MS: More Women Than Men?

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

MS: More Women Than Men?

Postby vesta » Mon Feb 11, 2013 9:05 am

On the site A to Z of MS it is noted that before puberty and after menopause, the male/female
ratio of incidence in MS is one to one. That is to say there is no
difference. Also, pregnant women, especially the last 3 months of pregnancy,
are less likely to have MS problems. In contrast, during her fertile years
women have 2 to 4 more times the incidence of MS than men.

Does it take a rocket scientist to see that female hormones
apparently increase the likelihood of developing MS?

It is being reported in France that third and fourth generation birth
control pills have doubled the risk of stroke in women taking them. There
have been Incidents of stroke, deep vein thrombosis, blood clots. Arterial
and Venous blood circulation problems dicate against birth control pills as
do Migraine headaches.

Leonard of Brussels on has brought to my attention the importance of damage
to the interior of the veins, their walls (endothelium) and their valves in impeding
blood circulation. I had been too focused on Dr. Zamboni's description of stenosed, twisted or
deformed veins as causing a blood reflux without considering that poor circulation INSIDE the vein
can have a similar effect. Leonard's Diabetes may well be the cause of his MS.
(It is well known that Diabetes causes poor blood circulation in the lower extremities. Why not the
neck and head as well?) Infections may also damage the veins. By detoxifying, taking nutritional suppements and maximizing nutrition one may try to heal the damaged veins in order to enhance blood circulation. For some reason female hormones must impact the veins negatively thus hampering blood circulation to the head and spine.

I took birth control pills for about two years 1967-69.
(Probably first generation?) The summer of 1969 pressure in my head built up
until I thought it would explode. I said to myself one night that if I
survived until morning I would never take another Pill. During the 1970’s I
developed migraine headaches which would be a contraindication of the Pill.
Then I developed MS. October 2012 I believe I suffered a very minor ischemic
stroke. (I do use estrogen cream.)

All these factors imply issues with the blood circulation in my
head linked to female hormones which might account for the increased
incidence of MS in women. The blood vessels themselves are somehow damaged
by female hormones.

Another factor - from puberty age 12 I experienced terrible,
monthly menstrual cramps. This alone could explain the higher incidence of
female MS since the cramps occur monthly and seize up the entire body,
including neck, back, and shoulders, potentially deforming their development.

Between age 18 and the breakdown at age 32 all my major health
problems were gynecological in origin. They caused stress, their treatment
led to toxicity. The drugs "poisoned" my intestines, by age 32 I had the
most rotten flatulence imaginable. From age 18 frequent bladder infections
required antibiotic treatment. The female anatomy favors cystitus subsequent
to intercourse, many women are subject to this problem. So right off we have
trauma in the pelvic region as well as stress through toxicity. I
developed endometriosis, a gynecological condition leading to intense pain
and cramping.. I was given DES stilboestrol, an endocrine disrupter, known to
lead to breast cancer and liver failure. Then I was given Danazol, a modified
testosterone, which can lead to ovarian cancer and liver problems.

When I detoxified and changed my diet at age 35, not only did the MS
disappear, but the endometriosis disappeared as well. (So did the foul
intestinal flatulence.) My gynecologist didn't want to believe this was
possible. He is wrong. The origin of endometriosis is unknown ( MS as well), but
think of the body absorbing foods (wheat) or medications (antibiotics) which
it finds toxic. It fights to evict the poison but can't. It fights its own
tissue where the toxins are imbedded, leading to all kinds of bizarre

To conclude, if more women than men develop MS it could well be because 1) female hormones
compromise the vascular system itself and 2) women have gynecological issues
which stress the body – menstrual cramps – and problems whose treatment poisons
(antibiotics, hormone therapy.) leading to further stress leading eventually to a blood reflux.

An epidemiological questionnaire should ask 1) if the woman experienced
menstrual cramps, starting when and with what severity 2) cystitus following
intercourse, treatment and frequency 3) birth control pills 4) endometriosis
5) any other gynecological disorder requiring hormone modifying treatment.
Gynecologists could expand on this.

So I think I need to back-track on the personality factor in female MS (suggested in earlier posts) and
simply consider 1) the negative impact of female hormones on the vascular
system and 2) the gynecological problems which cause stress and may require
treatment leading to toxicity.

Again we can consider MS to be a vascular disorder. For women the problem appears to be exacerbated by female hormones. So what to do?

