Quercetin is Probably Not a Useful Senolytic

Senolytic compounds are those that preferentially destroy senescent cells. Since these cells are one of the root causes of aging, there is considerable interest in finding and then quantifying the effectiveness of senolytic compounds. The known and alleged senolytics vary widely in effectiveness and quality of evidence, and quercetin is one of the more dubious examples. I don't think that anyone expects quercetin, on its own, to have a useful level of impact on senescent cells and their contribution to degenerative aging. The study here comes to the plausible conclusion that quercetin really can't achieve that goal. Yes, it is true that the 2015 mouse study of the chemotherapeutic dasatinib and quercetin demonstrated that the two together cleared more senescent cells than dasatinib alone, but synergy with other compounds is a very different story from unilateral effects. Quercetin is a widely used and extensively tested supplement compound. Any significant effect on health resulting from quercetin alone would likely have been discovered many years ago.

Previously, quercetin was reported to be a senolytic in irradiation-induced senescent human umbilical vein endothelial cells (HUVECs). HUVECs are derived from the umbilical cord of newborn babies, and for a long time were the only model of primary human endothelial cells (EC); however, these cells are not the best model of diseases associated with human arterial aging. HUVECs have been shown to differ substantially from primary endothelial cells derived from adult human vasculature. In the current study, we investigated whether quercetin is a senolytic in adult EC, and evaluated whether quercetin 3-D-galactoside (Q3G; hyperoside) would be a more selective senolytic.

Quercetin's low therapeutic/toxic ratio in the HUVEC study raised the possibility that quercetin could significantly injure non-senescent cells. It was unclear whether the proliferation of non-senescent cells could be compensating for some of the quercetin-mediated cell death, thus masking its toxicity to the young cells at the lower concentrations found to be selectively cytotoxic to senescent cells. We used adult human coronary artery endothelial cells (HCAEC), which are microvascular cells, as a relevant model, and generated two groups of cells from them to better understand the effect of quercetin: EP (early passage; young) and SEN (senescent), as a model of an aging tissue.

Our key findings are that quercetin at a concentration that reduced SEN EC also caused significant EP EC cell death, and that there was no evidence of senescent cell-specific cell death mediated by quercetin. Thus, quercetin is not a selective senolytic in adult human arterial endothelial cells, where both EP and SEN cells responded similarly to quercetin's toxicity.

To circumvent quercetin's toxicity on healthy, non-senescent cells, we investigated Q3G, a derivative of quercetin with limited toxicity to endothelial cells, which is processed by senescence-associated beta-galactosidase (SABG) enriched in senescent cells to release quercetin in situ. Q3G could act as a selective prodrug in senescent cells. However, Q3G had no significant toxicity to either EP or SEN EC. The lack of Q3G's toxicity in the current study may be due to Q3G being unable to enter the beta-galactosidase-rich lysosomes, or alternatively, Q3G being able to translocate to the lysosomes to release quercetin, which is further processed into an inert compound.

Link: https://doi.org/10.1371/journal.pone.0190374


i never used that. i am currently using life extension geroprotect ageless cell which was designed with insillico medicine

Posted by: scott emptage at January 16th, 2018 6:27 AM

It is more likely that quercetin is masking certain parts of SASP, such as CD38 for example.

Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome.

Flavonoid Apigenin Is an Inhibitor of the NAD+ase CD38

There is other supporting data but this will do for now. Quercetin does have a wide range of activity but I have been skeptical of its ability to remove senescent cells for quite a while now. It may have a place as a co-therapy in conjunction with true senolytics but alone I think it just masks some inflammatory cytokines.

Posted by: Steve Hill at January 16th, 2018 8:14 AM

This reinforces what I've been thinking. Finding safe and effective senolytics will involve many years of clinical trials.

