Aspirin Lowers Estrogen Levels / Load / Burden

haidut

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It is known that aspirin can inhibit the activation of the enzyme aromatase, which is activates by things like stress and prostaglandins. However, studies showing direct effects of aspirin on estrogenic burden / load in humans are lacking. Speaking of estrogenic burden / load, as I mentioned in a few other threads estrone (E1) and estrone sulfate (E1S) are the proper blood biomarkers for systemic estrogenic load. Blood estradiol and estriol really do not mean much unless you can also measure tissue levels. So, I was quite happy to find that aspirin lowers estrogen levels and especially the dreaded E1S. E1 and E1S are the primary prognostic biomarkers for breast and prostate cancer progression and survival. So much for prostate cancer being caused by excess androgens...
The results quotes below are from a low dose aspirin (<100mg daily) so presumably higher doses will have even bigger effects.

Analgesic use and sex steroid hormone concentrations in postmenopausal women
https://www.sciencedaily.com/releases/2010/03/100323133043.htm

"...Frequency of all analgesic use was inversely associated with estradiol, free estradiol, estrone sulfate and the ratio of estradiol to testosterone. Average estradiol levels were 10.5 percent lower among women who regularly used aspirin or non-aspirin NSAIDs. Similarly, free estradiol levels were 10.6 percent lower and estrone sulfate levels were 11.1 percent lower among regular users of aspirin or other NSAIDs. Among regular users of any analgesic (aspirin, NSAIDs or acetaminophen), levels of these hormones were 15.2 percent, 12.9 percent and 12.6 percent lower, respectively, according to Gates."
 

Tarmander

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Awesome. I tell everyone I know who has any issues that a little aspirin goes a long way.

Hey Haidut, I don't want to hijack your thread here, but do you know if Nrf2 is affected by aspirin? Have any info on Nrf2?

I found this: Aspirin induces Nrf2-mediated transcriptional activation of haem oxygenase-1 in protection of human melanocytes from H2 O2 -induced oxidative stress. - PubMed - NCBI Which, along with another study saying Resveratol activates Nrf2, leads me to believe that things that activate Nrf2 are not good.
 

paymanz

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interesting that testosterone level also raised,aromatase and its testosterone stealing shouldnt be the only reason for that as it converts very tiny amount of T to estrogen.

it improves steroidogenesis via increasing cell respiration and also camp, i guess.
 
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haidut

haidut

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interesting that testosterone level also raised,aromatase and its testosterone stealing shouldnt be the only reason for that as it converts very tiny amount of T to estrogen.

it improves steroidogenesis via increasing cell respiration and also camp, i guess.

Salicylic acid and of course aspirin also inhibit cortisol synthesis (by inhibiting 11β-HSD1) and this goes long way towards increasing T levels, in combination with the lowered estrogen.
11β-hydroxysteroid dehydrogenase type 1 - Wikipedia, the free encyclopedia
 
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haidut

haidut

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Awesome. I tell everyone I know who has any issues that a little aspirin goes a long way.

Hey Haidut, I don't want to hijack your thread here, but do you know if Nrf2 is affected by aspirin? Have any info on Nrf2?

I found this: Aspirin induces Nrf2-mediated transcriptional activation of haem oxygenase-1 in protection of human melanocytes from H2 O2 -induced oxidative stress. - PubMed - NCBI Which, along with another study saying Resveratol activates Nrf2, leads me to believe that things that activate Nrf2 are not good.

Not big fan of Nrf2. Cancer cells overexpress it as it provides defense against oxidative stress. Don't think aspirin affects it that much though as it can itself increase H2O2 production in higher doses and this is something Nrf2 is supposed to inhibit.
 

Ulysses

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Did some more digging and found this:

Effect of aspirin, flurbiprofen and indomethacin on porcine testicular steroidogenesis

232S.pdf-extract.jpeg


I don't have access to the full article but that is not, you know, an especially comforting preview image.

Not sure what to think, but I'm going to back off on the aspirin a bit, and start using it only occasionally. It took quite a bit of effort to find even this study, and I'm surprised by how little research there seems to be on this subject.
 
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haidut

haidut

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Did some more digging and found this:

Effect of aspirin, flurbiprofen and indomethacin on porcine testicular steroidogenesis

232S.pdf-extract.jpeg


I don't have access to the full article but that is not, you know, an especially comforting preview image.

Not sure what to think, but I'm going to back off on the aspirin a bit, and start using it only occasionally. It took quite a bit of effort to find even this study, and I'm surprised by how little research there seems to be on this subject.

