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Safety & Side Effects

What Adverse Event Reports Can and Cannot Tell You

FAERS and the Yellow Card scheme count reports, not cases, and a count with no denominator is not a rate. Here is what a spontaneous report can establish, and what it cannot.

A report is a numerator with no denominator

The FDA Adverse Event Reporting System and the MHRA Yellow Card scheme collect suspicions. Someone believed a medicine might have caused something and said so. That is the entire evidentiary content of a single report: not a verified diagnosis, not an adjudicated case, and not a finding that the drug was involved. Regulators say so plainly on their own public dashboards, because the alternative reading is so tempting.

The arithmetic is the core of the problem. To state how often something happens you need cases in the numerator and exposure in the denominator, and a spontaneous system supplies neither cleanly. The numerator is a filtered, self-selected fraction of events someone chose to write down. The denominator does not exist inside the database at all, because nothing about how many people were dispensed the drug, or for how long, is captured by the act of filing a report.

The consequence is immediate for the comparison readers most want to make. Ranking two drugs by raw report count tells you which was taken by more people, discussed more loudly and marketed more recently. Semaglutide and tirzepatide accumulated reports rapidly through the early 2020s largely because dispensing volumes for incretin drugs rose steeply over the same period. A curve that rises with prescriptions is not evidence that a drug became more dangerous.

Who files a report, and what actually gets stored

Two streams feed these databases. The first is mandatory: an authorisation holder that learns of a serious and unexpected suspected reaction must submit an expedited report within a short statutory window, with everything else flowing in periodically. The second is voluntary, covering clinicians, pharmacists and, since the mid-2000s in the United Kingdom, patients reporting directly. The mandatory stream dominates the volume, which is worth holding onto: the size of a drug's record depends heavily on whether a company exists that is obliged to keep it.

What gets stored is a coded version of the clinical narrative. Free text is mapped to standard terms from the MedDRA dictionary, and the mapping is lossy in both directions. One clinical picture can be split across several preferred terms, fragmenting a signal into pieces that individually look unremarkable, while a broad term can pool genuinely different problems into one impressive count. Anyone querying a public dashboard is querying coding decisions as much as patients. The same episode can also arrive three times over, from the patient, the prescriber and the manufacturer, and deduplication is imperfect.

Under-reporting is the normal state, and it is uneven

The best single estimate of how much is missed comes from a systematic review of thirty-seven studies across twelve countries, which found a median under-reporting rate of around ninety-four percent. The figure is old enough and variable enough to treat as an order of magnitude rather than a constant, but the direction is not in dispute: most adverse events that occur never enter any national system.

Uniform under-reporting would be survivable, since relative comparisons would still hold. What happens instead is differential under-reporting. Serious events are reported more often than mild ones, and unexpected events more often than labelled ones. A clinician seeing nausea in a patient on a GLP-1 receptor agonist is seeing what the prescribing information predicts and has little reason to file; the same clinician seeing an unfamiliar symptom may well file. The database is enriched for the surprising, which is useful for detection and disastrous for estimating frequency.

Time adds another distortion. The classical description, from work on non-steroidal anti-inflammatory drugs in the 1980s, is that reporting climbs after launch and falls away as prescribers grow familiar with a product. Later attempts to reproduce that pattern have been inconsistent, so hold it as a caution rather than a law. The narrower and defensible version still matters: a drug's position in its own publicity cycle affects its report count independently of its safety.

Stimulated reporting: attention manufactures data

Notoriety bias is the pharmacovigilance term for what happens when a suspected reaction becomes news. A regulator opens a review, a broadcast segment airs, a law firm buys advertising naming a drug and a condition, and reports for that pairing step upward within weeks. The step is often visible as a near-vertical line in the monthly counts, aligned to a date in the news rather than to anything about exposure. Once a pairing has been publicised, every count for it afterwards is partly a measurement of the publicity.

The clearest modern demonstration came through the Yellow Card scheme during the COVID-19 vaccination programme, when a campaign actively encouraging direct patient reporting produced volumes far above the baseline for ordinary medicines. That was a joint product of unprecedented exposure and unprecedented awareness, not a comparative risk ranking against products nobody was urged to report on.

