I read elsewhere that there is a negative interaction between Taurine and rapamycin. I have stopped taking taurine. At least you might consider avoid it around the time you take rapamycin.

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Thanks. I only take taurine on my lifting days as I understand it is anabolic. I don’t lift around my rapa dosing.

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It would be much more helpful if you gave a link to your source on this. Superificially this does not seem to have a rational basis in argument. However, if you gave a link to your source it would be worth spending a little time considering your source. In the absence of that why bother.

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It is true that I’ve been using chromium for a while (off and on since the 90’s). Now that I’ve lost faith in berberine I’ve gone back to my old insulin sensitizing friend Chromium Picolinate.

I did go through a phase of adding more and more supplements as I read papers, listened to influencers, and read personal anecdotes. I don’t know for sure that “too many” is actually bad but I decided I was losing the thread. We all already know what the big levers are…I decided to stop screwing around with most of those pills and powders that were doing me maybe a little bit of good. Instead I limit my supplements to put my attention on the big effect things:

(1) as much physical activity as possible (increasing over time as I adapt)
(2) increasing adaptive homeostasis (push on the extremes of temp, pH, fuels, etc)
(3) losing visceral fat (while keeping my muscle)
(4) sleeping well
(5) brain stimulation (social / cognitive challenge / purpose)

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@M_F Since you are new here I thought I’d give you a tip on how this forum (mostly) works. We like posters to share a study or an article that was the source of the information. My understanding of the logic is it is easier for the person posting information to share a source than for the reader to blindly look for a source. Even though one paper doesn’t prove anything it is better than “something I read on the internet” or an opinion of a layman that no one can vet.

For me anyway this discipline has turned out to be a step up in my thinking process.

Welcome to the party! We welcome new participants.

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Taurine taken in high dose (at least 6 grams at one time) does generate hours of mTORC1 inhibition is the only interaction I’d be aware of. Typically just skip Taurine days that Rapamycin levels will be >3.0 ng/mL.

Currently, there is no specific evidence or documented interaction between taurine and sirolimus. Taurine is primarily used as a supplement with potential cardiovascular benefits, such as lowering blood pressure and having antioxidant properties (ASHP Drug Compendium [Taurine; Cardiovascular]). Sirolimus, on the other hand, is an immunosuppressive agent used mainly in renal transplantation to prevent organ rejection (ASHP Drug Compendium [Sirolimus; Immunosuppressives]).

While taurine is metabolized in the liver and excreted through feces and urine, sirolimus is metabolized by the CYP3A4 enzyme and excreted primarily in feces. Given their different metabolic pathways, a direct pharmacokinetic interaction is unlikely. However, sirolimus has a wide range of potential interactions due to its metabolism via CYP3A4, and caution is advised when it is used with other substances that may affect this enzyme.

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Welcome… if you look like your avatar… you’re too young to be on this anti-aging site.

Hahaha.

We are all hunting information. Thanks.

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I saw this last night and tried 10mg right before bed. My Oura ring sleep metrics were significantly better than normal. HRV was also higher. I hope it wasn’t a fluke.

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1000mg melatonin. How’s that going?

Would love to hear about this again tomorrow to see if it continues.

I never really bothered to really look into MB but it’s becoming so popular that now I am too curious and might have to really dig into the research. I kind of avoided looking much into GLP1’s initially as well and then they became so popular that I did a deep dive and now I’m sold on those.

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In support of number #1, here’s an Outside Magazine article about a scientific paper that says….

“A new study from biostatisticians at the University of Colorado, Johns Hopkins University, and several other institutions crunched data from the long-running National Health and Nutrition Examination Survey (NHANES), comparing the predictive power of 15 potential longevity markers. The winner—a better predictor than having diabetes or heart disease, receiving a cancer diagnosis, or even how old you are—was the amount of physical activity you perform in a typical day“

Firewallwed paper: NHANES 2011-2014: Objective Physical Activity Is the Strongest Predictor of All-Cause Mortality - PubMed

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Looks most fine but the use of carnitine seems to raise the cardiovascular risk profile, at least there are issues around this:

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@David_King thanks. I hadn’t heard of this possibility. I take it for energy production. I don’t eat red meat so I haven’t been worried about excess carnitine. I’ll key an eye out for more on this topic.

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It’s crazy how the melatonin supplementation can range - Brad Stanfield takes 300 mcg, so that’s over 3000 times less.

Personally I use about 5 mg to help with sleep induction, I can’t sleep when my HRV drops below 50. My concern is endogenous melatonin suppression.

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If you mean suppression from supplementation (like the effect of TRT), here is a study that says there is no suppression (up to 50mg tested here). But it also says supplementation can affect the timing of natural production (is what I understand “phase shift” to mean).

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Consider this: Millions of people have been supplementing with melatonin daily doses ranging from mcg to grams. They have been doing this for many decades. I first started with 1 to 3 mg in the 1980s and have experimented with megadoses with no measurable harm. Currently, my dosage ranges from 20 to 80 mg nightly. The reason for this is that some of the melatonin cancer-prevention properties start at around 20 mg nightly, especially for women.

I can find no scientific papers that suggest melatonin supplementation causes any suppression of natural melatonin production.

@John_Hemming is apparently pursuing this for the protection of mitochondria if I understand him correctly.

In any case, I occasionally don’t take melatonin for one reason or another, and I still go to sleep at the same time as usual.

“There is no indication that melatonin supplementation causes suppression of endogenous melatonin.
The study by Rajaratnam et al. found that melatonin administration did not affect the duration of endogenous melatonin secretion.[1] This suggests that exogenous melatonin does not suppress the body’s natural production of the hormone. Additionally, the American Academy of Neurology’s guidelines for treating sleep disorders in children and adolescents with autism spectrum disorder do not report suppression of endogenous melatonin as a concern, further supporting the safety of melatonin supplementation in this regard.[2]
In summary, current evidence indicates that melatonin supplementation does not suppress endogenous melatonin production.”

Melatonin phase-shifts human circadian rhythms with no evidence of changes in the duration of endogenous melatonin secretion or the 24-hour production of reproductive hormones."

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Would reduce atorvastatin to
10 mg Monday /thursday
Start repatha 140 mg subcutaneous every 2 weeks
Follow glucose with CGM, and fasting insulin levels, hemoglobin A1C, consider adding metformin, in addition to acarbose,

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In one study, 7 days, and in another, 37 days— in my opinion, the duration of the studies was too short.

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Melatonin can also increase prolactin levels, which may, for example, reduce libido. I don’t believe moderate doses cause problems, but some individuals may be more sensitive.

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In early 2024 I was taking around 0.5 per night and then moved to around 1.5g per night around Summer time. Looking at these figures it seems reasonable without doing any calculations that prolactin is higher.

I think there is an argument that melatonin pushes up SHBG.

As I see it it tends to shift gene expression in the direction of prior to puberty. I have, however, not noticed anything that could equate to a metabolism operating actually prior to puberty. My hypothesis is that melatonin in slowing down mitochondrial damage does for pre-pubescent people delay puberty, but for adults I don’t think it can actually reverse puberty although in theory moving mitochondrial efficiency towards higher levels could put the body into that state from a MMP perspective.

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