2 replies to this topic

[Adam Karlovsky]

Berberine has a lot of potential - it has mechanisms that encroach on the territory of metformin, statins and aspirin, all in one. It's in my top 10 supplements for the prevention of disease and lifespan extension, perhaps even up there with rapamycin. We definitely need some rat lifespan studies done on berberine, and more disease treatment trials done for humans.

 

Berberine, a plant alkaloid with lipid- and glucose-lowering properties: From in vitro evidence to clinical studies.

 

https://www.ncbi.nlm...pubmed/26520899

 

 

Berberine (BBR) is an isoquinoline plant alkaloid endowed with several pharmacological activities, including anti-microbial, glucose- and cholesterol-lowering, anti-tumoral and immunomodulatory properties. The main mechanism by which BBR exerts a protective role in atherosclerosis relates to its cholesterol-lowering activity. BBR significantly increases hepatic low density lipoprotein receptor (LDLR) expression and reduces the expression and secretion of the LDLR modulator proprotein convertase subtilisin/kexin type 9 (PCSK9). In addition to this, several other atheroprotective effects have been ascribed to BBR, including anti-inflammatory and anti-oxidant properties, inhibition of vascular smooth muscle cell proliferation and improvement of endothelial dysfunction. BBR also increases glucose utilization in adipocytes and myocytes, while decreases glucose absorption in intestinal cells, resulting in a net hypoglycemic effect. In hypercholesterolemic animals, BBR significantly decreases LDL-C and total cholesterol (TC) levels and reduces aortic lesions, an effect similar to that of statins. In diabetic animals, BBR significantly reduces glucose levels, improves glucose tolerance, reduces body weight gain and adipose tissue mass. Several clinical studies have also tested the efficacy of BBR in humans. In hypercholesterolemic subjects, BBR induces a significant reduction of TC, triglycerides and LDL-C levels and a significant increase of HDL-C levels, without major adverse effects. BBR also reduces glycemia and plasma cholesterol in diabetic patients, improves lipid and glucose profile and decreases body mass index and waist circumference in subjects with metabolic syndrome. These findings, together with the good tolerability, suggest that BBR administration might be considered a potential therapeutic approach for the treatment of hypercholesterolemia or diabetes. Given the level of evidence available to date well-designed randomized controlled trials to test safety and efficacy of BBR are warranted.

 

Role of berberine in Alzheimer’s disease

 

https://www.ncbi.nlm...les/PMC5055107/

 

 

 

Berberine, an important protoberberine isoquinoline alkaloid, has several pharmacological activities, including antimicrobial, glucose- and cholesterol-lowering, antitumoral, and immunomodulatory properties. Substantial studies suggest that berberine may be beneficial to Alzheimer’s disease (AD) by limiting the pathogenesis of extracellular amyloid plaques and intracellular neurofibrillary tangles. Increasing evidence has indicated that berberine exerts a protective role in atherosclerosis related to lipid- and glucose-lowering properties, implicating that berberine has the potential to inhibit these risk factors for AD. This review also attempts to discuss the pharmacological basis through which berberine may retard oxidative stress and neuroinflammation to exhibit its protective role in AD. Accordingly, berberine might be considered a potential therapeutic approach to prevent or delay the process of AD. However, more detailed investigations along with a safety assessment of berberine are warranted to clarify the role of berberine in limiting these risk factors and AD-related pathologies.

 

[Attila Lajos Danko]

The lack of long term studies in animals and humans is a big problem with this one.  Certainly has promising potential, and I'm sure you have done a lot more study on it than me, but there are potential problems, as outlined here

 

http://diabetesupdat...ry-well-be.html

 

 

I'm staying with Metformin for now.  Then again, I haven't had the time to go through all the studies at all.  I totally agree we need more in vivo studies.

 

The history of drug discovery contains the graves of many drugs that had great effects on surrogate outcomes and biomarkers, even something as benign as salt reduction has a good effect on blood pressure, but it's not clear that people live longer from that.  Mortality and morbidity in humans is the ultimate measure and we are nowhere near any ability to assess that with Berberine, but we are on solid ground with Metformin.  I am reminded also of Torcetrapib; it worked fantastically at improving lipid profiles, but people died at higher rates.  There can be unpredictable off target effects that only become apparent after either big long studies or monitoring long term use.

[tunt01]

 

Berberine suppresses LPS-induced inflammation through modulating Sirt1/NF-κB signaling pathway in RAW264.7 cells.

Zhang H, e. (2017). Berberine suppresses LPS-induced inflammation through modulating Sirt1/NF-κB signaling pathway in RAW264.7 cells. - PubMed - NCBI . Ncbi.nlm.nih.gov. Retrieved 18 September 2017, from https://www.ncbi.nlm...pubmed/28888780

 

ABSTRACT:

Chronic inflammation is a major contributing factor in the pathogenesis of many diseases. Natural product berberine (BBR) exhibits potent anti-inflammatory effect in vitro and in vivo, while the underlying mechanisms remain elusive. Sirt1, a NAD+-dependent protein deacetylase, was recently found to play an important role in modulating the development and progression of inflammation. Thus, we speculate that Sirt1 might mediate the inhibitory effect of BBR on inflammation. In LPS-stimulated RAW264.7 macrophages, BBR treatment significantly downregulated the expression of proinflammatory cytokines such as MCP-1, IL-6 and TNF-α. Importantly, BBR potently reversed LPS-induced down-regulation of Sirt1. Consistently, the inhibitory effects of BBR on proinflammatory cytokines expression was largely abrogated by Sirt1 inhibition either by EX527, a Sirt1 inhibitor or Sirt1 siRNA. Further mechanistic studies revealed that BBR-induced inhibition of NF-κB is Sirt1-dependent, as either pharmacologically or genetically inactivating Sirt1 enhanced the IκΒα degradation, IKK phosphorylation, NF-κB p65 acetylation and DNA-binding activity. Taken together, our results provide the first evidence that BBR potently suppressed inflammatory responses in macrophages through inhibition of NF-κB signaling via Sirt1-dependent mechanisms.

 

 

Presumably metformin operates through a similar mechanism via SIRT1 in vivo and these effects are preventative of alzheimer's (inflammatory and perhaps other subtypes).