Posted by: NY2LA at January 16th, 2018 11:05 AM

@NY2LA unity should be publishing phase 1 of their clinical trial this year

Posted by: scott emptage at January 16th, 2018 11:28 AM

The only active senolytic trial in clinicaltrials.gov is the Mayo Clinic's Phase II study for Chronic Kidney Disease with Dasatinib and Quercetin


This should answer some of the above questions more definitively than in-vitro models

I see no trials for Unity beyond their completed exploratory biomarker work in the osteoarthritis


Posted by: Qing Song at January 16th, 2018 12:43 PM

@qing song they are starting trial this year and they should complete phase 1 this year too. That's what I heard

Posted by: Scott emptage at January 16th, 2018 1:26 PM

@Scott emptage

That does not sound right

FDA requires 6+ month data on disease modification in osteoarthritis

As they do not even have registered trial, let alone recruitment active, I question such a time line

Any evidence for a filed IND?

Posted by: Qing Song at January 16th, 2018 1:42 PM

The 2015 mouse study claims that quercetin does have "unilateral effects" in eliminating senescent mouse bone marrow stem cells, even slightly better than the dasatinib and quercetin combo.

Posted by: Florin Clapa at January 16th, 2018 2:02 PM

@Florin Clapa: True, but it is hard to argue against the evidence of decades of human use and studies with no sign of benefits to any of the health issues you'd expect to be positively affected by senolytic activity.

Posted by: Reason at January 16th, 2018 2:27 PM

The data in this study does show that Q selectively kills SC, just not selectively enough to qualify as a true Senolytic by the established criteria. Given that this is an in vitro study, Q is cheap, available, and has almost no side effects, I am going to continue using it. And, IMO, it is not unfathomable to image that the non scenescent cells Q killed in the study were in some way weaked, just not yet Scenescent.

Posted by: JohnD at January 16th, 2018 3:41 PM

Reason, I doubt any human studies got the dosage, frequency, and age ranges right. Even if all of those variables lined up correctly somehow, the effect of just using Q might be too subtle to detect (a somewhat lower cancer incidence over several decades, for instance), especially if you didn't know what to look for.

Posted by: Florin Clapa at January 16th, 2018 5:00 PM

I am taking Prosta-Q from Farr Laboratories. It contains Quercetin. Unfortunately, it's part of a proprietary blend of ingredients, so I don't know how much I've been taking.

Posted by: NY2LA at January 16th, 2018 6:38 PM

@Florin: their argument here is (a) the original Mayo Clinic study reported Q as senolytic in human umbilical cord vascular cells (HUVEC), which (i) "are derived from the umbilical cord of newborn babies" and are thus on their face" not the best model of diseases associated with human arterial aging", and (ii) "have been shown to differ substantially from primary endothelial cells derived from adult human vasculature," whereas these guys used the more relevant primary endothelial cells; and (b) as JohnD says, their selectivity is weak. Indeed, even the original Mayo Clinic report found a fairly narrow therapeutic window, and the new report said it was too small to be useful. Selectivity is really a core feature of a true senolytic: an agent that kills lots of senescent cells and also kills nearly as many normal ells at the same time is not really a senolytic, but a toxin.

Posted by: Michael at January 16th, 2018 9:35 PM

Michael, while Q might not be useful at eliminating senescent HCAECs (I never claimed that it was), it still might be useful in eliminating senescent BM-MSCs. As for Q's toxicity, I doubt it can kill a significant number of normal cells to matter (no toxic side effects were reported for mice, for instance), and even if Q isn't that selective at killing senescent BM-MSCs, it seems to kill enough of them to matter.

Posted by: Florin Clapa at January 16th, 2018 10:50 PM

@Florin: well, the only BM-MSC in which Q was tested Q were derived from Ercc1[-/Δ] mice, which have defects in DNA repair, great increases in the rate of senescence, and shortened lifespan - and, in particular, abnormal bones and bone marrow. So I wouldn't put too much stock in that result without more supporting data. As to the lack of side effects: well, we don't have the suitable controls of D or Q monotherapy in vivo. Possibly the dose of Q is too low to have much effect on either normal or senescent cells and D is responsible for all the observed effects, or possibly the effects would have been more positive without Q dragging them down - or the benefits of Q were balanced by deleterious effects, leaving it a wash. And they only did brief treatments, unlike some of the longer-term work with either genetic approaches, Navitoclax, or UBX0101.