Thanks, but a human study with big doses of aspirin found the exact opposite - aspirin increased testosterone and lowered cortisol.
Aspirin Decreases Cortisol And Increases Testosterone In Humans
 

koky

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aspirin is about the only thing that reduces my inflamed knees (meniscus tears), but gives me naseau over time
even with 1mg k2 for each 325 mg aspirin
suggestions please
 

Kunstruct

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aspirin is about the only thing that reduces my inflamed knees (meniscus tears), but gives me naseau over time
even with 1mg k2 for each 325 mg aspirin
suggestions please

Does this nausea include some acid reflux or increase in stomach acid also?
 

koky

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nothing but nausea when hungry before a meal
i had been increasing aspirin up to 3g per day, with improved antiinflamatory results
now down to 300-600mg/day and still too much inflamation
 

berk

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dammit, i recently noticed that i maybe have a salicylate sensitivity.
Must happen to me again...
 

tallglass13

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It is known that aspirin can inhibit the activation of the enzyme aromatase, which is activates by things like stress and prostaglandins. However, studies showing direct effects of aspirin on estrogenic burden / load in humans are lacking. Speaking of estrogenic burden / load, as I mentioned in a few other threads estrone (E1) and estrone sulfate (E1S) are the proper blood biomarkers for systemic estrogenic load. Blood estradiol and estriol really do not mean much unless you can also measure tissue levels. So, I was quite happy to find that aspirin lowers estrogen levels and especially the dreaded E1S. E1 and E1S are the primary prognostic biomarkers for breast and prostate cancer progression and survival. So much for prostate cancer being caused by excess androgens...
The results quotes below are from a low dose aspirin (<100mg daily) so presumably higher doses will have even bigger effects.

Analgesic use and sex steroid hormone concentrations in postmenopausal women
Another perk of painkillers? Decreased hormone levels may reduce cancer risk

"...Frequency of all analgesic use was inversely associated with estradiol, free estradiol, estrone sulfate and the ratio of estradiol to testosterone. Average estradiol levels were 10.5 percent lower among women who regularly used aspirin or non-aspirin NSAIDs. Similarly, free estradiol levels were 10.6 percent lower and estrone sulfate levels were 11.1 percent lower among regular users of aspirin or other NSAIDs. Among regular users of any analgesic (aspirin, NSAIDs or acetaminophen), levels of these hormones were 15.2 percent, 12.9 percent and 12.6 percent lower, respectively, according to Gates."
Ray Peat has said in a couple of interviews that Estrone is the least harmful of all the estrogens, is this not the case in your opinion?
 

Mito

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Abstract​

Background: Estrogen is involved in the pathogenesis of breast and gynecological cancers. Regular use of aspirin reduces estrogen levels. The present study aimed to evaluate the effect of aspirin on estrogen levels in postmenopausal women.

Methods: This double-blind, placebo-controlled parallel-group trial was conducted on postmenopausal women referred to an outpatient clinic at a women's hospital in Tehran. Volunteers were randomly assigned to receive aspirin 100 mg/day or placebo for 6 weeks. Estradiol, sex hormone-binding globulin (SHBG), and testosterone levels at baseline and at the end of the intervention were measured by ELISA. Data were analyzed using SPSS 20, Kolmogorov-Smirnov test, independent samples t-test, and Mann-Whitney U test.

Results: Twenty-seven and 28 participants were finally analyzed in the aspirin and placebo groups, respectively. There was no significant difference between the two groups in body mass index (BMI), age, or menopausal years. There was a statistically significant difference (p = 0.002) in the amount of change in estradiol levels of the intervention group (median=- 3.5 pg/ml) compared to the control group (median=1.5 pg/ml). In contrast, there were no significant differences between the two groups regarding testosterone and SHBG levels (p = 0.58, p = 0.32).

Conclusions: Since low doses of aspirin may decrease estradiol levels, it could be considered a promising adjunctive therapeutic candidate in postmenopausal women to decrease BC incidence. However, further studies with larger sample sizes, measurements of estrogen levels and its related compounds in different time points accompanied by long-term follow-ups are needed to better elucidate the potential mechanisms by which nonsteroidal anti-inflammatory drugs (NSAIDs) negatively affect breast cancer.

 

Lollipop2

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Abstract​

Background: Estrogen is involved in the pathogenesis of breast and gynecological cancers. Regular use of aspirin reduces estrogen levels. The present study aimed to evaluate the effect of aspirin on estrogen levels in postmenopausal women.

Methods: This double-blind, placebo-controlled parallel-group trial was conducted on postmenopausal women referred to an outpatient clinic at a women's hospital in Tehran. Volunteers were randomly assigned to receive aspirin 100 mg/day or placebo for 6 weeks. Estradiol, sex hormone-binding globulin (SHBG), and testosterone levels at baseline and at the end of the intervention were measured by ELISA. Data were analyzed using SPSS 20, Kolmogorov-Smirnov test, independent samples t-test, and Mann-Whitney U test.

Results: Twenty-seven and 28 participants were finally analyzed in the aspirin and placebo groups, respectively. There was no significant difference between the two groups in body mass index (BMI), age, or menopausal years. There was a statistically significant difference (p = 0.002) in the amount of change in estradiol levels of the intervention group (median=- 3.5 pg/ml) compared to the control group (median=1.5 pg/ml). In contrast, there were no significant differences between the two groups regarding testosterone and SHBG levels (p = 0.58, p = 0.32).

Conclusions: Since low doses of aspirin may decrease estradiol levels, it could be considered a promising adjunctive therapeutic candidate in postmenopausal women to decrease BC incidence. However, further studies with larger sample sizes, measurements of estrogen levels and its related compounds in different time points accompanied by long-term follow-ups are needed to better elucidate the potential mechanisms by which nonsteroidal anti-inflammatory drugs (NSAIDs) negatively affect breast cancer.

This is awesome. Thank you for posting.
 

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