Deep red, purple, and blue plant pigments, mostly taken apart by gut bacteria into the smaller compounds that do the work. Best supported: wider arteries, better cholesterol readings, lower blood sugar, almost entirely in people whose readings are already abnormal. Harms are mostly digestive upset. The realistic cautions are diabetes medication, reduced iron uptake, and product quality. (Full Review)
| Marker | Target | Why |
|---|---|---|
| LDL cholesterol | Below 100 mg/dL, ideally below 80 mg/dL | Primary lipid target anthocyanins move |
| HDL cholesterol | Above 55 mg/dL men, above 65 mg/dL women | Rises via blocked cholesterol transfer between lipoprotein particles |
| Triglycerides | Below 80 mg/dL | Sensitive to the sugar load of juice delivery forms |
| HbA1c | 4.8–5.4% | Average glucose over ~3 months; primary metabolic target |
| Fasting glucose | 75–86 mg/dL | Detects additive lowering when diabetes drugs are co-administered |
| Fasting insulin | Below 5 µIU/mL | Detects improved insulin signaling earlier than HbA1c |
| High-sensitivity C-reactive protein | Below 0.5 mg/L | The inflammation marker most responsive to anthocyanins |
| Ferritin | 50–150 ng/mL | Guards against the iron-binding effect rather than tracking benefit |
| Seated blood pressure | 110–120 / 70–75 mmHg | Detects both benefit and additive lowering with antihypertensives |
| Flow-mediated dilation | No established target; track change from own baseline | The mechanism most directly demonstrated for anthocyanins |
Cadence: Baseline before the first dose, then the full panel at 12 weeks, again at 24 weeks, then every 6–12 months while use continues. Fasting glucose weekly for the first 4 weeks where glucose-lowering drugs are co-administered, and standing blood pressure at 4 weeks where blood-pressure drugs are.