I have reported that Acupuncture could stop an MS attack, probably by enhancing blood circulation and reversing the blood reflux. However, the treatments exacerbated the Endometriosis "attacks", probably by stimulating the bleeding.
and the endometriosis then triggered MS attacks by cramping the muscles so intensely that they pressured the veins leading to a back jet of blood. (I kept a one year diary 1983-84 which well documented how my hormonal cycle impacted the MS.)

Chinese medicine did not heal the endometriosis - it only kept the MS under control. By following the Kinesiologists program of detoxification, optimal nutrition and supplements I was able to HEAL both the MS and the Endometriosis at the same time. In other words, they are the same disease - let's call it TOXIC REACTION DISORDER (misnamed Auto-Immune diseases) which manifest differently.

I believe menstrual cramps can deform the vascular system in a girls growing body. Whatever relieves the cramps of the back-shoulders-neck should help stop the reflux attack. Birth Control Pills have been used for women to prevent the stress of menstrual cramps. But since they apparently increase the risk of stroke, one should be aware of contraindications such as migraine headaches.

Another tip: Evening Primrose Oil is used to treat Pre-MenstrualStress in women as well as MS (in everybody) - diabetes etc. It was my first self prescribed supplement breakthrough. It takes about a month to smooth out the hormonal swings and feel more "balanced". Look it up under Evening Primrose Oil benefits, or Apparently the only other source of gamma-linoleic acid is mother's breast milk (I was not breast fed - a factor?)I still take 3 pearls a day and when I don't the insomnia starts and all the rest.

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Last edited by vesta on Wed Feb 13, 2013 10:47 am, edited 1 time in total.
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Re: MS: More Women Than Men?

Postby Anonymoose » Mon Feb 11, 2013 1:17 pm

Hi Vesta,

I think at least part of MS is hormone related as well. But it goes beyond female hormones. The fluctuations of hormones in the female reproductive cycle make us more susceptible to damage caused by excess hpa hormones. Progesterone blocks both cortisol and aldosterone...but its also a precursor to aldosterone. So, adding bcp w/progesterone could wind up causing more damage by feeding aldosterone synthesis. (btw, I think I might have taken bcp for a whole 3 mos of my life...not the culprit with me) During menstruation, our progesterone levels plummet, which for me results in pseudo flares. Does anyone else get that? In the last 3 months of pregnancy, there is so much circulating progesterone that even if aldosterone is also raised, it has greatly reduced opportunity to dock in MRs.

Estrogen actually protects our blood vessels (but can cause thrombi in the liver). Spironalactone, an estrogen-like aldosterone blocker, allows endothelial repair in male rats, but not female rats. I think this is because the females are already protected to some extent by estrogen.

I think MS progresses faster in women post-menopause because our progesterone and estrogen production dramatically drops and we lose our natural protection from cortisol and aldosterone. Another aldosterone-related condition, cardiovascular disease also increases post-menopause.

PwMS have a constantly activated hpa axis. We don't get a break from cortisol or aldosterone and I suspect our CYP450 aldosterone genes make it even worse by causing us to make excess aldosterone.

Cortisol shrinks regional gray matter (documented elsewhere on tims) and reduces ccsbfi of it.
The stress hormone cortisol acts onthe brain, supporting adaptation andtime-adjusted coping processes.Whereas previous research has focused on slow emerging, genomic effects of cortisol, we addressed the rapid, nongenomic cortisol effects on in vivo neuronal activity in humans. Three independent placebo-controlled studies in healthy men were conducted. We observed changes in CNS activity within 15 min after intravenous administration of a physiological dose of 4 mg of cortisol (hydrocortisone). Two of the studies demonstrated a rapid bilateral thalamic perfusion decrement using continuous arterial spin labeling. The third study revealed rapid, cortisol-induced changes in global signal strength and map dissimilarity of the electroencephalogram. Our data demonstrate that a physiological concentration of cortisol profoundly affects the functioning and perfusion of the human brain in vivo via a rapid, nongenomic mechanism. The changes in neuronal functioning suggest that cortisol acts on the thalamic relay of background as well as on task-specific sensory information, allowing focus and facilitation of adaptation to challenges.
The physiological origins of the observed changes in CBF can be twofold. One, GCs may hypothetically act on the vascular resistance on the levels of arterioles, which would influence the postarteriole blood flow (Gros et al., 2007). Another explanation lies in the effect on the metabolism of cells: a GC-mediated decrease in neuronal activity would decrease metabolic needs and cause reduced CBF. The specific endocrine pathways by which GCs can rapidly and nongenomically influence such changes in neuronal activity are still unknown (for a general overview of possible pathways in animal models, see Groeneweg et al., 2011).

