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Do Low-Carbohydrate Diets Negatively Affect Female Hormone Balance?

Key Findings

  • Carbohydrate restriction does not result in alterations of ovulation, menses, or other indicators of women’s hormonal health.
  • Low-carbohydrate diets have demonstrated positive benefits to women’s hormonal health.
  • Extreme calorie restriction is likely to affect women’s hormonal balance and health.
  • Those women who are leaner and exercise more are at greater risk of negative effects from excessive or prolonged energy restriction.

A common claim currently doing the rounds is that a low-carb or keto-diet will negatively affect either ‘female hormone balance’, menstrual cycles, or ovulation.

It is claimed that there is a minimum amount of carbohydrate (i.e. 200 g per day) required to preserve hormone status and ovulation, along with other indicators of hormonal health.

Does This Claim Stack Up?

There is no evidence that 200 g per day is required to preserve markers of female hormone balance. In fact, the most commonly cited study to support the idea that there is a minimum requirement for carbohydrate showed no such thing.


Read more and listen to the audio below

Luteinizing Hormone Pulsatility Is Disrupted at a Threshold of Energy Availability in Regularly Menstruating Women

Anna Loucks, Jean Thuma

The Journal of Clinical Endocrinology & Metabolism, Volume 88, Issue 1, 1 January 2003, Pages 297–311, https://doi.org/10.1210/jc.2002-020369

Abstract

To investigate the dependence of LH pulsatility on energy availability (dietary energy intake minus exercise energy expenditure), we measured LH pulsatility after manipulating the energy availability of 29 regularly menstruating, habitually sedentary, young women of normal body composition for 5 days in the early follicular phase.

Subjects expended 15 kcal/kg of lean body mass (LBM) per day in supervised exercise at 70% of aerobic capacity while consuming a clinical dietary product to set energy availability at 45 and either 10, 20, or 30 kcal/kg LBM per day in two randomized trials separated by at least 2 months. Blood was sampled daily during treatments and at 10-min intervals for the next 24 hours. Samples were assayed for LH, FSH, oestradiol (E2), glucose, β-hydroxybutyrate, insulin, cortisol, GH, IGF-I, IGF-I binding protein (IGFBP)-1, IGFBP-3, leptin, and T3.

LH pulsatility was unaffected by an energy availability of 30 kcal/kg LBM per day (p > 0.3), but below this threshold LH pulse frequency decreased, whereas LH pulse amplitude increased (all p < 0.04). This disruption was more extreme in women with short luteal phases (p < 0.01). These incremental effects most closely resembled the effects of energy availability on plasma glucose, β-hydroxybutyrate, GH, and cortisol and contrasted with the dependencies displayed by the other metabolic hormones (simultaneously p < 0.05).

These results demonstrate that LH pulsatility is disrupted only below a threshold of energy availability deep into negative energy balance and suggest priorities for future investigations into the mechanism that mediates the nonlinear dependence of LH pulsatility on energy availability.1

Comment

The paper itself makes for some difficult reading because what at first could be inferred to be a low-carbohydrate diet intervention, is in fact one that has both low energy availability and low carbohydrate availability because of adjustment for energy expenditure.

There is no evidence that 200 g of carbohydrate per day is required to preserve female hormone balance.

What did the study involve?

29 regularly menstruating, sedentary young women were measured for luteinising hormone (LH) pulsatility over a 5-day period (along with other blood outcome measures). They were randomised to receive an energy-sufficient diet matched to daily calorie expenditure (~ 2700 Kcal per day) or one of three calorie-restricted diets (~ 2000, 1500, 1100 Kcal per day respectively). (Figure 1.)

Figure 1. Energy intake and expenditure by group.

The diets were standardised by using a diet supplement drink (Ensure) which contains 28% fat, 15% protein, and 57% carbohydrate…

Yes, you read that right… 57% carbohydrate… Definitely not a low-carbohydrate modifier!

What did they find?

At energy availability under 30 Kcal/kg of lean body mass per day, there were significant alterations in LH pulse frequency and amplitude (Figure 2). In this case, the participants were eating 2000 Kcal per day or more than 700 Kcal per day under maintenance calories.

