A
allhers
Guest
Here’s a couple of pages to check out from your own source.
polycarp.org/how_does_the_pill_work.htm
polycarp.org/postfert_oc.htm
- Status
polycarp.org/how_does_the_pill_work.htm
polycarp.org/postfert_oc.htm
L
Lady_D_I
Guest
Thank you allhers. I found the site a couple of years ago and have these saved already. Some of the information is not current (such as the info on the IUD and EC) but still good to keep.
I really have researched this subject. You should see my reference list but y’all wouldn’t be as giddy as I with all the studies… most people find reviewing medical literature boring but I enjoy reading and critiquing.
I’m exiting this thread, but I do enjoy a thoughtful discussion or debate regarding the significance of endometrial receptivity and would return for that (if it is a good discussion). Thanks everyone who participated!
Blessings!
A
allhers
Guest
Wow, all that and still you aren’t convinced, perhaps its just in the wording for you.
On a side note, have you seen Fr. Frank Pavone’s you tube video’s? You can set up an account for free and subscribe to his video’s.
www.youtube.com/watch?v=us_y9GP_-DA - Dismemberment D&E Procedure
www.youtube.com/watch?v=QBOAPleF1t0 - Suction Abortion Procedure
On a side note, have you seen Fr. Frank Pavone’s you tube video’s? You can set up an account for free and subscribe to his video’s.
www.youtube.com/watch?v=us_y9GP_-DA - Dismemberment D&E Procedure
www.youtube.com/watch?v=QBOAPleF1t0 - Suction Abortion Procedure
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Lady_D_I
Guest
Who me? If you are asking me, you and I aren’t communicating. What do you think I should be convinced of?
I heard Fr. Pavone speak in St. Louis last October. I spoke to him briefly. He is an awesome man! God bless Fr. Pavone!
As a nurse, I have seen abortions performed
. But, I thought this was a discussion about the pill.
T
Texas_Roofer
Guest
let me guess you and Ms Brown decide who the “culture of death” is? Did I get that right. As you and she cast your condemnation nets please remember the teaching of Jesus and the Church on the subject
That is interesting how people now are shown to sign different things
interesting reference however problematic, it is much closer to honest than other references used so far. Let look at what the problems are :
B) *Could you present the evidence that some physicians and researchers give to support their claim that the pill is indeed an abortifacient? *
Before presenting the evidence
notice both the word “evidence” not requiring conclusive standards, and the overwhelming uh inability to answer directly.
*** F) Is there a technical or quantitative way to measure how much thinner a woman’s endometrium becomes when she uses BCPs?***
Yes, in 1991 researchers in the US performed MRI scans (Magnetic Resonance Imaging) on the uteri of women, some of whom were taking BCPs and some of whom were not 8. The BCP users had endometrial linings that were almost two millimeters thinner than that of the nonusers. Although this may sound like a small difference, it represented a 57% reduction in the thickness of the endometrial lining in women who used BCPs in this study.
Sounds good but is it true? read here acubalance.ca/node/508 and if you need more read this clinicalanswers.nhs.uk/index.cfm?question=6384 do you see the problem if 2 is a 57% reduction then lining have to be below 4 mm as at 4 a 50% reduction is 2 mm. Yet the others claim even postmenopausal women have liners over 5, so who is correct?
These videos did not address the pill
Sorry the post is a bit complex, however the fact is the parsing is a game to make statements which are exaggerations rather than simply tell the truth.
I still remain curious are you or Ms Brown going to declare female athletes as abortionists, abortion promoters, or parse them out of your net? (minor references
ivf.com/amenath.html
thinkmuscle.com/articles/volk/menstrual-cycle.htm
mesomorphosis.com/articles/volk/female-athletes-and-menstrual-irregularities.htm
T
Texas_Roofer
Guest
Thank you Mary Catherine the statement is clearly made however it is not proven.
A
allhers
Guest
I’ll end my time in this thread for now since we don’t seem to be getting across to one another.
I loved our Holy Father’s words today:
He called the Mass “a summons to move forward with firm resolve to use wisely the blessings of freedom, in order to build a future of hope for coming generations.”
And he repeated a core message of his six-day pilgrimage — that faith must play a role in public life, citing the need to oppose abortion.
The unwavering truth of the Roman Catholic message, he said, guarantees respect for the dignity of all “including the most defenseless of all human beings, the unborn child in the mother’s womb.”
I don’t see where that is happening here, so good-bye for now.
I’ll pray for you all who can’t seem to see clearly.