Peptide-adjacent signals have their own version. Online communities discuss a symptom, the discussion propagates, and a wave of reports follows it. The gastrointestinal motility reports associated with GLP-1 receptor agonists illustrate the difficulty: delayed gastric emptying is a real and expected pharmacological effect, severe cases are real, and the reporting surge nonetheless tracked media coverage and perioperative guidance closely enough that the curve cannot be read as an incidence curve. Attention works in reverse too: nobody campaigns for reports on compounds that were never approved.

How regulators turn a pile of reports into a signal

Signal detection asks a comparative question inside the database: is this drug reported with this event more often than expected, given how often each appears overall? The simplest implementations are the proportional reporting ratio and the reporting odds ratio. A widely used screening rule from the early 2000s requires a proportional reporting ratio of at least two, a chi-square of at least four, and at least three cases before a pairing warrants a human look.

Those thresholds exist because small numbers behave badly: two reports out of two produce a spectacular ratio and mean nothing. Bayesian shrinkage methods were built for this, including the empirical Bayes approach the FDA adopted for routine screening and the Bayesian confidence propagation neural network used on the global VigiBase collection. Both pull sparse estimates toward the null in proportion to how little data supports them, giving more stable rankings rather than more truthful ones.

The critical limitation is the comparator. Expected counts come from the rest of the database, so every result is relative to reporting behaviour rather than to the population. This produces masking, sometimes called competition bias: a heavily reported product dominating a class inflates the expected count for events in that class and can conceal a genuine excess in a smaller product beside it. In an area as concentrated as the incretin drugs, that is not theoretical.

Whatever emerges is a signal in the formal sense: information suggesting a possible causal association judged to warrant further evaluation. It is a hypothesis with a case count attached, and a screen calibrated to miss almost nothing will raise many that fail. Most do fail. That is the system working, not malfunctioning.

Three GLP-1 signals and what became of each

The pancreatitis signal is the cleanest worked example. A 2011 analysis of the FDA reporting database found disproportionate reporting of pancreatitis and of pancreatic and thyroid cancer for incretin-based therapies, and it received wide coverage. The FDA and the EMA then reviewed the full evidence base, including trial data, preclinical toxicology and epidemiological studies, and set out a joint assessment concluding that the available data did not support a causal association with pancreatic disease. The signal was correctly generated, properly evaluated and not confirmed.

The suicidal ideation signal followed the same arc a decade later. A small number of spontaneous reports from one national authority in 2023 prompted the European regulator's safety committee to open a formal review of GLP-1 receptor agonists. The FDA said its preliminary evaluation found no evidence of a causal relationship, and the European review concluded the evidence did not support one. Confounding by indication is severe here, since the treated population carries an elevated background rate of depression.

The third example runs the other way. Non-arteritic anterior ischaemic optic neuropathy is rare enough that spontaneous reports alone would have stayed ambiguous indefinitely. What moved the question was a retrospective cohort study published in 2024 in a specialty eye-centre population, reporting a substantially higher hazard among patients prescribed semaglutide than among matched patients on other agents. European regulators later treated it as a very rare adverse reaction and moved to reflect it in product information. The resolution came from a design with a denominator.

A fourth case never touched post-marketing reports at all. The boxed warning for thyroid C-cell tumours carried by several long-acting GLP-1 receptor agonists, including semaglutide and tirzepatide, originates in rodent carcinogenicity studies done before approval. Signals arrive from preclinical work, trials, registries and spontaneous reports, and the spontaneous stream is only one of the four.

Why grey-market peptides barely register at all

BPC-157 has no approved human indication in any major jurisdiction. Reviewing which bulk substances may be used in compounding, the FDA placed it in the category raising significant safety concerns, citing insufficient information to evaluate its risks. That status is the whole story for reporting purposes: with no approved product there is no authorisation holder, no expedited reporting obligation, and in most transactions no prescriber, pharmacy record or product identifier.

