics) attributed the episode to gastric irritation from the combined chili–vinegar acidity rather than a cardiac cause. The reaction resolved completely with Pepcid Complete (famotidine + antacid), confirming a gastrointestinal origin and establishing this as the upper safe limit  for this formulation. This clarified an important point: individuals with Balghami  (cold–moist) or Sawdawi  (cold–dry) temperaments—where metabolism is sluggish or mucosal sensitivity heightened—may react adversely to acidic preparations despite their benefits in others. Future formulations and studies will omit vinegar or strongly acidic components to improve tolerability across temperament types. The aim was to assess subjective changes in alertness, mental clarity, and overall cognitive function following short-term exposure to mild thermogenic and antioxidant agents. The working hypothesis was that mild neurostimulation from spice could activate cranial-nerve pathways, improving alertness and memory through adaptive neuroprotection, as suggested in studies linking capsaicin to neurogenesis and antioxidant effects. Initial outcome:  noticeable mental clarity and reduction in “brain fog.” Adjustment phase:  After initial subjective improvement, the dosage was deliberately increased to explore the upper tolerance range and potential dose–response relationship. Within 24 hours, transient retrosternal spasmodic anginal discomfort developed, prompting emergency evaluation. Cardiac workup, including ECG and biomarkers, echocardiogram was normal. A consulting cardiologist (with training in South Asian therapeutics) attributed the symptoms to gastric irritation from the combined chili–vinegar acidity, rather than a cardiac cause. The reaction resolved completely with Pepcid Complete (famotidine + antacid), confirming a gastrointestinal origin and establishing the upper safe limit for this formulation. This clarified an important point: individuals with Balghami (cold–moist) or Sawdawi (cold–dry) temperaments, where metabolism is sluggish or mucosal sensitivity heightened, may react adversely to acidic preparations despite their benefits in others. In future formulations and experiments, vinegar and other strongly acidic components will therefore be omitted to ensure broader tolerability across temperament types. This observation highlights a deeper truth about the philosophy of healing: that effective treatments often already exist within traditional or natural frameworks but are overlooked in favor of newer, more commercial options. Given the prevailing trend of monetization in modern medicine, new treatments may not be pursued unless they promise significant financial returns. As a result, potentially beneficial remedies are sometimes ignored simply because they do not fit the economic model of profitability. At this juncture, it is worth recalling a timeless medical principle beautifully expressed in the ḥadīth of the Holy Prophet ﷺ: The Prophet (ﷺ) said, “There is no disease that Allah has created, except that He also has created its treatment.”— Sahih al-Bukhari, Kitāb al-Tibb (Book of Medicine), Hadith 5678 https://sunnah.com/bukhari:5678 Comparable intuitions appear across several ancient healing traditions, each reflecting the recognition that nature carries within it both ailment and remedy. Hippocrates taught that “Nature itself is the best physician,” suggesting that the forces which disturb balance also contain the potential for its restoration. The Charaka Saṃhitā of Ayurveda records that “for every disease, there grows a herb that can cure it,” affirming divine provision through natural design. Likewise, the Huangdi Neijing of Chinese medicine describes health as harmony between yin and yang, where imbalance inevitably evokes its counterbalance. Even the Hebrew Scriptures (Ezekiel 47:12) echo this notion, describing leaves “for healing.” Yet, the ḥadīth of the Holy Prophet ﷺ transcends these intuitive philosophies. It frames healing not merely as a natural reciprocity but as a deliberate act of Divine wisdom, that for every illness permitted to exist, its cure was created within the same framework of mercy and balance. In light of this principle, it may be reasoned that the cure for every disease has existed since the very inception of that disease, both created within the same divine framework of balance and reciprocity. The true role of the physician and researcher, therefore, is not to wait for future invention, but to rediscover and apply time-tested remedies from historical knowledge, until a better, safer, or more refined one becomes available, a prospect increasingly limited by high cost of development and commercial priorities that favor profitability over genuine therapeutic discovery. Hence, one formula cannot fit all; treatment must always respect mizaj . Until modern medical science looks deeper into this philosophy, true success in healing may continue to elude us, and medicine will keep failing many whom it aims to serve. Temperaments and Their Scientific Echo Temperament Qualities Classical Description Modern Correlates 🟥 Damawi (دموی) Hot & Moist Cheerful, sociable, energetic; forgetfulness from distraction, not decay [1] Attention lapses ↔ working-memory overload [5] 🟦 Balghami (بلغمی) Cold & Moist Sluggish, pale, sleepy; prone to true memory loss [2] Metabolic-inflammatory profile (insulin resistance, raised CRP/IL-6) [11] 🟨 Safrawi (صفراوی) Hot & Dry Ambitious, restless, weakened by stress [1] Elevated cortisol, sympathetic over-activity, stress-induced hippocampal damage [7, 13] ⬛ Sawdawi (سوداوی) Cold & Dry Thoughtful, anxious, perfection-seeking [4] Depression-related hippocampal atrophy, rumination, serotonin imbalance [9, 10] Biochemical markers, such as cortisol, bilirubin, fasting glucose, CRP, and IL-6 — support that mizaj correlates with specific neuroendocrine and inflammatory profiles. What Unani called temperament aligns with modern “endophenotypes” in dementia research. Mizaj Is Not Limited to Alzheimer’s While this study centers on memory and cognition, mizaj underpins all bodily and psychological states. The same constitutional tendencies explain differential susceptibility to metabolic syndrome, cardiovascular disease, anxiety, and depression. Modern complementary medicine thus mirrors Unani’s call for personalized healing. Diagnosing Mizaj and Cognition A. Temperament Indicators (Simplified Overview) Category Damawī (Hot + Moist) Balghamī (Cold + Moist) Ṣafrāwī (Hot + Dry) Sawdāwī (Cold + Dry) Body & Color Reddish tone, warm skin Pale, cool, soft Lean, yellowish Dark, dry Energy High, steady Low, slow Quick, tense Variable, weak Digestion Strong Sluggish Acidic Sensitive Mood Cheerful, sociable Calm, steady Driven, impatient Cautious, analytical B. Cognitive Screening Tools Participants in Part 2 of this project are encouraged to complete one of these tests at baseline and repeat it after 4–6 weeks of temperament-guided therapy. Test Purpose (Lay Summary) Access MoCA – Montreal Cognitive Assessment Detects early memory loss and executive issues. mocacognition.com/paper SLUMS – St Louis University Mental Status Exam Screens for mild cognitive impairment or dementia. slu.edu/.../mental-status-exam.php M@T – Memory Alteration Test Quick 10-minute screen for early Alzheimer’s. PubMed 18063420 Validated Tools for Mizaj Assessment Tool Population / Setting Key Features