I loved our Holy Father’s words today:
He called the Mass “a summons to move forward with firm resolve to use wisely the blessings of freedom, in order to build a future of hope for coming generations.”
And he repeated a core message of his six-day pilgrimage — that faith must play a role in public life, citing the need to oppose abortion.
The unwavering truth of the Roman Catholic message, he said, guarantees respect for the dignity of all “including the most defenseless of all human beings, the unborn child in the mother’s womb.”
I don’t see where that is happening here, so good-bye for now.
I’ll pray for you all who can’t seem to see clearly.
M
MaryCatherine08
Guest
I am not sure what proof you would be looking for. Clinical studies maybe? How many babies were killed due to lack of implantation out of a few thousand pregnancies? For obvious reasons, that would be near impossible to do a major research study on. Which I think is why the drug manufacturer makes the statement.
But why would we even need proof if the chance is there? Which clearly it is.
L
Lady_D_I
Guest
Allhers,
Why do you not answer questions? Perhaps something productive would have come from this.
You are not going to convince people who are asking for evidence with what you’ve provided here.
In reply to one of your posts regarding the abortifacient effect, Texas Roofer replied “not a single documented case not one, not ever”. You asked him for sources to support his statement. You have been given sources.
Then, you began with these statements “what makes you think that you are supporting the Catholic Church’s position when clearly you aren’t” and “*t seems to me that if you were a faithful Catholic who did know the Cathechism that you would realize that ALL (American Life League) is faithful and clearly knows what they are talking about in spite of what others think”. If a person doesn’t believe, based on the available evidence, the pill is an abortifacient or potential abortifacient, how is this not supporting the Church’s position? Based on the available evidence, what if a person is convinced the pill never has and never will prevent implantation? *
After the direct evidence issue was http://bestsmileys.com/oneofakind/1.gif(thanks Newbe
), I offered to discuss the indirect evidence. I asked Based on the evidence you reviewed, what study or studies on endometrial receptivity convinced you the pill related changes prevent implantation? How do these changes demonstrate the pill is a “known abortifacient”? How do you know these changes have killed a baby? I am asking for studies that include study design, results, limitations, etc.
What about ovulatory pill cycles? Has anyone reviewed a study to answer this? “In a menstrual cycle on the “pill” in which ovulation occurs, what is the histology of the endometrium six days after ovulation (the time of implantation)? Certainly the hormone milieu and endometrial histology will be different from a menstrual cycle on the “pill” in which ovulation does not occur (i.e.,the typical atrophic, or “hostile,” endometrium). Source”
No response. I can support why I believe the pill may be an abortifacient. I can’t prove with direct evidence it is one, but I can state my case why I believe it is a potential or probable abortifacient. I can cite studies. Based on your posts, it seems you are convinced the pill is an abortifacient and has killed babies. I’ve asked you to support this with scientific studies studies that include study design, results, limitations, etc. You haven’t done that. Maybe you can’t… that is ok. Maybe medical evidence is not something you read and use (that is ok too), but that is what is requested when discussing evidence.
No one here has advocated the use of contraception. No one has advocated abortion.
Why do you not answer questions? Perhaps something productive would have come from this.
You are not going to convince people who are asking for evidence with what you’ve provided here.In reply to one of your posts regarding the abortifacient effect, Texas Roofer replied “not a single documented case not one, not ever”. You asked him for sources to support his statement. You have been given sources.
Then, you began with these statements “what makes you think that you are supporting the Catholic Church’s position when clearly you aren’t” and “*t seems to me that if you were a faithful Catholic who did know the Cathechism that you would realize that ALL (American Life League) is faithful and clearly knows what they are talking about in spite of what others think”. If a person doesn’t believe, based on the available evidence, the pill is an abortifacient or potential abortifacient, how is this not supporting the Church’s position? Based on the available evidence, what if a person is convinced the pill never has and never will prevent implantation? *
After the direct evidence issue was http://bestsmileys.com/oneofakind/1.gif(thanks Newbe
), I offered to discuss the indirect evidence. I asked Based on the evidence you reviewed, what study or studies on endometrial receptivity convinced you the pill related changes prevent implantation? How do these changes demonstrate the pill is a “known abortifacient”? How do you know these changes have killed a baby? I am asking for studies that include study design, results, limitations, etc.What about ovulatory pill cycles? Has anyone reviewed a study to answer this? “In a menstrual cycle on the “pill” in which ovulation occurs, what is the histology of the endometrium six days after ovulation (the time of implantation)? Certainly the hormone milieu and endometrial histology will be different from a menstrual cycle on the “pill” in which ovulation does not occur (i.e.,the typical atrophic, or “hostile,” endometrium). Source”
No response. I can support why I believe the pill may be an abortifacient. I can’t prove with direct evidence it is one, but I can state my case why I believe it is a potential or probable abortifacient. I can cite studies. Based on your posts, it seems you are convinced the pill is an abortifacient and has killed babies. I’ve asked you to support this with scientific studies studies that include study design, results, limitations, etc. You haven’t done that. Maybe you can’t… that is ok. Maybe medical evidence is not something you read and use (that is ok too), but that is what is requested when discussing evidence.
