Re: Re: CS - MANUKA HONEY & CFS

[Guest guest]

Hi

Ive copied the entire text - I hope it helps - it certainly has helped ME

clear the remaining digestive problems that i had where everything else I

tried failed.

Regards

CS

Manuka honey as a medicine

P. C. Molan, Honey Research Unit, University of Waikato, Hamilton, New

Zealand

E-mail: _p.molan@..._ (mailto:p.molan@...)

Honey - an ancient remedy " rediscovered "

The usage of honey as a medicine is referred to in the most ancient written

records, it being prescribed by the

physicians of many ancient races of people for a wide variety of ailments

(Ransome 1937). It has continued to be

used in folk medicine ever since, but in recent times there has been a

renaissance of the use of honey in the

medical profession: an editorial in the Journal of the Royal Society of

Medicine (Zumla and Lulat 1989)

discussing this expressed the opinion " The therapeutic potential of

uncontaminated, pure honey is grossly

underutilized. It is widely available in most communities and although the

mechanism of action of several of its

properties remains obscure and needs further investigation, the time has now

come for conventional medicine to

lift the blinds off this 'traditional remedy' and give it its due

recognition. " Some examples of the reports being

published are given here:

Cavanagh et al. (1970) described 12 cases of wound breakdown after radical

vulvectomy being dressed with

honey. The wounds, of a type notoriously difficult to keep free from

infection, were found to become sterile in 3–

6 days, have a clean healthy granulating (healing) appearance, required the

minimum of surgical removal of dead

tissue, and to not need skin grafting as would normally be required. Honey

was found to be non-irritant and much

more effective than topical antibiotics, the time in hospital being reduced

from the usual 7–8 to 3–4 weeks.

Efem (1988) reported clinical observations on the healing with honey of 59

cases of wounds and skin ulcers that

had not been healing for 1–24 months with conventional treatment. The wounds

were found to become sterile

and odourless in 1 week, pus and gangrenous tissue separating by themselves

painlessly. Swelling and exudation

of lymph subsided rapidly and there was rapid development of new tissue to

repair the wounds. The honey

caused no adverse reactions.

Efem (1993) reported a trial where 20 cases of Fournier's gangrene (a form

of necrotising fasciitis) were treated

by daily application of honey with no surgery, compared with 21 similar

cases treated by surgical removal of

infected tissue and systemic antibiotics. Similar outcomes were achieved

with both treatments but with a faster

response to treatment with honey, the wounds becoming sterile within 1 week

with honey, and with the group

treated with honey not requiring plastic surgery.

Subrahmanyam (1991) reported a randomised controlled trial in which honey

was compared with silver

sulfadiazine for efficacy as a dressing for burns. With silver sulfadiazine,

the most widely used agent to prevent or

clear infection in burns, 7% of the patients had infection in the burns

controlled within 7 days, whereas with honey

91% of the wounds were sterile within 7 days. Honey was observed to remove

dead tissue and offensive smell

from the burns. Healthy granulation tissue was observed to appear nearly

twice as fast with honey, and new skin

cover developed faster also. There was better relief of pain, less exudation

of lymph, and less irritation with

honey. Honey also gave a lower incidence of raised scars and contractures.

A detailed review of the published literature on the use of honey in wound

healing has been published by Molan

(1998). This literature provides a convincing body of evidence from clinical

observation, clinical trials and

experiments on animals for the effectiveness of honey as a wound dressing.

The published literature reporting

other therapeutic uses of honey has also been reviewed by Molan (1999b).

This review also cites historical and

traditional therapeutic uses of honey. Some examples of the modern

professional reports are given here:

Haffejee and Moosa (1985) reported a clinical trial in which honey was used

in place of glucose in a rehydration

fluid (solution of electrolytes) given to infants and children admitted into

hospital with gastroenteritis. The

treatment with honey gave a statistically significant reduction in the

duration of diarrhoea caused by bacterial

infection (58 hours cf 93 hours).

Salem (1981) reported a clinical trial in which 45 patients with dyspepsia

were given no medication other than 30

ml of honey before meals 3 times daily. After treatment with honey the

number of patients passing blood (from

peptic ulcers) in their faeces had decreased from 37 to 4; the number of

patients with dyspepsia had decreased

from 41 to 8; the number of patients with gastritis or duodenitis seen on

endoscopy had decreased from 24 to

15; the number of patients with a duodenal ulcer seen on endoscopy had

decreased from 7 to 2.

