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Manta, A.; Paschou, S.A.; Isari, G.; Mavroeidi, I.; Kalantaridou, S.; Peppa, M. Effects of Nutrition on Polycystic Ovary Syndrome. Encyclopedia. Available online: https://encyclopedia.pub/entry/54956 (accessed on 05 July 2024).
Manta A, Paschou SA, Isari G, Mavroeidi I, Kalantaridou S, Peppa M. Effects of Nutrition on Polycystic Ovary Syndrome. Encyclopedia. Available at: https://encyclopedia.pub/entry/54956. Accessed July 05, 2024.
Manta, Aspasia, Stavroula A. Paschou, Georgia Isari, Ioanna Mavroeidi, Sophia Kalantaridou, Melpomeni Peppa. "Effects of Nutrition on Polycystic Ovary Syndrome" Encyclopedia, https://encyclopedia.pub/entry/54956 (accessed July 05, 2024).
Manta, A., Paschou, S.A., Isari, G., Mavroeidi, I., Kalantaridou, S., & Peppa, M. (2024, February 09). Effects of Nutrition on Polycystic Ovary Syndrome. In Encyclopedia. https://encyclopedia.pub/entry/54956
Manta, Aspasia, et al. "Effects of Nutrition on Polycystic Ovary Syndrome." Encyclopedia. Web. 09 February, 2024.
Effects of Nutrition on Polycystic Ovary Syndrome
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This entry is adapted from the peer-reviewed paper 10.3390/nu15153483

Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by hormonal imbalances and various metabolic abnormalities linked to insulin resistance via a vicious cycle. Genetic and environmental factors underlie its pathogenesis and evolution. Nutrition, in terms of nutrient composition, dietary patterns, endocrine-disrupting chemicals, and food processing and preparation, has gained significant attention in the pathogenesis and therapeutic approach of polycystic ovary syndrome.

polycystic ovary syndrome anovulation hyperandrogenism menstrual disorders

1. Introduction

Polycystic ovary syndrome (PCOS) is a complex, polygenic metabolic condition and the most common endocrine disorder in women of reproductive age. According to the 2003 Rotterdam criteria, PCOS is defined as clinical or biochemical hyperandrogenism, an indication of oligo-anovulation and polycystic-appearing ovarian morphology on the ultrasound, excluding any other relevant conditions [1][2]. Currently, four recognized phenotypes of PCOS include all possible combinations of these characteristics: (1) hyperandrogenism, oligo-anovulation and polycystic ovarian morphology; (2) hyperandrogenism and oligo-anovulation with normal ovarian morphology; (3) hyperandrogenism and polycystic ovarian morphology with normal ovulation; and (4) polycystic ovarian morphology and oligo-anovulation without the presence of hyperandrogenism [3]. The most common PCOS symptoms are hirsutism, alopecia, and acne, all linked to hyperandrogenism, as well as menstrual irregularities, including oligomenorrhea and amenorrhea [3][4].

2. Effects of Dietary GI and GL Indexes on PCOS Risk

In addition to genetic and environmental factors, hyperinsulinemia due to IR, diabetes mellitus, obesity, family history for PCOS among first degree relatives, premature adrenarche, fetal androgen exposure, and low birth weight all constitute risk factors for PCOS [1][2][5]. Nutrition is considered another important determinant of PCOS risk, in terms of dietary patterns and specific nutrient intakes [6]. the amount of CHOs has especially been linked to increased PCOS risk [7].
Focusing on the dietary GI and GL indexes, it seems that women who follow high-GI and high-GL diets are more likely to develop PCOS [8][9]. According to a recent observational study, even the consumption of medium GI products increases the probability of PCOS by more than three-fold [10].
In addition, numerous studies have shown that PCOS patients consume noticeably more foods commonly high in GI or GL than healthy controls [9][10][11][12][13]. In comparison to patients of normal weight, obese PCOS patients consume foods with a higher mean dietary GI [14]. Obese and the classic PCOS phenotype are even considered age-independent predictors of higher dietary GI [13].

