#204

Give electrolytes a go. You can buy it premade, or make it yourself really cheap. I do equal parts salt, potassium chloride and then a bit of magnesium citrate and enough stevia/glycine to sweeten.

#205

It’s really strange it doesn’t mention doses. In my case, Nebivolol, 2.5 mg, reduces my BP much more than Telmisartan, 20. It also gives me dangerous bradycardia so I’m working on reducing Nebivolol dose even more, to 1.5-2 mg, and increase Telmisartan dose to 40. The right dose is everything, and it’s not that easy to calibrate it.

2 Likes
#206

Do you mean only 20 mg telmisartan/day?

#207

Yes, I’m taking telmisartan 20 mg in addition to two other medications - Nebivolol and amlodipine.

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#208

One more point for telmisartan:

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#209

Thank you, Antoine, it is now available on PMC:

Association of the protective effect of telmisartan on hearing loss among patients with hypertension

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#210

AI answer for someone with family history of hearing loss and personal history of hypertension now controlled with Telmisartan:

Your Blood Pressure Medication May Protect Your Hearing

This study provides encouraging evidence that telmisartan, the medication you’re taking for hypertension, may offer significant protection against hearing loss—a potential benefit beyond its primary purpose of controlling blood pressure.[1]

Study Overview

Researchers analyzed data from 860,103 patients with hypertension across three South Korean medical institutions, comparing those taking telmisartan with those on other blood pressure medications. After carefully matching patients to ensure fair comparison (accounting for age, other medications, and health conditions), they followed 6,012 patients for three years.[1]

Key Findings

Hearing Loss Risk Reduction: Patients taking telmisartan experienced significantly lower rates of hearing loss compared to those on other blood pressure medications—only 0.5% versus 1.5% over three years, representing a 63% reduction in risk.[2][1]

Type of Protection: The protective effect was most notable for bilateral hearing loss (affecting both ears) at 0.5% versus 1.2%, and for moderate hearing loss at 0.3% versus 0.9%. The benefits were consistent across different patient subgroups analyzed.[1]

How Telmisartan May Protect Hearing

Telmisartan works through a unique dual mechanism:[2][1]

Primary Action: As an angiotensin II receptor blocker, it controls blood pressure effectively (which you’re experiencing with your excellent 117/73 average).[1]

Secondary Action: Unlike most other blood pressure medications, telmisartan acts as a partial PPAR-gamma agonist, a property that appears protective against oxidative stress and inflammation in the inner ear’s delicate hair cells. Laboratory studies have shown this mechanism can protect auditory cells from damage caused by toxic substances and oxidative stress.[3][4][1]

Practical Implications

For Your Situation: Given your controlled hypertension and use of telmisartan, this research suggests you may be receiving dual benefits—blood pressure management plus potential hearing protection.[1]

Mechanism Matters: The cochlea (inner ear structure) contains high levels of PPAR-gamma receptors in hair cells, the very cells responsible for converting sound into nerve signals. Telmisartan’s ability to activate these receptors may reduce harmful reactive oxygen species and inflammation that typically damage hearing over time.[4][5][3][1]

Real-World Evidence: This represents the first large-scale clinical evidence (not just laboratory studies) demonstrating telmisartan’s association with hearing loss prevention in actual patients.[1]

Important Considerations

The researchers acknowledge this was a retrospective observational study, meaning it identified associations rather than proving causation. Factors like socioeconomic status and noise exposure weren’t captured in the medical records. Additionally, the study didn’t track specific dosages or examine whether higher doses provide greater protection.[1]

Bottom Line

While you’re taking telmisartan primarily for blood pressure control—which it’s managing excellently based on your numbers—this study suggests you may also be receiving an unexpected benefit in the form of hearing protection. This is particularly relevant since hearing loss affects approximately 13% of adults in developed countries and can significantly impact quality of life. Your current medication regimen appears well-chosen for both cardiovascular and potentially auditory health.[2][1]

