Nourish to Flourish: Harnessing Bio-Individual Nutrition to Support the Female Hormonal Milieu

This article was originally published in Nourishing Bites, the journal of the National Association of Nutrition Professionals (NANP).

 The female hormonal milieu relies on metabolic stability and nutrient sufficiency (Mashhadi et al., 2025). Insufficient or imbalanced macro- and micronutrient intake can destabilize reproductive and metabolic hormone levels, alter hormone metabolite profiles, and impair downstream signaling (Kumari et al., 2024; Słowińska-Lisowska & Jagielska, 2024). This article synthesizes current research to demonstrate how bio-individual macronutrient intake (adequate proteins, stable fats and judicious carbohydrate balance) paired with targeted micronutrient intake supports HPO signaling, insulin sensitivity and female specific needs.

The hypothalamic–pituitary–ovarian (HPO) axis is sensitive to nutritional status. When energy, protein, or other key nutrients are inadequate, HPO signaling can be negatively impacted, reducing ovulatory robustness or leading to anovulation (Cabré et al., 2022; Mashhadi et al., 2025). The implications extend beyond fertility: suboptimal ovulation limits corpus luteum production of progesterone and estradiol, hormones integral to metabolic health, mood, energy, and long-term well-being. Resulting imbalance may present as premenstrual symptoms, cycle irregularities (e.g., luteal insufficiency, oligomenorrhea, anovulatory cycles), weight gain (with estrogen–progesterone shifts influencing insulin sensitivity and muscle protein synthesis), low libido, poor metabolic markers, and syndromic patterns such as polycystic ovary syndrome, functional hypothalamic amenorrhea, and a shift toward catechol estrogen production (especially 4-hydroxylation) (Khalid et al., 2023; Kumari et al., 2024; Słowińska-Lisowska & Jagielska, 2024).

Additionally, nutritive overabundance, particularly from diets high in refined, high–glycemic-load carbohydrates and pro-inflammatory fats and oils (i.e., excess omega-6 relative to omega-3, shifting eicosanoid signaling toward initiation rather than resolution of inflammation) (Mariamenatu & Abdu, 2021; Valgimigli, 2023), creates a propensity for insulin resistance and the spectrum of metabolic syndrome. Resultant hyperinsulinemia and low-grade inflammation increase cardiometabolic risk (prediabetes, type 2 diabetes, hypertension, dyslipidemia characterized by low HDL, elevated triglycerides, and small, dense, oxidizable LDL particles). These same mechanisms may also perturb the female hormonal milieu. Dysglycemia and cytokine signaling can alter Gonadotropin-releasing hormone (GnRH) pulsatility and HPO axis tone (Athar et al., 2024). Lower sex hormone–binding globulin (SHBG) from hyperinsulinemia plus higher aromatase with adiposity can increase free sex steroids and shift estrogen balance, potentially contributing to oligomenorrhea, anovulation, short luteal phases, and PCOS-spectrum presentations (Coradini & Oriana, 2020; Ostinelli et al., 2022).

Diet is critical. Yet current Dietary Guidelines for Americans (DGA), with their high inclusion of refined grains and industrial vegetable oils, remain narrowly focused on lowering total cholesterol to improve cardiovascular risk—an increasingly outdated emphasis (Achterberg et al., 2022; Astrup et al., 2021). Contemporary analyses show that total cholesterol alone is a limited predictor of cardiovascular events, and even LDL-C’s clinical impact depends on subtypes and particle characteristics, with small, dense LDL more atherogenic than larger, buoyant particles (Liou & Kaptoge, 2020). More broadly, cholesterol reflects metabolic health within an inflammatory process rather than acting as a singular cause. The most predictive dyslipidemic profile combines low HDL-C, high triglycerides, and normal or elevated small, dense LDL—patterns that co-occur with dysglycemia and hyperinsulinemia. Even the American Heart Association’s newer PREVENT equations now assess total and HDL cholesterol together with blood pressure, diabetes, BMI, smoking, and kidney function to estimate 10- and 30-year cardiovascular risk (American Heart Association, 2023). This shift underscores a broader understanding of cardiometabolic health rather than LDL-C in isolation.

