Plants contain many constituents with local physical impact on body tissues. The topical use of herbal remedies is among the first emphases in the earliest and simplest traditions of healthcare. Wound healing was an obvious primal indication for which plant remedies appeared especially suitable.

From a modern perspective, direct effects on tissues are readily testable in research. Most antiseptic, anti-inflammatory and antitumour effects in the research literature relate to in vitro observations, of little direct application to anticipating the effects of oral consumption, but quite relevant to the prediction of topical activity.

Referral to Chapter 2 will provide much of the detail for this review. The following topical properties, however, can be highlighted.

Plant material often contains apparently soothing effects on physical contact and plant remedies must have been a very early instinctive application to wounds. Plants with high mucilage content form the basis of poultices and creams. Linum (linseed, flaxseed) is one of the most impressive poultices where the skin (or subdermal tissue in even unbroken skin) is painfully inflamed. Ulmus rubra (slippery elm bark) when powdered is one of the most obviously mucilaginous plant materials available for poultices. Stellaria (chickweed) in a cream base provides effective relief for many itchy conditions. Althaea (marshmallow root) and Trigonella foenum-graecum(fenugreek) have notably soothing reputations. The expressed juice of Aloe vera also has impressive topical demulcent properties when applied directly to broken or unbroken skin.^1–3

However, non-mucilaginous herbs like Alchemilla vulgaris (lady’s mantle) have also demonstrated topical healing effects, in this case on mouth ulcers.⁴ The anti-inflammatory remedy Boswellia has been shown topically to heal skin damaged by age and sunlight.⁵ The link between anti-inflammatory and healing properties is particularly well illustrated in an ex vivo study on an aqueous extract of Uncaria tomentosa (cat’s claw). The carboxy alkyl esters, in particular quinic acid esters, easily absorbed across the skin, have been shown to enhance DNA repair and skin resilience to UV damage through anti-inflammatory properties involving the inhibition of nuclear transcription factor kappaB (NF-kappaB).⁶

Perhaps the most thorough healing remedy is Symphytum (comfrey root) cream. When this is applied topically it combines an unparalleled local demulcent action, and tannins (see below) with an active promoter of repair, allantoin, which is known to be very rapidly absorbed into the subdermal tissue.⁷ Comfrey has demonstrated healing effects in controlled trials in ankle sprains,⁸ and even pain-relieving and anti-inflammatory effects (see below).

Tannins and related polyphenols are very common plant constituents with the simple property of curdling protein molecules into which they come in contact. The principle of tanning animal skins to make leather, most often using oak galls or oak bark, follows from this property. Simple washes with strong decoctions of high-tannin preparations (like broadleaved tree bark) are well-established country first-aid treatments for open wounds and third-degree burns and the technique was formally revived among ‘barefoot doctors’ in China after the Cultural Revolution in the 1960s. The aim here was to produce a sealing eschar over the exposed tissues formed from coagulated protein on the surface. In modern clinical application, suspensions of decoctions of high-tannin herbs in gum tragacanth or gum arabic can produce impressive healing effects in open wounds or skin lesions. Plants to be considered for this role include decoctions of Hamamelis (witchhazel bark), Potentilla tormentilla (tormentil root), Quercus (oak bark), Krameria (rhatany) and Geranium maculatum (American cranesbill root). The antioxidant effects of such preparations have also drawn attention.^9–11 Topically applied tea extracts have been shown to help to restore skin integrity in people with radiation-induced skin damage. On the basis of in vitro cell responses to various tea extracts, these effects are suggested to involve compounds other than the polyphenols.¹² The role of related polyphenols, the oligomeric proanthocyanidins (OPCs), in topical application has been suggested in a clinical study that pointed to a healing effect of combined oral and topical application of an OPC-rich pine bark extract in the treatment of ulcers of diabetic origin.¹³

The usefulness of application of green tea catechins for periodontal disease was investigated in a placebo-controlled trial.¹⁴ Strips containing the catechins as a slow release local delivery system were applied to oral pockets in patients once a week for 8 weeks. The pocket depth and amount of bacteria were markedly decreased in the tannin group, whereas there was no change for the placebo group.

A double blind study investigated the effect of chewing a green tea confectionery on gingival inflammation.¹⁵ A total of 47 volunteers (23 male, 24 female) were randomly assigned to chew either eight green tea or placebo candies per day for 21 days. While there was an improvement in the green tea group, the placebo group deteriorated slightly.

A number of plant constituents appear to possess topical anti-inflammatory effects, frequently in addition to their demulcent and astringent properties. They might be considered as alternatives to conventional steroidal and other anti-inflammatory prescriptions. For example, herbal Arnica extract compared well with topical non-steroidal anti-inflammatories in the relief of osteoarthritic pain.¹⁶ Calendula (marigold),¹⁷ at least when extracted in high-strength alcohol, and Matricaria recutita (German chamomile),¹⁸ both included in creams, have useful benefits in soothing inflamed skin lesions.¹⁹Berberis aquifolium²⁰ and Aloe vera²¹ have demonstrated efficacy in the treatment of psoriatic lesions. Echinacea applied topically appears to have local anti-inflammatory effects on minor wounds.²² Hypericum (St John’s wort) extracted in oil as a red pigment is a long-standing remedy for the relief of burns and skin pain, and a hyperforin-rich extract has shown benefit over placebo in relieving atopic dermatitis.²³ Other traditional remedies used topically for anti-inflammatory effects include Curcuma longa (turmeric), Juniperus (juniper oil) and Angelica archangelica (Angelica oil). Bruising is traditionally treated with external applications of Aesculus hippocastanum.²⁴ The antiseptic properties of tea tree oil (see below) are complemented with an observed topical antihistaminic effect.²⁵ Many of these applications are fully reviewed in the relevant monographs.

The comfrey ointment referred to above was evaluated for the treatment of knee arthritis.²⁶ In a large placebo-controlled clinical trial, 220 patients applied 2 g of ointment three times a day for 3 weeks to their painful knee joint. The ointment either contained comfrey or was a matching placebo. In terms of self-rated pain, there was a 55% drop in the comfrey group as opposed to a drop of only 11% in the placebo group. Similar results were also seen for other measures of osteoarthritis symptoms. Overall, pain was reduced, the mobility of the knee improved and quality of life increased.

Comfrey is also good for helping to relieve muscle pain. Two strengths of comfrey cream (10% and 1%) were tested in a double blind study involving 215 people with pain in either the upper or lower back.²⁷ The stronger cream caused significant improvements in pain on movement, pain at rest and pain on pressure.

A favourite herb for eczema and other forms of inflamed skin (dermatitis) and to promote healing is the Calendula marigold (Calendula officinalis). Radiation-induced dermatitis is a common side effect of radiation therapy. For approximately 80% of patients, irradiation induces dermatitis. Apart from the pain and inconvenience associated with the dermatitis, it can lead to interruption of the radiotherapy. There is no standard treatment for the prevention of radiation-induced dermatitis. A survey conducted in 2001 in France indicated that one-third of radiation oncologists prescribed a preventative topical agent for women undergoing irradiation for breast cancer; the most popular choice was the drug trolamine. Hence when French researchers initiated a trial of topical Calendula in patients receiving radiotherapy for breast cancer, they decided to compare its efficacy with that of trolamine.²⁸

Between July 1999 and June 2001, 254 patients who had been operated on for breast cancer and who were to receive postoperative radiation therapy were randomly allocated to application of either trolamine (128 patients) or Calendula ointment (126 patients) on the irradiated areas after each session. The occurrence of acute dermatitis of grade 2 or higher was significantly lower (41% versus 63%) with the use of Calendula than with trolamine. Patients receiving Calendula had less frequent interruption of radiotherapy and experienced significantly reduced radiation-induced pain. Calendula ointment was considered to be more difficult to apply, but self-assessed satisfaction was greater.

