Mounjaro Usage For Diabetes

I have been on Mounjaro about 4 months. I've moved from 2.5 to 10mg per week. The first 3 days my glucose level is great. Days 4-7 bg increases daily and I have use Soliqua for those days, to help lower. I am losing weight (15 lbs).

My question is does anyone else have issues with Mounjaro lasting a week?

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How long have you been taking the current dose?

Mounjaro may cause side effects, such as nausea, dizziness, hypoglycemia, and diarrhea.

Ref: Mounjaro Information

They do say that the initial starting dose is not intended to help with blood sugar control, you should experience better control once your dosage is raised.

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Soliqua I just looked up. It might be your actual problem. I'm not a medical professional, but have had to dig deep and learn about GLP-1 based drugs for my issues.

It says Soliqua contains lixisenatide, a short acting GLP-1 injectable agonist.

Our bodies naturally try to counter exogenous changes we make to it from drugs. We also have natural checks and balances of body chemistry. In the case of Mounjaro. It is a bias dual incretin agonist.
Mounjaro:
1. It is a full GIP agonist. Meaning it fully activates the GIP receptor. A full agonist in generaal, and known specifically in this case, causes receptor internalization. Reducing available receptors to reduce signaling potential. effectively desensitizing the receptors. These opposing actions by the body act as balancers, and /or counters to exogenous (source coming from outside the body) changes.
2. It is a bias partial GLP-1 agonist. Partial because it is not a full agonist, so it partially triggers GLP-1. Bias, because it results in intracellular cyclic adenosine monophosphate (cAMP) accumulation and avoids the recruitment of beta-arrestin.

Beta-arrestin, is the bodies natural counter to cAMP for GLP-1. cAMP pathways are responsible for signalling all the effects you see from GLP-1 meds (GIP is even better at increasing cAMP than GLP-1). GLP-1 and GIP peptides have a natural half life of just minutes. For Mounjaro, half life is 5 days, which means it builds up to a steady state and is always working. And "accumulates" cAMP. Vs the natural short acting spike in cAMP that goes away.

Beta-arrestin, is what shuts down GLP-1 receptors by causing them to internalize (take them out of play) so GLP-1 activation is limited by it. Checks and balances of the body. GIP does it too and gets downregulated by it. And beta-arrestin recruitment can affect other receptors within the cell and trigger downstream pathways, or potentially the other receptor on the cell. GLP-1 / GIP.

So, taking mounjaro or ozempic that have long half lives and built up effect, gradually accumulate cAMP levels. Gradual increase avoids receptor desensitization as much as acute spikes in activity do. (and can downregulate without beta-arrestin too). The stronger the spike in activity, the more potential for downregulation and desensitization. Even though it increases the effects you feel when you take it.

Soliqua, has acute (immediate, temporary) effect to manage after meal glucose spikes. It activates GLP-1 as a full agonist, which stimulates both cAMP and beta-arrestin increase. This spike in activity triggers the desensitization and receptor internalization (and can affect GIP and other receptors on the same cell). Wears off and stops agonism. In which case the body will undue the internalization / desensitization after a while, completing the cycle and getting ready for the next meals cycle.

**Here is what you are doing by adding Soliqua. Acute GLP-1 agonism, spikes activity which you see as positive effect. But, recruits beta-arrestin, that shuts down Soliqua activity, and gains Mounjaro has been working on toward a steady state and accumulated cAMP levels. When you are unable to undue acute tolerance fully, or cause other processes of downregulation, it is seen as long term tolerance. Which, is likely also affecting GIP to some degree on cells that also have GLP-1 receptors.

Soliqua also has a second drug in it that does stuff with insulin. Insulin also has checks and balances in the body (that I haven't looked into). Which Soliqua may "potentially" cause opposing processes of insulin, increased by Mounjaro, then spiked higher from there by Soliqua, to kick in. And may present as tolerance or more insulin resistance. Don't know if it does that or anything else in an opposing way. But, the way the body works it is not a stretch to think it might.

Soliqua does say not to take with other GLP-1 drugs. Now you know why (if you can decipher my poor writing).

You can take other diabetes drugs with Mounjaro that don't have mechanisms that get in the way. How is your tolerance for metformin? Metformin has actual long term health benefits of its own currently being studied for longevity and aging. And very cheap compared to others.

Metformin and Januvia had horribly intolerable side effects for me. I did some research and chose Jardiance based on side effects profile and which I prefer to avoid most. Turns out it has no noticeable side effects for my self. It works by making you pee out extra blood sugar. I actually took Mounjaro for the after dinner spikes that were not fully managed by Jardiance for me. Also, the Jardiance / Mounjaro combo probably saved my kidneys. They are both currently approved for kidney disease. Bonus. Mounjaaro, metformin, and Jardiance can be taken together if needed. Just watch for low blood sugar.

Again, not a medical professional. So obviously discuss with someone who is, even though they likely don't know this stuff either. Search Google for something like....Mounjaro bias duel incretin agonist....and a research article on its design should be in the results and explain a lot of what I just stated. And looked up other things I stated so you can show the doc legit sources and not pop health click bait websites they assume. Don't know about your doc, but they often have a knee jerk reaction to info from the web and immediately try to find ways to reject and dismiss it. Which is understandable as they probably spend a lot of time trying to explain why info a patient found and what someone believes is wrong and a mistake.

Like a therapist I mentioned SCT to and was told if it's not in the DSM guide, it doesn't exist. 6 months later it was diagnosed by a neuropsychiatrist who was familiar with it as he had colleagues researching it at the number 1 neurology hospital in the U.S. and worked with the guy who actually named it. When all the top SCT researchers are also the top ADHD researchers, and is 30 to 60% comorbid with millions of ADHD-I adults. And harder to manage than ADHD has been all my life. It does #%#!& exist!. So, be prepared when you go. And understand half their time is spent correcting wrong info found on the net.

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