Ovulation is the start of the process that hopefully ends in implantation, and ovulation is a dramatic event like a small volcano erupting! The “dominant follicle” that contains the egg fills rapidly with fluid, a blister forms on its surface and the egg is expelled in about 15ml of fluid.
The tentacle-like ends of the Fallopian tube “sweep” over the surface of the ovary to “catch” the egg and fertilization is close to the tube opening.
- The fertilized egg becomes an embryo when it divides into two cells, and division inside the egg’s shell continues until there are 70 to 100 cells
- The shell degenerates at this point, allowing the embryo to expand and enter the blastocyst stage with a fluid-filled cavity
- The embryo reaches the uterus after a week and must implant within a day to start a pregnancy
- When the embryo enters the ‘blastocyst’ stage, the cells differentiate into two types:
- The outer cells form the placenta, and these multiply rapidly during implantation. Sometimes these cells grow, but other embryonic cells don’t, causing a ”blighted ovum” to form
- The inner cells of the blastocyst grow to form the foetus
Stages of implantation
Implantation is a staged process of communication between the embryo and the lining of the uterus:
- Apposition is when cells in the embryo and the womb lining “line up” rather loosely
- Adhesion involves bonds forming between the two, with cells of the embryo penetrating the womb lining
- Invasion is the embryo cells burying further into the womb lining and reaching the basal membrane. They invade the uterine muscle, and the placenta (‘flat cake’ in Greek) grows until it contacts the maternal blood supply
The placenta releases ‘human chorionic growth hormone’ (hCG) when it implants. This stimulates the corpus luteum to increase progesterone production, which:
- Prevent new menstrual cycles
- Promotes growth of the womb lining
- Increases the blood supply to the uterus
- Triggers changes to the immune system that support pregnancy
Implantation failure causes around 70% of unsuccessful IVF cycles involving the transfer of healthy embryos.
For the womb to support implantation, the ‘functional layer’ becomes thicker, spongier, sticky and richer in its blood supply. There are two days called the ”window of implantation” when the proteins on the womb change, altering the bonding properties and increasing the likelihood of pregnancy. ii, iii
The womb environment is quite different during the ”window of implantation”, as the uterus fills with fluid to encourage the embryo to implant. The fluid is produced by:
- Secretions from glands in the womb wall
- Secretions from blood vessels
- Dead cells
Research into the makeup of the uterine ‘microbiome’ has recently raised the possibility that the microbes in the womb play essential roles in the implantation process.
The early nourishment of the embryo comes from stores of glycogen (a sugar)in the womb wall and glycoproteins from glands in the womb. iv These provide energy directly to the foetus during the first trimester when the blood supply is restricted.
The glycogen and glycoproteins stores are mainly from before conception rather than from food eaten during pregnancy. This strongly reinforces the importance of pre-conception nutrition and care, especially for women with Blood and Energy PFPs.
Other implantation issues
The depth of the womb lining
- The lining should be 8-15mm during the “fertile window”, and implantation is difficult if it’s too thin (usually a Blood, Hot and Energy PFP issue)
- If it’s too deep, there are other issues for implantation (usually due to drug stimulation or Cold or Fluids PFPs)
The freshness of the womb lining
- Incomplete shedding of the womb lining in periods can leave a “chequer-board” effect in the womb, with some areas of new and old lining
- Success rates are lower if an embryo tries to implant in “old” tissue
- Having a healthy period that entirely removes the functional layer is crucial, especially for Flow PFPs
- Some wombs have abnormal structures such as bicornate or septate, polyps, scars, and fibroids (myomas) that reduce pregnancy rates to varying degrees
ii ‘Molecular and cellular aspects of endometrial receptivity’ HM Beier 0 and K Beier-Hellwig Hum. Reprod. Update (1998) 4 (5): 448-458.
iii ‘Human Endometrium Ultrastructure During the Implantation Window – A New Perspective of the Epithelium Cell Types’
Carla Bartosch et al. Reproductive Sciences June 2011 vol. 18 no. 6 525-539
iv ‘Tracking nutrient transfer at the human maternofetal interface from 4 weeks to term’ C.J.P. Jones, R.H. Choudhury, J.D. Aplin. Placenta April 2015 Vol 36, Issue 4, Pages 372–380