Many in the bodybuilding and nutritional supplement industry had been following the personal injury lawsuit brought against Species Nutrition. Unfortunately, while it ended without a trial, we can safely infer that it didn’t end well for Species Nutrition; a confidential settlement was agreed upon. With that in mind, we can turn our attention from the legal case to the medical case.
The following article (a case study and literature review) was published in the Canadian Journal of Gastroenterology. Although it is well over a year old, it seems to have avoided being picked up by any of the major blogs or websites out there – so with that in mind, I present to you the published case study (edited and abbreviated with a link to the full study at the end) of the young woman who found herself in need of a liver transplant as a result (her Doctor’s conclusion, not mine) of taking Species Nutrition’s Somalyze and Lipolyze:
A previously healthy 28-year-old female bodybuilder with no risk factors for liver disease presented to her local emergency centre with fatigue, malaise, inability to exercise and new-onset jaundice. Her symptoms worsened over a span of one week before hospitalization. Initially, she was confused, and over two days became obtunded and eventually required intubation for airway protection before her transfer to The Mount Sinai Medical Center (New York, USA) for liver transplant evaluation.
The patient was a professional bodybuilder taking a multi-ingredient, nonstimulant health supplement and fat burner (Somalyze and Lipolyze, Species Nutrition, USA). Somalyze contains usnic acid (4 mg), propionyl-L-carnitine (167 mg), phosphatidylcholine/phosphatidylethanolamine (50 mg), gamma-aminobutyric acid (667 mg) and vitamin E (27 IU) per capsule. Lipolyze contains usnic acid (12 mg), propionyl-L-carnitine (500 mg), green tea extract (300 mg), guggulsterone Z and guggulster-one E (10 mg), cyclic adenosine monophosphate (2 mg) and vitamin E (20 IU) per capsul. She was taking one to two capsules of Somalyze at bedtime and one capsule of Lipolyze with meals three times a day as recommended for one month before illness. Her other medications included over-the-counter calcium and fibre supplements, and caffeine tablets.
On evaluation at The Mount Sinai Medical Center, there were no stigmata of chronic liver disease. Blood work revealed a total serum bilirubin level of 82.08 mmol/L (normal range 1.71 mmol/L to 20.5 mmol/L), a direct bilirubin level of 47.88 mmol/L (1.71 mmol/L to 13.6 mmol/L), a serum alanine aminotransferase level of 1220 U/L (1 U/L to 53 U/L), a serum aspartate aminotransferase level of 577 U/L (1 U/L to 50 U/L), an alkaline phosphatase level of 111U/L (30 U/L to 110 U/L), a gamma-glutamyl transferase level of 125 U/L (8 U/L to 35 U/L), an international normalized ratio of 2.6 and a serum creatinine level of 53.04 μmol/L (44.2 μmol/L to 106.2 μmol/L). Her hematological markers, electrolyte levels, metabolic profile, amylase levels and lipase values were unremarkable.
Etiological workup included the following: negative viral serology (hepatitis A virus immunoglobulin M, hepatitis B virus surface antigen and core antibody, hepatitis C virus antibody [polymerase chain reaction assay], cytomegalovirus DNA and Epstein-Barr virus immunoglobulin M); negative syphilis rapid plasma regain; negative autoimmune markers (antinuclear antibody, antiliver kidney muscle antibody, antimitochondrial antibody and antismooth muscle antibody); and normal serum gamma globulins. Extensive toxicology screening was negative, with no features of acetaminophen toxicity (acidosis, high lactate or renal failure). She had normal levels of ferritin, ceruloplasmin and alpha-1 antitrypsin. A pregnancy test was negative. A computed tomography scan of her abdomen revealed a normal size liver with a patent portal vein, hepatic artery, hepatic vein and normal biliary anatomy. Her spleen was normal and no ascites was noted.
The patient’s encephalopathy worsened and she remained unresponsive. A computed tomography scan of her head was normal. An intracranial pressure monitor was placed, which measured an intracranial pressure of 19 mmHg and a cerebral perfusion pressure of 77 mmHg to 82 mmHg. She underwent successful cadaveric orthotopic liver transplantation on hospital day 2. By postoperative day 4, she was awake and alert. She experienced no significant postoperative complications and was discharged home for outpatient follow-up.
Histopathological examination of the liver explant showed massive hepatic necrosis and parenchymal collapse, with a few islands of ductular regeneration.
Based on the temporal relationship between the use of the dietary supplements and onset of liver failure, literature supporting reports of hepatotoxicity associated with dietary supplements and exclusion of other causes, it is fair to assume that the patient developed fulminant hepatic failure due to dietary supplements. In view of the bulk of the literature, of all the ingredients, usnic acid may have been predominantly responsible for the hepatoxicity. Although usnic acid was the main hepatotoxic agent, its effect was possibly perpetuated by other hepatotoxins, including green tea and gum guggul, also contained in the dietary supplements taken by the patient.
Ok, so what I did here was give you the beginning of the case study and the end, because the doctors who wrote it up are a bit long winded, and get into a huge discussion about usnic acid and liver stuff, and it’s not terribly interesting to the narrative. But it’s there in black and white if you want to read the whole thing for yourself: