Depression

Unipolar depressive disorders (depression without a manic or hypomanic phase) not associated with medical illness are typically classified as follows in various diagnostic manuals:

• Major depression characterised by sadness, apathy, irritability, disturbed sleep, disturbed appetite, weight loss, fatigue, poor concentration, guilt and thoughts of death

• Dysthymic disorder, which consists of a pattern of chronic, ongoing mild depressive symptoms that are less severe than major depression

• Seasonal affective disorder (SAD), which is more common in women and related to seasonal changes. The prevalence increases with increasing latitude and it can be treated by light therapy. Symptoms include lack of energy, weight gain and carbohydrate craving.

The DSM-IV defines major depressive disorder (MDD) as a clinical depressive episode that lasts longer than 2 weeks and is uncomplicated by recent grief, substance abuse or a medical disorder.78 Various theories about the cause of MDD have been proposed, and include the monoamine-deficiency hypothesis (that underlies modern drug therapy) and a dysfunction in the hypothalamic-pituitary-adrenal (HPA) axis with an abnormal stress response.80 Elevated cortisol is consistently present in depressed patients. This overactivity of the HPA axis may be related to a conditioned response to traumatic events in childhood.

MDD has various degrees of expression, and phytotherapy is most appropriate for its mild to moderate manifestations. Patients experiencing severe MDD with acute suicidal thoughts or exhibiting other forms of self-endangerment should be referred to appropriate care. Impaired circulation to the brain, especially in elderly patients, is another cause of depression. Low systolic blood pressure was also associated with a poor perception of well-being in 50-year-old men81 and depression in men aged 60 to 89 years.82

The general considerations outlined in the treatment of anxiety also apply here. Patients suffering from depression should be treated as a whole with due attention to lifestyle, diet, drug use and mental hygiene (productive attitudes for coping with life events). Professional guidance and counselling is often appropriate, rather than the relegation of depression to just a biochemical imbalance to be corrected with pharmacological agents.

As noted above, phytotherapy is most appropriate for mild to moderate episodes of MDD, dysthymic disorder and SAD. Episodes of severe depression may require the more strident therapy offered by conventional drugs, although herbs can have a supportive role, especially in terms of boosting vitality. Herbs can also be relevant when the patient has improved and wishes to discontinue drug therapy.

Key elements of herbal treatment are as follows:

• The nervine tonic herbs are the mainstay of treatment, especially St John’s wort, which is a well-proven treatment for mild to moderate depression (see monograph). Other important herbs in this category include damiana, skullcap, Schisandra and Bacopa.

• Patients who are also anxious should be prescribed anxiolytic herbs. Valerian, passionflower and Zizyphus are also useful, but hops is traditionally contraindicated.

• Depressed patients are low in vitality, so adrenal restorative (licorice and Rehmannia), tonic and adaptogenic herbs are often indicated. Ginseng may have antidepressant activity, but it should be used cautiously if anxiety is present. Rhodiola, Withania and Siberian ginseng are better choices in these cases. Licorice and Schisandra also have exhibited some antidepressant activity in animal models. These herbs will also help correct the adverse long-term effects of stress on the physiology of the stress response.

• If required, herbs that improve circulation to the brain should be prescribed, especially Ginkgo.

• Recent research supports the value of lavender, Rhodiola and saffron (see above).

Example liquid formula

Valeriana officinalis 1:2 20 mL
Hypericum perforatum 1:2 25 mL
Rhodiola rosea 2:1 20 mL
Schisandra chinensis 1:2 20 mL
Glycyrrhiza glabra 1:1 15 mL
  total 100 mL

Dose: 5 mL with water three times a day.

Case history

A male patient, aged 72, came seeking help for depression following the death of his daughter from cancer about 6 months ago. He did not want to take conventional medication. He was prescribed St John’s wort extract 300 mg in tablets, 3 per day. Each tablet was standardised to 0.9 mg total hypericin and equivalent to 1500 to 1800 mg of flowering tops. There was a steady improvement in his mood over 6 to 8 weeks and he felt much better and more positive about life. The patient was maintained at 2 tablets per day with continued benefit.

Insomnia

Generally patients seek phytotherapy for insomnia that has become a chronic problem. The DSM-IV additionally requires that with chronic primary insomnia the patient’s sleep disturbance disrupts his or her daily performance and quality of life.78 It can be difficult in practice to differentiate primary insomnia from possible secondary causes such as alcohol and medical problems. Hence, it is more practical to address all the issues that might be contributing to the insomnia, while prescribing herbs as if it was primary insomnia. This approach therefore requires a detailed and careful case history and appropriate counselling of the patient.

Insomnia, or inadequate sleep, can be categorised for phytotherapy according to the difficulties experienced by the patient. These include difficulty falling asleep (sleep-onset insomnia), awakening during the night with difficulty falling back to sleep (sleep-maintenance insomnia), early morning awakening (sleep-offset insomnia) and a sense of not having enough sleep (non-restorative sleep). Patients can report a combination of these.

Major causes of sleep-onset insomnia include anxiety, pain or discomfort, caffeine and alcohol. Sleep-maintenance insomnia can be linked to depression, sleep apnoea, fibromyalgia syndrome, nocturnal hypoglycaemia, pain or discomfort and alcohol. If restless legs syndrome is a cause of insomnia, this should be addressed separately (see later in this section). Any obvious causes of the insomnia (such as pain) should also be treated separately.

It is important to ensure that the patient sleeps in a darkened, noise-free environment in a comfortable bed. The use of stimulants should be reduced, especially coffee, tea, guarana and cola drinks. Alcohol intake should also be reduced. Unwinding at night can be important and a few drops of lavender oil added to an evening bath can help this process. Where the insomnia has been precipitated by anxiety or other psychological problems, appropriate counselling or phytotherapy should be recommended. The key herbs for insomnia to be considered will depend on the pattern of the insomnia:

• Anxiolytic and hypnotic herbs are the mainstay of treatment. These can be taken throughout the day to prevent a build-up of tension or mental excitability that might result in insomnia. An additional dose is then recommended around 1 hour before bed. If the insomnia is not severe, then the herbs can be taken as a single dose before bed. Key herbs include valerian, kava, Zizyphus, hops, lemon balm, Magnolia, lavender, passionflower, California poppy and chamomile. Best results with valerian come from continuous use for at least 2 weeks (see monograph).

• Antidepressant and nervine tonic herbs are indicated, especially if the insomnia is associated with fibromyalgia or is sleep-maintenance insomnia. These include St John’s wort, saffron, skullcap, damiana, Rhodiola and Schisandra.

• If the patient is debilitated and suffers from sleep-maintenance insomnia, then adrenal restorative herbs such as licorice or Rehmannia are also indicated. These herbs will additionally help to maintain blood sugar levels during the night.

• Tonic and adaptogenic herbs used throughout the day can help to break the vicious cycle of non-restorative sleep in stressed patients. The safest and best herb to use in this context is Withania, although a small amount of ginseng will not be too stimulating for most patients. Also use of those herbs taken just before bed can tonify (and thereby improve) the sleep of patients experiencing non-restorative sleep.

• If pain interferes with sleep then analgesic herbs for pain management are indicated. For example, willow bark is useful for pain associated with inflammation, whereas Corydalis, cramp bark, kava and wild yam will help to alleviate pain associated with smooth muscle cramping. (See also the treatments for restless legs syndrome and nocturnal myoclonus.)

Recent research with Vitex (chaste tree) and melatonin represents a promising new development in the herbal treatment of maintenance insomnia (see monograph).

Example liquid formulas

image

Dose: 5 mL with water three times a day. Take the last dose 1 hour before bed.

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Dose: 5 mL with water three times a day. Take the last dose 1 hour before bed.

Case history

A male patient aged 47 complained of difficulty falling asleep some nights. He was prescribed kava tablets, 2 to 3 about 50 minutes before bed. Each tablet contained 200 mg of extract standardised to 60 mg of kava lactones and equivalent to about 1800 to 2000 mg of root. He found the tablets very effective, but did find that they caused early morning drowsiness on some, but not all, mornings after he used them.

Case history

A female patient, aged 59, suffered from fibromyalgia (which was treated with a herbal mixture taken during the day). However, a significant problem (typically associated with fibromyalgia) was her terrible insomnia. She claimed that some nights she only slept for about 1 hour. Valerian tablets and kava tablets were tried to no effect.

She was prescribed the following formula:

Zizyphus spinosa 1:2 30 mL
Scutellaria lateriflora 1:2 25 mL
Lavandula officinalis 1:2 20 mL
Corydalis ambigua 1:2 25 mL
  total 100 mL

Dose: 8 mL with water about 30 minutes before bed. Repeat a few hours later if still awake.

The above sleep mixture helped tremendously and, with the sleep improvement, her fibromyalgia also improved more rapidly.

Restless legs syndrome (and nocturnal myoclonus)

Restless legs syndrome (RLS) has been described as ‘the most common disorder you’ve never heard of’.83 It is an unusual sensation (paraesthesia) in the legs that typically occurs at bedtime and is a common cause of insomnia. The cause of RLS is not known. It is known to be associated with a number of medical conditions including iron deficiency, pregnancy and dialysis.

RLS is surprisingly common and plagues the sleep of many sufferers. Various estimates have ranged from 2% to 15% of the adult population, with the real number likely to be about 6%. It is more common in women.84 The older the person, the more likely he or she will suffer from restless legs. It is rare in young children, but for those older than 65 years around 10% to 28% are affected.

Lower iron levels in the brain affect dopamine metabolism, specifically inhibition of tyrosine hydroxylase needed for the synthesis of dopamine and requiring iron as a cofactor.85 In one study, 75% of patients with RLS had decreased iron stores. Iron concentrations in the blood drop by 50% to 60% at night. Ferritin concentrations of <50 ng/mL have been correlated with decreased sleep efficiency and increased leg movements in sleep in RLS. Oral supplementation of iron has resulted in significant clinical improvement in RLS. Some patients with RLS improve with folate supplementation, which is also involved in tyrosine hydroxylase production.84

Magnesium therapy (12.4 mmol/day=301 mg/day) has been shown to be beneficial.86 A placebo-controlled trial found that 800 mg/day Valerian root for 8 weeks improved RLS symptoms and daytime sleepiness.87 A recent pilot trial with Vitex (chaste tree) was also promising (see monograph). A number of lifestyle factors have been associated with RLS. These include heavy smoking, advanced age, obesity, hypertension, loud snoring, use of antidepressant drugs,83 diabetes and lack of exercise.88

Conventional medical treatment for RLS focuses on drugs for the nervous system, especially dopaminergic agents. Many of these drugs are quite powerful and dangerous and should be reserved for more severe cases.82 A study found that RLS was very common in people with varicose veins (22% incidence).89 After treatment for superficial varicose veins (sclerotherapy or vein stripping), 98% reported an immediate improvement in their restless legs.

When the blood is not circulating properly, the walls of the deeper veins can stretch, resulting in unpleasant sensations in the legs. The sluggish circulation can cause red blood cell aggregation that can further add to the paraesthesia and restless legs. Consistent with this, the condition is much more common during pregnancy.82 One survey of 500 women found that 19% reported RLS during pregnancy, that 7% described their symptoms as ‘severe’ and that the condition abated in 96% of affected women within 1 month of giving birth.82

Key herbs to consider for RLS are:

• anxiolytic and hypnotic herbs such as valerian, kava (especially), skullcap and passionflower to alleviate the nervous system imbalance that is part of RLS

• many of the factors involved in RLS (smoking, pregnancy, obesity, age, diabetes) all point to an involvement of the circulation. Hence venotonic herbs such as horsechestnut and butcher’s broom and herbs that enhance circulation such as Ginkgo have a key (but often neglected) role to play

• chaste tree and other herbs for insomnia may be of value.

Case history

A female patient aged 61 complained of sleep-onset insomnia and sleep latency largely brought about by restless legs at night. There was a history of anxiety and poor venous circulation. She was prescribed tablets (2 per day) containing Aesculus hippocastanum (horsechestnut) 1.2 g, Ginkgo biloba (Ginkgo) 1.5 g and Ruscus aculeatus (butcher’s broom) 800 mg and a magnesium supplement. Kava tablets (providing 120 to 180 mg kava lactones per day) were also to be taken as required.

This patient was successfully treated for about 2 years as above and then found that the treatment could be stopped for many months without problem. The treatment was started again if symptoms returned. This on and off approach was followed for 3 years.

Chronic tension headache

Chronic tension-type headache (TTH) is a neurological disorder characterised by frequent attacks of mild to moderate headache with few other symptoms.90 The headaches are typically bilateral, have a pressing (non-pulsatile) quality and are not aggravated by routine physical activity. They are not characterised by nausea or vomiting and no other causes are found. TTH affects up to 78% of the general population and 3% suffer from the chronic form.91

Peripheral factors are implicated in episodic TTH, whereas central factors probably underlie chronic TTH. Activation of hyperexcitable peripheral afferent neurons from head and neck muscles is the most likely explanation for infrequent headaches.90 Muscle and psychological tension are associated with and can aggravate TTH, but are not believed to be the cause. Abnormalities in central pain processing and a generalised increase in pain sensitivity are present in some patients with chronic TTH.90,92

The treatment of a single episode of tension headache is rarely an issue for a consultation for herbal treatment. The commonly encountered clinical situation is recurrent or chronic TTH, hence the approach to treatment described below is more aimed at the prevention of headaches, but many of the herbs below will also alleviate tension headache pain. Herbs with mild analgesic properties still have a role in this context because they generally also possess some relaxing or anxiolytic activity.

Aspects of herbal treatment that should be considered:

• If the headaches are related to trigger foods, or there are signs of problems with digestion, then bitter herbs to improve upper digestive and choleretic herbs to improve liver function should be included.

• Anxiolytic and nervine tonic herbs should be prescribed if appropriate, especially those which have some analgesic activity such as Corydalis and kava.

• Spasmolytic herbs, particularly those with an effect on the circulation can help to prevent tension headaches. These include wild yam, hawthorn, cramp bark and chamomile.

• Analgesic herbs include willow bark, California poppy and Corydalis. As well as its role in migraine, feverfew is a useful anti-inflammatory herb in TTH.

• If the headaches have a relationship with the menstrual cycle, then hormonal regulating herbs may be valuable, for example chaste tree if the headaches occur premenstrually.

• If eye strain is a factor then higher doses of bilberry (equivalent to at least 80 mg of anthocyanins per day) are indicated.

• In elderly people, cerebral ischaemia may contribute to headaches and can be treated with Ginkgo if there is evidence of its presence.

• Topical application of peppermint oil to the temples has been shown to relieve headache pain in clinical trials (see monograph).

• If the above approach does not give results then localised traction or compression of veins or nerves may be a cause, and anti-inflammatory and antioedema herbs such as horsechestnut and butcher’s broom should be tried in conjunction with St John’s wort (similar to the approach described next for trigeminal neuralgia).

• For headaches due to sinusitis, treatment should focus on this condition. An analgesic herb such as willow bark could also be recommended.

Example liquid formula

Corydalis ambigua 1:2 25 mL
Viburnum opulus 1:2 25 mL
Crataegus monogyna leaf 1:2 30 mL
Matricaria recutita (high in bisabolol) 1:2 20 mL
  total 100 mL

Dose: 8 mL with water twice a day.

Case history

A male patient, aged 74, complained of headaches and fatigue. He had experienced about one headache per week on and off for years. He had some sinus problems, with post-nasal drip at night and his nose could be blocked at times. He used to have migraines and his headaches were worse with stress. He worked long hours and was anxious and worried.

He was prescribed the following herbs:

Euphrasia officinalis 1:2 20 mL
Viburnum opulus 1:2 15 mL
Tanacetum parthenium 1:5 10 mL
Matricaria recutita 1:2 15 mL
Corydalis ambigua 1:2 20 mL
Crataegus monogyna leaf 1:2 20 mL
  total 100 mL

Dose: 5 mL with water three times a day.

