One of the main ways that dietary cholesterol enters your body is through the small intestine, where it absorbs plenty of it from your food. This group of drugs slows down the rate at which your small intestine can absorb cholesterol from your food.
So, this is where a good deal of the confusion regarding cholesterol comes in. All of the cholesterol that you actually need in your body is created in the liver. Any extra cholesterol floating around comes from the food you eat, such as fatty foods.
The main benefit of these substances is that they are combined with other drugs, like statins, to attempt to try and create a combined effect. On their own, they don’t reverse anything. But merely act as a stopgap to limit the results for the future.
Does CBD Lower Cholesterol?
The two options for cholesterol treatment are either to attempt to try and remove excess LDL cholesterol through medication or to try and improve general heart health.
Low-Density Lipoprotein: The first one, low-density lipoprotein, also known as LDL, is the typically maligned form of cholesterol. This type of cholesterol can build up in your bloodstream, causing blockages and reducing sufficient blood flow.
Cannabidiol (CBD) is a non-psychoactive plant cannabinoid that is clinically used in a 1:1 mixture with the psychoactive cannabinoid Δ(9)-tetrahydrocannabinol (THC) for the treatment of neuropathic pain and spasticity in multiple sclerosis. Our group previously reported that CBD exerts anti-inflammatory effects on microglial cells. In addition, we found that CBD treatment increases the accumulation of the endocannabinoid N-arachidonoyl ethanolamine (AEA), thus enhancing endocannabinoid signaling. Here we proceeded to investigate the effects of CBD on the modulation of lipid-related genes in microglial cells. Cell viability was tested using FACS analysis, AEA levels were measured using LC/MS/MS, gene array analysis was validated with real-time qPCR, and cytokine release was measured using ELISA. We report that CBD significantly upregulated the mRNAs of the enzymes sterol-O-acyl transferase (Soat2), which synthesizes cholesteryl esters, and of sterol 27-hydroxylase (Cyp27a1). In addition, CBD increased the mRNA of the lipid droplet-associated protein, perilipin2 (Plin2). Moreover, we found that pretreatment of the cells with the cholesterol chelating agent, methyl-β-cyclodextrin (MBCD), reversed the CBD-induced increase in Soat2 mRNA but not in Plin2 mRNA. Incubation with AEA increased the level of Plin2, but not of Soat2 mRNA. Furthermore, MBCD treatment did not affect the reduction by CBD of the LPS-induced release of the proinflammatory cytokine IL-1β. CBD treatment modulates cholesterol homeostasis in microglial cells, and pretreatment with MBCD reverses this effect without interfering with CBD’s anti-inflammatory effects. The effects of the CBD-induced increase in AEA accumulation on lipid-gene expression are discussed.