Access / Reference Mojahedi M, et al. (2014) — Reliability and Validity Assessment of Mizaj Questionnaire (Iran Red Crescent Med J. 16(3):e15924)* Adults (general) 10-item validated self-report; establishes hot/cold and wet/dry traits. PMC4005447 Salmannezhad H, Mojahedi M, et al. (2018) — Design and Validation of Mizaj Identification Questionnaire Adults Detailed scoring for compound temperaments. IRCMJ PDF Akhtari M, Mojahedi M, et al. (2024) — Elder Mizaj Questionnaire (60+) Older adults Tailored to geriatric use; reliable for dementia studies. PMC10921101 CCRUM “Know Your Mizaj” (Govt. of India) General public Official AYUSH screener mapping classical Unani axes. unanitemperament.ccrumapps.in Discussion: Tradition Meets Modern Science Classical Type Modern Parallel Key Insight Damawi Attentional lapses, multitasking fatigue Working-memory overload, dopamine balance [5] Balghami Metabolic sluggishness Insulin resistance, “Type 3 diabetes” hypothesis [11] Safrawi Stress-driven burnout Cortisol excess, hippocampal injury [7, 13] Sawdawi Mood-driven decline Depression and hippocampal shrinkage [9, 10] Thus, what in Unani medicine once called “imbalance of humors” is now measurable in biomarkers and neuroimaging. Noor Journal Mizaj (Temperament) Self-Assessment Form * (Based on the validated Mojahedi Mizaj Questionnaire, Iran J Public Health, 2014) Click below to print the form Reference:   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4005447/ Basic Information:  Name | Age | Gender | Date Mizaj (Temperament) Self-Assessment Instructions Read each statement carefully and mark Yes (✓) if it applies to you, or No (✗) if it doesn’t. At the end, count how many “Yes” responses you gave in each section.The sections with the highest Yes totals define your temperament (for example, Hot + Moist = Damvi). A. Hot (Garam) vs Cold (Sard) No. Statement Yes No Temperament 1 I usually feel warm or heat up quickly. ☐ ☐ Hot 2 I digest food quickly and feel hungry often. ☐ ☐ Hot 3 I prefer cool weather. ☐ ☐ Hot 4 I get irritated or excited easily. ☐ ☐ Hot 5 I sleep lightly and wake up early. ☐ ☐ Hot 6 I usually feel cold, and my hands or feet stay cool. ☐ ☐ Cold 7 I digest food slowly and rarely feel hungry. ☐ ☐ Cold 8 I prefer warm weather. ☐ ☐ Cold 9 I feel tired easily and need more rest. ☐ ☐ Cold 10 I remain calm and seldom get angry. ☐ ☐ Cold Hot (Yes) ____  Cold (Yes) ____ B. Moist (Tar) vs Dry (Khushk) No. Statement Yes No Temperament 1 My skin and hair feel soft or oily. ☐ ☐ Moist 2 I sweat more than most people. ☐ ☐ Moist 3 I have steady physical energy throughout the day. ☐ ☐ Moist 4 I sleep deeply and peacefully. ☐ ☐ Moist 5 My skin feels dry or rough. ☐ ☐ Dry 6 I sweat very little, even in heat. ☐ ☐ Dry 7 My lips or joints feel dry often. ☐ ☐ Dry 8 I tire quickly or need frequent rest. ☐ ☐ Dry Moist (Yes) ____  Dry (Yes) ____ Interpretation Combination Temperament Core Traits Hot + Moist Damvi (Sanguine) Warm, energetic, sociable Hot + Dry Safravi (Choleric) Active, decisive, focused Cold + Moist Balghami (Phlegmatic) Calm, steady, gentle Cold + Dry Saudavi (Melancholic) Thoughtful, analytical, deep Note: This self-assessment is for educational and lifestyle guidance only. For professional evaluation, consult a qualified Unani / Hikmat practitioner. Prepared by: Dr Qaisar Qayyum, MD. Chief Editor, Noor Journal of Complementary and Contemporary Medicine (NJCCM) Conclusion From Galen and Ibn Sina to Hakim Nuruddin ؓ, the guiding principle has remained constant: treatment must follow the temperament. Modern neurocognitive science now validates this ancient wisdom, recognizing that disease pathways vary by constitution, stress biology, and emotional tone. Unani medicine therefore stands not as an alternative, but as a complementary personalized model, harmonizing spiritual, physical, and neurobiological understanding. “True treatment consists of removing the causes in accordance with temperament.” — Hakim Nuruddin ؓ Acknowledgment: This article was written with AI assistance. All claims are supported by credible, peer-reviewed references, which were validated for accuracy and authenticity. The AI synthesized information were reviewed by authors, ensuring scientific integrity throughout. In the event of any inadvertent errors, the responsibility lies with the AI/authors, and corrections will be made promptly upon identification. I would like to express my sincere gratitude to Dr Tahira Khalid , for her thoughtful review and invaluable feedback, and Dr. Mohyuddin Mirza, Ph.D for his valuable feedback. Their expertise and guidance have played a pivotal role in refining and enhancing this article.   Conflict of Interest Statement: The author is the developer of a herbal formula and the owner of Dr. Q Formula/Insulinn LLC. However, this affiliation has not influenced the content, analysis, or conclusions of this article   Author’s Note on Scope and Intent: This article does not advocate the replacement of evidence-based conventional care modalities. All complementary interventions are intended to supplement, not supplant, standard clinical practice, and are implemented within a physician-governed, ethically reviewed, and fully documented medical framework. 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PLoS Medicine.  2006;3(6):e208. https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0030208 Prasher B, Negi S, Aggarwal S, Mandal AK, Sethi TP, Deshmukh SR, et al.  Whole-genome expression and biochemical correlates of Ayurvedic constitutional types. Journal of Translational Medicine.  2008;6:48. BioMed Central https://translational-medicine.biomedcentral.com/articles/10.1186/1479-5876-6-48 Akhondzadeh S, Sabet MS, Harirchian MH, Togha M, Cheraghmakani H, Razeghi S, Hejazi S, Yousefi MH, Alimardani R, Jamshidi A, Khani M.  Saffron in the treatment of patients with mild to moderate Alzheimer’s disease: A 16-week, randomized and placebo-controlled trial. Journal of Clinical Pharmacy and Therapeutics.  2010;35(5):581-588. DOI: 10.1111/j.1365-2710.2009.01133.x | PubMed Ownby RL, Crocco E, Acevedo A, John V, Loewenstein D.  Depression and risk for Alzheimer disease. Archives of General Psychiatry.  2006;63(5):530-538. https://pubmed.ncbi.nlm.nih.gov/16651510/ Koster EHW, De Lissnyder E, Derakshan N, De Raedt R.  Understanding depressive rumination from a cognitive science perspective: The impaired disengagement hypothesis. Clinical Psychology Review.  2011;31(1):138-145. DOI: 10.1016/j.cpr.2010.08.005 | PubMed Fadó R, López-Sanz P, Casado P, Pizarro-Delgado J, Sanz C, Bergantiños-López A, et al.  Feeding the brain: Effects of nutrients on cognition. Nutrients.  2022;14(21):4549. https://pmc.ncbi.nlm.nih.gov/articles/PMC9572450/ Genin E, Hannequin D, Wallon D, Sleegers K, Hiltunen M, Combarros O, et al.  APOE and Alzheimer disease: Semi-dominant inheritance. Molecular Psychiatry.  2011;16:903-907. https://pubmed.ncbi.nlm.nih.gov/21556001/ * Copyright and Usage Notice © 2025 Noor Journal of Complementary and Contemporary Medicine (NJCCM). This form may be used, reproduced, and adapted freely  for educational or clinical purposes, provided that proper credit is given as follows: Source: Noor Journal of Complementary and Contemporary Medicine (NJCCM) — Mizāj (Temperament) Self-Assessment Form, 2025. Developed by Dr Qaisar J. Qayyum, MD. Commercial use without permission is not allowed.

Dr. Qaisar J. Qayyum Chief Editor, Noor Journal of Complementary and Contemporary Medicine, Clinical Assistant Professor, Oklahoma, USA.   Email :   chiefeditor@njccm.org یہ کہانی ہے مسٹر اے ایس (Mr. A.S.) کی، جو امریکہ میں مقیم تھے اور جنہیں urothelial carcinoma with prostate extension  یعنی ایک خطرناک کینسر کی تشخیص ہوئی۔ مریض کو بایوپسی (biopsy) کے ذریعے بتایا گیا کہ کینسر ان کے bladder  سے بڑھ کر prostate  تک جا چکا ہے۔ عام فہم زبان میں وہ خود کو "prostate cancer" کا مریض سمجھتے رہے، کیونکہ علاج کرنے والے ڈاکٹروں نے کہا تھا کہ آپریشن میں دونوں اعضا (bladder اور prostate) نکالنے پڑیں گے۔ ابتدائی علاج 2016 میں انہیں chemotherapy  (gemcitabine + carboplatin) دی گئی۔ کچھ وقت کے لیے افاقہ ہوا مگر 2018 میں PET/CT scan پر پھر سے بڑی رسولی ظاہر ہوئی۔ ڈاکٹروں نے انہیں بڑا آپریشن (radical cystoprostatectomy) تجویز کیا، یعنی مثانہ اور پروسٹیٹ دونوں نکال دیے جائیں۔ مگر مریض نے اس تکلیف دہ آپریشن کو مسترد کر دیا۔ متبادل راستہ انہوں نے اپنی زندگی کا رخ موڑا اور ایک نیا طریقہ علاج اپنایا: Bitter apricot kernels (کریوی خوبانی کی گٹھلیاں):  شروع میں روزانہ تقریباً 30 گٹھلیاں پانچ حصوں میں تقسیم کر کے (7+7+7+5+4) کھاتے تھے۔ بعد میں آہستہ آہستہ خوراک کم کر کے 20، پھر 10 اور اب صرف 5 روزانہ لیتے ہیں۔ Amygdalin (B17) tablets:  500 mg کی تین گولیاں روزانہ ایک سال تک کھائیں۔ پھر خوراک کم کر کے آدھی گولی روزانہ کی اور اب تک یہی جاری ہے۔ غذا:  سخت vegetarian  اور sugar-free diet  اپنائی، ساتھ ہی دن میں دو بار ایک چمچ زیتون کا تیل لینا شروع کیا۔ مصنوعات کا ذریعہ (Product Source): مریض نے اپنے B17 (Amygdalin) کی گولیاں Cytopharma  سے حاصل کیں ( www.cytopharma.com )، اور کرُوے خوبانی کے بیج (bitter apricot kernels)   Amazon  سے خریدے ( link )۔ یہ سب چیزیں اُس نے باقاعدگی سے اپنی غذائی تبدیلیوں کے ساتھ استعمال کیں۔ نتیجہ اس نئے طریقہ علاج کے بعد ان کے کئی PET/CT scans (2019, 2020, 2023, 2024) میں بار بار ثابت ہوا کہ جسم میں کینسر بالکل ختم ہو چکا ہے۔ ان کے خون کے ٹیسٹ (Sept 2024) بالکل نارمل تھے: WBC: 7.0 × 10³/μL Hgb: 16.2 g/dL Platelets: 188 × 10³/μL CMP: نارمل سائیڈ ایفیکٹس کچھ وقتی اثرات ضرور ہوئے جیسے گٹھلیوں کا کڑوا ذائقہ، کبھی کبھار کمزوری، بھوک کم لگنا اور بلڈ پریشر گرنا۔ مگر کوئی دیرپا نقصان نہیں ہوا۔ موجودہ کیفیت (2025) آج وہ مکمل طور پر صحت مند ہیں، کینسر کے بغیر، فعال زندگی گزار رہے ہیں۔ ECOG 0  کے مطابق ان کی زندگی میں کوئی جسمانی پابندی نہیں رہی۔ https://www.njccm.org/post/remission-of-biopsy-proven-prostate-invasive-urothelial-carcinoma-after-failed-chemo-and-xrt-using-a References Shaker A. My Journey with Prostate Cancer and Laetrile (Urdu testimony).  YouTube. 2019. Available from: https://www.youtube.com/watch?v=y2rtnD8L4Ow

Dr. Qaisar J. Qayyum Chief Editor, Noor Journal of Complementary and Contemporary Medicine, Clinical Assistant Professor, Oklahoma, USA.   Email :   chiefeditor@njccm.org Original Case Report Abstract Background:  Amygdalin (laetrile, “vitamin B17”), derived from bitter apricot kernels, has long been controversial in oncology. Although dismissed by conventional guidelines, patients continue to report unexpected recoveries. Case Presentation:  We report the case of Mr. A.S., a U.S. patient with biopsy-proven, high-grade, muscle-invasive urothelial carcinoma with prostatic extension, which clinically, he believed he had “prostate cancer”. Following recurrence in 2018 despite chemotherapy and radiotherapy, his doctors offered radical surgery, which would remove both bladder and prostate. He declined radical cystoprostatectomy and adopted an alternative regimen of bitter apricot kernels, amygdalin (B17) tablets, and a strict vegetarian, sugar-free diet. Over six years of follow-up, repeated PET/CT scans documented complete remission, with normalization of hematology and chemistry labs. Methods:  Data were collected via direct patient interview, review of his Urdu video testimony on YouTube [1], and partial review of oncology notes, labs, and imaging reports. Not all laboratory results were available. Conclusion:  This case illustrates durable remission of a poor-prognosis malignancy, highlighting the need for unbiased investigation of amygdalin therapy and transparency regarding suppressed historical evidence [2,3]. Introduction Introduction Muscle-invasive urothelial carcinoma with prostatic extension is an aggressive disease, frequently requiring radical cystoprostatectomy after recurrence. Patient survival is limited, and treatment options beyond chemotherapy and radiotherapy are few. Amygdalin (laetrile, “vitamin B17”), a cyanogenic glycoside most concentrated in bitter apricot kernels , is also naturally found in bitter almonds, peach pits, apple seeds, cherries, and plums . Its widespread occurrence in seeds explains its use in folk remedies long before its controversial promotion in modern oncology. In the mid-20th century, amygdalin was popularized as an anti-cancer agent, but mainstream oncology dismissed it as ineffective [3]. However, historical evidence — including positive findings at Sloan Kettering later buried under institutional pressure [2,8] — and anecdotal patient testimonies continue to suggest possible benefit. The case of Mr. A.S. is particularly notable. Biopsy confirmed urothelial carcinoma with extension into the prostate, yet the patient himself understood it as “prostate cancer.” Later, he was told the surgical plan would remove both prostate and bladder. This dual framing reflects both histological accuracy and patient experience. Case Presentation Patient:  Mr. A.S., 71 y/o male, USA. Information Sources:  Direct telephone interview, Urdu YouTube testimony [1], and available oncology records. Not all laboratory results were accessible. Diagnosis (March 2016):  Biopsy-confirmed high-grade, muscle-invasive urothelial carcinoma with prostatic extension. Clinically, the patient believed he had prostate cancer, and that believe later was solidified since he was offered surgery, which would have included removal of both bladder and prostate. Initial Treatment (2016):  Four cycles of gemcitabine + carboplatin (Sept–Nov). Recurrence (April 2018):  PET/CT revealed a 6.3 × 5.5 cm hypermetabolic pelvic mass adjacent to prostate, with multiple pelvic lymph nodes. Radical cystoprostatectomy was recommended; patient refused. Additional Therapy (May–July 2018):  Pelvic radiotherapy with weekly cisplatin. Cystoscopy (Aug 2018):  Inflammation of prostatic urethra, no mass. Alternative Regimen (September 2018): Bitter apricot kernels: ~30/day in 5 divided doses (7,7,7,5,4) x 12 months, reduced to 20/day for few months, then to 10/day for few months. Currently taking 5 daily. Amygdalin tablets: 500 mg, 3 times/day × 1 year, tapered to ½ tablet daily, still