This recent research seems to indicate that the extra weight gain in TAF versus TDF users may well be related to increased metabolic impairment due to mitochondria toxicity in TAF versus TDF if I’m understanding things correctly? I mean it’d be an assumption but seems perhaps reasonable: https://www.metabolismjournal.com/article/S0026-0495(22)00273-6/fulltext
It seems mitoq can fix these effects though perhaps: A readily available dietary supplement may reverse organ damage caused by HIV and antiretroviral therapy | ScienceDaily
General disclaimer: This post is full of my own assumptions that I’m just trying to discuss and is not what the article itself says. Anyone else interested would just need to read the article and discuss their thoughts here
Thank you for your advice
I think this test-tube study may not necessarily reflect what is happening in a person and I don’t have access to the article to see if the amount of change they are observing would have any reasonable effect in people (particularly compared to other drivers of oxidative rate change like eating a meal). Moreover, there’s no evidence that taking that supplement would help anything in people (as mentioned in the article). I would take both with a grain of salt.
That’s terrible that one would be prescribed hiv med for hep b. Maybe it’s the same. I don’t know if hep b meds that are first line of prescription are also used for HIV patients as their first line.
The tenofovir in the HIV medications are sufficient to suppress HBV replication and is the same as the first line HBV treatment.
Got me wondering of the 3 main medication treatments for hep b, what other medication are in there. To treat something else
Yes, this is definitely a good point and it hasn’t escaped scientists’ notice. Many groups have tried drug library screens for hepatitis B using the entirety of FDA-approved drugs to see if there are other compounds already in clinical use that would help with hepatitis B. This is more of @john.tavis’ wheelhouse and he could probably provide more information on it, but I’m not sure this has been particularly productive.
My understanding is that the models of Hepatitis B are not set up in a way such that accurately screening thousands of samples can be done in a practical or economical manner. New approaches (e.g., easy and scalable manners of measuring how different parts of the virus life-cycle are affected) are the main avenues of research, so that this might yield better results.
The collections of approved drugs and those that have been tested in people and proven safe but were not approved for some reason have been extensively tested against HBV by many industrial and academic labs, with no really promising results. We did this against the RNaseH, and the only interesting results were about 4 that substantially increased replication (most definitely NOT what we were looking for!).
The big problem with these “repurposing” studies is that drugs are carefully designed to be specific for their intended target to avoid off-target causes of toxicity. Consequently, it is rare for this to work well. The best examples of successful repurposing are actually entecavir and tenofovir. They were designed against HIV and it is a happy accident that they work against HBV. That is due to the enzymatic similarities between the HIV and HBV reverse transcriptases.
It is possible to do high throughput screening against HBV, but that is remarkably slow and expensive.
Hope this helps.
Quick question, I know you are in Australia. I m in the USA. When you state FDA, is that your country or my country’s FDA?
When I talk about the FDA, that refers to the US FDA. The Australian equivalent is the therapeutic goods administration (TGA). My understanding is that the TGA and FDA have recognised each other as having similar standards, and will more readily accept approvals if already approved by the other party.