And these outdated dietary guidelines create a cascade of hormonal consequences. For one, when prediabetes is included, current CDC (2024) estimates suggest that roughly 50% of the adult population lies somewhere on the diabetes spectrum. This blanket high-carbohydrate dietary pattern, typically low in healthy fats and adequate protein, is a poor match for this metabolically vulnerable phenotype (Astrup et al., 2021). It fosters progression toward metabolic syndrome and the associated hormonal dysregulation of insulin and sex steroids (through increased aromatase activity in adipose tissue), as well as disturbances in hunger-regulatory hormones such as ghrelin and leptin (Coradini & Oriana, 2020; Ostinelli et al., 2022).

If followed rigidly, such guidelines may indeed lower total cholesterol, but they also eliminate or restrict many foods essential to women’s hormonal health (Mashhadi et al., 2025). Key nutrients at risk include bioavailable heme iron. Iron deficiency (ID) remains the most common nutrient deficiency globally, and maintaining robust iron stores during the menstruating years is critical to offset menstrual losses (MacLean et al., 2023). Low iron impairs oxygen delivery, thyroid hormone conversion (Swapnika et al., 2024), and energy metabolism, often manifesting as fatigue, reduced exercise tolerance, and impaired fertility status (Holzer et al., 2023). The best sources of heme iron include liver, red meat, shellfish, and dark poultry, while non-heme iron from plant foods is less bioavailable, often bound to lectins and phytates, and may require concurrent vitamin C intake to enhance absorption.

Preformed vitamin A from foods such as grass-fed liver, shellfish, and full-fat dairy, and its active metabolite, retinoic acid (RA), play critical roles in ovulation by supporting follicle development and maturation through granulosa cell proliferation and differentiation (Zhang et al., 2025). Additionally, within follicular fluid, vitamin A appears to play a dual role: acting as an antioxidant that protects the follicle and oocytes from oxidative stress, and finely tuning progesterone production through its influence on granulosa-cell steroidogenesis (Fonseca et al., 2023). Maintaining optimal retinoic acid levels—neither too high nor too low—therefore seems critical for healthy ovulation and oocyte development. While many nutrition professionals reflexively point to β-carotene as a substitute, conversion to retinol is highly variable and genetically influenced, and a substantial subset of women are low converters; thus, relying solely on provitamin A sources may be insufficient for some (Von Holle et al., 2024).

Another key nutrient that may become deficient on a low-cholesterol, low–animal-food diet is choline. It is critical for fertility, supplying methyl groups for phospholipid synthesis and participating in estrogen metabolism via estrogen-responsive PEMT activity which becomes even more critical for postmenopausal women when estrogen naturally declines (Van Parys, 2021). It also supports fetal neural tube development if conception occurs. In addition, choline contributes methyl groups (via betaine → SAM) that support phase II methylation pathways helping maintain a more favorable estrogen metabolite profile when hepatic function and methylation capacity are sufficient (Venter et al., 2025). While choline is available in limited quantities from some plant-based foods, the highest concentrations are found in animal foods, particularly egg yolks and organ meats (liver), with substantial amounts in shellfish, beef, poultry, and fish.

Lastly, zinc, a mineral required for numerous structural proteins and enzymes, is also essential for reproductive health in females. As Liu et al. (2024) point out, zinc is essential for follicle development and oocyte maturation; insufficiency is associated with suboptimal ovulatory function and reduced luteal progesterone output. Zinc deficiency has been linked to disrupted mitochondrial dynamics and increased oxidative stress within ovarian tissue. The richest sources include oysters, beef, lamb, poultry and eggs with lesser amounts found in legumes, nuts and whole grains and often bound to phytates.

For the aforementioned micronutrient considerations, as well as for the benefit of maximizing insulin sensitivity and supporting overall metabolic wellness in the quest to protect the female endocrine milieu, practitioners may find great value in approaching nutrition through a functional lens, one that honors ancestral food inclusion and the individual appropriateness of foods. This means moving beyond outdated dietary guideline dogma and embracing the whole, unprocessed foods that have nourished humans, and notably women, throughout millennia.

The following framework begins with the practical application of macronutrient categories, followed by additional considerations that shape a biochemically individualized approach to supporting and enhancing both the sex hormone environment and metabolic health, recognizing that there are many points of intersection between the two.