The topical effects of herbal remedies can include some antiseptic effects in vitro, although only a few whole preparations have significant clinical prospects. The antimicrobial effects of tea tree oil have been demonstrated in controlled clinical studies in acne vulgaris,²⁹ dandruff³⁰ and even methicillin-resistant Staphylococcus aureus (MRSA) infections.³¹ The oil also has established antifungal properties.^32,33 Another clinical study has demonstrated clinically relevant antifungal effects for a member of the Solanaceae (deadly nightshade) family.³⁴

Topical antiviral properties have been demonstrated for the concentrated extract of Melissa officinalis (lemon balm) in the relief of herpes infections.³⁵ One early study found an improved healing rate for 75% of patients, with the time between outbreaks prolonged in 50% of cases.³⁶ Compared with conventional treatments (at the time), the average healing time of lesions was halved to about 5 days and the time between outbreaks was approximately doubled.³⁶ In another multicentre study involving 115 patients, treatment of herpes lesions was commenced between 24 and 72 h from their outbreak.³⁷ It was found that lesions in 87% of patients were completely healed within 6 days of treatment. The time between outbreaks was increased for 69% of patients, and this was 2.3 months with lemon balm compared with 1.3 months for conventional drug treatments such as idoxuridine and tromantadine. Minor side effects were observed in only 3% of patients. The delay in new lesions occurring was without any prophylactic application, and it is possible that a preventative application of the cream to normally affected areas would further increase the time between outbreaks. Lemon balm cream can also be used to treat herpes simplex type 2 infection, and probably other similar viral skin infections, including shingles. The cream contained 1% of a concentrated 70:1 extract of lemon balm.

Rhubarb root (Rheum officinale) and sage (Salvia officinalis) also have activity against viruses, including herpes simplex type 1. In a double blind, controlled trial involving 49 patients, the results for creams containing either 2.3% sage, or 2.3% sage and 2.3% rhubarb, were compared against the conventional antiviral cream containing acyclovir. The average time for the herpes sores to fully heal was 7.6 days with the sage cream, 6.7 days with the rhubarb-sage cream and 6.5 days for acyclovir.³⁸ Hence, the herbal combination worked as well as the conventional drug.

Many herbs are used as a gargle, lozenge or throat spray to treat a sore throat. These include Calendula, sage, propolis, Echinacea root and golden seal. Acute viral pharyngitis is linked to the common cold and includes symptoms such as sore throat and fever. In a double blind, placebo-controlled clinical trial, the value of a sage throat spray was compared against a placebo spray in almost 300 patients with acute viral pharyngitis.³⁹ The throat spray was used for seven applications over 3 days, and each application consisted of three sprays. A 15% strength sage spray was found to be much better than placebo for relieving throat pain. Symptomatic relief occurred within 2 h of applying the spray.

For a further review of antimicrobial effects of herbal remedies see Chapter 2.

As well as the well-known effects on dental pain of topical Syzygium aromaticum (clove) oil,⁴⁰ and the impact on muscle pain⁴¹ and intractable itching⁴² of capsaicin preparations from Capsicum spp., there is now increasing evidence that comfrey (see above) also has pain-relieving properties in arthritis.⁴³

Fever is most often associated with viral and bacterial infectious illnesses of varying degrees of severity, such as ‘flu’, measles, rubella, rheumatic fever, pneumonia, malaria, scarlet fever, polio, tuberculosis and meningitis. It can also accompany a wider range of problems such as cardiovascular and autoimmune diseases, drug reactions and some cancers. Many cases, especially in children, remain mysterious.¹

It is therefore vital that the onset of any fever is diagnosed as accurately as possible, especially in the very young and elderly, pregnant women, among overseas travellers and those with immune disorders. Conventional drug therapy and even hospitalisation may be essential.

Perhaps because of the associations above, the fever process has come to be seen as a problem to be treated in its own right (‘We must bring the fever down’). The serious risks from hyperpyrexia (overheating) are well understood and the accompanying unpleasant symptoms are reason enough to regard fever with suspicion. However, if it is clear that fever is not part of a serious condition there are also good reasons for not suppressing the process unnecessarily. This view is gaining support in conventional medicine,^2,3 particularly in reaction to the fashion for using paracetamol, and previously aspirin, to treat common childhood fevers.⁴

A recent example of such concerns is the New Zealand study that investigated the association between infant and childhood paracetamol use and later atopy and allergic disease.⁵ Children given paracetamol before the age of 15 months were 3.6 times more likely to have atopy at age 6 years than infants who had not been given the drug. Paracetamol use between the ages of 5 and 6 years showed dose-dependent associations with wheeze and asthma.

Such modern reassessment of fever treatment echoes the older traditional view that fever was not the disease itself but the body’s extraordinary efforts to resist disease. It was therefore something to be supported, or at least managed, rather than unduly suppressed. In this view, a ‘good fever’, one which went through its natural course satisfactorily, would not only lead to better resolution of the immediate crisis but would actually rearm the body’s defences and increase its resistance to future onslaughts. Indeed, it was on this issue above all others that the revivalist practices of Samuel Thomson in the 19th century were based (see p. 11). It was common practice among ‘regular’ physicians to suppress fevers with mineral drugs based on mercury, arsenic and antimony. Thomson was moved by Indian practices, especially the sweat lodge, to vehemently challenge such principles and insist instead on the view that fever was a sign of healthy defences (the ‘natural heat’ of the body resisting ‘cold’ intrusion) and should be supported in its efforts rather than suppressed. To this end, he recommended the use of heating remedies, including cayenne, and other measures to support the body through the episode, managing excesses of the febrile condition along the way. Although Thomson’s message was simple (reflecting the predominance of fevers as the main clinical priority of the times), he identified a fundamental difference between traditional practices and the new direction of orthodox medicine – supporting body defences versus attacking disease processes.

Other traditional approaches to fever management were similar. Because fever was so common, the universal classification of remedies as heating or cooling was made very largely on the basis of their observed effects in this condition. Heating herbs would be used to support a flagging fever and, by promoting perspiration, were additionally seen as aiding elimination through the sweat glands (sweat glands do resemble primitive nephrons and can stand in for kidney function to some extent); cooling remedies would be used to temper excessive pyrexia. Herbs with subtle heating or cooling (such as the Galenic ‘hot in the first degree’) were seen as exerting a normalising effect, helping to steady body temperature. Other remedies were classified for their ability to reduce the impact of febrile convulsions, diarrhoea, vomiting and distress.

There is modern support for the traditional view.⁶ The body’s febrile response is accompanied by the arousal of powerful, unpleasant and debilitating defensive measures, the release of inflammatory chemicals, temperature-stimulated activity in the circulation and in various blood cells, including the scavenger white blood cells, and associated alterations in a wide range of other functions.^7,8 In many ways it is like inflammation, for which an analogous traditional view applies (see p. 152): it generally proceeds in defined stages, tends to be self-limiting and is directed to mobilising defensive resources to the rapid elimination of an intrusion into the tissues. Both inflammation and fever are accompanied by what may be regarded as guarding symptoms, in the case of fever often by nausea (leading to reduced eating and unnecessary digestive, eliminative and metabolic burdens), thirst (increasing fluid consumption and compensating for fever-induced dehydration), lassitude and exhaustion (ensuring adequate rest during the process) and photophobia (encouraging withdrawal to a darkened place so as to reduce visual and other stimulation).

In contrast to our forebears, modern practitioners can now accept the far superior diagnostic and treatment prospects that medicine can bring and be grateful that the killer fevers are largely in the past. Nevertheless, there is real value in revisiting some fundamental fever management approaches in the majority of feverish illnesses that do not present a serious threat. There is a real concern that suppressive measures like aspirin and paracetamol and pre-emptive (and often unsuitable) antibiotic treatments are aborting an important natural healing process. Earlier observers predicted that unresolved fevers would lead to recurrent low-grade problems thereafter. The current frequency of chronic catarrhal problems, sore throats, cervical lymphadenopathy (swollen glands), sinusitis, otitis media (glue ear) and atopic allergy, especially among children, reminds many modern practitioners of such a syndrome. Modern studies are beginning to validate these concerns (see above).