continuing. Vegetarian, sugar-free diet, one teaspoon olive oil twice/day. Product Source: The patient obtained his B17 (amygdalin) tablets from Cytopharma  ( www.cytopharma.com ), and used bitter apricot kernels purchased via Amazon  ( link ). These were taken consistently along with dietary modifications. Follow-up Imaging:  PET/CTs (Jan 2019, Jul 2020, Mar 2023, Sept 2024) documented complete remission, no recurrence or metastases. Latest Labs (Sept 2024):  WBC 7.0 × 10³/μL, Hgb 16.2 g/dL, Platelets 188 × 10³/μL, CMP normal. Side Effects:  Bitter taste, transient hypotension, asthenia, reduced appetite. No persistent toxicity noted. Current Status (2025):  Alive, cancer-free, active (ECOG 0: fully active, no restrictions). Mechanism of Action of Amygdalin (B17) Natural Occurrence: Amygdalin is a cyanogenic glycoside naturally present in various seeds and kernels such as apricot kernels, bitter almonds, apple seeds, peach pits, and plum kernels . Its content in seeds varies widely, e.g. Bolarinwa et al. quantified up to 17.5 mg/g in some Rosaceae species (14) Enzymatic Activation: Amygdalin can be hydrolyzed by β-glucosidase , releasing hydrogen cyanide, benzaldehyde, and glucose. Tumor tissues may express higher β-glucosidase activity, enhancing local cyanide release, while normal tissues detoxify via rhodanese [3,4,6]. Cytotoxicity: Hydrogen cyanide inhibits cytochrome oxidase, impairing oxidative phosphorylation and leading to apoptosis. Benzaldehyde Contribution: Benzaldehyde may contribute to cytotoxicity by promoting oxidative stress in malignant cells [5]. Metabolic Context: The patient’s strict sugar-free diet could enhance selectivity, because many tumors rely heavily on glycolysis (the Warburg effect) [4,5]. Discussion Mr. A.S.’s case demonstrates a prolonged remission in the setting of a poor-prognosis malignancy. While causality cannot be definitively proven, the close temporal association between the initiation of amygdalin therapy and the subsequent remission challenges the absolute dismissal of this agent [3–6]. In the absence of financial incentives, and given the durability of the response, common sense suggests that the alternative regimen likely contributed meaningfully, unless one attributes the outcome solely to a rare spontaneous remission, statistical chance, or divine intervention. Sloan Kettering Suppression The 1977 Sloan Kettering controversy, highlighted in The Lie of America’s War on Cancer  [2], revealed how positive experimental results with amygdalin, reported by Dr. Kanematsu Sugiura, were obscured within a “negative” overall conclusion [8]. “Every experiment that was done that came out positive had to be redone and retested… Sloan Kettering did something incredibly clever. They took his positive data and embedded it into the negative paper… They told him: ‘We’re going to have an overall negative conclusion, but to represent your position, we’ll put your data into the paper.’” This episode illustrates how institutional bias and external pressures can distort the scientific record and delay serious inquiry into potentially beneficial therapies. Quality of Life Considerations Standard management at recurrence would have required radical cystoprostatectomy, removing both bladder and prostate with permanent urinary diversion. Instead, the patient retained both organs, remained disease-free, and experienced only minor adverse effects from amygdalin therapy. For patients whose conventional choices are limited to severely mutilating surgery, poor quality of life, or death, investigating alternative approaches should not be dismissed; it represents a rational and humane option. Safety Considerations At the same time, it is essential to acknowledge safety concerns. According to the U.S. National Cancer Institute [3], the side effects of laetrile/amygdalin mirror cyanide poisoning and may include liver damage, neuropathy leading to difficulty walking, fever, coma, and even death. Laetrile is not approved for use in the United States. These warnings underscore the importance of careful monitoring and balanced risk–benefit assessment when considering patient reports such as that of Mr. A.S. Broader Evidence in Other Cancers Beyond urothelial carcinoma, experimental evidence suggests that amygdalin may exert anticancer effects across multiple malignancies. Christodoulou et al. reported that when combined with cisplatin, amygdalin enhanced cytotoxicity in breast cancer cell lines while simultaneously protecting normal breast epithelial cells and fibroblasts. This selective action points to a potential chemoprotective role  that could help preserve quality of life during chemotherapy [4]. In a murine breast cancer model, Mageid and Abdel-Rahman et al. demonstrated that amygdalin, administered alone or with tamoxifen, suppressed tumor biomarkers, strengthened antioxidant defenses, and activated apoptotic pathways, notably caspase-3 and p53  [11]. Complementing these findings, Zhu et al. reviewed broader data showing that amygdalin can induce apoptosis and inhibit proliferation in a range of cancers, including lung, breast, prostate, colorectal, cervical, and gastrointestinal tumors, largely through Bax/Bcl-2 modulation  and mitochondrial signaling pathways [12]. Research is also exploring novel delivery methods. Encapsulation approaches, including alginate-chitosan nanoparticles (ACNPs), are under investigation to enhance tumor-specific delivery of amygdalin while reducing systemic cyanide exposure [13]. Together, these studies suggest that amygdalin’s therapeutic potential may extend well beyond prostate-invasive urothelial carcinoma, justifying deeper investigation across oncology. Appendix — Selected Medical Record Excerpts Oncology Note (2018):  “Large hypermetabolic pelvic mass near right prostate gland… multiple pelvic lymph nodes.” Cystoscopy (2018):  “Inflammation in prostatic urethra but no mass.” Lab (2016):  WBC 2.5, Hgb 8.0, Plt 121. Lab (Sept 2024):  WBC 7.0, Hgb 16.2, Plt 188, CMP normal. CT (Sept 2024):  No recurrence or metastasis. Acknowledgment: This article was written with AI assistance. All claims are supported by credible, peer-reviewed references, which were validated for accuracy and authenticity. The AI synthesized information were reviewed by authors, ensuring scientific integrity throughout. In the event of any inadvertent errors, the responsibility lies with the AI/authors, and corrections will be made promptly upon identification. I would like to express my sincere gratitude to Dr Tahira Khalid , for her thoughtful review and invaluable feedback. Her expertise and guidance have played a pivotal role in refining and enhancing this article.   