Sources
[1] Association of the protective effect of telmisartan on hearing loss … Association of the protective effect of telmisartan on hearing loss among patients with hypertension - PMC
[2] Association of the protective effect of telmisartan on hearing loss … Association of the protective effect of telmisartan on hearing loss among patients with hypertension - PubMed
[3] Pioglitazone Represents an Effective Therapeutic Target … - Frontiers Frontiers | Pioglitazone Represents an Effective Therapeutic Target in Preventing Oxidative/Inflammatory Cochlear Damage Induced by Noise Exposure
[4] Effects of Peroxisome Proliferator Activated Receptors (PPAR)-γ and Effects of peroxisome proliferator activated receptors (PPAR)-γ and -α agonists on cochlear protection from oxidative stress - PubMed
[5] Noise-Induced Cochlear Damage Involves PPAR Down-Regulation … Noise-Induced Cochlear Damage Involves PPAR Down-Regulation through the Interplay between Oxidative Stress and Inflammation - PMC
[6] Association of the protective effect of telmisartan on hearing loss … https://www.semanticscholar.org/paper/Association-of-the-protective-effect-of-telmisartan-Cha-Yum/2e86ae211af53a3d9a92252b0fbb33969c099820
[7] Association of the protective effect of telmisartan on hearing loss … Association of the protective effect of telmisartan on hearing loss among patients with hypertension - Korea University Pure
[8] [PDF] Micardis, INN-Telmisartan - Europa.eu https://ec.europa.eu/health/documents/community-register/2024/20240912163922/anx_163922_en.pdf
[9] Can blood pressure drugs cause tinnitus? - Healthy Hearing https://www.healthyhearing.com/report/53446-Tinnitus-blood-pressure-medications-drugs
[10] [PDF] SUMMARY OF PRODUCT CHARECTERISTICS OF TELMISARTAN … https://admin.greenbook.nafdac.gov.ng/uploadImage/smpc_files/2024/11/28/20241128f5f26ea6-a413-501f-ae5e-7b2b4e2a460d.pdf
[11] Angiotensin-Receptor Blockers Prevent Vestibular Schwannoma … Angiotensin-Receptor Blockers Prevent Vestibular Schwannoma-Associated Hearing Loss - PubMed
[12] Ototoxic medications: Tinnitus and hearing loss: Treatment - Ototoxic medications: Tinnitus and hearing loss: Treatment -
[13] Drug to Treat Sudden Deafness Granted Orphan Drug Status by EMA Drug to Treat Sudden Deafness Granted Orphan Drug Status by EMA
[14] A real-world pharmacovigilance analysis of potential ototoxicity … A real-world pharmacovigilance analysis of potential ototoxicity associated with sacubitril/valsartan based on FDA Adverse Event Reporting System (FAERS) | Scientific Reports
[15] γ Activation Stimulates Keratinocyte Differentiation - ScienceDirect https://www.sciencedirect.com/science/article/pii/S0022202X15309106
[16] Is There a Link Between Tinnitus & Blood Pressure Medication? Is There a Link Between Tinnitus & Blood Pressure Medication? | Kampsen Hearing | Blog
[17] Peroxisome Proliferator-Activated Receptor-Gamma Agonists … Peroxisome Proliferator-Activated Receptor-Gamma Agonists Suppress Tissue Factor Overexpression in Rat Balloon Injury Model with Paclitaxel Infusion
[18] Can Lisinopril Cause Tinnitus? - Treble Health Can Lisinopril Cause Tinnitus? | Treble Health
[19] Preventing hearing loss in neurofibromatosis - Nature Preventing hearing loss in neurofibromatosis

4 Likes
#211

Anti-inflammatory potential of telmisartan compared to other antihypertensives: secondary outcomes from a randomized trial 2025

At baseline, hsCRP, IL-6, and TNF-α levels were comparable between groups. In the telmisartan group, hsCRP declined from 3.4 mg/L (IQR: 2.0, 13.7) to 1.8 mg/L (IQR: 1.2, 5.0), IL-6 from 4.3 pg/mL (IQR: 2.9,9.5) to 3.4 pg/ml (IQR: 2.2, 6.8), and TNF-α from 19.4 pg/ml (IQR: 8.9, 43.7) to 13.8 pg/ml (IQR: 3.5, 32.4). In the active control group, hsCRP changed from 3.1 mg/L (IQR: 1.7, 8.0) to 2.9 mg/L (IQR: 1.7, 4.9), IL-6 from 4.1 pg/ml (IQR: 3.0,7.6) to 4.2 pg/ml (IQR: 2.9, 7.8), and TNF-α from 20.2 pg/ml (IQR: 10.4, 48.6) to 16.9 pg/ml (IQR: 3.3, 30.3). The differences between groups at 12 weeks were not statistically significant for hsCRP (P = 0.07), IL-6 (P = 0.24), or TNF-α (P = 0.93).
The anti-inflammatory markers were reduced in both groups at 12 weeks without any statistically significant difference across groups. However, telmisartan was associated with greater reductions in hsCRP, IL-6, and TNF-α in patients with T2DM and hypertension following 12 weeks of treatment. These findings may indicate a potential anti-inflammatory effect of telmisartan that requires confirmation in adequately powered trials.