It is possible to retrieve some of the early measures as part of a new strategy of fever management, taking advantage of insights and technology unavailable to our forebears.

Fevers present serious challenges for any practitioner more used to dealing with modern chronic and low-grade conditions. Fevers can be dangerous. They can change rapidly and initial diagnoses can be wrong. It would be professionally negligent to take responsibility for managing a fever without the necessary personal medical qualifications and experience unless supported by an effective health team. The following suggestions can only be applied in such circumstances.

After best available medical diagnosis has determined that dangerous disease is unlikely, the phytotherapeutic approach to fever is to see the condition as something to be managed, even nurtured, to allow the body temperature to stay at acceptable febrile levels (usually the range 100–102°F or 37.8–38.9°C) until the fever breaks, then to switch to recuperative measures as required. During the fever the practitioner watches for dangerous symptoms (and ensures ongoing medical supervision as necessary), works with herbal and other measures to prevent body temperature rising too high and provides relief for ancillary symptoms like nausea, vomiting, diarrhoea, coughing, convulsions and general malaise and discomforts.

Many fever-causing bacteria and viruses either produce as metabolites, or present as surface antigens, trigger chemicals, referred to as exogenous pyrogens, that stimulate the temperature control mechanism in the hypothalamus – in effect, they ‘set the thermostat higher’. The result is a stimulus to the heat-generating and heat-conserving mechanisms of the body so that body temperature can rise to match the new setting in the hypothalamus. Such mechanisms include shutting down the blood flow to the surface (pallor), shivering and seeking warmth. In short, when the temperature is rising the patient feels cold.

This is the ‘chill’ phase of fever. When the body temperature rises to the level set by the hypothalamus, a new stability with balance of heat gain and loss returns. The symptoms of chill recede and a less uncomfortable phase commences.

With the rise in body temperature, blood flow through the tissues and the activity of the phagocytes increase. The body’s defences are alerted and mobilised. The intruder’s prospects are reduced, as eventually is its production of exogenous pyrogens. The upward stimulus on the hypothalamus is reduced and the thermostat setting falls. The outward sign of this change could be predicted from knowing that the body temperature will now be higher than that set in the thermostat so heat has to be lost. The circulation to the periphery opens up again, the sweat glands operate, clothing and coverings are thrown off. The temperature falls and for that reason the patient feels hot. In traditional terms, the fever has ‘broken’, ‘crisis’ has been reached and ‘lysis’ or resolution intervenes. With luck, the infection has been successfully rejected and recovery can commence.

There is a more complex story of course. For example, there are a range of cytokines, such as interleukin (IL)-1-(alpha and beta), IL-6 and tumour necrosis factor-alpha, produced by the body itself and known as endogenous pyrogens which, possibly interacting with prostaglandins, can induce relapsing and other complex fever patterns with no clear cause. More recently, it has been shown that inhibitors of cytochrome P450 exacerbate pyrexia and that inducing P450 arachidonic acid metabolism reduces fever.^9–11 There are also endogenous antipyretic mediators including neuroactive substances such as glucocorticoids, vasopressin, IL-10 and melanocortins.¹²

However, the summary account above provides an acceptable basis for a policy of fever management, in which basic principles of nursing can be augmented by herbal remedies.

The first requirement is for some means of monitoring the situation. A clinical thermometer is obviously central but its usefulness is greatly enhanced by knowing how to interpret its findings. Referring to the account of fever above will explain the following points:

With these clues and a thermometer, it is generally possible to assess progress through the fever. If, for example, the temperature was 104°F (40°C), its importance would depend on whether the patient was feeling hot or cold. In the former case, one would expect the temperature to fall; in the latter case, some quick treatment would be called for.

Apart from the usual techniques for bringing temperature down, such as cold wet face flannels or tepid baths, there is conventional aspirin.¹³ This, however, simply turns the thermostat controls down without attending to any other aspects of the fever; there is the risk of an unresolved problem with symptoms lasting for years.¹⁴

Its use in children has in any case been discontinued in recent years because of the incidence of serious side effects.^15,16 Paracetamol and ibuprofen¹⁷ are still used for similar purposes; there are reports of adverse effects in the case of paracetamol particularly,^18,19 but a recent systematic review indicates safety of these agents compared with nocebo effects is not a major concern.²⁰ The wider question is the wisdom of using such agents to bring down the fever, with consequent risks to antibody production and cell repair, when no other risk is present.²¹

Herbal remedies, by contrast, have a number of more complex effects on the body and on the febrile response. There are a number of peripheral antipyretic mechanisms associated with plant remedies,^22–24 including ginger,²⁵ fennel,²⁶ boldo²⁷ and Andrographis.²⁸ However, it is worth noting in the practical guides to fever management that follow, that the published evidence for efficacy in humans has been undermined by poor methodological quality of the studies.²⁹

Herbal treatments during fevers are best provided in the form of aqueous infusions or decoctions (see p. 126), either hot or warm depending on the wider context.

As a steadying influence, the peripheral vasodilators or diaphoretics are appropriate, including remedies such as Achillea (yarrow), Sambucus (elderflower), Matricaria (chamomile), Tilia (limeflowers), Nepeta cataria (catmint) and Eupatorium perfoliatum (boneset). Their effect in hot infusion, seen only in a febrile state, is subjectively to reduce chill and encourage cooling perspiration; they also have a variety of other useful benefits for the digestion, mucous membranes and neuromuscular system. They may be combined with peppermint tea for a more accelerated cooling effect.

For gentle but stronger reduction in febrile temperature, the cooling bitters, like Taraxacum (dandelion root), Gentiana (gentian root) and Cichorium (chicory root) and Erythraea (centaury), are favoured. They have the additional advantage of stimulating the otherwise dormant digestive system, thus helping to counter fermentation or infection arising from the gut. Throughout history some plants were particularly favoured for their fever-reducing properties; most were notable bitters as well as having a range of antipathogenic and anti-inflammatory properties. They are, however, inherently more powerful and should be applied with more caution and under closer supervision. They include Cinchona (Peruvian bark that later yielded quinine), various members of the Artemisia or wormwood family, Jateorhiza (calumba), Berberis vulgaris (barberry bark) and Hydrastis (golden seal).

Apart from body temperature, there are other symptoms of fever that need to be watched. Many, such as nausea, vomiting, diarrhoea, headaches, coughing, pains and spasms, can usually be controlled by the appropriate herbal remedy, covered elsewhere in this book. Accepting the potential value of the febrile reaction does not mean consigning the patient to unnecessary discomfort. There are of course danger signs as well (a pulse that does not rise with temperature as expected might herald meningitis; convulsions, although common enough in children, can disguise and exacerbate polio; a dry cough of measles can resemble that of pneumonia, which can also be heralded by rapid breathing rates; malaria remains impossible to diagnose without blood tests).³⁰ The untrained must not attempt to take full responsibility for any such treatment.

In addition to containing excessive body temperature, there may be a need to encourage it to rise. If it is clear that the fever is not adequately materialising and that there is no serious infection or underlying pathology, warming remedies might be chosen. This is a common scenario in affluent societies. Here, fevers are rare after childhood but unresolved low-grade chronic infections are not. In a case of persistent catarrh, for example, it is often useful to take advantage of a partial attempt by the body to raise the stakes, a cold or sore throat perhaps, and set a ‘therapeutic fever’ in train.

The patient should be advised to prepare properly. Bed rest, a minimal fresh diet and plenty of fluid are basic requirements. It is then possible to take one of the many circulatory stimulants, such as Cinnamomum zeylanicum (cinnamon,) Angelica archangelica (angelica), Zingiber (ginger), Allium (raw garlic) or even Capsicum (cayenne). A modest febrile process can then be nudged into existence, often to considerable advantage. Echinacea root, being both warming and stimulating to mucosal immune defences, may be particularly useful here.

