Which Supplements Have You Stopped Taking & Why

In the past 50 years, I have initiated and later stopped taking specific supplements for a variety of reasons. Many decades ago, I stopped taking dolomite for several reasons including its variable lead content. Perhaps a dozen supplements fit into this historical category. It is likely not worth thinking back to recall them because they are no longer common recommended supplements.

Recently, however, I stopped taking a supplement that many in our group still take. For a decade or more, I took berberine 500 mg. bid along with metformin 850 mg. in the evening. Based on mid-quality or better research, I felt that the two substances were synergistic for their impact on AMPK, their ability to modulate blood glucose levels over time, and other benefits pointed to in the literature. Two considerations caused me to stop taking berberine six months ago. First, the literature demonstrating the breadth and depth of functional control exerted by the intestinal biome is accelerating rapidly. Increasingly, it seems that the human gut executes some kind of executive function over much of human health. Second, a biochemist friend conducting research on probiotics shared his judgment that berberine’s antimicrobial actions on the gut could just as easily be net negative as net positive for a specific individual. In response, one might say that metformin also possesses antimicrobial actions. This is true but we have close to 75 years of cumulative data on metformin, literally thousands of studies from which to draw inferences, whereas we have only a handful on berberine.

I have stopped taking two other common supplements on a regular basis. I will follow up on them in the coming days.

resveretrol, pterostilbene, fisetin, quercitin, fadogia agrestis, nr, citrulline (this one just tastes too bad even though the science is sound), pqq. I stop supplements when they are expensive without much evidence and no personal benefit or they taste bad.

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Ashwagandha and related herbal supplements due to allergies.

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I also stopped taking ashwagandha. I also stopped NMN.

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Why did you stop them?

Ashwaghanha made me queasy and does not have a good evidence base. NAD boosting is a crutch rather than fixing the issue.

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My criteria for not taking or stopping a supplement is simply risk > benefit. For most of these the proven benefit is zero so easy for risk to outweigh.

NMN, NR, Niacin
Resveratrol, pterostilbene
fisetin
Metformin, Berberine
CoQ10
Pantethine
Vitamin C
Senolytics
Aspirin
Urolithin A
Quercitin
Dasatinib

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Ok what made it to your top list then?

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For me the reason for stopping is usually it is a waste of money or the benefit is so uncertain or small that it isn’t worth the polypharmacy risk.

The list of “dead to me for now” stuff is long. I keep adding (good marketing and everyone else loves it) but then removing (to stay within my control limits). This is why I have rigid limits.

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Have you experienced any polypharmacy issues such as liver function tests or subjective feelings of unwellness, etc. @Joseph_Lavelle?

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No. My concern started when the scientists I interviewed consistently said to be careful….That there are always interactions…that the effect of combinations of chemicals are impossible to predict, including even not knowing if the combined effect would be positive or negative. I decided I would be careful before I had a problem

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Good point. As I mentioned using L-Ergothioneine as an example, most of my supplements could be categorized as concentrated food extracts at levels that I could consume. Life Extension’s fisetin optimized for adsorbability is another example. On many occasions I have consumed more fisetin in a large bowl of strawberries. This might not fully eliminate issue of unanticipated adverse combinations but it might nudge it closer to being a food compatibility issue, where mother nature might have evolved at least some useful adaptations.

The substantive polypharmacy questions in my regimen are rapamycin, ezetimibe, metformin, and a sartin, where we know least about how well rapamycin actually plays with others with our patterns of use.

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I agree. I do not count food or food powders or spices or herbs that I sprinkle on my meals. Physiologic doses can be addressed by my liver. Pharmaceuticals are very powerful but at least they have been studied a lot and do not contain impurities (I expect).

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Discontinued NR some time ago due to lack of good supporting evidence, coupled with research finding a possible link with cancer. The high cost also made this decision easier. Discontinued niacin 500mg one week ago (was taking for putative ability to lower Lp(a), due to the recent research linking it with a pathway toward increased atherosclerosis. I actually liked the flushing response, especially when working out, but the benefit didn’t seem worth it weighed against the risk.

How about CoQ10 if taking a statin? The rationale is that statins inhibit the enzyme HMG-CoA reductase, which is both involved in synthesis of cholesterol and also endogenous CoQ10. Wouldn’t one want to replace this through supplementation?

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A times I think the uncertainty people like us face is due to being at the leading (and therefore possibly the bleeding) edge of human experimentation. But when I look carefully at mainstream medical research related to pharmaceuticals, supplements, diets, exercise, sleep and general healthspan, the certainty of often no greater but it does tend to be different. With very few exceptions RCTs trade off realism in order to gain precision, meaning they get very precise about exact conditions that may not generalize well back to humans overall. One need only read a random selection of the last 20 studies published on Vitamin-D to see this.

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There isn’t any good evidence to support that.

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No evidence to support statin’s inhibition of the enzyme (and that this in turn reduces CoQ10), no evidence that supplementation replaces a reduction in CoQ10 caused by statins, or no evidence there is any benefit to replacing CoQ10?

No good evidence that CoQ10 is of any benefit to people taking Statins. I would have to re-research to check on the mechanism.

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