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#212

What were the doses of telmisartan used? Given that there are pronounced different physiological effects of this drug at different doses, it’s crucial to include this information.

1 Like
#213

Trial ID is CTRI/2023/04/051878:

Intervention1: Telmisartan 40mg: Telmisartan is given 40mg orally once daily for 3 months as per the standard treatment guidelines in patients of T2DM newly diagnosed with hypertension
Control Intervention1: Any other anti-hypertensive in the standard dose: Any other anti - hypertensive like amlodipine 5 or 10mg once daily orally or ramipril 5mg or 10mg once daily orally or cilnidipine orally 10mg Once Daily or twice daily as per the physician choice and according to dose requirement as per the standard treatment guidelines is administered for 3 months in patients of T2DM with newly diagnosed hypertension.

Also, what are the “pronounced different physiological effects of this drug at different doses”? Telmisartan is almost exclusively used at 40 mg or 80 mg, and I don’t think there is a huge difference between these doses.

2 Likes
#214

It is my understanding that higher doses of telmisartan 80mg (and also 160mg) are used for pleiotropic effects apart from BP control, such as metabolic and other CVD effects, partially mediated by greater ppar gamma impact.

Telmisartan at 80 mg/day increases high-molecular-weight adiponectin levels and improves insulin resistance in diabetic patients

Long-term renoprotective effects of standard versus high doses of telmisartan in hypertensive nondiabetic nephropathies

In rats:

Telmisartan reduces progressive oxidative stress and phosphorylated α-synuclein accumulation in stroke-resistant spontaneously hypertensive rats after transient middle cerebral artery occlusion

More data on that one here:

Long-term amelioration of telmisartan on metabolic syndrome-related molecules in stroke-resistant spontaneously hypertensive rat after transient middle cerebral artery occlusion

High-dose treatment with telmisartan induces monocytic peroxisome proliferator-activated receptor-γ target genes in patients with the metabolic syndrome

Effect of High-dose Telmisartan on the Prevention of Recurrent Atrial Fibrillation in Hypertensive Patients

This is an example of differential impact of low vs high dose of telmisartan, including inflammatory factors (study in mice):

Nonhypotensive dose of telmisartan attenuates cognitive impairment partially due to peroxisome proliferator-activated receptor-gamma activation in mice with chronic cerebral hypoperfusion

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#215

Are the articles in rats relevant? Unless the doses tested were equivalent to 40 and 80 mg in humans?

The first one is interesting. I remember others for insulin resistance but I thought they tested 20 vs 40 mg.

In any case the paper I posted used 40 mg so… All good?

1 Like
#216

Rats/mice here are as relevant (or not) as animal models in other studies, including NDDs. Hypothesis generation, mechanism illustration etc. I cited studies in animal models because many of these can’t in practice be done in humans, or weren’t done.

Re: 40 mg vs 80 mg, well, it’s somewhat relevant because we have different effects even in BP control. The purely off target pleiotropic effects would start at something higher, like 160mg, because there are no longer significant BP effects above 80mg, where for primary indication there’s no reason to go higher. That’s where the other effects might be seen more prominently. Unfortunately there are very few studies using 160mg as that’s no longer a clinical dose for primary indication (BP) so we have to turn to animal models to look for signals (rats and mice in the above studies). But like I said, I would think it’s relevant whether it’s 40mg or 80mg, because there are different effects even on BP.

Telmisartan is one of the drugs that I’ve been doing a deep dive on (SGLT2i empagliflozin, statins pitavastatin, LLT bempedoic acid, ezetimibe, rapamycin, everolimus, pioglitazone), because I am interested in neuroprotection, NDDs (especially, but not limited to PD), and there most often the effect is obviously not the primary indication. So I have to look for off target effects and pathways, which often are strongly dose dependent. And unfortunately there are few direct studies, so you look to signals in animal models as a guide.