Posted by: Michael at January 17th, 2018 12:32 PM

@Reason I periodically take Q (500mg) but am somewhat concerned about its specificity for only getting rid of scenescent cells. Q does have some history of health benefits in that two very healthy food products used for hundreds if not thousands of years are known to have high Q content, including apples (an apple a day keeps the Dr. away) and onions. The peels of apple are have the highest concentration of Q, and I eat 1-3 apples a day.

Posted by: Biotechy at January 17th, 2018 12:36 PM

I hope everyone feel that small molecular approach in rejuvenation biothechology (and even in medicine as a whole) is a dead end. They are very expensive to design, to develop, to test and they hugely interfere with metabolism and thus have many side effects. Now it is just a waste of time and money to screen in the hope to find anything useful. We need to look forward and make things like Oisin targeted very efficient clearance systems.

Posted by: Ariel at January 17th, 2018 2:09 PM

Michael, SCs are SCs regardless of mouse strain, right? And as I've mentioned before, Q actually killed off more senescent BM-MSCs than either D or D+Q. While it's true that Q monotherapy wasn't tested in vivo, it's unlikely that there would be any big negative side effects at low doses and infrequent administration. So, the bottom line for me is that Q is low risk, and potentially high reward; it may (or may not) reduce senescent BM-MSCs without negative side effects.

Posted by: Florin Clapa at January 17th, 2018 7:25 PM

Well, "SCs are SCs" is a bit of an oversimplification even inside a single wild-type mouse, but leaving that aside, the main point is that a senescent cell with a hypomorphic Ercc1 gene (and in a milieu generated by other Ercc1 hypomorphic cells in a mouse that is actually rather young in narrow chronological terms) is not the same as a senescent cell with an intact gene and situated in an otherwise-normal but aging milieu. This was a question even in the original Van Deursen BubR1 hypomorphic mouse study, but at least in that study you could be confident that they were exclusively hitting p16-expressing cells because the mechanism of ablation was directly tied to p16 expression. Here, the idea is that the supplement is supposed to be working by selectively hitting the anti-apoptotic machinery on which senescent cells differentially rely, but the reality is that Q is a quite dirty drug with multiple MoAs, and could quite possibly be differentially toxic in cells that are both senescent and have sub-par nucleotide excision repair.

Posted by: Michael at January 19th, 2018 2:01 PM

The bioavailability of Q in humans is pretty bad. If the active senolytic species in rodents is the aglycone, then it's probably not going to work in humans. There are non-trivial difference in metabolism of polyphenols between humans and rodents. Humans knock out polyphenols very efficiently through glucuronidation and sulfation.

Posted by: george at March 15th, 2018 10:54 PM

I understand that the digestive tract breaks down quercetin very quickly to compounds that have no senolytic property. Is that true?

Posted by: Lenka at August 17th, 2018 6:04 AM

Interesting Quercetin (DHQ) study showing that DHQ appears safe to supplement with:


Toxicological and Genotoxicity Assessment
of a Dihydroquercetin-Rich Dahurian Larch
Tree (Larix gmelinii Rupr) Extract (Lavitol)