For an event to reach a national database, someone must present for care, disclose the compound, and have a clinician who recognises it and files. Every step leaks. Material bought as research-labelled powder is often not mentioned to a treating clinician, and a clinician who has never heard the name has little reason to attribute anything to it. Independent testing has also repeatedly found grey-market vial contents that do not match the label, so even a filed report may not identify the real exposure.

Compounded products sit awkwardly in between. A compounding pharmacy carries different reporting obligations than a new drug application holder, and the FDA has described receiving adverse event reports involving compounded semaglutide, including events arising from patients measuring their own doses from vials rather than from any property of the molecule. The database captures a product-and-practice combination, not the drug in isolation.

The practical rule follows. For an approved drug with high dispensing volume, an empty cell in the reporting database is weak evidence that an event is rare. For a compound sold outside the licensed supply chain, it is no evidence at all. Absence of reports is a property of the reporting pipeline before it is a property of the molecule, and for these compounds that pipeline is essentially closed.

What an individual report genuinely can establish

Spontaneous reporting is very good at one job nothing else does as cheaply: detecting rare, serious and clinically distinctive events that essentially do not occur at background in the treated population. The Yellow Card scheme exists because of exactly such an event, established in 1964 after the thalidomide disaster. Aplastic anaemia, anaphylaxis, angioedema, severe cutaneous reactions and characteristic congenital malformations have near-zero background rates, so a handful of well-documented cases can carry real weight.

At the level of a single case, certain features raise evidential value considerably. A positive dechallenge, where the event resolves after the drug is stopped, is informative; a positive rechallenge, where it recurs on restarting, is stronger. So are a plausible time to onset, the absence of a competing explanation, and a known mechanism that predicts the effect. Structured instruments such as the Naranjo algorithm and the WHO causality categories exist to make that judgement consistent across reviewers, not automatic.

The mirror weakness follows directly. Spontaneous reports are close to useless for common events in populations that already have them. Gallbladder disease, cardiovascular events, mood disorders and pancreatitis all occur at meaningful rates in people with obesity and type 2 diabetes whether or not they take anything, so the background swamps whatever the drug contributes.

That is the reasoning behind active surveillance. The FDA's Sentinel programme, built after 2007 legislation, runs pre-specified queries across large claims and health record populations where the denominator is known and an unexposed comparator exists. Regulators increasingly use spontaneous reports to raise questions and active surveillance, registries or trial safety databases to answer them.

Reading a safety dashboard without fooling yourself

A short set of habits prevents most common errors. Never compare counts between drugs without knowing something about relative exposure. Never read a rise over time as a rise in risk until you have checked what dispensing volumes did over the same window. When you see an inflection, look for a date: a regulatory announcement, a covered publication or a litigation campaign in the same month is the likeliest explanation.

Where narrative detail is available, read it rather than the coded term. A report documenting concomitant medicines, the indication, a plausible latency and a dechallenge is worth more than fifty consisting of a drug name and a symptom word. Counting treats those as equal; they are not.

Then ask whether anyone has studied the question properly. If a cohort study, registry analysis or pooled trial safety database addresses the same drug and event, that evidence supersedes the report count outright rather than sitting alongside it. The count did its job when it prompted the study.

Finally, allow a signal to stay unresolved. Much of what is flagged reaches neither confirmation nor refutation, because nobody funded the study that would settle it. The honest description is neither a confirmed harm nor a debunked scare: an open question with a known number of reports attached.

What we still don't know

Every claim above has a limit. These are the questions the current evidence does not answer.

  • The reporting fraction for events involving peptides bought outside the licensed supply chain has never been estimated, so the size of that blind spot is itself unmeasured.
  • Whether severe gastrointestinal motility cases reported with GLP-1 receptor agonists represent a distinct clinical entity beyond expected delayed gastric emptying, and at what frequency, is unresolved by the report data and by the cohort work published so far.
  • How much of the observed association between semaglutide and non-arteritic anterior ischaemic optic neuropathy is attributable to the drug rather than the underlying metabolic disease remains open, since the cohort evidence comes from selected specialty populations.
  • Nobody has tested whether disproportionality screening performs as well for peptide drugs as for small molecules, given that peptides cluster into a few crowded classes where masking between products is most likely.

