Choosing the correct IVF protocol

My response to the IVF protocol, the agonist flare protocol, where I got a microdose of lupron from day 2 continuously followed by stims (with a mix of follistim and menagon, which contains equal amounts of both FSH and LH), was truly awful- we got a lot of eggs (11 eggs from 13 follicles), but most of them were immature and failed to mature and fertilize and even though we produced one 'good' Day 5 embryo, that failed to implant.


Why was this? I've always thought that maybe my protocol was not best suited for me, but never thought I'd be able to find a good (or any) explanation as to why and how.

However, I just found a recent opinion by Geoffrey Sher, which gave a plausible explanation of what may have been the issue:

Some background- there are two ways to shut down the pituitary gland, which is the master remote controller of ovulation:

1. The first method developed is through agonists- these work by a weird method- they first stimulate the pituitary gland, but such a strong stimulation however later shuts it down completely.
2. The second developed method is antagonists, which directly shut down pituitary activity (or is it just LH secretion?)

Dr. Sher makes that the point that if you start the agonist at day 2 or 3, it first produces a spike of LH at this point,  and THEN shuts it completely. His theory is that this increase in LH, on CD2/3  (which is, importantly, also out of time with this natural process, though he does not put it this way), may be bad, especially in vulnerable populations like PCOS patients or older women.

I really think this point makes sense for one reason, and here it is: What is associated with annovulatory PCOS? A really high ratio of LH to FSH, on CD3. This is a hallmark of this syndrome and if his interpretation that agonist use first causes that LH spike is right, it may actually mimic the natural situation that produces annovulation in PCOS, if first given on CD2/3.

He makes several other less important, and less strong, nonetheless plausible points:

Ideal curve of LH in a healthy ovulatory cycle, courtesy Wikipedia.

• Menagon (which is equal doses of FSH and LH) may be less than idea- This may be true- it deviates the natural bell shaped curve of LH found in nature in health, but nonetheless, it clearly works for many.
• Femara may also increase LH at the wrong point

Dr Sher's opinion really makes for interesting reading- I'm very glad I came across it. See above the bell shaped curve of LH in the natural cycle- maybe protocols that deviate from this may not serve optimally. Maybe too much LH at the spike or any other point may be bad too- its difficult to say

All i know is, if I'm doing IVF, I need to go away from what was done the last time. Based on what he said, I've also decided to avoid Femara and Clomid.

I may go straight to low dose FSH from an early point. I'm going to figure out if I want to use antagonists or not. The reason I'm vacillating on this point is that LH IS important- the gradual increase of this as ovulation nears, resulting in that spike, may be a good thing. But too much LH may be a problem too, and the reason pituitary shutdown was introduced was that 51 % of women had a premature LH surge which resulted in cycle cancellation.

Trying natural cycle IVF is so very alluring- except I have 2 IUI and 1 IVF vial of swimmers, and the really steep costs of IVF come in during the pickup and fertilization. Finances are not a problem, yet nor can I act like money grows on trees.

There are many choices to be made, but the good news is, right now, I'm pursuing the next option without the angst and hand-wringing and feeling that time crunch. Other people are always telling me my attitude is awesome, and I have to say, I'm impressing myself at this point.