I believe there’s a period of adjustment. You could go super slow, gradually escalating over weeks to 50, 60, 70, 80 (obv. tricky splitting pills!) and your body will adjust. Of course you might have huge BP variation throughout the day, but it’s less likely with telmisartan, as it’s supposed to get your BP to be less variable.
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5 months.
I agree splitting them in half-ish seems easy but smaller quarters would be a challenge.
But I suspect the consensus would be making the daily dose the same (e.g., 60mg) rather than alternating between 40mg and 80mg EOD.
In my observation there is a behavioral component associated to ARBs, at least with telmisartan. This facet can continue to favorably modulate the variance in BP over a much longer period than is required for the biochemical stabilization. If you can tolerate it, there are well researched ASCVD and renal benefits associated to the 80 mg. dose. Telmisartan reduces the rate of decline in kidney function by as much as 49%. Likely less in younger people with normal kidney function but still geroprotective.
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Olmesartan superior to telmisartan in certain contexts? Olmesartan 40mg lowered inflammatory markers such as hsCRP and IL-6 while telmisartan 80mg did not, and lowered SBP/DBP more than telmisartan - old Japanese paper, small number of subjects:
Comparison of Effects of Olmesartan and Telmisartan on Blood Pressure and Metabolic Parameters in Japanese Early-Stage Type-2 Diabetics with Hypertension
https://www.nature.com/articles/hr2008303
This was confirmed in lower dosages olmesartan 20mg and telmisartan 40mg:
Comparison of Effects of Olmesartan and Telmisartan on Blood Pressure and Metabolic Parameters in Japanese Early-Stage Type-2 Diabetics with Hypertension
https://www.nature.com/articles/hr2008303
And again, this time also showing lower albuminuria in olmesartan users:
Difference in the effects of switching from Candesartan to Olmesartan or Telmisartan to Olmesartan in hypertensive patients with type 2 diabetes: the COTO study
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Good find. What is the half life of Olmesartan and are there any downsides?
Roughly half, a little over half of telmisartan, about 13 hours (10-18). But once you’ve adjusted to it, it can typically be taken once daily and be effective for 24 hours. Telmisartan is likely safer, because olmesartan can in rare cases cause severe diarrhea. Telmisartan is a more straightforward and more predictable drug, while olmesartan has a more complicated mode of action. The pleiotropic effects (i.e. apart from BP impact) is different, with telmi more effective for CV and lipid issues.
All in all, it depends on your particular needs. For me, telmi is better, as I don’t need stronger BP control or help with inflammation. But for others olme might be a more interesting choice. It’s good to be aware of options, which is why I posted this.
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Olmesartan doesn’t cross BBB so you lose that benefit of Telmi. I personally prefer Telmi.
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Telmisartan increases systemic exposure to rosuvastatin after single and multiple doses, and in vitro studies show telmisartan inhibits ABCG2-mediated transport of rosuvastatin
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Could Telmisartan be causing elevated SHBG, low DHEA-s, and low Free Test?
I’ve been taking Telmisartan since discussing it here about 15 months ago as my BP remained elevated even after weight loss to normal BMI. Started at 40mg then increased to 80mg which normalized my BP to 115-125/75-83.
However, during the same time frame my hormones have been out of range (through normal before Telmi):
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SHBG elevated 70-95 nmol/L, averaging around 83.
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Free T low (7-11mg/dL by direct and calculated measures) like as results of elevated SHBG
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DHEA-s low at 76-95 ug/dL
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LH elevated 7-11 mIU/mL
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Total Test remains normal or even elevated (600-945ng/dL) so I can produce T, it just gets bound by SHBG resulting in like free T / low bioavailable T.
Prior to Telmi my SHBG WAS 26.1 nmol/L (normal or optimal range) for several months, though that’s as far back as my data goes.
Gemini says Telmi is causing the high SHBG:
“Patient is in state of drug-induced functional hypogonadism and chronic hyponatremia. Longitudinal analysis of his 2024–2025 health records identifies Telmisartan as the pharmacological driver of his endocrine dysregulation.
The Mechanism of Toxicity:
Telmisartan functions as a partial agonist of PPAR-γ. While beneficial for insulin sensitivity, chronic PPAR-γ activation transcriptionally upregulates SHBG synthesis in the liver. Simultaneously, Telmisartan inhibits adrenal CYP17 enzymatic activity, throttling the production of DHEA-S.
