Menopause at 38?

[mindersue]

Hello,
I'm new here. I've learned so much from my visits here, thank you all!

I'm at the point in my treatment where I must decide on hormone therapy. I've read the posts on Tamoxifen vs. Suppression of ovary function + aromatase inhibitor. From that I concluded that removal of ovaries + a.i. would be the most aggressive approach and therefore the one that I should consider. My gynecologist is reluctant to remove my ovaries at my age (38) based on quality of life issues (severe hot flashes, mood swings, etc.).

Anyone out there who had their ovaries removed and would like to share their experience with side effects?

I was diagnosed 12/26/05. I'm stage II (3 pos. nodes), lumpectemy, done with chemo (Taxotere & carboplatin), 1/2 done with Herceptin (1 year total), 2/3 done with radiation. I'll start hormone therapy after radiation.

Thanks!

Hi Mindersue,

I was Stage II also. I was 38 at diagnosis. I had my ovaries removed 3 weeks after my last chemo treatment. I am taking Arimidex for 5 years.
My onc recommended the surgery, even though there is no proven survival benefit. I have three children, and my tumors were strongly hormone receptive. I wanted the most aggressive treatment.

My menopausal symptoms are similar, albeit somewhat less severe, to my chemopause. I have mild night sweats and joint pain. I had trouble with insomnia at first, is better now that I am taking it first thing in the morning. I have not had any sexual side effects, thank goodness. The risks are there for going into menopause at a young age. I am taking fosamax to preserve my bone density.

It is a very personal decision. I know of many women that have severe side effects on the ai's and it affects their quality of life.

[saleboat]

I've been to three Oncs, and no one will recommend anything besides Tamox for me, Stage IIIC and 35 y.o.-- and I've been to two major cancer centers in NYC.

Maybe you could try the shots at first to shut down your ovaries?-- it could give you an idea of what menopause will be like before you remove your ovaries.

I've pestered my Onc about this, and she is adamant that there is no evidence that convinces her that ovary shut-down/removal will help me beyond all the treatment that I've already received...and she's pretty sure that I'll have bone and heart problems in the future if I go that route.

So lots of debate out there on this issue.

Good luck with everything. Wish I had the answer!

Jen

[Becky]

I had my ovaries removed at age 46. My menses returned just when I would have started hormone therapy. I wanted to be on an AI with Herceptin and since my dad's mom died of ovarian cancer, I wanted that out of the equation too.


I had some hot flashes and night sweats. No joint pain but I did get bladder infections (a menopause problem for some women due to the thinning tissues - if you have this potential side effect, it is worse if menopause is abrupt as in oophorectomy. Then the AI makes estrogen nonexistant so its even worse (for me - this is an uncommon side effect)).

I am very happy with the decision I made and I would make it again (as I gulp my cranberry extract supplements).

Kind regards

Becky

[Bev]

Hi Sue,

It seems to me the older studies said doing 2 yrs tamox, followed by an AI worked nicely. Those 2 years would give you some time to reflect on it all. It seems some of the newer stuff suggest Herceptin/AI synergies.

So run a search on this web site and get at least 2 doc opinions. Best of luck. BB

[Bev]

Hi, my computer just did something. OK. maybe was me, hoping I don't post twice. If your'e BRAC pos, I would do the oophrectomy. Otherwise get 3 opinions. Most docs do the same as others. Think about you. If you did chemopause OK. you'll do menopause OK. This cancer thing makes you feel old, and you're too young to feel that way. Either way. it will work out.

[R.B.]

I am a man and non sufferer.

I am not an expert.

I am only trying to provoke thought based on various bits I have seen in my journeys over the last year. I wish I had time to really look at this area. At the moment I have my time fully used looking at fats diet and health which includes BC.

It is important to appreciate the ovaries are not the only source of oestrogen. The cells of the bodies are like mini production plants and one of the things many of those plants do is make oestrogen hormones etc. A trigger for that is the COX 2 pathway which is dependent on omega six derivatives.

Fat cells store hormones including oestrogen and I think I have seen it stated that they are the largest source of oestrogen in post menopausal women.

I cannot recall if I saved it but I recollect a trial where breast levels of oestrogen where higher than those in the body fat. This for me raises the question if on site eostrogen production in the breast is greater factor than that produces by the ovaries.

There is also significant evidence that the fat balance is intimately tied up with hormone and oestrogen production. I posted a trial in the Greek diet post which suggested that the levels of receptors dropped significantly (a factor of six?) in animals where omega six consumption was reduced.

http://www.her2support.org/vbulletin...ad.php?t=24410

The trial below has a chapter Aromatase in breast cancer issues with a graph between cox 2 and aromatase which shows a straight line relationship. It is a complex read but worth struggling. It is also though provoking in that it underlines that much of what we eat contains nautual aromatse inhibitors, and the importance of local production in the breast.