A few things caused by excess aldosterone:
-suspected na/k pump/tight junction/bbb disruption (related to osmotic demyelination in CAH...cute little early MS looking lesions)
-upregulation of several immune system "bad guys" associated with MS
-likely muscle tension...spasticity (definitely causes "tense" cardiac muscles) Inhibiting aldosterone/cortisol eliminated my problem with tense neck and shoulder muscles.
-several vitamin/mineral deficiencies common in MS (excess cortisol associates with several too)

I'm *trying* to quit harping on this but I can't keep quiet when I see something so closely related posted. My apologies if you are tired of hearing this old song.
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Re: MS: More Women Than Men?

Postby blossom » Mon Feb 11, 2013 10:10 pm

hi anonymoose and vesta, not gonna even try to put all the med. terms etc. i'm more of just a plain jane with most things. i get the drift and agree with you two on many things maybe not all things. but that's what it's about here. we are all different looking for a sameness and i always have felt as vesta--different causes and one thing seems to help some but not all and on and on. anyhooooooo----------------------------

a few questions maybe you guys could answer--me, great health all my life, active, thin never had a problem with weight back in the day yada yada. had a bad fall all this bull shit started. had a hysterectomy about a yr. later was told i had very bad endometriosis probably why i never got pregnant. as like vesta i was on the pill late 60's-but no problems. vesta, it seems i read somewhere that endometriosis can relocate elsewhere in the body-what's your take on that?

anonymoose and vesta--this thread is why more women than men. through my life deserts were a must-no life if not for sweets i was a hands down chocoholic. although i did always eat the veggies etc. friends and family were in awe the chocolate i would eat and not overdose. never had a problem so far at 66 no diabetis no cholesterol problems. for age everything is not bad. i just can't f------ move. i have cut back and i am no longer skinny. anyhoooooooooooooooooooooo-----------------

"i always noticed girls seemed to go for the sweets more than most boys." i know this is crazy maybe and it won't fit everyone "but what does?" but the whole hormone thing and some feel there's an insulin connection.

for the first 8 yrs. after the fall i had tremendous stress in my life no time or money to really try to get well. but afterwards tried different diets etc.even went so far for a few yrs. that chocolate was only in my dreams.

don't know if i'm making any sence here but what the heck does anything at times?
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Re: MS: More Women Than Men?

Postby blossom » Mon Feb 11, 2013 11:25 pm

here you go endometrosis can go to other body parts- ... s/endo.htm

now this is freaky as hell-note blood vessels brain etc.

read it is also more in white women than black women------

oh how the plot thickens--if we weren't crazy before--trying to figure it out can drive you crazy. sorry the one link did not come up but anyone with a curiosity can explore. note that there are many women with endrometriosis that have little symptoms and are unaware. i was one of those until after the fall and who knows what all got jarred and discombobiled????
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Re: MS: More Women Than Men?

Postby Anonymoose » Tue Feb 12, 2013 10:07 am


I think targeting hormone balance whichever way you want to do it is a good idea. They are only just recently starting to uncover all of the nongenomic effects of hormones and they are a plenty. My mother, sister, and I all have "autoimmune" disorders. Mother-thyroid issues, endometriosis, varicose veins, hypertension, type II diabetes with neuropathy and macular degeneration. Sister-sarcoidosis (hysterectomy because of had spread to her stomach), peripheral neuropathy, mild hypertension, gestational diabetes, thyroid issues, very minor varicose veins, premature ventricular contractions. Me-luteal phase defect/progesterone deficiency, premature ventricular contractions (gone??), MS.

To me, this points to genetic hormonal aberrations as each of our issues could be attributed in part to hormone irregularities. Other factors are likely involved but would our "autoimmune" issues be triggered in absence of the hormone issues?

But, none of that matters if you aren't eating chocolate. I do hope you plan to indulge yourself in a big ol' heart shaped box of chocolates this week. Sometimes being bad feels so da*n good! :twisted:
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Re: MS: More Women Than Men?

