Clinician reference tool — not medical advice. This is a clinical decision-aid intended for healthcare professionals: it gives deterministic suggestions to think with, not a diagnosis or a prescription. If you’re a patient, you’re welcome to look around — but please review anything here with your own doctor; it isn’t a substitute for personalized medical care.

Evidence: American Diabetes Association 2026 · sources last checked 2026-08-20

Reference tool — not medical advice. Thresholds, targets, and first-line agents differ by guideline body and change over time — switch the lens to compare. Clinician judgement, dosing/monitoring, contraindications, and live coverage always required. Runs entirely in your browser — no data is collected.

Diabetes agent selector

Choose the guideline lens (Diabetes Canada / ADA / ADA-EASD), enter comorbidities, glycemic status and renal function — get a comorbidity-driven agent across the full range: metformin, SGLT2i, GLP-1 RAs (oral & injectable), tirzepatide, DPP-4i, sulfonylurea, pioglitazone, and insulins (basal → basal-bolus). Organ protection drives the choice irrespective of A1c; marked hyperglycemia drives insulin.

Guideline lens

Comorbidities (drive the choice, irrespective of A1c)

Glycemic statuschoose one

Marked hyperglycemia / symptoms drive insulin

Renal function (eGFR)choose one

Priorities / constraints

Main driver

No compelling driver — individualize (cost, hypoglycemia, A1c)

Diabetes Canada framing

Metformin baseline; add cardiorenal-protective agents if indicated; incretins before insulin.

Notes

  • • Escalation (ADA): a GLP-1 RA is generally preferred over insulin. Incretins now include oral (Rybelsus) and injectable GLP-1 RAs and tirzepatide (dual GIP/GLP-1, most potent). Do not combine a DPP-4 inhibitor with a GLP-1 RA.

Suggested drug classesPer Diabetes Canada 2024.

Select any comorbidities and renal function to begin.

e.g. HF → SGLT2i; CKD → SGLT2i; ASCVD → GLP-1/SGLT2i; weight → tirzepatide/GLP-1; markedly high A1c / symptomatic → basal insulin; avoid injections → oral agents (incl. Rybelsus).

Should I be tested?

Last reviewed 2026-09-23

Testing concerns patients raise about insulin resistance and reactive hypoglycemia, usually after a naturopathic visit or an online read — what genuinely raises suspicion, what does not, and what to order instead.

Insulin resistance

Clinical diagnosis — no single test

Also called: insulin resistance, pre-diabetes I can't see yet, high fasting insulin, HOMA-IR

Patients hear 'insulin resistance' from an ND after a fasting insulin level or a calculated HOMA-IR score, from online calculators, or from a relative with type 2 diabetes. The underlying worry, that the body is struggling with blood sugar before a diabetes diagnosis is obvious, is legitimate and worth taking seriously. The specific test used to name it is the part that is not standardized.

Raises suspicion

  • • Increased waist circumference or abdominal weight gain
  • • Acanthosis nigricans (dark, velvety skin at the neck or armpits)
  • • High blood pressure
  • • High triglycerides or low HDL cholesterol
  • • Fatty liver on imaging or a persistently elevated ALT
  • • Polycystic ovary syndrome
  • • A strong family history of type 2 diabetes, or a personal history of gestational diabetes

Does not raise suspicion

  • • Fatigue or difficulty losing weight on their own, without other metabolic risk factors
  • • A single elevated fasting insulin or HOMA-IR result in someone with no other metabolic risk factors: there is no agreed cut-off that turns this into a diagnosis

Red flags

  • • Symptoms of high blood sugar itself, such as increased thirst, frequent urination, or unexplained weight loss: these need glucose or A1c testing now, not a wait-and-see approach

