Appetite suppression through dopamine modulation Central appetite control: Tesofensine acts on hypothalamus Affects arcuate nucleus (appetite center) Different pathway from GLP-1 receptors Direct neurotransmitter modulation Rapid onset (hours not days) Dopamine's role in eating: Mediates food reward (hedonic eating) High-dopamine = reduced food seeking Decreases obsessive food thoughts Reduces binge eating tendencies Similar to ADHD medication effects Subjective appetite changes reported: Reduced hunger (moderate, not as strong as semaglutide ) Less food preoccupation Earlier satiety (smaller portions satisfying) Reduced cravings especially for high-calorie foods More mental focus on non-food activities Appetite suppression comparison: Why dopamine approach different: Addresses psychological/behavioral eating Reduces food as reward behavior Helps with emotional eating Less GI side effects than GLP-1s But creates stimulant-like dependency risk Clinical trial results and efficacy Evidence from human studies
Dipali Ladkat | Mohanish Wagh | Rubina Mandlik | Dr.Shital Bhor To view or add a comment, sign in 1,713 followers
Patient B: Jennifer, 43 Starting weight: 242 pounds Height: 57 Exercise approach: No resistance training, some walking, protein intake around 50-60g daily After 11 months: Weight: 168 pounds (74 pounds lost) Body fat: 34% (down from 43%) DEXA scan: 47 pounds fat lost, 27 pounds muscle lost Resting metabolic rate: Dropped 280 calories from baseline Clothing size: 22 to 12 Strength: Not assessed (no baseline) Jennifer looked deflated
Although GI AEs are common across all GLP-1 RAs, differences in formulation, dosing, and dual agonism with tirzepatide can influence how well patients tolerate therapy
This is when the effects are strongest
In the obesity trial, maximal WL was achieved with retatrutide 12 mg after 48 weeks: -24.2% vs
