#155

Can you say more about these two statements? I wonder if this applies to me too.

As someone whose sympathetic response is above average, there are theoretical reasons why an ARB might increase HRV

How do you know your sympathetic response is above average?

Why do you think an ARB would increase your HRV if you have an above average sympathetic response?

#156

I know a girl who drinks abut a pitcher a day and lowered her BP by 10 points.

I have labile hypertension on telmisartan, but I also had it on lisinopril. I think an amlodipine add-on is more stabilizing, but not at the lower doses.

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#157

That might lead to too high aluminum and manganese.

#158

A complete answer would require more time than I have before I have to travel @Barnabas. White Coat hypertension can be a common indicator of an exaggerated sympathetic response. There are many others for which, over a lifetime, one observes that their sympathetic system takes over when, objectively, there may be no need.

The theory and research discipline has yet to consolidate but if you Google terms like Telmisartan, HRV, blood pressure, ARBs, stress, sympathetic system, etc. you will uncover an interesting trail of research suggesting that HRV declines when parasympathetic/sympathetic control favors the latter and that stressors (both real physiological and perceived meditated by cognition) are associated with this condition (the actual causal chain can be comp[lex and run in both directions). This is why these two control systems are known as “rest and digest” and “fight or flee.”

If you precede your searches with “SITE: *.GOV” you will mostly retrieve research articles.

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#159

Thanks

Still, another cheap intervention to try.

It has higher customer ratings on Amazon, not that it means anything, but most enjoy the tea.

It looks like there are studies to back up the benefits claims. Pub Med has many articles establishing its benefits

"Various review articles have highlighted other potential benefits of hibiscus tea, including:

Several studies have demonstrated the potential of hibiscus tea in lowering blood pressure:

A randomized controlled trial ([2]) found that consuming hibiscus tea for 6 weeks significantly reduced systolic blood pressure (SBP) by 7.2 mmHg compared to placebo in pre- and mildly hypertensive adults.

A systematic review and meta-analysis ([3]) showed a significant reduction in both systolic and diastolic blood pressure with hibiscus supplementation, with greater effects observed in individuals with higher baseline blood pressure levels.

Neuroprotective effects and potential benefits in Alzheimer’s disease ([1])

Nephroprotective, antianemic, antioxidant, anti-inflammatory, and anti-xerostomic activities ([5])

Potential therapeutic applications in cancer and inflammatory diseases ([6])

Antimicrobial and antioxidant activities

Several studies have suggested that hibiscus tea may have beneficial effects on lipid profiles:

A review article ([4]) indicated that hibiscus extracts can improve lipid profiles by reducing total cholesterol, LDL cholesterol, and triglycerides.

A review article ([5]) highlighted the antidyslipidemic effects of hibiscus preparations reported in clinical trials.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9033014/

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#160

It seems like a beta-blocker medication (rather than ARB or other BP med classes), especially a B-blocker with low side effects such as nebivolol, would be the ideal antidote for someone with an overly active sympathetic nervous system, since we’re directly targeting receptors for adrenaline/epinephrine. It’s strange to me why there isn’t more research specifically in this area.

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#161

For the study @adssx cited Neuroglia | Free Full-Text | Telmisartan Reduces LPS-Mediated Inflammation and Induces Autophagy of Microglia
here is the mechanism summary of Telmisartan by Gemini:

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#162

What dose did your mother take?

#163

On the Hawthorn she is taking the Healths Harmony Hawthorn 4:1 Extract, 1 capsule (665 mg concentrated from 2660 mg) daily.
The price is right - on Amazon 4 months for $15.

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#164

Independent paper on Aktiia in the Journal of Human Hypertension: Wearable cuffless blood pressure tracking: when will they be good enough? 2024

To understand the challenges of currently accepted methods and cuffless devices, I performed a 24-h blood pressure monitoring self-test, including measurements when awake, asleep and watching an intense match of the Rugby World Cup final, with the purpose to demonstrate the challenges and opportunities we face. Blood pressure was monitored using five different devices simultaneously: validated left and right arm cuff blood pressure, and three cuffless wearable devices (wrist-band, chest patch and a ring). Whilst none of these devices proved to be perfect in capturing a physiologically challenging measure, namely blood pressure, it emphasised that our current practice of a single blood pressure measurement in clinical practice should be revisited.

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The Aktiia device (Fig. 1 Panel B) produced comparable systolic blood pressure when awake (p = 0.73) and during the rugby match (p = 0.54), but reported higher values when asleep (p < 0.001). This finding aligns with our previous independent comparison study in 41 patients.

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Where a patient can usually only endure one 24-h cuff-based blood pressure measurement at a time, cuffless devices are used for weeks and months without the user being aware that readings are taken. The benefit of weeks or months’ worth of data compared to a single 24-h period, is perhaps underestimated.

With blood pressure changing all the time, it is likely that when more readings are taken, it may be better than fewer. In fact, when reflecting on current clinical practice mostly relying on a single snapshot clinic blood pressure taken (often imprecisely) for decision-making, one cannot help but wondering whether it is time to completely overhaul how blood pressure is measured in primary care. Current blood pressure measurement practices across thousands of busy clinics is certainly not ‘good enough’—the question is when cuffless readings will be good enough?

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Pressão arterial ideal que devemos atingir? Sistólica abaixo de 110 ou 100?
Blood Pressure monitors
#165

Hawthorn has lowered my BP by ten points and counting.