Emarah (1982) reported treating with honey 102 patients with a variety of

ophthalmological disorders not

responding to conventional treatment, such as keratitis, conjunctivitis and

blepharitis. The honey was applied

under the lower eyelid as eye ointment would be applied. Improvement was

seen in 85% of the cases, with no

deterioration seen in any of the other 15%. There was reported a transient

stinging sensation and redness of the

eye soon after putting honey in the eye, but never enough to stop the

treatment in any of the cases.

Getting honey accepted as a respectable medicine

Despite the many published clinical reports of the therapeutic effectiveness

of honey there is a tendency for some

practitioners to dismiss out of hand any suggestion that treatment with

honey is worthy of consideration as a

remedy in modern medicine. An editorial in Archives of Internal Medicine

assigned honey to the category of

" worthless but harmless substances " (Soffer 1976). Other medical

professionals have clearly shown that they are

unaware of the research that has demonstrated the rational explanations for

the therapeutic effects of honey

(Editorial 1974, Condon 1993). Many have attributed the therapeutic action

of honey to just the osmotic effect

of its sugar content (Seymour and West 1951, Keast- 1980, Mossel 1980,

Bose 1982, Green 1988,

Somerfield 1991, Tovey 1991, Condon 1993). There has also the long-standing

suspicion in the medical

profession of any remedy that has a reputation for being a " cure-all " , and a

suspicion of the claims made for the

plethora of " alternative remedies " that are being promoted in modern times.

Therefore many practitioners demand

a much higher standard of evidence of effectiveness for honey than is the

case for products of the pharmaceutical

industry.

Quen (1975), in a discussion of the ethics of running trials on remedies for

which there is no rational explanation

for how they work, has expressed the opinion: “The premature acceptors, and

the premature rejectors, are

equally anti-scientificâ€. With a world-wide move under way towards

evidence-based medicine it is important that

more clinical trials are run on the use of honey, that give results that

cannot be refuted by sceptics. But to get the

interest of the medical profession to run such trials it has been necessary

to find rational explanations for why

honey has the therapeutic effects that are observed. The published

literature on the experimental observations that

explain how honey exerts its therapeutic effects has been reviewed by Molan

(2001b). But it has taken more than

this to get the medical profession interested in using honey as a

therapeutic agent. The problem is best

summarised by a quotation: " Prejudice is a great time saver — it enables one

to form opinions without bothering

to get the facts. " (Australian Bee Journal, January 1944). It has needed a

major educational campaign to make

people aware of the facts: besides informational articles written for

medical journals (Molan 1998, Molan 1999a,

Molan 2000a, Molan and Betts 2000, Molan and 2000, Molan 2001a) and

professional magazines for

nurses (Molan 2000b, Betts and Molan 2001a, Molan and Betts 2001), 10 papers

have been presented at

medical conferences, 14 lectures have been given to medical professionals,

41 lectures to community groups, 5

items for science or medical TV programmes have been filmed, 16 articles

have been written for magazines and

newspapers for the general public, 42 interviews have been given for radio

stations, 20 interviews for TV news

have been given, and 112 interviews have been given for print media and web

news sites. These have all been

spread across many different countries. As well as that an informational

website on the medicinal properties of

honey has been set up (_http://honey.bio.waikato.ac.nz_

(http://honey.bio.waikato.ac.nz) ).

With all of these educational opportunities the emphasis has been put on

explaining how honey exerts its

therapeutic effects, rather than just trying to persuade people that it

gives good therapeutic outcomes. Mostly it

has been in the context of honey being used in wound healing as that is

where most of the evidence is to be

found.

The bioactivity of honey in wound healing

There are many reasons why honey has such a good therapeutic effect on

wounds, particularly on infected nonhealing

wounds. These have been discussed in detail by Molan (2001b), and are just

briefly outlined here:

The physical properties of honey play a part in its effectiveness as a wound

dressing. Because of its viscosity

honey provides a protective barrier which prevents cross-infection. Also,

because of its osmolarity drawing fluid

out from tissues it creates a moist healing environment. That gives optimum

healing as tissue growth not slowed

by drying, fibroblasts are able to pull wound closed, and epithelial cells

grow level with the skin surface so there

is no pitted scar resulting. It also means that dressings do not stick to

the surface of wounds as they sit on a layer

of diluted honey. Also that there is no growth of new tissue into dressing,

so there is no pain when changing

dressings and the new tissue is not torn away. The osmotically induced

outflow also creates " drainage', flushing

away from the tissues in the wound any harmful substances from bacterial

contaminants. The sugar content of

honey also aids in the rapid removal of malodour from wounds that is

observed, as bacteria use glucose in

preference to amino acids and thus produce lactic acid instead of

bad-smelling amines and mercaptans.

