Why Women With Diabetes Should Know Their Menstrual Cycle – and What Puberty Has to Do With It
People living with diabetes quickly learn that blood glucose is influenced by much more than food, physical activity, and insulin. Hormones also play an important role. In women, the hormonal environment changes substantially over the course of life and, during the reproductive years, throughout each menstrual cycle.
These hormonal fluctuations can affect insulin sensitivity and insulin requirements, particularly in women with type 1 diabetes. Modern continuous glucose monitoring (CGM) systems make these changes much easier to recognize than was possible in the past.
This article explains which hormones are involved, why insulin requirements may vary during the menstrual cycle and different stages of life, and how these observations can be incorporated into individualized diabetes management.
Insulin is the central hormone regulating the uptake and utilization of glucose in insulin-sensitive tissues. How strongly the body responds to insulin is referred to as insulin sensitivity. When insulin sensitivity is high, less insulin is required to achieve a given metabolic effect. Reduced insulin sensitivity is referred to as insulin resistance.
The predominant estrogen during the reproductive years is estradiol. Estrogens influence glucose and lipid metabolism through several organ systems and estrogen receptors. Experimental and clinical studies suggest that physiological estrogen exposure generally has favorable metabolic effects, although these relationships are complex and cannot be reduced to a simple “more estrogen means better insulin sensitivity” model. [1,2]
Estrogen signaling appears to influence several metabolically important tissues:
However, these effects should not be oversimplified. Both very low and abnormal hormonal states can be associated with adverse metabolic effects, and insulin sensitivity is determined by many factors in addition to estrogen.
After menopause, changes in body composition, visceral fat accumulation, muscle mass, physical activity, aging, genetics, and other hormonal changes all contribute to alterations in glucose metabolism. The metabolic changes occurring during and after menopause therefore cannot be attributed to declining estrogen concentrations alone.
Estrogen does not act in isolation. Numerous hormones influence glucose metabolism, and it is misleading to classify them simply as “good” or “bad” hormones.
Progesterone
Progesterone rises after ovulation during the luteal phase of the menstrual cycle. In some women, insulin sensitivity decreases during this phase.
Studies in women with type 1 diabetes suggest that higher glucose levels and increased insulin requirements may occur particularly during the late luteal phase, in the days immediately preceding menstruation. However, the magnitude and timing of these changes vary considerably between individuals, and progesterone is unlikely to be the only factor involved. [3–7]
Changes in appetite, food intake, sleep, physical activity, mood, and premenstrual symptoms may contribute as well.
Androgens
Androgens such as testosterone are also present in women. Excess androgen activity is often associated with insulin resistance.
A typical example is polycystic ovary syndrome (PCOS), in which hyperandrogenism and insulin resistance frequently occur together.
The relationship is bidirectional. Hyperinsulinemia can reduce hepatic production of sex hormone-binding globulin (SHBG), thereby increasing the proportion of biologically active free testosterone. Insulin resistance and hyperandrogenism can therefore reinforce one another.
In men, the relationship differs: low testosterone concentrations are frequently associated with obesity, insulin resistance, and an increased risk of type 2 diabetes, although these associations are also influenced by age, body composition, and underlying disease.
Growth Hormone
Growth hormone is particularly important during puberty. Increased secretion of growth hormone and changes in the growth hormone–IGF-1 axis contribute substantially to the physiological reduction in insulin sensitivity observed during adolescence. [8]
Stress and Other Hormones
Stress hormones such as cortisol can increase hepatic glucose production and reduce insulin sensitivity.
Prolactin and several pregnancy-related hormones can also influence glucose metabolism and insulin requirements.
Thyroid Disease
The thyroid should not be classified as a direct “antagonist” of insulin.
However, autoimmune thyroid disease is considerably more common in people with type 1 diabetes than in the general population. Thyroid dysfunction can also influence glucose control and insulin requirements.
For this reason, current diabetes guidelines recommend thyroid screening in children and adolescents with type 1 diabetes. Thyroid-stimulating hormone (TSH) should be measured at diagnosis when the patient is clinically stable or after glycemic control has improved. If results are normal, reassessment is generally suggested every one to two years, or earlier in the presence of thyroid antibodies, symptoms, abnormal growth, goiter, or unexplained glycemic variability. [9]
Insulin sensitivity is not constant throughout a woman’s life.
It is generally high during childhood, decreases substantially during puberty, improves again after adolescence, and is relatively more stable during the reproductive years.