No one here has advocated the use of contraception. No one has advocated abortion.
L
Lady_D_I
Guest
Thank you Mary Catherine. This provides an opportunity to clarify my position.
We err on the side of life. I can’t prove the pill IS an abortifacient with the available evidence, but no one can prove it isn’t. There is evidence it may be an abortifacient based on our current understanding of reproduction.
T
Texas_Roofer
Guest
would this not mean these statements never were supported? Maybe less babies were killed?
There is a chance of everything, everywhere, everyday this is a standard were do not use unless we are hunting for an excuse to follow our desires! Just as others rationalize their desires whatever they may be, this issue is the same.
L
Lady_D_I
Guest
Could you elaborate on this statement?
If not, that is ok.
L
Lady_D_I
Guest
I’ve been reading the through the links you posted Texas Roofer. This is what I read.
HOW DO THE PILL AND OTHER CONTRACEPTIVES WORK? states the endometrial linings were almost 2 mm thinner. Nonusers had a 3.22 mm + or – 0.99 and users had a 1.36 mm + or – 0.41. (Source) This is a difference of ~ 1.86. BTW, “[t]he normal endometrial thickness varies with the menstrual cycle, and ranges on MRI from 1-3 mm during the early proliferative phase to 5-7 mm during the mid-secretory phase” (Source)
Clinical Answers reports this:
“Transvaginal ultrasound: After the menopause, or during ovulatory suppression, (e.g. oral contraceptive usage), the endometrium is inactive, and is seen as a thin layer of under 5 mm in thickness".
According to Accubalance,
“[e]ndometrial thickness between 6mm-14mm is ideal. Pregnancies do occur when the endometrial thickness is < 6mm or >14mm but it seems not as often”. I read this to mean the thining of the endometrium reduces the likelihood of implantation … but it is not impossible. IMO, the pill’s pescribing information is stating the changes in the endomterium reduce the likelihood of implantation, which is not claiming implantation is impossible.
The study referened by Dr. Taylor found “a marginally significant trend toward decreasing rates of spontaneous pregnancy loss with increasing endometrial thickness". So, rates of implantation increase with increasing endometrial thickness.
The normal ranges are different for ultrasound, which was used in the postmenopausal women. I would like you to elaborate on the significance of the findings in postmenopausal women. What is the correlation in your opinion? BTW, an endometrium >5mm in postmenopausal women may be abnormal. “The reported normal range for this bilayer endometrial thickness is up to 5 mm in asymptomatic postmenopausal women not receiving hormones and up to 8 mm in asymptomatic postmenopausal women on HRT. (Source)
Just want to add that endometrial thickness is not the only factor in endometrial receptivity AND there is much to learn.
HOW DO THE PILL AND OTHER CONTRACEPTIVES WORK? states the endometrial linings were almost 2 mm thinner. Nonusers had a 3.22 mm + or – 0.99 and users had a 1.36 mm + or – 0.41. (Source) This is a difference of ~ 1.86. BTW, “[t]he normal endometrial thickness varies with the menstrual cycle, and ranges on MRI from 1-3 mm during the early proliferative phase to 5-7 mm during the mid-secretory phase” (Source)
Clinical Answers reports this:
“Transvaginal ultrasound: After the menopause, or during ovulatory suppression, (e.g. oral contraceptive usage), the endometrium is inactive, and is seen as a thin layer of under 5 mm in thickness".
According to Accubalance,
“[e]ndometrial thickness between 6mm-14mm is ideal. Pregnancies do occur when the endometrial thickness is < 6mm or >14mm but it seems not as often”. I read this to mean the thining of the endometrium reduces the likelihood of implantation … but it is not impossible. IMO, the pill’s pescribing information is stating the changes in the endomterium reduce the likelihood of implantation, which is not claiming implantation is impossible.
The study referened by Dr. Taylor found “a marginally significant trend toward decreasing rates of spontaneous pregnancy loss with increasing endometrial thickness". So, rates of implantation increase with increasing endometrial thickness.