For the fatigue he was also prescribed 2 tablets per day, each containing Withania root 600 mg and ginseng main root 125 mg. The eyebright was included in the treatment because of the possible association of the headaches with his sinus condition. After 8 weeks on the herbal treatment he was relatively free from headaches.

Trigeminal neuralgia

Trigeminal neuralgia, also known as tic douloureux, is a frequent cause of facial pain that involves the trigeminal nerve and occurs almost exclusively in middle-aged or elderly people. The pain is severe and fleeting and may be so severe that the patient winces (hence the term tic). Pain attacks tend to occur in clusters that can go on for several weeks.93

The pathogenesis of trigeminal neuralgia is speculated to be an ephaptic conduction caused by segmental demyelination and artificial synapse formation (in other words the trigeminal nerve becomes cross-wired due to demyelination). The cause of the demyelination might be multiple sclerosis, vascular degeneration or ageing. However, one recent review suggested that the most common aetiology is vascular compression of the trigeminal nerve root entry zone that leads to a focal demyelination.94 The blood vessels involved are said to be aberrant or tortuous.92 Studies have demonstrated proximity of the nerve root to such vessels, usually the superior cerebellar artery.

Under a relatively new classification from the International Headache Society, for the diagnosis of classical trigeminal neuralgia no cause of symptoms other than vascular compression can be found. In contrast, symptomatic trigeminal neuralgia has the same clinical picture, but an underlying cause such as multiple sclerosis, amyloid filtration, small brain infarcts or bony compression is identified.92

Relevant herbs to consider include the following:

• A key herb is St John’s wort, which is traditionally prescribed for any neuralgia related to nerve irritation or compression.

• The health of large blood vessels and the microcirculation can be improved with grape seed and pine bark extracts and bilberry, Ginkgo, garlic, gotu kola and hawthorn.

• Any compression caused by oedema associated with inflammation or tortuous vessels can be treated with horsechestnut. The venous-toning effect of this herb may also be of value.

• Anti-inflammatory herbs could be tried, such as Boswellia and turmeric.

• Analgesic herbs such as Corydalis or willow bark can be prescribed for the painful episodes.

• Effects from demyelination can be somewhat improved by ensuring adequate intake of essential fatty acids (for example evening primrose oil, which is also anti-inflammatory) and improving the microvasculature (see above).

• A published case history described the successful use of consumption of 30 to 60 mL/day of Aloe vera juice for 3 months. The patient’s pain diminished significantly within 2 weeks of initiating therapy. When she stopped the Aloe juice her pain returned and it went within a few days of starting it again.95

Case history

A male patient, aged 77, presented with trigeminal neuralgia on the right side of his face. He had had the condition for about 9 years and it was first diagnosed as a dental problem. His episodes of attacks numbered 2 to 3 per year and each episode lasted 3 weeks to 3 months. While he was experiencing attacks he found it difficult to shave or wash his face. He was told by a specialist that a blood vessel was impinging on the trigeminal nerve (he had a history of atherosclerosis of the carotid arteries and angina pectoris). He was prescribed carbamazepine for the trigeminal neuralgia, but was concerned that this medication made him feel sluggish. His case history revealed that he suffered from hayfever with bouts of sneezing and he drank an enormous amount of tea each day (which he was advised to reduce).

He was prescribed the following herbal treatments:

• Grape seed extract tablets 100 mg/day

• Tablets (3 per day) containing the following herbs:

• horsechestnut extract equivalent to dry seed 1.2 g containing escin 40 mg
• butcher’s broom extract equivalent to dry root and rhizome 800 mg
• Ginkgo extract 30 mg equivalent to dry leaf 1.5 g containing Ginkgo flavone glycosides 7.3 mg

• Liquid formulation:

Scutellaria baicalensis 1:2 30 mL
Hypericum perforatum 1:2 30 mL
Crataegus monogyna leaf 1:2 30 mL
Ginkgo biloba (standardised extract) 2:1 10 mL
  total 100 mL

Dose: 5 mL with water twice a day.

(The Ginkgo in the liquid supplemented the amount in the tablets containing horsechestnut and butcher’s broom.) Over the ensuing months the intensity and frequency of the neuralgia abated and after 6 months he was free of pain and not taking carbamazepine. Continued treatment maintained the freedom from neuralgia. He was also sneezing less.

Rationale

Given the association with circulation, grape seed extract and Ginkgo were prescribed to boost the integrity of the microvascular circulation, hawthorn for the arteries and horsechestnut and butcher’s broom for any pressure on the nerve associated with oedema or venous congestion.

Baical skullcap and grape seed were to help reduce the sneezing and St John’s wort was given for the irritated trigeminal nerve.

Migraine

Results from the American Migraine Prevalence and Prevention Study indicate that the cumulative lifetime incidence of migraine in the USA is 43% for women and 18% for men. This frequency is likely to be reflected in most Western countries and, given that the diagnostic criteria used were relatively stringent, the incidence may be even greater.96

A migraine is a complex brain event that can produce a wide array of neurological and systemic symptoms. Although the term migraine is derived from the word hemicrania, meaning one side of the head, the pain is not necessarily one-sided. Symptoms include extreme and prolonged head pain, photophobia, nausea and vomiting. Sometimes the migraine is preceded by sensory (especially visual) or motor symptoms (the aura). More commonly there is no aura.

The vascular theory of migraine was proposed by Wolff and others in the 1930s. It attributes migraine to an initial intracranial vasoconstriction (which accounts for the aura) followed by an extracranial vasodilation (the headache). However, this theory was not consistent with later experimental observations.

There has been further movement away from the concept of migraine as a primarily vascular disorder.96 Although intracranial vasodilation is an appealingly simple explanation for migraine pain, this hypothesis has never been capable of explaining the wide range of symptoms that may precede, accompany, or follow the pain. Multiple imaging studies have now confirmed that vasodilation is not required for migraine headache. In fact cortical hypoperfusion during the headache is more characteristic.

A corollary of the vascular hypothesis of migraine is the concept that vasoconstriction is a primary mechanism by which caffeine, ergotamines and triptans exert their therapeutic effect. But experimental studies do not support this understanding and suggest that the mode of action of each drug class is complex and distinct.96 However, the vascular hypothesis still has its supporters as well as detractors.97

Migraine is currently hypothesised by some researchers as an episodic disorder of brain excitability, akin to epilepsy and episodic movement disorders. Waves of altered brain function, such as cortical spreading depression could be responsible for translating changes in cellular excitability into a migraine attack.96 This suggests a role for sedative and antiepileptic herbs.

Another suggestion is that migraine is an episode of local sterile meningeal inflammation and the subsequent activation of trigeminal neurons that supply the intracranial meninges and related large blood vessels.98 Meningeal mast cells could be involved here as triggers, suggesting a role of Scutellaria baicalensis, given the neurological and mast cell activities of its flavonoids.

Epidemiological studies suggest that migraine is associated with disorders of the cerebral, coronary, retinal, dermal and peripheral vasculature. There is evidence that migraine is associated with vascular endothelial dysfunction and impaired vascular reactivity, both as a cause and a consequence.99 This suggests a role for microvascular herbs and could explain the role of feverfew in migraine, including this herb’s possible effects on platelet function (see the feverfew monograph).

Migraine is a potentially progressive disorder, and progression of episodic migraine to chronic migraine (migraine chronification) is associated with a range of co-morbidities and risk factors, that could represent either cause or effect. Hypertension is one such co-morbidity,100 others include obesity, excessive use of medications, caffeine overuse, stressful life events, depression, sleep disorders, cutaneous allodynia,101 temporomandibular disorders,102 white matter lesions in the brain,103 cardiac and vascular problems, psychiatric disorders,104 head injury, pro-inflammatory states and prothrombotic states.105

The higher frequency of migraine in women has already been noted, and menstrual migraine, which occurs before or during menstruation, is believed to be associated with the fall of oestrogen.106 In other women, oral contraceptive use can trigger migraines.105 At menopause, migraine can regress, worsen or remain unchanged.105

Other factors linked to migraine development or migraine attacks include prolonged stress,107,108 and trigger foods such as cheese, coffee, chocolate or citrus fruits. Alcohol drinks, especially red wine, can also act as a trigger. About 40% of migraine sufferers tested positive for Helicobacter pylori, and eradicating this organism resulted in a significant clinical improvement.109

As well as trigger foods it has been suggested that other food allergies could also be a factor in migraine headaches. Commonly implicated foods include cow’s milk products, wheat and eggs.110 Poor body alignment and the benefits of spinal manipulation are particularly relevant to this condition.

In general, patients seeking phytotherapy for migraine will be sufferers of chronic migraine. Hence therapy is best aimed at preventing attacks, although a separate formula to abort attacks if taken early can be prescribed. This abortive treatment could include herbs such as feverfew, willow bark, ginger and Corydalis, all in relatively high doses.

Considerations for preventative herbal treatment include selection from the following:

• Anxiolytic and nervine tonic herbs are used for the effects of stress, especially those having some analgesic activity such as Corydalis. St John’s wort may be particularly valuable, as will herbs with some antiepileptic properties such as kava, Bacopa, Withania and valerian.

• Feverfew works well as a migraine prophylactic, but it must contain good levels of parthenolide. It takes about 4 to 6 months to fully work (see feverfew monograph). Since its primary effect may be on platelets, its role may be supported by antiplatelet herbs such as ginger and turmeric.

• If the migraines are related to trigger foods or there are signs of problems with digestion, then herbs to improve upper digestive and liver function should be included. Phytotherapy places an emphasis on the relationship between migraine headaches and liver function. It is good practice to include a liver herb in a migraine preventative formula, be it a choleretic herb such as globe artichoke or ones that aid hepatic detoxification such as turmeric or Schisandra. In France, this liver connection is acknowledged by phytotherapists, as evidenced by a study of migraine treated by the liver herb Fumaria officinalis (fumitory).111Helicobacter pylori can be treated with bitters, garlic, sage, thyme, Nigella and golden seal (see also pp. 321–322).

• Menstrual migraine should be treated with herbs with oestrogenic effects such as shatavari, wild yam and Tribulus. Premenstrual migraine may be alleviated by prescribing chaste tree.

• Ginkgo should be included in a preventative formula, given that cortical hypoperfusion is associated with migraine. The anti-PAF activity of Ginkgo (PAF is platelet activating factor) may also be an advantage.

• Spasmolytic herbs, particularly those with an effect on the circulation, can help to prevent a migraine. These include hawthorn, cramp bark and chamomile. The spasmolytic herb butterbur is used in Europe for migraine prophylaxis. (Caution: butterbur contains toxic pyrrolizidine alkaloids, but these compounds have been removed from products permitted for sale in Europe.)

• Given that a pro-inflammatory cascade might be involved in the aetiology of migraine, anti-inflammatory herbs such as Boswellia, turmeric and ginger could be of value as preventive agents.

• Herbs for microvasculature and promoting endothelial health could be of value. These include garlic, bilberry, pine bark and grape seed extracts, Ginkgo, green tea, turmeric, and Polygonum cuspidatum (as a source of resveratrol).

Example liquid formula

Tanacetum parthenium 1:5 20 mL
Hypericum perforatum or Bacopa monniera 1:2 30 mL
Schisandra chinensis 1:2 25 mL
Zingiber officinale 1:2 10 mL
Viburnum opulus 1:2 20 mL
  total 105 mL

Dose: 8 mL with water twice a day.

Case history

A female patient aged 43 suffered from about two severe migraines a month. There did not appear to be any association with trigger foods and they tended to occur premenstrually. She was prescribed the following treatments:

• Feverfew tablets 150 mg standardised to contain 900 μg parthenolide, 2 tablets per day

• Three tablets per day of an anti-inflammatory formula containing Boswellia extract 200 mg equivalent to dry gum resin 2400 mg containing boswellic acids 135 mg, celery seed oil equivalent to dry seed 3000 mg, and ginger rhizome 300 mg

• Chaste tree 500 mg tablets, 2 tablets on rising.

Over a period of about 4 to 6 months the migraines reduced substantially in frequency and severity. She found that conventional analgesics such as aspirin could better abort or allay an attack than previously (this is a common finding with feverfew therapy).

Enhancing cognition

Although not a health issue, there is considerable interest in herbs that may be able to effect cognition enhancement, for example among students studying for exams or older people whose memories are weakening. In addition, these herbs form a central part of the treatment of more serious conditions such as Alzheimer’s disease.

On current evidence, Ginkgo has been shown to improve cognitive function, although there have been some negative findings (see Ginkgo monograph). In particular, the combination of Ginkgo and ginseng seems to be particularly powerful at improving cognition in both acute and long-term studies (see the ginseng monograph).

The Ayurvedic herb Bacopa monniera, also known as brahmi in India, has a strong traditional reputation for improving cognitive function and intelligence.112 Several clinical trials have found that various Bacopa extracts (typically at around 300 mg/day) improved cognitive function in healthy volunteers, usually when given over 90 days.113–115 Features of some of these trials included effects being maximal at 90 days and Bacopa decreasing the rate of forgetting of new information. A short-term trial (2 hours) on Bacopa showed no benefit.113

In a 12-week randomised, double blind trial conducted in the USA, the effect of 300 mg/day of Bacopa on cognitive function was investigated in healthy elderly volunteers. The main outcome was measured by the delayed recall score from the AVLT (Auditory Verbal Learning Test) word memory task. Also measured was the Stroop Task which assesses the ability to ignore irrelevant information. The following results were obtained:116

• Bacopa significantly enhanced AVLT delayed word recall memory scores

• Stroop results were similarly significant, with the Bacopa group improving and the placebo group unchanged

• Depression and anxiety scores and heart rate significantly decreased over time for the Bacopa group, compared to an increase in the placebo group

• No effects were found on the DAT (Divided Attention Task).

A team of British and Australian scientists, including Professor Andrew Scholey now at Swinburne University, have undertaken a series of investigations on sage (Salvia officinalis) because of its traditional reputation as a tonic for the nervous system and memory. For example, the 16th century English herbalist John Gerard wrote about sage: ‘It is singularly good for the head and brain and quickeneth the nerves and memory’. The investigators used a randomised, placebo-controlled, double blind, crossover design to investigate the effects of a single dose of sage in healthy older volunteers over a 6-hour period.117 Compared with the placebo phase (which generally exhibited the characteristic decline in performance over the 6-hour test period), the 333 mg extract dose of sage caused a highly significant enhancement of secondary memory at all testing times. Secondary memory is longer term memory where, in this case, recently supplied information is processed. There were also significant improvements in accuracy of attention following this dose, but not for the other doses. The extract used in the study was also shown to inhibit cholinesterase in test tube experiments. The authors concluded that the overall pattern of results was consistent with a benefit to pathways involved in efficient processing of information and/or consolidation of memory, rather than enhanced efficiencies in retrieval or working memory. The optimum sage dosage of 333 mg (about 2.5 g of herb) improved secondary memory by about 30 units. The decline with age for the healthy group tested (compared to healthy 18 to 25 year olds) was around 40 units. Hence the benefits seen in the present study reflect a substantial temporary reversal of the deterioration in secondary memory that typically occurs with about 50 years of normal ageing.

Other herbs demonstrated to improve cognitive function include gotu kola (see monograph), Schisandra and Rhodiola. In two sets of experiments, young (21 to 24 year old) telegraph-operators were asked to transmit Morse code at maximum speed for a period of 5 minutes.118,119 Following treatment with a single dose of Schisandra extract (3 g herb) the test was repeated. The error frequency was within the range 84% to 103%, whilst that of the control group (treated with a placebo of glucose or 70% ethanol) was 130%. It was concluded that Schisandra prevented or reduced exhaustion-related errors. By using a test method involving the correction of texts in which fatigue affected the accuracy but not the speed of work120 it was demonstrated that 38 (65%) of a group of 59 students treated with Schisandra showed an improvement in performance. Of these, seven presented an increase in the amount of work performed, 14 exhibited an enhancement in the quality of correction, and 17 showed improvements with respect to both of these.

