On the Road Again!

DH and I have not been traveling for pleasure as much as we normally have in the past – another lifestyle change FOR SURE.  I am a travel advisor, after all – being on the road in far flung places is my jam!  But not now, not when we are worried about my cycle and ovulatory times and doctors appointments and blood draws.

However, Wednesday we are happily headed to San Francisco for a few days!  We’ll be driving through Napa over the weekend.  I am curious to see the damage from the 6.0 earthquake.  So glad that so few people were severely injured.  From there, we go on to north Tahoe, then Deer Valley, then Livingston MT and finally Jackson Hole.  Who knows, we may have to bop down to Denver at the end of the trip for our ODWU.  It all depends on my cycle.  Doesn’t it always?  Sheesh.

I will be posting from the road – and it will feel more like a travelog in lieu of a trip through infertility.  But again, it is both.  In our case, as we sadly have no living children, we are “free to move about the country” and even further afield with a fair amount of ease.  Trust me, I look forward to the day when I can say, “Whew – so many kids, I really need a getaway but I can’t do it!”

The age of 40, that magical, arbitrary age when your egg quality seems to go from bad to really bad, never seemed to bother me.  Now it is a dreaded specter on the horizon.  But I won’t think about it now.  I will simply pack my scary large supplement regime, hope I don’t get stopped by the TSA, and enjoy our 5 year anniversary and a fantastic family wedding.

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More About MTHFR

MTHFR – are you tired of reading about it yet? I am tired of having to think about it, and more importantly, I am tired of doctors pooh-poohing my hetero status.  If you are a doctor and you are reading this (which I am sure you are not because you are too busy reading marketing material from Big Pharma about the latest and greatest way to poison the population), listen up: MTHFR IS REAL, it may effect your patients in ways you may not yet know or understand.  OR it may not.  Be open to the possibility.

Dr. Ben, who I have mentioned before, has a great basic protocol for C677T hetero and homo individuals.

The biggest differences in recommendations between these two types of mutations are:

  1. folic acid needs to be avoided more seriously by homozygous individuals
  2. the amount of methylfolate required for homozygous mutations is greater
  3. the blood thinning requirement is greater for homozygous individuals

Here are the common recommendations for supporting those with C677T MTHFR mutations:

  1. Limit ingestion of folic acid in fortified foods as you cannot process folic acid well. – Done
  2. Limit or cease taking supplements or drugs with folic acid in them. Talk with your doctor before stopping. – Done
  3. Avoid folic acid blocking drugs such as birth control or Methotrexate. – Um, not relevant to me at this time. If I have to down-regulate with BCP before IVF I will discuss with doctors.
  4. Avoid drugs which increase homocysteine such as Nitrous Oxide (most used in dentistry) – LOL
  5. Avoid antacids as they block absorption of vitamin B12 and other nutrients – Oy! Catch you later, Zantac!
  6. Begin understanding which of your symptoms may be related to the C677T MTHFR mutation.
  7. Measure homocysteine levels – properly!
  8. Inform your family members so they can also test for the MTHFR mutation – I am pretty certain MTHFR is on both sides of my family.  No one has tested yet.
  9. Find a doctor who is knowledgeable about MTHFR or is willing to learn
  10. If you are pregnant, find an OB/GYN or midwife who is knowledgeable about MTHFR.
  11. Eliminate Gluten from your diet – especially wheat. – Why is this? Is it because all conventional wheat products are fortified? I do not believe that I have a gluten sensitivity, but I am open to discussing this.
  12. Eliminate or reduce dairy from your diet. If you must have dairy, use goat milk. – um, I only have dairy in my coffee which will soon go away, and the occasional cheese in a salad, which is typically goat. This isn’t too hard.
  13. Sauna or sweat somehow (epsom salt baths, sports, yoga..) at least once to three times a week. – Love this!
  14. Limit intake of processed foods – Been doing this for years to the best of my ability, but sometimes, I just have to have a Canada Dry ginger ale, and it kills me that it is made with high fructose corn syrup.  Might as well be made with Round Up! directly into the drink.  Bleh....
  15. Increase intake of whole foods and home-prepared meals. – Difficult with travel and a DH who LOVES to eat out.
  16. Eat the Rainbow of colors from fruits and vegetables – daily
  17. Castor Oil Packs over your abdomen daily during times of pain, soreness, cramps – ???
  18. Vegetable/Fruit Juice Diet with Chia Seeds during times of pain, soreness, cramps
  19. Limit intake of high methionine-containing foods if homocysteine elevated
  20. Coffee Enemas during times of detoxification or pain – no.
  21. Filter chlorine from your drinking water, shower and bath. – sigh, really?
  22. Drink at least two liters of filtered water daily mixed with vitamin C and electrolytes.
  23. Eat smaller, but more frequent meals, throughout the day with some form of protein.
  24. Limit protein intake to approximately 0.7 grams protein per kilogram of body weight.
  25. Remove mercury amalgams and root canals with a trained biological dentist.
  26. Avoid cooking, drinking, storing and heating in any type of plastic container. – done, gross
  27. Use an air purifier in your home and office
  28. Eliminate carpets from your home and install low VOC wood or tile flooring.
  29. Eat grass-fed beef, free range, hormone free and antibiotic meats and eggs – done
  30. Cook with electric stove and oven and remove gas stove and oven. – Never, and I mean, never going to happen.