Safety assessment is reported of an orally ingested dihydroquercetin-rich extract (Lavitol) derived from the Dahurian larch tree, used as a food additive and as a dietary supplement ingredient. Dihydroquercetin, a potent antioxidant, is also known as taxifolin.
The results of genotoxicity and toxicological tests (Comet assay, micronucleus test in human lymphocytes, chromosomal aberration test, subacute 7-day oral toxicity study, subchronic 90-day toxicology study with histopathologies, and, prenatal and postnatal developmental toxicity studies) on the extract provide further support for the safety of its consumption as a food supplement and food additive.
The deciduous coniferous Dahurian larch tree, Larix gmelinii
Rupr and syn Larix dahurica Turoz (Pinaceae), is indigenous to
central Siberia and found growing from the Yenisei Valley in
the east of Siberia, west to Kamchatka, Russia. Larix gmelinii
is a hybridized Larch species of Larix sibirica Leder1 and the
most northerly growing tree in the world.2 Compounds found
in the heartwood have been studied to determine what role
they might play in order to adapt to the extremely stressful
environmental conditions the tree is subjected to.
Bioassays have revealed that this tree's resiliency to stress
conditions is likely due to a high concentration of the flavonoid,
dihydroquercetin (DHQ; (2R,3R)-2-(3,4-dihydroxyphenyl)-
3,5,7-trhydoxy-2, 3-dihydrochromen-4-one), also known as
taxifolin. The concentration of DHQ is higher than that found
in onions, Douglas fir bark, French maritime bark, or milk thistle,
all foods found to contain this compound and studied for
their medicinal properties.3
The finding of a high concentration of DHQ in L. gmelinii.
led to the development and manufacture of a DHQ-rich extract,
Lavitol (Ametis JSC, Blagoveshchensk, Amur Oblast, Russia),
which over a period of more than 10 years secured regulatory
approval for use as a food additive and dietary supplement
ingredient in Russia. One of the beneficial properties of Lavitol
demonstrated in vivo is as an oral radioprotective agent, which
has been attributed to its preferential uptake of the compound
by the liver to assist in attenuating the damaging effect of
radiation exposure.4,5 Given the recent incidences of significant
human exposure to radiation (I-131, Cs-134, and Cs-137),
as has been experienced at the Fukushima Nuclear Power Plant
in Japan,6 and nuclear reactors in Chernobyl, Russia, along
with the realization that the potential for more such events
exist, there is a need to determine whether oral radioprotective
agents such as Lavitol are safe to ingest. Experimental evidence
indicates taxifolin displays hepatoprotective, cardioprotective,
and neuroprotective properties. There is an indication that taxifolin
stimulates fibril formation and promotes stabilization of
fibrillar forms of collagen. Also, taxifolin inhibits the cellular
melanogenesis as effectively as arbutin, one of the most widely
used hypopigmenting agents in cosmetics.
The same authors also reported on a chronic 6-month toxicity
study of diquertin given to 48 white male rats (150-165 g),
divided into 3 groups of 16 rats each that received either a 1%
starch solution serving as controls or 2 experimental groups
that received either 150 or 15000 mg/kg of diquertin administered
into the stomach. The same investigators also studied the
safety of the same preparation in another chronic 6-month
study on mongrel dogs (10-16 kg), divided into 2 groups that
either received 190 mg/kg/d diquertin in their food or the same
diet without the test substance. In both the rat and dog studies,
no evidence of diquertin toxicity was shown. Except for slight
variations in some functional tests, the safety of the preparation
was supported by evaluation and analyses of the animal's
organs and tissues.

In addition, the authors reported in the same article an
evaluation of the immunomodulatory properties of diquertin
administered to CBA mice. The experimental substance did
not affect antibody-forming cells of the spleen or alter the
hemagglutinin titer in the serum or result in any delayedtype
hypersensitivity or graft versus host reactions. Previous
studies reported by Zhanataev et al,29 that assessed DHQ's
genotoxicity in the chromosome aberration test and the DNAcomet
assay, found a lack of evidence of the compound's
genotoxicity. In their studies, DHQ was administered 5 times
at 0.15 or 1.5 mg/kg, or in a single dose of 15, 150, or 2000
mg/kg, in 8- to 12-week-old male and female C57B1/6 mice
(18-20 g) and found to induce no DNA damage in bone
marrow, or blood, liver, and rectal cells. The single administration
study at either a dose of 150 or 2000 mg/kg had no
effect on the level of chromosome aberrations in mouse bone
marrow cells compared to controls. As was seen in our studies
of Lavitol, the DHQ in a wide dose range exhibited no clastogenic
or DNA-damaging effects in organs or tissues of the
animals so studied.
Article in International Journal of Toxicology · April 2015
DOI: 10.1177/1091581815576975 · Source: PubMed