Who to test

  • Adults with metabolic risk factors (abdominal weight, high blood pressure, dyslipidemia, fatty liver, PCOS, or a family history of type 2 diabetes): HbA1c and fasting glucose (diabetes screening) (Situation-specific)Risk-based screening with A1c and/or fasting glucose, guided by a validated risk calculator such as CANRISK, is the recommended way to find diabetes-level or prediabetes-level risk. Fasting insulin and HOMA-IR are not part of this pathway.
  • Metabolic risk factors present: Lipid panel (total cholesterol, HDL, LDL, triglycerides) (Situation-specific), Liver panel (ALT, AST, GGT, ALP, bilirubin, albumin) (Situation-specific)A lipid panel and ALT (with a FIB-4 score if ALT is abnormal) capture the cardiovascular and fatty-liver risk that goes along with insulin resistance, and are things we can act on directly.
  • Specifically asking about a 'high insulin' or HOMA-IR result: Fasting insulin (Rarely indicated)Fasting insulin and HOMA-IR have no standardized reference range or validated diagnostic threshold for individual clinical use; they are research and epidemiological tools. What changes management is the A1c/glucose, lipid, blood pressure and liver picture, not the insulin number itself.

More likely instead

  • • Diabetes (an already-diagnosable prediabetes or type 2 diabetes on glucose/A1c criteria, which is what actually drives management)
  • • Cholesterol
  • • fatty liver disease captured on the liver panel
  • • PCOS, when applicable
  • • weight gain and lifestyle factors without a distinct, separately diagnosable metabolic condition

Counselling script

“If you have risk factors like weight around your middle, high blood pressure, or high triglycerides, your metabolic risk is real and worth acting on regardless of any insulin number. I wouldn't rely on a fasting insulin or HOMA-IR result to make that call, since there's no agreed threshold for diagnosing insulin resistance from it in one person. What I'd rather do is check your blood sugar, cholesterol, and liver enzymes, and build a plan from those.”

Chart snippet (OSCAR-safe plain text)

Concern discussed, not tested

Concern re: insulin resistance discussed, raised by patient or ND.
Discriminating features: abdominal obesity, hypertension, dyslipidemia, fatty liver, PCOS, family history of type 2 diabetes; reviewed.
Red flags: absent.
Assessment: no standardized diagnostic threshold for fasting insulin or HOMA-IR in routine care; metabolic risk better assessed with glucose/A1c, lipids, blood pressure, waist circumference and liver enzymes.
Plan: fasting insulin and HOMA-IR not ordered.
Ref: Diabetes Canada Clinical Practice Guidelines, chapters 3 and 4; Canadian Task Force on Preventive Health Care 2012.
Patient given info page: https://diabetes.ajaxharwoodclinic.com/patient#insulin-resistance
Revisit if: symptoms of hyperglycemia develop, or metabolic risk factors change.

Testing ordered

Concern re: insulin resistance discussed.
Discriminating features: metabolic risk factors present (specify: abdominal obesity, hypertension, dyslipidemia, fatty liver, family history).
Assessment: risk-based metabolic screening indicated.
Plan: A1c and/or fasting glucose, lipid panel, and ALT (with FIB-4 if abnormal) ordered; fasting insulin and HOMA-IR not ordered, as neither has a validated diagnostic threshold.
Ref: Diabetes Canada Clinical Practice Guidelines, chapters 3 and 4; Canadian Cardiovascular Society dyslipidemia guideline 2021; AASLD/AGA fatty liver pathway.
Patient given info page: https://diabetes.ajaxharwoodclinic.com/patient#insulin-resistance
Revisit if: results show prediabetes- or diabetes-range glucose, or symptoms of hyperglycemia develop.

Revisit if

  • • Symptoms of hyperglycemia develop (increased thirst, frequent urination, unexplained weight loss)
  • • A1c or glucose returns in the prediabetes or diabetes range
  • • New or worsening metabolic risk factors (weight gain, rising blood pressure, abnormal lipids or liver enzymes)

