Estrogen (estradiol) Is The Cause Of Varicose Veins

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,799
Location
USA / Europe
Another confirmation of something Ray has been saying for years, and the medical establishment has been denying for years. The authors of this study actually expected to see a relationship between testosterone and varicose veins, but found that estrogen (estradiol) is the likely culprit. Their suggestion is to try aromatase inhibitors for the condition, but in theory anything that inhibits the action of estrogen should work as well. Topical progesterone should be very helpful as well as the fat-soluble vitamins K, A, D, E.

http://ang.sagepub.com/content/60/3/283.abstract

"...About 21 symptomatic varicose men (VM [C ≥ 2] mean age of 40.3/+6.9 years) and 13 healthy men (HM [C ≤ 1] mean age of 38.1/+ 7.4 years) were analyzed. The serum E2:fT ratio (VM 2.83/+ 0.79 and HM 2.32/+0.63) was significantly different (P < .05) between the two groups. No major differences were seen on the serum levels of the sex hormones. In summary, our results demonstrate a changed serum E2:fT ratio among men with varicose veins compared to healthy men. By the fact of a small study sample, the interpretabillity of this result is limited."
 

north

Member
Joined
Dec 21, 2013
Messages
156
Is it possible to measure estrogen (or estradiol) properly? Peat says serum E doesn't reflect tissue E. Which tests is most likely to reflect accurate estrogen levels? (Asking cause I am looking into which blood tests to get)
 
OP
haidut

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,799
Location
USA / Europe
north said:
Is it possible to measure estrogen (or estradiol) properly? Peat says serum E doesn't reflect tissue E. Which tests is most likely to reflect accurate estrogen levels? (Asking cause I am looking into which blood tests to get)

Here is something that confirms Peat's statements:
http://www.ncbi.nlm.nih.gov/pubmed/3160722

"...Except for dehydroepiandrosterone (DHEA) sulfate (DHEAS), there existed a positive tissue/plasma gradient for all steroids studied (testosterone, androstenedione, DHEA, androstenediol, estrone, and estradiol), suggesting androgen uptake and estrogen synthesis in situ. Androgen concentrations did not vary according to site of origin of fat tissue, except that the DHEAS concentration was significantly lower in abdominal sc and omental fat than in breast, pericardial, or sc pubic fat. Tissue androgen concentrations were positively correlated with their plasma concentrations, but tissue and plasma estrogen concentrations were not correlated. All tissue steroid concentrations, with the exception of estradiol in men, decreased with age.

So, basically androgens decrease with age and estrogen stays constant or increases. So much for the theory of menopausal women being low in estrogen...
You can measure prolactin and serotonin, which are tightly correlated with tissue estrogen. So, high prolactin would almost definitely mean high estrogen in tissues. In addition, I think PUFA status is also a good predictor of estrogen in tissues. You can estimate PUFA status by measuring iodine. High iodine means high PUFA in tissues and consequently high estrogen. High iodine plus abdominal fat is also close to a guarantee for high estrogen, since it means the fat deposits are unsaturated.
 

Ben

Member
Joined
Dec 13, 2013
Messages
497
It is not new to me that estrogen is the cause of varicose veins, but the fact that testosterone-estrogen ratio makes a difference in that surprises me. I have low SHBG, which means high active testosterone but high active estrogen, and I have huge veins and varicose veins in my testicles. I thought that increasing the production of testosterone, or reducing SHBG, would increase varicose veins.

Another theory is that huge veins and varicose veins stem from too much parasympathetic nervous activity in comparison to sympathetic. Estrogen does increase parasympathetic activity, so it would still be valid. My dentist said I metabolize adrenalin, which she uses as a nerve blocker, 2-3x more quickly. I also don't sweat much in response to stress or get drymouth, and if do, it is usually very short-lived, in response to short-lived intense fear. What do you think of this Haidut, and what do you think the likely mechanism is, high MAO?

Both of my theories may be correct because estrogen stimulates the PSNS, but testosterone does not stimulate the SNS. Unless, it inhibits the PSNS-stimulating effect of estrogen. But I have minimized aromatase very much and increased testosterone very much and my veins are not smaller. They only get smaller if it's cold or from hypoglycemia, when there is strong constant adrenalin stimulation.

So maybe testosterone is only correlated because concentrations are higher if not converted to estrogen. And apparently some people will get varicose veins no matter what, unless perhaps they inhibit the PSNS more directly with atropine or anti-histamines. I do have a high tolerance for atropine. And btw, people with high histamine, low methylation, high metabolism but with lots of glycolysis, lipolysis, etc, they do have larger veins. So the truth appears clear: PSNS overactivity causes varicose veins, which estrogen can contribute to.
 