Conflict of Interest Statement: The author is the developer of a herbal formula and the owner of Dr. Q Formula/Insulinn LLC. However, this affiliation has not influenced the content, analysis, or conclusions of this article   Author’s Note on Scope and Intent: This article does not advocate the replacement of evidence-based conventional care modalities. All complementary interventions are intended to supplement, not supplant, standard clinical practice, and are implemented within a physician-governed, ethically reviewed, and fully documented medical framework. References Shaker A. My Journey with Prostate Cancer and Laetrile (Urdu testimony).  YouTube. 2019. Available from: https://www.youtube.com/watch?v=y2rtnD8L4Ow The Lie of America’s War on Cancer.  YouTube documentary. 2010. Available from: https://www.youtube.com/watch?v=RQfls0RzzCM PDQ® Integrative, Alternative, and Complementary Therapies Editorial Board. Laetrile/Amygdalin (Health Professional Version).  Bethesda (MD): National Cancer Institute; 2022. Available from: https://www.ncbi.nlm.nih.gov/books/NBK65988/ Christodoulou P, et al. Amygdalin as a chemoprotective agent in co-treatment with cisplatin: effect on normal and cancer cells. Front Pharmacol.  2022;13:1013692. Available from: https://www.frontiersin.org/articles/10.3389/fphar.2022.1013692/full Cecarini V, Selmi S, Cuccioloni M, et al. Targeting proteolysis with cyanogenic glycoside amygdalin induces apoptosis in breast cancer cells. Molecules.  2022;27(21):7591. Available from: https://www.mdpi.com/1420-3049/27/21/7591 Albogami S, et al. Evaluation of the effective dose of amygdalin on antioxidant gene expression and suppression of oxidative damage in mice. Saudi J Biol Sci.  2020;27(12):3258-64. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC7246030/ Dang T, et al. Severe cyanide toxicity from amygdalin tablets ingestion: a case report. Case Rep Med.  2017;2017:1-4. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC5587935/ Stock CC, Martin DS, Sugiura K, et al. Antitumor tests of amygdalin in spontaneous animal tumor systems. J Surg Oncol.  1978;10(2):89-123. PubMed PMID: 347176 - https://pubmed.ncbi.nlm.nih.gov/642516/ Moss RW. The Cancer Industry.  Brooklyn, NY: Equinox Press; 1996. Griffin GE. World Without Cancer: The Story of Vitamin B17.  Westlake Village, CA: American Media; 1974. Abdel Mageid AD, Abdel-Wadoud IM, Salim EI, Aljutaily T, Barakat H, Aljumayi H, Radhi KS, Almutairi SO, Ebeid TA. The protective and chemotherapeutical role of amygdalin in induced mammary cancer in experimental mice and upregulation of related genes. Sci Rep.  2025;15:9131. Available from: https://www.nature.com/articles/s41598-025-93620-2 Zhu H, et al. Pharmacological insights into amygdalin: apoptosis induction and antitumor effects in multiple cancers. Int J Mol Sci.  2023;24(18):14270. Available from: https://www.mdpi.com/1422-0067/24/18/14270 Rashid F, Ahmed Z, Hussain A, Batool R, Iqbal R, Majeed R, et al. Amygdalin: A review on its characteristics, antioxidant potential, gastrointestinal microbiota intervention, anticancer therapeutic and mechanisms, toxicity, and encapsulation. Front Nutr . 2022;9:959971. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC9599719 Bolarinwa IF, Orfila C, Morgan MR. Amygdalin content of seeds, kernels and food products commercially available in the UK. Food Chem.  2014;152:133–9. Available from: https://doi.org/10.1016/j.foodchem.2013.11.002

Dr. Qaisar J. Qayyum Chief Editor, Noor Journal of Complementary and Contemporary Medicine, Clinical Assistant Professor, Oklahoma, USA.   Email :   chiefeditor@njccm.org Kamarkas ( Butea monosperma  gum) N-of-1 Case Report Abstract Back pain is a leading global cause of disability. Postpartum women are especially vulnerable, with up to 75% reporting new or worsened pain immediately after delivery, and many continuing to suffer years later. Traditional South Asian medicine prescribes Kamarkas ( Butea monosperma  gum) as a musculoskeletal tonic during the postpartum period. We present an N-of-1 self-observational case conducted by a physician with a long-standing history of recurrent back pain and thoracic spasm. Over four weeks, Kamarkas was self-administered in doses of 0.5–2 g daily, first as a tea (soaked and boiled gum) and later as a puffed–capsule preparation. The tea was effective but poorly tolerated due to bitterness, while the puffed–capsule method was well tolerated. C linical outcomes included gradual reduction of mid-thoracic spasm (approximately T8–T10) and improvement in chronic back pain, along with resolution of a recurrent upper mid-back pain episode. A recent acute lower-back pain attack , unresponsive to prior herbal remedies, also resolved rapidly  during treatment. These observations support the hypothesis that Kamarkas relaxes musculature, allowing the body to repair itself. Experimental literature confirms anti-inflammatory and analgesic effects of Butea monosperma , but no prior clinical report has proposed or documented a direct spasm-relieving effect of the gum. This case reinforces the traditional role of Kamarkas in musculoskeletal health and highlights the need for systematic trials. Introduction Back pain is one of the most common health problems globally and remains the leading cause of years lived with disability (YLDs)  worldwide, affecting more than 619 million people  as of 2020 [1,2]. In women, the burden of back pain increases during and after pregnancy. A systematic review estimates a 40.5% global prevalence of pregnancy-related back pain  [3]. Postpartum, up to 75% of women report new or worsened back pain immediately after delivery , and many continue to suffer well beyond the puerperium [4]. Longitudinal data confirm that postpartum low back pain can persist well beyond the puerperium , with a significant proportion of women reporting symptoms two years after delivery [5]. Traditional South Asian medicine addresses this vulnerability through dietary and herbal formulations. Kamarkas ( Butea monosperma  gum) is a central component of sweet Panjiri/Laddu  preparations given for 30–40 days postpartum  (the chilla ) to strengthen back and pelvic tissues [6–8]. While ethnomedical texts and pharmacognosy sources describe Kamarkas as a “back tonic,” modern clinical reports are rare. This case report presents a physician self-experiment with Kamarkas, motivated by a history of chronic recurrent back pain and thoracic spasm unresponsive to standard herbal remedies. Case