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Astaxanthin plus berberine: a nutraceutical strategy for replicating the benefits of a metformin/fibrate regimen in metabolic syndrome
  1. James J DiNicolantonio1,
  2. Mark McCarty2 and
  3. James OKeefe3
  1. 1Department of Preventive Cardiology, Mid America Heart Institute, Kansas City, Kansas, USA
  2. 2Catalytic Longevity, Encinitas, California, USA
  3. 3Saint Luke’s Mid America Heart Institute, University of Missouri-Kansas City, Kansas City, Missouri, USA
  1. Correspondence to Dr James J DiNicolantonio; jjdinicol{at}

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Berberine is a nutraceutical activator of AMP-activated kinase

The phytochemical berberine, a constituent of certain herbs used in traditional Chinese medicine, has long been in use in China as a well-documented therapy for type 2 diabetes.1 2 Mechanistic studies demonstrates that, like metformin, it activates AMP-activated kinase (AMPK); this is thought to be the chief basis of its utility in diabetes.3–5 The typical therapeutic regimen is 500 mg two or three times per day, or 850 mg two times per day. The most common side effect is constipation, which tends to remit during continuing treatment.6 Unlike metformin, however, berberine upregulates the hepatic expression of LDL receptors, through a mechanism that is complementary to that of statins or red yeast rice (RYR); whereas statins increase transcription of the gene coding for LDL receptors, berberine increases the half-life of LDL receptor mRNA.7 Hence, the combination of berberine plus RYR—a natural low-potency source of monacolin K (lovastatin) and other monacolins that has moderate hypocholesterolaemic activity in a standardised dose that is well tolerated in most patients who don’t tolerate pharmaceutical statins8–10—has been recommended as a nutraceutical alternative to pharmaceuticals in the management of hypercholesterolaemia.11

The carotenoid astaxanthin can act as a PPARα agonist

The natural carotenoid astaxanthin is extraordinarily effective—more so than tocopherols—for conferring radical-scavenging antioxidant protection to biological membranes.12 It may be particularly beneficial for blunting the feedforward loop whereby mitochondria subjected to oxidative stress—as during ischaemia-reperfusion injury—become greater sources of oxidants owing to damage to their respiratory chains.13 However, in both clinical and rodent studies, oral astaxanthin has ameliorated the …

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