The remarkably rapid effect of honey in cleaning up wounds, an autolyic

debridement in which adherent dead

cells and fibrin clots, a rich breeding ground for bacteria, are digested

free by protease activity in the wound

tissue and lift off easily, is due to a combination of the osmotic outflow

and a bioactive effect of honey. Honey

contains the enzyme glucose oxidase which becomes active when honey is

diluted and produces hydrogen

peroxide (Molan 1992a). Change in the conformation of protein molecules

brought about by oxidation by low

levels of hydrogen peroxide is a physiological switching mechanism between

active and inactive forms of some

proteins. There are two types of protein-digesting enzyme involved in wound

tissues: the matrix metalloproteases

of the connective tissue ( et al. 1982), and the serine proteases

produced by the neutrophils (Tonnesen

et al. 1988). The serine proteases are normally inactive because of the

presence of an inhibitor, but hydrogen

peroxide inactivates the inhibitor, so the protease becomes active (Ossanna

et al. 1986). The metalloproteases

are normally present in an inactive conformation, but hydrogen peroxide

changes the conformation of these and

makes them active (Weiss et al. 1985, Peppin and Weiss 1986).

A similar mechanism switching nuclear transcription factors within cells to

their active forms. There is a large

amount of evidence for hydrogen peroxide being involved in many cell types

in the body as a stimulus for cell

multiplication (Burdon 1995). It is a normal part of wound healing, where

the inflammatory response that is a

natural consequence of injury or infection produces hydrogen peroxide, and

this serves to stimulate the growth of

fibroblasts and epithelial cells to repair the damage (Burdon 1995). Burdon

(1995) has proposed that low

concentrations of hydrogen peroxide might be used to stimulate wound

healing, rather than the expensive cell

growth factors produced by biotechnology for this purpose. But it has been

pointed out by Chung et al. (1993)

that this is feasible only if the concentration could be carefully

controlled. Honey provides such a controlled

delivery of hydrogen peroxide, the enzymic production giving a slow release

achieving equilibrium concentrations

of 20 - 95 µmol/l (Buntting 2001). This would account for the

" kick-starting " the healing process seen to occur

when honey is applied to wounds that have remained unhealed for a long time.

The hydrogen peroxide produced in honey would also be a factor responsible

for the rapid rate of healing

observed when wounds are dressed with honey. Additional to the actions

mentioned above, low concentrations

of hydrogen peroxide activate insulin receptor complexes (Czech et al. 1974,

Helm and Gunn 1986, Koshio et

al. 1988). This activation triggers a chain of molecular events in the cell

that stimulates the uptake of glucose and

amino acids, and promotes anabolic metabolism, giving cell growth. But there

appears to be an additional factor

involved, as Tonks et al. (2001) have reported that honey stimulates

cytokine release from monocytes (the start

of the normal sequence that gives rise to activation of tissue repair), and

that greater stimulation resulted from a

honey with a low production of hydrogen peroxide than from one with a higher

production. Additional to these

effects promoting tissue growth, honey provides vitamins, minerals, amino

acids and sugars for the growing cells.

The provision of glucose to the wound tissues is important also for allowing

maximal activity of phagocytes to

clear infecting bacteria. Glucose is essential for the ‘respiratory burst’

in macrophages, the reaction that generates

hydrogen peroxide, the dominant component of the bacteria-destroying

activity of these cells ( and Majno

1977). Also, honey provides substrates for glycolysis, the major mechanism

for energy production in the

macrophages. This would allow them to function in damaged tissues and

exudates where the oxygen supply is

often poor ( and Majno 1977). Additional to this nutritional

optimisation of the body's immune system,

honey enhances immunity through a bioactive effect. Abuharfeil et al. (1999)

have found that concentrations of

honey as low as 0.1% stimulate the proliferation of lymphocytes in cell

culture and activate phagocytes from

blood, and Tonks et al. (2001) have found that that honey at a concentration

of 1% stimulates monocytes in cell

culture to release cytokines which activate the many facets of the immune

response to infection.