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Most likely not.
What telmisartan is (and isn’t) known to do hormonally
- Total testosterone: In at least one controlled clinical study of telmisartan in men, telmisartan had a neutral effect on total testosterone (no meaningful change). Wiley Online Library+1
- “Anti-androgen” effects: There are reports in women with PCOS where telmisartan was associated with lower androgen levels (case series). That’s a very different physiology than an older male, and it doesn’t prove the same effect occurs in men. PMC
- SHBG specifically: I did not find good evidence that telmisartan reliably raises SHBG. SHBG is largely a liver-produced binding protein, strongly influenced by thyroid status, liver function, estrogen balance, and insulin/nutritional state. PubMed
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I’m suspicious Gemini has led me down a speculative path. It also referenced the same studies but provides the plausible PPAR-y mechanism.
I had a liver concern around the same time (since resolved, was DILI from a since stopped medication) but in reality the endocrine dysfunction preceded the Telmi. I’m trying to narrow down possible causes.
United States: In 2023, there were an estimated 2.7 million prescriptions filled for telmisartan, serving approximately 661,000 patients in the U.S. alone.
Your symptoms are not even included in the rare side effects. You should look elsewhere for your problems.
Uncommon and Rare Medical Side Effects
These effects occur in fewer than 1% of patients but are recognized in official clinical data:
- Sprue-like Enteropathy: A rare but severe condition characterized by chronic diarrhea and significant weight loss. Symptoms can appear months or years after starting the drug and resolve only after discontinuation.
- Musculoskeletal Issues: Rare instances of rhabdomyolysis (severe muscle breakdown) and tendon pain or inflammation (tendonitis).
- Skin Reactions: Rare reports of lichenoid keratosis (small, scaly skin bumps), eczema, and toxic skin eruptions.
- Sensory Changes: Patients occasionally report dysgeusia (distortion of taste), tinnitus (ringing in the ears), or blurred vision.
- Systemic Infections: There is a slightly increased, though uncommon, risk of sepsis, particularly in patients with specific comorbidities.
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It is pretty clear in the literature that the long term use of Telmisartan may reduce bioavailable testosterone in some individuals, primarily by increasing SHBG, rather than by directly inhibiting testicular testosterone production. With older individuals whose preexisting levels may be toward the lower end of the distribution, an effect might be seen. This said, whether the slight increase in SHBG (with the possible slight decrease in free testosterone) is beneficial or harmful is an incredibly complex discussion that does not admit to any simple generalizations that I can see. Rare, one-off effects exist for virtually all drugs, including aspirin. To complicate matters even more, such effects might exist only in the presence of another unique substance in your diet or supplement stack. The only way to accurately assess your causalities @zebit0, is via a time-consuming test in which you document and compare effects over multiple baselines with reversals looking for regression discontinuities. Figuring this out in N=1 cases generally exceeds the time, patience, interest, or ability of most users. When confronted with the choice myself, I usually opt for a simpler, less rigorous solution, such as ignoring the issue or changing the drug.
Switching to Amlodipine and will track with labs
On reflection Gemini speculated/extrapolated too far from limited info. I’ll work on improving the prompts for that. Claude’s critical analysis appears more sound:
The claim fails at multiple mechanistic levels:
- PPAR-γ actually represses SHBG—the opposite of the claim. Selva & Hammond (2009) showed rosiglitazone reduced SHBG 20-25%, while PPAR-γ antagonists increased it 2-3x. When TZDs raise SHBG clinically, it’s indirect (improved insulin sensitivity → ↑HNF-4α).
- Telmisartan’s PPAR-γ effect is pharmacokinetically negligible. EC50 is 4.5 µmol/L; free drug after 80mg is ~1,000-fold below this. ONTARGET (N=25,620) found no metabolic advantage over ramipril.
- DHEA-S has zero SHBG affinity—it binds albumin. No feedback pathway exists from SHBG to adrenal synthesis. This part is biochemically impossible.
- Testosterone dynamics are more complex. SHBG-transgenic mice showed elevated SHBG increased total T ~200-fold via HPG feedback, not simple “sequestration.”
Conclusion: If SHBG rose on telmisartan, attribute it to improved insulin sensitivity or metabolic changes (ARB class effects), not PPAR-γ. The proposed mechanism contradicts established molecular biology.
