Menstrual Cycle & Weight

It is common to hear women speak to sudden weight gain at particular points in the month, even when they have been sticking to their caloric deficit religiously. In this article, we will investigate how weight loss can be influenced by the menstrual cycle.

Does the menstrual cycle lead to weight gain?

Yes. The menstrual cycle, as it nears closer and closer to menstruation, leads to greater water retention [1].

How much water weight gain?

While this could vary slightly as the study that investigated this exact question was not exactly rigorous or powered for population applicable reliability (n = 1), it is safe to say weight gain can be anywhere up to ~2.3kg (~5lbs) [3]. This weight gain/bloating tends to begin mild, then increases in severity over the week leading up to menstruation [1][21]. Once menstruation occurs, water retention begins to dissipate over the following days, up to another week [1][3].

Understanding the 
Physiology

This has been one of the most irritating headaches to overcome, but here is the understanding of the physiology of the weight gain during menstruation. Nothing about this will be self-explanatory, so you will need to pay attention and keep in mind, this is merely my interpretation of the literature and is not as set in stone as many other articles I have written.

With that said, we break up the menstrual cycle into 2 sections (one could easily complicate this further) of time: the follicular phase (pre-ovulation) and the luteal phase (post-ovulation). In the beginning of the follicular phase, or one might identify it as “pre-follicular” or “early follicular”, menstruation occurs. It is the days leading up to this event (late luteal), and the days following (early follicular) that the most fluid retention occurs, with the highest level at menstruation [1][3]. So, what hormones are at play during this time?

 

In the luteal phase, progesterone and estrogen are both upregulated, but in the late luteal, they both dip dramatically [4]. This is a point of extreme confusion, because estrogen is shown to act on estrogen receptors in the hypothalamus of the brain [5]. These receptors promote the release of vasopressin (aka, anti-diuretic hormone) from the pituitary gland of the brain [5]. However, while this may make some sense in the details, if we take a step back, it does not.

Since water retention is maximal around menstruation, one would imagine estrogen to be high around this point of time, yet it is not [4]. So, the mechanism described above seems to have a problem – low estrogen, less vasopressin release at a time when they should be high (by this described mechanism).

However, progesterone could be a player, and is, but only in the luteal phase (just like estrogen), and is found in lower quantities during menstruation [4]. Also, progesterone leads to increased diuresis (less water retention) [6]. So, neither of these hormones seems to explain this increase in weight during menstruation, or do they?

Estrogen may, yet.

Estrogen does act on estrogen receptors found on the hypothalamus, but these receptors come in two forms: Estrogen receptor alpha (ERa) and estrogen receptor beta (ERb) [5]. ERa stimulates the release of vasopressin, and ERb inhibits its release [5]. Notably, there is 50 times more ERb than ERa present in the hypothalamus, and substantially more in women than in men [7]. Interestingly, ERb may also have a lower ability to bind to estrogen compared to ERa – so, ERa is quantitatively lower, yet binds estrogen more easily [5]. This leads to a fascinating scenario.

It may be that when estrogen levels are high, as in the luteal phase, estrogen binds to ERa and ERb, and as there are far greater amounts of ERb, the end result is an inhibition of vasopressin. Not only that, estrogen may decrease the sensitivity of the kidneys to react with vasopressin, making it less likely to carry out the role of vasopressin [8]. However, when estrogen is in low quantities, one would not see the inhibition through ERb, because what estrogen is available binds more easily to ERa, effectively releasing vasopressin. This would also lead the kidneys to have a greater sensitivity relative to high estrogenic state.

This would all work nicely, yet vasopressin is not significantly different across phases of the menstrual cycle and slightly increases only in correlation with estrogen [9][10]. So, assuming estrogen binding to ER (regardless of subtype) leads to vasopressin release, then the logical explanation is the effect estrogen has on the kidneys by desensitizing them to vasopressin [8][11].

 

So, low estrogen (in menstruation) promotes the release of vasopressin, and the possible lack of inhibition by progesterone may add to the issue, yet estrogen is not in high enough quantity to suppress vasopressin’s action on the kidneys, so water retention occurs in menstruation. Then, in the luteal phase, there is an increase in estrogen and, yet, there is still a release of vasopressin, yet due to the high estrogen levels, the kidneys are desensitized, so we see less water retention. So, overall, estrogen may be a large player, yet one might not know it, considering its actionable consequences result in the same release of vasopressin; so, it’s real impact is on the kidneys by either desensitizing them or not. Oddly enough, the addition of estrogen and/or progesterone shows no change in body weight and the evidence clearly shows the largest increase in water retention pre-menstruation, peaking at menstruation, and decreasing post [1][16].