Tonks et al. (2001) also found that monocytes already activated by exposure

to mitogens had their production of

reactive oxygen species reduced by honey. This is an important bioactivity

of honey, as a feedback loop (see

Figure 1) allows the reactive oxygen species produced as a consequence of

the inflammatory response to destroy

bacteria to initiate a greater inflammatory response which can be very

deleterious to the healing process. Apart

from inflammation creating pain, it causes opening of the circulation which

leads to exudation of lymph from open

wounds which can be difficult to manage, and oedema in surrounding tissue

which can restrict circulation through

capillaries and increase diffusional distances from capillaries to tissue

cells. This reduces the availability of oxygen

and nutrients to cells and thus restricts the cell growth necessary to

replace tissues to repair wounds.

Furthermore, the reactive oxygen species, being or giving rise to free

radicals, are very damaging to the

surrounding tissues, such that a wound will not heal if excessively

inflamed. A further problem that comes from

prolonged inflammation, where it is not sufficient to stop healing, is that

it can give rise to over-growth of

fibroblasts such that keloid scars, contractures and fibrosis can result.

Figure 1. The inflammatory response to bacterial infection. (ROS = reactive

oxygen species.)

mitogens on bacteria

inflammatory response by leukocytes

prostaglandins ROS

produced produced

pain, oedema & exudate tissue damage

It is probably the very effective anti-inflammatory activity of honey that

is responsible for the minimisation of

scarring by honey dressings on wounds, although it may also be the

antioxidants in honey removing free radicals

that is involved. Honey has a direct anti-inflammatory effect, not a

secondary effect resulting from the antibacterial

action removing inflammation-causing bacteria. The anti-inflammatory effects

of honey have been demonstrated in

histological studies of experimental wounds in animals where there was no

infection involved (Burlando 1978,

Kandil et al. 1987, El-Banby et al. 1989, Gupta et al. 1992, Postmes et al.

1997, Oryan and Zaker 1998). A

direct demonstration of the anti-inflammatory properties of honey, where

honey decreased the stiffness of

inflamed wrist joints of guinea pigs, has also been reported (Church 1954).

Honey has been found to have a

significant antioxidant content (el et al. 1998), measured as the

capacity of honey to scavenge free radicals.

The antioxidant activity of honey has also been demonstrated as inhibition

of chemiluminescence in a xanthinexanthine

oxidase-luminol system that works via generation of superoxide radicals (Ali

and Al-Swayeh 1997). It

also sequesters iron and thus inhibits the formation of free radicals from

hydrogen peroxide through the Fenton

reaction (Buntting 2001). But its antibacterial activity rapidly clearing

infecting bacteria which provoke an

inflammatory response would also play a large part.

The antibacterial activity of honey

Two millennia before bacteria were identified as the cause of disease

physicians were aware that particular types

of honey were best for treating particular ailments. Dioscorides, c.50 AD,

stated that a pale yellow honey from

Attica was the best, being “good for all rotten and hollow ulcers†(Gunther

1934), and Aristotle , 384-322 BC,

discussing differences in honeys, referred to pale honey being “good as a

salve for sore eyes and wounds "

(Aristotle 350 BC). Although this wisdom has long been forgotten by medical

professionals it has continued in

folk medicine around the world (Molan 2001b). It was because of the

reputation of manuka honey in New

Zealand folk medicine for its antiseptic properties (K. Simpson, personal

communication) that the research on it

was started at the University of Waikato. This one bioactivity, the unusual

antibacterial activity found in it, has

made manuka honey world famous.

The antibacterial activity of honey was first recognised in 1892, by van

Ketel (Dustmann 1979). The studies

carried out on this since have been reviewed by Molan (1992b, 1992a). It has

been found that mostly the activity

is due to the hydrogen peroxide produced enzymically in honey, but there

have been some reports of minor

additional antibacterial components. A survey of 345 samples of New Zealand

honeys from 26 different floral

sources carried out by et al. (1991) found that when catalase was

added to destroy hydrogen peroxide the

honey from only one of the floral sources, manuka (Leptospermum scoparium),

had any significant amount of

antibacterial activity remaining. This was unique amongst the many reports

on other honeys around the world in

that this non-peroxide component was a major contributor to the

antibacterial activity, although a subsequent

survey of 340 samples of Australian honeys from 78 different floral sources

(C. , Queensland Department

of Primary Industries: personal communication) made a similar finding for

honey from jellybush (Leptospermum

polygalifolium).