As important as any other part of the treatment is adequate convalescence (see p. 86) after it is all over. There are a range of remedies traditionally used for post-fever recuperation. These include some of the warming and cooling remedies above, those with additional tonic reputations, like Inula helenium (elecampane), Cardamomum (cardamom seed), Echinacea, Taraxacum (dandelion root) and Gentiana (gentian root).

A modern observer might presume that one area where traditional herbal medicine could not be claimed as a useful model is in the area of infections. It is generally accepted that until Pasteur’s germ theory of disease and the isolation of effective antimicrobials, humanity had seriously missed the plot. The history of pestilences and plagues, the decimation caused by the killer infections such as smallpox, cholera, typhoid and scarlet fever, the waking medieval nightmares of tuberculosis and syphilis, the Russian roulette that every mother and infant played with perinatal mortality, along with the near universal ignorance of the dangers of living in filth and squalor along with dark mutterings about ‘contagions’ and ‘toxins’ in lieu of simple hygienic measures, all looks rather bad for traditional medicine.

Much of this is undeniable. There is no doubt that healthcare shifted beyond recognition with public hygiene measures like clean water and separate sewage systems from the 19th century and the discovery of penicillin in the early decades of the 20th. Herbal practitioners can admit this gracefully and be grateful they no longer have to attempt to thwart life-threatening infectious diseases.

Nevertheless, the herbal cupboard is not entirely bare. Most of the horrors referred to above were features of life in cities and towns, of crowded squalid conditions, far from sources of fresh food (and with no refrigerated delivery) and clean water. The historical and archaeological evidence available suggests that life was more equable in traditional rural communities, that, leaving perinatal mortality aside, average lifespans in the ancient world differed little from those reached until the middle of the 20th century^1–3 and that longevity was not uncommon where land was fertile.⁴ In such circumstances, the case against the traditional remedies used by country people is harder to sustain.

Furthermore, if the killer diseases are taken out of the picture and more ordinary everyday infections are considered, the balance shifts in favour of historical treatment. There are a number of traditional remedies that appear to support the body in its battle against infections. From an exhaustive review of traditional cooking practices and recipes and correlation with exposure to infections, it has been concluded that the pungent spices were adopted as flavourings, consciously or unconsciously, at least in part because of their protective effect against enteric infections, with the hottest used where there is greatest exposure.⁵ There are other indications that chillies in particular are antimicrobial in moderate doses.^6,7

As another example of a dietary antimicrobial, various publications indicate that garlic extract also has broad-spectrum antimicrobial activity against many genera of bacteria and fungi. This activity, particularly in respect of Gram-negative bacteria, seems to be stronger than that of other members of the onion family.^8,9 Allicin was the early candidate as the most active constituent in garlic.¹⁰ In terms of the phytochemical world it has been verified as a potent antibacterial agent, but even then its activity is relatively modest compared with conventional antibiotics.¹¹ Later research has demonstrated that ajoene, the prominent metabolite of allicin, also conveys particular antimicrobial activity, including against such Gram-negative bacteria as Escherichia coli and Klebsiella pneumoniae. The disulphide bond in ajoene appeared to be necessary for this activity, since reduction by cysteine, which reacts with these bonds, abolished its antimicrobial activity.¹² This activity is, however, significantly exceeded by another metabolite, 10-devinylajoene, marked by substitution of the allyl group in ajoene by a methyl group and sulfinyl group.¹³ These findings might explain why a garlic extract was observed to have a more potent anti-staphylococcal activity than an equivalent amount of allicin.¹¹

The incidence of stomach cancer is lower in individuals and populations with high allium vegetable intakes. To investigate this further, an aqueous extract of garlic cloves was standardised for its thiosulfinate concentration and tested for its antimicrobial activity on Helicobacter pylori. Minimum inhibitory concentration was 40 µg/mL thiosulfinate. This study may have detected a particular sensitivity of H. pylori to garlic constituents as Staphylococcus aureus tested under the same conditions was not susceptible to garlic extract up to the maximum thiosulfinate concentration tested (160 µg/mL).¹⁴ However, clinical trials of the use of garlic in eradicating H. pylori have been disappointing, although this might reflect on the form of garlic used.^15,16 Systemic antifungal activity has been supported in a study where commercial garlic extract was given intravenously to two patients with cryptococcal meningitis and three patients with other types of meningitis. Plasma titres of anti-Cryptococcus neoformans activity rose two-fold over preinfusion titres.¹⁷

The position with other plant constituents is less clear. Essential oils have demonstrated antimicrobial effects in vitro (see, for example references^18–20 and also Chapter 2). In one study, for example, the antimicrobial effects of some essential oils on oral bacteria were surveyed. Tea tree oil, peppermint oil and sage oil proved to be the most potent essential oils, whereas thymol and eugenol were potent essential oil components.²¹ Tea tree oil has demonstrated a number of antimicrobial effects, even against MRSA.²² More studies on tea tree oil are reviewed in Chapter 2. In research on antifungal effects, those of phenolics such as iso-eugenol, cinnamaldehyde, carvacrol, eugenol and thymol were linked to the presence of a free hydroxyl group linked to an alkyl substituent.²³ However, all these studies generally refer to isolated oils rather than to the whole plant and it is difficult to infer from these that traditional treatments had much antimicrobial efficacy.

On the other hand, ethnobotanical reviews of traditional plants (often reported in the excellent Journal of Ethnopharmacology) have shown in vitro efficacy of whole-plant preparations (for example references^24–27) and in one study a high correlation was demonstrated between traditional use and in vitro antisepsis among plants in North America.²⁸ It is possible that modest antimicrobial effects may lie in other plant constituents: tannins (especially tannic acid and propyl gallate) have demonstrated such properties. This activity is suggested as being associated with the hydrolysis of ester linkage between gallic acid and polyols, hydrolysed after the ripening of many edible fruits. Tannins in these fruits thus may serve as a natural defence mechanism against microbial infections.²⁹

There were other particular remedies, generally at least a few in each tradition, with a role of directly helping the body resist infections. Raw garlic in Europe, Echinacea and Baptisia (wild indigo) in North America, Picrorrhiza in Asia and Andrographis in China were all accorded great respect in their respective cultures. Some were mobilised in managing the fevers that often resulted, others were used to support recovery and the hopefully increased defensive strength of the well-managed convalescence. There is little evidence that any of these are antibiotics in the modern sense: most were understood as supporting some defensive function or other. This list would also contain other supporters of host resistance:

For the many non-serious infections in everyday life, the deathbed recantation attributed to Pasteur is increasingly relevant. No seed can develop without le terrain, the soil to nourish it, no infections can establish without the body, by deficit, enabling a sympathetic environment for colonisation to occur. There are very few genuinely aggressive pathogens; there are always some people, usually the majority, unaffected in even the most notorious epidemics. The normal environment, food, air, skin, mouth and gut lining, is full of theoretically pathogenic bacteria (legally allowable counts in many foods are still in the millions of bacteria per milligram). In the absence of supporting immune defences, it is likely that the drive to kill pathogens has gone too far. While antibiotics have changed the prospects for bacterial infections beyond traditional recognition, and antifungals, antiprotozoals and antiviral medicines have played important parts in the management of other infections, it is also clear that infectious diseases remain major clinical problems in even the most modern societies. In particular, there is concern about the increasing resistance of many pathogens to new drugs. Antibiotic resistance is causing particular worries, with the spectre of ‘super-bugs’ now occupying the attention of the popular press. In Britain the government instructed doctors in September 1998 to avoid prescribing antibiotics in minor self-limiting infectious conditions such as colds and sore throats or when infections are likely to be viral in origin.