A combination of Rhodiola, Siberian ginseng and Schisandra, used either in single or repeated doses, significantly increased the mental working capacity of healthy volunteers (computer operators on night duty).121 A relatively low dose of Rhodiola extract at 170 mg/day for 2 weeks improved five different tests of cognitive function in a double blind, placebo-controlled trial in 56 young, healthy doctors on night duty.122

Cognition-enhancing herbs can also be of value in children, including those suffering attention deficit hyperactivity disorder (ADHD), and Bacopa is a good example of this. BR-16A is an Ayurvedic herbal formulation containing Bacopa as the main ingredient. It was evaluated for its efficacy in an open label trial in 25 children aged between 4 and 14 years having hyperkinetic behavioural problems. The duration of the problem ranged from 6 months to 3 years. Fifteen children were mentally disadvantaged and amongst them 10 had a history of brain damage. The herbal syrup brought about ‘marked improvement’ in five children as judged by both parents and doctors. No side effects were noted.123

In terms of controlled trials in ADHD, two have been conducted: one with BR-16A and the other using Bacopa alone. A randomised, double blind, placebo-controlled trial was undertaken to evaluate the efficacy of BR-16A in school-going children with ADHD. A total of 195 children were screened, out of which 60 satisfied the medical criteria for ADHD. Among those enrolled in the study, 30 received herbal treatment and 30 received placebo. An assessment of academic functioning along with psychological tests was done before and after the treatment. Statistical analysis was carried out in only 50 children and showed improvement in these tests in the herbal group compared with the placebo group. However, none of these differences achieved statistical significance because of the low number of trial participants.124

The study of Bacopa in ADHD was a small pilot study only published in abstract form. In this trial, a double blind, randomised, placebo-controlled design was employed. A total of 36 children were involved. Of these, 19 received Bacopa extract 100 mg/day for 12 weeks and 17 were given placebo. The active herbal treatment was followed by a 4-week placebo administration, making the total duration of the trial 16 weeks in both groups. One child in the Bacopa group and six in the placebo group dropped out. The mean ages were 8.3 years and 9.3 years in the Bacopa and placebo groups respectively. The children were evaluated on a battery of tests including mental control, sentence repetition, logical memory and word recall. Evaluation was undertaken before, during and at the end of the study. Data analysis revealed a significant improvement with sentence repetition, logical memory and learning following 12 weeks’ administration of Bacopa. This improvement was maintained at 16 weeks. During the clinical trial Bacopa exhibited excellent tolerability and no treatment-related adverse effects were reported.125

Pycnogenol, a proprietary, standardised extract of French maritime pine bark (Pinus pinaster) has shown promising results in ADHD and the clinical trial data in children is more robust than for Bacopa. Initial positive case reports stimulated the interest to study this extract further.126–128 However, a double blind, placebo-controlled comparative study in adults with ADHD failed to yield significant results.129 No significant differences were found between placebo, the drug methylphenidate and pine bark extract. However, the sensitivity of this study can be questioned since it also found no activity for the reference drug.

A pilot study found a significant improvement in ADHD for the pine bark extract in children at 1 mg/kg/day.130 This then led to a double blind, placebo-controlled study in 61 children, using the same dose over 4 weeks.131 Patients were examined at start of trial, 1 month after treatment and 1 month after the end of treatment period by standard questionnaires: CAP (Child Attention Problems) Teacher Rating Scale, Conner’s Teacher Rating Scale (CTRS), the Conner’s Parent Rating Scale (CPRS) and a modified Wechsler Intelligence Scale for children. Results showed that 1 month of the pine bark extract caused a significant reduction of hyperactivity and improved the attention, coordination and concentration of children with ADHD. No positive effects were found in the placebo group. A relapse of symptoms was noted 1 month after termination of treatment.

Example liquid formulas

For stress-associated memory impairment:

Glycyrrhiza glabra 1:1 20 mL
Rhodiola rosea (standardised extract) 2:1 25 mL
Ginkgo biloba (standardised extract) 2:1 40 mL
Panax ginseng (standardised extract) 1:2 20 mL
  total 105 mL

Dose: 8 mL with water twice a day.

For acutely improving short-term memory and cognitive function (the student or speaker’s friend):

Ginkgo biloba (standardised extract) 2:1 60 mL
Panax ginseng (standardised extract) 1:2 40 mL
  total 100 mL

Dose: 8 mL twice within a 1 hour period about 1 to 2 hours before an exam or lecture.

For age-associated cognitive decline:

Ginkgo biloba (standardised extract) 2:1 35 mL
Salvia fruticosa 1:2 30 mL
Panax ginseng (standardised extract) 1:2 15 mL
Rhodiola rosea (standardised extract) 2:1 25 mL
  total 105 mL

Dose: 8 mL with water twice a day.

Combine with tablets containing an extract of Bacopa capable of providing the equivalent of at least 10 g of herb per day (100 mg bacosides).

Case history

A student studying for university exams requested a formula to improve performance in the exam and concentration and memory while studying. She was prescribed the following formula:

Ginkgo biloba (standardised extract) 2:1 20 mL
Eleutherococcus senticosus 1:2 30 mL
Schisandra chinensis 1:2 25 mL
Bacopa monniera 1:2 25 mL
  total 100 mL

Dose: 8 mL with water twice a day. (Note: The Siberian ginseng was prescribed for the stressful effects of studying as well as its effects on performance.)

The student reported improved concentration and memory and less fatigue while studying. She passed her exams.

References

1. Hsieh MT, Peng WH, Wu CR, et al. Review on experimental research of herbal medicines with anti-amnesic activity. Planta Med. 2010;76(3):203–217.

2. Leung JW, Xue H. GABAergic functions and depression: from classical therapies to herbal medicine. Curr Drug Targets CNS Neurol Disord. 2003;2(6):363–374.

3. Johnston GA. GABA(A) receptor channel pharmacology. Curr Pharm Des. 2005;11(15):1867–1885.

4. Ko FN, Wu TS, Lu ST, et al. Ca(2+)-channel blockade in rat thoracic aorta by protopine isolated from Corydalis tubers. Jpn J Pharmacol. 1992;58(1):1–9.

5. Low AM, Berdik M, Sormaz L, et al. Plant alkaloids, tetrandrine and hernandezine, inhibit calcium-depletion stimulated calcium entry in human and bovine endothelial cells. Life Sci. 1996;58(25):2327–2335.

6. Kwan CY. Vascular effects of selected antihypertensive drugs derived from traditional medicinal herbs. Clin Exp Pharmacol Physiol. 1995;22(suppl 1):S297–S299.

7. Yamahara J, Kobayashi G, Matsuda H, et al. Vascular dilatory action of the Chinese crude drug. II. Effects of scoparone on calcium mobilization. Chem Pharm Bull (Tokyo). 1989;37(2):485–489.

8. Yu SM, Ko FN, Su MJ, et al. Vasorelaxing effect in rat thoracic aorta caused by fraxinellone and dictamine isolated from the Chinese herb Dictamnus dasycarpus Turcz: comparison with cromakalim and Ca2+ channel blockers. Naunyn Schmiedebergs Arch Pharmacol. 1992;345(3):349–355.

9. Sun RY, Yan YZ, Zhang H, Li CC. Role of beta-receptor in the radix Angelicae sinensis attenuated hypoxic pulmonary hypertension in rats. Chin Med J (Engl). 1989;102(1):1–6.

10. Isono T, Oyama T, Asami A, et al. The analgesic mechanism of processed Aconiti tuber: the involvement of descending inhibitory system. Am J Chin Med. 1994;22(1):83–94.

11. Kimura M, Muroi M, Kimura I, et al. Hypaconitine, the dominant constituent responsible for the neuromuscular blocking action of the Japanese–sino medicine ‘bushi’ (aconite root). Jpn J Pharmacol. 1988;48(2):290–293.

12. Chen Z, Duan X. Mechanism of the antiasthmatic effect of total coumarins in the fruit of Cnidium monnieri (L.) Cuss. Chung Kuo Chung Yao Tsa Chih. 1990;15(5):304–305, 320.

13. Huang ZH, Yang DZ, Wei YQ. Effect of atropine on the enhancing action of Fructus aurantii immaturus on the myoelectric activity of small intestine in dogs. Chung Kuo Chung Hsi I Chieh Ho Tsa Chih. 1996;16(5):292–294.

14. Anekonda TS, Reddy PH. Can herbs provide a new generation of drugs for treating Alzheimer’s disease? Brain Res Rev. 2005;50(2):361–376.

15. Yamada K, Hayashi T, Hasegawa T, et al. Effects of Kamikihito, a traditional Chinese medicine, on neurotransmitter receptor binding in the aged rat brain determined by in vitro autoradiography (2): Changes in GABAA and benzodiazepine receptor binding. Jpn J Pharmacol. 1994;66(1):53–58.

16. Sugiyama K, Kano T, Muteki T. Intravenous anesthetics, acting on the gamma-amino butyric acid (GABA) A receptor, potentiate the herbal medicine ‘saiko-keishi-to’-induced chloride current. Masui. 1997;46(9):1197–1203.

17. Kuang P, Wu W, Zhu K. Evidence for amelioration of cellular damage in ischemic rat brain by radix salviae miltiorrhizae treatment – immunocytochemistry and histopathology studies. J Tradit Chin Med. 1993;13(1):38–41.

18. Hu Y, Ge Y, Zhang Y, et al. Treatment of 100 cases of nerve deafness with injectio radix salviae miltiorrhizae. J Tradit Chin Med. 1992;12(4):256–258.

19. Chang HM, Chui KY, Tan FW, et al. Structure–activity relationship of miltirone, an active central benzodiazepine receptor ligand isolated from Salvia miltiorrhiza Bunge (Danshen). J Med Chem. 1991;34(5):1675–1692.

20. Kuang P, Xiang J. Effect of radix salviae miltiorrhizae on EAA and IAA during cerebral ischemia in gerbils: a microdialysis study. J Tradit Chin Med. 1994;14(1):45–50.

21. Tao Y, Kuang P, Zuo P. Inhibitory effect of 764-3 on Ca2+ uptake in rat brain synaptosomes. J Tradit Chin Med. 1996;16(4):288–292.

22. Chen LW, Wang YQ, Wei LC, et al. Chinese herbs and herbal extracts for neuroprotection of dopaminergic neurons and potential therapeutic treatment of Parkinson’s disease. CNS Neurol Disord Drug Targets. 2007;6(4):273–281.

23. Kasture S, Pontis S, Pinna A, et al. Assessment of symptomatic and neuroprotective efficacy of Mucuna pruriens seed extract in rodent model of Parkinson’s disease. Neurotox Res. 2009;15(2):111–122.

24. Shen XL, Witt MR, Dekermendjian K, Nielsen M. Isolation and identification of tetrahydrocolumbamine as a dopamine receptor ligand from Polygala tenuifolia Willd. Yao Hsueh Hsueh Pao. 1994;29(12):887–890.

25. Reimeier C, Schneider I, Schneider W, Schäfer HL, Elstner EF. Effects of ethanolic extracts from Eschscholtzia californica and Corydalis cava on dimerization and oxidation of enkephalins. Arzneimittelforschung. 1995;45(2):132–136.

26. Schäfer HL, Schäfer H, Schneider W, Elstner EF. Sedative action of extract combinations of Eschscholtzia californica and Corydalis cava. Arzneimittelforschung. 1995;45(2):124–126.

27. Kleber E, Schneider W, Schäfer HL, Elstner EF. Modulation of key reactions of the catecholamine metabolism by extracts from Eschscholtzia californica and Corydalis cava. Arzneimittelforschung. 1995;45(2):127–131.

28. Hanus M, Lafon J, Mathieu M. Double blind, randomised, placebo-controlled study to evaluate the efficacy and safety of a fixed combination containing two plant extracts (Crataegus oxyacantha and Eschscholtzia californica) and magnesium in mild-to-moderate anxiety disorders. Curr Med Res Opin. 2004;20(1):63–71.

29. Herbert JM, Augereau JM, Gleye J, Maffrand JP. Chelerythrine is a potent and specific inhibitor of protein kinase C. Biochem Biophys Res Commun. 1990;172(3):993–999.

30. Meller ST, Dykstra C, Gebhart GF. Acute thermal hyperalgesia in the rat is produced by activation of N-methyl-D-aspartate receptors and protein kinase C and production of nitric oxide. Neuroscience. 1996;71(2):327–335.

31. Yashpal K, Pitcher GM, Parent A, et al. Noxious thermal and chemical stimulation induce increases in 3H-phorbol 12,13-dibutyrate binding in spinal cord dorsal horn as well as persistent pain and hyperalgesia, which is reduced by inhibition of protein kinase C. J Neurosci. 1995;15(5 Pt 1):3263–3272.

32. Fundytus ME, Coderre TJ. Chronic inhibition of intracellular Ca2+ release or protein kinase C activation significantly reduces the development of morphine dependence. Eur J Pharmacol. 1996;300(3):173–181.

33. Shah BH, Shamim G, Khan S, Saeed SA. Protein kinase C inhibitor, chelerythrine, potentiates the adrenaline-mediatated aggregation of human platelets through calcium influx. Biochem Mol Biol Int. 1996;38(6):1135–1141.

34. Pavlakovic G, Eyer CL, Isom GE. Neuroprotective effects of PKC inhibition against chemical hypoxia. Brain Res. 1995;676(1):205–211.

35. Granger I, Serradeil-le Gal C, Augereau JM, Gleye J. Benzophenanthridine alkaloids isolated from Eschscholtzia californica cell suspension cultures interact with vasopressin (V1) receptors. Planta Med. 1992;58(1):35–38.

36. Boegge SC, Kesper S, Verspohl EJ, Nahrstedt A. Reduction of ACh-induced contraction of rat isolated ileum by coptisine, (+)–caffeoylmalic acid, Chelidonium majus, and Corydalis lutea extracts. Planta Med. 1996;62(2):173–174.

37. Kim DK, Lee KT, Baek NI, et al. Acetylcholinesterase inhibitors from the aerial parts of Corydalis speciosa. Arch Pharm Res. 2004;27(11):1127–1131.

38. Chernevaskaja NI, Krishtal OA, Valeyev AY. Inhibitions of the GABA-induced currents of rat neurons by the alkaloid isocoryne from the plant Corydalis pseudoadunca. Toxicon. 1990;28(6):727–730.

39. Ma ZZ, Xu W, Jensen NH, et al. Isoquinoline alkaloids isolated from Corydalis yanhusuo and their binding affinities at the dopamine D1 receptor. Molecules. 2008;13(9):2303–2312.

40. Kurahashi K, Fujiwara M. Adrenergic neuron blocking action of dehydrocorydaline isolated from Corydalis bulbosa. Can J Physiol Pharmacol. 1976;54(3):287–293.

41. Matsuda H, Tokuoka K, Wu J, Shiomoto H, Kubo M. Anti-inflammatory activities of dehydrocorydaline isolated from Corydalis Tuber. Nat Med. 1997;51(4):293–297.

42. Matsuda H, Tokuoka K, Wu J, Shiomoto H, Kubo M. Inhibitory effects of dehydrocorydaline isolated from corydalis tuber against type I-IV allergic models. Biol Pharm Bull. 1997;20(4):431–434.

43. Liu L, Li G, Zhu Y, et al. Comparison of analgesic effect between locally vinegar-processed preparation of fresh rhizoma Corydalis and traditionally vinegar-processed rhizoma Corydalis. Chung Kuo Chung Yao Tsa Chih. 1990;15(11):666–667, 702.

44. Wang Y, Zhu F, Zhang J, et al. Chemical evaluation of vinegar-processing method for fresh rhizoma Corydalis. Chung Kuo Chung Yao Tsa Chih. 1990;15(9):526–528.

45. Yamahara J, Yamada T, Kitani T, Naitoh Y, Fujimura H. Antianoxic action and active constituents of evodiae fructus. Chem Pharm Bull (Tokyo). 1989;37(7):1820–1822.