1 Like
#217

I don’t get your point: are you looking at taking 160 mg? Or even more? Just take 80 mg and that’s it?

#218

I’m taking 80mg/day at present. I am considering 160mg/day pending further research. Should I decide to take 160mg, the earliest that would occur is June 2026, after several months of low dose (7.5mg/day) of pioglitazone. There are many reasons to consider the simultaneous use of pioglitazone and telmisartan, which I have explored in the pioglitazone thread, and dosage is important in that context. There are some additional considerations in that I also take 25mg/day of empagliflozin. When looking at polypharmacy, dosages of the individual drugs become even more important (such as the stacking of BP effects among others).

3 Likes
#219

I wish I could take Telmisartan 20 mg, but I can’t as it lowers my BP too much. However, I did start taking Tadalifil, and that does not cause my blood pressure to go too low. I feel good overall without having the effects of too low a BP. The benefits of Tadalifil for my prostate is also a bonus.

1 Like
#220

Preprint: Telmisartan reduces systemic inflammation and alters the renin-angiotensin system in mild COVID-19 2025

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#221

@adssx I dropped that study into Gemini and (while I haven’t been following Telmisartan much at all due to my good blood pressure numbers), this caught my eye (see below). What do you think of the broader research around Telmisartan as a anti-inflammaging and fibrosis medication?

From the summary of the paper you posted today:

Researchers from the University of Southern California and the University of Hawaii have provided clinical and molecular evidence that the antihypertensive drug Telmisartan acts as a potent metabolic switch during acute viral stress. While the study focused on mild COVID-19, the implications extend far beyond viral defense into the core mechanisms of inflammaging and vascular fibrosis.

The central finding is that Telmisartan does more than lower blood pressure; it fundamentally alters the “software” of the Renin-Angiotensin System (RAS). In untreated patients, the RAS system is often hijacked to favor Angiotensin II, a peptide that drives vasoconstriction, inflammation, and aging. Telmisartan treatment (40 mg/day) successfully blocked this pathway and upregulated the “pro-resolving” arm of the system: ACE2 and MasR. This shift increased levels of Angiotensin(1-7), a peptide known for tissue repair and anti-inflammatory effects.

Then I queried about the broader scientific and clinical research around telmisartan and any possible benefits for inflammaging and fibrosis, and got the following result.

I know you’ve looked more closely at this, but does all this sound accurate to you?

While the provided study highlights acute inflammatory modulation in viral infection, broader research paints a more compelling picture of Telmisartan as a systemic geroprotector. It is distinct among the “sartan” class (Angiotensin Receptor Blockers, or ARBs) because it possesses a dual mechanism: it is both an AT1 receptor blocker and a partial PPAR-gamma agonist. This unique pharmacological profile allows it to target two central pillars of aging: inflammaging (chronic sterile inflammation) and vascular fibrosis (tissue stiffening).

1. Inflammaging: The “SASP” Silencer

Research indicates that Telmisartan acts as a senomorphic agent—a compound that does not necessarily kill senescent cells but suppresses their toxic secretions (the Senescence-Associated Secretory Phenotype, or SASP).

  • The AMPK/mTOR Autophagy Switch: Unlike other ARBs (e.g., valsartan, candesartan), Telmisartan has been shown to uniquely activate AMPK and inhibit mTOR in microglial cells. This is the “holy grail” mechanism of fasting and rapamycin. By flipping this switch, it induces autophagy, allowing immune cells to clear cellular debris rather than spewing inflammatory cytokines like IL-6 and TNF-alpha.
  • Neuro-Inflammaging: Because Telmisartan is highly lipophilic (it dissolves in fats), it crosses the blood-brain barrier more effectively than older ARBs like Losartan. Once in the brain, its PPAR-gamma activity reduces neuroinflammation, protecting against the cognitive decline associated with “inflamed” aging.
  • Systemic Cytokine Blockade: Beyond the viral context, Telmisartan inhibits the NF-kB pathway, a master regulator of inflammation. In models of colitis and systemic endotoxin stress (LPS), it significantly blunts the release of pro-inflammatory cytokines, acting as a metabolic shield against chronic immune overactivation.

