Considering Going the Opposite Way with Supplements

dragonsnake · May 2016

Dear wise Owl, I'm indeed waiting for the pathology results. All my previous live did not prepare me for that. Thank you for your kindness and understanding.

dragonsnake · May 2016

Solfeo, I also have been to a therapist before, after my unstoppable panic attacks that turned to be a reaction to antibiotics and my leaky gut rather than my mental state. No medical professional saw a connection. Therapy was not helpful. Therapist just listened my rambling about my past and dodged all my questions trying very hard not to offer any solutions. From that prospective, I can annoy my husband for free, although poor thing does not deserve it. My body reacted badly to antidepressants increasing the severity of my panic attacks. I managed to put together my own course of treatment, and stuck to it. It took me a couple of years to heal my stomach. What a disaster would it be to impart a standard bc treatment on it.

I was raised in an atheist society. It is very hard to find faith if you are not raised in faith. Same goes for love. It took me 50 years of my life to recognize love, and I finally know what it is. It's a wonderful feeling.

Graduation is a huge thing in everyone's life. Please take good care of yourself during the trip.

Thank you for reaching out to me.

dragonsnake · May 2016

Cowgirl, you say it, and I believe it. You understand. Thank you for being there for me.

I was raised in a pretty violent society that does not value human lives. I'm overwhelmed with your guys kindness . Thank you.

BarredOwl · May 2016

dragonsnake:

Sending wishes for the best possible pathology results for you!

BarredOwl

ChiSandy · May 2016

dragonsnake, sending you healing wishes for a good result.

I'm on tenterhooks myself--after spending my entire adult life slathering on the sunscreen, wearing long sleeves & pants, and avoiding the sun almost as much as Dracula, I am waiting on the results of two biopsies yesterday: a possible basal/squamous on my face; and a probable (derm said 50-50) melanoma on my back (hoping it's stage 0 so that removal w/margins did the trick). I am in general (except for the pity-party I seem to have been throwing myself since dx) a low-carb eater--lost 50 lbs. on it but comfort food cravings put back 20 lbs. and letrozole another 5-7. I see obese (some “morbidly" so) omnivorous sun-worshipping regularly-imbibing sedentary friends never get cancer (heck, nearly all my relatives successfully thumbed their noses at the fates--the only ones who got cancer of any kind were my dad's alcoholic sister, who drank and smoked herself into esophageal cancer; and his half-sister, who got melanoma but didn't know about it till it had metastasized to her liver and killed her within months of dx....and she too had smoked). I have friends who do everything “right" but still got bc--including a friend's wife who is a slender teetotaling vegan triathlete but still got high-grade bilateral widely-disseminated DCIS and needed a bmx. And my morbidly obese friend who just had a bmx for DCIS and ADH had ER- cancer.......has been eating heart-healthy since her first angioplasty 15 yrs ago, hits the gym daily, avoids caffeine and sugar, and has never touched a drop of alcohol in her life.

I think that by the time most of us have read about how to lower our “modifiable" risk factors, the die has already been cast--the prevention train has left the station, and we probably can't prevent recurrence with lifestyle changes alone: what supposedly “gave" us bc in the first place is also the gremlin that only adjuvant treatments and luck of the draw can defeat. I was lucky in that my ODX was low enough that the “poison" part of the treatment algorithm was not necessary (at least for what they found)--I was able to get by with “slash/burn/starve" (i.e., deprive any remaining micromets of the estrogen on which they depend for their proliferation and even survival).

Which leads me to the misconception, or at least oversimplification--that despite nonfunctioning or missing ovaries, one's fat cells and adrenal glands still “make estrogen." True, those are the sources of whatever estrogen continues to be produced after menopause (natural, surgical or chemical). But those glands only “make" a hormone, androstenedione, that is actually an androgen (the same class as testosterone, and what Mark McGwyre and Sammy Sosa “juiced" with--legally at the time, available OTC), not an estrogen. In order to be converted to estradiol (a form of estrogen), androstenedione needs an enzyme called aromatase, which is produced in the liver. Aromatase inhibitors block the action of aromatase, so the androstenedione can't become estrogen. The side effects of AIs are due to the deprivation of estrogen in a body already deprived of actual ovarian estrogen--the “andro" converted by aromatase into estradiol was what the postmenopausal female body normally depends on to keep joints from deteriorating, hair from thinning, metabolism high enough, arteries from clogging (or plaques from forming), the hypothalamus from irregularly raising body temperature and temporarily stimulating apocrine sweat glands (the ones all over the body that produce odorless sweat in response to exertion and perception of body heat) from causing hot flashes and/or night sweats, and endorphins at normal levels (keeping mood at an even keel). Deprive the already-estrogen-reduced female body of aromatase--keeping adrenal and fat-cell andro from becoming estradiol, and you get classic AI side effects that essentially are Menopause 2.0. And unopposed andro causes hair to thin, just as it does in men. (Men with male-pattern-baldness, especially before late middle-age, tend to have higher testosterone levels than their full-head-of-hair brethren--there's some truth to “solar sex-panel," the boastful nickname for a bald pate). And cruelly, it makes us hornier at the same time the lack of estrogen dries out our vaginas & vulvas.