So, other contributors people might jump to are cortisol and sodium retention, both of which are commonly held as culprits in general weight gain. However, while cortisol can rise, during menstruation cortisol is at its lowest point [14]. Sodium retention is minimal, but may occur when estrogen is present as estrogen acts on the tubules of the kidneys and directly stimulates sodium retention [15]. Progesterone antagonizes this action by inhibiting sodium retention through blocking the kidneys from retention, which may be a reason little weight gain is seen during the luteal phase although estrogen is elevated [17][18]. Progesterone also induces the production of aldosterone from the adrenal gland, yet blocks it at the kidneys (as well as cortisol) via blocking mineralocorticoid receptors that normally allow water retention to occur [19].

Speaking to aldosterone, it is found in lower concentrations during menstruation (highest in the luteal phase), so either it is not a factor in our water weight gain, or the lack of progesterone allows aldosterone to act on the kidneys uninhibited [20].

Finally, while all these hormones act on sodium retention in the kidneys, looking simply at water retention (without considering hormonal activity), there is evidence plasma sodium levels are higher in the follicular phase compared to the luteal phase as sodium excretion is increased during the luteal phase [21]. However, there is also evidence that plasma sodium does not change between phases [22].

As a side note, vasopressin is released, not only for water retention (presumably to maintain blood pressure during menstruation), but it acts on the uterus and promotes uterine contractions for the expulsion of the endometrium [12][13]. Interestingly, progesterone may protect against these contractions in the luteal phase.

Now, with all that said, there seems to be a massive factor that has not yet been revealed – premenstrual syndrome (PMS). Apparently, only some women suffer from PMS, which changes their hormone profile compared to non-PMS women in the same phase of the menstrual cycle. Estrogen is decreased, in the luteal phase, of PMS women, and possibly more importantly, in the late luteal phase (the onset of PMS symptoms), there is a substantial increase in aldosterone [23]. This means that some women, but not all, may experience a rise in water retention, because aldosterone levels rise, yet progesterone is not present to inhibit its action on the kidneys – voila!

Not only that, PMS (and potentially non-PMS) leads to edema (increase in size due to fluid retention) across the body, so there is a substantial shift in water distribution [24].

SUMMARY

I realize that everything you just read may have made your head spin, so let us break this down into more digestible pieces.

Some women, but not all, gain water weight pre-menstruation (late luteal), during menstruation, and lose it post-menstruation (early follicular) [3]. More common, but not universally, women redistribute their water peripherally around this time, as well [1][24]. In some women, there is mild water retention in the luteal phase [1].

If a woman has water retention issues in the usual time frame (late luteal to early follicular), it is likely due to a combination of factors, but chiefly due to increased aldosterone in the absence of progesterone [23]. Other factors may be a small contribution of vasopressin in the absence of estrogen. As for small increases in water retention across the late follicular or mid luteal phases, those can likely be attributed to an interplay between estrogen on vasopressin and aldosterone, and progesterone on the kidneys as an antagonist to estrogen diuretic effects. This means the greatest potential for the lowest body weight and water retention in women is immediately after ovulation (early luteal phase).

Author: Nicolas Verhoeven
References
[1] White, C. P., Hitchcock, C. L., Vigna, Y. M., & Prior, J. C. (2011). Fluid Retention over the Menstrual Cycle: 1-Year Data from the Prospective Ovulation Cohort. Obstetrics and Gynecology International, 2011, 1-7. doi:10.1155/2011/138451

[2] Stachenfeld, N. S. (2008). Sex Hormone Effects on Body Fluid Regulation. Exercise and Sport Sciences Reviews, 36(3), 152-159. doi:10.1097/jes.0b013e31817be928

[3] SWEENEY, J. S. (1934). MENSTRUAL EDEMA. Journal of the American Medical Association, 103(4), 234. doi:10.1001/jama.1934.02750300008003

[4] Reed, B. G. (2000). The Normal Menstrual Cycle and the Control of Ovulation. In Endotext. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK279054/

[5] Stachenfeld, N. S. (2008). Sex Hormone Effects on Body Fluid Regulation. Exercise and Sport Sciences Reviews, 36(3), 152-159. doi:10.1097/jes.0b013e31817be928

[6] Stachenfeld, N. S. (2014). Hormonal Changes During Menopause and the Impact on Fluid Regulation. Reproductive Sciences, 21(5), 555-561. doi:10.1177/1933719113518992

[7] Sladek, C. D., & Somponpun, S. J. (2004). Oestrogen Receptor beta: Role in Neurohypophyseal Neurones. Journal of Neuroendocrinology, 16(4), 365-371. doi:10.1111/j.0953-8194.2004.01187.x

[8] Stachenfeld, N. S., & Keefe, D. L. (2002). Estrogen effects on osmotic regulation of AVP and fluid balance. American Journal of Physiology-Endocrinology and Metabolism, 283(4), E711-E721. doi:10.1152/ajpendo.00192.2002