//end of my discussion of MTHFR for the foreseeable future

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Supplements upon Supplements – Everything else…

Back in the day, I’d be poppin’ bottles not poppin’ supplements.  Out with the old, in with the new.  I really do miss champagne.  Krug, Veuve, Tattinger – I lived in France for a number of years and love the way the French toast to pretty much everything (a new baby, an engagement, 6pm, Thursdays) with champagne.

Long before I had thought about IVF or even before I suspected diminished ovarian reserve (DOR) – which, by the way, is only inferred due to my low AMH number (oh, and all of those miscarriages) – I had started a very serious supplementation regimen.  I guess it started when I was trying to get more breast milk when pumping for Nash, so I was on domperidone, blessed thistle, fenugreek seed, vitamin D3, vitamin C, DHA and others.  In fact, I will do a post on DHA after this.  I owe a big thank you to two people who got me started with DHA just a few days after Nash was born and I attribute his fast healing IVH (intraventricular hemorrage), grade III and grade IV which are considered the most serious, to the DHA supplementation.

Before I start my list, I must mention that I am not a doctor, and this is not advice.  Please do research and discuss with your physician before starting an extensive supplement regimen. For my suspected ovarian quality and quantity issue I take the following (and the brands are listed on my supplements page), reasoning below:

MORNING:

25mg DHEA (to be discussed), 2 caps DHA/EPA, 200mg CoQ10 Ubiquinol, 1000mg l-arginine, 2mg myo-inositol, 1000mg vitamin C, 5000iu vitamin D3, 200mg freeze dried açai powder capsules

NOON:

25mg DHEA, 200mg CoQ10 Ubiquinol, 400iu vitamin E, 100mg pycnogenol, 100mg freeze dried açai powder capsules

NIGHT:

25mg DHEA, 200mg CoQ10 Ubiquinol, 2 caps DHA/EPA, 3mg melatonin, 2mg myo-inositol, prenatals, low dose aspirin, 4mg 2mg methylfolate, 5000mg active B12, 100mg freeze dried açai powder capsules

At the end of the day, this is all snake oil and magic beans until you get your take home baby.  With science, results must be replicated before they can be considered a “rule”.  Any woman will tell you that their cycles differ month to month, each pregnancy is different, so many functions are in flux at any one time, that it is difficult to know what will work for one woman from month to month, let alone *many* women at any given moment in their fertility journey.  These links are the best I could find to justify my supplement choices.


