The first part of this review is concerned with the balance between N input and output as urinary urea. I start with some observations on classical biochemical studies of the operation of the urea cycle. According to Krebs, the cycle is instantaneous and automatic, as a result of the irreversibility of the first enzyme, carbamoyl-phosphate synthetase 1 (EC 6.3.5.5; CPS-I), and it should be able to handle many times the normal input to the cycle. It is now generally agreed that acetyl glutamate is a necessary co-factor for CPS-1, but not a regulator. There is abundant evidence that changes in dietary protein supply induce coordinated changes in the amounts of all five urea-cycle enzymes. How this coordination is achieved, and why it should be necessary in view of the properties of the cycle mentioned above, is unknown. At the physiological level it is not clear how a change in protein intake is translated into a change of urea cycle activity. It is very unlikely that the signal is an alteration in the plasma concentration either of total amino-N or of any single amino acid. The immediate substrates of the urea cycle are NH3 and aspartate, but there have been no measurements of their concentration in the liver in relation to urea production. Measurements of urea kinetics have shown that in many cases urea production exceeds N intake, and it is only through transfer of some of the urea produced to the colon, where it is hydrolysed to NH3, that it is possible to achieve N balance. It is beginning to look as if this process is regulated, possibly through the operation of recently discovered urea transporters in the kidney and colon. The second part of the review deals with the synthesis and breakdown of protein. The evidence on whole-body protein turnover under a variety of conditions strongly suggests that the components of turnover, including amino acid oxidation, are influenced and perhaps regulated by amino acid supply or amino acid concentration, with insulin playing an important but secondary role. Molecular biology has provided a great deal of information about the complex processes of protein synthesis and breakdown, but so far has nothing to say about how they are coordinated so that in the steady state they are equal. A simple hypothesis is proposed to fill this gap, based on the self-evident fact that for two processes to be coordinated they must have some factor in common. This common factor is the amino acid pool, which provides the substrates for synthesis and represents the products of breakdown. The review concludes that although the achievement and maintenance of N balance is a fact of life that we tend to take for granted, there are many features of it that are not understood, principally the control of urea production and excretion to match the intake, and the coordination of protein synthesis and breakdown to maintain a relatively constant lean body mass.

The current application and future potential of near infrared (NIR) spectroscopy in the evaluation of foods for domesticated animals and humans is enormous. Where used, NIR spectroscopy has revolutionized the analysis and nutritional evaluation of animal feeds and human foods by providing a rapid means of examination. The availability of accurate and rapid methods of evaluation is becoming increasingly important to meet the nutritional requirements of animals for meat, milk, wool and egg production. This is essential for efficient and economic animal production, to maintain animal health and to minimize environmental impact. Accurate evaluation methods are also needed in relation to national and international legislation that regulates the circulation, trade and inspection of foods and feeds, aids effective functioning of the market and guards the safety of animals and humans. The aim of this review is to outline the theory and principles of NIR spectroscopy and to focus primarily on its application in the field of animal nutrition. The vital role NIR spectroscopy is playing in the prediction of biologically meaningful feed characteristics, including data derived in vivo, is demonstrated particularly through its application to forage evaluation, but also in the examination of raw materials and compound feeds. While the applications of NIR spectroscopy to different foods and drinks are extensive, this review gives an overview only of selected reported applications including its use for predicting nutritive value (mainly water, protein, fat, sucrose and starch content), monitoring food processing and for food authentication. The review provides clear evidence that the future application of NIR spectroscopy will undoubtedly increase, playing a vital role in the authentication of the quality and origin of foods and feeds and enabling the complex methods of feed evaluation required in the future to be put into widespread use.

The central nervous system undertakes the homeostatic role of sensing nutrient intake and body reserves, integrating the information, and regulating energy intake and/or energy expenditure. Few tasks regulated by the brain hold greater survival value, particularly important in farmed ruminant species, where the demands of pregnancy, lactation and/or growth are not easily met by often bulky plant-based and sometimes nutrient-sparse diets. Information regarding metabolic state can be transmitted to the appetite control centres of the brain by a diverse array of signals, such as stimulation of the vagus nerve, or metabolic ‘feedback’ factors derived from the pituitary gland, adipose tissue, stomach/abomasum, intestine, pancreas and/or muscle. These signals act directly on the neurons located in the arcuate nucleus of the medio-basal hypothalamus, a key integration, and hunger (orexigenic) and satiety (anorexigenic) control centre of the brain. Interest in human obesity and associated disorders has fuelled considerable research effort in this area, resulting in increased understanding of chronic and acute factors influencing feed intake. In recent years, research has demonstrated that these results have relevance to animal production, with genetic selection for production found to affect orexigenic hormones, feeding found to reduce the concentration of acute controllers of orexigenic signals, and exogenous administration of orexigenic hormones (i.e. growth hormone or ghrelin) reportedly increasing DM intake in ruminant animals as well as single-stomached species. The current state of knowledge on factors influencing the hypothalamic orexigenic and anorexigenic control centres is reviewed, particularly as it relates to domesticated ruminant animals, and potential avenues for future research are identified.