Common questions

Can I use FAERS to work out how often a side effect happens?
No, and this is the most common misuse of the database. Calculating a frequency requires a numerator and a denominator. FAERS provides an incomplete, self-selected numerator and no denominator at all, since nothing in it records how many people were dispensed the drug or for how long. Any percentage derived from FAERS counts is arithmetic performed on a number never designed to support it.
Does a large number of reports for semaglutide mean it is more dangerous than older drugs?
Not by itself. Report volume is driven by three things unrelated to per-patient risk: how many people take the drug, how recently it launched, and how much public attention it has drawn. Incretin drugs score highly on all three. Showing that one drug is more dangerous than another requires exposure-adjusted comparison, ideally from trials or cohort studies with a defined denominator and a comparator group.
Why are there almost no adverse event reports for BPC-157?
Because the reporting pipeline for it barely exists. There is no approved product, so no company carries a legal duty to report; most transactions involve no prescriber and no pharmacy record; and users often do not tell a clinician what they took. Grey-market material also frequently fails to match its label, so even a filed report may not identify the actual exposure. The empty record describes the pipeline, not the compound's safety.
What is the difference between a safety signal and a proven side effect?
A signal is a hypothesis: a pattern in reported data suggesting a possible causal association that warrants investigation, and nothing more. A proven adverse reaction has survived evaluation against trial data, epidemiological studies, biological plausibility and often a time or dose relationship. Many signals are evaluated and dismissed, as the incretin pancreatitis signal was. Treating a signal as confirmed harm skips the entire evaluation step.
How do reviewers judge whether one report was actually caused by the drug?
They look at case-level features rather than counts. Did the event resolve when the drug was stopped, and did it return if the drug was restarted? Was the time to onset biologically plausible? Is there an alternative explanation such as another medicine or the underlying disease? Is there a known mechanism? Structured tools including the Naranjo algorithm and the WHO causality categories exist to apply those questions consistently across reviewers.
If these systems cannot prove causation, why do regulators keep them?
Because they catch a class of problem nothing else catches affordably. Spontaneous reporting covers every patient taking every marketed drug, indefinitely, which no trial can do. For rare, serious and distinctive events with a near-zero background rate, a small number of well-documented cases can be decisive. The Yellow Card scheme was created in 1964 precisely because no such early warning existed when thalidomide was in use.

What this is based on

Named sources, with what each one actually showed. We link live literature searches rather than a frozen citation list, so you can check the current record yourself.

  1. Hazell L, Shakir SAW. Under-reporting of adverse drug reactions: a systematic review — Reviewed thirty-seven studies across twelve countries and found a median under-reporting rate of about ninety-four percent for adverse drug reactions. find on PubMed
  2. Evans SJW, Waller PC, Davis S. Use of proportional reporting ratios for signal generation from spontaneous adverse drug reaction reports — Proposed the combination of a proportional reporting ratio of at least two, a chi-square of at least four and at least three cases that is still used as a screening benchmark. find on PubMed
  3. DuMouchel W. Bayesian data mining in large frequency tables with an application to the FDA spontaneous reporting system — Introduced the empirical Bayes shrinkage approach the FDA adopted for routine disproportionality screening of its reporting database. find on PubMed
  4. Bate A et al. A Bayesian neural network method for adverse drug reaction signal generation — Described the Bayesian confidence propagation neural network used by the WHO collaborating centre to screen the global VigiBase collection. find on PubMed
  5. Elashoff M, Matveyenko AV, Gier B, Elashoff R, Butler PC. Pancreatitis, pancreatic, and thyroid cancer with glucagon-like peptide-1-based therapies — Reported disproportionate adverse event reporting for pancreatitis and pancreatic cancer with incretin therapies, generating the signal that regulators later evaluated. find on PubMed
  6. Egan AG et al. Pancreatic safety of incretin-based drugs: FDA and EMA assessment — Joint regulatory review of trial, preclinical and epidemiological evidence concluding that the available data did not support a causal association with pancreatic disease. find on PubMed
  7. European Medicines Agency PRAC review of GLP-1 receptor agonists and suicidal ideation — Formal safety review opened in 2023 on the basis of spontaneous reports and concluded in 2024 that the available evidence did not support a causal association. find on PubMed
  8. Hathaway JT et al. Risk of nonarteritic anterior ischemic optic neuropathy in patients prescribed semaglutide — Retrospective cohort study in a specialty eye-centre population reporting a substantially higher hazard of the condition among patients prescribed semaglutide. find on PubMed
  9. Naranjo CA et al. A method for estimating the probability of adverse drug reactions — Established the structured causality algorithm that weights dechallenge, rechallenge, timing and alternative explanations for individual case assessment. find on PubMed
  10. WHO-UMC system for standardised case causality assessment — Defines the certain, probable, possible, unlikely, conditional and unassessable categories used to grade individual spontaneous reports. find on PubMed
  11. CIOMS Working Group VIII: Practical aspects of signal detection in pharmacovigilance — Sets out the working definition of a safety signal as information suggesting a possible causal association that warrants further evaluation. find on PubMed
  12. FDA Sentinel Initiative — Active surveillance system established under 2007 legislation that queries large claims and electronic health record populations where a denominator and comparator exist. find on PubMed
  13. FDA evaluation of BPC-157 for the 503A bulk drug substances list — Placed BPC-157 in the category of substances raising significant safety concerns for compounding, citing insufficient information to evaluate its risks. find on PubMed
  14. Weber JCP. Epidemiology of adverse reactions to nonsteroidal anti-inflammatory drugs — Original description of the post-launch rise and decline in reporting rates that later work has reproduced only inconsistently. find on PubMed