With every new epidemic, be it SARS, bird flu, swine flu or an outbreak of antibiotic-resistant bacteria, it becomes increasingly obvious that the conventional approach to preventing and treating infection is beginning to fail our communities. The hero antibiotics of yesteryear are being rendered next to useless by resistant organisms, with the cost and challenges of developing new antibiotic drugs ensuring that future prospects are relatively bleak. The role for phytotherapy in infectious diseases is likely to increase rather than diminish under these circumstances.

It is worthwhile reviewing the considerations for the herbal management of infections. These are as follows:

Patients with poor immunity and/or recurrent infections should receive treatment selected from the following groups:

Echinacea alone, either the root of E. angustifolia or E. purpurea, or their combination, has helped countless patients prone to infection in doses equivalent to 2.5 to 7.5 g/day (5 to 15 mL of a 1:2 preparation). The treatment protocol is as follows (equivalent doses in tablet or capsule form can also be used):

See also the Echinacea root monograph.

The skeletal and connective tissues of the body are primarily designed to cope with wear and tear and have a range of impressive repair mechanisms to reduce consequent problems for the organism, at least until late in life. By far their most frequent problems therefore involve disturbances of the inflammatory and immunological mechanisms. As well as the familiar inflammations of the skin (dermatitis, including eczema and psoriasis) and joints (arthritis), these include those of other connective tissues: arteritis, cellulitis, chondritis, meningitis, osteitis, pericarditis, phlebitis, pleurisy and vasculitis. Chronic inflammatory disturbances also involve glandular tissue: epididymitis, oöphoritis, pancreatitis, prostatitis and thyroiditis, as well as endodermal tissue: Crohn’s disease, gastritis and ulcerative colitis. Inflammatory changes in the blood vessel walls have also been shown to be key elements in the chronic deterioration associated with atherosclerosis, and more broadly with several stages in the path through late-onset diabetes, increasing insulin resistance and the later vascular complications of the illness.

In many of these long-term inflammatory conditions, there are also wider disturbances of the immune system, so that mechanisms designed to cope with foreign material begin to attack the body’s own tissues. These ‘autoimmune’ exacerbations in turn provoke their own inflammatory responses. In many chronic inflammatory diseases, there are multiple pathological elements to disentangle. The practitioner rarely has a clear target.

The modern approach to most inflammatory and immunological disturbances is to suppress the manifestations with anti-inflammatory drugs, either steroids or the non-steroidal anti-inflammatories (NSAIDs), or coal-tar products in the case of topical applications to the skin. When steroidal drugs based on cortisone became widely available in the early 1950s, the transformation these made to the prognosis for arthritic, skin and other connective tissue diseases was dramatic. For two decades, any challenge to these drugs would have been derided. However, it then became apparent that both steroids and their non-steroidal counterparts based on aspirin were associated with a range of side effects and diminishing therapeutic returns that now lead physicians to limit their prescription much more than in the past. There is again a demand for other approaches, especially in the case of those sufferers otherwise condemned to a lifetime of powerful and potentially dangerous drugs.

Traditional herbal practice approached these conditions in radically different, although surprisingly consistent, ways. Even though there is very little modern clinical evidence of efficacy, their consistency justifies a rational review, not least because some of the traditional insights concur with the latest findings about the aetiology and mechanisms of inflammatory and immunological diseases. It will be useful to look at some relevant pathophysiological mechanisms.

Chronic low-grade systemic inflammation has come to be defined as a term for a wide variety of conditions marked by a two- to three-fold increase in the systemic concentration of C-reactive protein (CRP) and increased systemic levels of some cytokines. Cytokines are small polypeptides, which were originally discovered to have immunoregulatory roles. The local response to infections or tissue injury involves macrophage activation (often by certain toxins) that causes them to produce cytokines. Some of these facilitate an influx of lymphocytes, neutrophils, monocytes and other cells. The initial cytokines in the cytokine cascade are (in order) tumour necrosis factor (TNF)-alpha, IL-1, IL-6, IL-1 receptor antagonist (IL-1ra) and soluble TNF-alpha receptors. In response to an acute infection or trauma, the cytokines and cytokine inhibitors may increase several-fold and decrease when the infection or trauma is healed.

The key interface in the inflammatory response is the endothelium, the cell lining of the blood vessels, through which the white blood cells that mediate both inflammation and immunity have to pass. Endothelial cells secrete various factors influencing vessel tone, platelet function, coagulation and fibrinolysis and which initiate inflammatory responses. Clinical problems develop when these processes are imbalanced.

In the early stages of the inflammatory response, TNF-alpha and IL-1, among other cytokines, stimulate the endothelial cells to express the cell surface adhesion molecule P-selectin. Within a couple of hours, a second surface adhesion molecule, E-selectin, is produced. Together E- and P-selectin slow the motion of leukocytes through the bloodstream by causing them to roll along the endothelial surface, allowing other molecules to interact with the slowed leukocytes to stop them and promote their movement into the tissues (described as analogous to throwing a tennis ball at a Velcro surface). Tight adhesion to the rolling leukocyte is performed by two endothelial cell ligands, intercellular adhesion molecule-1 (ICAM-1) and vascular cellular adhesion molecule-1 (VCAM-1), which arrest the motion of the rolling leukocyte.¹ Stopping the leukocyte allows it to enter the tissues by secreting proteases to breach the endothelial basement membrane, a process known as diapedesis.

There are a number of other mediators of endothelium-mediated inflammation. The major cause of the endothelial dysfunction is thought to be decreased availability of nitric oxide (NO), either due to decreased production or enhanced breakdown due to increased oxidative stress.² It is the major factor in large arteries mediating endothelial dependent relaxation and inhibits platelet aggregation, cell adhesion and smooth muscle cell proliferation. A number of plant remedies hold promise as promoters of NO activity at the endothelium.³ The activation of nuclear transcription factor-kappa B (NF-kappaB) has also been linked with a variety of inflammatory diseases. Kappa B kinase catalyses NF-kappaB activation and is implicated in the effects of excessive free fatty acids on the induction of insulin resistance, in atherogenesis, and other inflammatory disorders.

The above are among a number of mechanisms involved in altering endothelial function in the inflammatory response. They therefore represent potential mechanisms in any inflammatory-modulating strategy, and, as will be seen below, there are many plant constituents with this potential.⁴ In the case of chronic deteriorations such as increased insulin resistance, diabetes and atherosclerosis, there is the prospect that many dietary plants may have long-term protective effects. The warming spices like ginger,⁵ cinnamon⁶ and turmeric⁷ may share cholinergic ‘endothelium-dependent’ vasodilator effects mediated by NO and counteracted for example by high glucose levels. Garlic⁸ and even daily beverages of tea^9,10 and coffee,¹¹ have been shown to benefit endothelial markers associated with reduced inflammation in atherosclerosis and diabetes. Among its well-attested benefits on microvascular function,¹² chocolate also reduces inflammatory markers like CRP.¹³

Many commonly consumed herb and spice constituents may inhibit extravasation in the inflammatory response. See Table 8.1.

Table 8.1 Inhibition of extravasation

Others may inhibit migration through inflamed endothelial cells. See Table 8.2.

Table 8.2 Inhibition of invasion

However, it must be kept in mind that this research is identifying prospects only until such effects are also demonstrated in humans after oral doses. Nonetheless, there can be no harm in increasing the dietary intake of such phytochemicals in cases of chronic inflammation as a background therapy. For a fuller discussion of herbal compounds able to target defined biochemical and molecular mediators of inflammatory, autoimmune arthritis (at least from experimental models), the reader is referred to an excellent recent review.⁴³

It is, however, obvious that chronic inflammatory diseases are among the most demanding indications. It is likely that only individual treatments have been truly effective in the past and, apart from the undoubted power of the placebo effect, these are not very amenable to simple recipes or over-the-counter treatments (fish oils in arthritic disease are perhaps the main exception). The required complexity and individualisation of treatments also renders controlled clinical trials near impossible to conduct.