Presentation and Methods Subject The subject was a physician with chronic recurrent back pain, including frequent mid-thoracic (T8–T10) spasms  and episodic acute lower-back attacks . Prior herbal regimens had provided inconsistent benefit, prompting a structured self-trial of Kamarkas gum. Preparation and Administration Two methods of preparation were tested: Tea method : Gum soaked overnight, boiled in the morning, consumed as tea (~0.5–2 g equivalent). Effective but poorly tolerated due to bitterness and mucosal adhesion. Puffed–capsule method : Gum was exposed to very hot oil for 10–15 seconds , both to sterilize and kill potential contaminants, and to cause swelling/puffing. The puffed gum was then crushed, powdered, and encapsulated. Avoided bitterness; well tolerated. This process also likely reduces microbial contamination, a traditional concern addressed by frying in ghee during Panjiri preparation. Duration and Dose 4 weeks  total. Dose: 0.5 g → gradually increased to 2 g daily. Results Muscle spasm: Thoracic T8–T10 paraspinal spasm gradually decreased. Chronic back pain: Spasm reduction was accompanied by improvement in chronic back pain, including resolution of a recurrent upper mid-back T8–T10 pain episode  that had been long-standing and frequently recurred even just by streching. Acute lower-back pain: A recent acute lower-back pain episode , which had occurred prior to the trial and had not responded to previously effective herbal remedies, resolved rapidly after initiation of Kamarkas. Causation and activity relapse: Back pain improved within a few days of starting Kamarkas, which allowed resumption of usual activities such as climbing stairs. However, this early return of activity led to a recurrence of pain and spasm. With a more cautious approach, restricting activity until completion of the 30-day course, improvement was sustained. Tolerance: Tea form: poorly tolerated. Puffed–capsule form: well tolerated, no adverse effects. Duration: At the end of the 30-day trial, approximately 80% reduction in T8/10 spasm and pain was achieved. Based on the observed trend, a further 10 days of treatment is expected to bring complete resolution. Extending the course to 40 days also coincides with the traditional chilla  ( چِلّہ  ) period during which Kamarkas is prescribed in South Asian postpartum care. Discussion This N-of-1 case suggests that Kamarkas may have a novel role as a muscle relaxant , providing a therapeutic window for intrinsic repair of musculoskeletal tissue. Experimental studies support related properties of Butea monosperma : Anti-inflammatory activity  demonstrated in flower extracts [9]. Analgesic and anti-inflammatory effects of gum extract  confirmed in rodent models [10]. Neuropathic pain modulation  shown in chronic constriction injury models [11]. Traditional pharmacognosy texts describe the gum as a pelvic and back tonic  in menstruation, pregnancy, and postpartum states [8]. No prior study has documented gum-derived Kamarkas  as a spasm-relieving agent in humans. By combining ethnomedical background with self-observed outcomes, this case adds clinical plausibility to the hypothesis. Activity restriction: This experiment also highlights a practical clinical consideration. Although pain relief occurred quickly, premature resumption of full activity (e.g., climbing stairs) caused recurrence of pain and spasm. Sustained improvement was only achieved when activity was restricted until the end of the treatment course. This observation suggests that Kamarkas should be combined with a period of light, restricted activity to allow time for repair and prevent relapse. The principle mirrors traditional postpartum guidance in South Asia, where women are advised to avoid strenuous activity during the 40-day chilla . Tradition and therapeutic timeframe: Interestingly, the 30-day trial produced about 80% relief in thoracic spasm and pain, with projection that a full 40-day course may lead to complete resolution. This coincides with the traditional chilla  period prescribed in South Asian postpartum care, where Kamarkas is routinely administered for 30–40 days. The convergence of observed clinical benefit with ethnomedical practice supports the hypothesis that Kamarkas acts as a muscle relaxant, allowing the body to engage its own repair mechanisms. Conclusion This N-of-1 physician self-experiment with Kamarkas gum suggests a dual benefit: Gradual improvement of chronic thoracic spasm and pain. Rapid resolution of an acute lower-back pain attack resistant to prior herbal remedies. At the end of the 30-day trial, approximately 80% reduction in thoracic spasm and pain was achieved, with expectation that a full 40-day course may lead to complete resolution. This observation aligns with the traditional chilla  period of 40 days during which Kamarkas has historically been prescribed in postpartum care. The convergence of modern self-observation with longstanding ethnomedical practice suggests that the 40-day duration may represent not only a cultural convention but also a physiologically meaningful therapeutic window. Controlled clinical studies are warranted to further evaluate this possibility. Clinical Significance This N-of-1 case highlights Kamarkas ( Butea monosperma  gum) as a potential adjunct for recurrent musculoskeletal pain. A 30-day course provided approximately 80% relief of thoracic spasm and pain, with projected full resolution by 40 days. Importantly, early resumption of normal activity led to relapse, emphasizing that recovery requires both the herbal intervention and a period of light, restricted activity. The observed therapeutic window mirrors the traditional 40-day chilla  period used in South Asian postpartum care, suggesting that longstanding ethnomedical practice may reflect an optimal physiological timeframe. While preliminary, this observation supports further clinical evaluation of Kamarkas as a muscle relaxant and restorative agent in back pain management. Acknowledgment: This article was written with AI assistance. All claims are supported by credible, peer-reviewed references, which were validated for accuracy and authenticity. The AI synthesized information were reviewed by authors, ensuring scientific integrity throughout. In the event of any inadvertent errors, the responsibility lies with the AI/authors, and corrections will be made promptly upon identification. I would like to express my sincere gratitude to Dr Tahira Khalid , for her thoughtful review and invaluable feedback. Her expertise and guidance have played a pivotal role in refining and enhancing this article.   