Can the Ketogenic Diet Help With Fertility?

Summary

Background: Infertility affects about 15% of the population in developed countries [1]. Polycystic ovary syndrome (PCOS) affects up to 20% of reproductive-age individuals and is strongly linked to obesity [2]. Because insulin resistance and excess weight are common in PCOS, researchers have asked whether a ketogenic diet (KD) could improve metabolic, hormonal and reproductive measures.

Scope: This article is a narrative summary of published meta-analyses, clinical studies and laboratory studies on ketogenic diets, PCOS and fertility in women and men. It is not a systematic review.

What the evidence shows: In meta-analyses of small studies in women with PCOS and overweight or obesity, ketogenic diets were associated with weight loss and with lower glucose, insulin, HOMA-IR, LH, LH/FSH ratio and testosterone, and higher SHBG [3, 7, 8, 9]. Most included studies were not randomized; in two randomized trials that compared ketogenic diets with low-calorie diets, body weight did not differ significantly [8]. Reports of pregnancy outcomes come from small retrospective analyses and case series without control groups [2, 10, 11].

Conclusions: Ketogenic diets are a promising research area for women with PCOS and overweight or obesity, but the evidence is described by its own authors as low quality and heterogeneous, and larger high-quality randomized trials are needed to determine clinical efficacy [9]. The ketogenic diet is not an established fertility treatment, and its safety during pregnancy has not been established [15]. Anyone considering it while trying to conceive should work with their clinician.

Introduction and Epidemiology of Infertility and PCOS

Infertility affects approximately 15% of the population in developed countries, and its prevalence is increasing [1]. Modifiable factors such as diet may influence both female and male fertility [1]. PCOS is the most common endocrine disorder in women, and it is diagnosed when at least two of the following are present: hyperandrogenism, oligo-anovulation and polycystic ovaries [3]. It affects up to 20% of reproductive-age individuals and is strongly linked to obesity [2].

Obesity is associated with greater menstrual irregularity and with PCOS, and individuals with obesity often show higher testosterone and fasting insulin and lower sex hormone-binding globulin (SHBG), a pattern similar to PCOS [4]. Obesity in adolescence is linked to later gynecologic and obstetric complications, including infertility [4]. These overlaps have prompted interest in dietary approaches that address both metabolic and reproductive health.

Pathophysiology of Insulin Resistance and Its Impact on Fertility

Insulin Resistance in PCOS and Female Fertility

Obese women show decreased insulin sensitivity and persistent hyperinsulinemia, which may be involved in the development of PCOS [5]. Metabolic disorders such as diabetes, obesity and hyperlipidemia are suspected to affect fertility either by direct damage to oocyte health or by interfering with the hypothalamic-pituitary axis [5]. Reducing insulin secretion through dietary change is therefore considered an attractive non-drug approach [5].

Male Fertility and Metabolic Dysfunction

In men, obesity and low testosterone are linked in both directions: hypogonadism is more common in men with obesity, and weight loss raises testosterone [13].

The Ketogenic Diet: Mechanisms of Action in Metabolic and Reproductive Health

Dietary Composition and Metabolic Induction

The ketogenic diet restricts carbohydrate enough to induce ketosis, in which ketone bodies become a major fuel. The PCOS studies used several versions, including very-low-calorie ketogenic diets (VLCKD), low-calorie ketogenic diets (LCKD), classic ketogenic diets (CKD) and a Mediterranean eucaloric ketogenic diet (KEMEPHY) [3]. These protocols differ widely in calories and carbohydrate, which makes studies hard to compare.

Much of the metabolic benefit seen in these studies accompanies weight loss. The ketone body β-hydroxybutyrate also has direct biological effects: in cells and mice it inhibits class I histone deacetylases, increases expression of the oxidative-stress resistance genes Foxo3a and Mt2, and protects mice against oxidative stress [6]. Whether these effects contribute to fertility outcomes in people has not been tested.