If you go to the link and click on the blue icon you will get the full article.

I do not know if there is any merit / possibility in a watching breif in terms of monitoring oestradiol levels in the breast. I have seen reports where women have relied on natural aromatase inhibitors diet etc and monitored oestradoil. Try the "Annie Appleseed" BC site and search under oestradiol etc.

At a very personal and still confused level I still have a large number of question on the involvement of oestrogen. Oestrogen is a antioxidant it is reported so presumably helps guard against oxidative stress. Oxidative stress is what causes the degredation of the genes that is a factor leading to cancers. Omega six and three seem to control some of the mechanisms that make oestrogen. There is a growing recognition that some tumours are "stem" cell related. It is a whole very complex subject on its own. For me there is significant room for risk reduction through diet.

The young sufferer group report the highest disatisfaction levels. As you more than me will be aware the QOL issues are significant particularly in respect of fertility and femininity issues.

If I can find any stats I have saved I will post them. It would be worth trying to see what you can find.

It is also worth checking the stats on tamoxifen. I was surprised at the low additonal protection in percentage terms of tamoxifen as an addition over RT and boost in overall terms (which is not the same as for particular groups which could be better or worse). Tamoxifen also has some serious side effects for the few. Part of Tamoxifens action is intrvention in the fat pathways. Part of herceptins action is intervention in the fat pathways.

BUT all of this wittering is just that and things depend on your personal diagnosis aspirations, fears, outlook on life etc.

I can only suggest from my reading and as a male that you should do all the research and reading you can before making this decsion with your medical advisors.

This is a very though provoking link, and the MOJO link is worth checking out for a huge history of the female pespective on the subject, and between the lines the impact on their lives.

http://www.her2support.org/vbulletin...highlight=mojo
http://community.breastcancer.org/ub...page=2&fpart=1
http://www.her2support.org/vbulletin...ad.php?t=23891

I wish you the best with these hugely difficult personal decisions.


RB







http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum

1: Endocr Rev. 2005 May;26(3):331-45. Epub 2005 Apr 6.Click here to read Links
Aromatase inhibitors in the treatment of breast cancer.

* Brueggemeier RW,
* Hackett JC,
* Diaz-Cruz ES.

College of Pharmacy, The Ohio State University, 500 West 12th Avenue, Columbus, Ohio 43210-1291, USA. Brueggemeier.1@osu.edu

Estradiol, the most potent endogenous estrogen, is biosynthesized from androgens by the cytochrome P450 enzyme complex called aromatase. Aromatase is present in breast tissue, and intratumoral aromatase is the source of local estrogen production in breast cancer tissues. Inhibition of aromatase is an important approach for reducing growth-stimulatory effects of estrogens in estrogen-dependent breast cancer. Steroidal inhibitors that have been developed to date build upon the basic androstenedione nucleus and incorporate chemical substituents at varying positions on the steroid. Nonsteroidal aromatase inhibitors can be divided into three classes: aminoglutethimide-like molecules, imidazole/triazole derivatives, and flavonoid analogs. Mechanism-based aromatase inhibitors are steroidal inhibitors that mimic the substrate, are converted by the enzyme to a reactive intermediate, and result in the inactivation of aromatase. Both steroidal and nonsteroidal aromatase inhibitors have shown clinical efficacy in the treatment of breast cancer. The potent and selective third-generation aromatase inhibitors, anastrozole, letrozole, and exemestane, were introduced into the market as endocrine therapy in postmenopausal patients failing antiestrogen therapy alone or multiple hormonal therapies. These agents are currently approved as first-line therapy for the treatment of postmenopausal women with metastatic estrogen-dependent breast cancer. Several clinical studies of aromatase inhibitors are currently focusing on the use of these agents in the adjuvant setting for the treatment of early breast cancer. Use of an aromatase inhibitor as initial therapy or after treatment with tamoxifen is now recommended as adjuvant hormonal therapy for a postmenopausal woman with hormone-dependent breast cancer.

PMID: 15814851 [PubMed - indexed for MEDLINE]
Related Links

* Aromatase inhibitors: new endocrine treatment of breast cancer. [Semin Reprod Med. 2004] PMID: 15083379
* Aromatase, aromatase inhibitors, and breast cancer. [Am J Ther. 2001] PMID: 11550075
* Aromatase inhibitors in breast cancer therapy. [Expert Rev Anticancer Ther. 2002] PMID: 12113240
* Where do selective estrogen receptor modulators (SERMs) and aromatase inhibitors (AIs) now fit into breast cancer treatment algorithms? [J Steroid Biochem Mol Biol. 2001] PMID: 11850229
* Use of aromatase inhibitors in breast carcinoma. [Endocr Relat Cancer. 1999] PMID: 10732791
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