Prioritizing Protein

Protein, meaning “of first importance,” is a critical component of the diet. Unlike fats and carbohydrates, which are primarily used for energy, protein serves as the body’s main structural building material. The amino acids that make up protein are used to form hormones, neurotransmitters, tissues, and enzymes, all of which enable the body’s processes to function efficiently. Protein supports numerous physiological roles, including the synthesis of gastrointestinal hormones such as leptin and ghrelin, which regulate hunger and satiety (Kohanmoo et al., 2020); the production of insulin and glucagon, which work together to maintain blood sugar balance and, in turn, support female hormonal regulation; and the stabilization of postprandial blood glucose through its ability to slow gastric emptying and moderate the rise in blood sugar after meals (Wolever et al., 2024).

This regulation of metabolism, as well as the synthesis of metabolic hormones, is critical for female hormonal balance, as protein’s role in preventing insulin resistance helps protect against inflammation, which can act as physiological static noise, disrupting hormonal signaling and creating imbalances in the female hormonal cascade (Athar et al., 2024; Püschel et al., 2022). Additionally, as women enter perimenopause and beyond, declining estrogen makes it increasingly difficult to maintain muscle mass; adequate protein intake, especially with advancing age, is essential for stimulating muscle protein synthesis (Simpson et al., 2022). Dietary protein supports training adaptations, helping maintain lean body mass and metabolic health.

It is not only the quantity of protein that matters but also the quality, specifically, obtaining a complete array of amino acids, both essential and conditionally essential. Without these building blocks, protein synthesis becomes limited due to insufficient raw materials. While recent trends have sought to downplay the importance of animal foods, these remain the most efficient and balanced sources of essential amino acids. Although certain plant foods, such as soy, quinoa, buckwheat, and spirulina, are considered complete proteins, their amino acid ratios and digestibility scores are generally less optimal for stimulating muscle protein synthesis (van Vliet, Burd, & van Loon, 2015). Animal proteins, in contrast, provide higher levels of branched-chain amino acids (particularly leucine), which play a central role in muscle protein synthesis and, by extension, in maintaining lean mass, metabolic health, and hormonal balance in women (Lim, Pan, Toh, Sutanto, & Kim, 2021). Additionally animal foods are the only source of naturally occurring creatine in the diet. One illustrative example comes from an NHANES review that examined female hormonal disruption in relation to creatine, a compound synthesized from amino acids and found predominantly in meat, particularly red meat and fish. Women with creatine intakes below 13 mg/kg of body weight were 26% more likely to require hormone replacement therapy, 33% more likely to report irregular menstrual cycles, 42% more likely to undergo hysterectomy, and 68% more likely to experience pelvic infection (Ostojic et al., 2024). The takeaway is clear: adequate protein is not simply a concern for athletes; it exerts profound effects on fertility, hormonal balance, and women’s health at large.

Lastly, it is important to address the persistent claims that protein is “bad for the bones” or “hard on the kidneys.” Much research from the past decade indicates the opposite. Protein has been shown to enhance osteoblastic activity and bone formation through improved calcium absorption in the gut. Furthermore, both researchers and professional organizations have recognized that advances in nitrogen balance methodology since the 2005 dietary guidelines have clarified earlier misconceptions. These updates correct for prior overestimations of nitrogen intake and underestimations of nitrogen loss, which previously led to misleading conclusions. In addition, current insights into amino acid metabolism suggest that while the body can adapt to low protein intake, such compensation is functional rather than optimal (Weiler et al., 2024). Regarding renal health, recent evidence demonstrates that higher protein intake does not impair kidney function in healthy individuals and may, in fact, confer benefits. A study published in JAMA Network Open found that greater consumption of total, animal, and plant protein was associated with lower mortality in older adults, including those with chronic kidney disease (Kovesdy et al., 2023).