Posted by: Eugene at November 9th, 2018 3:41 AM

I just started using 15mg Bio-Quercetin phytosome (providing 5 mg quercetin [from Japanese sophora concentrate (flower bud)], phosphatidylcholine complex [from sunflower]) daily in my Two per Day multi + 29 mg. Bio-Quercetin upon waking 10 mg quercetin [from Japanese sophora concentrate (flower bud)], phosphatidylcholine complex [from sunflower])

Once a week I take Bio-Quercetin phytosome 74 mg (providing 25 mg quercetin [from Japanese sophora concentrate (flower bud)], phosphatidylcholine complex [from sunflower]) combined with Theaflavins [from decaffeinated black tea extract (leaf)] 275 mg.

Most things are effected by dose vs lean body weight & I am 65 years old, 6' 6" tall & not under 220 pounds since my early 20's.

I have been self experimenting with substances specifically including but not limited to their potential benefit on these cells for about a decade.

I am adding a very recient cover story from Bill Faloon as an explanation of my reasoning on that new way of getting more quercetin into the cell.

It is pretty darn cheep too especially since I buy @ wholesale or half retail price.

Life Extension Magazine 2018
Cover Story
Removal of Senescent Cells "Might Transform Medicine"
By William Faloon

On July 9, 2018, the world awoke to news from the Mayo Clinic that many age-related afflictions can be reversed by eliminating senescent cells from old mice.1
In addition to regaining aspects of youthful health, the old mice whose senescent cells were selectively removed lived 36% longer.1
This is not the first study showing these effects. What makes it exceptional is the meticulous way it was conducted.
The first part of the study involved transplanting a few senescent cells into young mice. This caused the young mice to endure physical decline characteristic of degenerative aging. When senescent cells were transplanted into old mice, the same toxic effects occurred and the mice died sooner.
But with oral administration of compounds that remove senescent cells, physical dysfunction was alleviated and lifespan markedly increased.
The incredible news is that novel ways are being developed to help remove senescent cells from aging humans today!
Why Senescent Cells Accumulate

As cells age, most undergo a beneficial elimination process known as apoptosis.
If all aged cells properly self-eliminated, we would see improvements in healthy lifespans.2
Instead, too many senescent cells linger. These aged cells emit signals that promote inflammation, injure healthy cells, and block regenerative factors that may improve one's health.3
This scenario occurs inside our bodies, whereby senescent cells fail to undergo apoptosis (normal cell elimination). These pesky senescent cells emit inflammatory-type signals that spread to healthy cells and cause them to deteriorate.
Senolytics Extend Healthy Lifespan

Rodent study shows senolytics
dasatinib + quercetin:
Improve frailty symptoms (gait, grip strength)
Enhance hair color appearance
Improve cardiac/arterial function
Reduce tremors and urinary incontinence
Decrease osteoporosis
Increase exercise endurance
Improve kidney/liver age scores
Extend healthy lifespan
Does anyone NOT want these benefits?
Aging Cell. 2015 Aug;14(4):644-58. doi: 10.1111/acel.12344. Epub 2015 Apr 22.
An Old Problem with New Solutions
I was informed about senescent cells in the late 1990s by a brilliant researcher. He made it clear that if we were to achieve meaningful control over aging, we had to selectively remove senescent cells that accumulate and create metabolic havoc.
The problem back then was there was no valid approach to accomplish this.
Starting around year 2014, scientists at the Mayo Clinic and Scripps Research Institute began investigating senolytics, which are compounds that induce normal elimination of senescent cells.4
Remarkable Results
The box on the previous page is from a presentation I give to advocate for accelerated age-reversal research. This slide highlights findings from a groundbreaking (year 2015) animal study that found remarkable rejuvenation effects in response to aggressive senolytic therapy.
This 2015 study4 was followed by another study funded in part by the National Institutes of Health (NIH) published in 2017.5
The 2017 study looked at age-accelerated mice treated with a senolytic compound. The findings showed improvements in grip strength, coat condition, movement, and overall health. This study also revealed improvement in a biomarker of senescent cells in the kidney compared with control mice.5
Favorable Media Coverage