[9] Punnonen, R., Viinamäki, O., & Multamäki, S. (1983). Plasma Vasopressin during Normal Menstrual Cycle. Hormone Research, 17(2), 90-92. doi:10.1159/000179681

[10] Vokes, T. J., Weiss, N. M., Schreiber, J., Gaskill, M. B., & Robertson, G. L. (1988). Osmoregulation of thirst and vasopressin during normal menstrual cycle. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 254(4), R641-R647. doi:10.1152/ajpregu.1988.254.4.r641

[11] Cheema, M. U., Irsik, D. L., Wang, Y., Miller-Little, W., Hyndman, K. A., Marks, E. S., … Norregaard, R. (2015). Estradiol regulates AQP2 expression in the collecting duct: a novel inhibitory role for estrogen receptor α. American Journal of Physiology-Renal Physiology, 309(4), F305-F317. doi:10.1152/ajprenal.00685.2014

[12] Arkelund, M. (1998). Uterine contractions in non-pregnant women. How are they handled? what is their significance? Lakartidningen, 95(4), 284-287. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/9469963

[13] Åkerlund, M. (1993). The role of oxytocin and vasopressin in the initiation of preterm and term labour as well as primary dysmenorrhoea. Regulatory Peptides, 45(1-2), 187-191. doi:10.1016/0167-0115(93)90204-l

[14] GENAZZANI, A. R., LEMARCHAND-BÉRAUD, T., AUBERT, M. L., FELBER, J. P., MULLER, A., LAVANCHY, M., & GOMEZ, J. (1975). Pattern of Plasma ACTH, hGH, and Cortisol During Menstrual Cycle. The Journal of Clinical Endocrinology & Metabolism, 41(3), 431-437. doi:10.1210/jcem-41-3-431

[15] Stachenfeld, N. S., & Keefe, D. L. (2002). Estrogen effects on osmotic regulation of AVP and fluid balance. American Journal of Physiology-Endocrinology and Metabolism, 283(4), E711-E721. doi:10.1152/ajpendo.00192.2002

[16] Stachenfeld, N. S., & Taylor, H. S. (2004). Effects of estrogen and progesterone administration on extracellular fluid. Journal of Applied Physiology, 96(3), 1011-1018. doi:10.1152/japplphysiol.01032.2003

[17] Stachenfeld, N. S., Silva, C., Keefe, D. L., Kokoszka, C. A., & Nadel, E. R. (1999). Effects of oral contraceptives on body fluid regulation. Journal of Applied Physiology, 87(3), 1016-1025. doi:10.1152/jappl.1999.87.3.1016

[18] Myles, K., & Funder, J. W. (1996). Progesterone binding to mineralocorticoid receptors: in vitro and in vivo studies. American Journal of Physiology-Endocrinology and Metabolism, 270(4), E601-E607. doi:10.1152/ajpendo.1996.270.4.e601

[19] Szmuilowicz, E. D., Adler, G. K., Williams, J. S., Green, D. E., Yao, T. M., Hopkins, P. N., & Seely, E. W. (2006). Relationship between Aldosterone and Progesterone in the Human Menstrual Cycle. The Journal of Clinical Endocrinology & Metabolism, 91(10), 3981-3987. doi:10.1210/jc.2006-1154

[20] MICHELAKIS, A. M., YOSHIDA, H., & DORMOIS, J. C. (1976). PLASMA RENIN ACTIVITY AND PLASMA ALDOSTERONE DURING THE NORMAL MENSTRUAL CYCLE. Obstetrical & Gynecological Survey, 31(6), 507. doi:10.1097/00006254-197606000-00021

[21] Olson, B. R. (1996). Relation between Sodium Balance and Menstrual Cycle Symptoms in Normal Women. Annals of Internal Medicine, 125(7), 564. doi:10.7326/0003-4819-125-7-199610010-00005

[22] Pechère-Bertschi, A., Maillard, M., Stalder, H., Brunner, H. R., & Burnier, M. (2002). Renal segmental tubular response to salt during the normal menstrual cycle. Kidney International, 61(2), 425-431. doi:10.1046/j.1523-1755.2002.00158.x

[23] Rosenfeld, R., Livne, D., Nevo, O., Dayan, L., Milloul, V., Lavi, S., & Jacob, G. (2008). Hormonal and Volume Dysregulation in Women With Premenstrual Syndrome. Hypertension, 51(4), 1225-1230. doi:10.1161/hypertensionaha.107.107136

[24] Tacani, P., De Oliveira Ribeiro, D., Barros Guimarães, B. E., Perez Machado, A. F., & Tacani, R. E. (2015). Characterization of symptoms and edema distribution in premenstrual syndrome. International Journal of Women's Health, 297. doi:10.2147/ijwh.s74251

 

"CLICK" for Most Recent