# Hepatotoxicity of dietary supplements containing Garcinia gummi-gutta (L.) N. Robson

## TL;DR

This paper reviews case reports linking Garcinia dietary supplements to liver damage, highlighting serious health risks.

## Contribution

The study compiles and analyzes over 200 cases of Garcinia-induced liver injury, including confirmed causality via rechallenge.

## Key findings

- Over 200 cases of liver injury linked to Garcinia dietary supplements were identified.
- 17 cases had causality scores indicating possible to highly probable liver damage from Garcinia.
- Hydroxycitric acid in Garcinia may cause liver injury through oxidative stress and mitochondrial inhibition.

## Abstract

Botanical dietary supplements derived from the fruit of the tree Garcinia gummi-gutta (L.) N. Robson (commonly known as Garcinia cambogia or Garcinia) are used to support weight loss but are increasingly linked to adverse events and case reports of liver injury.

Clinical case reports of liver injury associated with Garcinia dietary supplements were reviewed that had prompted the United States Pharmacopeia (USP) to revise the USP Garcinia family of dietary ingredient monographs to include a cautionary statement regarding potential risk of liver damage.

The terms ‘Garcinia cambogia,’ ‘Garcinia gummi-gutta,’ or ‘Garcinia’ were searched in multiple databases of adverse events. PubMed and Google Scholar were searched for peer-reviewed papers describing preclinical and clinical studies of Garcinia toxicity.

More than 200 adverse events of liver injury resulting from Garcinia consumption were identified. A total of 34 case reports of Garcinia hepatotoxicity indicated one death and nine liver transplants, with 17 cases receiving CIOMS/RUCAM scores that indicated possible to highly probable causality due to Garcinia dietary supplements. In one case, causality was confirmed by rechallenge with Garcinia.

Garcinia toxicity was consistent with drug-induced liver injury and included elevated serum liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase with a high ratio of ALT to alkaline phosphatase. Proposed mechanisms of toxicity include genetic predisposition to immune-mediated reactions involving the human leucocyte antigen HLA-B*35:01 allele, induction of hepatocyte oxidative stress and inflammation, and hepatocyte apoptosis caused by the active constituent, hydroxycitric acid, which inhibits mitochondria ATP-citrate lyase.