How does young pregnancy decrease breast cancer risk?

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Decicco

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I know it supposedly has something to do with decreasing the patient's exposure to estrogen, but isn't estrogen high during pregnancy (pp484 First Aid)?
 
Fewer periods = less breast cancer risk. Pregnancy is 9 months without periods. Same idea with earlier onset of menses = higher breast Ca risk.
 
Fewer periods = less breast cancer risk. Pregnancy is 9 months without periods. Same idea with earlier onset of menses = higher breast Ca risk.

My understanding was that all of these things increase breast cancer risk because of an increased lifetime exposure to unopposed estrogen (ie, estrogen without progesterone): anovulatory cycles, polycystic ovarian syndrome, granulosa cell tumors, early menses, late menopause. If this is true, then I'm not sure how pregnancy fits into this. I agree it decreases the # of periods a woman has, but what about estrogen exposure?
 
pregnancy = super duper ridiculously high progesterone. so sure you have estrogen, but it is totally overwhelmed by having tons of progesterone vs the follicular phase of a woman's cycle where there is estrogen more or less unopposed by progesterone
 
Fewer periods = less breast cancer risk. Pregnancy is 9 months without periods. Same idea with earlier onset of menses = higher breast Ca risk.

Not to single you out, we all do this from time to time, but this is why I hate the paradigm of medical education exemplified by stuff like First Aid. Explaining things by circular logic with no substance or deeper understanding and then acting like that's a definitive answer. You haven't explained anything at all, no pathophys, no mechanism, not even outlining what exactly is going on. Just strung together a bunch of associations and called it a day.
 
I believe it has to do with the different types of estrogen. During pregnancy, E3 (estriol), the mildest form of estrogen is elevated during pregnancy and replaces estradiol, the more potent form involved in the menstrual cycle. The greater the exposure to Estradiol, the greater the risk of endometrial CA.
 
Not to single you out, we all do this from time to time, but this is why I hate the paradigm of medical education exemplified by stuff like First Aid. Explaining things by circular logic with no substance or deeper understanding and then acting like that's a definitive answer. You haven't explained anything at all, no pathophys, no mechanism, not even outlining what exactly is going on. Just strung together a bunch of associations and called it a day.

Outline of what is going on: You are a tool.

Mechanism: Busting out a holier-than-thou attitude and making it well known.

Pathophysiology: Some deep seated confidence problems. Maybe you were the smartest person in your high school or even in some of your college classes. Now acting from the almighty experience of a second year medical student you attempt to parade around with a smug sense of superiority because you can preach about what you believe is wrong with medical education and how everyone except you obviously just doesn't get it. Stupid people like the rest of us obviously have no idea what is going on in physiology, obviously have no idea about progesterone:estrogen counterregulation, and are just stupid sheep mindlessly reciting lines from First Aid. Or... maybe I just didn't feel like typing out a six paragraph answer if it wasn't necessary when it was getting late at night and I was tired.

Good enough for you?
 
If you want to take it personally that's on you. But you just prove my point. More periods = more risk is only going to help me as a last-ditch guideline on an exam, it's not the sort of thing you say to someone who was just diagnosed, or something you use to understand cancer.

But in a world where misinformation runs rampant: http://thatmarriedcouple.blogspot.com/2010/10/how-to-prevent-breast-cancer-have.html

It would be nice if as doctors we had a solid grounding in telling women what goes on during pregnancy that lowers their risk of breast cancer, assuming it is known. And it would be even nicer if I could read that article and countless others which I will be exposed to in my lifetime, and either have an idea of where it was wrong or know where to find it.

There's a lot of groups out there furthering very legit sounding "research" with zero science behind it, and despite being sent out by some crack pot anti abortion activists ( http://en.wikipedia.org/wiki/Abortion-breast_cancer_hypothesis ) it's all over the internet.

And if there's no consensus on breast cancer risk then that's what should be taught. But if we as doctors don't have answers then somebody else will gladly take that role, and the next thing you know they're using homeopathy and woo woo to treat their cancer. But maybe I just deal with more hippies on a daily basis than you do.
 
Ok, so I'm studying for the boards now as well, and this whole progesterone thing is driving me nuts. But let me summarize what I did come up with.

1st point- There are certain types of BreastCA that are estrogen receptor positive and then there are those that are progesterone receptor positive. They can both be positive at the same time, negative at the same time, and/or one can be positive while the other is negative.

2nd Point- Estrogen is mainly involved in breast tissue proliferation/"hyperplasia," while progesterone is mainly involved in breast tissue "differentiation."

3rd Point- When on combined oral contraceptives treatment (estrogen and progestin) women are at higher risk for developing breast cancer than women on estrogen therapy alone.

Ok.. So as I understand it, but keep in mind that I'm still a bit confused, is that progesterone (given exogenously via OCP) actually increases your risk of developing breast cancer. I'm not entirely sure how this happens yet, especially since progesterone is a cell "differentiator" not proliferator. Maybe its acting on the progesterone receptor + types of BreastCA?...

So here's the big question then. How does nulliparity increase your risk of Breast cancer? So most of you are right in that in pregnancy, your progesterone levels are very high. Progesterone (endogenous) in pregnancy is causing an increased breast tissue differentiation in preparation for lactation. Because there are more breast cells differentiated, there are less stem cells that are available for neoplastic division. (so endo progesterone lower risk of BreastCA, while progestin OCP increases the risk?)

Listen up to this point though. So many of you, might be confusing nulliparity and its association with ENDOMETRIAL cancer. So here, the pathophys is different. In nulliparity, you do have less estrogen levels than pregnant women, but the key difference here is that you also have less progesterone. So the problem with nulliparity is that you do not have the PROTECTIVE effect of progesterone on endometrial cells.

Summary:
Nulliparity in BreastCA- less progesterone for tissue differentiation.
Nulliparity in EndometrialCA- less progesterone to counteract estrogen's negative role on endo hyperplasia
OCP with added Progestin- increased risk of BreastCA (don't quite understand why)

I used a combo of Robbins and uptodate to find most of this stuff. I'm giving this answer not as a final statement on the subject, but more as a summary as how I understand what is going on. Please feel free to comment and edit any areas that might be wrong.
 
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