Postby vesta » Wed Feb 13, 2013 10:41 am

Hi Anonymoose and Blossom :
On my post I mistakenly suggested one look up Evening Primrose Oil on Wikipedia without knowing what was there. Not much. Check out or anything under Evening Primrose Oil benefits and many of the problems you mention are helped by these “pearls” , including endometriosis, multiple sclerosis, diabetes, many things. Apparently the only other source of gamma-linoleic acid is mothers breast milk (which I didn’t get – I wonder if not being breast fed is a factor?) Anyway, I began taking EPO for PMS and multiple sclerosis in 1983 and it smoothed things out. (Insomnia another problem when the hormones are out of balance.)
Most all of the disorders you mention are related to food intolerances and I believe the genetic factor is simply an intolerance for glutens, modern diet. I’m glad I brought up the subject of endometriosis. Yes the lesions can grow anywhere.
Good to hear from you. Vesta

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Re: MS: More Women Than Men?

Postby 1eye » Wed Feb 20, 2013 4:06 pm

I can't help thinking that we are staring at the solution to this conundrum and not seeing it, if it's a single thing. A question I don't have an answer for, is: what one thing do twice or more as many women have, that men have, too, but only half or fewer, or half or less of it?

That one thing is not estrogen, and it's been around a lot longer than birth control pills.

It's not menstruation, or anything that applies only to women.

It could be a hormone that women also have, and it protects against "MS", and they have less of it (in a similar ratio), than men. Or it might assist "MS", but men have half as much of it, or it could be something that men are half as likely to be exposed to, and it protects against "MS", or something that both are likely to be exposed to, but men twice as likely, and it assists "MS".
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Re: MS: More Women Than Men?

Postby Anonymoose » Wed Feb 20, 2013 5:09 pm

The male to female ms ratio increased from 1.4 to 2.3 between 1955 and 2007.

Is this the result of women's lib...the increased stress of balancing work, home and children?
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Re: MS: More Women Than Men?

Postby vesta » Thu Feb 21, 2013 2:08 am

I read somewhere that in Scotland the male/female ratio of MS incidence has widened to the point there are 4 times as many women as men who develop the disease. Why? Because besides being subject to male dominance in general (let's not pretend that misogyny has vanished) the Scotswoman now has success stress fear to deal with, the injunction to succeed professionally while being disadvantaged by gender in the race. And having the triple load of motherhood, home responsibility and work requirements. More stress.
Marc Stecker of Wheelchair Kamikaze reports as well that studies of urbanization in Crete show a rise of MS in women who move to the cities. The most obvious reason for this in my opinion is the added stress of finding work in a more competitive environment. Ah yes, the higher socio-economic strata of society is the most affected. Again Success Stress.

Then look at another study - of MS incidence among various populations in Israel. Same latitude and climate. Israeli born Jews and Jewish immigrants from Europe/North America show the highest MS incidence, of middling incidence are Jewish immigrants from Africa and Asia as well as Christian Arabs, the lowest incidence being among Moslem Arabs, Druze and Bedouin. Forget the sunlight argument and other material factors, the Success Stress Culture strikes me as the most critical factor.
Israeli born Jews are the most afflicted with MS in Israel.. Let's look at this phenomenon again in light of Chinese Medical Theory. Remember, it is said that fear (and cold) "injure" the Kidneys. When their Yang protector the Bladder Meridian mobilizes to protect the Kidneys, the back and neck muscles tense up affecting blood circulation to the head and spine. Israelis don't suffer from a cold climate, it must be the Fear factor. It may be that Israeli children really do grow up with a heightened sense of survival fear which affects their health.

Someone should think of doing an epidemiological comparison of MS incidence among the various religious groups. In other words, study the role of belief and or behavior in the rearing of children. Up to now, I believe one has been too preoccupied with purely material factors - genes, UVB radiation, viruses etc. Stress is as much an emotional/ psychological factor as material. The necks, shoulders and backs of stressed individuals seize up with tension, and it is exactly this phenomonen which I believe damages the vascular system in children leading eventually to adult Multiple Sclerosis.

A fuller development of these ideas can be found under the Blog subject Success Stress June 1, 2012 on my site
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Re: MS: More Women Than Men?

Postby Cece » Thu Feb 21, 2013 7:41 am

With the advent of the use of MRI in diagnosing MS, now more subtle cases of MS are identified and diagnosed. Before these subtle cases would have gone undiagnosed. These more subtle cases are more likely to be in women. Men, when they have MS, tend to get worse faster and the MS is not subtle. Adding in these previously undiagnosed subtle cases tips the balance even more towards more women than men having MS.
It's a theory, anyway.
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Re: MS: More Women Than Men?

Postby Anonymoose » Thu Feb 21, 2013 11:00 am

Is there any data comparing the relative success of ccsvi PTA between men and women? I'm pondering the lack of estrogen, an endothelial protection factor, in men. If ccsvi is less successful (less dramatic results in men) perhaps its because PTA can't compensate enough for the greater endothelial damage in men.