The traditional understanding of inflammatory diseases notably involved ideas of ‘toxicity’ and, particularly but not exclusively, in Chinese herbal therapeutics, meteorological concepts of ‘damp’, ‘wind’, ‘heat’ and ‘cold’ (see also p.158). These apparently quaint medieval notions are metaphors for clinical insights into the way the body appears to behave in such illnesses that can indeed inform a modern review. This will now be attempted.

Modern research into the causes of inflammatory diseases has uncovered, in particular, disturbed reactions to infections and significant events in the digestive tract.

At the turn of the 20th century, the rheumatoid-like condition ankylosing spondylitis was regarded as a venereal disease, though 20 years later the wider association with urinary infection had been made. This, however, was lost by the time steroids transformed the prospects for the condition.

An interesting later brush with ancient notions by modern medical research was seen in an issue of The British Medical Journal.⁴⁴ It was reported that patients with RA had a significantly higher incidence or history of pulmonary disease than the wider population. It was pointed out that the lungs remain sub-clinically infected, almost indefinitely in many cases, after the incidence of pneumonia, bronchitis and pleurisy, and this persistence is obvious in conditions like emphysema and bronchiectasis. The findings were dramatic and led a linked editorial to speculate, probably reluctantly, that ‘toxins’ in the infected lung base might provoke the inflammatory changes in the rheumatoid joints.

Modern rheumatology has now taken such notions into orthodoxy, although gratefully abandoning any primitive imagery. Rather than ‘toxic’ influences, the role of ‘immunological cross-reactivity’ has emerged as a leading factor in the aetiology of rheumatic diseases. In this view, the autoimmune nature of these diseases is reinforced; it had long been understood that the body’s own immune defences were the main cause of many connective tissue inflammations (the term ‘collagen diseases’ was used to embrace a wide range of such conditions). In immunological cross-reactivity, the immune system is provoked and then confused by the similarity between bacterial, viral or other antigens and those of its own tissues and attacks both. In fact, a survival imperative drives invading organisms to resemble their host, at least at a molecular level, in order to escape immune detection. This phenomenon of ‘molecular mimicry’ drives immunological cross-reactivity.

Infectious agents are now (controversially) regarded as the major environmental factors that may cause arthritic inflammation in genetically susceptible hosts. Retroviruses, urinary and pulmonary, and especially enteric bacteria are the provocateurs most often discussed.^45–48Helicobacter pylori has been associated with diseases such as autoimmune gastritis, Sjögren’s syndrome, atherosclerosis, immune thrombocytopenic purpura, inflammatory bowel diseases and autoimmune pancreatitis, in each of which it seems to play a pathogenic role in some cases. On the other hand, it has also been suggested that it may help to protect against the development of autoimmune gastritis, multiple sclerosis, systemic lupus erythematosus and inflammatory bowel diseases.⁴⁹

Molecular mimicry has been found between a white blood cell protein, HLA-B27, and two molecules, nitrogenase and pullulanase D, in the anaerobic gut bacterium Klebsiella pneumoniae among ankylosing spondylitis patients,⁵⁰ and between HLA-DR1/DR4 and the haemolysin molecule in another gut anaerobe, Proteus mirabilis, among RA patients.⁵¹ Molecular mimicry between HLA-B27 and K. pneumoniae molecules in the aetiology of ankylosing spondylitis patients has been extensively studied. It was first proposed by Dr Alan Ebringer in 1976. K. pneumoniae was isolated in stool samples more frequently in active phases of the disease and was linked to relapses. High antibody levels in ankylosing spondylitis patients directed against K. pneumoniae were found in several studies. Some of these antibodies were shown to cross-react with HLA-B27 as well as spinal collagens. Specific anti-Klebsiella antibodies in ankylosing spondylitis patients have now been reported from 18 different countries. ‘B27 disease’ is the new terminology proposed by Ebringer.⁵²

In another growing association, patients with long-standing active RA have a substantially increased frequency of periodontal disease compared with that among healthy controls. High levels of oral anaerobic bacteria antibodies (such as from Porphyromonas gingivalis, Tannerella forsythensis, and Prevotella intermedia) have been found in the serum and synovial fluid of such patients. Appropriate antibiotics have been shown to be effective against the arthritis⁵³ (leading to intriguing prospects for herbal oral antiseptics such as gum myrrh). Autoimmunity in RA has been characterised lately as an antibody response to citrullinated proteins. There is an association with periodontitis that is largely, but not exclusively, caused by Porphyromonas gingivalis infection. The citrullination of proteins by P. gingivalis and the subsequent generation of autoantigens that drive autoimmunity in RA represent a possible causative molecular mimicry link between these two diseases.⁵⁴ As noted above, a further link with the aetiology of RA is with Proteus infection in the urinary tract.⁵⁵ Both bacteria can be found as secondary infections elsewhere in the body and prospects for future control of rheumatoid diseases by antibiotic therapy have been raised.⁵⁶

There are some strong indications from archaeology for an infectious trigger for RA. Examinations of skeletal remains from antiquity in Europe do not show signs of RA. In contrast, specimens dating back several thousand years from Native American tribes in North America show clear evidence of the disease. The prevalence of RA in this ethnic group today remains extraordinarily high, with over 5% of individuals affected in some groups. Evidence of RA in Europe first appeared in 17th century art, especially by the Dutch Masters, and the first case report was published in 1676. RA could well be linked to an infectious agent brought from the New World to the Old World.⁵⁷

The site of the trigger for ankylosing spondylitis is not necessarily always the bowel. An association between ankylosing spondylitis and chronic bacterial prostatitis has long been observed. The incidence of chronic prostatitis in male ankylosing spondylitis patients was 83%, compared with 33% in patients with RA.⁵⁸ This association was confirmed in a later study.⁵⁹ The fact that the prostate may harbour bacteria that contribute to ankylosing spondylitis could explain the higher incidence of this disorder in males. Evidence of Chlamydial urinary tract infection is frequent in female patients with ankylosing spondylitis.⁶⁰

Gut inflammation is a prime candidate for having a bacterial origin (see also below). Johne’s disease, which occurs in cattle and other ruminants, is very similar to Crohn’s disease and is caused by Mycobacterium avium subspecies paratuberculosis (MAP). In 1984, Chiodini and co-workers reported the isolation of a strain resembling MAP from the intestinal tissue of three patients with Crohn’s disease.⁶¹ This report initiated interest and controversy about a mycobacterial aetiology for Crohn’s disease that is still ongoing. MAP has also now been cultured from human milk, faeces, intestinal tissues and peripheral blood of patients with Crohn’s disease.⁶² Ebringer has also implicated Klebsiella in Crohn’s disease and advised a low starch diet (see later).⁶³ In terms of Crohn’s disease, one group of researchers reflected: ‘The mycobacterial theory and the autoimmune theory are complementary; the first deals with the aetiology of the disorder, the second deals with its pathogenesis. Combined therapies directed against a mycobacterial aetiology and inflammation may be the optimal treatment …’.⁶⁴ The levels of MAP found in Crohn’s disease patients is not high, so its presence does not represent a bacterial infection per se. Rather it is best viewed as a form of dysbiosis.