Putting It All Together: Considerations for Practitioners

Much expert opinion asserts that protein needs are likely higher than the 0.8 g/kg body weight recommended by the recommended dietary allowance (RDA) (Burstad et al., 2025; Weiler et al., 2023). High quality contemporary analysis suggests higher intakes for specific populations—typically in the range of 1.2–2.0 g/kg body weight—particularly during times of increased metabolic demand such as preconception, pregnancy, lactation, injury, and athletic training (Burstad et al., 2025; Stephens et al., 2015). Clinicians should pay special attention to periods of hormonal transition. During the luteal phase, higher progesterone favors nutrient partitioning toward the endometrium rather than muscle tissue, increasing the importance of adequate protein intake (Wohlgemuth et al., 2021). Similarly, during perimenopause and menopause, declining estrogen reduces muscle protein synthesis efficiency and impairs insulin sensitivity, creating a greater need for dietary protein to preserve lean mass and metabolic stability (Black & Matkin-Hussey, 2024). Pregnant and lactating women also require higher protein intake to support fetal growth and milk production, as amino acid demands substantially rise in these stages (Burstad et al., 2025; Weiler et al., 2023).

Fats for Endocrine Health

The late-20th-century “low-fat era” saw manufacturers remove fat from foods and replace it with refined sugars, grains, and flavor enhancers to restore palatability. This shift was not solely industry-driven; it reflected early, incomplete hypotheses (e.g., Ancel Keys’ work and the Seven Countries Study), federal policy, and a public increasingly concerned about rising coronary mortality (Teicholz, 2014). Despite limited evidence directly linking total or saturated fat to cardiovascular disease, the Dietary Goals for the United States (1977) promoted broad fat reduction. In the decades that followed, low-fat eating patterns coincided with rising dysglycemia and metabolic disorders. Even as Americans reduced intake of several “off-limits” foods, the metabolic burden increased; today, approximately half of individuals aged 13 years or older are estimated to be on the pre-diabetes and diabetes spectrum (Centers for Disease Control and Prevention, 2024). High-quality evidence over the past decade has not demonstrated the robust, causal relationship between saturated fat intake and cardiovascular disease risk that was historically assumed. Where benefits are observed, they are generally modest and depend on the nutrient replacement (e.g., polyunsaturated fats vs. refined carbohydrates) (Achterberg et al., 2022; Astrup et al., 2021). Notably, a 2020 Cochrane review estimated that about 56 people would need to reduce saturated fat for four years for one person to avoid a CVD event, with no reduction in all-cause or coronary mortality observed (Hooper et al., 2020).

Why Fats Matter for Female Physiology

Dietary fatty acids are essential for the synthesis of steroid hormones, including estrogen, progesterone, testosterone, and cortisol, which all derive from the parent molecule pregnenolone. Pregnenolone itself is synthesized from a cholesterol backbone, and adequate dietary fat helps ensure sufficient substrate for both steroidogenesis and cellular signaling.

A recent systematic review by Colebatch, Fuller, Mantzioris, and Hill (2025) examined the relationship between dietary fat intake and bone stress injury risk in women, finding that lower-fat diets were significantly associated with higher bone stress injury risk. The authors suggested that this may be due, at least in part, to reduced estrogen production secondary to diminished steroidogenesis, as estrogen plays a key role in osteoblastic bone remodeling and bone density maintenance.

Notably, earlier studies, many of which severely restricted dietary fat intake (15-20% total energy) compared with more moderate reductions used in recent research, found that women with ovulatory irregularities consumed substantially less dietary fat than women with regular cycles (Laughlin, Dominguez, & Yen, 1998). Controlled feeding studies also demonstrated that low-fat diets, independent of fiber intake, lowered circulating levels of estrogen, progesterone, and luteinizing hormone (Rose et al., 1987). While strategic fat reduction may be appropriate in select cases of estrogen excess or dyslipidemia, it should be carefully balanced against potential impacts on estrogen and progesterone, which more commonly trends low in the context of modern stress and nutrient insufficiency. In short, adequate dietary fat is essential for maintaining female hormonal balance.

At the cellular level, fats form the phospholipid bilayer of all cells. Unsaturated fats provide membrane fluidity, while saturated fats contribute stability and structure, and both are essential for receptor function, hormone signaling, and inflammatory balance. Because all sex steroids are synthesized from cholesterol, adequate fat intake supports substrate availability for hormone production. Although the body can compensate to some degree through endogenous cholesterol synthesis, human studies have shown that even a single statin dose can acutely inhibit steroidogenesis and reduce circulating steroid hormone precursors, reinforcing the link between cholesterol metabolism and hormone synthesis (London et al., 2020).