46. Yamahara J, Yamada T, Kitani T, Naitoh Y, Fujimura H. Antianoxic action of evodiamine, an alkaloid in Evodia rutaecarpa fruit. J Ethnopharmacol. 1989;27(1–2):185–192.

47. Yu LL, Liao JF, Chen CF. Effect of the crude extract of Evodiae fructus on the intestinal transit in mice. Planta Med. 1994;60(4):308–312.

48. Chiou WF, Liao JF, Chen CF. Comparative study of the vasodilatory effects of three quinazoline alkaloids isolated from Evodia rutaecarpa. J Nat Prod. 1996;59(4):374–378.

49. Hibino T, Yuzurihara M, Kase Y, Takeda A. Synephrine, a component of Evodiae Fructus, constricts isolated rat aorta via adrenergic and serotonergic receptors. J Pharmacol Sci. 2009;111(1):73–81.

50. Shoji N, Umeyama A, Takemoto T, Kajiwara A, Ohizumi Y. Isolation of evodiamine, a powerful cardiotonic principle, from Evodia rutaecarpa Bentham (Rutaceae). J Pharm Sci. 1986;75(6):612–613.

51. King CL, Kong YC, Wong NS, et al. Uterotonic effect of Evodia rutaecarpa alkaloids. J Nat Prod. 1980;43(5):577–582.

52. Chiou WF, Liao JF, Shum AY, Chen CF. Mechanisms of vasorelaxant effect of dehydroevodiamine: a bioactive isoquinazolinocarboline alkaloid of plant origin. J Cardiovas Pharmacol. 1996;27(6):845–853.

53. Yang MC, Wu SL, Kuo JS, Chen CF. The hypotensive and negative chronotropic effects of dehydroevodiamine. Eur J Pharmacol. 1990;182(3):537–542.

54. Yu LL, Liao JF, Chen CF. Effect of the crude extract of the Evodiae Fructus on the intestinal transit in mice. Planta Med. 1994;60(4):308–312.

55. Kim HJ, Jang YP, Kim YC. A constituent from Evodiae fructus having inhibitory effect on acetylcholinesterase. Seoul Univ J Pharm Sci. 1995;20:1–11.

56. Park CH, Kim SH, Choi W, et al. Novel anticholinesterase and antiamnesic activities of dehydroevodiamine, a constituent of Evodia rutaecarpa. Planta Med. 1996;62(5):405–409.

57. The Symbolism of the Passion Flower. <http://www.paghat.com/passiflorasymbolism.html>. accessed 9.09.2011.

58. Bone K. Clinical Guide to Blending Liquid Herbs. In Herbal Formulations for the Individual Patient. USA: Churchill Livingstone; 2003. pp. 362–365

59. Akhondzadeh S, Naghavi HR, Vazirian M, et al. Passionflower in the treatment of generalized anxiety: a pilot double blind randomized controlled trial with oxazepam. J Clin Pharm Ther. 2001;26(5):363–367.

60. Kammerer E, Wegener T. Schlafstörungen und deren Behandlung: stellenwert hochdosierter pflanzlicher Kombinationen. Nat Med. 1995;10(2):1–8.

61. Mollenhauer C. Anwendung eines hochdosierten Schlafsaftes aus Passionsblumenkraut and Baldrianwurzelextrakt (Dormo-Sern®) in der ambulanten Praxis bei Patienten mit Ein- und Durchschlafstörungen (EDS). Z Phytother Abstractband. 1995:22.

62. Schulz H, Jobert M, Hubner WD. The quantitative EEG as a screening instrument to identify sedative effects of single doses of plant extracts in comparison with diazepam. Phytomedicine. 1998;5(6):449–458.

63. Akhondzadeh S, Kashani L, Mobaseri M, et al. Passionflower in the treatment of opiates withdrawal: a double blind randomized controlled trial. J Clin Pharm Ther. 2001;26(5):369–373.

64. Movafegh A, Alizadeh R, Hajimohamadi F, et al. Preoperative oral passiflora incarnata reduces anxiety in ambulatory surgery patients: a double blind, placebo-controlled study. Anesth Analg. 2008;106(6):1728–1732.

65. Chaudhry HR, Taj R, Saeed N, et al. Effectiveness of a combination of Hypericum and Passiflora for the treatment of depression with concomitant anxiety. Eur Neuropsychopharmacol. 2007;17(suppl 4):S394.

66. Ngan A. Conduit R. A double blind, placebo-controlled investigation of the effects of Passiflora incarnata (Passionflower) herbal tea on subjective sleep. Phytother Res. 2011;25(8):1153–1159.

67. Lee IS, Lee GJ. Effects of lavender aromatherapy on insomnia and depression in women college students. Taehan Kanho Hakhoe Chi. 2006;36(1):136–143. (Article in Korean)

68. Akhondzaheh S, Kashani L, Fotouhi A, et al. Comparison of Lavandula angustfolia Mill. tincture and imipramine in the treatment of mild to moderate depression: a double blind, randomized trial. Prog Neuropsychopharmacol Biol Psychiatry. 2003;27(1):123–127.

69. Akhondzaheh S, Tahmacebi-Pour N, Noorbala AA, et al. Crocus sativus L. in the treatment of mild to moderate depression: a double–blind, randomized and placebo-controlled trial. Phytother Res. 2005;19(2):148–151.

70. Moshiri E, Basti AA, Noorbala AA, et al. Crocus sativus L. (petal) in the treatment of mild-to-moderate depression: a double blind, randomized and placebo-controlled trial. Phytomedicine. 2006;13(9–10):607–611.

71. Akhondzadeh S, Fallah-Pour H, Afkham K, et al. Comparison of Crocus sativus L and imipramine in the treatment of mild to moderate depression: a pilot double blind randomized trial [ISRCTN45683816]. BMC Complement Altern Med. 2004;4:12.

72. Noorbala AA, Akhondzadeh S, Tahmacebi-Pour N, et al. Hydro-alcoholic extract of Crocus sativus L versus fluoxetine in the treatment of mild to moderate depression: a double blind, randomized pilot trial. J Ethnopharmacol. 2005;97(2):281–284.

73. Akhondzadeh Basti A, Moshiri E, Noorbala AA, et al. Comparison of petal of Crocus sativus L and fluoxetine in the treatment of depressed outpatients: a pilot double blind randomized trial. Prog Neuropsychopharmacol Biol Psychiatry. 2007;31(2):439–442.

74. Darbinyan V, Aslanyan G, Aroyan E, et al. Rhodiola SHR-5 extract and the treatment of depression. Planta Med. 2007;73:813–814.

75. Darbinyan V, Aslanyan G, Amroyan E, et al. Clinical trial of Rhodiola rosea L. extract SHR-5 in the treatment of mild to moderate depression. Nord J Psychiatry. 2007;61(5):343–348.

76. Della Loggia R, Tubaro A, Redaelli C. Evaluation of the activity on the mouse CNS of several plant extracts and a combination of them. Riv Neurol. 1981;51(5):297–310.

77. PellaLoggia R, Zilli C, Del Negro P, et al. Isoflavones as spasmolytic principles of Piscidia erythrina. Prog Clin Biol Res. 1988;280:365–368.

78. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th ed. Arlington: American Psychiatric Association, 2000.

79. Starcevic V. Have anxiety disorders been disowned by psychiatrists? Aust Psychiatry. 2011;19(1):12–16.

80. Belmaker RH, Agam G. Major depressive disorder. N Engl J Med. 2008;358(1):55–68.

81. Rosengren A, Tibblin G, Wilhelmsen L. Low systolic blood pressure and self perceived wellbeing in middle aged men. BMJ. 1993;306(6872):243–246.

82. Barrett-Connor E, Palinkas LA. Low blood pressure and depression in older men: a population based study. BMJ. 1994;308(6926):446–449.

83. Clark MM. Restless legs syndrome. J Am Board Fam Pract. 2001;14(5):368–374.

84. Ohayon MM, Roth T. Prevalence of restless legs syndrome and periodic limb movement disorder in the general population. J Psychosom Res. 2002;53(1):547–554.

85. Patrick L. Restless legs syndrome: pathophysiology and the role of iron and folate. Altern Med Rev. 2007;12(2):101–112.

86. Hornyak M, Voderholzer U, Hohagen F, et al. Magnesium therapy for periodic leg movements-related insomnia and restless legs syndrome: an open pilot study. Sleep. 1998;21(5):501–505.

87. Cuellar NG, Ratcliff SJ. Does valerian improve sleepiness and symptom severity in people with restless legs syndrome? Altern Ther Health Med. 2008;15(2):22–28.

88. Phillips B, Young T, Finn L, et al. Epidemiology of restless legs symptoms in adults. Arch Intern Med. 2000;160(14):2137–2141.

89. Kanter AH. The effect of sclerotherapy on restless legs syndrome. Dermatol Surg. 1995;21(4):328–332.

90. Loder E, Rizzoli P. Tension-type headache. BMJ. 2008;336(7635):88–92.

91. Bendtsen L, Jensen R. Tension-type headache. Neurol Clin. 2009;27(2):525–535.

92. Cathcart S, Winefield AH, Lushington K, Rolan P. Stress and tension-type headache mechanisms. Cephalalgia. 2010;30(10):1250–1267.

93. Krafft RM. Trigeminal neuralgia. Am Fam Physician. 2008;77(9):1291–1296.

94. Cheshire WP. Trigeminal neuralgia: for one nerve a multitude of treatments. Expert Rev Neurother. 2007;7(11):1565–1579.

95. Hayes SM. Tic douloureux: report of successful treatment. Gen Den. 1984;32(5):441–442.

96. Charles A. Advances in the basic and clinical science of migraine. Ann Neurol. 2009;65(5):491–498.

97. Panconesi A, Bartolozzi ML, Guidi L. Migraine pain: reflections against vasodilatation. J Headache Pain. 2009;10(5):317–325.

98. Levy D. Migraine pain, meningeal inflammation, and mast cells. Curr Pain Headache Rep. 2009;13(3):237–240.

99. Tietjen GE. Migraine as a systemic vasculopathy. Cephalalgia. 2009;29(9):987–996.

100. Barbanti P, Aurilia C, Egeo G, Fofi L. Hypertension as a risk factor for migraine chronification. Neurol Sci. 2010;31(suppl 1):S41–S43.

101. Aguggia M, Saracco MG. Pathophysiology of migraine chronification. Neurol Sci. 2010;31(suppl 1):S15–S17.

102. Bevilaqua Grossi D, Lipton RB, Bigal ME. Temporomandibular disorders and migraine chronification. Curr Pain Headache Rep. 2009;13(4):314–318.

103. Kruit MC, van Buchem MA, Launer LJ, et al. Migraine is associated with an increased risk of deep white matter lesions, subclinical posterior circulation infarcts and brain iron accumulation: the population-based MRI CAMERA study. Cephalalgia. 2010;30(2):129–136.

104. Negro A, D’Alonzo L, Martelletti P. Chronic migraine: comorbidities, risk factors, and rehabilitation. Intern Emerg Med. 2010;5(suppl 1):S13–S19.

105. Bigal M. Migraine chronification – concept and risk factors. Discov Med. 2009;8(42):145–150.

106. Silberstein SD. Migraine and women. Postgrad Med. 1995;97(4):147–153.

107. Klingler D, Bauchinger B. Migraine – summary of diagnostic and therapeutic strategies. Wien Med Wochenschr. 1994;144(5–6):117–120.

108. Sauro KM, Becker WJ. The stress and migraine interaction. Headache. 2009;49(9):1378–1386.

109. Gasbarrini A, De Luca A, Fiore G, et al. Beneficial effects of Helicobacter pylori eradication on migraine. Hepatogastroenterology. 1998;45:765–770.

110. Pizzorno JE, Jr., Murray MT, Joiner-Bey H. Chapter 55: Migraine headache. In In: The Clinician’s Handbook of Natural Medicine. 2nd ed. Edinburgh: Churchill Livingstone; 2008. pp. 502–520

111. Barre Y. Migraine and Fumaria officinalis. Sem Ther. 1967;43(5):307–308.

112. Bone K. Clinical Applications of Ayurvedic and Chinese Herbs. Warwick: Phytotherapy Press, 1996. pp. 101–102

113. Stough C, Lloyd J, Clarke J, et al. The chronic effects of an extract of Bacopa monniera (Brahmi) on cognitive function in healthy human subjects. Psychopharmacology (Berl). 2001;156(4):481–484.

114. Roodenrys S, Booth D, Bulzomi S, et al. Chronic effects of Brahmi (Bacopa monnieri) on human memory. Neuropsychopharmacology. 2002;27(2):279–281.

115. Stough C, Downey LA, Lloyd J, et al. Examining the nootropic effects of a special extract of Bacopa monniera on human cognitive functioning: 90 day double blind placebo-controlled randomized trial. Phytother Res. 2008;22(12):1629–1634.

116. Calabrese C, Gregory WL, Leo MJ, et al. Effects of a standardized Bacopa monnieri extract on cognitive performance, anxiety, and depression in the elderly: a randomized, double blind, placebo-controlled trial. Altern Complement Med. 2008;14(6):707–713.

117. Scholey AB, Tildesley NTJ, Ballard CG, et al. An extract of Salvia (sage) with anticholinesterase properties improves memory and attention in healthy older volunteers. Psychopharmacology (Berl). 2008;198:127–139.

118. Lebedev AA. On the pharmacology of Schizandra. In: Lazarev NV, ed. Materials for the Study of Ginseng and Schizandra. Moscow: Far East Branch of USSR Academy of Science; 1955:178–188.

119. Lebedev AA. Schizandrin – a new stimulant from Schizandra chinensis fruits. Dissertation for a Degree in Medicine. Tashkent, Tashkent University, 1967. p. 16.

120. Kochmareva LI. The effect of Schizandra chinesis and Ginseng on processes of concentration. In: Lazarev NV, et al, eds. Materials for the Study of Ginseng and Schizandra. Leningrad: Far East Branch of USSR Academy of Science; 1958:12–17.

121. Vezirishvili MO, Roslyakova NA, Wikman G. The experience in developing an up-to-date biologically active supplement. Med Altera. 1999:44–46.

122. Darbinyan V, Kteyan A, Panossian A, et al. Rhodiola rosea in stress induced fatigue – a double blind cross-over study of a standardized extract SHR-5 with a repeated low-dose regimen on the mental performance of healthy physicians during night duty. Phytomedicine. 2000;7(5):365–371.

123. Shah LP, Seth GS. An open clinical trial of mentat in hyperkinetic children. Probe. 1992;31(2):125–129.

124. Kalra V, Hina Z, Pandey RM, Kulkarni KS. A randomized double blind placebo-controlled drug trial with Mentat in children with attention deficit hyperactivity disorder. Neurosci Today. 2002;6(4):223–227.

125. Negi KS, Singh YD, Kushwaha KP, et al. Clinical evaluation of memory enhancing properties of memory plus in children with attention deficit hyperactivity disorder. Indian J Psychiatry. 42(suppl 2), 2000.

126. Hanley JL. Attention Deficit Disorder. Green Bay: Impact Communication Inc., 1999.

127. Passwater RA. All about Pycnogenol®. New York: Average Publishing Group; 1998.

128. Masao H. Pycnogenol®’s therapeutic effect in improving ADHD symptoms in children. Mainichi Shimbun (Japan). 2000.

129. Tenenbaum S, Paull JC, Sparrow EC, et al. An experimental comparison of Pycnogenol® and methylphenidate in adults with attention-deficit/hyperactivity disorder (ADHD). J Atten Disord. 2002;6:49–60.

130. Trebaticka J, Skodacek I, Suba J, et al. Treatment success of ADHD by Pycnogenol®. In: Hoikkala A, Soidinsal O, Wahala K, eds. XXII International Conference on Polyphenols Polyphenols 2004. Finland, Jyvaskyla: Gummerus Printing; 2004:179–180.