Estrogen may be the reason women typically have a slower progression.
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Re: MS: More Women Than Men?

Postby Cece » Thu Feb 21, 2013 11:24 am

Data, data...
Women showed greater improvement than did men on the physical scale at 6 months (P = .01).

That's from Dr. Hubbard/Dr. Ponec's study on 259 MS patients.
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Re: MS: More Women Than Men?

Postby Anonymoose » Thu Feb 21, 2013 1:08 pm

Thanks Cece,
You give google some pretty stiff competition. I love it! :)

Back to the topic...could this be why women have a higher incidence of MS than men? Estrogen seems to be both a blessing and a curse. It's a well known endothelium protector but not so well known for causing glucocorticoid receptor insensitivity. Which could cause problems with the negative feedback loop governing stress response. Isn't estrogen in birth control pills??
The effect of estrogen (E) on the hypothalamic-pituitary-adrenal axis was investigated in female Sprague-Dawley rats. Animals were bilaterally ovariectomized (OVX), and a Silastic capsule (0.5 cm) containing 17 beta-estradiol was sc implanted. Control animals received a blank capsule. Animals were killed 21 days later. In E-treated rats, we found significantly higher corticosterone (CORT) peak levels 20 min after a 5-sec footshock (1.0 mamp) or exposure to ether vapors (P less than 0.05) compared to those in OVX controls. In addition, the recovery of the ACTH and CORT responses to footshock stress was significantly prolonged (P less than 0.05) in the presence of E. Furthermore, the ACTH and CORT secretory responses to ether stress could be suppressed by exogenous RU 28362 (a specific glucocorticoid receptor agonist; 40 micrograms/100 g BW for 4 days) in OVX controls (P less than 0.05), but not in E-treated animals. These data suggest that E can impair glucocorticoid receptor-mediated delayed or slow negative feedback. Consequently, we examined the influence of E on mineralocorticoid and glucocorticoid receptor concentrations using in vitro binding assays. E did not alter mineralocorticoid or glucocorticoid receptor concentrations in any of the brain regions examined. The administration of RU 28362 (40 micrograms/100 g BW for 4 days) to OVX control or E-treated rats significantly down-regulated hippocampal glucocorticoid receptor (P less than 0.02) in control rats only. In contrast, aldosterone administration (40 micrograms/100 g BW for 4 days) significantly down-regulated hippocampal glucocorticoid receptor (P less than 0.0008) in both control and E-treated animals. Thus, E treatment results in a loss of the glucocorticoid receptor's ability to autoregulate; this suggests that E may cause a functional impairment of the glucocorticoid receptor even though receptor binding appears normal. These findings suggest that hyperactivation of the hypothalamic-pituitary-adrenal axis after stress in E-treated rats is due in part to impaired glucocorticoid receptor-mediated slow negative feedback.

And for the estrogen deficient boys (and girls because it's our problem too, though to a lesser extent until menopause). This isn't an "if" situation. We all have a constantly activated hpa-axis. We all have errant aldosterone circulating in our bloodstreams 24/7. The levels don't have to be outside of "normal" ranges to cause damage. It's the constant secretion that causes cumulative damage. The anti-hypertensive drugs that have been shown to be protective and that are currently in trial, in some way work to counteract the effects of excess aldosterone. CCSVI less successful in men and in older MS because endothelial damage is obstructing perfusion and maybe even csf drainage? Couldn't endothelial damage affect the arachnoid villi? Inexpensive and relatively harmless medications can manage the excess secretion. My clonidine has a $0.00 co-pay. They have shown that aldosterone blockers can reverse endothelial damage in males. You *could* get some things back. ... 194.x/full (full text)
Aldosterone exerts actions in the vascular endothelium through acute, non-genomic and chronic, genomic effects that modulate vascular resistance and blood flow. Aldosterone-induced vasculopathy is characterized by a reduction of endothelial NO synthesis and bioavailability and by increased generation of superoxide radicals that degrade endogenous NO. The present article describes how endothelial function is altered by acutely administered aldosterone and in addition compares it with the effect of chronic exposure to aldosterone in humans, experimental animals and isolated endothelial cells. We will discuss the mechanisms of its unwanted actions and the interactions between aldosterone and ET-1, Ca2+ flux through T-type Ca2+ channels and sodium, with reference to the bioavailability of endothelial NO. Therapeutic efficacies of MR inhibitors, ETA receptor antagonists, and T-type Ca2+ channel blockers through beneficial actions of NO on blood flow against inappropriately elevated plasma aldosterone concentrations or aldosteronism and resistant hypertension are also summarized.