These studies generated worldwide headlines, with scientists describing the potential of senolytic compounds to reverse aging in humans.
In a review published by The American Geriatrics Society (2017), senolytics were described as having potential to:
"…transform geriatric medicine by enabling prevention or treatment of multiple diseases and functional deficits in parallel, instead of one at a time."2
The authors of this review explained how reducing the "senescent cell burden" can lead to less inflammation with enhanced function of stem cells.2
The review went on to describe how senescent cells destroy the knee joints of healthy mice.6 These findings have encouraged people with osteoarthritis to self-experiment with senolytic compounds, with encouraging results being reported.
Of interest is that senolytics do not have to be used continuously to derive benefits. This corroborates current strategies whereby people are using senolytics intermittently ("on" and "off" periods).
This 2017 review concluded that after clinical trials are completed:
"…it is conceivable that the rapidly emerging repertoire of senolytic agents might transform medicine as we know it."2
Researchers have further remarked that the introduction of senolytics into clinical practice could be transformative when stating:
"Our goal is to achieve the same success in humans as we have in preclinical animal models in efforts to prevent or delay the conditions associated with aging."7
Human senolytic studies are being pursued by a number of physician/scientists. We look forward to reporting on them after more long term data is gathered.
Practical Senolytic Approaches

Early stage research on senolytics indicates that intermittent dosing may be an ideal approach. In other words, the strategy is to selectively induce senescent cell apoptosis for a limited time, and then cease until more senescent cells accumulate.
Drugs that purge senescent cells are being clinically studied. Some individuals are self-experimenting today with senolytic drugs + high-dose quercetin.
In a cell culture study, the drug dasatinib eliminated human senescent fat cell progenitors.4 Quercetin was more effective against senescent human endothelial cells and bone marrow stem cells.4
Improving circulation via enhanced endothelial function and enabling more potential stem cell release from bone marrow is important. Removing fat-cell progenitors is desirable, since these cells can negatively impact surrounding tissue and are linked to metabolic dysfunction.8
Until recently, people seeking to achieve senolytic benefits were challenged to take large-doses of quercetin, and many don't yet want to try dasatinib. A new quercetin phytosome eliminates the need to ingest large amounts of quercetin.
Another discovery suggests that a tea extract containing theaflavins provides some of the same senolytic properties targeted by dasatinib,9-11 and other senolytic drugs.12
How to Purge Senescent Cells Today

A new quercetin phytosome provides approximately 50 times greater oral bioavailability compared to typical quercetin supplements.13
This enables 74 mg of this quercetin phytosome (providing 25 mg quercetin) to deliver a dose approximately equivalent to about 1,250 mg of typical quercetin. This empowers more people to achieve greater amounts of intact and unmodified quercetin into their bloodstream.
In addition to having a similar mechanism of action as dasatinib,9-11 preclinical evidence indicates the senolytic potential of black tea theaflavins.14 Based on our interpretation of the current research findings, we suggest most people over age 35 consider taking a once weekly dose of:
74 mg of quercetin phytosome
275 mg of theaflavins
Those taking lower doses of regular quercetin for its other benefits may continue to do so and use the new phytosome delivery formula on an intermittent schedule. The article on page 6 of this issue describes this low-cost and novel approach to removing senescent cells by taking theaflavins and quercetin phytosome just one time each week.
The cost of this once-weekly senolytic nutrient approach is less than $7 a month.