Dietary fat also helps stabilize postprandial glucose by slowing gastric emptying and moderating glycemic excursions, thereby supporting HPO-axis stability and insulin sensitivity (Słowińska-Lisowska & Jagielska, 2024). In addition, fats facilitate the absorption and delivery of fat-soluble vitamins; preformed vitamin A (retinol) and vitamin D are predominantly found in animal-sourced foods, while vitamin E is abundant in high-quality plant oils and vitamin K is present as K₁ in leafy greens and as K₂ in certain animal and fermented foods. Finally, essential fatty acids (omega-3 and omega-6) are required for eicosanoid and specialized pro-resolving mediator production, which shape immune balance and the inflammation–resolution cycle relevant to ovarian and endometrial health (Mohammadi et al., 2022).

The Problem with Seed Oils: Clinical Considerations for Overall Health

Vegetable oils, also known as seed oils, are a relatively new addition to the human diet, with large-scale use beginning in the early 20th century through hydrogenation technologies that produced shelf-stable fats such as Crisco (Teicholz, 2014). Although industrial trans fats have since been banned in the United States, non-hydrogenated polyunsaturated seed oils remain widely used in processed foods.

Polyunsaturated fatty acids (PUFAs) are especially prone to lipid peroxidation, generating oxidative by-products that impair membrane integrity and can amplify systemic inflammation. Because bis-allylic hydrogens in PUFAs are highly susceptible to radical attack, peroxidation proceeds in orders of magnitude faster than in mono- or saturated fats (Mariamenatu & Abdu, 2021; Valgimigli, 2023). From a culinary-historic perspective, most traditional cooking fats were richer in mono- and saturated fatty acids which are more oxidation-stable under heat than PUFA-rich oils. While both omega-6 and omega-3 fatty acids are essential, their relative proportion shapes the inflammatory milieu: evolutionary analyses estimate ancestral intakes near 1–2:1 (n-6:n-3) (Kuipers et al., 2010), whereas modern Western patterns often exceed 15–20:1(Djuricic & Calder, 2021), favoring pro-inflammatory eicosanoid pathways.

Uncovering the true health risk of industrialized, high-omega-6 seed oils is complicated by the fact that most intervention trials are short term, often only a few weeks, and therefore capture only transient shifts in mid-range biomarkers. Some short-term studies show modest improvements in lipid or inflammatory markers, while others show harm. And importantly, these studies rarely account for the slow turnover of cellular membranes; it can take years of dietary exposure for linoleic acid and other omega-6 fatty acids to accumulate to levels that meaningfully influence oxidative stress liability or disease risk (Guyenet & Carlson, 2015). Consequently, brief trials provide limited insight into outcomes that develop over decades, such as increased cancer or all-cause mortality risk (O’Keefe, DiNicolantonio, & Lavie, 2018).

Long-term evidence warrants concern. Adding weight to the picture, a large 2024 population cohort of 179,230 UK adults found that participants with higher plasma omega-6:omega-3 ratios had significantly greater risks of cancer mortality, cardiovascular mortality, and all-cause mortality over years of follow-up (Zhang et al., 2024). This recent data mirrors the only truly long-term trials we have on potential seed-oil harm, often called the classic “core” diet-heart trials from the 1960s–70s. These include the Sydney Diet Heart Study (re-analysis of recovered data: higher-LA safflower oil increased all-cause, CHD, and CVD mortality) (Ramsden et al., 2013), the Minnesota Coronary Experiment (no mortality benefit despite cholesterol lowering; each 30 mg/dL drop in total cholesterol linked to higher death risk) (Ramsden et al., 2016), and the Los Angeles Veterans Trial (signal for higher cancer incidence in the high-PUFA arm) (Pearce & Dayton, 1971). In parallel, reevaluation of randomized controlled trials underlying the historic 10 % saturated-fat cap indicates that, while lowering saturated fat may reduce LDL-cholesterol, the effect on cardiovascular or all-cause mortality is smaller than previously thought or nonsignificant (Hooper et al., 2020; Astrup et al., 2020). Additionally, linoleic acid (LA) is the predominant oxidized fatty acid in LDL, and individuals with coronary artery disease (CAD) show higher absolute LA concentrations in serum cholesteryl esters and phospholipids, raising the question of whether increasing omega-6–rich oils is truly cardioprotective despite lowering LDL-C (O’Keefe, DiNicolantonio, & Lavie, 2018).