3. Effect of Dietary GI and GL Indexes on PCOS Pathophysiology

3.1. Effect of Dietary GI and GL Indexes on Glucose and Insulin Homeostasis

Glucose homeostasis in the whole body is dependent on the insulin secretion and action. IR is a complex phenomenon, due to its molecular and cellular aspects, leading to the disruption of insulin metabolism and elevated glucose levels. IR has been extensively studied and has been linked to numerous cardiometabolic and cognitive disorders and cancer [15][16][17].
IR can be driven by a number of hereditary and lifestyle factors, with diet being one of the main contributors. Macronutrient composition, particularly the intakes of CHOs, proteins, and fats, can influence insulin sensitivity. High-CHO diets, especially those rich in processed CHOs and sugars, may trigger rapid spikes in blood glucose levels, leading to IR. Dietary fiber consumption is also essential for regulating insulin metabolism. Whole grains, fruits, vegetables, and legumes are examples of high-fiber diets that slow down the digestion and absorption of carbs, reducing blood sugar rises and promoting improved insulin regulation [18][19].
IR is one of the major pathophysiologic mechanisms implicated in PCOS and can be present regardless of adiposity, body composition, and androgen levels [1][2][20][21]. Overall, IR is present in 75% of lean women and 95% of obese women with PCOS [21]. IR can exacerbate PCOS symptoms, leading to even more difficulties in weight management, excessive production of androgens, and disrupted ovulation [1][2][20][22].
The effects of different dietary patterns on glucose and insulin homeostasis in PCOS patients have been studied considerably. An overly high-fat diet, especially one high in saturated fat, raises the likelihood of developing IR and worsens its negative consequences [23]. CHOs have been linked to disturbed insulin homeostasis and IR, whereas a modest decrease in dietary CHO content was found to reduce fasting glucose, insulin, and IR while increasing insulin sensitivity [24][25][26]. Reduced dietary CHO consumption also appears to affect pancreatic β-cell responsiveness, which is a measure of insulin secretion, by increasing the first-phase response and decreasing the basal β-cell response [24].
Focusing on GI and GL indexes, there is a clear association between high dietary GI and GL values, insulin levels, and IR, as expressed by the Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) [10]. Women with PCOS and IR were found to consume more GL, compared to those without IR [27].
In regards to dietary interventions, adherence to a low-GI diet was linked to a significant increase in insulin sensitivity [28][29] and a reduction in insulin levels [30], as well as a reduction in HOMA-IR [31], whereas a short-term low-GI intervention had no effect on measures of glycemia [28]. The Dietary Approaches to Stop Hypertension (DASH diet), which is actually a low-GI diet, was initially proposed for the management of hypertension [32]. This diet was studied in overweight and obese women with PCOS and was found to lead to a significant reduction in insulin levels and HOMA-IR [33][34][35], as well as an increase in the quantitative insulin sensitivity check index [35]. Alongside calorie-restricting diets, the DASH diet might be one of the most effective options for reducing IR in PCOS patients [36].

3.2. Effects of Dietary GI and GL Indexes on Inflammation Biomarkers

Chronic inflammation refers to a persistent state of subclinical low-grade inflammation in the body that can promote the development and progression of various diseases, including CV disease, cognitive dysfunction, and certain malignancies [37][38].
Diet plays a crucial role in either promoting or mitigating chronic inflammation. Poor nutritional habits have been recognized as a component of the environmental triggers for chronic inflammation, due to their link to the abnormal activation of the innate immune system, resulting in low-grade systemic inflammation [39][40].
Food intake is known to cause a postprandial inflammatory reaction, the extent of which correlates with the level of IR. The caloric and CHO contents, as well as the lipid profile of a meal, are some of the nutrient-dependent parameters that affect postprandial inflammation [41]. Particularly complex CHOs are associated with inflammation through abnormal postprandial rises in glucose and lipids [6]. Dietary intakes of fat, protein, cholesterol, and sodium have also been found to be positively correlated with high-sensitive C-reactive protein (hs-CRP) levels, whereas a low-fiber diet is associated with increased inflammation [42].
Obesity is also a key factor for low-grade chronic inflammation, independently of specific nutrients, through a mechanism that involves adipocytes, macrophages, and the expression of pro-inflammatory receptors [43].
Chronic low-grade inflammation is considered to be involved in PCOS pathogenesis. A number of studies have found increased CRP levels in PCOS patients, although it is still unclear whether the inflammation is brought on by PCOS itself or by IR and obesity [44]. Inflammation is a cause of hyperandrogenism and can also exacerbate IR and affect ovulation via several pathways involving pro-inflammatory compounds [22].
Focusing on the dietary GI and GL indexes, the combination of high-protein and low-GL foods caused a significant decrease in hs-CRP levels, compared to a standard hypocaloric diet [30]. In overweight and obese women with PCOS, the DASH diet, a classical low-GI diet, resulted in a significant reduction in hs-CRP levels [33]. Adherence to a low-GI diet for 3 months was found to substantially decrease inflammation, as indicated by rising uric acid levels and glutathione peroxidase activity [45].