 

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Supplements upon Supplements – MTHFR edition

This is a big lifestyle change: pill popping.  When I fell pregnant with Nash, I was caught with my pants down, so to speak!  The only thing I was taking at the time was copious amounts of wine and coffee.  DH and I were off of red meat, and that left plenty of room for more wine.

I had to rush out and buy prenatals and folic acid.  I took A LOT of folic acid – to the tune of an additional 800ug (micrograms) per day on top of the recommended 400ug already found in the prenatals I was taking.  Little did I know, as a heterozygous carrier of MTHFR C677T folic acid is toxic to me.  There is some debate as to how much folic an MTHFRer can process, certain sources say a hetero carrier can absorb 60% of folic acid (in the synthetic form, not from natural foods, natural foods are easiest to absorb), others say 35-40%, and this Dr. Ben guy says zero.

In fact, this simple gene polymorphism is found in almost 50% of the American population, but we only just “discovered” it in 1998.  Since 1998, folic acid fortification has been mandatory in our foods.  Good luck finding ANYTHING in the grocery store made with wheat flour that is not fortified. I’ve spent a small fortune at Whole Foods doing my best to avoid folic acid fortification.  I do however take L-5-Methylfolate (see below), and that is how I get the much needed folate, which is the natural form of “folic acid” – which, let me repeat, is SYNTHETIC folate.

{…could this be the source of the rise in gluten intolerance that was not seen in prior to recent years? … most wheat products have folic fortification AND gluten…}

Thanks to the March of Dimes, we know that folic acid supplementation in women of child bearing age helps limit gestational developmental problems like neural tube defects.  What has NOT been widely disseminated are these other interesting items: MTHFR polymorphisms (those carriers who have synthetic folic acid to folate conversion dysfunction) have been linked to autism spectrum disorders, psychiatric disorders, congenital heart defects (like Nash), pulmonary hypertension with heart defects/disease, and on and on.  With regard to ASDs, I would suspect that infants who developed in utero with highly enriched, folinated environments who then are born and either do not get breast milk or when they are weaned from enriched breast milk (from mom who is still taking folic/folate), then the lack of supplementation might cause a disruption.  There is a lot of research happening around this right now.  This is just a small sampling:

The point is: we are still learning about MTHFR, folate metabolism and how it effects our fertility and other functions.  I will say, in late February of this year I switched from a B-100 complex with folic acid to a 5-MTHF methylfolate and my energy went through the roof.  I had been heavily supplementing with something that was super toxic to my system.

MTHFR folks do tend to have elevated homocysteine and that in turn raises the risk for blood clots.  Pregnant women are also more prone to blood clots, which is a greater risk when you have elevated homocysteine levels.  But MTHFR researcher, Dr. Ben Lynch, says it isn’t enough to look at homocysteine levels when dealing with pregnancy complications and loss. My homocysteine levels are perfect – and here I sit with a very thick medical record jacket and a very complicated obstetrical history.

Andrea, at MTHFRLiving, writes the following:

It is important to remember that MTHFR gene mutations are inherited. Therefore, depending on what mutations are present in the mother and father, the fetus is likely to inherit MTHFR in some form. The baby can inherit problems in its own DNA, which present symptoms, and can also suffer from the nutritional deficiencies of the mother that are caused by her gene mutations. The most common problem is the risk of neural tube defects because of the mother’s inability to convert folic acid into l-methylfolate. Before I was aware of MTHFR, I was ingesting copious amounts of folic acid. This just blocks a person with MTHFR’s ability to absorb and assimilate natural folate and methylfolate. It is a major failing of current widespread prenatal advice that more women are not aware of the problems of folic acid for so many members of the population. A lack of folate and/or B12 can cause everything from spina bifida to anencephaly to Down’s Syndrome. Elevated homocysteine can cause low birth weight and premature birth.