This novel antibacterial activity has been subsequently studied to determine

the potential usefulness of manuka

honey as a therapeutic agent. In this research it has been compared with

honey that has the usual type of

antibacterial activity due to hydrogen peroxide. In the survey carried out

by et al. (1991) a large number of

the samples of honey from the different floral sources were found to be of

low activity (36% of the samples had

activity near or below the level of detection in an agar diffusion assay),

the rest having almost a Gaussian

distribution over a thirty-fold range of activity. The non-peroxide activity

in the samples of manuka honey was

found to be similarly distributed. Consequently in the studies on the

effectiveness of the antibacterial activity a

representative manuka honey and a honey with activity due to hydrogen

peroxide were selected to be each near

the median level of their respective type of activity. The manuka honey was

also selected to have a low level of

activity due to hydrogen peroxide, and in some of the studies catalase was

added to break down any hydrogen

peroxide that may have been formed.

The results are summarised as follows, expressed as the minimum

concentration of honey (% v/v) that will completely stop the growth of each

species of microorganism:

Seven common wound-infecting species of bacteria (Willix et al. 1992):

manuka honey: 1.8–10.8% other honey: 2.6–7.1%

20 isolates of Pseudomonas from infected wounds ( and Molan 1999):

manuka honey: 5.5–8.7% other honey: 5.8–9.0%

58 clinical isolates of Staphylococcus aureus ( et al. 1999):

manuka honey: 2–3% other honey: 3–4%

82 epidemic strains of MRSA ( et al. 2000):

manuka honey: 4–7% other honey: 3–7%

56 strains of VRE ( et al. 2000):

manuka honey: 5–10% other honey: 8–20%

16 clinical isolates of ? -haemolytic streptococci ( RA, Halas E and

Molan PC: paper in preparation):

manuka honey: 4.5–9.7% other honey: 5.3–9.8%

20 strains of Burkholderia cepacia isolated from the sputum of cystic

fibrosis patients ( et al. 2000):

manuka honey: 2.1–5.0% other honey: 2.8–5.3%

Seven species of dermatophytes commonly causing tineas (Brady et al. 1997):

manuka honey: 10–50% other honey: 5–20%

7 isolates of Helicobacter pylori from biopsies of gastric ulcers(Al Somai

et al. 1994):

manuka honey: 5% other honey: >40%

Twelve species of bacteria commonly causing gastroenteritis (Brady NF and

Molan PC: paper in preparation):

manuka honey: 2–11% other honey: 3–8%

Seven species of bacteria commonly causing mastitis in dairy cattle (

and Molan 1997):

manuka honey: 5–10% other honey: 5–10%

These results all show that the activity is sufficient to expect a good

therapeutic antibacterial action if the honey

were used clinically. But they showed that in most cases the manuka honey

was not much different in its

effectiveness as a honey with the usual sort of antibacterial activity.

However, there are several reasons why

manuka honey could be expected to be more effective than other honey when

used therapeutically. The enzyme

catalase which breaks down hydrogen peroxide is present in the tissues and

serum of the body, so activity of

honey due to hydrogen peroxide will be less than is seen in laboratory

testing in media without catalase. Also, the

enzyme which produces hydrogen peroxide is inactive until honey is diluted,

and its activity is low at the acidic pH

of honey. Although the two types of honey antibacterial activity may be seen

to be fairly equal in laboratory

testing where the honey is diluted and neutralised by the culture medium, in

therapeutic use there would be a

much higher activity diffusing into body tissues from manuka honey that from

other honey if the honey is not

substantially diluted and neutralised by body fluids.

However it should be borne in mind that the results tabulated above were ob

tained with honeys with median

levels of activity. As people became aware of the special antibacterial

activity in manuka honey it became

apparent that there was a lot of manuka honey with undetectably low levels

of this antibacterial activity being

purchased for therapeutic use in ignorance of the fact that not all manuka

honey was active. An easily understood

activity rating system was devised so that purchasers could know the

antibacterial potency of the honey being

purchased. This is based on an agar diffusion assay of antibacterial

activity using Staphylococcus aureus ATCC

9144 as the test species and phenol as the reference standard ( et al.