3.3. Effects of Dietary GI and GL Indexes on Oxidative Stress Biomarkers

An imbalance between pro-oxidants and antioxidants leads to oxidative stress (OS). Oxidative compounds, such as reactive oxygen species (ROS) and reactive nitrogen species (RNS), are involved in a number of processes, including those that regulate signaling, cell growth, and differentiation. Excess ROS accumulation can induce cell, protein, and lipid damage [22][42].
In a similar way to low-grade systemic inflammation, OS can be induced by postprandial hyperglycemia and is highly influenced by eating habits. Among the pro-inflammatory dietary patterns, CHOs are deemed responsible for the induction of OS, as demonstrated by large studies focusing on different populations [6]. On the other hand, dietary modifications can have an impact on the redox state, particularly in individuals with diabetes, hypertension, obesity, or dyslipidemia. Dietary antioxidants, hypocaloric diets that cause adipose tissue loss, and the substitution of animal protein for plant protein all enhance the antioxidant status of patients with these disorders [46].
Various circulating biomarkers of OS are abnormal in PCOS patients, regardless of weight status, indicating that OS plays a role in the etiology of the condition [47]. PCOS patients have markedly greater levels of homocysteine, malondialdehyde, asymmetric dimethylarginine, and superoxide dismutase activity, compared to healthy women. They also have lower levels of glutathione and paraoxonase-1 activity [47]. However, the mechanism of this link is not entirely clear, considering that PCOS patients frequently present with IR, obesity, and hyperandrogenemia, which also promote OS [48]. Nutritional supplementation is considered beneficial for OS related to PCOS and its accompanying disorders. Vitamin D, flavonoids, selenium, probiotics, vitamin E, folate, and omega-3 fatty acids are among the supplements being studied for their capacity to decrease OS and its detrimental effects on patients’ hormonal and lipid profiles [49].
Regarding the GI and GL indexes, the low GI DASH diet seems to have antioxidant properties that increase the total antioxidant capacity, 2,2-Diphenyl-1-picrylhydrazyl (DPPH) activity, glutathione, and nitric oxide [34][35][50] and decrease malondialdehyde levels [35].