Aldosterone has detrimental effects on various peripheral vascular beds. In the cerebral vasculature, it reduced blood flow and therefore promoted cerebral ischaemia (Rigsby et al., 2005). When cerebral ischaemia was induced experimentally, the volume of the resultant infarct was greater in SHRSP than in Wistar Kyoto rats. The infarct size was reduced by spironolactone treatment to an extent similar to that seen in Wistar Kyoto rats (Dorrance et al., 2001). The lumen diameter of middle cerebral arteries was greater in the spironolactone-treated (6 weeks) aldosterone SHRSP than in the control SHRSP. Spironolactone had no effect on systolic blood pressure (Rigsby and Dorrance, 2004). Chronic aldosterone appears to participate in impairment of cerebral blood perfusion. There was a cerebrovascular protective effect of spironolactone in the absence of lowered blood pressure in saline-drinking SHRSP (Rocha et al., 1998). High plasma aldosterone concentration is a risk factor of cognitive impairment in hypertensive patients (Yagi et al., 2011), and cerebral hypoperfusion is associated with later cognitive decline (Kitagawa et al., 2009). Vascular endothelial dysfunction via high aldosteronaemia may participate in cerebral hypoperfusion that is associated with cognitive decline. Reduced cerebral blood flow associated with impairment of endothelial function and NO bioavailability leads to the generation and development of Alzheimer's disease (Toda and Okamura, 2012).

In contrast to these detrimental effects, aldosterone or MR activation in the brain may be required for neuronal survival by inhibiting cell death via the expression of anti-apoptotic genes (Macleod et al., 2003; Rigsby et al., 2005). Aldosterone facilitates neuronal damage through deleterious actions on vasculature. Conversely, MR activation in the brain may inhibit cell death.

Taken together, aldosterone non-genomically impairs or enhances endothelial function in humans, whereas it increases endothelial function in most instances of experimental animals in situ and in isolated preparations (Table 1). This discrepancy may not be explained by different doses of aldosterone used in humans and animals, use of different animal species in the experiments and use of in vivo or in vitro preparations. Differences in ambient redox or sodium status during experiments and in involvement of NO-independent (PLC, ET, PKC and sodium–proton exchanger) or MR-independent mechanisms may participate in the different actions of aldosterone. Chronic exposure to high aldosterone milieu is harmful to endothelial functions. Aldosterone-induced endothelial dysfunction and hypoperfusion in the brain seem to participate in the genesis of cognitive decline. An imbalance between NO synthesis and actions and superoxide anion generation plays an important role in endothelial dysfunction elicited either by acute or chronic exposures to aldosterone.

So...I got slightly off topic again. lol It does have to do with the difference between man-MS and woman-MS though. :P
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Re: MS: More Women Than Men?

Postby ljelome » Fri Feb 22, 2013 2:51 am

Hi! i found an interesting relationship between hormone (progesterone) and venous disease. Maybe could help u in some way of thinking.
I quoted from a book found on the web "Medicographia95, The Venous Valve and Primary Chronic Venous Disease", by J. Bergan :
(I have a link of the book in the "venous valve" topic)

Primary venous insufficiency
A dysfunctional venous system is caused for the main part by functional failure of venous valves.
The molecular mechanisms uncovered recently that enter into functional valve failure are mentioned
above. Other factors are traditionally cited as contributing to venous valve failure; these
include female sex, pregnancy, obesity, a standing occupation in women,7 and heredity.8,9 An increase
in vein diameter is one cause of valve dysfunction and reflux. Progesterone inhibits smooth
muscle contraction. This is useful in preventing uterine contraction and spontaneous abortion
in pregnancy. However, preventing vein wall smooth muscle contraction allows passive dilation
of veins and when a critical diameter is reached, a functioning venous valve becomes dysfunctional
or incompetent. As half of a women’s adult lifetime is under the influence of progesterone,
and this is exacerbated markedly during pregnancy, it is no wonder that primary venous insufficiency
is twice as common in women than in men
Warm regards,

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Re: MS: More Women Than Men?

Postby Anonymoose » Fri Feb 22, 2013 8:15 am

That's interesting! "They" seem to be pretty convinced that the valve issues are of a congenital nature rather than something being developed over time. I don't fully understand it but I bet someone else here could explain it better. :)
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