If you had to take either Telmisartan or Tadalifil, which would be better? I’m afraid that I can’t take them both without killing myself.
I’m interested in neuroprotection and the evidence is strong for telmisartan and weak for tadalafil. So telmisartan. For other endpoints: I don’t know.
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But isn’t this dose dependent? At what dose do you expect to see neuroprotection and in what aspect of neuroprotection? I am preparing to start telmisartan early next year and so have been looking at the literature. Neuroprotection is a very broad term.
By neuroprotection I mean “beneficial for AD, PD, depression and anxiety”. The PD trial is using 40 mg. It seems to be dose–dependent indeed. I’m taking 80 mg.
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What happens if you take both?
I will probably pass out due to low blood pressure based on past experiences.
Could try Telmisartan every other day and Tadalafil on the other alternate days.
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Unfortunately for me, I can’t tolerate telmisartan (gives me serious brain fog even at low doses), but I do great with irbesartan, so that’s the one I take. Good to know that irb is 2nd-best for adiponectin.
What’s your usual blood pressure now and how low does it go when you get symptoms? I’m curious.
When I was taking Telmisartan 40 mg daily, my SBP would vary between 90 and 125. I didn’t measure it when I passed out because I was unconscious at 3 am in the morning, lying on the bathroom floor. I did feel extreme nausea at that time, which is why I was going to the bathroom as I felt like vomiting. In the future, if I feel that way again, I’ll just stay in bed and call for help instead.
I reported this before but am repeating it as an update months later. For me telmisartan 80 mg has been an amazing drug. Setting aside the potential longer term cardiac benefits, it significantly lowered my BP readings from a former daily range from 112/75 to 145/85 to a current typical range of 110/68 to 120/70, with most readings now clustering toward the lower end. I find that telmisartan has other observable effects as well. Reporting purely subjectively, it seems to alter the cause of those daily variations, I have always been somewhat reactive to events for at least the first few seconds until my rational processes take over. That reactivity is no longer a part of my typical reactions but not in the way a tranquilizer might dampen one’s reactions. The effect is much more subtle and “natural” than that. My theory – for which there is some empirical evidence – is that the sartans modulate sympathetic-adreno-medullar axis, the hypothalamic-pituitary-adrenal (HPA) axis, and the immune system. I’ll post more later on this when I have had time to track some issues down.
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Thanks for that report, RobTuck. I’m researching telmisartan as my BP has been climbing the last few years, now getting readings over SBP 120 dr office, at home 115. I’m onlining meds one by one at the moment with copious tests, and have telmisartan scheduled for May 2026 - takes awhile as I’m testing combos too. Hope my BP can hold on not too high until then. I was thinking of starting with a 20mg/day dose and seeing how it goes. Admittedly DeStrider’s passing out experience on 40mg has me somewhat spooked.
I would be interested in any further reports of experiences you may have.
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The literature calls attention to possible dizziness, especially when starting the drug. I started with 40 mg/day and experienced no side effects of any kind. After a few months, I went to 80 mg/day to realize some of the secondary benefits. As far as I can tell, I have never had a side effect of any kind, even a minor one. In the way I described above, I actually feel better for taking telmisartan.
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This is my thinking as to why some of us report subtle positive effects when taking telmisartan.
Basis for speculating positive impact on the sympathetic-adreno-medullar axis is reduced Ang II-mediated sympathetic activation and confirmed reduction in SNS tone.
Basis for speculating positive impact on the hypothalamic-pituitary-adrenal is reduced Ang II-driven CRH-ACTH-Cortisol signaling leading to lowered cortisol levels.
Basis for speculating positive positive immune modulation is inhibition of AT1-mediated inflammatory signaling leading to reduced cytokines and NF-κB signaling.
You can see the synergy here. With reduced CRH-ACTH-Cortisol signaling, for example, there could be a form of learning taking place that would result in increased benefits over time. Of course, the opposite could be true.
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Clonidine anyone? Lowers BP, enhances sleep, reduces pain, inhibits anxiety, and manages ADHD. Not without side effects, but what isn’t?
I use Clonidine only in rare extreme situations when BP suddenly skyrockets (usually stress related). It works fast, however if you start taking it it’s not safe to stop abruptly. The smallest dose 0.1 mg is too big for me. I need 0.025 mg to bring my BP down. I also tried Clonidine patch 0.1 mg/week. It works better than a pill for me.
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I can see how a patch would be better. Tapering a tablet down to less than 25 mcg could be tricky.
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