3.4. Effects of Dietary GI and GL Indexes on Androgen Levels

Sex hormones are essential for growth, sexual development, and reproduction. They are also associated with metabolic parameters and relevant diseases. Low levels of circulating androgens have been associated with obesity and visceral adiposity in males, whilst excessive levels of androgens have also been connected to metabolic abnormalities in women. According to research, nutrition is known to influence androgen levels. A particular nutrient’s effects or other metabolic pathways, such as diet-induced changes in the context of obesity or IR, may mediate such an effect [51]. Regarding nutritional patterns, intermittent fasting was found to be beneficial for lowering androgen levels (testosterone and the free androgen index (FAI)) while raising sex hormone-binding globulin (SHBG) levels in premenopausal obese women [52].
The majority of PCOS patients with oligo-amenorrhea also have biochemical hyperandrogenemia, with the ovaries being the primary source of this androgen excess [3].
Androgen production is directly influenced by pro-inflammatory stimuli, while biomarkers of OS and inflammation are closely linked to circulating androgens [1][2][3][20]. In PCOS women, insulin levels have an impact on circulating androgens, independently of changes in gonadotropin secretion [53]. Nevertheless, ovarian androgen production in PCOS patients arising from dietary-induced inflammation may not be reliant on excessive body fat or IR [20]. Various dietary interventions have been promising in regulating androgen levels in PCOS patients. In obese PCOS individuals with anovulatory infertility, a hypocaloric high-protein diet and an exercise regimen decreased serum androgens, namely SHBG, androstenedione, and dehydroepiandrosterone sulphate [54].
However, the association of dietary GI and GL indexes specifically with androgen levels in PCOS is not clear. In overweight women with PCOS, a low-GI diet resulted in a significant reduction in total testosterone and an increase in sex hormone-binding globulin [12], while a reduction in dietary CHO content also significantly reduced total testosterone [24]. The low-GI DASH diet had a significant reduction in serum androstenedione [50] and significant increases in sex hormone-binding globulin [35][50] and anti-Müllerian hormone (AMH) [35]. A low-GI diet had a significant but similar decrease in testosterone in obese PCOS patients, compared to the effects of a conventional hypocaloric diet [30].
On the contrary, a 3-month low-GI diet intervention had no effect on androgen levels [55]. Wong et al. compared the impact of a low-GL diet with a low-fat diet in overweight and obese adolescents with PCOS and also found no difference in testosterone after either intervention [56].

3.5. Effects of Dietary GI and GL Indexes on Weight Status

Obesity is a serious public health issue that affects both children and adults, with a high prevalence globally.
This trend is also seen in PCOS, as 30% to 70% of women are overweight or obese. Abdominal obesity, in particular, affects and accentuates all metabolic and reproductive manifestations of PCOS [57].
Weight loss is recommended as an essential component of treatment for PCOS patients with an elevated BMI. Physical activity and maintenance of a healthy weight status are crucial components of the treatment of metabolic dysfunction related to PCOS [2][3][20]. Adherence to a hypocaloric diet and weight reduction of as little as 5% have been shown to improve clinical, metabolic, and reproductive abnormalities [58][59]. In women with PCOS, improved fatty acid oxidation, weight loss, and prevention of further weight gain may result from dietary changes that lower postprandial hyperglycemia and hyperinsulinemia [60].
Independent of calorie restriction, a reduction in CHO consumption has been associated with a greater decrease in adipose tissue and an impact on body composition [25]. These impacts may be related to changes in insulin release [61]. A reduced CHO diet for 8 weeks in women with PCOS significantly increased body fat loss, compared to the standard diet. The diet induced a decrease in subcutaneous-abdominal, intra-abdominal, and thigh-intermuscular adipose tissues [25]. Previous research also showed that females with PCOS had a lower risk of being overweight and obese when their daily consumption of plant protein was increased by 10 gr [62].
Regarding the GI and GL indexes, healthy but also PCOS women consuming high-GI or high-GL diets were found to have a higher BMI and waist circumference [12][13]. A significant inverse association between dietary GL and waist-to-hip ratio in women with PCOS was also reported [63].
In PCOS women, a low-GI diet decreased body mass, BMI, and waist, hip, and arm circumferences [64][65] and affected several indexes of body compositions [64]. A vegan low-GI diet had a greater decrease in energy and fat intake and a significant weight loss at 3 months, but not at 6 months, compared to conventional low-calorie diets [66]. The low-GI DASH diet appears to be an effective dietary strategy, as it was found to considerably reduce body weight, BMI [34][35], waist and hip circumferences [33], and fat mass [50], even when compared to a standard calorie-restricting diet [34].
Nevertheless, several studies reported an increased adherence to a low-GI diet quite similar to other diets, whether hypocaloric [30], low-fat [56], or designed to decrease hypercholesterolemia [31].

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Subjects: Nutrition & Dietetics
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Aspasia Manta
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Stavroula A. Paschou
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Georgia Isari
,
Ioanna Mavroeidi
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Sophia Kalantaridou
,
Melpomeni Peppa
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Update Date: 17 Feb 2024
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