The metabolic syndrome is an important risk factor for type 2 diabetes mellitus and CVD. Epidemiological studies have now suggested protective effects of dairy product consumption on the development of this syndrome. Here we review the physiological effects and possible mechanisms involved of three main dairy constituents (Ca, protein, fat) on important components of the metabolic syndrome. Ca supplements improve the serum lipoprotein profile, particularly by decreasing serum total and LDL-cholesterol concentrations. They also lower systolic and diastolic blood pressure. Insufficient evidence exists for a significant role of Ca supplements or dairy in body-weight management. Effects of Ca may be related to intestinal binding to fatty acids or bile acids, or to changes in intracellular Ca metabolism by suppressing calciotropic hormones. Dietary proteins may increase satiety in both the short and longer term, which may result in a reduced energy intake. They have also been reported to improve the serum lipoprotein profile as compared with carbohydrates. Dairy proteins are precursors of angiotensin-I-converting enzyme-inhibitory peptides, which may lower blood pressure. Such effects, however, have inconsistently been reported in human studies. Finally, conjugated linoleic acid, which effectively lowers body weight in animals, has no such effect in humans in the quantities provided by dairy products. To reduce the intake of SFA, the consumption of low-fat instead of high-fat dairy products is recommended. In conclusion, more research is warranted to better understand the physiological effects and the mechanisms involved of dairy products in the prevention and treatment of the metabolic syndrome.

CVD are the leading cause of death worldwide. Hypertension, a major controllable risk factor of CVD, is intimately associated with vascular dysfunction, a defect which is also now recognised to be a major, modifiable risk factor for the development of CVD. The purpose of the present review was to critically evaluate the evidence for the effects of milk proteins and their associated peptides on blood pressure (BP) and vascular dysfunction. After a detailed literature search, the number of human trials evaluating the antihypertensive effects of casein-derived peptides (excluding isoleucine-proline-proline and valine-proline-proline) was found to be limited; the studies were preliminary with substantial methodological limitations. Likewise, the data from human trials that examined the effects of whey protein and peptides were also scarce and inconsistent. To date, only one study has conducted a comparative investigation on the relative effects of the two main intact milk proteins on BP and vascular function. While both milk proteins were shown to reduce BP, only whey protein improved measures of arterial stiffness. In contrast, a growing number of human trials have produced evidence to support beneficial effects of both milk proteins and peptides on vascular health. However, comparison of the relative outcomes from these trials is difficult owing to variation in the forms of assessment and measures of vascular function. In conclusion, there is an accumulating body of evidence to support positive effects of milk proteins in improving and/or maintaining cardiovascular health. However, the variable quality of the studies that produced this evidence, and the lack of robust, randomised controlled intervention trials, undermines the formulation of firm conclusions on the potential benefits of milk proteins and peptides on vascular health.

Dietary deficiencies in Fe and Zn are globally widespread, causing serious health problems such as anaemia, poor pregnancy outcomes, increased risk of morbidity and mortality, stunted growth and impaired physical and cognitive development. Edible insects, of which a diversity of over 2000 species is available, are dietary components for about 2 billion individuals and are a valuable source of animal protein. In the present paper, we review the available information on Fe and Zn in edible insects and their potential as a source of these micronutrients for the rapidly growing human population. The levels of Fe and Zn present in eleven edible insect species that are mass-reared and six species that are collected from nature are similar to or higher than in other animal-based food sources. High protein levels in edible insect species are associated with high Fe and Zn levels. Fe and Zn levels are significantly positively correlated. Biochemically, Fe and Zn in insects occur predominantly in non-haem forms, bound to the proteins ferritin, transferrin and other transport and storage proteins. Knowledge gaps exist for bioavailability in the human alimentary tract, the effect of anti-nutritional factors in other dietary components such as grains on Fe and Zn absorption and the effect of food preparation methods. We conclude that edible insects present unique opportunities for improving the micronutrient status of both resource-poor and Western populations.

