Charting

Due to the often significant timeframes encountered when treating patients with PCOS, tools such as charting may be employed to observe hormonal status changes over time. Menstrual cycle charting based on basal body temperature (BBT) has been traditionally used in naturopathic practice to ascertain changes in levels of hormone levels in reproductive females (see Figure 20.3). It is thought to reflect the menstrual cycle in two ways: (1) within 1–2 days before LH surge there should be a low point in BBT; and (2) following ovulation women should generally see a sustained increase in BBT of between 0.2 and 0.5°C.¹⁴ This rise is most likely due to the thermogenic effect of a metabolite of progesterone.

Figure 20.3 The ‘normal’ chart (left) shows a concordance in temperature with expected levels of progesterone and an immediate strong rise in temperature, giving a strong indication of ovulation. The PCOS chart (right) shows an anovular cycle with no pattern differentiating follicular and luteal phases. Mucus changes may be evident in this case and may represent follicular activity and surges in oestrogen that do not result in ovulation.

There has been some contention as to the effectiveness of BBT charting in pregnancy outcomes; however, its use in naturopathy has been extended more broadly to the menstrual cycle in general.

It should be noted that focusing on individual components of charting is very often inadequate.¹⁴ However, when integrated they can form a useful clinical tool that provides a broad overview of reproductive function and actively involves patients in their treatment. Despite the fact that more specific and accurate investigations currently exist, charting may still have a role to play in clinical practice as it is inexpensive, non-invasive and generally reliable. It also actively involves the patient in the therapeutic and diagnostic process. However, interpretation can be subjective and difficult and in more complex cases other investigative techniques may be more appropriate.

Temperature should be taken (sublingually) immediately upon rising. Several factors—including alcohol consumption the night before, restless sleep, variations in waking time and illness—may affect temperature and should be noted on the chart.

Sustained temperature rise shows the most likely day of ovulation (the actual rise begins 12 hours before ovulation during the LH surge).

Consistently low temperature (under 36.5°C) may indicate a hypothyroid condition, which may play a role in poor reproductive function (see Chapter 17 on thyroid abnormalities).

Follicle stimulating hormone and luteinising hormone regulation

Some herbal medicines may affect levels of FSH and LH and may therefore proffer some benefit in the treatment of PCOS. Despite its status as a phytoestrogen, Cimicifuga racemosa does not seem to affect the release of prolactin and FSH, though it does reduce LH, in the limited research currently conducted.¹⁵ This central effect is thought to be due to its role on dopaminergic regulation of reproductive hormones rather than its effects on oestrogen receptors.^16,17 The British Herbal Pharmacopeia lists C. racemosa’s main actions as being useful in ovarian dysfunction and ovarian insufficiency.¹⁸

Vitex agnus-castus has had conflicting results, with some studies showing no change in FSH or LH, and another suggesting increased LH release.^19–21 V. agnus-castus is thought to have antiandrogenic properties. Humulus lupulus also reduces LH with continued use and may therefore be useful to reduce androgens in PCOS.²² A review of soy studies suggests that soy consumption has no effects on FSH or TSH.²³

Unpublished (though publicly available) data suggest that supplementation with the herb Tribulus terrestris for 3 months may normalise ovulation and result in pregnancy in women with endocrine infertility.²⁴ Mentha spicata (via tea therapy—2 cups per day for 5 days) use has been associated with increases in LH, FSH and oestrogen levels in women with PCOS.²⁵

Glycyrrhiza glabra is a commonly used herb in the treatment of PCOS. Though trials for its stand-alone treatment in PCOS are lacking, there exists a theoretical basis behind its use. G. glabra has been demonstrated to reduce testosterone levels in healthy women.²⁶ Various forms of Glycyrrhiza has been used in a combination product (as the key ingredient with Paeonia lactiflora) in the treatment of PCOS in some small trials that showed reduction in FSH:LH ratio, ovarian testosterone production and improvements in ovulation.^27,28 However, the situation in the combination product has been confused further by the fact that while this research has focused on G. uralensis clinical application is still dominated by G. glabra. The clinical effects of these minor differences are unknown. G.racemoza may also exert further potent phytoestrogenic activity independent of these effects.²⁹ Glycyrrhiza glabra is also demonstrated to reduce body fat mass in normal weight subjects.³⁰ A Paeonia lactiflora and Glycyrrhiza glabra combination has been found to have numerous effects on PCOS, including regulating FSH:LH ratios (possibly through stimulation of pituitary dopamine receptors),²⁷ lowering testosterone levels and improving oestradiol to testosterone ratios.^28,31

Exogenous melatonin has been demonstrated to enhance LH secretion, LH pulse amplitude and LH sensitivity to GnRH.^32–34 This was thought to be the result of melatonin supplementation mimicking the effects of PCOS—possibly due to the effects of melatonin on increasing cortisol levels. This effect is known to increase in hypo-oestrogenic states.³⁵ However, while most studies have been in postmenopausal or older women, melatonin supplementation in younger women has been associated with return to menstrual regularity, as well as the reduction of LH levels in younger women with high baseline levels, in clinical settings.^36,37 This has led to calls for a possible role of melatonin in the treatment of PCOS and, despite its popularity in some streams of naturopathic medicine, it remains unclear at this stage what role it may play; further research is required.³⁸ Other factors known to affect melatonin levels should also be considered (see Chapter 14 on insomnia).