Interactome

Member
Joined
Sep 13, 2015
Messages
193
Age
44
Location
Copenhagen
In my case, my veins came out during a few times when I tried to eat a lot of fruit, sugar and honey. I got very warm and they started bulging more than normally, and now whenever they get full, they assume their new extra-bulgy size. I still don't have an explanation. It happened very quickly... we're talking minutes. So the question is, is it the sugar, or certain polyphenols or other compounds in the fruit, or is it some other background hormones in the body that are pro-vein bulging, so that when we eat a lot of carbs and body temperature increases and the veins are stretched, they adapt to a larger size due to those background hormones.

If it's the background hormones, then fixing those might reverse the veins. I don't know about my intracellular estrogen and progesterone, but the serum ones were low. But I never had blood drawn right after eating a large amount of fast carbs, so I don't know how hormones change during feeding. But I did have high renin and aldosterone on one blood test. Those are also stress hormones according to Peat, so if we could find a way to lower those by addressing the underlying issues and then see what happens with the veins after a while...

If it's due to the sugar getting into the cells and drawing water into them, then emptying the veins of the glycogen should bring them back to their previous size. Going low carb for to see if the glycogen stores are slowly depleted could be an experiment.

I don't see how they could have gotten injured by high blood sugar, since it happened so quickly... that would be quite extreme. Unless the high sugar feeds some bugs that created a lot of endotoxin which triggered the immune system that then bombed stuff all around, including the veins, or produced a lot of NO which caused local adaptation in the veins...

Anyone out there that can confirm/disprove some of this stuff?
 

Interactome

Member
Joined
Sep 13, 2015
Messages
193
Age
44
Location
Copenhagen
And btw, people with high histamine, low methylation, high metabolism but with lots of glycolysis, lipolysis, etc, they do have larger veins.
Hi. How do you mean that low methylation could contribute to larger veins? Would methylfolate help?
 

dookie

Member
Joined
May 5, 2015
Messages
517
@haidut

Are those the main substances you consider anti-estrogenic: progesterone, vitamins A D E K?

Of the fat-soluble vitamins, which do you consider the most anti-estrogenic? What doses are necessary?

Besides progesterone, are there other things which can remove estrogen from the tissues? Do aromatase inhibitors effectively remove estrogen from the tissues, where it can get "stuck" according to Peat ?
 
OP
haidut

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,799
Location
USA / Europe
@haidut

Are those the main substances you consider anti-estrogenic: progesterone, vitamins A D E K?

Of the fat-soluble vitamins, which do you consider the most anti-estrogenic? What doses are necessary?

Besides progesterone, are there other things which can remove estrogen from the tissues? Do aromatase inhibitors effectively remove estrogen from the tissues, where it can get "stuck" according to Peat ?

From the fat-solubles, E is most directly anti-estrogen, followed by A/K and then D. The doses are listed in various studies I have posted on the forum. Besides progesterone, aspirin and caffeine are capable of getting estrogen out of the cell, as well as potentially magnesium. Caffeine can even destroy the estrogen "receptor" in higher doses so the estrogen would not have any effects even if it is inside the cell.
Caffeine is a potent anti-estrogen; can block estrogen "receptor" completely
 

DaveFoster

Member
Joined
Jul 23, 2015
Messages
5,027
Location
Portland, Oregon
Right. Around 5 grams of caffeine will destroy the receptor. The good ol' days. Highly do not recommend.
 
OP
haidut

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,799
Location
USA / Europe
Right. Around 5 grams of caffeine will destroy the receptor. The good ol' days. Highly do not recommend.

Aromatase inhibitors would not get estrogen out of the cell. DHT would though. Caffeine is not needed in 5g doses. Taken in lower doses (600mg - 800mg daily) would also do the trick over longer periods of time. The production of estrogen receptor depends mainly on stress, so the lower the stress the less ability your cells will have to even react to estrogen. I would venture a guess that pregnenolone may also be able to get estrogen out of the cell but I do not have studies on that. Finally, there is an old Indian study on cyproheptadine I have been trying to get saying cypro is an estrogen antagonist and aldosterone antagonist. What that means for the cellular levels I am not sure.
 