Selected biochemical evidence suggests a potential role for n-3 long-chain PUFA (n-3PUFA) in the regulation of mood and behaviour. The present paper reviews the relevant evidence, to date, from epidemiological studies, clinical studies and intervention trials. Most evidence is available investigating a role for n-3PUFA in depression, depressive illness and suicidal behaviour, but work is also available on anxiety and anxiety-related disorders, fatigue and fatigue-related disorders, aggression, hostility and anti-social behaviour, inattention, impulsivity and attention deficit hyperactivity disorder and schizophrenic disorders. For all these aspects of mood and behaviour, the evidence available is currently limited and highly inconsistent, both in terms of study methodology and study findings. There is a clear need for further work in this area.

Resistant starch (RS) is defined as ‘the sum of starch and products of starch degradation not absorbed in the small intestine of healthy individuals’. This basic definition includes different types of starches that (1) are physically inaccessible, usually due to an encapsulation in intact cell walls, or (2) are naturally highly resistant to mammalian α-amylase, or (3) have been modified by hydrothermic treatments then retrograded. Interest in RS has increased significantly during the last two decades, mostly due to its capacity to produce a large amount of butyrate all along the colon. Butyrate has been observed to have a range of effects on cell metabolism, differentiation and cell growth as well as inhibition of a variety of factors that underlie the initiation, progression and growth of colon tumours. The physiological definition of RS, which seems to be nearly consensual, raises a difficulty in proper analytical quantification of RS. A number of methods have, however, been proposed and provide similar values for the RS content in most of the starch types and starchy foods. It seems, however, that some starches, proven to be partly resistant according to in vivo investigations on ileostomy subjects, could not be quantified by most of these methods. This may be due to a widespread use of glucoamylase during the first steps of these methods. Accordingly, there is an international debate on health aspects of RS and on how to quantify the RS content of food products. The present review describes aspects of classification of RS, past and current consumption, physiological effects and analytical aspects, and concludes with impacts on food and product labelling.

Thiamin plays a key role in the maintenance of brain function. Thiamin diphosphate is cofactor for several enzymes involved in glucose metabolism whereas thiamin triphosphate has distinct properties at the neuronal membrane. Thiamin metabolism in the brain is compartmented between neurons and neighbouring glial cells. Thiamin deficiency is commonly encountered in severe malnutrition associated with chronic alcoholism, HIV–AIDS and gastrointestinal disease where it frequently results in Wernicke's encephalopathy (the Wernicke–Korsakoff syndrome). Wernicke's encephalopathy is severely underdiagnosed according to clinical criteria in both alcoholic and HIV–AIDS patients. Magnetic resonance imaging reveals bilateral ventricular enlargement, mammillary body atrophy and cerebellar degeneration indicative of selective neuronal loss that is characteristic of Wernicke's encephalopathy. Several mechanisms have been proposed to explain this selective loss of neurons including a cerebral energy deficit resulting from reductions in activity of thiamin diphosphate-dependent enzymes, oxidative stress and N-methyl-D-aspartate receptor-mediated excitotoxicity. Both microglia and perivascular endothelial cells are sources of NO and oxidative stress in thiamin deficiency. Decreased activities of thiamin diphosphate-dependent enzymes (in particular α-ketoglutarate dehydrogenase) have also been reported in neurodegenerative diseases such as Alzheimer's and Parkinson's diseases independent of patient malnutrition. In these cases, decreased activities result from direct toxic actions of oxidative stress and β-amyloid produced as part of the neuronal cell death cascade in these disorders.

Dietary intake and tissue levels of carotenoids have been associated with a reduced risk of several chronic diseases, including cardiovascular diseases, type 2 diabetes, obesity, brain-related diseases and some types of cancer. However, intervention trials with isolated carotenoid supplements have mostly failed to confirm the postulated health benefits. It has thereby been speculated that dosing, matrix and synergistic effects, as well as underlying health and the individual nutritional status plus genetic background do play a role. It appears that our knowledge on carotenoid-mediated health benefits may still be incomplete, as the underlying mechanisms of action are poorly understood in relation to human relevance. Antioxidant mechanisms – direct or via transcription factors such as NRF2 and NF-κB – and activation of nuclear hormone receptor pathways such as of RAR, RXR or also PPARs, via carotenoid metabolites, are the basic principles which we try to connect with carotenoid-transmitted health benefits as exemplified with described common diseases including obesity/diabetes and cancer. Depending on the targeted diseases, single or multiple mechanisms of actions may play a role. In this review and position paper, we try to highlight our present knowledge on carotenoid metabolism and mechanisms translatable into health benefits related to several chronic diseases.

