2,4-Dinitrophenol (DNP): A Weight Loss Agent with Significant Acute Toxicity and Risk of Death

doi:10.1007/s13181-011-0162-6

Paper

2,4-Dinitrophenol (DNP): A Weight Loss Agent with Significant Acute Toxicity and Risk of Death

Published Jul 8, 2011 · J. Grundlingh, P. Dargan, M. El-Zanfaly

Journal of Medical Toxicology

Q2 SJR score

382

Citations

18

Influential Citations

Full textSemantic Scholar

Abstract

Abstract2,4-Dinitrophenol (DNP) is reported to cause rapid loss of weight, but unfortunately is associated with an unacceptably high rate of significant adverse effects. DNP is sold mostly over the internet under a number of different names as a weight loss/slimming aid. It causes uncoupling of oxidative phosphorylation; the classic symptom complex associated with toxicity of phenol-based products such as DNP is a combination of hyperthermia, tachycardia, diaphoresis and tachypnoea, eventually leading to death. Fatalities related to exposure to DNP have been reported since the turn of the twentieth century. To date, there have been 62 published deaths in the medical literature attributed to DNP. In this review, we will describe the pattern and pathophysiology of DNP toxicity and summarise the previous fatalities associated with exposure to DNP.

Literature Review

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Study Snapshot

2,4-Dinitrophenol (DNP) is a rapid weight loss agent with significant acute toxicity and risk of death, with 62 reported fatalities in medical literature since the turn of the twentieth century.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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2,4-Dinitrophenol (DNP): A Weight Loss Agent with Significant Acute Toxicity and Risk of Death

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References

2, 4-dinitrophenol poisoning caused by non-oral exposure

2, 4-DNP poisoning can cause death through skin absorption and respiratory tract inhalation, with common symptoms including excessive sweating, hyperthermia, tachycardia, clouded consciousness, and asystole.

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Dinitrophenol, an unlicensed drug available online, is a potential risk for accidental poisoning due to obesity prevalence and its availability through mail-order websites.

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The SIGN guideline recommends that health professionals should identify and manage obese individuals, focusing on prevention, early intervention, and early intervention for obesity-related comorbidities.

Deliberate poisoning with dinitrophenol (DNP): an unlicensed weight loss pill

Dinitrophenol (DNP) is an illegal weight loss agent that can cause fatal hyperthermia, and its use is common among bodybuilders.

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DNP has general and reproductive/developmental toxicity, but not teratogenicity, with a NOAEL of 10 mg/kg bw/day in rats.

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Dinitrophenol's popularity as a weight-loss drug in the 1930s led to thousands of deaths before mainstream physicians realized its risks outweighed its benefits.

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2,4-DNP toxicity is a potential cause of death in individuals who use it for weight loss, despite its illegal use.

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Dinitrophenol, a dangerous chemical used as an insecticide, has resurrected interest as a weight loss agent, highlighting the danger of this product and its easy accessibility.

Citations

Unsymmetric hydroxylamine and hydrazine BAM15 derivatives as potent mitochondrial uncouplers.

Hydroxylamine BAM15 derivatives are more potent than hydrazine ones, with potential for obesity treatment and low exposure and short half-life in mice.

Case report: Fatal long-term intoxication by 2,4-dinitrophenol and anabolic steroids in a young bodybuilder with muscle dysmorphia

A young bodybuilder with muscle dysmorphia died after 6 months of repeated 2,4-DNP intoxication, suggesting the need for primary care professionals to be trained in detecting and managing such cases.

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Low resting metabolic rate is associated with weight gain, making it a crucial target for obesity treatment and understanding its effects on treatment outcomes.

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Obesity management involves a tiered approach, with first-line therapies including lifestyle changes and second-line therapies including antiobesity medications.

A Spatiotemporally Controlled and Mitochondria-Targeted Prodrug of Hydrogen Sulfide Enables Mild Mitochondrial Uncoupling for the Prevention of Lipid Deposition.

The mitochondria-targeted H2S prodrug M1 effectively induces mild mitochondrial uncoupling, preventing lipid deposition and improving metabolic syndrome by increasing cellular energy expenditure.

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Morphological findings, such as yellowing of the skin, sclera, mucosa, internal organs, and urine, are a characteristic indication of 2,4-DNP ingestion and, if localized to the skin, indicate prolonged consumption.

Exploring the role of mitochondrial uncoupling protein 4 in brain metabolism: implications for Alzheimer’s disease

UCP4, a key regulator of brain metabolism, may play a protective role against neurodegeneration and aging, and activating UCPs may offer therapeutic interventions for Alzheimer's disease and other neurodegenerative diseases.