Avoiding peanuts is two interventions. With confirmed peanut allergy, removing peanut protein is the only reliable way to stop an immediate reaction, though accidental exposures still occur. Without allergy, the case rests on mould toxins and an untested blood-borne peanut protein, set against lower cholesterol particle counts and death rates with regular intake. Infants kept away face the largest harm. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Ara h 2 specific IgE | <0.35 kU/L | Confirms or excludes true peanut allergy before a lifelong restriction begins |
| Peanut skin-prick wheal | <3 mm above saline control | Independent second confirmation of sensitisation |
| Apolipoprotein B | <80 mg/dL, or <60 mg/dL with established atherosclerosis | Detects the lipid cost of removing peanuts without substitution |
| Low-density lipoprotein cholesterol | <100 mg/dL, or <70 mg/dL with atherosclerosis | Simplest marker of the forgone lipid benefit of peanut intake |
| Red-blood-cell magnesium | 4.2–6.8 mg/dL | Peanuts supply roughly 50 mg magnesium per 30 g serving |
| Serum alpha-tocopherol | 20–30 µmol/L | Peanuts are a leading dietary vitamin E source, lost on removal |
| Aflatoxin B1–albumin adduct | No established optimal target; track the fall from the pre-avoidance value | Confirms that avoidance actually reduced mould-toxin exposure |
| High-sensitivity C-reactive protein | <1.0 mg/L | General inflammatory context when diet composition changes substantially |
Cadence: Baseline before peanuts are removed; lipid markers rechecked at 8–12 weeks, then at 6 and 12 months and annually thereafter; micronutrient status at 6 months and annually; aflatoxin adducts no sooner than 3 months; allergy testing repeated only when reintroduction is being considered.