During the menopausal transition, fluctuating ovarian hormone concentrations, changes in body composition, aging, physical activity, sleep, and other factors may make glucose management less predictable.
There is therefore no single hormonal pattern that applies to every woman.
Puberty: Physiological Insulin Resistance
Puberty is associated with a marked physiological reduction in insulin sensitivity.
Studies suggest that insulin sensitivity in adolescents with type 1 diabetes may be approximately 33–42% lower than in prepubertal children or compared with children without diabetes at corresponding stages. The main hormonal contributors appear to be increased growth hormone secretion and changes in the GH–IGF-1 axis. [8,10]
This physiological insulin resistance has important consequences for adolescents with type 1 diabetes.
Insulin requirements frequently increase substantially during puberty and can exceed requirements seen before or after adolescence. The precise dose, however, varies widely depending on pubertal stage, body weight, diet, physical activity, residual insulin secretion, and individual insulin sensitivity.
For this reason, insulin treatment should always be based on the individual glucose pattern rather than on a predefined number of units per kilogram.
Several challenges are particularly common during adolescence:
Higher Morning Glucose Levels
Growth hormone is released in pulses, particularly during sleep. Together with other counter-regulatory hormones, this can contribute to the dawn phenomenon, with rising glucose concentrations during the early morning hours.
Insulin pumps and automated insulin delivery systems may help compensate for these predictable changes in insulin requirements.
Menarche and Irregular Cycles
The onset of menstruation introduces another source of hormonal variability. Menstrual cycles are frequently irregular during the first years after menarche, and some early cycles are anovulatory.
This makes cycle-related changes in glucose control less predictable.
Transition to Adult Diabetes Care
The transition from pediatric to adult diabetes care is an important period. Some adolescents and young adults disengage from regular medical follow-up during this phase.
Structured transition programs can help maintain continuity of diabetes care.
Youth-Onset Type 2 Diabetes
When type 2 diabetes develops during adolescence, its course can be particularly aggressive.
Beta-cell function may decline more rapidly than in many adults with type 2 diabetes, and metformin monotherapy is often insufficient to maintain long-term glycemic control.
Long-term data from the TODAY study demonstrated that hypertension, diabetic kidney disease, dyslipidemia, neuropathy, and retinopathy may already develop during young adulthood in a substantial proportion of people with youth-onset type 2 diabetes. [11]
Early, intensive treatment of glycemia and cardiovascular risk factors is therefore particularly important.
A Sensitive Issue: Insulin Restriction for Weight Control
Some adolescents and young women with type 1 diabetes intentionally reduce or omit insulin in an attempt to lose weight.
The term “diabulimia” is sometimes used informally to describe this behavior. However, it is not a formal medical diagnosis.
More accurately, it can be described as intentional insulin restriction or omission for weight control in the context of disordered eating or an eating disorder.
This behavior can be extremely dangerous. Insufficient insulin may lead to severe hyperglycemia, diabetic ketoacidosis, recurrent hospital admission, and an increased risk of early diabetes complications.
Because affected individuals may be reluctant to discuss the problem spontaneously, diabetes teams should address eating behavior and insulin manipulation in a sensitive, nonjudgmental manner.
The Diabetes Eating Problem Survey–Revised (DEPS-R) is a short diabetes-specific screening questionnaire that can help identify individuals who may have problematic eating behaviors. It is a screening tool, not a diagnostic test, and abnormal findings require appropriate clinical and psychological assessment. [12,13]
During the reproductive years, glucose control may vary across the menstrual cycle.
The typical textbook model is approximately as follows:
Menstrual-cycle phase | Typical hormonal pattern | Possible change in insulin sensitivity | Possible effect on glucose |
Early follicular phase / beginning of menstruation | Estrogen and progesterone relatively low | May be higher in some women | Insulin requirements may fall; hypoglycemia may occur if insulin has previously been increased |
Late follicular phase / around ovulation | Estradiol rises and reaches a peak | Often relatively preserved | Glucose may be relatively stable, although individual responses vary |
Luteal phase | Progesterone rises together with a secondary rise in estrogen | May decrease | Glucose levels and insulin requirements may increase |
Late luteal / premenstrual phase | Estrogen and progesterone subsequently fall | Reduced insulin sensitivity is reported by some women | Higher glucose levels and increased insulin requirements may occur |
This table describes a possible population-level tendency, not a rule.