Figure 2. Luteinising hormone pulse frequency and amplitude.

Therefore, based on these results, it is reasonable to conclude in this study, a calorie restriction to ~26% less than your daily energy requirement (the combination of energy intake from food and what you expend over a day) is likely to impair LH pulsatility. As you can see in Figure 2, there was no effect above 30 Kcal per kilogram of bodyweight. There might be an effect of relative carbohydrate availability, but it appears to be mostly related to fuel availability, not whether a diet is ‘low-carb’ simply because these diets were not.

Calorie restriction to ~26% less than your daily energy requirement is likely to impair LH pulsatility.

What does the research say about low-carb and hormone balance?

There are relatively few studies on low-carbohydrate (or other diets) and female hormone balance. In fact, female health has been typically underserved in research. There are, however, a few studies that are very informative for whether low-carbohydrate diets are arbitrarily ‘bad’ for women and they were reviewed in 2017 by Melanie McGrice and Judi Porter.

The Effect of Low Carbohydrate Diets on Fertility Hormones and Outcomes in Overweight and Obese Women: A Systematic Review

Melanie McGrice, Judi Porter

Nutrients 20179(3), 04; https://doi.org/10.3390/nu9030204

Abstract

Background

Medical interventions including assisted reproductive technologies have improved fertility outcomes for many sub-fertile couples. Increasing research interest has investigated the effect of low carbohydrate diets, with or without energy restriction. We aimed to systematically review the published literature to determine the extent to which low carbohydrate diets can affect fertility outcomes.

Methods

The review protocol was registered prospectively with Prospective Register for Systematic Reviews (registration number CRD42016042669) and followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Infertile women were the population of interest, the intervention was low carbohydrate diets (less than 45% total energy from carbohydrates), compared to usual diet (with or without co-treatment). Four databases were searched from date of commencement until April 2016; a supplementary Google scholar search was also undertaken. Title and abstract, then full-text review, were undertaken independently and in duplicate. Reference lists of included studies and relevant systematic reviews were checked to ensure that all relevant studies were identified for inclusion. Quality assessment was undertaken independently by both authors using the Quality Criteria Checklist for Primary Research. Outcome measures were improved fertility outcomes defined by an improvement in reproductive hormones, ovulation rates and/or pregnancy rates.

Results

Seven studies fulfilled the inclusion criteria and were included in the evidence synthesis. Interventions were diverse and included a combination of low carbohydrate diets with energy deficit or other co-treatments. Study quality was rated as positive for six studies, suggesting a low risk of bias, with one study rated as neutral. Of the six studies which reported changes in reproductive hormones, five reported significant improvements post-intervention.

Conclusion

The findings of these studies suggest that low carbohydrate diets warrant further research to determine their effect. These randomised controlled trials should consider the effect of carbohydrates (with or without energy deficit) on hormonal and fertility outcomes.

Comment

In this review, six of seven studies assessed changes in reproductive hormones, with all but one reporting significant improvements and one showing no meaningful difference between groups.

Four of the seven studies reported on menstrual cycles; frequency of menses and/or ovulation rates. All studies showed significant improvements in menstrual cyclicity (normalisation of menstrual cycles) and/or improvements in ovulation rates with a low-carbohydrate diet.

It should be noted that Palomba et al. demonstrated an improvement in menses frequency and ovulation rates compared to the start of the intervention, but the results were not as significant as the usual diet plus structured exercise training. 2

All studies showed significant improvements in menstrual cyclicity and/or improvements in ovulation rates with a low-carbohydrate diet.

Also observed by Moran et al. was that two amenorrhoeic (not menstruating) participants had a resumption of menses or improvement in ovulation after commencing a low-carbohydrate diet.3

Four studies also reported pregnancy outcomes. Three out of four studies showed improved pregnancy rates in low-carbohydrate intervention groups. This would not be an expected result if hormonal dysfunction was a natural consequence of a low carbohydrate diet.

It should also be noted that all of these studies were energy-restricted, ranging from around 600 (followed by habitual calories) to 1400 calories per day, and with the intervention group (low carb) in the Palombo studies eating 800-1000 calories less than requirement per day. The comparison groups all consumed their usual diets. 