The normal ranges are different for ultrasound, which was used in the postmenopausal women. I would like you to elaborate on the significance of the findings in postmenopausal women. What is the correlation in your opinion? BTW, an endometrium >5mm in postmenopausal women may be abnormal. “The reported normal range for this bilayer endometrial thickness is up to 5 mm in asymptomatic postmenopausal women not receiving hormones and up to 8 mm in asymptomatic postmenopausal women on HRT. (Source)
Just want to add that endometrial thickness is not the only factor in endometrial receptivity AND there is much to learn.
T
Texas_Roofer
Guest
Yes pretty much, I was reorganizing this when you posted
From polycarp.org/how_does_the_pill_work.htm
*F) Is there a technical or quantitative way to measure how much thinner a woman’s endometrium becomes when she uses BCPs?
Yes, in 1991 researchers in the US performed MRI scans (Magnetic Resonance Imaging) on the uteri of women, some of whom were taking BCPs and some of whom were not 8. The BCP users had endometrial linings that were almost** two millimeters thinner **than that of the nonusers. Although this may sound like a small difference, it represented a **57% *reduction in the thickness of the endometrial lining in women who used BCPs in this study.
But from acubalance.ca/node/508*
In general, as endometrial thickness after IVF stimulation increases so does pregnancy rate. Endometrial thickness between 6mm-14mm is ideal. Pregnancies do occur when the endometrial thickness is** < 6mm or >14mm **but it seems not as often. To this end, we sometimes cancel/postpone/modify treatment if the endometrial thickness is outside this range………*. - Dr. Beth Taylor
She further references :
Richter KS, Bugge KR, Bromer JG, Levy MJ Rellationship between endometrial thickness and embryo implantation, based on 1,294 cycles of in vitro fertilization with transfer of two blastocyst-stage embryos. Fertil Steril. 2007 Jan;87(1):53-9…
Additionally on this site and several others you will see verses versions of statements that linings under 6mm are associated with pregnancy problems. Similarly often cited is a minimum thickness of 7.5mm before IVF procedures are recommended
From clinicalanswers.nhs.uk/index.cfm?question=6384*
The reported normal range for this bilayer endometrial thickness is up to 5 mm in asymptomatic postmenopausal women*
So in summary is the reported change of under 2mm a 57% reduction? Probably not because giving an extremely generous attempt to model that let’s use 1.9mm change and go backwards to achieve a 57% reduction that number is 4.4mm. So 4.4 mm the normal thickness of a lining? Is it reduced by 1.9 mm a 57% to 2.5 mm? no, study after study, doctor after doctor report much thicker linings. According to various doctors some linings may be too thick and thus could benefit from medicines which reduce the lining thickness. In summary the objective is to show studies and doctors are not in agreement on many supporting facts, and thus conclusions are not really available.
hope that helps
From polycarp.org/how_does_the_pill_work.htm
*F) Is there a technical or quantitative way to measure how much thinner a woman’s endometrium becomes when she uses BCPs?
Yes, in 1991 researchers in the US performed MRI scans (Magnetic Resonance Imaging) on the uteri of women, some of whom were taking BCPs and some of whom were not 8. The BCP users had endometrial linings that were almost** two millimeters thinner **than that of the nonusers. Although this may sound like a small difference, it represented a **57% *reduction in the thickness of the endometrial lining in women who used BCPs in this study.
But from acubalance.ca/node/508*
In general, as endometrial thickness after IVF stimulation increases so does pregnancy rate. Endometrial thickness between 6mm-14mm is ideal. Pregnancies do occur when the endometrial thickness is** < 6mm or >14mm **but it seems not as often. To this end, we sometimes cancel/postpone/modify treatment if the endometrial thickness is outside this range………*. - Dr. Beth Taylor
She further references :
Richter KS, Bugge KR, Bromer JG, Levy MJ Rellationship between endometrial thickness and embryo implantation, based on 1,294 cycles of in vitro fertilization with transfer of two blastocyst-stage embryos. Fertil Steril. 2007 Jan;87(1):53-9…
Additionally on this site and several others you will see verses versions of statements that linings under 6mm are associated with pregnancy problems. Similarly often cited is a minimum thickness of 7.5mm before IVF procedures are recommended
From clinicalanswers.nhs.uk/index.cfm?question=6384*
The reported normal range for this bilayer endometrial thickness is up to 5 mm in asymptomatic postmenopausal women*
So in summary is the reported change of under 2mm a 57% reduction? Probably not because giving an extremely generous attempt to model that let’s use 1.9mm change and go backwards to achieve a 57% reduction that number is 4.4mm. So 4.4 mm the normal thickness of a lining? Is it reduced by 1.9 mm a 57% to 2.5 mm? no, study after study, doctor after doctor report much thicker linings. According to various doctors some linings may be too thick and thus could benefit from medicines which reduce the lining thickness. In summary the objective is to show studies and doctors are not in agreement on many supporting facts, and thus conclusions are not really available.
hope that helps
L
Lady_D_I
Guest
FIrst, thank you for replying to my questions. I do appreciate it!