So taking an AI can (and usually does) make us gain weight--though some of that weight is muscle, thanks to the unopposed andro--but the adrenals and the fuller (hypertrophic obesity) or newly-acquired (hyperplastic obesity) fat cells make only more andro, not estradiol--so long as either the liver either fails to make enough aromatase and the aromatase it makes is blocked by the action of the drug. I suspect that researchers who cite statistical retrospective studies that fatter women are more susceptible to ER+ bc will eventually admit that obese women taking AIs don't necessarily have a greater chance of recurrence so long as their livers continue to fail to produce aromatase and what aromatase they make is rendered powerless by AIs. And I also suspect that alcohol's supposed unhealthful effect on ER+ bc is due to its relatively high caloric content (7 per gm., as opposed to 4 for protein and carb--but 9 for fat) and therefore, the higher caloric intake of women who imbibe regularly--but again, the studies tend to reflect retrospective risk for development of bc, for excessive drinking up until dx; and not prospective risk for recurrence in moderately-drinking women on AIs. And here's food for thought: it is universally agreed that alcohol does impair liver function.....can one of those impaired functions be production of aromatase? Epidemiological (statistically retrospective) researchers say that an impaired liver can't effectively clear estrogens from the bloodstream.....but what if there isn't any estrogen left to be cleared because the AIs are working as intended?

I'm not giving up my one pint of wine per week--many doctors cite 3 drinks a week, with a “drink" being a 12-oz. beer, a 1-oz.. shot of spirits, or a 5-oz. glass of table (<14% abv, not fortified dessert) wine, as the safe limit for women dxed with bc. I prefer to allocate that as five 3-oz. glasses of wine (or seven 2-oz. tasting portions) a week, since I only drink wines that go with the food I'm eating (and when the food's been eaten, I often don't finish what's in my glass). I don't need or even like the buzz, so if the only wine around is less than wonderful, I'm not drinking it, period.

Hopeful82014 · May 2016

I've just read the following:

"Women who carry common gene variants linked to breast cancer can still reduce risk of the disease by following a healthy lifestyle, according to research published online May 26 in JAMA Oncology.

The results were based on records from 42,912 women tested for 24 gene variants previously linked to breast cancer risk. The researchers created a model for predicting a woman's risk of breast cancer, using that genetic information plus other factors. Those other factors included ones that can't be changed, such as age and genetics, as well as modifiable lifestyle habits. The researchers then estimated the effects of 68 other gene variations that the women weren't tested for.

The researchers found that four lifestyle factors were key: maintaining a healthy weight; not smoking; limiting alcohol; and not using hormone therapy after menopause. The team estimated that if all white U.S. women did those things, 28.9 percent of breast cancer cases could be avoided. And a majority of those averted cancers would be among women at increased risk because of family history and the gene variants they carry.

"Lifestyle factors may be even more important for women at higher genetic risk than for those at low genetic risk," senior researcher Nilanjan Chatterjee, Ph.D., a professor at the Johns Hopkins Bloomberg School of Public Health in Baltimore, told HealthDay."

I realize I am only one woman and am NOT trying to invalidate the above; I think it's very important information. However, I observed all of the above recommendations, among others - exercised hard and regularly, ate lots of fruits & veggies, little meat but still managed to fall into that 70% whose cancers weren't averted. Cancer is sneaky, unpredictable and unfair - at best. We can waste a lot of time and energy comparing ourselves to others, wondering what we did "wrong" and (in my opinion) trying to treat it without Western medical therapies. Just my .02.

Sandy - I'm sorry to hear about your biopsies. I hope you get the best possible news - and soon. My husband (also an atty. and a musician) deals with the same issues and I know what he goes through. Wishing you the best.

dragonsnake · May 2016

Dear ChiSandy,

Thank you for sharing. It's truly torturous to wait and look into abyss of the unknown.