Technology-based dietary assessment offers solutions to many of the limitations of traditional dietary assessment methodologies including cost, participation rates and the accuracy of data collected. The 24-h dietary recall (24HDR) method is currently the most utilised method for the collection of dietary intake data at a national level. Recently there have been many developments using web-based platforms to collect food intake data using the principles of the 24HDR method. This review identifies web- and computer-based 24HDR tools that have been developed for both children and adult population groups, and examines common design features and the methods used to investigate the performance and validity of these tools. Overall, there is generally good to strong agreement between web-based 24HDR and respective reference measures for intakes of macro- and micronutrients.

The present review examines the importance of choline in dairy cow nutrition. Choline is an essential nutrient for mammals when excess methionine and folate are not available in the diet. The requirement for choline can be met by dietary choline and by transmethylation reactions. Two types of functions for choline are known: functions of choline per se; functions as a methyl donor. The two principal methyl donors in animal metabolism are betaine, a metabolite of choline, and S-adenosyl-methionine, a metabolite of methionine. Choline and methionine are interchangeable with regard to their methyl group-furnishing functions. In adult ruminants, choline is extensively degraded in the rumen; for this reason dietary choline contributes insignificantly to the choline body pool and methyl group metabolism is generally conservative with a relatively low rate of methyl catabolism and an elevated rate of de novo synthesis of methyl groups via the tetrahydrofolate system. In dairy ruminants, the dietary availability of choline is still low, but the output of methylated compounds in milk is high, and precursors from the tetrahydrofolate pathway are limiting, especially at the onset of lactation. Therefore choline may be a limiting nutrient for milk production in high-yielding dairy cows.

Mounting evidence substantiates the central role of the endocannabinoid system (ECS) in the modulation of both homeostatic and hedonic elements of appetite and food intake. Conversely, feeding status and dietary patterns directly influence activity of the ECS. Following a general introduction on the functioning of the ECS, the present review specifically addresses its role in the modulation of hedonic eating. Humans possess strong motivational systems triggered by rewarding aspects of food. Food reward is comprised of two components: one appetitive (orienting towards food); the other consummatory (hedonic evaluation), also referred to as ‘wanting’ and ‘liking’, respectively. Endocannabinoid tone seems to influence both the motivation to feed and the hedonic value of foods, probably by modifying palatability. Human physiology underlying hedonic eating is still not fully understood. A better understanding of the role of the ECS in the rewarding value of specific foods or diets could offer new possibilities to optimise the balance between energy and nutrient intake for different target groups. These groups include the obese and overweight, and potentially individuals suffering from malnutrition. Examples for the latter group are patients with disease-related anorexia, as well as the growing population of frail elderly suffering from persistent loss of food enjoyment and appetite resulting in malnutrition and involuntary weight loss. It has become clear that the psychobiology of food hedonics is extremely complex and the clinical failure of CB1 inverse agonists including rimonabant (Accomplia®) has shown that ‘quick wins’ in this field are unlikely.

Maintaining a correct balance of N is essential for life. In mammals, the major sources of N in the diet are amino acids and peptides derived from ingested proteins. The immediate endproduct of mammalian protein catabolism is ammonia, which is toxic to cells if allowed to accumulate. Therefore, amino acids are broken down in the liver as part of the ornithine–urea cycle, which results in the formation of urea – a highly soluble, biochemically benign molecule. Mammals cannot break down urea, which is traditionally viewed as a simple waste product passed out in the urine. However, urea from the bloodstream can pass into the gastrointestinal tract, where bacteria expressing urease cleave urea into ammonia and carbon dioxide. The bacteria utilise the ammonia as an N source, producing amino acids and peptides necessary for growth. Interestingly, these microbial products can be reabsorbed back into the host mammalian circulation and used for synthetic processes. This entire process is known as ‘urea nitrogen salvaging’ (UNS). In this review we present evidence supporting a role for this process in mammals – including ruminants, non-ruminants and man. We also explore the possible mechanisms involved in UNS, including the role of specialised urea transporters.