Effects on Female Fertility: Hormonal and Metabolic Parameters

PCOS-Specific Outcomes and Hormonal Balance

A meta-analysis of seven studies in women with PCOS and overweight or obesity reported results as standardized mean differences (SMD, a unitless effect size) [7]. After a ketogenic diet, women had lower body weight (SMD 1.31, 95% CI 0.45 to 2.17), BMI (SMD 1.27, 95% CI 0.71 to 1.83), blood glucose (SMD 1.36, 95% CI 1.08 to 1.64), insulin (SMD 1.15, 95% CI 0.60 to 1.70), HOMA-IR (SMD 1.84, 95% CI 0.72 to 2.96) and triglycerides (SMD 1.11, 95% CI 0.53 to 1.68) [7]. LH and the LH/FSH ratio fell, FSH rose, free and total testosterone fell, and SHBG rose [7]. Data on pregnancies were too scarce to analyze [7].

A second meta-analysis of 10 studies (three randomized trials, one non-randomized intervention study, four cohort studies and two case series) found improvements after ketogenic diets compared with baseline, and lower glucose, HOMA-IR and LH than with low-calorie diets [8]. However, the two randomized trials that compared ketogenic diets with low-calorie diets found no significant difference in body weight [8]. A 2026 meta-analysis found that ketogenic diets were associated with lower total testosterone and LH/FSH ratio and higher SHBG, but its authors judged the available studies to be of low quality and heterogeneous and called for larger, high-quality randomized trials [9].

Menstrual Regularity and Ovulation Restoration

In a retrospective review of the records of 30 women with PCOS who followed a ketogenic diet for at least 3 months at the Cleveland Clinic, all 30 had restoration of regular menstrual cycles [2]. The study had no control group, so it cannot show how much of this was caused by the diet.

Weight Loss, Body Composition Changes, and Metabolic Improvements

VLCKD Before Assisted Reproduction

In a prospective case series, 52 women with overweight or obesity scheduled for assisted reproductive technology (ART) were enrolled in a meal-replacement VLCKD (less than 800 kcal/day for 3 months), followed by a 6-month transition with gradual carbohydrate reintroduction and a Mediterranean-style maintenance diet [10]. Of the 40 women who started the VLCKD, 27 (68%) lost at least 10% of body weight while preserving lean mass [10]. BMI, fat mass, waist circumference, glucose metabolism, lipid profile and liver function improved, and no adverse events were reported [10]. The study had no comparison group.

Effects on Male Fertility and Testicular Function

Testosterone and the Hypothalamic-Pituitary-Testicular Axis

A meta-analysis of seven studies (230 participants) found that total testosterone rose after ketogenic diets, more so with VLCKD, and that the rise was correlated with age and with the amount of weight lost [13]. In 22 men with obesity, 28 days of VLCKD raised total testosterone and SHBG, while calculated free testosterone and LH did not change [14].

Effects on bioavailable hormones are not uniformly favorable. In a three-week randomized crossover study of 11 middle-aged adults with obesity (five men), a ketogenic diet increased SHBG in men and women and lowered the free androgen index and free estradiol index in both [12]. Total testosterone in men did not differ significantly from the standard diet (20.2 ± 1.23 vs 18.2 ± 1.23 nmol/l, p = 0.1), while the free androgen index decreased (0.65 ± 0.05 vs 0.74 ± 0.05, p = 0.04) [12]. The clinical impact of this reduction has not been studied [12].

Spermatogenesis and Sperm Quality

We did not find controlled human studies showing that a ketogenic diet improves sperm quality or male fertility outcomes. Any effect on male fertility remains unproven.

Assisted Reproductive Technology Outcomes

Implantation and Pregnancy Outcomes with Ketogenic Diet Preparation

A retrospective study evaluated 12 women with PCOS and insulin resistance who had a previous failed IVF cycle [11]. They followed a ketogenic diet of 50 g total carbohydrate and 1,800 calories per day for 14 ± 11 weeks before another IVF cycle. Carbohydrate intake fell from 208 ± 50.5 to 41.71 ± 10.1 g/day, weight fell by 7.9 ± 1.1 kg, and fasting glucose, triglycerides, fasting insulin and HOMA-IR decreased [11].