William Faloon

Xu M, Pirtskhalava T, Farr JN, et al. Senolytics improve physical function and increase lifespan in old age. Nat Med. 2018;24(8):1246-56.
Kirkland JL, Tchkonia T, Zhu Y, et al. The Clinical Potential of Senolytic Drugs. J Am Geriatr Soc. 2017;65(10):2297-301.
Zhu Y, Armstrong JL, Tchkonia T, et al. Cellular senescence and the senescent secretory phenotype in age-related chronic diseases. Curr Opin Clin Nutr Metab Care. 2014;17(4):324-8.
Zhu Y, Tchkonia T, Pirtskhalava T, et al. The Achilles' heel of senescent cells: from transcriptome to senolytic drugs. Aging Cell. 2015;14(4):644-58.
Fuhrmann-Stroissnigg H, Ling YY, Zhao J, et al. Identification of HSP90 inhibitors as a novel class of senolytics. Nat Commun. 2017;8(1):422.
Xu M, Bradley EW, Weivoda MM, et al. Transplanted Senescent Cells Induce an Osteoarthritis-Like Condition in Mice. J Gerontol A Biol Sci Med Sci. 2017;72(6):780-5.
Available at: https://www.sciencedaily.com/releases/2017/09/170904093428.htm. Accessed August 6, 2018.
Tchkonia T, Morbeck DE, Von Zglinicki T, et al. Fat tissue, aging, and cellular senescence. Aging Cell. 2010;9(5):667-84.
Noberini R, Koolpe M, Lamberto I, et al. Inhibition of Eph receptor-ephrin ligand interaction by tea polyphenols. Pharmacol Res. 2012;66(4):363-73.
Noberini R, Lamberto I, Pasquale EB. Targeting Eph receptors with peptides and small molecules: progress and challenges. Semin Cell Dev Biol. 2012;23(1):51-7.
Ting PY, Damoiseaux R, Titz B, et al. Identification of small molecules that disrupt signaling between ABL and its positive regulator RIN1. PLoS One. 2015;10(3):e0121833.
Leone M, Zhai D, Sareth S, et al. Cancer prevention by tea polyphenols is linked to their direct inhibition of antiapoptotic Bcl-2-family proteins. Cancer Res. 2003 Dec 1;63(23):8118-21.
Supplier Internal Study. A randomized and crossover pharmacokinetic study of Quercetin 500mg., Quercetin Phytosome 500 mg. and Quercetin Phytosome 250 mg. administered in a single dose to healthy volunteers under fasting conditions. Data on File. 2017.
Han X, Zhang J, Xue X, et al. Theaflavin ameliorates ionizing radiation-induced hematopoietic injury via the NRF2 pathway. Free Radic Biol Med. 2017;113:59-70.

All Contents Copyright ©2019 Life Extension® All rights reserved

Posted by: Danney Hendrix at January 5th, 2019 1:52 PM

"A new quercetin phytosome provides approximately 50 times greater oral bioavailability compared to typical quercetin supplements.13

This enables 74 mg of this quercetin phytosome (providing 25 mg quercetin) to deliver a dose approximately equivalent to about 1,250 mg of typical quercetin. This empowers more people to achieve greater amounts of intact and unmodified quercetin into their bloodstream.
In addition to having a similar mechanism of action as dasatinib,9-11 preclinical evidence indicates the senolytic potential of black tea theaflavins.14 Based on our interpretation of the current research findings, we suggest most people over age 35 consider taking a once weekly dose of:

74 mg of quercetin phytosome
275 mg of theaflavins

Those taking lower doses of regular quercetin for its other benefits may continue to do so and use the new phytosome delivery formula on an intermittent schedule. The article on page 6 of this issue describes this low-cost and novel approach to removing senescent cells by taking theaflavins and quercetin phytosome just one time each week.

The cost of this once-weekly senolytic nutrient approach is less than $7 a month."

I've been using this from LEF for maybe 3 weeks...except for the first dose...no noticeable effects so far.

* If I start wearing diapers...then I'll know it's working...getting younger?

Posted by: bob at January 9th, 2019 6:26 AM

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