Before buying CBD, always check your state’s cannabis laws.
In hypercholesterolemia, cholesterol buildup damages the blood vessel walls. It also sets off an inflammatory response that attracts more immune cells to the site. The more immune cells that go to the damaged blood vessel, the narrower the blood vessel becomes as more debris accumulates. If a chunk breaks off, it could travel to other parts of the body as a blood clot and cause a stroke or congestive heart failure .
Hypercholesterolemia is a condition where there’s an unhealthy level of serum total cholesterol (more than 200 mg/dl). The causes may either be genetics or acquired (eating high-cholesterol food and a sedentary lifestyle, for example). High cholesterol levels may also be worsened by medications and chronic medical illnesses like chronic kidney disease and diabetic diseases.
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As the plaque grows, it increases the risk of blood clot formations. These can block the blood vessel or get dislodged and travel to other parts of the body, causing a heart attack or a stroke.
There may be some minor side effects such as eye and mouth dryness, change in bowel movements, drowsiness, and even fatigue, but these are usually well-tolerated by CBD users. These side effects also disappear once the body gets used to CBD.
Reduces Inflammation of the Blood Vessel Walls
While these medications help reduce high cholesterol levels, they also produce side effects like:
This article talks about CBD and cholesterol, how CBD affects hypercholesterolemia, and how to use CBD for this health concern.
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.