Menopause: Estrogen and Its’ Direct Relationship to Insulin Resistance

Menopause, Estrogen, and Insulin Resistance: Exploring Their Connection

40 year old woman holding yoga mat

By Laura Cipullo, RD, CDCES, CEDS-S

The inevitable happens when women hit their mid 40’s to 50’s. Hot flashes start; our menstrual cycles can become heavy, long and sporadic. This all comes to a “climax” when we cease menstruation altogether with both progesterone and estrogen levels plummeting indefinitely. What does this mean for women and their health, most specifically, their metabolic health and blood sugar management? 

 

What Is Menopause and Its’ Relationship with Estrogen?

 

The National Institute on Aging defines menopause as the time stamp marking 12 months after a women’s last menstrual cycle. The years before and after are also affected by hormonal changes, specifically the decrease in estrogen which ultimately leads to insulin resistance. (1) Perimenopause, menopause and post menopause are all consistent with “low circulating levels of estrogen due to a decrease in ovarian function” (2). Consequently, this time in life is also associated with metabolic, bone and cardiovascular co morbidities. (3)

 

How to Eat for Menopause?

 

The loss of lean body mass, and bone as well as an increase in fat mass (3) can all be balanced with dietary changes. The decrease in muscle mass automatically decreases basal metabolic rate so women need to adjust for this change by decreasing overall intake. It is recommended to increase dietary protein and anti-inflammatory plant foods to further counter the loss of lean body mass and combat any cardiovascular risks associated with a decrease in estrogen.(7) Following a plant heavy Mediterranean diet during the postmenopausal time is also associated with the prevention of bone loss. 

 

 

What is Insulin Resistance and What Does it Have to Do With Menopause?

 

A lower level of circulating estrogen decreases the glucose uptake by muscles resulting in higher blood sugar and a decreased ability of the liver to respond to insulin.(6) All of this leads to insulin resistance. IR is defined as the inability of the cells to recognize the hormone insulin which would normally uptake sugar from circulation into insulin-sensitive tissues and organs. IR is also partly responsible for the body’s skeletal muscle’s decreasing ability to create protein and or build muscle. Thus, having a diet higher in protein can provide for more muscle synthesis and possibly allow for a more efficient metabolism.(4) The net effect of low estrogen is less muscle mass, slower metabolism, increased resistance to insulin and higher blood sugar. 

 

Menopause and Continuous Glucose Monitoring, Should You Try It?

If menopause puts women into this prediabetes like state, would women benefit from moderating their blood sugar with the use of a continuous glucose monitor? Since 2017, RD’s specializing in diabetes have been using continuous glucose monitors to help individuals with Type 1 and Type 2 manage their blood sugar. In the past few years, CGM use has been extended/additionally used by to individuals with insulin resistance and prediabetes. One population that naturally falls into the insulin resistance category are women who are in perimenopausal, have reached menopause or are now post-menopausal. The ZOE PREDICT 1 study used continuous glucose monitors to study the postprandial or after meal blood glucose levels of women post menopause. For all meals, the post menopause women had a higher blood sugar response regardless of the macronutrient distribution (5). In another study of 24 healthy volunteers, continuous glucose monitoring revealed that meals higher in fiber, protein and fat better helped to manage insulin resistance. These particular meals resulted in a slower and lower overall rise in blood sugar after eating the meal. (8)

 

In conclusion, insulin resistance is experienced by women as a postmenopausal consequence of decreased estrogen. While there are dietary changes to combat decreases in lean body mass, bone and an increase in fat mass, it may benefit women to use a continuous glucose monitor to better learn how their metabolism responds to meals and manage their blood sugar in a tighter range. 

 

  1. https://www.nia.nih.gov/ health/menopause/what-menopause
  2. Chopra S, Sharma KA, Ranjan P, Malhotra A, Vikram NK, Kumari A. Weight Management Module for Perimenopausal Women: A Practical Guide for Gynecologists. J Midlife Health. 2019 Oct-Dec;10(4):165-172. doi: 10.4103/jmh.JMH_155_19. PMID: 31942151; PMCID: PMC6947726.
  3. Silva TR, Oppermann K, Reis FM, Spritzer PM. Nutrition in Menopausal Women: A Narrative Review. Nutrients. 2021 Jun 23;13(7):2149. doi: 10.3390/nu13072149. PMID: 34201460; PMCID: PMC8308420.
  4. Simpson SJ, Raubenheimer D, Black KI, Conigrave  AD. Weight gain during the menopause transition: Evidence for a mechanism dependent on protein leverage. BJOG. 2023; 130(1): 4–10. https://doi.org/10.1111/1471-0528.17290
  5. eBioMedicine 2022;85: 104303 Published online 18 October 2022 https://doi.org/10.1016/j. ebiom.2022.104303. Menopause is associated with postprandial metabolism, metabolic health and lifestyle: The ZOE PREDICT study https://www.thelancet.com/action/ showPdf?pii=S2352-3964%2822%2900485-6
  6. Yan H, Yang W, Zhou F, Li X, Pan Q, Shen Z, Han G, Newell-Fugate A, Tian Y, Majeti R, Liu W, Xu Y, Wu C, Allred K, Allred C, Sun Y, Guo S. Estrogen Improves Insulin Sensitivity and Suppresses Gluconeogenesis via the Transcription Factor Foxo1. Diabetes. 2019 Feb;68(2):291-304. doi: 10.2337/db18-0638. Epub 2018 Nov 28. PMID: 30487265; PMCID: PMC6341301.
  7. Raubenheimer David and Simpson Stephen J.2023Protein appetite as an integrator in the obesity system: the protein leverage hypothesisPhil. Trans. R. Soc. B3782022021220220212 http://doi.org/10.1098/rstb.2022.0212
  8. Freckmann G, Hagenlocher S, Baumstark A, Jendrike N, Gillen RC, Rössner K, Haug C. Continuous glucose profiles in healthy subjects under everyday life conditions and after different meals. J Diabetes Sci Technol. 2007 Sep;1(5):695-703. doi: 10.1177/193229680700100513. PMID: 19885137; PMCID: PMC2769652.

 

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