131. Trebaticka J, Kopasova S, Hradecna Z, et al. Treatment of ADHD with French maritime pine bark extract, Pycnogenol®. Eur Child Adolesc Psychiatry. 2006;15(6):329–335.

Female reproductive system

Scope

Apart from their use to provide non-specific support for recuperation and repair, specific phytotherapeutic strategies include the following.

Treatment of:

• irregular menstruation and dysmenorrhoea (painful periods)

• some cases of menorrhagia (heavy menstrual bleeding)

• premenstrual syndromes

• menopausal syndrome

• impaired lactation

• postnatal syndromes

• some cases of infertility

• functional ovarian cysts

• some cases of vaginitis, cervicitis, vulvitis.

Management of:

• fibroids and endometrial polyps

• endometriosis and pelvic inflammatory diseases

• polycystic ovary syndrome.

Because of its use of secondary plant products and for ethical and legal reasons, particular caution is necessary in applying phytotherapy in cases of:

• delayed menstruation

• pregnancy and lactation

• venereal disease

• ovarian cancers

• hormone antagonist treatment for cancer (e.g. tamoxifen).

Orientation

Introduction

The female reproductive system provides perhaps the most substantial challenge to modern medical procedures and at the same time potentially the richest prospects for an inspired phytotherapy. Modern medicine finds disorders of the system difficult to treat conservatively. The reproductive structures themselves are the most dramatic examples of structure following function and, indeed, a function that is notably rhythmic. Beyond this is the historical and social reality: the experience of women has been neglected in medical science and their illnesses poorly charted. On the other hand women have often been the health care practitioners in society, they have necessarily had to focus a great deal on matters of their own reproductive health, fertility and, as midwives, childbirth and child-rearing. They have mastered the skills of intuitive diagnosis and treatment of functions that are notably difficult to isolate and measure and have developed some non-medical approaches to them. Nowadays they may feel particularly aggrieved about the medicalisation of their reproductive functions and are receptive to a new appreciation of their own insights.

The medical challenge

It has proven difficult to devise modern treatments for disorders of the female reproductive system that are genuinely appropriate to the task. It has always been hard to get a true measure of the job in the first place. Many problems start with dysfunctions in menstrual cycles or with hormonal disruptions, for which treatment outcome measures are not agreed and where subjective distress is not matched by technological monitoring. Even pathologies are more variable than consistent. Endometriosis and fibroids remain largely inexplicable; there are more categories of ovarian cysts and tumours than can easily be grasped; pelvic inflammatory conditions are almost defined by their unchartability.

Treatments therefore tend to bluntness. The primary recourse is to hormones, hormone analogues or hormone antagonists. These often have a crude effect on reproductive tissues that can be beneficial. However, they cannot interact comfortably with the astonishing choreography of multiple hormonal interactions that shape normal reproductive functions. They work by blocking this complexity, changing the force of negative feedback from subtle rhythm generation to the dictator of an artificial regime. As with almost everything else in this area, clear indicators of the wider impact of such treatments are hard to obtain but many women do not feel happy with them. Other conventional treatments are even more intrusive. Surgery is probably used for gynaecological and obstetric problems more extensively than for any other area of medicine. Although the days of routine hysterectomies, ovariectomies and mastectomies may be passing, it is still the case that surgery is undertaken too quickly for many sufferers, simply for want of any alternatives. Other measures – antibiotics for pelvic inflammatory disease, short-wave diathermy, dilation and curettage and laser ablation – appear often to be used without a clear treatment strategy and without an evidence base of efficacy.

One only needs to review the social history of obstetrics in the modern world, the move by women in many countries to reclaim home births, the move to less medicalised labour wards in hospitals, the increasing restoration of the midwife as arbiter of labour management and the exceptionally high professional liability insurance premiums required of obstetricians, to see that medicine has not always served women’s needs well. There appears to be a case for a different approach to their healthcare, one ideally that involves them better.

Structures and functions

Neither reproductive functions nor structures are fixed through life. In the case of the female, there is additional variability due to the need to ensure ideal conditions for pregnancy. In most mammals ovulation, and the associated transformation of the reproductive system, only occurs in certain situations and at certain times of the year (early hunter nomad women also probably ovulated only when food and circumstances were acceptable). Nevertheless, there is in the human female the mechanism for constant menstrual cycles that switches on in adolescence and, circumstances permitting (adequate food is still important), is maintained to the sixth decade of life. The menstrual cycle is a transformative cycle, generated by the interplay of secretory sites, the hypothalamus, the anterior pituitary and the ovaries, and of the hormones they produce. It leads to real changes in reproductive structures so that the relevant anatomy actually changes through the month. The hormone secretions appear to be the outcome of a rhythmic pulse.1 The anatomical changes in the ovarian hormone secretors, the development and ripening of the follicle to ovulation and the formation of the new secretory apparatus, the corpus luteum, out of the remnants of the follicle are rate-limiting elements in the equation and, with the functional pulsation, can be seen to provide the structural mechanism for the ‘ovarian clock’. If pregnancy occurs the corpus luteum is enabled to increase its activity, so priming the whole body towards the major shifts in both structure and function required to support a developing embryo and eventually give birth.

The main characteristic of the female reproductive system, therefore, is its mobility and changeability. Many disorders of it are thus functional disorders and most start that way. Dysfunctions are medical challenges in their own right. There is by definition no physical damage or pathological change to observe, as functional measures (for example biochemical markers such as metabolite and hormone levels) are notoriously unreliable in complex systems. There is a more subjective impression than objective monitoring. For example, relative dominance of oestrogen or progesterone is as much determined by symptoms as by blood tests. Oestrogen dominance may be implicated by sore breasts, heavier periods, increased fat distribution in hips and thighs, and presence of fibrocystic changes in the breast, fibroids and endometriosis. Progesterone lack may be seen in spotting between periods, increased premenstrual symptoms and early premenopause.

Treatments that aim to correct such dysfunctions can do so in two ways: suspend normal activity, in this case often with hormonally active agents – the contraceptive pill or hormone replacement therapy, for example, or hormonal antagonists; or, secondly, engage the causes of dysfunction at source. In this case treatments should be interactive, should support rather than interfere with normal checks and balances and should in part be guided by the woman herself. Even when treating actual pathologies, a strategy that also supported the return to underlying functional rhythms could be commended. In modern times exposure to oestrogens in the diet and environment has added a significant new factor to reproductive health in both women and men.

The herbal strategy: prompts to self-organisation

As there is a particular paucity of hard scientific data for the herbal treatment of female reproductive problems, practitioners have to be guided by case evidence. In treating menstrual disorders, this can be striking. Typically, a woman suffering dysmenorrhoea, irregular menstruation, premenstrual syndrome or menorrhagia will be given a mixture of traditional women’s remedies. For 1 or 2 months there are likely to be unfamiliar changes in the menstrual cycle, occasionally even a worsening of the original problem. Then from the third or fourth cycle there is often a real sense that a normal rhythm is emerging. It is as if the original software programme has been rebooted: the disturbance is diminished or even disappears. Most importantly, it is often possible to stop the medication soon after this point without relapse.

Such cases, and there are many in practice, are very illuminating. Whatever mechanisms are involved, and these can only be speculative, there appears to be a strong self-corrective tendency to the menstrual cycle. It is of course very robust and consistent among women all over the world and in all sorts of circumstances. A tendency to self-organisation would be consistent with the behaviour of other complex dynamic systems in biology. It is also highly reassuring. It suggests that to return to normal, menstrual function requires only the lightest nudge, even a placebo nudge (see p. 91). (It is also striking, however, how often women through the ages spontaneously chose plants with high levels of steroidal molecules for this work.)

The herbal nudge to self-correction is a feature of other gynaecological treatment strategies. Menopausal disturbances are another example. A typical scenario might involve a woman in her late 40s with increasing menstrual difficulties, premenstrual syndrome, congestive dysmenorrhoea and/or emotional turbulence. She thinks they may be signs of impending menopause but of course cannot be sure. A herbal treatment that might include Vitex agnus-castus (chaste berry) and Hypericum (St John’s wort) could be given, with one of two possible endpoints. Either periods stop and a smooth menopause, with hopefully few symptoms, could be underway in a few months or normal menstrual cycles could be resumed over the same time frame. The treatment seems to prompt the body to revert to its programme, whatever that might be. Again, there is the assumption of self- organisation, extended in this context to the view that menopause is programmed to be a smooth transition, that menopausal syndrome is an aberration (this could be argued if even one woman had a quiet and positive menopause; in fact a good proportion of women do).

Similar assumptions underpin the traditional herbal treatment of infertility, difficulties after childbirth and with lactation, and even of more overtly pathological states, functional ovarian cysts, some cases of endometriosis and the management of fibroids and pelvic inflammatory disease. Even when faced with more serious pathologies where conventional medical treatment is already underway, such as breast and cervical cancers, polycystic ovaries or the aftermath of hysterectomies, provided that there is some prospect of returning normal ovarian-pituitary dialogue and rhythms, then herbal prompts to this end are plausible and attractive strategies towards improved health.

Emmenagogues and abortifacients

Women in earlier times lived very different lives with radically different aspirations compared with their descendants in modern societies. Childbirth and child-rearing were generally more central to their lives. Infertility was one of the worst social problems a woman could suffer, often seriously threatening her position in the community. In all cultures considerable effort was put into treatments to improve fertility. These might well have worked to the principles set out above. Nevertheless, childbirth needed to be paced. For those who were normally fertile the priority became birth control. The absence at the due time of a period was not always welcome and there would be a regular demand in most communities for remedies that could prompt menstruation when delayed: emmenagogues. These would clearly need to be uterine stimulants and might need to be taken in heroic dosages. In modern times they might be classified as abortifacients.

Many herbs passed down as ‘women’s remedies’ were probably for this purpose, although the term ‘emmenagogue’ has come in popular books to refer to menstrual regulators in general and is no longer a reliable pointer to such an effect. In reviewing the modern application of traditional women’s remedies, it will be useful to keep this category of remedies in mind, however. Although generally taken in small doses in modern times, they may be contraindicated in pregnancy or where pregnancy is being sought and may be more stimulating than the menstrual modulators described earlier. In the Anglo-American tradition, emmenogogues could include Caulophyllum (blue cohosh), Actaea racemosa (black cohosh), Mitchella repens (squaw vine), Ruta graveolens (rue), Thuja occidentalis (arbor-vitae), Mentha pulegium (pennyroyal), Gossypium herbaceum (cotton root), Artemisia spp. (the wormwoods) as well as the stimulating laxatives and cathartic remedies. Uterostimulant action has also been shown for Chinese herbs Carthamus tinctorius, Angelica sinensis and Leonurus sibiricus with H1 and alpha-adrenergic receptors as postulated mediators.2 Some traditional effects on reproductive structures and functions have been linked with herbal activities on various prostaglandin receptors and functions that may also constitute stimulation of this type.3

The use of emmenagogues as abortifacients cannot be recommended in this text. Ethicolegal issues aside, getting the dose and timing right to terminate an early pregnancy was undoubtedly either a skilled or a messy affair and the possibility of embryo-damaging mistakes is high.

Phytotherapy in gynaecological and obstetric conditions

Note: The first edition of this book often cited the remedy Chamaelirium luteum (helonias or false unicorn root) as a major remedy in ‘rebooting’ normal menstrual cycles. This plant with its steroidal saponins was one of the more dramatic legacies of indigenous women’s medicine in North America. However it has not fared well in recent decades and is now in danger in the wild. There are programmes to grow the plant commercially and a few reliable sources of supply are available, but at the time of writing these are in the minority and the majority of stock on the market is likely to arise from wild harvesting. One possible substitute is shatavari (Asparagus racemosus) from the Ayurvedic tradition. Hence on the few occasions where false unicorn is mentioned in the following sections, it should be read in the context that it is only being recommended if sustainable sources are available.

Premenstrual syndrome

Premenstrual syndrome (PMS) is a variety of psychological, behavioural and physical symptoms which occur in the luteal phase of the menstrual cycle. Up to 85% of menstruating women report having one or more premenstrual symptoms, and 2% to 10% report these as disabling. More than 200 symptoms have been associated with PMS, but irritability, tension and dysphoria are the most prominent and consistently described. Of a number of potential causes that have been considered, evidence points to two being particularly significant:4

1. Enhanced sensitivity to progesterone in women with underlying serotonin deficiency

2. An inability to convert linoleic acid to prostaglandin precursors.

In anovulatory cycles, symptom cyclicity (PMS) disappears, and there exists a consensus that the cyclical changes are provoked by factors from the corpus luteum.5 The nature of the provoking factor, however, is unknown; but the ovarian steroids, 17beta-oestradiol and progesterone, are suspected.6,7 The response systems within the brain known to be involved in PMS symptoms are the serotonin (as noted above) and GABA systems. Progesterone metabolites, especially allopregnanolone, are neuroactive, acting via the GABA system in the brain. Allopregnanolone has similar effects to benzodiazepines, barbiturates and alcohol.6,7

The symptoms experienced vary from woman to woman and Abraham has created five distinct subgroups (Table 9.3).8 This classification is relevant since a pilot clinical trial conducted in England found that the herb Vitex agnus-castus (chaste berry) gave good results for PMS-A, PMS-D and PMS-H. A second larger clinical trial with Vitex found no statistical significance over placebo, although there was a tendency to improvement for breast tenderness and symptoms of fluid retention (see also the chaste tree monograph).9

Table 9.3 Abraham’s five PMS subgroups and symptoms

image

Since then the evidence for chaste tree has improved. A systematic review of herbal treatments for PMS found that chaste tree was the most investigated treatment and, after excluding trials because of poor quality or unsuitable diagnostic criteria, identified four eligible trials involving 500 women.10 The review concluded that chaste tree was useful for PMS. Several other trials showing benefit in premenstrual mastalgia have also been published, including one that demonstrated that it lowered prolactin levels, another possible factor implicated in PMS (see chaste tree monograph).

The aims of herbal treatment in PMS are as follows:

• Correct any hormonal imbalance. Vitex is often prescribed throughout the cycle on a long-term basis. (See monograph for dosage recommendations and discussion.) Actaea (black cohosh) and Paeonia (white peony) can also have a role here

• Correct essential fatty acid status, especially with evening primrose oil at doses of 3000 to 4000 mg/day. According to Abraham it is particularly indicated in PMS-C, which is associated with a prostaglandin deficiency

• Treat the main physical symptoms as they occur, for example treat fluid retention with diuretics such as Taraxacum leaves (dandelion), aches and pains with herbal analgesics such as Salix (willow bark) and sweats with Salvia (sage). Ginkgo throughout the cycle was found to be useful for breast symptoms. Sometimes symptomatic treatment will not be necessary if the other aims are addressed. Ruscus (butcher’s broom) has also shown benefits for the congestive symptoms in a clinical trial (see butcher’s broom monograph)

• Treat the emotional disturbances. This can often be the most important part of the therapy. Treatment is usually throughout the cycle. Nervine tonics such as Hypericum (St John’s wort) have been shown in double blind controlled trials directly to reduce symptoms of PMS, even after excluding non-luteal depression,11and sedatives such as Valeriana (valerian) for anxiety or insomnia are also valuable

• Compensate for the adverse effects of stress on the body using adaptogenic herbs such as Schisandra, Eleutherococcus (Siberian ginseng) and Withania. Sources of stress should be examined and dealt with if possible and diet should be balanced and mainly consist of unprocessed foods

• Treat the liver if signs of sluggishness are apparent, for example difficulty digesting fats, tendency to constipation, history of liver disease, tendency to nausea, preference for light or no breakfasts, etc. The liver is the site of the breakdown of female hormones and a sluggish liver may contribute to hormonal imbalance. Herbs to use include Taraxacum root and Silybum (St Mary’s thistle), but especially those that promote hepatic detoxification such as Schisandra and Curcuma (turmeric)

• In some cases oestrogen-modulating herbs such as Asparagus (shatavari) and Dioscorea (wild yam) can be beneficial (especially for PMS-D).