Viruses may also be involved in triggering an autoimmune response. For the past 25 years, a potential role of Epstein-Barr virus (EBV) in the pathogenesis of RA has been suspected. The QKRAA amino acid sequence of HLA-DRB1, a tissue marker that carries susceptibility to RA, is found in the EBV envelope. Sera from patients with RA contained higher levels of antibodies to latent and active EBV antigens.⁶⁵ RA patients have more EBV-infected B cells than normal controls. Patients with RA have a 10-fold higher EBV load than healthy controls. EBV DNA is detected more frequently in immune cells, synovial fluid and saliva from RA patients than from controls.⁶⁵

In contrast to Crohn’s disease, studies over 40 years have associated ulcerative colitis with cytomegalovirus (CMV).⁶⁶ A clear association between onset of ulcerative colitis and primary CMV infection was confirmed by viral studies in two patients.^67,68 Higher frequency and amount of antibodies to CMV were found in patients with ulcerative colitis.⁶⁶ The simultaneous presence of DNA from several herpes viruses, including CMV, was much greater in ulcerative colitis patients compared to those with Crohn’s disease or normal controls.⁶⁹ While it is debated that CMV infection may be a causative factor in ulcerative colitis, it is recognised by many clinicians as a complicating event that can increase its severity.⁷⁰

There is increasing evidence of damage to the gut wall in a range of autoimmune diseases. One category of diseases, classified as spondylarthropathies, involve inflammatory damage of the joints and the skeleton, the eyes, gut, urogenital tract, skin and sometimes the heart.^71,72 Ankylosing spondylitis is the prototype example of this condition; other examples include reactive arthritis, psoriatic arthritis and arthritis in patients with inflammatory bowel disease. In a series of investigations, histological signs of gut inflammation were found in a high proportion of patients with spondylarthropathies.⁷³ Most of these patients did not present any clinical intestinal manifestations. Remission of the joint inflammation was always connected with a disappearance of the gastrointestinal inflammation. Persistence of locomotor inflammation was mostly associated with the persistence of gastrointestinal inflammation. It was proposed that some patients with a spondylarthropathy had a form of subclinical Crohn’s disease in which the locomotor inflammation was the only clinical expression.⁷⁴ Further genomic work substantiates the unique relationship between gut and joint inflammation.⁷⁵ These data suggest that spondylarthropathies and Crohn’s disease should be scientifically and clinically considered as distinct phenotypes of common immune-mediated inflammatory disease pathways, rather than as separate disease entities.⁷⁶

This hypothesis is supported in prospective long-term studies in which ileocolonoscopied patients were reviewed over periods of up to 9 years. About 6% of spondylarthropathy patients who did not present any sign of Crohn’s disease at first investigation (but did show gut inflammation on biopsy) developed full-blown Crohn’s disease within 9 years. Electron microscopy of these lesions demonstrated an increase in the number of membranous (M) cells in inflamed mucosa. Necrosis and rupture of these M-cells, with lymphocytes entering the gut lumen, was observed. Such evidence of damage to the gut mucosa could be responsible for an increase in local antigenic stimulation and could readily lead to secondary systemic immunological disorders.⁷⁷

Pathogenic forms of Escherichia coli with specific hairs or pilli adhere to the gut mucosa. In 1988, it was first demonstrated that E. coli isolated from patients with ulcerative colitis and Crohn’s disease showed a significantly greater index of adhesion when compared with normal controls.⁷⁸ A new term adherent-invasive Escherichia coli (AIEC) was coined to describe this aggressive form. They can replicate intracellularly and survive within macrophages. AIEC strains were found (predominantly in the ileum) in 21.7% of Crohn’s disease chronic lesions versus 6.2% of controls.⁷⁹ Crohn’s disease patients with anti-E. coli antibodies were more likely to have internal perforating disease and to require small bowel surgery.⁸⁰ Because AIEC can cross and breach the intestinal barrier, move to deep tissues and continually activate macrophages, they can generate persistent inflammation.⁸¹

As mentioned above, AIEC are found in significant amounts in patients with ulcerative colitis compared with controls.⁷⁸ Several workers have shown that isolates of E. coli obtained from patients with ulcerative colitis can degrade mucins and produce toxins. Results from one study suggested that connective tissue exposed by bowel ulcerations may result in selection of E. coli strains able to bind to them.⁸² Compared with healthy people, ulcerative colitis patients have increased levels of IgG directed against their normal flora.⁸³ There may be an increased number of bowel bacteria in ulcerative colitis, but reduced counts of ‘protective’ bacteria such as Lactobacilli and Bifidobacteria.⁸³ Lactobacilli numbers were certainly found to be lower in ulcerative colitis patients during the active phase.⁸⁴ This was confirmed in another study that also found the bacterial diversity decreased during a relapse.⁸⁵

In patients with active ulcerative colitis there is an over-production of hydrogen sulphide, which is toxic to the intestinal mucosa by competing with short-chain fatty acids.⁸⁶ This appears to be due to an excess (or greater activity) of sulphate-reducing bacteria (SRB), such as Desulfovibrio desulfuricans.⁸⁶ In a pilot study, a low sulphur diet for 12 months was associated with a remarkable clinical improvement in four patients with chronic ulcerative colitis.⁸⁷ A recent review concluded that there is evidence to implicate SRB in the pathogenesis of ulcerative colitis.⁸⁸

As noted in a Lancet review: ‘The long-standing assumption that ulcerative colitis is an autoimmune disease has been revised to incorporate evidence suggesting that commensal microflora and their products are autoantigens, and that ulcerative colitis is caused by loss of tolerance towards otherwise harmless components of the normal intestinal flora’.⁸⁹

Hormonal factors in rheumatoid disease are well accepted. Risk factors include reduced childbearing and breastfeeding; these apparently contradictory influences are both associated with high prolactin levels.⁹⁰

Several autoimmune diseases have been linked to higher levels of prolactin in the blood, including lupus,⁹¹ RA,⁹² Sjögren’s syndrome⁹³ and juvenile arthritis.⁹⁴ For systemic lupus erythematosus (SLE), serum prolactin concentrations have been correlated with both clinical activity and remission.^91,95 On the other hand, preeclampsia and breast cancer have a negative association with rheumatic and other autoimmune diseases.⁹⁶

Such links are confusing and even contradictory, but a defective response of the neuroendocrine system to inflammatory stimuli has been proposed as one feature of RA.⁹⁷

The use of willow bark for rheumatism in traditional medicine is a reminder that where remedies clearly provided symptomatic relief, they were used. More recently, there has been a huge research effort to find new anti-inflammatory activities in the plant world. Many chemical subgroups from plants have shown promising experimental activity, including terpenoids and steroids, phenolics and flavonoids, fatty acids, polysaccharides and alkaloids.⁹⁸ Most of this work remains on the laboratory bench as interesting markers for the effect of the whole plant; the evidence is more persuasive when demonstrated in clinical trials. For long the potential benefit of sea buckthorn (Hippophae rhamnoides) for inflammatory conditions has been assumed on the basis of its high levels of antioxidants but reinforced by clinical trials.⁹⁹ Herbal remedies that have shown efficacy in clinical trials for osteoarthritis include Harpagophytum procumbens (devil’s claw),¹⁰⁰Rosa canina (rosehip),¹⁰¹Uncaria tomentosa (cats claw)¹⁰² and Boswellia serrata. RA has also been relieved by Boswellia.¹⁰³ The benefits of Tripterygium wilfordii in the same condition were found to be associated with an in vitro suppression of antigen-stimulated T-cell production, immunoglobulin production by B-cells¹⁰⁴ and reduction of IL-2 production and activity.¹⁰⁵ However, while it is a promising intervention in inflammatory disorders, this herb is potentially toxic and has been associated with serious side effects.¹⁰⁶ The effect of the Chinese herbal formulation found effective in London trials in the treatment of atopic eczema has been shown to be associated with changes in a number of immunological functions, such as decreasing the higher levels of circulating IgE complexes and IL-2 receptors and vascular cell adhesion molecules in atopic eczema patients.¹⁰⁷

Topical anti-inflammatory activity has been observed in clinical studies of Matricaria recutita (wild chamomile) in mucositis,¹⁰⁸ and Melaleuca alternifolia (tea tree) oil in histamine-induced skin inflammation.¹⁰⁹ (See earlier in this chapter regarding topical anti-inflammatory treatments.)