BarredOwl · May 2016

Hi ChiSandy:

Hoping for benign results for you. 🍀

I've been known to make that simplification, and did so earlier today, saying: "This is because tissues other than the ovary can make estrogen (e.g., adipose (fat) tissue)." Not the whole story, but not false in my understanding. As explained below, adipose cells do contain aromatase and can produce estrone, which is considered an "estrogen" and is a precursor of estradiol.

You noted: "Which leads me to the misconception, or at least oversimplification--that despite nonfunctioning or missing ovaries, one's fat cells and adrenal glands still "make estrogen." True, those are the sources of whatever estrogen continues to be produced after menopause (natural, surgical or chemical). But those glands only "make" a hormone, androstenedione, that is actually an androgen (the same class as testosterone, and what Mark McGwyre and Sammy Sosa "juiced" with--legally at the time, available OTC), not an estrogen. In order to be converted to estradiol (a form of estrogen), androstenedione needs an enzyme called aromatase, which is produced in the liver."

I agree that the adrenal glands are the primary source of the estrogen precursor "androstenedione". However, this article indicates that adipose tissue, among some others, does express the enzyme aromatase and can mediate the enzymatic conversion of androstenedione "of adrenal origin" to estrone, a precursor of estradiol.

http://pharmrev.aspetjournals.org/content/57/3/359.full#title5

"In the human, aromatase is expressed in a number of cells, including the ovarian granulosa cell, the placental syncytiotrophoblast, the testicular Leydig cell, and various extraglandular sites, including the brain and skin fibroblasts (Simpson et al., 1994). The principal product of the ovarian granulosa cells during the follicular phase is estradiol (-17β). Additionally, aromatase is expressed in human adipose tissue. Whereas the highest levels of aromatase are in the ovarian granulosa cells in premenopausal women, the adipose tissue becomes the major aromatase-expressing body site after menopause (Fig. 2) (Grodin et al., 1973; Bulun and Simpson, 1994). Although aromatase level per adipose tissue fibroblast may be small, the sum of estrogen arising from billions of adipose tissue fibroblasts in the entire body makes a physiologic impact. The principal product of the ovary is the potent estrogen estradiol. In adipose tissue, estrogenically weak estrone is produced from androstenedione of adrenal origin in relatively large quantities. However, at least half of this peripherally produced estrone is eventually converted to estradiol in extraovarian tissues (Fig. 2) (MacDonald et al., 1979)."

According to this image and legend, the liver also expresses aromatase and contributes to the process:

https://www.pharmgkb.org/pathway/PA145011117

"In addition, aromatase is also present at lower levels in several nonglandular tissues that include subcutaneous fat, liver, muscle, brain, normal breast and breast cancer tissue 4. Estrogen production after menopause is solely from nonglandular sources, particularly subcutaneous fat."

The legend also notes: "In all tissues, hydroxysteroid (17-beta) dehydrogenase (HSD17B) converts . . . estrone to estradiol," suggesting the adipose tissue (or other tissues) can complete the conversion from estrone to estradiol, in a second step mediated by a second enzyme (HSD17B).

BarredOwl

dragonsnake · May 2016

BarredOwl,

Do you know if a total hysterectomy for pre-menopausal women can substitute treatment with tamoxifen? What is the lesser of two evils in terms of cognitive abilities, focusing and concentration?

BarredOwl · May 2016

Hi dragonsnake:

Even with bilateral oophorectomy, patients who have undergone breast conserving therapy (lumpectomy) for DCIS and/or IDC are still likely to receive a recommendation for endocrine therapy under current treatment guidelines from the NCCN. However, with a bilateral oophorectomy, they are considered to be post-menopausal, and will have the added option of an aromatase inhibitor. I posted more on this question today:

https://community.breastcancer.org/forum/5/topics/844630?page=1#post_4723511

What is the lesser of two evils in terms of cognitive abilities, focusing and concentration? I don't know. However, as it does not obviate endocrine therapy, oophorectomy (specifically, bilateral salpingo oophorectomy, including ovaries and fallopian tubes) is not routinely recommended for lower risk patients. This reflects in part some benefits of having ovaries versus not having them for other health reasons.

BarredOwl

ShetlandPony · June 2016

Dragonsnake, if things don't improve for you once your treatment plan is in place, I encourage you to consider solfeo's idea of cognitive-behavioral therapy. CBT is different from the talk therapy you found so unhelpful, and even a limited number of sessions can be a very effective.

Considering Going the Opposite Way with Supplements

Comments

Categories