Case history

A woman, aged 34, with one child, aged 3, experienced severe depression, irritability, anxiety, fluid retention and breast tenderness that began about 7 days before the onset of menstruation and persisted until the first day of bleeding. Questioning revealed a history of viral hepatitis and increased levels of stress and devitalisation caused by caring for a young child. Initial treatment consisted of the following:

Valeriana officinalis 1:2 20 mL
Hypericum perforatum 1:2 30 mL
Silybum marianum 1:1 30 mL
Withania somnifera 1:1 25 mL
  total 105 mL

Dose: 5 mL with water three times a day

Tablets containing 500 mg Vitex agnus-castus extract were prescribed at 2 per day.

After 4 weeks there was a mild improvement. After another 3 months of treatment there was a substantial improvement. The breast and fluid symptoms were gone and her emotional symptoms and energy levels were considerably better. Treatment was continued. After some time of consistent benefit the patient continued on chaste tree only (as above) and remained virtually symptom-free.

Dysmenorrhoea

There are two types of dysmenorrhoea (painful menstruation) recognised:

1. Spasmodic or primary dysmenorrhoea in which the pain is directly related to the onset of menstruation and is uterine in origin. A widely prevalent and common complaint among young women, estimated to be present in 40% to 50%, with severe forms giving rise to work or school absenteeism in 15%. Prevalence is highest in the early 20s and decreases progressively thereafter. It only occurs in ovulatory cycles. Advances in the last three decades suggest that in primary dysmenorrhea there is abnormal and increased secretion of proinflammatory prostaglandins, thromboxane A2, prostacyclin and leukotrienes, which in turn induce abnormal uterine contractions similar to the way they induce contractions in labour. The contractions reduce uterine blood flow, leading to uterine hypoxia and pain, analagous to that of angina in the heart.12 Unlike endometriosis, primary dysmenorrhoea can be relieved by non-steroidal inflammatory drugs and usually the contraceptive pill.

2. Secondary or congestive dysmenorrhoea, which occurs before or late in menstruation and may arise in the uterus or in some other organ.

Since primary dysmenorrhea usually only causes problems for 1 to 2 days each month, it makes sense to use herbs that can help to control the pain at these times. Treatment throughout the whole menstrual cycle is best reserved for severe cases only.

Short-term treatment consists of uterine spasmolytics, analgesics, sedatives and herbs that decrease prostaglandin production. They can be given at around the onset of menstruation. However, these remedies are usually more effective for severe pain when given prior to the onset of menstruation by a few days. High doses need to be recommended to control acute symptoms.

Overall treatment focusses on the following herbs:

• Since Vitex (chaste berry) might enhance progesterone production, it could aggravate spasmodic dysmenorrhoea and should not be used. However, if a woman with spasmodic dysmenorrhoea also suffers from PMS with congestive symptoms (e.g. breast tenderness), Vitex can help both disorders when used as a long-term treatment.

• Herbs that support oestrogen function in the body (they may not be intrinsically oestrogenic themselves) can be indicated and include Asparagus (shatavari) and Dioscorea (wild yam). These herbs will help long term.

• Lamium (white dead nettle) is a specific that may decrease the condition when given long term.

• Short-term treatment consists of uterine spasmolytics and herbs that decrease prostaglandin production. The former include Angelica sinensis (dong quai), Dioscorea, Rubus (raspberry leaves) and Viburnum species (cramp bark or black haw). Achillea (yarrow) is spasmolytic and will check excessive bleeding if taken long term. Fennel has shown value in a clinical trial (see monograph). The latter include Zingiber (ginger), Curcuma (turmeric) and Salix (willow bark). Ginger at 1 g daily dose has been shown in early controlled trials to be particularly effective here.13 Actaea (black cohosh) is an anti-inflammatory and hormonal herb that can also be indicated and Corydalis and Eschscholtzia (California poppy) are useful analgesics.

• Aromatherapy with herbal oils of lavender, clary sage and rose has been shown to be an effective option in managing dysmenorrhoea symptoms.14

• For congestive dysmenorrhoea, herbs that help reduce localised oedema are indicated, including Aesculus (horsechestnut) and butcher’s broom.

Example liquid formulas
Spasmodic dysmenorrhoea

About 3 to 4 days before the period is due, start the following herbal formula:

Corydalis ambigua 1:2 25 mL
Dioscorea villosa 1:2 30 mL
Viburnum opulus 1:2 35 mL
Zingiber officinale 1:2 10 mL
  total 100 mL

Dose: 5 mL with water twice a day. Then just before menstruation, increase to 5 mL with water six times a day and stop treatment when pain has gone.

Not all women experience dysmenorrhoea. Hence it is not an inevitable consequence of menstruation. If the patient desires to treat the underlying condition an additional long-term hormonal-balancing formula can be tried. In more severe cases of spasmodic dysmenorrhoea, this hormonal-balancing treatment throughout the cycle is an essential requirement. An example is as follows:

Cimicifuga racemosa 1:2 10 mL
Zingiber officinale 1:2 15 mL
Angelica sinensis 1:2 40 mL
Dioscorea villosa 1:2 35 mL
  total 100 mL

Dose: 5 mL with water two times a day. Symptomatic treatment should also be used as above, but taken just prior to menstruation.

Chaste tree 1:2 liquid (1 to 2 mL with water on rising) so long as PMS or congestive symptoms are also present.

Congestive dysmenorrhoea

Vitex agnus-castus 1:2 20 mL
Aesculus hippocastanum 1:2 25 mL
Dioscorea villosa 1:2 30 mL
Angelica sinensis 1:2 25 mL
  total 100 mL

Dose: 8 mL with water twice a day.

Abnormal uterine bleeding

Excessive or abnormal bleeding from the uterus is a symptom, not a disease. The pattern of bleeding can vary, as can the cause. Metrorrhagia, where the bleeding is irregular in amount, acyclical in nature and often prolonged in duration, is usually due to a pathological condition of the uterus. A number of conditions, largely dysfunctional in nature, can respond to herbal treatment and are described below. Where abnormal bleeding is due to an organic cause, treatment should be directed at that cause. Such problems may be beyond the scope of herbal treatment.

A key herb for dysfunctional uterine bleeding is shepherd’s purse (Capsella bursa-pastoris). This is antihaemorrhagic and astringent, traditionally used to treat chronic menorrhagia and uterine haemorrhage.15,16 European herbalists regarded shepherd’s purse as useful for heavy bleeding associated with fibroids.17,18 In the late 19th century, and during World War I in Europe, shepherd’s purse was commonly used as a substitute for ergot in uterine bleeding.19–21 (Ergot is the product of a fungus (Claviceps purpurea) that grows on grain, especially rye. By the end of the 19th century, ergot was a standard drug used to induce contractions during labour. It was also used to treat postpartum haemorrhage.22) Ethanolic extracts of shepherd’s purse were also found to have a haemostatic action in a clinical setting in Japan.23,24

Menorrhagia

This is excessively profuse or prolonged bleeding occurring with a normal cycle. The iron status of women with menorrhagia should always be checked. Fibroids (see below) are the most likely cause, but other underlying causes must be investigated. In severe cases herbs can be taken throughout the cycle with doses increased to acute levels just prior to menstruation. In milder cases herbs can be commenced at acute doses just prior to menstruation only and continued until it has ceased.

Treatment may include Vitex (chaste berry), Paeonia (white peony) and antihaemorrhagic herbs, for example Achillea (yarrow), Panax notoginseng (Tienchi ginseng) and Equisetum (horsetail) and uterine antihaemorrhagics such as Capsella (shepherd’s purse) and Trillium (beth root).

Functional secondary amenorrhoea

This is the absence of menses for 6 months or for longer than three of the patient’s normal menstrual cycles. First exclude pregnancy, lactation, drugs, premature menopause, polycystic ovary syndrome (PCOS), poor diet or excessive exercise as causes. Other organic causes should also be excluded.

Herbal treatment of amenorrhoea is aimed at:

• correcting hypothalamic malfunction and the resultant hormonal imbalance using herbs such as Vitex (chaste berry), Asparagus racemosus (shatavari) and Caulophyllum (blue cohosh)

• treating the effects of any co-morbid depression with nervine tonics such as Hypericum (St John’s wort)

• treating the effects of stress with adaptogens, nervine tonics and sedative herbs

• treating debility with tonic herbs such as Withania and Panax ginseng; Angelica sinensis (dong quai) is specifically indicated where amenorrhoea follows menorrhagia or is associated with anaemia.

Difficulty with conception

This has a number of causes, many of which are not treatable by herbs. It should first be established if the problem truly exists with the woman. If this is the case, then the cause or causes should be isolated, if possible. Endometriosis and PCOS are common causes that will be treated as separate subjects below.

Some categories of difficult conception are listed below with the corresponding herbal approach to treatment:

• With anovulatory cycles, first establish the cause. Obesity or being underweight and overall health may determine whether ovulation occurs or not. Serious liver or kidney disease and other metabolic disorders all affect ovulation. Thyroid disease, even when mild, is a common problem affecting fertility. Lifestyle factors such as stress, excessive or too little exercise, diet, tea, coffee, alcohol, smoking and drugs should all be investigated. Treat the underlying cause and additionally give Vitex (chaste tree). Nervine tonics are frequently called for. Actaea (black cohosh, at higher doses) and Angelica sinensis (dong quai) may also be tried to establish ovulation. Tribulus and other saponin-containing oestrogen-modulating herbs are often appropriate and can either be given during the follicular phase of the menstrual cycle or for the whole cycle. Paeonia (white peony) can normalise folliculogenesis.

• Defective luteal function may be the problem, possibly associated with latent or frank hyperprolactinaemia. Treat mainly with Vitex and oestrogen-modulating herbs such as Tribulus. Paeonia may alternatively be of value.

• Cervical mucus may be too viscous. Cervical mucus may be ‘hostile’ for reasons other than hormonal. If this is suspected, recommend an alkaline diet (low protein, high fruit and vegetables). Lifestyle factors should be addressed (see below) and alkalinising herbs such as Apium (celery seed) prescribed together with oestrogen-promoting herbs (Dioscorea, Tribulus, and Asparagus) which will help to stabilise vaginal flora.

• Immunological rejection of sperm can occur. Sperm carries foreign proteins and a woman will often mount an immunological reaction against the sperm of her partner. With a consistent partner, this reaction usually abates but sometimes it does not. Treat with immune-regulating herbs such as Echinacea. Also attend to any factors which may be causing immune system dysregulation (see Chapter 8 under Autoimmunity).

• After investigation of difficulty with conception, no known factor can be identified in 20% to 30% of cases. Emotions can affect hypothalamic-pituitary hormone secretion and release. Stress and other emotional stimuli are known to increase prolactin release, which may affect reproductive function. Emotional factors may be involved in producing oviductal spasm which is sometimes observed in diagnostic tests. Obesity or being underweight and overall health may determine whether conception occurs or not. Lifestyle factors such as excessive or too little exercise, diet, tea, coffee, alcohol, smoking and drugs should be investigated. Treatment should be based on the above considerations and could include Vitex, Caulophyllum (blue cohosh), Actaea (higher doses) Tribulus and Asparagus for the hormonal side, Viburnum opulus for oviductal spasm and tonics, adaptogens, nervine tonics and sedatives as appropriate.

Example liquid formula

Chaste tree 1:2, 1 to 2 mL with water on rising each day and the following:

Asparagus racemosus 1:2 30 mL
Dioscorea villosa 1:2 30 mL
Cimicifuga racemosa 1:2 10 mL
Angelica sinensis 1:2 30 mL
  total 100 mL

Dose: 8 mL with water twice a day.

Pelvic inflammatory disease

Pelvic inflammatory disease is infection of the uterus, fallopian tubes and adjacent pelvic structures not associated with surgery or pregnancy. It is also known as chronic salpingitis. The most common organisms involved are Chlamydia trachomatis and Neisseria gonorrhoeae. There may be an original or current venereal origin, which if possible should be elicited. Misdiagnosis by the woman or by the practitioner of vaginal infections, with symptoms including discharge, irritation, dyspareunia, urinary complaints, and malodour may lead to secondary infections or pelvic inflammatory disease. Three likely causes, bacterial vaginosis, vulvovaginal candidiasis and trichomoniasis, should be distinguished and appropriate treatment instituted.25

Any vaginal infection provides a possible topical treatment route to a pelvic infection. The healthy vagina is an impressive barrier to infection and first steps should be to maintain its healthy microenvironment of lactic-acid-producing commensal bacteria (whose activity is maintained by moderate levels of oestrogen). Excessive douching, common among some women, is a known factor in bacterial vaginitis and should be discouraged.

For pelvic inflammatory conditions uncomplicated by vaginal infection the following systemic approaches can be tried:

• Immune-enhancing herbs such as Echinacea, Andrographis and Astragalus

• Dioscorea and Asparagus to support the female organs

• Hydrastis (golden seal) is a mucous membrane tonic useful for chronic infections of the oviducts

• Corydalis may assist to relieve the pain.

The above approach to treatment is compatible with and will actually assist conventional antibiotic treatment.

Uterine myoma (fibroids)

Uterine fibroids are benign, slow-growing smooth muscle tumours. They are probably the most common neoplasm in women. They are made up of myometrial cells that, under various hormonal and unknown stimuli, express increased aromatase activity and thus increase local oestrogen production; this further increases local tissue growth. Medically they are treated by gonadotrophin releasing hormone (GnRH) agonists or by surgery or ablation. The most common problem they cause is menorrhagia, but this disorder may be suspected in any combination of symptoms of lower abdominal congestion such as bloating, urinary frequency, painful intercourse, as well as infertility and complications of pregnancy.

A significant inverse association between risk of fibroids and age at menarche was reported. Compared with women who were 12 years of age at menarche, those who were ≤10 years of age at menarche were at increased risk (relative risk, RR, 1.24), whereas women who were age ≥16 years of age at menarche were at lower risk (RR 0.68).26,27

Several studies have shown an inverse relationship between the number of pregnancies and the risk of fibroids.26 One explanation is that pregnancy reduces the time of exposure to unopposed oestrogens. The reduced risk of fibroids requiring surgery in postmenopausal patients is probably due to tumour shrinkage in the reduced oestrogen environment following menopause.26

The role of the use of oral contraceptives is controversial and may depend on the actual components of the pill used.26 A significantly elevated risk of fibroids has been reported among women who first used oral contraceptives in their early teenage years (13 to 16 years of age) compared with those who had never used them.26,27 In contrast, hormone replacement therapy may not only prevent the shrinkage of fibroids after menopause, it may even stimulate their growth (or at least the growth of some of the tumours in women with multiple tumours).26 While tamoxifen is anti-oestrogenic, in breast tissue it probably exerts oestrogenic effects on the uterus. Hence it has been linked to promoting fibroid growth in a percentage of women in several clinical studies.26

Several studies have found a marked association between obesity and an increased incidence of fibroids.26 This may be related to hormonal factors, especially excess oestrogen. In obese premenopausal women, decreased metabolism of oestradiol by the 2-hydroxylation route reduces the conversion of oestradiol to inactive metabolites, which could result in a relatively hyperoestrogenic state.26,28 (See the studies cited later on how linseed may help to correct this effect.) A prospective study from the UK found that the risk of fibroids increased approximately 21% for each 10 kg increase in body weight.29 A large US study found a correlation between BMI and fibroid risk.30

One study has addressed the question of dietary influences on the prevalence of fibroids. In an Italian population, 843 women with fibroids were compared with 1557 women without. A diet weighted toward green vegetables was protective (RR 0.5), whereas a higher intake of meat was associated with a greater incidence of fibroids (RR 1.7).31,32 It is known that vegetarians have lower plasma oestrogen levels compared with non-vegetarians, so this fact could explain this observation. Also low fat diets are known to reduce oestrogen levels.26

Several studies have shown a reduced risk of fibroids associated with current smoking, but not past smoking.26 Again this has been attributed to the reputed anti-oestrogenic effect of cigarette smoking. One study found no change in risk for caffeine consumption and an increased risk for more than seven drinks of beer per week.33

A case-control study of 318 women found, after adjustment for other known risk factors, that the incidence of uterine fibroids was positively correlated with a history of pelvic infection.31,34 A history of three separate episodes of pelvic inflammatory disease conferred a relative risk of 3.7. Similarly a history of infection with Chlamydia gave a relative risk of 3.2.