Compared with each woman's previous failed cycle, oocyte number, fertilization rate and viable embryos did not differ, while implantation (83.3% vs 8.3%), clinical pregnancy (66.7% vs 0%) and ongoing pregnancy/live birth (66.7% vs 0%) rates were higher [11]. Because each woman was compared only with her own earlier failed cycle and there was no control group, these results cannot show that the diet caused the improvement.

Pregnancy Rates in Natural Conception and Fertility Restoration

In the Cleveland Clinic review, 10 of the 18 women who wanted to become pregnant (55.6%) did so [2]. The pregnancy rate was 38.5% in women taking metformin and 100% in those who were not (P = 0.036), and 62.5% with ovulation induction agents versus 50.0% without (P = 0.66) [2]. Percent weight change did not differ significantly between women who became pregnant and those who did not [2].

In the VLCKD case series, 11 women conceived naturally during or after the diet, and 12 more became pregnant among the 22 who underwent ART, a 58% pregnancy rate among the 40 who began the VLCKD [10]. Without a comparison group, these figures show feasibility rather than efficacy.

Comparison with Other Dietary Approaches

Ketogenic vs. Mediterranean and Other Dietary Approaches

The Mediterranean diet is widely regarded as a gold-standard healthy diet [1], and a Mediterranean diet aimed at maintaining normal body mass may help preserve ovarian health [5]. Where ketogenic diets have been compared directly with low-calorie diets in randomized trials, weight loss did not differ significantly [8]. There is not enough evidence to say that a ketogenic diet is better for fertility than other weight-loss or healthy-eating approaches.

Safety Considerations and Pregnancy-Related Concerns

Safety Profile During Preconception

No adverse events were reported in the medically supervised VLCKD case series [10], but small uncontrolled studies cannot establish safety. Very-low-calorie protocols in these studies were run under medical supervision.

Ketogenic Diet During Pregnancy

The safety of a ketogenic diet during pregnancy has not been established. In mice, a ketogenic diet during the second half of pregnancy reduced litter size and litter mass, reduced the proportion of female offspring, and shortened the lifespan of male offspring [15]. The authors note that results in mice may not translate to humans, but they raise concern that even a partial maternal ketogenic diet in pregnancy may harm offspring [15].

Transition Protocols

The VLCKD case series used a three-phase program before ART [10]:

Phase	Duration	Description
VLCKD	3 months	Meal-replacement very-low-calorie ketogenic diet, less than 800 kcal/day
Transition	6 months	Gradual carbohydrate reintroduction
Maintenance	Ongoing	Mediterranean-style diet

Limitations and Future Research Directions

Study Design and Evidence Quality

The evidence on ketogenic diets and fertility consists mainly of non-randomized studies, such as cohort studies, case series and retrospective reviews, with few randomized trials [8]. Protocols differ widely [3], most studies enrolled women with PCOS and overweight or obesity, and few report live births. The authors of the most recent meta-analysis describe the available studies as low quality and heterogeneous and state that larger, high-quality randomized trials are essential [9].

Personalization and Clinical Implementation

Women with PCOS and overweight or obesity are the group in which ketogenic diets have been studied, and results may not apply to lean women or to other causes of infertility. Anyone considering a ketogenic diet while trying to conceive, or who takes medicines such as metformin, should plan it with their clinician.

Conclusion

In small studies of women with PCOS and overweight or obesity, ketogenic diets are associated with weight loss, improved insulin resistance, lower testosterone and LH/FSH ratio, and higher SHBG [7, 8, 9]. Reports of restored menstrual cycles and of pregnancy after a ketogenic diet come from retrospective studies and case series without control groups [2, 10, 11]. Randomized trials have not shown greater weight loss than with low-calorie diets [8], and the overall evidence is low quality [9].

In men, ketogenic diets, especially VLCKD, raise total testosterone in proportion to weight loss [13], but a three-week ketogenic diet lowered the free androgen index [12], and no controlled human studies show improved sperm quality or fertility. The safety of a ketogenic diet during pregnancy has not been established, and animal data raise concerns [15].

A ketogenic diet may be worth studying further as part of weight management for women with PCOS who are planning a pregnancy, but it is not an established fertility treatment. Anyone considering it should do so with their clinician.

References

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