The relationship between meat consumption and breast cancer has been the focus of several epidemiological investigations, yet there has been no clear scientific consensus as to whether red or processed meat intake increases the risk of breast cancer. We conducted a comprehensive meta-analysis incorporating data from several recently published prospective studies of red or processed meat intake and breast cancer. In the meta-analysis utilising data from the Pooling Project publication (includes data from eight cohorts) combined with data from nine studies published between 2004 and 2009 and one study published in 1996, the fixed-effect summary relative risk estimate (SRRE) for red meat intake (high v. low) and breast cancer was 1·02 (95 % CI 0·98, 1·07; P value for heterogeneity = 0·001) and the random-effects SRRE was 1·07 (95 % CI 0·98, 1·17). The SRRE for each 100 g increment of red meat was 1·04 (95 % CI 1·00, 1·07), based on a fixed-effects model, and 1·12 (95 % CI 1·03, 1·23) based on a random-effects model. No association was observed for each 100 g increment of red meat among premenopausal women (SRRE 1·01; 95 % CI 0·92, 1·11) but a statistically significant SRRE of 1·22 (95 % CI 1·04, 1·44) was observed among postmenopausal women using a random-effects model. However, the association for postmenopausal women was attenuated and non-significant when using a fixed-effects model (SRRE 1·03; 95 % CI 0·98, 1·08). The fixed- and random-effect SRRE for high (v. low) processed meat intake and breast cancer were 1·00 (95 % CI 0·98, 1·01; P value for heterogeneity = 0·005) and 1·08 (95 % CI 1·01, 1·16), respectively. The fixed- and random-effect SRRE for each 30 g increment of processed meat were 1·03 (95 % CI 1·00, 1·06) and 1·06 (95 % CI 0·99, 1·14), respectively. Overall, weak positive summary associations were observed across all meta-analysis models, with the majority being non-statistically significant. Heterogeneity was evident in most analyses, summary associations were sensitive to the choice of analytical model (fixed v. random effects), and publication bias appeared to have produced slightly elevated summary associations. On the basis of this quantitative assessment, red meat and processed meat intake does not appear to be independently associated with increasing the risk of breast cancer, although further investigations of potential effect modifiers, such as analyses by hormone receptor status, may provide valuable insight to potential patterns of associations.

Autism spectrum disorder (ASD) is characterised by deficits in the ability to socialise, communicate and use imagination, and displays of stereotypical behaviour. It is widely accepted that ASD involves a disorder in brain development. However, the real causes of the neurodevelopmental disorders associated with ASD are not clear. In this respect, it has been found that a majority of children with ASD display gastrointestinal symptoms, and an increased intestinal permeability. Moreover, large differences in microbiotic composition between ASD patients and controls have been reported. Therefore, nutrition-related factors have been hypothesised to play a causal role in the aetiology of ASD and its symptoms. Through a review of the literature, it was found that abnormalities in carbohydrate digestion and absorption could explain some of the gastrointestinal problems observed in a subset of ASD patients, although their role in the neurological and behavioural problems remains uncertain. In addition, the relationship between an improved gut health and a reduction of symptoms in some patients was evaluated. Recent trials involving gluten-free diets, casein-free diets, and pre- and probiotic, and multivitamin supplementation show contradictive but promising results. It can be concluded that nutrition and other environmental influences might trigger an unstable base of genetic predisposition, which may lead to the development of autism, at least in a subset of ASD patients. Clear directions for further research to improve diagnosis and treatment for the different subsets of the disorder are provided.