Conflict of Interest Statement: The author is the developer of a herbal formula and the owner of Dr. Q Formula/Insulinn LLC. However, this affiliation has not influenced the content, analysis, or conclusions of this article   Author’s Note on Scope and Intent: This article does not advocate the replacement of evidence-based conventional care modalities. All complementary interventions are intended to supplement, not supplant, standard clinical practice, and are implemented within a physician-governed, ethically reviewed, and fully documented medical framework. References WHO. Low back pain fact sheet . WHO website . Wu A, et al. Global Burden of Low Back Pain: Estimates from the GBD 2020 study.   Lancet Rheumatology.  2023. Lim ZX, et al. Global prevalence of pregnancy-related low back pain: a systematic review and meta-analysis.   BMC Pregnancy Childbirth.  2023. Corso M, Grondin D, Weis CA. Postpartum Low Back Pain: It is not always What You Think.   Obstet Gynecol Cases Rev.  2016;3:079. To WWK, Wong MWN. Persistence of back pain symptoms after pregnancy and bone mineral density changes as measured by quantitative ultrasound — a two-year longitudinal follow up study.   BMC Musculoskelet Disord.  2011;12:55. LeMasters K, et al. Maternal depression in rural Pakistan: role of postpartum period.   BMC Public Health.  2020. Chandra N, et al. Postpartum practices in India.   Women’s Health Reports.  2023. Jain A, et al. Butea monosperma.   Res J Pharmacogn Phytochem.  2010;2(1):7–13. Shahavi S, Desai S. Anti-inflammatory activity of Butea monosperma flowers.   Fitoterapia.  2008;79(2):82–85. PMID: 17904309 . Sharma V, Chaudhary R, et al. Evaluation of anti-inflammatory and analgesic activity of Butea monosperma gum.   Pharmacology Online.  2010;1:536–544. Thiagarajan VRK, et al. Ameliorative potential of Butea monosperma on chronic constriction injury (CCI) of sciatic nerve induced neuropathic pain in rats.   An Acad Bras Cienc.  2012;84(4):1091–1104. PMID: 23011113 .

Dr. Qaisar J. Qayyum Chief Editor, Noor Journal of Complementary and Contemporary Medicine, Clinical Assistant Professor, Oklahoma, USA.   Email :   chiefeditor@njccm.org Abstract Constipation affects nearly one-third of individuals over age 60. While general advice often includes increasing fiber, water, avoidance of offending drugs and physical activity, these strategies are frequently ineffective in older patients with comorbidities or frailty. This article outlines a low-risk, clinically observed protocol combining regularly timed defecation with early morning hydration, lemon-honey infusion, bed-based exercises, and topical coconut oil. Consistent improvements in one older individual (also the author) over six months revealed novel insights involving hydration timing, honey storage material, sensory activation, and perianal microtrauma healing. Introduction Chronic constipation remains a highly prevalent issue among older adults, with rates estimated at 33% in adults over 60 years of age [1]. The elderly are especially vulnerable due to age-related changes in colonic motility, polypharmacy, sedentary lifestyle, and impaired fluid intake. While conventional advice, fiber, fluids, and laxatives, may suffice in healthier populations, they often fail or cause discomfort in frail elderly patients. This article presents a practical case-based protocol developed and tested by the author, a physician experiencing age-related constipation, over a six-month period. The approach incorporates: Timed defecation Timed hydration prior to defecation Lemon-honey infusion (with glass-stored honey) Supine lower body exercises Topical virgin coconut oil for sphincter tone modulation Some elements of this protocol introduce novel clinical hypotheses not widely explored in mainstream gastroenterology literature. The integration of personal observation, physiologic rationale, and reflection make this a valuable autoethnographic case study  for further research. Case Overview: Managing Constipation in Later Life: A Physician’s Self-Experimentation Case Report The subject, a physician in his late sixties with diabetes, hypertension, and coronary artery disease, had struggled with persistent constipation, characterized by infrequent, hard stools and incomplete evacuation. Standard remedies, including fiber supplements and stool softeners, provided only intermittent relief and often led to bloating or unpredictability. Over a six-month period, the subject self-tested and refined a multi-step daily protocol. All elements were chosen for safety, affordability, and physiologic plausibility. Subjective improvements included: More regular and complete bowel movements Less straining Marked reduction in sensation of rectal pressure or incomplete evacuation Description of the Protocol 1. Timed Early Morning Hydration (60–70 Minutes Before Attempted Defecation) One glass of 500 ml of room-temperature water was consumed immediately upon waking, 60–70 minutes prior to planned defecation. Hypothesis : The delayed window allows water to reach the colon, softening stool, rather than simply stimulating upper GI motility. Clinical Benefit : Timing hydration ahead of evacuation consistently improved stool consistency and reduced straining. 2. Lemon and Honey Mixture (Without Water) – Glass-Stored Honey Instead of traditional lemon water, the patient consumed a thick emulsion of: 1 tablespoon of honey (stored in a glass  bottle) 1 teaspoon of fresh lemon juice No water was added ; the consistency was intentionally kept thick. Observation : Plastic-stored honey was noticeably less effective. Glass-stored honey reliably softened stool and triggered defecation more consistently. Possible Mechanisms : Leaching of microplastics or degradation of honey bioactives in plastic [2] Electrostatic or enzymatic alterations Changes in flavor profiles known to affect TRP receptor activation (discussed below) 4. Topical Virgin Coconut Oil Application Post-Defecation After each bowel movement and daily after showering, a small amount of virgin coconut oil was rubbed to the anus and perianal area. Rationale : Repeated microabrasions caused by hard stool likely trigger increased sphincter tone. Hypothesis : Soothing the skin and local tissue may interrupt the cycle of: Minor trauma → increased tone → impaired evacuation → more trauma Clinical Insights and Emerging Hypotheses A. Hydration Timing Enhances Colonic Access Rather than stimulating upper GI motility reflexively, hydration 60–70 minutes before attempting to evacuate may allow water to directly reach