References

  1. 1. Diabetes Canada. Diabetes Canada Clinical Practice Guidelines: Screening for Diabetes in Adults (2018)Diabetes Canada's screening pathway is built on fasting plasma glucose and/or A1C, not a fasting insulin level or HOMA-IR calculation
  2. 2. Diabetes Canada. Diabetes Canada Clinical Practice Guidelines: Definition, Classification and Diagnosis of Diabetes, Prediabetes and Metabolic Syndrome (2018)Prediabetes is defined by impaired fasting glucose, impaired glucose tolerance, or an A1C of 6.0% to 6.4%, not by an insulin or HOMA-IR value
  3. 3. Canadian Task Force on Preventive Health Care. Recommendations on screening for type 2 diabetes in adults (2012)— older guidelineRisk-based, validated-calculator-guided A1C screening (e.g. CANRISK) is recommended over routine screening in adults at low risk
  4. 4. Canadian Cardiovascular Society. 2021 Canadian Cardiovascular Society Guidelines for the Management of Dyslipidemia for the Prevention of Cardiovascular Disease in Adults (2021)Lipid screening in adults over 40, or at any age with a risk condition, is part of assessing the same metabolic risk profile
  5. 5. Ajmera et al., Hepatology (validation cohort describing the AGA/AASLD NAFLD clinical pathway). Validation of AGA clinical care pathway and AASLD practice guidance for nonalcoholic fatty liver disease in a prospective cohort of patients with type 2 diabetes (2024)A risk-based pathway starting with ALT, and FIB-4 if abnormal, is the current approach to finding metabolic dysfunction-associated liver disease in people with metabolic risk factors
Evidence notes

Tag rationale: B, not borderline. Insulin resistance is a real, mechanistically well-described physiological state and a genuine risk marker for type 2 diabetes, but it has no validated clinical diagnostic test or agreed threshold in routine primary care; prediabetes and diabetes themselves are defined by glucose/A1c criteria [2], not by an insulin or HOMA-IR value. Gap: this session tried to independently verify a source specifically stating that HOMA-IR is not standardized for individual clinical/diagnostic use (attempted Wallace/Levy/Matthews 'Use and Abuse of HOMA Modeling', Diabetes Care 2004) but could not fetch a verbatim, substring-matchable quote from an accessible copy (Diabetes Care and the PDF mirrors returned HTTP 403). Per the batch instructions this falls back to [1], whose screening pathway simply does not include fasting insulin or HOMA-IR, which supports the same clinical conclusion (insulin-based testing is not part of the standard diagnostic pathway) without directly asserting a standardization critique; flagged as an honest gap rather than a fabricated citation. Per batch notes, the linked cortisol-serum, leptin and igf-1 test records were reviewed: none has a validated role in evaluating insulin resistance. They are sometimes bundled with fasting insulin into an ND 'metabolic' or 'hormone' panel for fatigue or weight-gain complaints, but each test's own record documents a validated role only for its specific indication (adrenal insufficiency/Cushing's for cortisol, congenital leptin deficiency for leptin, acromegaly for IGF-1), none of which is insulin resistance; not cited as formal references here since the claim is drawn from those tests' own already-verified records rather than a new source. Host is 'diabetes' per batch instruction (this renders as a new section in the existing ahc-diabetes tool); the host choice between diabetes. and glp. is pending Dr. Yu's decision per docs/ecosystem-survey.md, and should not be built until he confirms which subdomain gets the new section. Resolved 2026-09-23: Dr. Yu confirmed hosting on diabetes., not glp. (decision 10).

Reactive hypoglycemia (sugar crashes after eating)

Defined testing criteria

Also called: reactive hypoglycemia, sugar crashes, low blood sugar after meals, postprandial hypoglycemia

Patients describe shakiness, sweating, irritability, hunger, or brain fog one to a few hours after eating, and an ND or their own research labels this 'reactive hypoglycemia' or a 'blood sugar crash,' sometimes after an ND-ordered oral glucose tolerance test (OGTT). These symptoms are real and common. Whether they reflect a true drop in blood sugar is a separate question, and one that needs to be answered with the right test.