With telmisartan 40 and amlodipine 5, I got my BP down to 123. Hawthorn bumped it down to 114. The ScienceDirect paper says it has been shown to be safe for up to two years. High BP can do some damage in two years.

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#166

How long does it take for Telmisartan to lower BP? I’ve been on it for about a month and my BP is about the same.

#167

About 2 weeks. How do you measure your BP? How often? Which dose are you using?

#168

I use the BP machine at a doctors clinic. I’m usually in the 120s. I did measure it after work and it is about 37 C outside. So maybe the weather?

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#169

Measure it at home using this protocol (2024 European guidelines):
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Before eating or drinking coffee. So for instance after waking up before breakfast and in the afternoon or evening before dinner.

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#170

Association between risk of Alzheimer’s disease and related dementias and angiotensin receptor Ⅱ blockers treatment for individuals with hypertension in high-volume claims data 2024

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If people still needed to be convinced by telmisartan, massive study on 6 million people:

From 6,390,826 individuals with hypertension, there were 1,839,176 ARB users, 3,366,841 non-ARB AHM users, and 1,184,809 AHM non-users. The unadjusted KM curve showed that ARB users had lower cumulative hazard than other AHM users or AHM non-users (P < 0.0001). In Cox PH analysis, ARB users showed a 20% lower adjusted hazard of developing ADRD compared to angiotensin-converting enzyme inhibitor (ACEI) users and a 29% and 18% reduced hazard when compared to non-ARB/ACEI AHM users and AHM non-users (all P < 0.0001). Consumption of BBB-crossing ARBs was linked to a lower hazard of ADRD development than non-BBB-crossing ARBs, undetermined ARBs, and non-consumption of AHMs by 11%, 25%, and 31% (all P < 0.0001).

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#171

Not sure how much this has been addressed in this thread, but administration of ACEI drugs appears to block the RAS activation from empagliflozin. This does not occur with ARB co-administration.

Angiotensin pathways under therapy with empagliflozin in patients with chronic heart failure - PMC).

Here are some relevant quotes from the paper:

In addition, we performed an exploratory comparison of systemic haemodynamic parameters in patients treated with empagliflozin who received either ARB (23 patients) or ACEI (19 patients) co‐medication. Change in PWV from baseline to 1 as well as 3‐months therapy with empagliflozin was greater in the ARB (−1.05 and −0.42 m/s) compared with the ACEI (−0.006 and 0.30 m/s) group (P = 0.002, P = 0.014). Furthermore, change in central diastolic BP from baseline to 1 as well as 3 months (trend) therapy with empagliflozin was also greater for patients with ARB (−7.65 and −4.15 mmHg) compared with ACEI (−5.76 and 0.02 mmHg) co‐medication (P = 0.049, P = 0.064).

In patients with CHF, 1 and 3 months of therapy with empagliflozin lead to a rise in Ang I and Ang II as well as Ang‐(1‐7) and Ang‐(1‐5) compared with baseline, which was not present in the placebo group. Thus, our results indicate an activation of both the Ang I–ACE–Ang II receptor axis and the Mas axis. Most interestingly, the activation of both the Ang I–ACE–Ang II receptor axis and the Mas‐axis pathway after initiating treatment with empagliflozin was only observed in patients with ARB co‐medication. Patients with ACEI co‐medication did not show any empagliflozin‐induced activation of either pathway of the RAS.

We believe that the finding of the empagliflozin‐induced activation of both the Ang I–ACE–Ang II receptor axis (which still is blocked by the ARB medication) and the protective Mas axis only in patients with ARB co‐medication could have important implications for the treatment of CHF patients with SGLT2 inhibitors nowadays as first‐line treatment in patients with CHF.

In light of this, taking a ACE inhibitor in combination with a SGLT2 inhibitor may not be advisable as it will negate some of the positive effects of the SGLT2i activation of RAS (cardioprotective effects from the activation of the Mas-axis)

Taking a SGLT2i such as empagliflozin with an ARB such as telmisartan seems like a good combination, retaining the positive effects of each:

  • Blood pressure regulation (key points from this study is ARB+SGLT2i was better in reducing PWV and central DBP than ACEi+SGLT2i)
  • Metabolic benefits (reduces blood glucose, increased insulin sensitivity via PPARγ activation)
  • Renal protection (intraglomerular pressure, CKD progression)
  • Cardioprotection (via Mas-axis)
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#172

This paper also points to potential synergies with valsartan + empagliflozin: Combining renin-angiotensin system blockade and sodium-glucose cotransporter-2 inhibition in experimental diabetes results in synergistic beneficial effects 2024

RAS blockade and SGLT2 inhibition display synergistic beneficial effects on BP, kidney injury and cardiac hypertrophy in a rat with hypertension and diabetes. The synergy does not involve upregulation of angiotensin-(1–7), but may relate to direct RAS-independent effects of empagliflozin in the heart and kidney.

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#173

An Open-Label, Non-randomized, Drug-Repurposing Study to Explore the Clinical Effects of Angiotensin II Type 1 (AT1) Receptor Antagonists on Anxiety and Depression in Parkinson’s Disease

This small sample of ARB-treated PD patients displayed lower levels of anxiety. Randomized clinical trials are warranted.

Many of us reported lower anxiety with telmisartan. This study in people with PD seems to confirm the benefits.

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#174

I wonder if one would get similar effects with telmisartan +empa instead of valsartan+empa. I ask selfishly, since I have a ton of telmi on hand😅.

It’s in rats, but still interesting. There’s got to be a lot of people who take these drug combos, so there’s probably some clinical effects seen incidentally in some human studies.

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