cbd and liver enzymes

Researchers presented initial results from a study to the FDA in March suggesting there is no evidence of liver disease from the use of hemp-derived CBD products.

Investigators report to FDA no evidence of liver toxicity in 839 adults consuming oral CBD

CBD, short for cannabidiol, comes from the cannabis plant. It is one of two most commonly known compounds of cannabis (marijuana), the other being delta-9-tetrahydrocannabinol (THC). It’s the THC that is associated with a “high,” not CBD.

Michigan’s guidance on CBD and industrial hemp

The study of 839 people was completed between August 2020 and February 2021.

Cbd and liver enzymes

Female Sabra mice (34–36 g), 8 to 10 weeks old, were assigned at random to different groups of 10 mice per cage and were used in all experiments. All cages contained wood-chip bedding and were placed in a temperature-controlled room at 22°C, on a 12 h light/dark cycle (lights on at 07h00min). The mice had free access to water 24 h a day. The food provided was Purina chow and the animals were maintained in the animal facility (Specific Pathogen Free Organism unit) of the Hebrew University Hadassah Medical School, Jerusalem. Mice were killed after each treatment by decapitation between 10h00min and 12h00min. Animals were kept at the animal facility in accordance with NIH guidelines and all experiments were approved by the institutional animal use and care committee, No. MD-89.52-4.

Introduction

TAA-treated animals showed the typical TAA-induced liver necrosis lesions that have been described in detail previously (Avraham et al., 2008a). The statistical analysis of liver histopathology scores did not reveal significant differences in the extent and severity of necrotic lesions between CBD-treated and untreated mice (data not shown).

Results

Previous work from our laboratory has demonstrated an impaired neurological and motor function 3 days, and impaired cognition 12 days after TAA injection to mice (Avraham et al., 2006; 2008a; 2009;). These results were reproduced in the present study ( Figures 1–3 ). In a more recent study from our laboratory, cognitive and motor deficits were observed 21 days after bile duct ligation, a chronic model of liver disease (Magen et al., 2009). The different durations of the development of HE symptoms in the two models apparently result from their different characteristics – an acute versus a chronic model of HE. In the latter model, CBD was found to improve cognition and locomotor activity, in accordance with our present data (Magen et al., 2009). However, in sharp contrast to the findings reported here no evidence for astrogliosis was found in that study (data not reported); in our acute model induced by TAA we observed astrogliosis after 3 days ( Figure 4C ). Those mice with histopathological alterations displayed an increased neurological score and decreased activity level, and 5 mg·kg −1 CBD reversed both the increase in the number of GFAP(+) cells, an index of neuroinflammation ( Figure 4E ), and the neurological and locomotor impairments ( Figures 1 and ​ and2), 2 ), suggesting a link between neuroinflammation and motor and neurological deficits. Similar results were reported by Jover et al. (2006) who demonstrated a decrease in motor activity in bile duct-ligated rats on a high-protein diet, in association with astrogliosis, and by Cauli et al. (2009), who reported that treatment with an anti-inflammatory restored the motor activity in HE. In the work of Jover et al. (2006), astrogliosis was found only in the bile duct-ligated rats on a high protein diet, but not in the bile duct-ligated rats on a regular diet, similar to our previous findings (Avraham et al., 2009) This suggests that TAA causes more severe damage to the brain than bile duct ligation, and that hyperammonaemia is required to worsen the damage in bile duct-ligated rats to an extent that is equivalent to that observed in TAA mice. The reason for this may be that in chronic liver disease induced by bile duct ligation, compensation mechanisms are activated, which moderate the brain damage, while in the acute model induced by TAA, no such mechanisms can come into action because of the severity of the liver insult and the short interval of time between the induction of liver damage and the histopathological examination.