Raises suspicion

  • • Symptoms one to three hours after eating together with a documented low glucose reading at that time, relieved by eating (Whipple's triad)
  • • Symptoms of this kind after bariatric or gastric surgery, which can cause a real, sometimes severe, form of post-meal hypoglycemia (late dumping)
  • • Hypoglycemia while fasting or during exercise, rather than only after meals
  • • Unexplained weight gain alongside the episodes, which raises concern for an insulin-secreting tumour (insulinoma), though this is rare

Does not raise suspicion

  • • Shakiness, irritability, hunger, or brain fog one to a few hours after meals without ever having a documented low glucose reading at the time: this is common and is usually 'idiopathic postprandial syndrome,' not true hypoglycemia
  • • Symptoms that only ever happen when a meal is skipped or delayed, or after caffeine

Red flags

  • • A documented glucose under 3.0 mmol/L together with confusion, seizure, or loss of consciousness (neuroglycopenia)
  • • Hypoglycemia while fasting, not just after meals
  • • Hypoglycemia with neuroglycopenic symptoms in someone who has had bariatric or gastric surgery
  • • Unexplained weight gain together with hypoglycemia in someone without diabetes

Who to test

  • Symptoms plausibly reflecting true hypoglycemia, especially after bariatric or gastric surgery, or with fasting or exertional symptoms: Fasting insulin (Rarely indicated)Best captured by measuring glucose, insulin, and C-peptide during a spontaneous symptomatic episode, or with a supervised mixed-meal test (no TestSelect entry; specialist-directed) or supervised fast. A standard oral glucose tolerance test should not be used to evaluate this.
  • Typical postprandial symptoms without a documented low readingChecking a home glucose reading during a symptomatic episode is a practical first step; a normal reading at that time points toward idiopathic postprandial syndrome rather than true hypoglycemia.

More likely instead

  • • anxiety or panic attacks
  • • caffeine
  • • skipped or delayed meals
  • • idiopathic postprandial syndrome (symptoms without a documented low glucose)
  • • dumping syndrome
  • • pots (orthostatic symptoms mistaken for a sugar crash)

Counselling script

“If we can catch your blood sugar during one of these episodes and it's genuinely low, with symptoms that improve once you treat it, that's true hypoglycemia and worth a proper work-up. Without a documented low reading, your symptoms are still real, but they're more likely to be idiopathic postprandial syndrome, which isn't dangerous. If you've had bariatric surgery, I'd take this more seriously and look into it sooner rather than waiting.”

Chart snippet (OSCAR-safe plain text)

Concern discussed, not tested

Concern re: reactive (postprandial) hypoglycemia discussed, raised by patient or ND.
Discriminating features: documented low glucose during symptoms (Whipple's triad), prior bariatric or gastric surgery, fasting or exertional symptoms, unexplained weight gain; reviewed.
Red flags: absent.
Assessment: symptom pattern consistent with idiopathic postprandial syndrome; no documented hypoglycemia at time of symptoms.
Plan: home glucose check during a symptomatic episode advised; oral glucose tolerance test not ordered, as it is not a valid test for this indication.
Ref: Endocrine Society hypoglycemic disorders guideline 2009.
Patient given info page: https://diabetes.ajaxharwoodclinic.com/patient#reactive-hypoglycemia
Revisit if: a documented low glucose reading during symptoms, neuroglycopenic symptoms, or fasting hypoglycemia develop.

Testing ordered

Concern re: reactive (postprandial) hypoglycemia discussed.
Discriminating features: symptoms plausibly reflecting true hypoglycemia, or prior bariatric/gastric surgery; red flags absent.
Assessment: work-up indicated to establish Whipple's triad.
Plan: glucose, insulin, and C-peptide ordered to be drawn during a spontaneous symptomatic episode, or supervised mixed-meal test arranged; oral glucose tolerance test not used for this purpose.
Ref: Endocrine Society hypoglycemic disorders guideline 2009; Salehi et al. 2018 post-bariatric hypoglycemia review.
Patient given info page: https://diabetes.ajaxharwoodclinic.com/patient#reactive-hypoglycemia
Revisit if: neuroglycopenic symptoms, fasting hypoglycemia, or unexplained weight gain develop.

Revisit if

  • • A glucose reading below 3.0 mmol/L is documented during symptoms, especially with confusion, seizure, or loss of consciousness
  • • Symptoms occur while fasting or with exertion, rather than only after meals
  • • Unexplained weight gain accompanies the episodes
  • • Symptoms begin or worsen after bariatric or gastric surgery

References

  1. 1. Endocrine Society. Evaluation and Management of Adult Hypoglycemic Disorders: An Endocrine Society Clinical Practice Guideline (2009)— older guidelineHypoglycemic disorders should be evaluated only when Whipple's triad is documented, with glucose, insulin, C-peptide, proinsulin and beta-hydroxybutyrate measured during an episode
  2. 2. Salehi, Vella, McLaughlin, Patti; Journal of Clinical Endocrinology & Metabolism (mini-review). Hypoglycemia After Gastric Bypass Surgery: Current Concepts and Controversies (2018)Post-bariatric hypoglycemia can be severe, with neuroglycopenia leading to falls, motor vehicle accidents, and job and income loss
Evidence notes

Tag rationale: A, not borderline, for true hypoglycemia: the Endocrine Society 2009 guideline defines it by Whipple's triad with a documented low plasma glucose, which is a defined testing criterion [1]. A judgment call worth flagging for Dr. Yu: the everyday patient label 'reactive hypoglycemia' actually covers two different things, held together in this one A-tagged record rather than split out, (1) true, documented postprandial or post-bariatric hypoglycemia, which is tag-A material, and (2) 'idiopathic postprandial syndrome,' which is common, has symptoms without a documented low glucose, and is not itself a defined diagnosis with its own criteria. The brief's instruction is that a not-a-real-diagnosis label gets its own C-tagged record hosted inside the real condition's page; idiopathic postprandial syndrome was kept as a paragraph inside this A record instead of spun out as a separate C record, because it is the explanation for a negative work-up rather than a distinct self-applied label patients bring in by name the way 'adrenal fatigue' is. Escalate if Dr. Yu would rather it be a standalone C record. [1] is flagged older_than_10y (2009); no more recent Endocrine Society or Diabetes Canada guideline specifically on adult hypoglycemic disorders was located this session, so it remains the standard-cited framework. Gap: the record and chart snippets state that a standard OGTT should not be used to evaluate suspected postprandial hypoglycemia. This session read that exact recommendation in the Endocrine Society 2009 guideline full text ('An oral glucose tolerance test should never be used for the evaluation of suspected postprandial hypoglycemia'), but could not mechanically re-verify it through scripts/verify_sources.py: the guideline page (academic.oup.com) returns HTTP 403 to the automated fetch, and the sentence is in the guideline body, not the PubMed abstract text pulled by the pipeline's pubmed method. Rather than register an unverifiable source, that specific quote was dropped from references; the OGTT-avoidance guidance is kept in the record as confident, guideline-based physiology per the 'confident but unsourced goes in evidence_notes' rule, resting on the already-verified [1] entry's Whipple's-triad framework (diagnosis requires a documented low glucose during a spontaneous episode, which an OGTT does not provide) rather than a directly quoted OGTT-specific sentence. Flagged for reviewer re-check against the full guideline text if a verifiable copy becomes available. No TestSelect entry exists for a mixed-meal test or a supervised fast, noted as free text per instructions. Host is 'diabetes' per batch instruction; the host choice between diabetes. and glp. is pending Dr. Yu's decision per docs/ecosystem-survey.md. Resolved 2026-09-23: Dr. Yu confirmed hosting on diabetes. and tag A (decision 10).

Guidelines

References

  1. [1]Diabetes Canada. Pharmacologic Glycemic Management of Type 2 Diabetes in Adults — 2024 Update (Ch.13). Can J Diabetes 2024;48:415. link
  2. [2]American Diabetes Association. Standards of Care in Diabetes — 2026 (Ch.9 Pharmacologic Approaches; Ch.11 CKD). Diabetes Care 2026;49(Suppl 1). link
  3. [3]Davies MJ, et al. Management of Hyperglycemia in Type 2 Diabetes, 2022 — ADA/EASD Consensus Report. Diabetes Care 2022;45:2753. link