The most common application of counter-irritation was to inflamed arthritic joints and the technique is discussed further in the appropriate chapter (see p. 304). Nevertheless, the approach was also used for other subdermal inflammations, notably in pleurisy and other chest infections, mastitis and other cellulitis conditions. (A traditional treatment of mastitis and pleurisy involved making poultices with cabbage leaves, a relative of mustard.) Heating of inflammations was not always considered appropriate, however. As discussed below, some inflammatory diseases are excessively ‘hot’ and can react violently to additional heat. Some rheumatic joints can behave in this way.

One of the persistent dietary notions in European tradition in the case of degenerative diseases, particularly arthritis, has been the distinction between ‘acid’ and ‘alkaline’ foods. The view is that as metabolites tend to be acidic, as acid-buffering agents are a major constituent of the body fluids and as eliminatory channels (lungs, kidney, bile and bowel) pass mainly acidic materials, inflammatory diseases may be marked by, and even result from, greater acidosis. Overt metabolic acidosis is well characterised in medicine and may follow excessive alcohol consumption, laxative abuse, excessive vitamin D and NSAIDs (most often prescribed in arthritis) and salicylate use, among other drugs.¹¹⁰ The case for a more subtle effect is considered further in the section on joint disease in Chapter 9. In addition to the prospects for therapy that could, for example, include diuretic herbal remedies, there are associated dietary observations that reinforce the potential for benefit in some chronic inflammatory diseases. There was, for example, a widespread traditional instinct in many inflammatory diseases to reduce animal protein, although chicken and other fowl were a common exception.

There is modern support for this approach in rheumatic diseases. A combination of fasting and vegetarian diets has been shown to reduce the ability of the urine to support the growth of Proteus mirabilis and Escherichia coli.¹¹¹ A substantial placebo-controlled trial has confirmed that gamma-linolenic acid, (GLA), a component mainly of plant-based foods, has antirheumatic activity.¹¹² The possibility of cross-reaction between dietary collagen found in animal products and the sufferer’s connective tissue has also been postulated.^113,114 The effects of a low-starch diet in reducing the gut levels of anaerobic bacteria such as Klebsiella and serum IgA antibody levels in both normal subjects and those suffering ankylosing spondylitis, and in benefiting symptoms in the latter, have been supported by clinical evidence.¹¹⁵ Nevertheless, the quality of the research on this issue is too limited to draw firm conclusions on the value of dietary changes on RA.¹¹⁶

Damp was the universal metaphor for toxic congestion, recalling the notions of stagnation, brackishness and mould. As expected, it tended to occur in conditions of poor circulation, most often associated with cold but with a hot ‘humid’ variant as well. Damp is exacerbated and to some extent caused by external climatic dampness (as the Romans noted, a feature of Britain and the Britons). Associated with cold, it tends to gravitate to the lower regions of the body and can be associated with sluggish digestion and congested abdomen. Associated with heat, it involves the liver, with intolerance to fats, rich food and alcohol and perhaps a history of jaundice/hepatitis. Naturally, it would need treatment with ‘drying’ remedies: warming aromatics for cold-damp and bitters for hot-damp conditions.

The tendency of rheumatic and some skin problems to fluctuate and move rapidly around the body was obvious. Chinese medicine in particular invoked the universal metaphor of change, wind, to characterise this phenomenon. Wind of course occurs with the juxtaposition of hot and cold and implies that there was similar imbalance within the body. Apart from the fluctuation of symptoms, signs of wind might include, when deep seated (a common occurrence in rheumatic disease) wandering, sudden pains in joints. In Chinese medicine, there were a number of remedies specifically reputed to calm the wind but the deeper view might be that attendance to the underlying imbalances of hot and cold would be the more lasting strategy.

As the obvious vital sign, heat was seen as a mark of vigorous defence (as in fever and inflammation) and in its place was even encouraged. When stuck, however, or marked by destructive symptoms like allergic reactions or eczema, it signified blocked poisons which needed clearing, perhaps with local cooling as well. When coupled with dryness, there would be respiratory symptoms like asthma, allergic rhinitis or hayfever, dry eczema and/or constipation; when coupled with damp, the liver and digestion would be involved as above. It might also be localised to an organ like the lungs or kidneys or to some other part of the body. Heat was often diagnosed on the basis of simple palpation or by the presence of flushing, and a preference for cool drinks, cool weather or cold applications. The tongue might be more red in colour, with less saliva (if associated with dryness) or with a coloured coating (if associated with damp). A range of cooling remedies were used to help clear such hot spots and help with a wider strategy to improve circulation.

Cold is the symptom of diminished vitality and death and marks a condition where the metabolic furnace has faltered, either generally or locally. The patient would prefer heat, in food and drink or as hot applications, abhor cold and might be listless, pale and withdrawn. The tongue might be pale and wet and (if associated with damp) the coating would be white. As long as debility was not too extreme, heating remedies like the spices were indicated either systemically or as hot topical applications.

The modern concepts of immunological diseases as disturbed responses to infection or disrupted gut barriers entirely accord with the intuitive and systematised traditional focus on toxicities. In the particular remedies below, their relevant properties are also listed. Not all plants are ascribed temperaments like warming or drying: some, like diuretics and astringents, were considered to have neutral temperaments; in other cases some Western herbs have no consistent tradition that would allow these qualities to be safely ascribed.

A large number of remedies are effective for intestinal wall problems (see p. 156). The following are immediately obvious options in arthritic, skin and other chronic inflammatory diseases:

Many herbs are rich in stigmasterol and other potentially anti-inflammatory phytosterols, or saponins with anti-inflammatory activity. Some also have reputations for hormone balancing and all those below have a traditional reputation in the treatment of inflammatory diseases:

The traditional herbal approach includes anti-inflammatories in the modern medical sense (like NSAIDs). These remedies are, perhaps with a few exceptions, less clinically powerful than modern drugs and are most useful as adjuncts to the therapeutic measures listed above:

The use of anti-inflammatory herbs is inappropriate when there is already prescription of strong anti-inflammatory medication, unless they are acting by a different mechanism to the drug and/or are aimed to gradually replace the drug.

Faced with a highly complex condition like a chronic inflammatory disease, the traditional practitioner might of course proceed entirely intuitively to clear the obstacles, using remedies such as the above in their own favoured ways. However, where strategies are systematised, notably in the Chinese tradition, a consistent pattern emerges. There is an almost geological approach. Pathogenic influences are envisaged as penetrating to different strata of the body, becoming more disturbed, disruptive and persistent the deeper they go. In chronic inflammations, by definition, the pathologies are deeply rooted and very intermingled. Looking for a way to disentangle the complexity, the traditional approach was often compared with peeling the layers of an onion, starting from the outside. Any opportunity to use effective ‘superficial’ eliminative measures would be taken up.

Chronic inflammatory diseases are often, almost by definition, accompanied by compromised defences and reduced vigour and there may be hot spots of relatively violent inflammations, for example rheumatic joints or skin eruptions. It is thus possible that treatments may be unduly provocative and exacerbations may occur. Contrary to some popular opinion (‘Things must get worse before they get better’), these ‘healing crises’ are rarely a good idea; indeed, they may worsen the condition in the long term. (Therapeutic exacerbations may be justified under carefully controlled conditions to expedite a blocked inflammation or fever but only when the patient is in a sufficiently robust state and the inflammation concerned is relatively simple.) Thus a good practitioner will peel the onion layers with care, only proceeding at a pace the body can stand, avoiding unnecessary exacerbation (for example with remedies that are too heating or cooling or with too strong an eliminative effect) and using remedies that calm and soothe. The practitioner will often take special care to apply strategies that aid recuperation and restoration of a robust and balanced immune system. This may mean, for example, adopting convalescent dietary principles (see p. 87) and combining these with appropriate digestive or hepatic remedies.

Anti-inflammatory remedies are best taken before or, if there is any stomach irritation, after meals.

Long-term therapy with anti-inflammatory remedies is usually acceptable, although this should be kept under review.

Although the conditions involved are sometimes very complex there should still be early endpoints to aim for. The obvious is relief of the symptoms, but there may be stages along the way as well.