High blood pressure is known to damage the smooth muscle lining of the arteries, and atherosclerosis is in part a proliferative condition of blood vessel walls. A prospective study of hypertension and risk of uterine fibroids found that diastolic blood pressure was an independent risk factor.31,35 Hypertensive women were 24% more likely to report fibroids, and for every 10 mgHg increase in diastolic blood pressure the risk for fibroids increased 8% to 10%.

It is widely accepted that oestrogen and the interaction with oestrogen receptors in the nucleus of the smooth muscle cell influence the growth of uterine fibroids. At menopause, fibroids begin to shrink in most patients; hence ovarian hormones are thought to play a key role in fibroid growth.36 While there are a considerable amount of both experimental results and clinical findings to support this connection, not the least being the use of GnRH agonists as treatments for fibroids, the mechanism remains poorly understood.36 Oestrogen may directly increase proliferation of leiomyoma cells or might indirectly increase growth by augmenting the effects of progesterone.36

As noted above, the enzyme aromatase is present in fibroids. This enzyme governs the conversion of androstenedione into oestrone and testosterone into oestradiol. Also 17beta-hydroxysteroid dehydrogenase (17beta-HSD), which converts oestrone into oestradiol (the active form of oestrogen), is overexpressed.37

The growth promoting effects of oestrogen and progesterone on the uterine smooth muscle cells is probably mediated by various locally produced growth factors.26 In particular, TGF-beta appears to be the only factor overexpressed in fibroid cells that is hormonally regulated.38 Other growth factors have also been extensively investigated, but their role remains unclear.26

One interesting observation is the connection with prolactin.26 Prolactin is produced by uterine tissues as well as the pituitary gland, and is a known growth promoter for vascular smooth muscle.26 While this is speculative at this stage, it does provide further support for the use of Vitex (chaste tree), which has been shown to decrease circulating prolactin levels in clinical trials.39

Treatment

The aim of herbal treatment for uterine fibroids is to minimise any further growth of the tumours and to manage any associated symptoms, especially the menorrhagia. It is unlikely that herbal treatments will substantially shrink fibroids (although see the study cited below). Treatment needs to be trialled for at least 3 months and combined with attention to those lifestyle issues identified by the risk factors listed above. In particular, attention should be given to achieving a healthy body weight and diet.

One review observed that no controlled trials of complementary treatments for uterine fibroids could be found in the literature.40 However, a traditional Chinese herbal formula also used in Kampo was found by Japanese medical scientists to shrink uterine myomas.41 The formula, known in Japanese as Keishi-bukuryo-gan (KBG) and in Mandarin as Kuei-chih-fui-ling-wan, contains Cinnamomum cassia, Paeonia lactiflora, Prunus persica seeds, Poria cocos and Paeonia suffruticosa. In English it is known as cinnamon and hoelen combination. This formula is frequently used in gynaecological disorders such as pelvic inflammatory disease, menopausal symptoms, and menorrhagia and dysmenorrhoea related to venous congestion of the pelvic region.

In an open study, 110 premenopausal women, average age 43.2 years (ranging from 27 to 52 years) were treated with the equivalent of 22.5 g/day of the dried herb formula administered as a freeze-dried decoction (1.5 g) for 12 weeks or more. These women had symptomatic uterine myomas all less than 10 cm in diameter. Clinical symptoms of menorrhagia and dysmenorrhoea were improved in more than 90% of cases, with shrinkage of the fibroids in about 60% of patients.

There is evidence to suggest that linseed supplementation causes a change in oestrogen metabolism that may be favourable for inhibition of uterine fibroids. Oestradiol is the biologically active oestrogen that drives the tumour growth. It is metabolised in the liver by the CYP450 enzymes 2-hydroxylase and 16alpha-hydroxylase into 2-hydroxyoestrone and 16alpha-hydroxyoestrone, respectively. The latter is still potently oestrogenic, with uterotropic activity similar to oestradiol. Hence excessive formation of 16alpha-hydroxyoestrone contributes to oestrogen excess. Controlled clinical studies have shown that supplementation with linseed (10 to 25 g/day) significantly reduced the relative formation of 16alpha-hydroxyoestrone in both pre- and postmenopausal women.42,43

The most enlightened approach to controlling fibroid growth would be to reduce oestrogen levels and especially aromatase activity. Factors that stimulate aromatase include excessive adipose tissue, high insulin levels (associated with insulin resistance), and levels of the proinflammatory prostaglandin PGE2. Obesity includes all these negative factors (adipose tissue also produces many proinflammatory cytokines). A number of herbs and herbal constituents are considered to have aromatase inhibitory properties, including Serenoa (saw palmetto) and Linum (linseed or flax seed) and flavonoids in general.44 However, much of this represents in vitro data and clinical research is needed. Other approaches may include reducing exposure to dietary oestrogenic sources by choosing organic diets. To modify the effects of oestrogen, the intake of (oestrogen-blocking) phyto-oestrogens and oestrogenic lignans (e.g. from soya and linseed) should be increased (see above).

Vitex (chaste tree) is a major part of herbal treatment and can be given in high doses (e.g. 5 mL twice a day) if the fibroids are severe. Paeonia can potentially exert anti-oestrogenic and other favourable hormonal effects. Liver herbs, especially Schisandra, may help the breakdown and elimination of excessive oestrogen. Antihaemorrhagic and uterine antihaemorrhagic herbs are indicated for the menorrhagia (see above). Herbs that have been traditionally used to control benign growths include Echinacea, Thuja (arbor-vitae) and Chelidonium (greater celandine). Ginkgo biloba standardised extract can relieve pain associated with fibroids. Other immune herbs may also be beneficial. Oestrogen-promoting herbs such as Dioscorea and Tribulus are best avoided.

Example liquid formula

Capsella bursa-pastoris 1:2 20 mL
Equisetum arvense 1:2 20 mL
Echinacea purpurea/angustifolia root 1:2 20 mL
Panax notoginseng 1:2 20 mL
Paeonia lactiflora 1:2 20 mL
  total 100 mL

Dose: 8 mL with water twice a day.

And chaste tree 1:2, 4 to 6 mL with water once a day.

Case history

A patient aged 43 presented with uterine fibroids characterised by menorrhagia and pain, especially with menstruation. She did not want surgery and asked for herbs to control her symptoms.

Treatment was as follows (based on 1 week):

Capsella bursa-pastoris 1:2 20 mL
Achillea millefolium 1:2 25 mL
Thuja occidentalis 1:5 20 mL
Echinacea angustifolia root 1:2 20 mL
Panax notoginseng 1:2 15 mL
  TOTAL 100 mL

Dose: 5 mL with water 3 times a day.

She was also prescribed Vitex 1:2, 2.5 mL with water twice a day, with the first dose on rising in the morning. Ginkgo biloba 50:1 standardised extract, 40 mg per tablet, 2 tablets per day, was also prescribed.

After 10 weeks of treatment there was considerable improvement in the menorrhagia and pain. Herbal treatment was maintained for continued symptom control.

Case history

A female patient aged 41 presented with multiple uterine fibroids and heavy bleeding. A few of the tumours were quite large (>8 cm). She was placed on the following treatment:

Astragalus membranaceus 1:2 20 mL
Paeonia lactiflora 1:2 30 mL
Hypericum perforatum 1:2 25 mL
Withania somnifera 1:2 35 mL
  total 110 mL

Dose: 5 mL with water twice a day.

Chaste tree 1:2 liquid. Dose: 4 mL with water on rising.

This patient also regularly took Echinacea root 1:2 liquid at 5 mL per day.

The Hypericum and Withania were for the stress the patient was experiencing due to other issues. Over the ensuing 5 years of treatment her fibroids grew slightly (but not rapidly) but she now experiences normal uterine bleeding. Her gynaecologist cannot understand why this is so. Note that, unlike the previous case, this patient received no uterine antihaemorrhagic herbs.

Endometriosis

Endometriosis is the presence of functioning endometrial tissue in an abnormal location. This may occur between the muscle fibres of the myometrium (uterine endometriosis) or in various locations in the pelvic cavity. The ectopic endometrium forms a cyst that can often rupture, resulting in inflammation and formation of multiple adhesions. Unlike normal endometrial tissue, the ectopic cells contain aromatase and are thus able to generate and be further stimulated by oestrogen (like cells that make up fibroids). The prostaglandin PGE2 is a potent stimulant of aromatase in endometriosis, emphasising the inflammatory factors in the origin of this condition.

Treatment

The most important herb for the treat of endometriosis is Vitex agnus-castus (chaste tree). Higher doses may be necessary, similar to those recommended for uterine fibroids (see chaste tree monograph).

Because of the prostaglandin abnormalities, evening primrose oil can also be indicated. Other herbs indicated for the symptoms include:

• Viburnum opulus (cramp bark), Corydalis, Angelica sinensis (dong quai), Rubus idaeus (raspberry leaf) and Zingiber (ginger) for dysmenorrhoea and chronic pelvic pain

• Pulsatilla for ovarian and ovulation pain

• Centella asiatica (gotu kola) and Saliva miltiorrhiza (dan shen) to reduce formation of adhesions

• antihaemorrhagic and uterine antihaemorrhagic herbs for the menorrhagia

• sedative, nervine tonic and adaptogenic herbs for the exacerbating effects of stress

• anti-inflammatory herbs such as Zingiber (ginger), Curcuma (turmeric), Boswellia, Bupleurum, Vitis (grape seed extract), Pinus (pine bark extract), Glycyrrhiza (licorice) and Rehmannia.

Herbs that may influence the underlying pathology include:

• Vitex, because of its regulating effect on ovarian function

• liver herbs, especially Schisandra to accelerate the breakdown of oestrogen, supported by hepatotrophorestoratives such as Silybum (St Mary’s thistle)

• immune-enhancing herbs to help prevent and resolve endometrial cysts (e.g. Echinacea, Astragalus and Phytolacca (poke root))

• herbs to control benign growths (e.g. Thuja (arbor-vitae) and Echinacea).

To modify the effects of oestrogen, the intake of phyto-oestrogens and oestrogenic lignans should be increased.

Polycystic ovary syndrome

Full recognition and understanding of this most common cause of infertility has been slow, with international conferences in 1990 and 2003 marking landmarks in definition and clinical approach. PCOS affects up to 7% of young women with a combination of intermittent or absent ovulation, hyperandrogenism and very often insulin resistance and hyperinsulinaemia. This last connection is significant as 60% of sufferers are obese, half of even normal weight PCOS sufferers also have insulin resistance, and there is also an increased risk of type 2 diabetes and associated cardiovascular conditions among PCOS sufferers later in life. Insulin-sensitising drugs like metformin are now common treatments to stabilise cycles. Anovulatory cycles and relatively excessive androgen and luteinising hormone (LH) production are normal features of puberty for young girls, a product of spurts in growth hormone. Early weight gain is now regarded as a potent factor in the development of fully fledged PCOS from this normal stage of development.45

The most common symptoms of PCOS are hirsutism and other signs of hyperandrogenism, such as oily skin and acne.

The evidence of a link between PCOS and insulin resistance, although not universal, now dominates clinical approaches. Any moves that can reduce adipose tissue levels and other causes of hyperinsulinaemia appear to be merited. Other hormonal interventions are less clear (the use of the contraceptive pill disguises rather than prevents PCOS in adolescence).

Key biochemical features of PCOS are as follows:

• Increased serum androgen (testosterone, androstenedione, dehydroepiandrosterone sulphate (DHEAS))46 with or without hyperinsulinaemia

• Decreased SHBG (sex hormone binding globulin) levels46

• Increased LH levels and serum LH:FSH (follicle stimulating hormone) ratio >246

• Increased prolactin levels in some cases46

• Increased oestrone levels. Oestradiol can be increased, but is typically low or normal47

• Increased fasting insulin or fasting glucose.46

Due to long-standing unopposed oestrogen stimulation, there is increased risk for endometrial carcinoma.48 Women with PCOS also have many abnormalities in lipid profiles, and are at increased risk of cardiovascular disease.48

A combination of white peony (Paeonia lactiflora) and licorice roots has been used in Chinese and Japanese traditional medicine and has the following names: Shaoyao Ganchao Tang (Chinese), Shakuyaku-Kanzo-To (SKT, Japanese) and TJ-68 (a Japanese proprietary product). In these combinations Glycyrrhiza uralensis is used, but Glycyrrhiza glabra would also be suitable, since in traditional Chinese medicine G. uralensis, G. glabra and G. inflata are medicinally interchangeable species.49 The combination has also been evaluated in uncontrolled clinical trials in PCOS.

SKT significantly decreased serum testosterone in women with defined PCOS, and in those described as infertile, oligomenorrhoeic or amenorrhoeic. All women had high serum testosterone levels. The dosage of extract was 5 to 7.5 g/day (equivalent to 4 to 6 g of dried white peony root and 4 to 6 g of dried licorice root), and given for periods ranging from 2 to 8 weeks up to 24 weeks. The extent of the reduction in mean testosterone is illustrated by the before and after values in two trials: 137 to 85 ng/dL (p<0.001) and 94 ng/dL dropping to below 70% of this value at 4 and 6 weeks (p<0.005). In some cases regular ovulation was established and some women conceived. Several trials documented that no side effects were observed.50–52 SKT (7.5 g/day, equivalent to 6 g of dried white peony root and 6 g of dried licorice root, and taken for 12 weeks) also significantly decreased serum free testosterone compared to baseline values in women with acne vulgaris. The herbal treatment significantly decreased the number of comedomes. No difference was observed for the other hormones measured: total testosterone, dihydrotestosterone, DHEAS and SHBG.53 The white peony and licorice combination may also be of benefit in lowering raised prolactin levels. A rapid decrease in prolactin levels was observed in 10 anovulatory women with elevated serum prolactin after administration of SKT (7.5 g/day). The decrease reached significance 2 weeks after the start of treatment.54 In case observation studies SKT (7 g/day) successfully treated drug-induced hyperprolactinaemia in men and a woman.55,56

Herbal treatment is centred on the following strategy:

• If appropriate, address central obesity as the driver of insulin resistance with Coleus and licorice

• If appropriate, address insulin resistance with St Mary’s thistle, Gymnema, ginseng, pine bark, Korean ginseng, Polygonum and berberine-containing herbs

• Chaste tree for hormonal regulation, doses depending on androgen and especially prolactin levels (see monograph)

• Licorice and white peony are clinically proven in PCOS and especially help to restart ovulation

• Tribulus and shatavari will improve fertility if that is a goal

• Support adrenal function with licorice and Rehmannia.

Example liquid formula

Vitex agnus-castus 1:2 20 mL
Glycyrrhiza glabra 1:1 15 mL
Paeonia lactiflora 1:2 30 mL
Gymnema sylvestre 1:1 25 mL
Schisandra chinensis 1:2 20 mL
  total 110 mL

Dose: 8 mL with water two to three times daily.

When a cycle has been initiated, add Tribulus concentrated extract, equivalent to furostanol saponins (as protodioscin) 300 to 400 mg/day on days 5 to 14 of the cycle to ensure cyclic regularity and fertility.

Case history

‘Karen’ was 27 years old and was diagnosed with PCOS when she was 18. Her periods were very irregular, usually between 60 and 90 day cycles, she had no hirsutism and was of normal weight.

Prior to her period she developed severe sugar cravings, depression, became very anxious and did not sleep well. Her diet was poor (‘Karen’ described herself as a vegetarian, but mostly ate junk food, chocolate and fruit) containing very low levels of vegetables, protein and complex carbohydrate.

