{"id":52489,"date":"2020-07-15T11:55:32","date_gmt":"2020-07-15T15:55:32","guid":{"rendered":"https:\/\/asweetlife.org\/?p=52489"},"modified":"2020-07-15T12:09:49","modified_gmt":"2020-07-15T16:09:49","slug":"a-diabetes-researcher-thinks-he-may-have-just-solved-covid-19","status":"publish","type":"post","link":"https:\/\/asweetlife.org\/?p=52489","title":{"rendered":"A Diabetes Researcher Thinks He May Have Just Solved Covid-19"},"content":{"rendered":"

Potentially big news from Israel: Professor Yaakov Nahmias<\/a> of Jerusalem\u2019s Hebrew University believes that he may have discovered a breakthrough treatment for Covid-19. Remarkably, the potential cure is a common prescription drug, Fenofibrate, that is already known to be tolerated by adults without significant side effects. Fenofibrate is widely available in both branded and generic forms; many take it as a cholesterol-lowering medication.<\/p>\n

Working with Dr. Benjamin tenOever<\/a> of New York\u2019s Mount Sinai Medical Center, Professor Nahmias was able to show that in lab tests on human lung tissue, Fenofibrate<\/a> seriously impeded the coronavirus\u2019 ability to reproduce itself, hugely reducing the severity of infection and its resulting damage. The team is enthusiastic, and told another media source<\/a> that \u201cwithin a few months, treatment with our drug could be turning Covid-19 into a type of common cold.”<\/p>\n

The theory still needs to be confirmed in human trials, but there is hope that it can be evaluated as a treatment for Covid-19 very quickly. Because the drug is already safe and well-understood, researchers will be able to fast-track clinical trials. And retrospective data, which his lab is currently reviewing, should show whether Covid-19 patients that are already taking Fenofibrate have superior outcomes.<\/p>\n

We have followed Professor Nahmias\u2019 work for years through his diabetes research<\/a>. When ASweetLife reached to him, he gladly agreed to explain his potential breakthrough.<\/p>\n

Any virus needs to \u2018hijack\u2019 host cells in order to replicate itself, and Nahmias observed that the way the novel coronavirus does so appears to be \u201cunique\u201d: \u201cWe see a lot more lipid droplets in human lung cells as well as massive membrane complexes that the virus uses to replicate, essentially factories to produce new viruses.\u201d<\/p>\n

\u201cThe new corona virus enters lung cells and produces viral proteins that seem to stick to different parts of the cells.\u00a0A few of those virus proteins shut down the mitochondria, the part of the cell that burns sugar into energy.\u00a0This causes the cells to take up more sugar and start make new fatty acids and phospholipids.\u201d<\/p>\n

\u201cPhospholipids turn into the membrane replication complexes and spread throughout the cells. New viruses\u00a0start being produced and packaged inside the lung cells, then released to infect other lung cells.\u201d<\/p>\n

The bottom line is that the virus causes an unusual amount of fat to build up on the inside of lung cells, fat that it requires to reproduce.<\/p>\n

This mechanism also may help explain why both diabetes and non-diabetic hyperglycemia appear to be such significant risk factors<\/a>: \u201cWe see that virus-infected lung cells use much more glucose and convert it to lipids that the\u00a0virus needs to propagate. It makes sense that patients with high glucose levels would be more prone to lung damage\u00a0and higher viremia due to this mechanism.\u201d<\/p>\n

The virus, therefore, appears to feast on high blood sugar. And when a patient\u2019s blood sugar rises in response to Covid-19, while it \u201clooks like insulin resistance, it is actually mitochondrial dysfunction. Virus proteins seem to bind\u00a0specific genetic elements that shut down the mitochondria. Without it, lung cells can\u2019t burn glucose into energy.\u201d<\/p>\n

If a medication were able to interrupt the dysfunctional metabolic processes triggered by the virus, it could stop Covid-19 in its tracks. Professor Nahmias\u2019 team experimented with several medications that could plausibly get the job done, including statins, but when they evaluated the results it was clear that there was \u201cnothing like Fenofibrate.\u201d<\/p>\n

\u201cThe virus shuts down PPARA<\/a>, blocking the cell\u2019s ability to burn fat. Fenofibrate specifically activates PPARA,\u00a0specifically reversing the virus\u2019 effect.\u201d<\/p>\n

The team\u2019s work was published yesterday in a preprint<\/a>, and has not yet been peer reviewed.<\/p>\n","protected":false},"excerpt":{"rendered":"

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