Friday, February 14, 2014

Clarifying Confusion about OCPs [Serge]

Over at Soulation (a great site, btw), a commenter named Marie has responded to some of my writing here as well as a recent interview that I had with Life Report regarding the mechanism of action of certain contraceptives.  I thought I would respond here in order to help others who may also be confused regarding this, well, complex and confusing issue.  Marie's response is very long, so I will be responding to specific quotes.  Her entire response can be found here.  I wish to remind everyone that we are discussing the ethical implications of contraception, but the medical mechanism of action.

 and since we know that the progestin in the pill is a synthetic form of progesterone which does not act like natural progesterone to prepare the uterus for implantation, it ends up working like a slower, low dose mifepristone. Yes, mifepristone has double the binding site affinity as normal progesterone and progestins and therefore it works much more harshly and quickly, but they are both "progesterone Narcan" as far as filling progesterone receptors but yet blocking the function of the woman's natural progesterone to prepare the uterus for implantation. A woman's own progesterone works best to prepare the uterus and maintain a pregnancy, that's why so many doctors and others have switched to bioidentical progesterone for treating infertility/miscarriage/menopause.

The assertion here is that LNG, the progestin found in Plan B, works as a competitive antagonist for progesterone receptors like Narcan works for opioid receptors.  She doesn't provide evidence for this, and I believe there are at least three reasons why it is very unlikely.

First, the amount of progesterone secreted by the corpus luteum after ovulation is far greater than that exogenous progestin absorbed by taking Plan B.  The notion that the small amount of oral progestin that effects the endometrium would overcome the huge surge of natural progesterone secreted in the luteal phase of the cycle is highly unlikely and would need evidence to be compelling.

Second, if LNG acts as a "weak" mifipristone (RU-486), then it should also have the effect of exhausting the progesterone receptors after inplantation has occurred.  In all studies, LNG has had no effect on pregnancies after implantation.  Why not?

Third, and I believe most compelling, is that other progestins are used in order to treat luteal insufficiency.  When a women does not produce enough progesterone during the luteal phase of her cycle it has been shown that progestins have had a positive effect on preventing spontaneous miscarriage.  It is true that bioidentical progesterone has been shown to be the best supplement for the insufficient natural progesterone in these patients (not surprisingly), but synthetic progestins did not have a negative effect, but a positive one.

In short, the assertion that the LNG in Plan B acts as a competitive antagonist is not only not supported in the literature, there is a number of reasons see that the evidence shows it is highly unlikely.

I'll respond to Marie's other comments in a future post.

4 comments:

  1. If emergency contraception causes abortions, it has huge implications for our cause. Emergency contraception is as cheap as a dinner at Chili's, as easy to take as a Tylenol, and is as convenient as the nearest Walgreens. There's no doctor, no clinic, and not even a statically tally marking it as an abortion. It would mean that abortion is out of the hands of politicians, doctors, and the Supreme Court. It would mean we're barricading the barn door after the horses have already escaped.

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  2. "the amount of progesterone secreted by the corpus luteum after ovulation is far greater than that exogenous progestin absorbed by taking Plan B"

    Wow, and that is very significant because the progestin in Plan B is a much higher dose than BCPs would give.

    "In all studies, LNG has had no effect on pregnancies after implantation."

    For sure it would have to have some post-implantation effect if it really worked that way, and all studies for sure show that it doesn't work after implantation.

    "other progestins are used in order to treat luteal insufficiency"

    It is compelling that other progestins are effective at treating threatened miscarriage, and not just "minimally effective" as one of my Chinese herbalism teachers told us. But she was probably going by her "personal experience", which would be basically anecdote.

    I am not sure if it was my nursing teacher or herbalism teacher who put forth this "progestin narcan" theory, maybe more likely the herbalism teacher. Good to know that this isn't supported at all in the literature either. The herbalism teacher was very adamant about us learning how to direct patients to use progesterone cream for infertility/miscarriage/menopause. For infertility/miscarriage she recommended that we have the patient buy and use a saliva sample kit where the patient collects saliva samples over the period of one cycle and then send away the kit to a lab for analysis. But she said that nearly all women are estrogen dominant, and that it's very rare that a woman is estrogen deficient. She said this was directly because of environmental estrogens and BCP use. But it's probably pretty likely that women seeking treatment for infertility from a Chinese doctor would have a low progesterone condition causing this, and so it is likely that most of the test kit results she sees would show women with this specific imbalance.

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  3. http://lti-blog.blogspot.com/2008/06/does-thin-uterine-lining-support-pill.html

    This is the blog post that I needed to disprove "the pill kills" theory. Thanks!

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  4. Stellar post. Looking forward to reading the rest.

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