Lactation results in a number of physiological adaptations which exert direct effects on maternal health, some of which may confer both short and long term advantages for breast feeding mothers. Breast feeding in the early postpartum period promotes a more rapid return of the uterus to its prepregnant state through the actions of oxytocin. Breast feeding may also lead to a more rapid return to prepregnancy weight. Among studies that had good data on duration and intensity of lactation, the majority show a significant association between lactation and weight loss. However, there is no evidence that lactation prevents obesity. Lactation also affects glucose and lipid metabolism. The long term effects of these adaptations are unknown but may have implications for preventing subsequent development of diabetes and heart disease. Lactation delays the return of ovulation and significantly reduces fertility during the period of lactational amenorrhoea. This process is linked with feeding patterns and may therefore be affected by practices such as scheduled feedings and the timing of introduction of complementary foods. While the evidence from epidemiologic studies is mixed, several large studies have shown that extended lactation is associated with reduced risk of premenopausal breast, ovarian and endometrial cancers. Although bone mineralization declines during lactation, repletion takes place after weaning. As a result, breast feeding does not appear to cause long term depletion of bone nor does it increase risk of osteoporosis. Many of the physiological effects of lactation are dependent on the stimulation of the hypothalamic-pituitary axis and milk removal and thus may vary with infant feeding practices. Well controlled studies are needed that include detailed information regarding infant feeding practices in addition to the total duration of any breast feeding. Future feeding recommendations should reflect careful consideration of how such practices affect both infant and maternal health.

The rumen is the site of significant interactions between Cu, S and Mo. It also shows reactions between Cu, S and Fe. The interaction between Mo and S results in the formation of thiomolybdates, which in the absence of adequate quantities of rumen Cu are absorbed into the animal and bind to Cu in biological compounds. This is the cause of thiomolybdate toxicity, often misleadingly called Cu deficiency. The effects of thiomolybdates being absorbed into the animal are considered, especially how thiomolybdates bind to Cu-containing compounds such as enzymes, decreasing their activity without removing the active Cu component. The sources of Cu, Mo, Fe and S are examined, including the impacts of water and soil on the animal's intake. Within the present review we have been able to provide evidence that: all classes of thiomolybdates are formed in the rumen; in the absence of available Cu all thiomolybdates can be absorbed into the animal rapidly though the rumen wall or via the small intestine; thiomolybdates bind to Cu in biological compounds and are able to cause problems; effects of thiomolybdate are reversible in vivo and in vitro on cessation of thiomolybdate challenge; the tetra-thiomolybdate form is the most potent Cu binder with decreased potency with decreasing S in the compound. Fe will exacerbate a thiomolybdate problem but will not directly cause it.

It is important to pay attention to weight management before and between pregnancies, as women have an increased risk of weight gain during the reproductive years. Having a baby is a life-changing event for women and the challenge of weight management amidst this period of major physiological, psychological and social change should not be underestimated. However, the postpartum period offers an opportune time for lifestyle interventions, as women may have heightened awareness of their own and their wider families’ health. Systematic reviews indicate that interventions including both diet and physical activity along with individualised support and self-monitoring are more likely to be successful in promoting postpartum weight loss. However, high levels of attrition and poor engagement have been an issue in previous trials in this area. Since postpartum women are difficult to reach and retain, future research must consider how to make weight-management interventions an attractive and attainable proposition for women who are juggling multiple, competing demands on their time. Ideally, intervention approaches need to be flexible and allow sustained contact with women, to facilitate a focus on maintenance of weight loss, as well as opportunities for re-engagement after life events that may disrupt weight-management progress. Using technology to deliver or support interventions holds promise but trials are needed to generate a range of appealing, effective and scalable options for postpartum women. What works at other life stages may not necessarily work here owing to specific barriers to weight management encountered in the postpartum period.

Despite the much improved therapeutic approaches for cancer treatment that have been developed over the past 50 years, cancer remains a major cause of mortality globally. Considerable epidemiological and experimental evidence has demonstrated an association between ingestion of food and nutrients with either an increased risk for cancer or its prevention. There is rising interest in exploring agents derived from natural products for chemoprevention or for therapeutic purposes. Honey is rich in nutritional and non-nutritional bioactive compounds, as well as in natural antioxidants, and its potential beneficial function in human health is becoming more evident. A large number of studies have addressed the anti-cancer effects of different types of honey and their phenolic compounds using in vitro and in vivo cancer models. The reported findings affirm that honey is an agent able to modulate oxidative stress and has anti-proliferative, pro-apoptotic, anti-inflammatory, immune-modulatory and anti-metastatic properties. However, despite its reported anti-cancer activities, very few clinical studies have been undertaken. In the present review, we summarise the findings from different experimental approaches, including in vitro cell cultures, preclinical animal models and clinical studies, and provide an overview of the bioactive profile and bioavailability of the most commonly studied honey types, with special emphasis on the chemopreventive and therapeutic properties of honey and its major phenolic compounds in cancer. The implications of these findings as well as the future prospects of utilising honey to fight cancer will be discussed.