Dr. Ben Bikman – ‘GLP-1 Drugs: Consequences and Considerations’
Dr. Benjamin Bikman earned his Ph.D. in Bioenergetics and was a postdoctoral fellow with the Duke-National University of Singapore in metabolic disorders. He is currently a professor of pathophysiology and a biomedical scientist at Brigham Young University in Utah.
Dr. Bikman's professional focus as a scientist and professor is to better understand chronic modern-day diseases, with a special emphasis on the origins and consequences of obesity and diabetes, with an increasing scrutiny of the pathogenicity of insulin and insulin resistance. He frequently publishes his research in peer-reviewed journals and presents at international science meetings.
Dr. Bikman has long been an advocate of a ketogenic diet in light of the considerable evidence supporting its use as a therapy for reversing insulin resistance. His website InsulinIQ.com promotes dietary clarity, healing, and freedom through evidence-based science about insulin resistance. Employing cell-autonomous to whole-body systems, Dr. Bikman's recent efforts have focused on exploring the intimate associations between the metabolic and immune systems.
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What about berberine? Can you share your thoughts please?
Excellent video. Thanks.
My BMI is 21 and I’m very athletic. My a1c is stubbornly at 5.8
I’m starting 10% carbs eating. I hope it works
Seems to me these drugs should be avoided at all costs.
Thank you professor Bikman. You gave a very clear and up-to-date summary of the effects, benefits and problems of GLP-1 drugs.
Excellent presentation.
The comment about type 1 diabetes people not being able to retain weight absent insulin regardless of calories is an ultimate nail in the CICO coffin
As always, Ben is a wealth of information and wisdom
Interesting
Thanks Ben. Insightful, as usual.
23:00 AUC of insulin is lower, under GLP-1 treatment, but insulin nadir (160-270 min) is higher.
Insulin signalling doesn’t just relocate GLUT4 to the plasma membrane, it also potentiates the transcription of and activation of acetyl-CoA carboxylase, which catalyzes the conversion of cytosolic citrate to palmitate. The first step of that process produces malonyl-CoA which inhibits long chained fatty acid (LCFA) import into the mitochondria. We can infer then that the insulin nadir is the point of the maximal transport of LCFA across the mitochondrial membranes. Raise the insulin nadir and the fuel line of fatty acids is crimped. Reduce supply of fatty acids and the mitochondria is required to supplement from alternative fuels to support the ATP:ADP ratio. 2 hours after a meal glucose available from circulation has dropped. Where does the mitochondria find fuel when glucose has run low, and fatty acid supply is inhibited. The labile amino acid pool.
Now take a process (circulating GLP-1) that was evolutionary conserved to have a half-life of 2 mins, and mess with its degradation so it has a half-life of 2 weeks. And re-dose every week. Of course it causes outsized lean mass loss. How could it do anything else?
The best interpretation of the carbohydrate insulin model of obesity must include not just the hormones effect on the source (adipocytes) but also on the sink (LCFA import into beta-oxidation).
Brilliant as usual!
As usual, Dr. Bikman explained this so well.
Brilliant presentation, thanks for sharing.
Thank you Ben for your service and efforts
I could listen to Dr. B for hours
Incredible presentation!
Always looking fwd to your next classroom discussions 🤓
Cheers from Switzerland
Ben is a genius! ❤
Brilliant as always thank you Dr. Bikman.
Monkeying around with nature’s exquisite balancing with pharmaceuticals seldom leads to a good outcome.
Thank you Ben!