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🩸 GLP-1 vs Insulin Therapy Decision Simulator

An interactive model for choosing between GLP-1 receptor agonists and insulin therapy in type 2 diabetes based on HbA1c levels, beta-cell function, and cardiovascular risk.

Type 2 Diabetes & Insulin Resistance2DModerate60 FPS
glp1-vs-insulin-therapy-decision-simulator ↗ Open standalone

When Oral Agents Stop Being Enough

Metformin and add-on orals no longer hold glucose targets.

  • HbA1c > goal: Trigger for escalation (despite oral therapy)
  • GLP-1 / Insulin: Two leading options (injectable step-up)
  • 3 factors: Decision inputs (HbA1c, beta-cell, CV risk)
  • Individualized fit: Goal (not one-size-fits-all)

Why escalation happens

Oral agents plateau; beta-cell decline continues over time.

Two divergent mechanisms

GLP-1 boosts endogenous insulin; exogenous insulin replaces it directly.

HbA1c Level Sets the Urgency

Higher HbA1c demands a more potent, predictable glucose-lowering tool.

  • 7–8%: Mild elevation (either class often works)
  • 9–10%: Marked elevation (insulin gains an edge)
  • >11%: Severe elevation (insulin often preferred)
  • 1–1.8%: GLP-1 typical drop (placeholder estimate)

Ceiling effect of GLP-1

GLP-1 lowering has a ceiling; very high HbA1c may exceed it.

Insulin's unlimited titration

Insulin dose can be titrated upward with no pharmacologic ceiling.

How Much Insulin-Secreting Capacity Remains

GLP-1 agonists need residual beta-cell function to work well.

  • >60%: Well-preserved (GLP-1 mechanism intact)
  • 30–60%: Moderately reduced (GLP-1 response weaker)
  • <30%: Severely depleted (favors insulin replacement)
  • C-peptide: Marker used (placeholder proxy measure)

GLP-1 mechanism dependency

GLP-1 stimulates the pancreas; an empty reserve limits benefit.

Insulin bypasses the pancreas

Insulin works regardless of remaining beta-cell secretory capacity.

Established Cardiovascular Disease Shifts the Balance

GLP-1 agonists carry proven cardiovascular outcome benefits.

  • Positive: CV outcome trials (placeholder trial summary)
  • ~14%: MACE reduction (placeholder relative risk)
  • Loss: Weight effect (GLP-1 vs. insulin gain)
  • Lower: Hypoglycemia risk (with GLP-1 vs. insulin)

Proven cardioprotection

Large trials show GLP-1 agonists reduce major cardiac events.

Insulin is CV-neutral

Insulin controls glucose but offers no independent cardiac benefit.

Three Factors, One Weighted Recommendation

HbA1c, beta-cell reserve, and CV risk combine into a verdict.

  • Low score: GLP-1 favored (good reserve, CVD present)
  • High score: Insulin favored (high HbA1c, low reserve)
  • Mid score: Either reasonable (mixed or balanced factors)
  • Shared decision: Real-world practice (placeholder clinical note)

Weighing, not ranking

No single factor decides alone; all three are weighed together.

A living decision

Recommendation shifts as HbA1c, reserve, or risk profile changes.

⚙ Under the hood

An interactive model for choosing between GLP-1 receptor agonists and insulin therapy in type 2 diabetes based on HbA1c levels, beta-cell function, and cardiovascular risk.

CanvasBiomedicine

2D · HTML5 Canvas 2D · 60 FPS target · runs fully client-side, no install

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