The Implantation Dip
The "implantation dip" is not a validated clinical phenomenon and does not represent a reliable marker of implantation timing or success. While some fertility tracking literature has described a transient drop in basal body temperature around the time of presumed implantation, this observation lacks scientific validation and should not be used for clinical decision-making.
What Actually Happens During Implantation
Estrogen levels do not consistently dip during implantation. Instead, estrogen plays a critical regulatory role in establishing and maintaining the window of uterine receptivity:
- Estrogen within a narrow physiological range determines the duration of the window of uterine receptivity, with lower estrogen levels keeping the window open longer and higher levels causing it to close more rapidly 1
- Implantation in mammals (including giant pandas with delayed implantation) is associated with rising pregnanediol glucuronide (PdG) levels, not estrogen dips—PdG increases from baseline to 60-80 ng/mg creatinine coincident with implantation 2
- Urinary estrone-3-glucuronide (E1G) primarily reflects follicular growth, with peak E1G occurring pre-ovulation; post-ovulatory E1G patterns are variable and do not show a consistent "dip" at implantation 3, 4
Hormonal Patterns Around Implantation
The actual hormonal signature of implantation involves progesterone metabolites, not estrogen dips:
- Pregnanediol glucuronide (PdG) rises after ovulation from less than 5 ng/mg creatinine to 15-30 ng/mg creatinine, then shows further increases (to 60-80 ng/mg creatinine) approximately 114 days after mating in species with delayed implantation, presumably coincident with implantation 2
- E1G excretion rates provide direct measurement of follicular growth but do not reliably indicate implantation timing 3
- Estrogen and progesterone together regulate endometrial receptivity through complex molecular mediators including pinopodes, cell adhesion molecules, cytokines, and growth factors 5
Clinical Implications
Do not rely on temperature or hormone "dips" to diagnose or time implantation:
- The window of uterine receptivity is regulated by precise estrogen levels within a narrow range, not by transient dips 1
- Elevated estrogen levels (as seen with controlled ovarian hyperstimulation) can have detrimental effects on the endometrium and implantation success 5
- Monitoring E1G and PdG excretion rates can help navigate ovarian activity patterns (anovulatory vs. ovulatory cycles, luteal phase adequacy), but these do not show consistent "dips" at implantation 3
Common Pitfalls to Avoid
- Do not interpret random temperature fluctuations as implantation markers—these lack scientific validation and can lead to false reassurance or unnecessary anxiety
- Do not expect E1G to show a consistent pattern during the luteal phase—E1G primarily reflects follicular activity, and post-ovulatory patterns are highly variable 4
- Do not confuse the post-ovulatory PdG rise with implantation timing—the initial PdG rise reflects corpus luteum function after ovulation, not implantation itself 2, 3