Forgive me I"m repeating myself… I read this to mean the thining of the endometrium reduces the likelihood of implantation … but it is not impossible. IMO, the pill’s pescribing information is stating the changes in the endomterium reduce the likelihood of implantation, which is not claiming implantation is impossible.
*
Nonusers had a 3.22 mm + or – 0.99 and users had a 1.36 mm + or – 0.41. (Source) This is a difference of ~ 1.86 (almost 2mm). Doesn’t this reflect almost a 57% reduction? Or is my math off? (which is highly possible)
Oh, MRI was used to measure endometrial thickness in the study showing the 57% reduction. “The normal endometrial thickness varies with the menstrual cycle, and ranges on MRI from 1-3 mm during the early proliferative phase to 5-7 mm during the mid-secretory phase” (Source)
"Pregnancies do occur when the endometrial thickness is < 6mm or >14mm but it seems not as often***".
Forgive me I"m repeating myself… I read this to mean the thining of the endometrium reduces the likelihood of implantation … but it is not impossible. IMO, the pill’s pescribing information is stating the changes in the endomterium reduce the likelihood of implantation, which is not claiming implantation is impossible.
*
I referenced the study abstract here: “[t]he study referened by Dr. Taylor found “a marginally significant trend toward decreasing rates of spontaneous pregnancy loss with increasing endometrial thickness”. So, rates of implantation increase with increasing endometrial thickness.
I’m missing your point. I’m sorry.
I’m not sure how the endomteriums of postmenopausal women correlates to the endometriums of reproductive age women. In addition, endomterial thickness is one factor in endometrial receptivity. What about the other measurements of endometrial receptivity in the postmenopausal group? That is why I don’t see a correlation.
I linked the study. These are the numbers:
Nonusers had a 3.22 mm + or – 0.99 and users had a 1.36 mm + or – 0.41. (Source) This is a difference of ~ 1.86 (almost 2mm). Doesn’t this reflect almost a 57% reduction? Or is my math off? (which is highly possible)
Oh, MRI was used to measure endometrial thickness in the study showing the 57% reduction. “The normal endometrial thickness varies with the menstrual cycle, and ranges on MRI from 1-3 mm during the early proliferative phase to 5-7 mm during the mid-secretory phase” (Source)
T
Texas_Roofer
Guest
You did well
There are many issues: to include it would seem likely measurement nor reporting are standardized. Notice the reference reports a 3.32mm for non users while those numbers do not fit data by others. Additionally they show about 35% std deviation. General 6 std deviation are considered the general range so that 0-105% above listed average. The study you reference does show a 57% reduction in their measurement in one column. Please notice that is one set of measurements 7 women in total. I am not out to disparage the report. The issue is the numbers on this subject is all over the place so all we know is we do not know, at least yet.
There are many issues: to include it would seem likely measurement nor reporting are standardized. Notice the reference reports a 3.32mm for non users while those numbers do not fit data by others. Additionally they show about 35% std deviation. General 6 std deviation are considered the general range so that 0-105% above listed average. The study you reference does show a 57% reduction in their measurement in one column. Please notice that is one set of measurements 7 women in total. I am not out to disparage the report. The issue is the numbers on this subject is all over the place so all we know is we do not know, at least yet.
L
Lady_D_I
Guest
Thank you!
I am assuming the 3.22 mm is late luteal, when the endometrium begins to breakdown, and may be one explanation for the difference in measurement. The first column is the measurement of the endometrium. The other columns are junctional zone & the myometerium (musle layer). This is a small sample; however, the changes in the edometrium of pill users are documented in the medical literature.
I’m not sure what numbers you mean (so I may change my opinion), but to me it seems the findings are consistent and consistently the research shows implantation rates decrease with thinning of the endometrium. I would really like to see a study on the endometrium in ovulatory pill cycles. :yup:
Just a thought… some of the differences in the measurements could be related to the technology. Ultrasound tech is improving. It will be interesting to see what 3D u/s shows.
I know you are taking a critical look at the information. I appreciate and respect that.
Thank you again for the discussion.
- Status