Lastly, emerging clinical evidence supports the role of omega-3 fatty acids in modulating the menstrual cycle and improving premenstrual symptoms, likely through anti-inflammatory and hormone-regulatory effects (Mohammadi et al., 2022). These findings underscore the importance of rebalancing fatty acid intake rather than indiscriminately reducing all dietary fat. This is relevant because many common seed oils (soybean, corn, peanut, sunflower) have omega-6:omega-3 ratios heavily weighted toward omega-6, which can shift eicosanoid pathways toward unresolved inflammation (Mariamenatu & Abdu, 2021).

Putting It All Together: Considerations for Practitioners

From a functional nutrition perspective, prioritizing stable, ancestral, minimally processed fats such as olive oil, avocados, grass-fed dairy, pastured animal foods, and certain tropical oils, while moderating omega-6–dense seed oils, can better support women’s metabolic and hormonal health. Because women tend to rely more on fat oxidation in the luteal phase, very low-fat intakes during menstruating years warrant caution (Wohlgemuth et al., 2021). As a practical floor, about 25% of total calories from fat helps maintain steroidogenesis, satiety, and metabolic flexibility. A commonly effective working range for many women is 30–45% of calories from fat, adjusted to individual metabolic status and energy needs. In insulin resistance and PCOS, it may be clinically useful to trial higher fat intakes—up to 60% of calories within a well-formulated ketogenic approach—to reduce testosterone, improve insulin sensitivity, and support ovulation, with dosing individualized and monitored for response (Athar et al., 2024; Pandurevic et al., 2023).

It is often useful to consider carbohydrate tolerance first, based on glycemic control and metabolic status. After that, fat is adjusted to meet energy needs while protein remains prioritized for tissue repair and maintenance. In short: set protein, then set carbohydrates to the individual’s threshold, and allocate the remainder to fat, not dropping below 25%, with emphasis on fatty-acid quality and micronutrient density.

Carbohydrates: Finding the Personal Carbohydrate Threshold

Carbohydrates are sugars and starches used for readily available energy. They’re present in nearly all plant foods and range from nutrient-dense, low-glycemic sources to highly processed, high-glycemic varieties. Whole-food carbohydrates provide vitamins, minerals, phytochemicals, and fiber that support the gut microbiome, including the estrobolome, the subset of commensal gut microbes capable of metabolizing estrogens through the action of β-glucuronidase enzymes (Ervin et al., 2019). These bacteria influence circulating estrogen levels by modulating deconjugation and reabsorption of estrogen metabolites. Such dietary fibers also help stabilize blood glucose, reduce glycemic variability, and improve cholesterol ratios (Seal et al., 2021).

 Though not technically essential, small-to-moderate carbohydrate intake can support hormone regulation in some women. Short-term ketogenic feeding in healthy adults has been reported to shift thyroid indices (lower TSH, lower T3) and lower insulin (Majid et al., 2022). Clinically, this underscores biochemical individuality: women with low T3/thyroid output may tolerate, or even benefit from, slightly higher whole-food carbohydrate intake within their personal threshold, whereas women with hyperinsulinemia or PCOS often benefit from lower-carbohydrate targets to reduce insulin and downstream androgen production (Athar et al., 2024). Carbohydrate needs should therefore be individualized to a personal carbohydrate threshold that avoids dysglycemia and metabolic disruption. When exceeded, dysglycemia contributes to insulin resistance, diabetes, cardiovascular disease, and hormonal imbalances such as estrogen dominance and PCOS (Purwar & Nagpure, 2022; Athar et al., 2024).

Some clinicians promote high-carbohydrate diets to “support” hormonal balance, yet much of this literature conflates carbohydrate restriction with overall caloric restriction. It is well established that caloric deprivation, rather than carbohydrate reduction alone, lowers estrogen and progesterone (Słowińska-Lisowska & Jagielska, 2024). Insulin sensitivity also varies across the menstrual cycle and tends to decline in the luteal phase (Gamarra & Trimboli, 2023). NHANES data from over 1,900 women show cyclical shifts in glucose, triglycerides, and insulin sensitivity independent of BMI across the menstrual cycle (MacGregor, Gallagher, & Moran, 2021). In women with PCOS, ketogenic interventions reduce the LH/FSH ratio and free testosterone by 36% and 30%, respectively (Khalid et al., 2023).