She was placed on a ‘grazing’ diet to improve possible glucose tolerance: small, frequent meals, no refined carbohydrates and emphasis on a better balance of food groups.

Herbal formula

Paeonia lactiflora 1:2 40 mL
Glycyrrhiza glabra 1:1 30 mL
Taraxacum officinale root 1:2 30 mL
  total 100 mL

Dose: 5 mL three times daily.

After 3 months she had experienced three menstrual cycles at 27 day intervals and was feeling very well with no PMS. Her herbal formula was continued for another two cycles.

Benign breast disorders

Many terms have been used in the past to describe benign breast disorders. These include such descriptions as benign mammary dysplasia, cystic mastopathy, chronic cystic mastitis and cystic epithelial hyperplasia. Often they were grouped under the term ‘fibrocystic breast disease’ but this nomenclature is considered to be inappropriate and benign breast disease can be more appropriately categorised as the following:

• Fibroadenoma (FA)

• Cystic disease of the breast (fibrocystic changes, breast cysts).

One novel concept has been proposed to describe benign breast disorders. They are seen as aberrations of normal breast development and involution (ANDI). This is based on the fact that most benign breast disorders are not neoplastic growths, but rather arise on the basis of normal changes occurring in the breast throughout the various stages of reproductive life. They are no more benign neoplasms than is endometriosis.57

FA is a common, usually single lesion, typically seen in patients between ages 20 and 40. This lesion may enlarge during pregnancy, but usually becomes smaller as patients age. Clinically, FAs are usually sharply demarcated, with well-circumscribed smooth borders.58

Fibrocystic changes are commonly seen in the breast.58 The term describes pathological changes seen under the microscope and should not be used to describe clinical findings. The histological changes include varying amounts of fibrosis and cyst sizes. If predominantly fibrosis is present, the lesion may be referred to as fibrous mastopathy. Calcification may be seen in association with fibrocystic changes.

FA is classified in most surgical texts as a neoplasm. However, evidence supports the fact that FAs come under the category of ANDI.57 The natural history of FA is unlike that of benign tumours. The average FA grows to a diameter of 1 to 1.5 cm and then remains static. It regresses at menopause. FA are more hormonally responsive than most benign tumours, they lactate during pregnancy. FA-like lesions occur in most women’s breasts. In fact, histologically there is a complete spectrum from normal lobules to large lobules, to subclinical FA, to clinical FA. Moreover, a FA develops from a single lobule, not a single cell.

FA accounts for about 12% of all palpable symptomatic breast masses. They are quite common in women under 25 years and rare in women over 40. As noted, FA is probably an aberration of normal lobule development, a process which begins in the early stages of reproductive life. They can be removed surgically, usually after a period of observation.

Mechanisms controlling FA development and growth are poorly understood. In addition to the role of oestrogen and progesterone receptors expressed by epithelial cells, recent studies describe a possible role for growth factors and their receptors in the pathogenesis and growth FA, suggesting that multiple receptor signalling pathways could be involved in the growth and differentiation of benign breast lesions.59 However, concerning the risk of development of subsequent breast cancer, one large retrospective study has concluded that there is no increased risk for a woman with a simple FA and no family history of breast cancer.

Discrete palpable breast cysts are most common in the 40 to 50 year age group and are uncommon below 30 and over 54. A breast cyst is probably an aberration of lobular involution, a process that begins in the later stages of reproductive life.59 Some studies have looked at breast cancer risk in patients with palpable breast cysts.60 There may be an increased risk of between 2 to 4 times average, but this finding may be exaggerated.60 Patients with macrocysts do appear to have a higher risk of later developing breast cancer,61 although terminology and classifications have confused the issue.59

Elimination of caffeine and other methylxanthines from the diet (tea, coffee, chocolate and cola) can result in considerable clinical improvement in women with benign breast disorders.62 Some women may also respond to a diet low in tyramine (i.e. remove aged cheese, wine, mushrooms, bananas and aged and processed meats).62 Nicotine also contributes to the disorder.62 The common biochemical link between these observations is the enhancement of catecholamine release and increase of circulating catecholamines (epinephrine and norepinephrine).62 This also underlines the role of physical and emotional stress. Women with benign breast disease had a significantly higher level of urinary catecholamines than women without breast disease.63

Treatment for fibroadenoma

Vitex is the main treatment, because of its regulating effect on ovarian function. Herbs for growths such as Thuja (arbor-vitae) and Echinacea are also indicated. Oestrogen-promoting herbs such as Asparagus (shatavari) and Paeonia may be beneficial because an FA is an aberration of normal lobule development. Any stress aspects should also be addressed by prescribing nervine tonics, sedatives or tonics as the case history dictates.

Case history

‘Jenny’ was 31 and had a breast lump which was diagnosed as an FA. Her GP recommended 3 months’ observation but the surgeon wanted the lump removed. Being concerned at the prospect of surgery, she decided to try herbal treatment during the observation period.

Treatment was as follows (based on 1 week):

Echinacea angustifolia root 1:2 30 mL
Scutellaria lateriflora 1:2 30 mL
Paeonia lactiflora 1:2 25 mL
Thuja occidentalis 1:5 15 mL
  total 100 mL

Dose: 5 mL with water three times a day.

Vitex 1:2, 2 mL with water on rising, was also prescribed.

Treatment was continued for 3 months. When she returned to the surgeon, he could find no trace of the FA.

Treatment for breast cysts

The herbal treatment of breast cysts is similar to the approach used for FA, except that oestrogen-promoting herbs are best avoided. Vitex is the most important herb and the alleviation of the negative physiological effects of stress should also be emphasised. Abstinence from stimulants, as described above, should also be observed. To modify the effects of oestrogen, intake of phyto-oestrogens and oestrogenic lignans should be increased. This could also reduce any risk of breast cancer. Ginkgo could help control mastalgia symptoms (see Ginkgo monograph).

Menopause

The climacteric or menopause is a period of waning ovarian function that marks the end of the reproductive lifespan. As such, it is a normal event in the life of a woman and should not be regarded as a disease. Menopause is a retrospective diagnosis usually made after 12 months of amenorrhea.64 The average age for the menopause is around 51 years and has changed little in the last century. The average age of onset of the perimenopause is about 46 to 47 years and it lasts about 4 years.

The aim of herbal treatment is to assist the adjustment to this important change and provide symptomatic alleviation of the effects of oestrogen withdrawal. It is not intended that herbal treatment for the menopausal change should be prescribed indefinitely, although it may be required for several years until the body has adapted to the new hormonal levels. The principle form of circulating oestrogen in postmenopausal women is oestrone, synthesised by the peripheral conversion of androstenedione (mainly from the adrenals, with a small amount from the postmenopausal ovary) in the liver and adipose tissue.

Many symptoms are associated with menopause, but the two that are the most distressing are hot flushes (which often cause insomnia) and vaginal dryness. These are experienced by over 70% of women and are directly related to the drop in oestrogen.64 Hot flushes typically last for 6 months to 5 years, but may persist for as long as 15 years.64 Other physical symptoms include night sweats, headaches, bone and joint pain, tiredness and breast tenderness. Psychological symptoms associated with the menopause include depression, poor memory, irritability and loss of confidence. Whether these are directly related to the fall in oestrogen is controversial.

Hot flushes tend to persist longer and are more severe in women who have had a surgically induced menopause.64 They occur most often in the first year after the final period. Symptoms consist of sweating on the face, neck and chest as well as peripheral vasodilation. There is a rise in skin temperature of several degrees Celcius and a transient increase in heart rate. The body’s core temperature falls slightly. Symptoms last for 4 to 5 minutes each time.

The aetiology of the hot flush is unknown.65,66 Probably the rate of change of plasma oestrogen influences the thermoregulatory system via the hypothalamus. Neurotransmitter activity, especially in the serotonergic and noradrenergic pathways, is altered. Hot flushes occur in conjunction with the pulsatile release of LH. There is a suggestion that women who experience more extreme hot flushes may have a less healthy cardiovascular system.67

An emerging conclusion from clinical practice is that the extent of distress in menopause is directly associated with conditions and circumstances that would imply adrenal exhaustion. One could suggest that during reproductive life the woman has two steroid-producing pairs of glands working in tandem (and overlapping considerably). With menopause the loss of one pair is felt considerably harder. Strategies that support adrenal function and relieve stress burdens on the body are well justified.

Treatment

There are many remedies sold in the open market for the treatment of menopause. However, the results of rigorous clinical trials have so far not been overly encouraging for the most popular such as Actaea (black cohosh)68 and Trifolium pratense (red clover).69 A positive result for a Hypericum and Actaea combination70 has been limited by lack of controls and other methodological defects (see the black cohosh monograph). However, recent results of a placebo-controlled study for St John’s wort point to a benefit.71 In fact, phytotherapists often rely on different herbs to these for the management of the menopausal transition.

The main aims of herbal assistance with the menopausal change are as follows:

• To assist the body to adapt to the new hormonal levels by reducing the effects of oestrogen withdrawal. This is achieved by prescribing saponin-containing herbs such as Tribulus, Chamaelirium luteum (helonias root), Asparagus (shatavari), Dioscorea (wild yam) and Actaea (black cohosh) (see Chapter 2). Alchemilla vulgaris (ladies mantle) is also indicated in this context and can be a useful backup when other herbs fail to deliver the expected result. Some recent clinical studies with hops (Humulus lupulus) are encouraging. Panax (ginseng) is a tonic saponin-containing herb with some disputed evidence for oestrogenic activity; however, it may aggravate irritability and insomnia and should be used cautiously

• To provide support for the nervous system and adrenal function using tonic and nervine tonic herbs with adaptogens and adrenal restoratives. Hypericum (St John’s wort) is almost a specific for menopausal depression. Avena (oats) is also popular. Rehmannia, Panax (ginseng), Eleutherococcus (Siberian ginseng), Glycyrrhiza (licorice) and Withania are all potentially indicated

• To abate the intensity of the hot flushes or sweating. The important herb here is Salvia (sage), although cardiovascular herbs such as Crataegus (hawthorn) and Leonurus (motherwort) also can be useful

• Vitex has a role to play for the perimenopausal woman with PMS-like symptoms (which may or may not be premenstrual due to menstrual irregularity). Some herbalists are of the opinion that Vitex also helps allay other menopausal symptoms such as flushes (see Vitex monograph). Its influence on pituitary function might be the key here

• Phyto-oestrogen intake should be increased through soya products, linseeds and herbal teas, but it should not be excessive as this may interfere with the main herbal treatment.

Despite its popularity, there is little traditional or clinical evidence to support the claim that Angelica sinensis (dong quai) has a specific role in menopause, although it has been helpful in combination (see dong quai monograph). Its tonic effect will also be of some value. Evening primrose oil appears to have no place in a therapeutic regime for the menopause.

The above approach will reduce the severity of menopausal symptoms in a majority of cases. Many women will find that, although hot flushes still occur, their intensity and frequency are so reduced as not to be a problem. A small percentage of women cannot be helped by the above approach, presumably because their levels of oestrogen are too low or have dropped too rapidly. Often these are women who have received extensive hormone replacement therapy in the past. After menopause, oestrogen is manufactured in fat and muscle tissue from adrenal hormones. Such unresponsive cases may eventually respond to adrenal support.

Case history

A woman 47 years old presented with hot flushes, sweating, depression and interrupted sleep caused by the hot flushes. She was irritable, low in energy and under stress at work. The hot flushes had started 18 months ago.

The following formula was prescribed (based on 1 week):

Hypericum perforatum 1:2 20 mL
Chamaelirium luteum 1:2 20 mL
Dioscorea villosa 1:2 20 mL
Crataegus oxyacantha (fruit) 1:2 15 mL
Withania somnifera 1:2 25 mL
  total 100 mL

Dose: 5 mL with water three times a day.

After 1 month of treatment there was little change, but by the end of the second month there were considerable reductions in the frequency and severity of the hot flushes. She was less irritable and depressed. After 1 year of treatment the herbs were stopped and no return of menopausal symptoms occurred.

Case history

A 49-year-old woman was experiencing hot flushes. It had been 8 months since her last period. She was waking up one to two times a night and having five or six flushes a day, including with sweating. Herbal tablets containing Dioscorea villosa (wild yam) 400 mg, Asparagus racemosus (shatavari) 400 mg, Actaea racemosa (black cohosh) 100 mg, Hypericum perforatum (St John’s wort) 600 mg, Salvia fruticosa (sage) 290 mg and Panax ginseng 75 mg were prescribed at 3 tablets per day.

After 5 weeks she reported a lower severity and frequency of flushes; that outcome was maintained through the following months.

Therapy during pregnancy

After taking into account the professional reluctance to prescribe herbs in pregnancy, there are nevertheless a number of herbs invaluable for the treatment of some common problems of pregnancy.

Morning sickness

In the first trimester, Zingiber (ginger) can provide effective relief in mild to moderate cases of morning sickness (see monograph). About 10 drops (approx 0.3 mL) of a 1:2 extract with water can rapidly relieve nausea. This can be repeated up to nine times more in a day if required. More severe cases may require liver herbs such as Silybum (St Mary’s thistle) and Taraxacum (dandelion root). Mentha piperita (peppermint), Filipendula (meadowsweet), Gentiana and Ballota (black horehound) are also useful herbs. For morning sickness and nausea that extends into the second trimester, Rubus (raspberry leaf) is usually an effective treatment.

Threatened miscarriage

Vitex (chaste berry) is indicated for threatened miscarriage if progesterone levels are relatively low (at the lower dosage end). Other herbs usually indicated include Dioscorea (wild yam), Viburnum opulus or prunifolium for cramping or bearing down sensations and Capsella (shepherd’s purse) for bleeding.

Varicose veins

Varicose veins are more likely to develop during pregnancy, probably because of the weakening effect on connective tissue of higher levels of female hormones. The main basis of treatment is therefore to maintain connective tissue; safe herbs which do this include Vaccinium (bilberry) and Crataegus (hawthorn). A cream containing Aesculus and Hamamelis (witchhazel) can be applied to problem areas.

Preparation for childbirth

To help the mother prepare for birth, Rubus idaeus (raspberry leaf) and Mitchella (squaw vine) can be taken continuously after the first trimester. It is not known how these herbs act, but Rubus probably builds up the strength of the myometrium (uterine muscle), which leads to an easy birth. The value of Rubus in pregnancy has been proven in many cases and there is no evidence for any deleterious effect. During labour, Rubus should be taken with increased frequency, up to six 5 mL doses in a day. Viburnum opulus (cramp bark) may also be prescribed if there is a problem with dilation of the cervix, as can Mitchella and Actaea.

Therapy following pregnancy

Herbs and breastfeeding

Herbs that promote milk include: Galega (goats rue), Asparagus (shatavari), Silybum marianum, Foeniculum (fennel), Trigonella (fenugreek), Verbena (vervain), Urtica (nettles) and Euphorbia pilulifera. The role of chaste tree is controversial and only low doses should be used.

Herbs that decrease milk include Salvia (sage), Mentha piperita (peppermint) and Lycopus (gypsywort or bugleweed).

Some herbal components may be passed in the milk. A breastfed baby can sometimes be effectively treated by medicating the mother, especially if there is infant colic.

Postnatal depression

Postnatal depression is caused by a combination of female hormonal effects with the adrenal depletion that can follow pregnancy and childbirth. Treatment is based around Vitex, tonics and nervine tonics.

A typical treatment is as follows (based on 1 week):

Panax ginseng 1:2 10 mL
Hypericum perforatum 1:2 25 mL
Glycyrrhiza glabra (high in glycyrrhizin) 1:1 15 mL
Withania somnifera 1:2 30 mL
Rhodiola rosea 2:1 20 mL
  total 100 mL

Dose: 5 mL with water three times a day.

Also Vitex 1:2, 1 to 2 mL with water once a day on rising.