and soften colonic contents. This strategy departs from the classic "drink water and go" model, suggesting a physiological delay between hydration and colonic benefit. B. Container Material Affects Honey’s Clinical Efficacy Subjective reporting showed that glass-stored honey outperformed plastic-stored honey. Food science literature supports this , noting increased enzymatic degradation and flavor loss in plastic containers [2]. C. Neurogenic Modulation and TRP Channel Involvement A noticeable softening of stool and urge to defecate occurred within 5–15 minutes of ingesting the lemon-honey mixture. This rapid onset suggests mechanisms beyond delayed osmotic action and points toward sensory-neurogenic modulation. One plausible mechanism involves TRP (Transient Receptor Potential) channels , which are known to mediate chemosensory input from the oral cavity and upper gut to the enteric nervous system. These channels are sensitive to a variety of stimuli such as heat, acidity (as in lemon), osmolarity (as in honey), and certain natural compounds. Their activation can initiate neural reflexes that influence gut motility, secretion, and visceral sensitivity, even before the ingested substance reaches the colon. In particular, TRPV1  and TRPA1  subtypes have been studied for their role in modulating gastrointestinal responses to chemical and thermal stimuli. Lemon juice, due to its citric acid content, and honey, through its high osmolarity and sugar content, may synergistically activate these pathways, resulting in prompt peristaltic stimulation/secretomotor responses. This mechanism is consistent with prior hypotheses involving orally mediated TRP activation  in other contexts, including mustard (6) ingestion for leg cramps, where chemosensory signaling was proposed to induce systemic neuromuscular effects via cranial and enteric reflex arcs [5]. While not yet established in mainstream constipation guidelines, such TRP-mediated effects represent a compelling target for further exploration, particularly in interventions that rely on small quantities of potent, natural substances. Additional Hypothesis: Sphincter Tone as a Feedback Loop While sphincter spasm is a known response to anal fissures, this case suggests a subclinical loop : Hard stool → microabrasions of the anal canal → Increased sphincter tone as a protective response → Reduced evacuation and increased stool dehydration → Further hard stools and worsening constipation This feedback loop is not widely discussed in literature but could represent a missing physiologic contributor in chronic constipation. Proposed Disruption : Gentle perianal rubbing of virgin coconut oil seems to help break this cycle by soothing tissues, reducing local irritation, and allowing for sphincter relaxation and improved defecation dynamics. Conclusion This reflective case study introduces a simple, home-based regimen for managing chronic constipation in elderly individuals, emphasizing: Key Clinical Insights and Emerging Hypotheses Fixed Timing of Defecation to Promote Predictability Establishing a regular morning schedule for bowel movements may entrain the gut to respond more reliably, aligning with circadian regulation of colonic motility. Hydration Timing as a Modifiable and Underexplored Variable Deliberate early morning fluid intake—60 to 70 minutes before attempted defecation, may directly influence colonic stool hydration, offering a non-pharmacologic mechanism to ease stool passage. Impact of Storage Material on Natural Product Efficacy Preliminary clinical observations suggest that honey stored in glass may retain greater properties than that stored in plastic, possibly due to preservation of enzymatic or antioxidant activity. Sensory-Gut Signaling via TRP Channels or Similar Receptors Rapid onset of gastrointestinal response following ingestion of lemon-honey mixture may be mediated by sensory receptors such as transient receptor potential (TRP) channels, which are known to activate enteric neural circuits and modulate motility. Anal Sphincter Tone as a Reinforcing Element in the Constipation Cycle Recurrent passage of hard stool may cause microabrasions in the anal canal, triggering a protective increase in sphincter tone. This heightened tone can impair evacuation, promote further stool dehydration, and perpetuate a self-reinforcing cycle of constipation, an underrecognized mechanism in current literature. Topical Use of Virgin Coconut Oil for Perianal Soothing and Healing Application of a small amount of virgin coconut oil around the anal area after defecation and bathing may help reduce irritation, promote local healing, and disrupt the feedback loop of sphincter hypertonicity. This low-cost intervention offers potential benefit with minimal risk, particularly in elderly or post-surgical patients. Each of these interventions has demonstrated individual effectiveness when applied in the context of a balanced diet. However, the author sees added value in combining them, particularly when single interventions yield suboptimal responses. Although this report is based on a single-subject experience, the clinical insights and observed synergies may serve to generate hypotheses for larger studies and support safe, patient-centered experimentation in routine practice . Acknowledgment: This article was written with AI assistance. All claims are supported by credible, peer-reviewed references, which were validated for accuracy and authenticity. The AI synthesized information were reviewed by authors, ensuring scientific integrity throughout. In the event of any inadvertent errors, the responsibility lies with the AI/authors, and corrections will be made promptly upon identification. I would like to express my sincere gratitude to Dr Tahira Khalid , for her thoughtful review and invaluable feedback. Her expertise and guidance have played a pivotal role in refining and enhancing this article.   Conflict of Interest Statement: The author is the developer of a herbal formula and the owner of Dr. Q Formula/Insulinn LLC. However, this affiliation has not influenced the content, analysis, or conclusions of this article   Author’s Note on Scope and Intent: This article does not advocate the replacement of evidence-based conventional care modalities. All complementary interventions are intended to supplement, not supplant, standard clinical practice, and are implemented within a physician-governed, ethically reviewed, and fully documented medical framework. Reference List Bharucha AE, Pemberton JH, Locke GR. 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