What does this all mean?

We already know from previous research that a relative energy deficiency syndrome (REDS) is detrimental to the creation and release of many hormones and is especially concerning for women for menstruation and ovulation, and other aspects of female hormone balance.

But the study by Louks and Thuma does not show that low-carb diets are the culprit. In this case, even the low-calorie diets that have been suggested as ‘low-carb’ were relatively rich in carbohydrate (ranging from ~156 g of carbohydrate per day, up to 385 g per day). The results may have been misread by some commentators due to the authors listing in a table the ’24-hr Carbohydrate availability’ (40-230 g per day from lowest to highest group). However, this figure was derived from a calculation of the daily carbohydrate intake minus carbohydrate usage during the prescribed exercise regime. We would expect in a high energy expenditure situation, with relatively high-calorie restriction, that carbohydrate availability would be low. However, I must restate, the diets were not low carbohydrate (except as a function of severe energy restriction overall) by any accepted measure.

In this study, there was a negative effect on luteinising hormone pulsatility and frequency at a calorie restriction of more than 700 calories less than maintenance (< 30 calories per kilogram of body weight).

There are several points to consider when evaluating these results.

  1. The participants in the Loucks and Thuma study were of normal body composition, so they may have had less energy availability (from stored bodyfat) than the overweight and obese participants in the studies reviewed by McGrice and Porter.
  2. The participants in the Loucks and Thuma study were exercised to expend on average 896 calories per day, which would have significant effects on recovery and stress, apart from the calorie deficit created.
  3. Overweight and obese people are more likely to benefit from low-carbohydrate interventions.

How can we apply these findings?

Relative energy availability, or conversely, energy deficiency, is becoming a major talking-point in nutrition. It is clear from research on athletes that a relative energy deficiency syndrome (REDS) is a major risk for over-reaching, overtraining, and hormonal dysregulation and this is becoming more widely accepted as a causative factor in over-stress and fatigue in non-athletes.

Relative energy deficiency syndrome (REDS) is a major risk for over-reaching, overtraining, and hormonal dysregulation

Much of our ‘framing’ in health and nutrition is geared towards methods to help people reduce calories, due to the epidemics of obesity and metabolic syndrome. But the growing awareness of the importance of energy sufficiency to thrive, and the clinical observation that there are a significant minority of people who are habitual under-eaters, shows the importance for clinicians and practitioners to recognise the importance of sufficient energy intake for long term health.

This is especially true when other demands (like exercise and career workload, or other stressors) are also providing for an increase in both energy expenditure AND resulting in other stress-related effects; such as increased catecholamines, increased tissue breakdown, reduced availability of substrate for hormone production, and effects on sleep, essential micronutrient intake, and mind-state. (Figure 3.)

Energy restriction should, therefore, be limited in time, in order to accomplish results, and the magnitude of energy restriction should be modified based on other factors.

Carbohydrate allotment in the diet should be based on the needs of the individual, not on an arbitrary idea that carbohydrates are required in a certain amount to preserve hormonal status.

References

1.         Loucks AB, Thuma JR. Luteinizing Hormone Pulsatility Is Disrupted at a Threshold of Energy Availability in Regularly Menstruating Women. The Journal of Clinical Endocrinology & Metabolism. 2003;88(1):297-311.

2.         McGrice M, Porter J. The Effect of Low Carbohydrate Diets on Fertility Hormones and Outcomes in Overweight and Obese Women: A Systematic Review. Nutrients. 2017;9(3).

3.         Palomba S, Falbo A, Giallauria F, Russo T, Rocca M, Tolino A, et al. Six weeks of structured exercise training and hypocaloric diet increases the probability of ovulation after clomiphene citrate in overweight and obese patients with polycystic ovary syndrome: a randomized controlled trial. Human Reproduction. 2010;25(11):2783-91.

4.         Moran LJ, Noakes M, Clifton PM, Tomlinson L, Norman RJ. Dietary Composition in Restoring Reproductive and Metabolic Physiology in Overweight Women with Polycystic Ovary Syndrome. The Journal of Clinical Endocrinology & Metabolism. 2003;88(2):812-9.

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