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This may seem of pretty marginal relevance to most biohackers, but nonetheless it’s a small win for ARBs (so telmisartan too) for those who may need to undergo ACDF surgery. As someone who recently underwent just such a surgery, I found this result of interest and relevance (at least to me, as I take telmisartan). A key variable is the speed and rate of spinal fusion - the faster and more thorough the better. And here an interesting phenomenon is present. It appears that antihypertensive agents influence the rate of spinal fusion in a differential way based on drug class. If we compare patients who are not taking any antihypertensive drugs, and are normotensive to patients taking ARBs, then the ARB taking patients experience better rates of spinal fusion, while those who take ACEi drugs experience worse rates. That’s a win for ARBs (and so, presumably telmisartan) in this very specific context. This is based on the following study (not the most stellar p values, but the signal is there):
A retrospective cohort analysis of the effects of renin-angiotensin system inhibitors on spinal fusion in ACDF patients
Quote:
“In the analysis of fusion rates, patients treated with ARBs exhibited a higher fusion rate, while those treated with ACEIs displayed a lower fusion rate compared to untreated nonhypertensive patients (p = .04 and .02, respectively). The difference in fusion rates between ARBs and ACEIs was also significant, with the former displaying higher rates (p < .001).”
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So, the theory would be that ARBs are selective antagonists of the Angiotensin II Type 1, and blocking AT1 diverts angiotensin II to bind to the Angiotensin II Type 2 receptor, the activation of which has been shown to promote osteoblast differentiation, bone formation, and reduce bone resorption.
Whooda thunk it! Was this known or speculated in advance?
Not that I know of. And btw. the way I found this paper was a total fluke. The cervical spine is exceptionally poorly vascularized and I was brainstorming ways to facilitate my spinal fusion. The thought occurred to me that perhaps there might be a similar mechanism I could deploy as happens with elderly people whose blood pressure rises due to stiffening endothelium and vascular stenosis - the older people did better with higher BP because it was easier to perfuse the tissues in that situation (bringing nutrients, growth factors etc.). So analogous to that I wondered if higher BP might better perfuse the poorly vascularized cervical spine and assist with the fusion process. In that situation I might want to hold off on getting back on a BP lowering med like my telmisartan. So I decided to do a search of the literature to see if there was any signal for antihypertension agents and spinal fusion rates. That’s how I found this paper.
And I discovered that ineed there is a signal, but it has nothing to do with BP - since two classes of meds both of which lower BP have opposite effects on the rate of spinal fusion. Which means that the mechanism of action is biochemical in nature, not mechanical, which sent me down a different rabbit hole - but that’s a different story🤓.
Oh, and incidentally AI (Gemini 3 Thinking Deep Research mode), was utterly useless in finding ways to enhance spinal fusion - just the usual superficial slop. I asked for all papers that identify factors which impact spinal fusion rates and it did not find this paper. As always it’s up to the human to do the heavy lifting. YMMV.
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Oldie, but interesting in how these concepts have evolved since the publication of this paper.
Angiotensin II blockade: how its molecular targets may signal to mitochondria and slow aging. Coincidences with calorie restriction and mTOR inhibition
https://journals.physiology.org/doi/full/10.1152/ajpheart.00459.2014
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Does anyone have any experience with different brands of Telmisartan? I have been taking 80 mg Sandoz from Canada but recently switched to ‘Telmikind’ manufactured by Mankind Pharma in India and shipped from there. I have had good luck with direct to India pharma but I’m not familiar with this brand. For some reason, I’m wondering about it. I still have some Sandoz so I may do an A/B test.
Ha, that’s interesting! Please let us know! I have a different brand of telmi from India - TeleAct 40 (Sun Pharma), and since I went up to 80mg/day, I have to take 2 pills a day (I take both in the evening). Recently I decided to top up my stash of telmi and came across 80mg pills, Telmikind (Mankind Pharma). So now I have a bunch of those. Before I bought them, I did some checking around and it looked to me like Mankind Pharma has a pretty good reputation and I didn’t come across any recalls or scandals - they are also expanding internationally, so presumably will try to maintain some standards. But of course, you never know. So I’d be very interested in your experiences. I have so far not taken any Telmikind, but the TeleAct seemed to work OK more or less in line with my expectations of effect on BP and no side effects that I could tell. I have still not tried the Telmikind.
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