This has been discussed before;

I use Azithromycin.

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What dose? What is your protocol?

What is your protocol, weekly, monthly, semi-annually?

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Once a quarter{ever 3 month/12 weeks]

I do the modified DAV therapy/procedure, as was discussed in the other thread

For one week/seven days

250mg of azithromycin once ever 72 hours
100mg of doxycycline twice a day{100mg every 12 hours]
And 2.4g of vitamin C - I use fat soluble, a mix of liposomal C and ascorbyl palmitate {AP] - 4 to 6 hours after taking either the azithromycin or the doxycycline.

A slightly modified version of Professor Michael Lisanti published paper.

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and

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I have upped my dose of taurine to 8 mg a day in my afternoon coffee along with 2 g of magnesium citrate. The dosing is based on the taurine video in the taurine linked below. I try to space it 4 hours after my Glycine and collagen coffee to avoid receptor conflicts.

Although caffeine also blocks the taurine receptor, there were studies that showed them to have synergistic qualities as well. I also need the strong taste of coffee to cover up the not so pleasant taste of taurine.

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How long the aftertaste last?

The taste of taurine isn’t too bad. It’s just mildly unpleasant. So coffee covers it well. A smoothie would work too. I just don’t like it in plain water.

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Thanks Chris! Then we should optimize for impact and not count the taste?

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Yes. Optimize for impact.

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Can you expound a bit more?

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Watch the video I linked 4 posts above this one. It’s the best guide to taurine I have found yet. It discusses the best dose to take based on our current knowledge.

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A new video:

Dr. Kirkland shares insights into the science of cellular senescence and how targeting these cells could revolutionize the treatment of age-related chronic diseases. He sheds light on the mechanisms behind senolytics and their promise for extending healthspan. The discussion also touches on the importance of lifestyle factors like diet and exercise in managing senescent cells. Dr. Kirkland also discusses geroscience, a research paradigm that seeks to understand the mechanisms that make aging a major risk factor for and driver of common chronic conditions and diseases of older people. This knowledge can be used to slow the rate of aging, reverse its effects, delay or even cure age-related diseases, and extend healthspan. The conversation also highlights the emerging evidence and potential of using gerotherapeutics (treatments) that target aging biology to combat aging-related diseases and increase healthspan and lifespan. Dr. Kirkland also covers the challenges and opportunities in translating these scientific discoveries into clinical applications, emphasizing the critical role of interdisciplinary efforts in advancing our understanding and management of aging. This is an enlightening episode with Dr. Kirkland on aging research and the opportunities to revolutionize healthcare by combating aging-related diseases and increasing people’s healthspan and lifespan.

Introduction: 00:00-03:49
What led Dr. James Kirkland to become a physician-scientist and become interested in aging research?: 03:50-05:24
What is geroscience, and what are fundamental aging processes?: 05:25-09:17
What are the differences between targeting aging vs. the traditional medical system of waiting to treat illnesses or diseases after they occur?: 09:18-12:39
What are gerotherapeutics, and what is their relevance for healthspan and lifespan?: 12:40-16:10
What are senescent cells? What is the impact of senescent cells on the body and aging: 16:11-26:39
What are senolytics? How do senolytics work to target senescent cells to remove them?: 26:40-35:05
How Dr. James Krikland discovered senolytics such as fisetin, quercetin, and dasatinib? What clinical trials on the effects of senolytics in humans have been done? 36:06-40:47
Discovering biomarkers for senescent cells: 40:48-42:37
What are some important factors to consider on the effects of gerotherapeutics and senolytics on lifespan and healthspan in model organisms compared to humans?: 40:38-47:39
The potential for geroscience and gerotherapeutics, such as senolytics, to transform healthcare. What is the importance and what are some challenges of conducting clinical trials on gerotherapeutics, such as senolytics, to improve healthspan in humans?: 47:40-56:15
What is the Translational Geroscience Network, and what are its goals?: 56:16-01:02:01
How might senolytics be used clinically in the future if proven safe and effective? What conditions might they benefit?: 01:02:0201:05:57
What are the effects of lifestyle, such as diet and exercise, on senescent cells?: 01:05:58-01:06:52
What excites Dr. James Kirkland the most about the potential for extending people’s healthspan and lifespan with therapies, drugs, or interventions in the coming years?: 01:06:53-01:07:41

Dr. Kirkland’s top tip for health? 01:07:42-01:12:13 (end)

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Senescence caught my eye in 2018 when I read a head line that went something like this “Zombie cells may be killing you”. A catchy headline for a zombie fan and science geek so I had to know what it was all about.

After reading a fair bit on this in these articles and studies I decided to have some fun :slight_smile:

This is a good overview of the field but is somewhat out dated now after only 5 years of continued research. I see that James Kirkland is referenced in previous posts in this thread.

Targeting Senescent Cells for a Healthier Aging: Challenges and Opportunities

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7709980/

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Here are 2 studies that demonstrated in Phase 1 trials that clearing senescent cells appeared to have a benefit for 2 very different conditions. These 2 trials clearly demonstrated that the “hit and run” D+Q protocol does clear senescent cells and reduces SASP

Senolytics decrease senescent cells in humans: Preliminary report from a clinical trial of Dasatinib plus Quercetin in individuals with diabetic kidney disease

https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(19)30591-2/fulltext

Senolytics in idiopathic pulmonary fibrosis: Results from a first-in-human, open-label, pilot study

https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(18)30629-7/fulltext

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Most of the headlines, after interesting results like this, where quite “hopeful” and many people decided to try the D+Q protocol.

Most people missed the very high doses of Quercitin or failed to understand what effect a liposomal form of Quercetin, as used in these 2 trials, means relative to dosing.

Why is this important? because dose matters.

The liposomal form of Q used in these 2 trials as provided by Thorne is highly bio-available. As demonstrated in this clinical evaluation.

The form of Q used is up to 20 times more bioavailable that “regular” Quercetin. Lets just use 10x as an example. What impact does that have on the results?

If we consider that the high amount used in these studies, 20mg/kg of body weight = 20mg x 70kg = 1,400mg bio-availability really does matter. My body weight = 70kg.

Because of the highly bio-available form of Quercetin used, one would need to take at minimum 14,000mg or 14 grams of “regular” Quercetin to come close to the actual dose used in these 2 trials that demonstrated that the D+Q protocol works.

This is why I focused on increasing bio-availability for my personal use.

I’ve been using my little formula for over 4 years, 4 “cycles” per year.

My personal objective is to achieve a “youthful” level of senescence and am seeking to maintain my “threshold” of senescence :slight_smile:

threshold_theory_of_senescence

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So Steve_C what is your exact Protocol?

And can you provide link to the Quercetin you use?

I use “regular” Quercetin but in my little formula there are a number of bio-availability enhancers. So it’s a bit more complicated than just Quercetin.

There are 9 compounds in our formula, all to enhance the performance of the 2 key compounds, Quercetin and Fisetin.

One could always purchase the brand used in the successful trials, Thorne.

Also I’d be happy to offer anyone on this forum a discount off our product of 80%

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