There are also additional risks once the baby is born, which makes testing for methylation gene defects important. MTHFR has been linked to congenital heart disease, autism, ADD/ADHD and a host of other illnesses. As Dr. Kendal Stewart reminds us, it’s possible to use epigenetics to bypass the harmful effects of these mutations in your child, but only if you know which mutations he has. Ensuring proper methylation in a baby will prevent impaired immunity and virus and heavy metal accumulation from birth. This is an essential component to preventing autism and other serious health conditions.

I take 4mg – that’s right, FOUR MILLIGRAMS – of 5-MTHF-methylfolate with 5000ug of active B12 containing methylcobalamin and adenosylcobalamin for better absorption.  Folgard, which is commonly and mistakenly prescribed to MTHFR gals, has 2.2mg of folic acid, and I am essentially doubling that intake.  I may cut my dose in half and see how I do.  Since we are not TTC-ing this month I do not see any harm in it, AND I have been on 4mg for at least 2 miscarriages, so this clearly is not the key to my infertility.

Lovenox becomes a natural part of this discussion, but is beyond the scope of this post.  I will discuss it in future posts, so if you are interested just click on the *lovenox* tag to the right and you should see all associated posts as I publish more.

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A Little Bit About Asherman’s Syndrome

Asherman’s Syndrome.  Have you heard of it? I had not, until I started Googling “no period after D&C”. I am so glad I did.

After Nash was born, his placenta did not pass, so I needed a D&C to remove the placenta. Now, the doctor on call that night would argue that she could have pulled it out.  But after all I had just been through, that fact that she was wrist deep into my vagina really rubbed me the wrong way (no pun!) and I grabbed her arm and said, “No. More.” She protested for like a nano-second.  Apparently, even after tragedy, my patented withering glare remained intact.

After losing our identical twins at 6 and 7 weeks, I was not quite up to miscarrying naturally.  Doctors offered me a D&C again, so I said, “sure”.  It went really smoothly and I respect my doctor.  I know she did a good job, but with two procedures within 8 months of each other paired with my scar overgrowth problem (I scar easily and create just a little extra scar tissue) it was a recipe for trouble.

I expected my cycle to return 4-5 weeks later.  When it didn’t, but I had cyclical pain, I thought, well, next month will be the month.  My husband and I were in New Orleans the following month – I’ll never forget it.  Again, the cyclical pain came and this time worse.  Pressure plus cramps.  And no blood.  I had been tracking my cervical mucus, and I had figured I had ovulated, but why no menses?  I stayed up all night searching for answers with Dr. Google.  I searched with terms like: cyclical pain no menses, no period after D&C, problems after D&C. What I learned was terrifying.

Asherman’s Syndrome, also know as adhesions or scarring, is an acquired uterine condition, characterized by the formation of scar tissue inside the uterus and/or the cervix. In many cases the front and back walls of the uterus stick to one another. I feel so lucky that this was not my situation.  However, at the time, I had no idea what my condition was.

In other cases, adhesions only occur in a small portion of the uterus or cervix – and this latter case was mine. The extent of the adhesions defines whether the case is mild, moderate, or severe. They are usually not vascular, which is an important when it comes to treatment.  Many, many women have scarring MUCH worse than I did.  However, in my case, with the cervix scarred shut I was at risk for retrograde menses that cause endometriosis and all kinds of other problems.  Again, I did not know this to be the case until after my appointments with Dr. Isaacson at Newton-Wellesley.

Most patients with Asherman’s Syndrome have really light or absent periods, but some have normal periods. Some patients have no periods but feel pain at the time that their period would normally arrive each month, as I did. This pain may indicate that menstruation is occurring but the blood cannot exit the uterus because the cervix is blocked by adhesions. I can’t tell you how strange a feeling it was.  It was a slightly painful pressure that felt like I needed to push or squeeze to release the bloating feeling.  Recurrent miscarriage and infertility could also be symptoms.

It was through the Yahoo Group that I found Dr. Isaacson.  He is what they call an “A-Lister”, which is to say he not only has some of the best outcomes, but uses the gold-standard of treatment: micro-scissors.  Let me say, it is not a very comfortable procedure.  As I had minimal scarring, the procedure was done in his office, and I was awake. And I got to watch the whole procedure on the big screen!