Peptides covered here

Terms used in this article

FDA Adverse Event Reporting System (FAERS)
FAERS is the FDA database of spontaneous adverse event reports for drugs and therapeutic biologics, a hypothesis-generating tool with no denominator and therefore no incidence rates.
Yellow Card Scheme
The Yellow Card Scheme is the United Kingdom's spontaneous reporting system, run by the MHRA, for suspected adverse drug reactions, vaccine and device problems and defective medicines.
Medicines and Healthcare Products Regulatory Agency (MHRA)
The Medicines and Healthcare products Regulatory Agency is the United Kingdom's medicines and device regulator, licensing products, classifying their supply and running national safety surveillance.
The Incretin Effect
The incretin effect is the larger insulin response to oral glucose than to intravenous glucose matched for the same blood glucose profile, and it is mediated mainly by GLP-1 and GIP.
Medical Dictionary for Regulatory Activities (MedDRA)
MedDRA is the standardised hierarchical terminology used to code adverse events for regulators, mapping a reporter's words onto a Preferred Term within a System Organ Class.
Systematic Review
A systematic review answers a defined question using a prespecified protocol, an explicit multi-database search, stated eligibility criteria and formal risk-of-bias assessment, unlike a narrative review.
Adverse Event (AE)
An adverse event is any untoward medical occurrence in someone receiving a medicine, recorded whether or not the drug caused it, which is why an event table is not a harm table.
Prescribing Information and the Label
Prescribing information is the regulator-approved labelling that defines a drug's authorised indications, dosing, warnings and pharmacology, and is the reference point for what a product may claim.
Agonist
An agonist is a ligand that binds a receptor and stabilises its active conformation, producing a biological response rather than merely occupying the binding site.
Glucagon-Like Peptide-1 (GLP-1)
Glucagon-like peptide-1 is an incretin hormone released by intestinal L-cells after a meal that stimulates glucose-dependent insulin secretion and suppresses appetite.
Pharmacovigilance
Pharmacovigilance is the science and practice of detecting, assessing, understanding and preventing adverse effects of medicines once they are in real-world use.
Gastric Emptying
Gastric emptying is the rate at which stomach contents pass into the duodenum, a major determinant of postprandial glucose and of incretin therapy tolerability.

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This article is educational information, not medical advice. It cannot account for your medical history, medications, or risk factors. Do not start, stop or change any treatment based on it. Speak to a qualified healthcare professional who knows your case. We publish no dosing protocols for unapproved compounds and link to no supplier.

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