Iodolactones, Prostaglandins, and the Menstrual Cycle

Decreasing menstrual cycle length as a proxy for stored/ intake of PUFA and iodine on the low iodine diet.

I will add more to this later, but wanted to get these ideas out for the general discourse!

Could iodolactones be behind why many women report iodine/ iodide supplementation restores their menstrual cycle length - both follicular and luteal? And why there are anecdotes of decreasing menstrual cycle length when on the low iodine diet?

Areas of low iodine intake also report shorter cycle lengths - these areas can of coure have other factors at play.

The low iodine diet is being used to address thyroid disorders like hashimotos, and is remarkedly successful! The changes in menstrual cycle length are independent of changes to thyroid hormone (same lab values) - there is the possibility of the lowered antibodies, inflammation, receptor density, cell signaling, etc. causing the change. However, I am exploring another path -

Prostaglandins are one of the eicosanoids that are made from PUFA (polyunsaturated fatty acids).

Decreasing prostaglandins increases the menstrual cycle length. This is because prostaglandins increase luteolysis - the breakdown of the corpus luteum. This means less prostaglandins will allow the corpus luteum to maintain progesterone production for a longer period. So decreasing luteolysis increases the luteal phase. Prostaglandins also inhibit follicular growth, so decreasing prostaglandins would allow the follicles to grow and mature more. This can then lead to an increase in estrogen producton which promotes follicular growth and maturation and delaying the selection of the dominant follicle, leading to a longer follicular phase.

Iodolactone production from prostaglandins obviously means a reduction in the overall prostaglandin pool, leading to the above. They also seem to have some regulatory effect directly on the thyroid.

When on the low iodine diet, there is now less iodine to convert the prostaglandins to iodolactone. This can be a proxy for insufficient iodine intake, recycling, or showing the body is sequestering the iodine (probably in the thyroid) for some reason, and less is now available for the conversion. This would be exacerbated if one was consuming a diet that superseded the threshold for their body’s ability to handle PUFA. Or if lipolysis was adding too much PUFA to the free fatty acid, etc. pool. Yes, there are other routes PUFA can take that are not the eicosanoid pathway, so there are of course other considerations.

The body is a complex interconnection of pathways. While we think we are addressing one, and only one pathway, they all are impacted - “the rising tide lifts all boats".” (And yes, I am aware that President JFK stated that about government economic policy - please stop DMing me about it, the idea remains). In the same way, the ebbing/ receding tide lowers all boats. Many quickly figured this out when it came to “supporting methylation,” etc.

Some practical takeaways -

1. Consider how much PUFA you are eating.

2. Consider your PUFA intake history - the ratio of PUFA released during lipolysis.

3. Block PUFA conversion to eicosanoids - aspirin and NSAIDs are commonly used, but I have my concerns. Cortisol also does this (I know, the horror), so maybe if one isn’t constantly calling on cortisol to maintain blood glucose. Mg, Zn, vit B6, and vit B3 all seem to reduce the activity of COX-2. Ginger and vit E seem to inhibit/ reduce COX-1 activity. Antioxidants and potentially ALCAR seem to reduce COX-3 activity. I am not one to spam supplements, so are you getting 100+% of the theoretical RDAs?

4. Minimum effective intake of iodine that allows for sufficient reduction in prostaglandins via converting them to iodolactones, but also allows for lowering of iodine to address the thyroid issues.