Have you had a D&C and did your cycle never return OR not return in a way that you feel it should have?  Asherman’s Syndrome is NOT AS RARE as doctors let on, mostly because they perhaps feel that implicates their work.  And sometimes it does!  And sometimes it does not.  But, in lieu of a D&C, I strongly recommend Cytotec and passing the POC yourself unless you are very concerned about testing.  If you suspect you may have Asherman’s, I urge you to seek consultation with one of the doctors recommended in the Yahoo group.  Run, DO NOT WALK, to the very best doctor you can get to.  DO NOT let doctors use lasers, or any other method of lysing the adhesions other than micro-scissors.  Your fertility hangs in the balance.

Dr. Isaacson’s office is at the Newton Wellesley hospital, so not at all in Boston proper.  However, it is about a 20 minute commute on the train.  I stayed in central Boston both times (in the Back Bay area, once at the Hilton and once at the Ritz Carlton – don’t judge, I am a travel advisor and do a lot of biz with RC, so naturally I would stay with a partner property) and commuted out on the Green Line.  Each time was a one night stay, with the earliest appointment possible so I could catch the last flight out of Boston bound for Nashville if things ran over.

Resources:

Ashermans.org, Yahoo Support Group, Asherman’s Syndrome Awareness and Support

 

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Research: It goes with everything this season

I feel like ever since Nash was born, all I do is lean on my scientific background (B.S. Evolution, Ecology and Organismal Biology – focus on microbiology) to learn as much as possible about whichever current Hell I am living through.

With Nash’s pulmonary hypertension, I was constantly worried, studying Nitric, Sildenafil, Iloprost, outcomes, developmental delays, etc.

With regard to my endocrine picture, I have had a field day doing deep dives into supposed diminished ovarian reserve (DOR).  With a normal CD3 FSH of 4.4 but an abnormally low AMH of 0.49 for my age, I have freaked out about what could possibly be wrong with my eggs and how to improve potential response with IVF.  Yet, I get pregnant all of the time.  The uterus over here is clearly not very choosy.

My best guess is that Dr. Schoolie at CCRM will put me on Protocol 6 (EPP or estrogen priming protocol) when I cycle there.  The normal FSH is throwing me, because EPP is kind of the bazooka.  My antral follicle count is an incomplete picture at this point.  Dr. W at NFC only saw 4 on my right ovary but could not find my left ovary at all, which is a total cop out.  My left is slightly bigger and does all the ovulation.  On my Femara cycle there were 3 decent sized follies maturing on the left, so I am guessing my AFC is closer to 8.  Not stellar.

Happily, a brilliant and *organized* Calcotje has collected all of the links in one place:

Poor Responder Links
  1. Ovarian volume and antral follicle count for the prediction of low and hyper responders with in vitro fertilization.pdf 
  2. Pretreatment with transdermal testosterone may improve ovarian response to gonadotrophins in poor-responder IVF patients with normal basal concentrations of FSH
  3. Ovarian Stimulation for IVF in Low Responders Microflare Protocol Using Microdose Lupron (“short” protocol)
  4. Antagonist/letrozole protocol in poor ovarian responders for intracytoplasmic sperm injection: a comparative study with the microdose flare-up protocol
  5. http://www.fertilityfriends.co.uk/forum/index.php?topic=230320.40
  6. http://www.fertilityfriends.co.uk/forum/index.php?topic=230320.0
  7. Flexible GnRH antagonist versus flare-up GnRH agonist protocol in poor responders treated by IVF: a randomized controlled trial 
  8. Adjuvant L-arginine treatment in controlled ovarian hyperstimulation: a double-blind, randomized study
  9. Gonadotropin-releasing hormone agonist/antagonist conversion with estrogen priming in low responders with prior in vitro fertilization failure
  10. Docs Assess Three Therapy Approaches for Poor IVF Responders 
  11. http://www.ivf-indiana.com/education/why-does-ivf-fail/stimulation-protocols.html
  12. Expected poor responders on the basis of an antral follicle count do not benefit from a higher starting dose of gonadotrophins in IVF treatment: a randomized controlled trial 
  13. Adjuvant L-arginine treatment for in-vitro fertilization in poor responder patients
  14. GnRHa flare and IVF pregnancy rates.
  15. http://www.resolve.org/diagnosis-management/infertility-diagnosis/poor-responder.html
  16. Are poor responders patients at higher risk for producing aneuploid embryos in vitro? 
  17. Antioxidant Deficiencies And Infertility 
AMH Links
  1. Anti-Mu¨llerian hormone: clairvoyance or crystal clear?
  2. Anti-Mu¨llerian hormone—is it a crystal ball for predicting ovarian aging?
  3. Age-specific serum anti-M€ullerian hormone values for 17,120 women presenting to fertility centers within the United States
  4. AMH: why it is so useful 
  5. The clinical significance of anti-Müllerian hormone evaluation in gynecological endocrinology
  6. http://www.drmalpani.com/amh.htm
  7. http://haveababy.com/fertility-information/the-abc-of-ivf/anti-mullerian-hormone-amh-test/
  8. http://www.ivf1.com/AMH-Ovarian-Reserve/
  9. Antral follicle count, anti-mullerian hormone and inhibin B: predictors of ovarian response in assisted reproductive technology? 
  10. Serum anti-Müllerian hormone predicts ovarian response and cycle outcome in IVF patients 
  11. Circulating basal anti-Müllerian hormone levels as predictor of ovarian response in women undergoing ovarian stimulation for in vitro fertilization. 
  12. http://www.mindfood.com/at-amh-blood-test-conception-naturopathy.seo
  13. The DHEA and AMH paradox
  14. Serum antimüllerian hormone levels best reflect the reproductive decline with age in normal women with proven fertility- a longitudinal study.pdf 
  15. The role of antimullerian hormone in prediction of outcome after IVF- comparison with the antral follicle count 
  16. Assessing Egg Quantity with Anti-Mullerian Hormone 
  17. AMH Levels by Age.pdf 
Egg Quality Links
  1. An expert patient reviews the medical literature on how to improve egg quality
  2. http://uscfertility.org/fertility_options/fertility_basics/egg_quality.php
  3. http://news.harvard.edu/gazette/story/2011/07/cut-calories-increase-egg-quality/
  4. http://www.thedailybeast.com/newsweek/2007/12/01/fat-carbs-and-the-science-of-conception.print.html
  5. Science behind Oocyte/egg quality
  6. How to Improve Egg Quality
  7. Fat, Carbs and the Science of Conception / http://www.huffingtonpost.com/2013/05/06/fertility-diet-pregnancy_n_3209511.html
  8. How to Increase Your Egg Health in 90 Days
  9. Prevention of maternal aging-associated oocyte aneuploidy and meiotic spindle defects in mice by dietary and genetic strategies. 
  10. http://ivfover40.blogspot.com/2012/05/post-13-hokus-pokus.html
  11. http://ivfover40.blogspot.com/2013/03/fertility-supplements-for-women-and-men.html
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Welcome!

I have decided to create this blog to help consolidate information about our infertility journey and its many twists and turns.  I will openly share our first pregnancy at (my) age 37, which ended with pPROM at 27 weeks, a 5 month NICU stay, a 1 month PICU stay, 28 days on ECMO, child loss, subsequent recurrent pregnancy loss x 4, Asherman’s Syndrome, and next steps that will include immune testing and IVF.  Some of the topics will be difficult to read, especially if you too have suffered through any of the above. 

Infertility is a lifestyle – I didn’t choose it, but it is my way of life.  For now.

Posted in Endocrinology, Immunology, Infertility, IVF | Tagged | 3 Comments