There is considerable variation between women. Some experience clear and reproducible changes, others only minor changes, and some show little or no consistent menstrual-cycle effect.
Even in the same woman, the pattern may vary between cycles.
What CGM Data Show
Continuous glucose monitoring has made cycle-related glucose changes much easier to study.
A 2026 study examined women with type 1 diabetes using the MiniMed 780G automated insulin delivery system. Glycemic differences between phases of the menstrual cycle were relatively small but measurable.
Time in Range was slightly lower during the late luteal phase than during the follicular phase, while time above range and mean glucose were modestly higher.
Importantly, the differences were seen predominantly in meal-related insulin requirements, whereas basal insulin delivery and automated correction boluses did not show major differences.
These results suggest that modern AID systems can compensate for some menstrual-cycle-related changes, but they do not necessarily eliminate them completely. [7]
Other studies have also found cycle-related changes, but results are heterogeneous. A systematic review concluded that the evidence remains limited and that there is currently no universal glucose or insulin pattern that can be applied to all women with type 1 diabetes. [3]
Menstrual-Cycle Effects Also Occur Without Diabetes
Cycle-related changes in glucose are not limited to women with diabetes.
In a study using continuous glucose monitoring in women without diabetes, glucose concentrations varied modestly across the menstrual cycle and were associated with reproductive hormone patterns. [6]
The absolute differences were small in metabolically healthy women because endogenous insulin secretion can compensate for changing insulin sensitivity.
In type 1 diabetes, this automatic physiological compensation is absent, which may make similar hormonal changes clinically more noticeable.
The most useful approach is not to assume that a woman will follow a textbook menstrual-cycle pattern, but to determine whether she has a reproducible individual pattern.
Menstrual-cycle dates can be documented for several months and compared with CGM and insulin data.
Useful questions include:
Tracking at least several cycles may help distinguish a genuine recurring pattern from random glucose variability.
If a reproducible cycle-related pattern is identified, insulin therapy may sometimes be adjusted.
Depending on the insulin delivery method, this might involve changes in:
However, there is currently no evidence-based universal percentage by which basal insulin should routinely be increased during the luteal phase.
Some women may require substantial adjustments, while others require little or none.
Any planned changes should therefore be based on the individual’s CGM and insulin data and discussed with the diabetes care team.
In women who experience increased insulin requirements before menstruation, insulin sensitivity may improve rapidly once menstruation begins.
If previously increased insulin doses are continued unchanged, hypoglycemia may occur.
Recognizing this individual transition can therefore be as important as managing premenstrual hyperglycemia.
Not every premenstrual glucose change is caused directly by ovarian hormones.
Other factors frequently change during the menstrual cycle, including:
All of these can influence glucose levels and insulin requirements.
In studies of women without diabetes, for example, food cravings were independently associated with higher glucose concentrations during parts of the menstrual cycle. [6]
What Automated Insulin Delivery Can – and Cannot – Do
Modern automated insulin delivery systems continuously adjust insulin delivery according to CGM glucose values and glucose trends.
This provides an important advantage when insulin sensitivity changes gradually during the menstrual cycle.
However, current AID systems generally do not directly know which phase of the menstrual cycle a woman is in.
Small qualitative studies of women using open-source AID systems have shown that many users recognize reproducible cycle-related changes and sometimes make manual adjustments despite automation. [14]
Future AID systems may potentially integrate menstrual-cycle information and use pattern recognition to anticipate recurring changes in insulin requirements.
At present, however, treatment should remain individualized and based on the woman’s own CGM and insulin patterns.
Female reproductive hormones can influence glucose metabolism and insulin requirements, but the relationship is more complex than a simple opposition between estrogen and progesterone.
During puberty, increased growth hormone and changes in the GH–IGF-1 axis produce pronounced physiological insulin resistance. During the reproductive years, some women with type 1 diabetes experience reproducible changes in insulin sensitivity across the menstrual cycle, particularly during the luteal and premenstrual phases.
At the onset of menstruation, insulin requirements may decrease again in some women, which can increase the risk of hypoglycemia if previously increased insulin doses are not adjusted.
Modern CGM and automated insulin delivery systems make these patterns easier to recognize and may compensate for part of the hormonal variability.
The most important message, however, is that the individual’s pattern matters more than the textbook pattern.
By comparing menstrual-cycle information with CGM and insulin data over several months, women and their diabetes care teams may be able to identify recurring changes that previously appeared unexplained and incorporate them into individualized diabetes management.