For most women, a moderately low to moderate carbohydrate range of 20–45% of total calories, below the typical Western 45–65%, balances nutrient sufficiency with metabolic stability. Historically, many traditional populations appear to have consumed less carbohydrate than current DGA recommendations while maintaining robust fertility (Cordain et al., 2000; Giangregorio et al., 2024; Price, 2009). Individual tolerance varies by genetics, gut health, stress, metabolic history, and activity; women with insulin resistance, PCOS, or gut dysbiosis often do better on the lower end, whereas those with high insulin sensitivity or higher training loads may thrive with more.

While many benefit from moderating carbohydrate intake, extreme or prolonged carbohydrate reduction without adequate total energy can reduce glucose availability and signal energy scarcity to the hypothalamic–pituitary–ovarian (HPO) axis, suppressing reproductive output. Sustained energy deficits on very low-carbohydrate diets can elevate cortisol and blunt GnRH, LH, FSH, and free T3 signaling (Słowińska-Lisowska & Jagielska, 2024).

Conversely, excessive carbohydrate intake, particularly refined/high-glycemic sources, promotes inflammation, insulin resistance, and hormonal imbalance. Chronic hyperinsulinemia increases ovarian androgen production and is strongly associated with PCOS (Athar et al., 2024). High-carbohydrate patterns can also drive reactive hypoglycemia, triggering cortisol release and HPO-axis dysregulation (Tada et al., 2025; Koukoubanis et al., 2023), perpetuating fatigue, cravings, and hormonal instability.

In sum, individualized carbohydrate balance supports hormonal and metabolic stability when aligned with whole-food proteins and healthy fats.

Putting It Together: Personal Carbohydrate Threshold

For practitioners, it is important to emphasize whole-food carbohydrate sources alongside fat and protein to limit postprandial excursions and reduce dysglycemia. Within carbohydrate choices, promote fiber-rich options to slow gastric emptying and intestinal absorption, thereby protecting glycemic control.

Carbohydrates must be matched to biochemical individuality. If carbohydrate intake is too low or too high for an individual’s physiology, the body may interpret inadequate or unstable energy availability (Athar et al., 2024). This can present as unstable glycemia (either from excessively low carbohydrate intake or from reactive hypoglycemia driven by excessively high intake), increased cortisol, and lowered T3 production, all of which can negatively impact HPO-axis function.

In the luteal phase, it may be helpful for female clients to prioritize fats and proteins while including some high-quality carbohydrates to support the endometrial lining (a glucose-rich tissue relevant to potential implantation) (Chen & Dean, 2023), help regulate cravings and support serotonin via insulin-mediated selective uptake across the blood–brain barrier (Sacher et al., 2023), and maintain stable energy while minimizing dysglycemia.

For insulin-resistant, sedentary, or stress-sensitive individuals, a carbohydrate intake of about 20–35% of total calories often helps to support or improve metabolic function. In cases of significant insulin resistance or PCOS, therapeutic ketogenic approaches (<15–20% of calories, or <50 g/day) may further improve insulin sensitivity, ovulation, and androgen balance when well-formulated and nutrient-sufficient (Khalid et al., 2023). Reproductive-age women who are moderately active and metabolically healthy may do well with 30–45% of calories from carbohydrates. High-performing athletes, breastfeeding mothers, or very active women may require 45–55% of calories from carbohydrate for optimal performance (but this is not universal), drawn primarily from whole-food sources.

Intermittent Fasting and the Female Body

Intermittent fasting (IF) is a common nutritional strategy that limits eating to a defined window within a 24-hour period. Popular forms include 16:8 (fasting for 16 hours, eating during an 8-hour window), 12:12 (a 12-hour overnight fast), or OMAD (one meal a day). When implemented thoughtfully, fasting can maintain adequate calorie and nutrient intake; however, when used primarily for rapid weight loss, it often results in reduced energy and micronutrient insufficiency. Pushing the first meal too late in the day can make it difficult to meet caloric and nutrient needs required for optimal female hormonal function.