Other factors may also affect LH levels. Various human studies have suggested that inadequate nutrition or short periods of fasting reduces LH pulsing, though not always LH levels.^39–41 This is thought to be due to relative increases in cortisol caused by these states.⁴² Animal studies seem to suggest that increased endotoxin load can reduce plasma LH levels.⁴³

HPO and hypothalamic–pituitary–adrenal (HPA) axis interaction

It is well known that women with PCOS exhibit abnormalities in cortisol metabolism as well as higher levels than controls.⁴⁴ It is also known that a return to states of normal cortisol from high cortisol level in women with amenorrhoea or menstrual disturbances often precedes the resumption of normal ovarian activity.⁴⁵ These findings further support the role for stress reduction in regulating LH and FSH function in the treatment of reproductive disorders such as PCOS.

The reproductive axis is inhibited at all levels by various components of the HPA axis. Corticotrophin-releasing hormone (CRH) can either directly or indirectly (through β-endorphin) suppress gonadotrophin-releasing hormone. Glucocorticoids may also exert inhibitory effects by rendering target tissues resistant to reproductive hormones, inhibiting GnRH and LH secretion and inhibiting ovarian oestrogen and progesterone biosynthesis.⁵ The effects of the HPA axis interaction with the female reproductive system can result in idiopathic or hypothalamic amenorrhoea (for example, that associated with stress, depression, anxiety or eating disorders) in its own right, or result in the hypogonadism associated with Cushing’s syndrome,⁵ though it may also result in further indirect complication of other disorders of hormonal dysregulation like PCOS.

Figure 20.4 Interactions of the HPO and HPA axes. CRH = corticotrophin-releasing hormone; GnRH = gonadotropin-releasing hormone; LH = luteinising hormone; E₂ = ovarian estradiol; α-MSH = melanocyte-stimulating hormone; ACTH = adrenocorticotropic hormone; AVP = arginine-vasopressin; FSH = follicle-stimulating hormone; NE (α) = norepinephrine stimulation via α-noradrenergic receptors; POMC = proopiomelanocortin; solid line = stimulation; dotted line = inhibition

However, these interactions can also be bidirectional. Corticotrophin-releasing hormone, for example, is regulated to some extent in reproductive tissue by oestrogen. Corticotrophin-releasing hormone is responsible for a number of functions in reproductive tissue (see Table 20.1), and disorders or events (such as chronic stress adaptation) that affect these levels may also have clinically relevant effects on reproductive function. Due to this bidirectional activity, a multifaceted approach to disorders, focusing on regulation of both reproductive and adrenal hormones, may be more successful in conditions such as PCOS rather than targeting one system alone, particularly considering PCOS may often be a disorder of oestrogen excess (via adipose tissue) as well as androgen excess. For this reason, generalised hormone-balancing protocols may also be beneficial in PCOS. Further information on balancing reproductive hormones can be found in Chapter 19 on endometriosis.

Table 20.1 Reproductive corticotrophin-releasing hormone, potential physiological roles and potential pathogenic effects⁴⁶

Weight management

Although not all people presenting with PCOS are overweight, in those that are, weight loss is an essential part of PCOS treatment. Not only can realistic weight loss result in dramatic improvement in the condition, but being overweight can also make treatment less effective.^47,48 Weight loss also proffers more effectiveness than current medication

for insulin resistance and related disorders.⁴⁹ Specific individual pharmacotherapy of any kind—including that of dietary and herbal supplements—is generally clinically ineffective in weight loss in the insulin-resistant individual⁵⁰ and therefore therapy should focus on an integrated approach to weight management.

As little as 2–5% reduction in weight can be enough to improve metabolic and reproductive indices in women with PCOS.⁵¹ This modest improvement can restore ovulatory function and improve insulin sensitivity by over 70%.⁵² A 5–10% reduction in weight can reduce central fat stores by 30% and weight loss also increases SHBG concentration, reduces testosterone concentration and androgenic stimulation of the skin (resulting in reduction in hirsutism), improves menstrual function and conception rates and reduces miscarriage rates in women with PCOS.^53–59

High protein diets are typically associated with excellent weight loss results in insulin-resistant and PCOS women.^60,61 Although higher-protein or lower-carbohydrate diets are often successful in weight loss in women with PCOS, this weight loss may not automatically equate to improvements in insulin parameters or ovarian function.⁶² However, Mediterranean-style diets have been associated with both weight loss and improved insulin parameters in both generic insulin resistant and PCOS patients.^63,64

An Israeli study comparing three common diets—low-fat, low-carbohydrate and Mediterranean—found that all diets were effective.⁶⁵ However, the low-carbohydrate and Mediterranean diets appeared to be more effective than the low-fat diet over 2 years. This suggests that dietary interventions may best be individualised to patient needs rather than protocol-driven.

Long-term modest weight loss is far more important in PCOS than acute weight loss. In fact drastic weight loss in women with PCOS may have negative effects on reproductive function.⁶⁶ Patient compliance may be improved in low-carbohydrate or higher-protein diets compared to low-fat diets. This is evidenced by a systematic review of dietary interventions that suggested that participant attrition was higher in low-fat diet

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