1991). By analogy with the familiar

sunscreen protection factor rating (SPF), a 'UMF' rating is used on the

labels of manuka honey. ('UMF' is the

'unique manuka factor' – the non-peroxide antibacterial activity.) The

numbers used in the 'UMF' rating are the

concentration of phenol with the same antibacterial activity as the honey.

(E.g. 'UMF 15' honey has the same

activity against the S. aureus test species as a solution of 15% phenol

has.) " UMF' was registered as a

trademark by the producers of the active manuka honey to stop its misuse,

with testing standards having to be

complied with for permission to be granted for use of the trademark.

Results from clinical usage of manuka honey

With high-activity manuka honey being available commercially, especially

that which has been sterilised by

gamma-irradiation (a process that does not reduce the activity: Molan and

1996), there have been several

clinical cases published where the results have been remarkable. Three,

using 'UMF 12' manuka honey, have

reported healing wounds infected with MRSA (Dunford et al. 2000b, Betts and

Molan 2001b, Natarajan et al.

2001). Another, using 'UMF 12' manuka honey, reported rapidly healing

widespread serious skin ulcers resulting

from meningococcal septicaemia that were heavily infected with Pseudomonas,

Staphylococcus aureus and

Enterococcus and had not responded to all modern conventional treatments

over a period of 9 months in

intensive care (Dunford et al. 2000a). Also, et al. (2001) have

reported a case of hidradenitis

suppuritiva that had been giving recurrent abscesses for 22 years and had

given a non-healing wound for the past

3 years that had had three attempts at surgical removal of infected tissue

and a wide range of antibiotics,

antiseptics and wound dressings. This was healed (with no recurrence of

infection in the two years since) within 1

month by dressing with 'UMF 13' manuka honey. Another case reported was of a

large wound from surgical

removal of an area of necrotising fasciitis which was heavily infected with

Pseudomonas after surgery so could

not have a skin graft applied: this was rapidly cleared of infection by

application of a dressing of 'UMF 12'

manuka honey then successfully skin-grafted (Robson et al. 2000). Betts and

Molan (2001b) have reported a

trial using 'UMF 12' manuka honey on a wider range of types of infected

wounds (venous leg ulcers, leg ulcers of

mixed aetiology, diabetic foot ulcers, pressure ulcers, unhealed graft donor

sites, abscesses, boils, pilonidal

sinuses, and infected wounds from lower limb surgery). Infection was rapidly

cleared and all wounds were healed

successfully other than ones where there was an underlying failure in

arterial blood supply creating non-viable

tissue.

Research still to be done on the bioactivity of honey

Because of the tendency of many medical professionals to cling to the belief

that only pharmaceutical products

are of value, it is necessary to provide a higher standard of evidence of

effectiveness than is usually provided to

gain acceptance of new forms of treatment. Consequently, a clinical trial

comparing honey with best modern

practice for the healing of leg ulcers is under way at Aintree Hospital,

Liverpool. Also there is a trial under way in

the Ophthalmology Department at Christchurch Hospital using honey to treat

blephatitis; in the Department of

Oral Surgery at the University of Illinois, Chicago, using honey to prevent

the development of dry socket after

removal of impacted third molars; and at the Dental School at the University

of Otago using honey to decrease

dental plaque and gingivitis. A clinical trial is being discussed to

investigate the use of honey in palliative care of

cancerous wounds. Also, veterinary trials are being planned for treating

mastitis in dairy cows, and for preventing

gastroenteritis in pigs, chickens and calves.

Research is under way assaying the antioxidant and anti-inflammatory

activities in honey with a view to being able

to select for marketing honeys with high levels of these activities, and to

identify the components responsible for

these bioactivities. Further research is still to be done to identify the

components of honey that stimulate the

immune response and stimulate wound tissue growth, and the component

responsible for releasing bacteria from

skin cells and mucosa. The development of assays for these bioactivities

will allow selection for marketing honeys

with high levels of these also.

Conclusion

The establishment by research that there are bioactive components in honey,

and the wide dissemination of this

knowledge, has led to a general acceptance that honey is a respectable

therapeutic agent, and to a rapidly

increasing uptake of its usage by clinicians as well as by the general

public. The finding that there are multiple

bioactive components involved in the therapeutic action makes it a much more

attractive option to use the natural

product rather than to attempt to identify individual active components and

use synthesised copies of those.

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