2. Vascular Fibrosis: The “De-Stiffening” Agent

Aging is characterized by the stiffening of arteries, driven by the replacement of elastic fibers with rigid collagen—a process controlled by TGF-beta. Telmisartan appears to directly intervene in this calcification of the vascular tree.

  • Blocking the Fibrosis Master Switch (TGF-beta1/Smad3): Research confirms that Telmisartan downregulates the TGF-beta1/Smad3 signaling pathway. In hypertensive models, this prevents the differentiation of vascular fibroblasts into myofibroblasts (the scar-forming cells), effectively halting the structural remodeling that leads to “old,” stiff vessels.
  • Reversing Arterial Stiffness (Pulse Wave Velocity): Clinical data backs the mechanism. In a study of hypertensive type 2 diabetics, Telmisartan significantly reduced **Carotid-Femoral Pulse Wave Velocity (cf-PWV)**by 0.95 m/s compared to placebo. A reduction in PWV is a functional biomarker of “vascular rejuvenation,” indicating that the arteries have become more compliant (elastic).
  • MMP Regulation: As hinted at in the provided PDF, Telmisartan modulates Matrix Metalloproteinases (MMPs). By balancing MMP activity (specifically inhibiting pathological MMP-2 and MMP-9 in some contexts while modulating MMP-1), it preserves the structural integrity of the extracellular matrix, preventing the “saggy” and “stiff” phenotype of aged tissues.

3. The PPAR-gamma “Goldilocks” Effect

The defining feature of Telmisartan in longevity research is its Partial PPAR-gamma Agonism.

  • Metabolic Synergy: Full PPAR-gamma agonists (like the diabetes drug Rosiglitazone) are powerful metabolic regulators but come with dangerous side effects like weight gain, fluid retention, and heart failure. Telmisartan activates the receptor to only ~25–30% of its maximum potential.
  • The Sweet Spot: This partial activation is sufficient to improve insulin sensitivity, boost mitochondrial biogenesis, and lower inflammation, but it avoids the severe side effects associated with full agonism. It acts as a “metabolic modulator,” improving the way the body handles glucose and lipids without the toxic overhead.

Full Gemini Analysis: https://gemini.google.com/share/769856293e99

2 Likes
#222

I am on 160 mg Of Telemisartan for nearly a year now. I am taking it for the PPAR agonism. Monitored potassium - initially it went upto 5, now it has settled at 4.75. Pleased with it. I am experimenting to increase my insulin sensitivity but no clear cut outcome. I am also on Pioglitazone 7.5mg and the polypharmacy muddles the picture and now the peptides are muddling it more. There will be light at the end of the tunnel!

3 Likes
#223

I have read that telmisartan is used to prevent kidney decline in those with CKD (chronic kidney disease) even with a normal BP. Based on graphs I’ve seen of kidney function over time, specifically Cystatin C with age, basically everyone gets CKD eventually without any intervention.

Activation of the renin-angiotensin-aldosterone system (RAAS), especially angiotensin-2 is involved in CKD pathogenesis and its cardiovascular complications.[10] Drugs interfering with the renin-angiotensin system, i.e. angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor antagonists (ARBs) are of choice as they have a blood pressure-independent antiproteinuric effect. During therapy with ACE inhibitors, angiotensin II escape prevents complete RAAS inhibition, due to alternative non-ACE pathways. However, ARBs overcome this limitation by selective blockade of the AT1 receptor and therefore angiotensin II escape observed with an ACEI do not occur with an ARB.[11,12] They are used to maximize RAAS inhibition and more effectively reduce proteinuria and decrease in GFR in diabetic and nondiabetic renal disease.[10] ARBs reduce protein excretion by approximately 35% to 40%, which is greater than other antihypertensive agents.[13] As CKD continues to rise, measures to prevent disease progression is an important goal. Among RAAS inhibitors, ARBs are preferred because of advantage discussed earlier and also because of the fact that ACE inhibitors are known to cause dry cough in a higher proportion of the Asian population. Literature search did not reveal specific study with telmisartan carried out in real-life setting in Indian patients. The aim of the present study was to examine the effects of telmisartan in patients with CKD.

Telmisartan is used to prevent kidney decline in CKD? But it can also cause renal injury? Does anyone know if a drug like this could be preventative to try and slow down kidney aging / EGFR decrease over time independent of BP effects? I know Peter Attia had trouble some while ago finding a nephrologist working in prevention.

1 Like