DaveFoster

Member
Joined
Jul 23, 2015
Messages
5,027
Location
Portland, Oregon
If anyone chooses to take cyproheptadine, be sure to consume a much larger amount of salt on a daily basis (as in 2-3 times greater than normal, or more [5-10 grams to start]). The aldosterone antagonism will cause sodium excretion. I was having adrenaline rushes and severe dehydration from cypro without the salt.
 

mirc12354

Member
Joined
Jan 8, 2016
Messages
279
Gotu Kola herb (Centella Asiatica) is the only thing that offered my mother some relief form varicose veins.
@haidut : have you perhaps seen any research about the herb being antiestrogenic?
 

dookie

Member
Joined
May 5, 2015
Messages
517
Aromatase inhibitors would not get estrogen out of the cell. DHT would though. Caffeine is not needed in 5g doses. Taken in lower doses (600mg - 800mg daily) would also do the trick over longer periods of time. The production of estrogen receptor depends mainly on stress, so the lower the stress the less ability your cells will have to even react to estrogen. I would venture a guess that pregnenolone may also be able to get estrogen out of the cell but I do not have studies on that. Finally, there is an old Indian study on cyproheptadine I have been trying to get saying cypro is an estrogen antagonist and aldosterone antagonist. What that means for the cellular levels I am not sure.

How long time would one need to take coffee, at 600-800 mg per day, to get estrogen out of cells?

Also how much is 600 mgs of caffeine in terms of espresso shots?
 

Interactome

Member
Joined
Sep 13, 2015
Messages
193
Age
44
Location
Copenhagen
Aromatase inhibitors would not get estrogen out of the cell. DHT would though. Caffeine is not needed in 5g doses. Taken in lower doses (600mg - 800mg daily) would also do the trick over longer periods of time. The production of estrogen receptor depends mainly on stress, so the lower the stress the less ability your cells will have to even react to estrogen. I would venture a guess that pregnenolone may also be able to get estrogen out of the cell but I do not have studies on that. Finally, there is an old Indian study on cyproheptadine I have been trying to get saying cypro is an estrogen antagonist and aldosterone antagonist. What that means for the cellular levels I am not sure.
Hi.

Do you know if cyproheptadine also lowers renin? I'm experimenting with it right now, but only taking 1mg at night.
 
OP
haidut

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,799
Location
USA / Europe

Interactome

Member
Joined
Sep 13, 2015
Messages
193
Age
44
Location
Copenhagen
I think it does. Here is one study that shows it does but in higher doses (~8mg daily).
Cyproheptadine inhibition of stimulated plasma renin activity. - PubMed - NCBI

Thank you. So it seems that renin has something to do with serotonin. As I see, serotonin is related to blood clotting and both vasoconstriction and vasodilation (confusing stuff).

I'll have to see if I dare increase my Cypro dose. I'm extra cautious right now. It probably depends on why my renin and aldosterone are high. But I think it's somehow related to the veins. I don't know if all cases of swollen veins are due to the same reason.

Do you think gut irritation/endotoxin could cause clotting/serotonin induced vasoconstriction around the kidneys which might cause them to think there's too little blood and thereby ramp up renin and aldosterone? I also have a feeling that vit K causes blood clotting in me so I don't dare touch it again.
 

Danmcakes

Member
Joined
Jan 6, 2016
Messages
7
If anyone chooses to take cyproheptadine, be sure to consume a much larger amount of salt on a daily basis (as in 2-3 times greater than normal, or more [5-10 grams to start]). The aldosterone antagonism will cause sodium excretion. I was having adrenaline rushes and severe dehydration from cypro without the salt.

I think another way of saying that is that if you are having issues with adrenaline (or dehydration) one thing you can experiment with is increasing your intake of salt. 5-10g is not really a large amount (unless you are going by official recommendations). Cypro helps improve metabolic function in many different ways and will likely help protect against the excessive wasting of sodium that is often associated with hypothyroidism and related hormones.
Cypro (Periactin) by improving metabolic function can increase fuel requirements etc., and this could potentially cause an adrenaline reaction if you are highly susceptible or under fueled.

As far as the aldosterone connection is concerned, Ray Peat has said that "Aldosterone causes less sodium to be lost in the urine and sweat, but it achieves that at the expense of the increased loss of potassium, magnesium, and probably calcium."...so I don't know if I would say that lowering aldosterone increases your requirements for salt...it seems more likely that it would help the alkaline minerals to be used more appropriately...if anything I think that insufficient intake of salt, or the wasting of salt associated with hypothyroidism is the real issue...the need for more salt may be there but that is really a separate issue...in the long run cyproheptadine will likely decrease salt requirements rather than increase them.
 
Joined
Mar 10, 2021
Messages
21,516
“Experiments have shown that progesterone relieves anxiety, improves memory, protects brain cells, and even prevents epileptic seizures. It promotes respiration, and has been used to correct emphysema. In the circulatory system, it prevents bulging veins by increasing the tone of blood vessels, and improves the efficiency of the heart. It reverses many of the signs of aging in the skin, and promotes healthy bone growth.” -Ray Peat
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

Similar threads

Back
Top Bottom