Aggressive fasting programs marketed toward women raise concern because undereating is one of the most well-established causes of ovulatory dysfunction and hormonal disruption (Saadedine et al., 2023). The female endocrine system is highly sensitive to perceived energy deficits. During times of low intake, interpreted biologically as potential famine, the body prioritizes survival over reproduction. This adaptive response involves several regulatory systems. The HPO axis downregulates gonadotropin release, lowering luteinizing and follicle-stimulating hormone and, in turn, reducing estrogen and progesterone (Saadedine et al., 2023). The hypothalamic-pituitary-adrenal (HPA) axis becomes overactive, raising cortisol, while thyroid function may downshift to conserve energy. Collectively, these changes can lead to fatigue, oligomenorrhea, luteal phase defect (LFD) and in some cases, worsening body composition (decreased lean mass and increased central adiposity) despite caloric restriction.

Nevertheless, intermittent fasting does have potential benefits when applied judiciously. Our ancestors likely experienced fasting periods without constant food availability. Short, structured fasting windows may help improve insulin sensitivity and glycemic stability, particularly in women with insulin resistance or polycystic ovary syndrome (PCOS), where metabolic improvement is often observed (Silva et al., 2023).

A balanced approach allows women to reap the metabolic benefits of time-restricted eating without compromising hormonal health. Practitioners can encourage clients to align food intake with circadian rhythms by front-loading nutrition earlier in the day. Individuals may be more insulin-sensitive earlier in the day and transiently more insulin-resistant toward evening due to effects of melatonin, a physiological rhythm that promotes stable blood glucose during overnight fasting (Garaulet et al., 2020). Shifting food intake earlier helps moderate morning cortisol and enhances nutrient utilization when the body is most metabolically efficient.

For most cycling women, maintaining an eating window of 8–12 hours supports both metabolic and hormonal stability. Clinically, the author has observed that narrower fasting windows often suit men better, whereas reproductive-aged women typically benefit from slightly longer eating periods and adequate energy intake to maintain total daily energy expenditure (TDEE).

A well-planned intermittent fasting approach can be safe for many women, provided key warning signs are monitored. Indicators that fasting may not be well tolerated include irregular cycles, missed or light periods, mid-cycle spotting, worsened PMS, a shortened luteal phase, or consistently low basal body temperatures. Longer intermittent fasting should not be utilized during pregnancy, for those with a history of disordered eating, or in cases of hypothalamic amenorrhea.

Nourish with Nutrient Density: Ancestral Wisdom in a Modern Context

While macronutrient balance matters, it should never displace the foundational principle of eating real, nutrient-dense food. Historically, humans prioritized nutrient density and bioavailability over dietary dogma, practicing nose-to-tail eating and preparing plant foods through cooking, soaking, sprouting, and fermentation to enhance absorption. In the 1930s, Weston A. Price documented the robust health of traditional, ancestral populations, noting the ease of childbearing and robust fertility of the pre-industrialized women, and found their diets provided substantially higher concentrations of fat-soluble and water-soluble vitamins and minerals compared with modern fare; when these groups adopted “displacing foods of commerce,” dental health and broader markers of vitality deteriorated (Price, 2009).

For women, the loss of nutrient density may be especially consequential. Adequate intakes of fat-soluble vitamins (A, D, E, K), bioavailable minerals (calcium, magnesium, iron, zinc, iodine, selenium), and high-quality proteins support ovarian function, thyroid health, adrenal balance, and the synthesis and regulation of estrogen, progesterone, and other hormones. Insufficiency across these nutrients is associated with irregular cycles, more severe PMS, low progesterone, relative estrogen dominance, reduced fertility, and metabolic instability (Mashhadi et al., 2025). Emphasizing nutrient-dense whole foods including pastured animal products, properly prepared plant foods, organ meats, fermented foods, and mineral-rich bone broths broadly supports hormonal balance, builds metabolic resilience, and enhances energy and overall health.

In summary, guiding women across the lifespan, from early fertility through perimenopause, menopause, and beyond, requires micronutrient-dense foods and macronutrient ratios tailored to biochemical individuality. Standard guidelines can serve as a starting point, but they are rarely precise enough to address the complexity of the female sex-hormone milieu or the widespread metabolic resistance affecting multiple systems, including reproduction. With thoughtful practitioner oversight, a personalized framework can integrate these considerations to restore or improve hormonal balance, strengthen metabolic resilience, and support longevity while reducing the symptom burden of imbalance.

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