Minerals fulfil a wide variety of functions in the optimal functioning of the immune system. This review reports on the minerals that are essential for the immune system’s function and inflammation regulation. We also discuss nutritional aspects of optimized mineral supply. The supply of minerals is important for the optimal function of the innate immune system as well as for components of adaptive immune defense; this involves defense mechanisms against pathogens in addition to the long-term balance of pro- and anti-inflammatory regulation. Generally, a balanced diet is sufficient to supply the required balance of minerals to help support the immune system. Although a mineral deficiency is rare, there are nevertheless at-risk groups who should pay attention to ensure they are receiving a sufficient supply of minerals such as magnesium, zinc, copper, iron, and selenium. A deficiency in any of these minerals could temporarily reduce immune competence, or even disrupt systemic inflammation regulation in the long term. Therefore, knowledge of the mechanisms and supply of these minerals is important. In exceptional cases, a deficiency should be compensated by supplementation; however, supplement over-consumption may be negative to the immune system, and should be avoided. Accordingly, any supplementation should be medically clarified and should only be administered in prescribed concentrations.

The monoamine model of depression has long formed the basis of drug development but fails to explain treatment resistance or associations with stress or inflammation. Recent animal research, clinical trials of ketamine (a glutamate receptor antagonist), neuroimaging research, and microbiome studies provide increasing evidence of glutamatergic dysfunction in depression and other disorders. Glutamatergic involvement across diverse neuropathologies including psychoses, neurodevelopmental, neurodegenerative conditions, and brain injury forms the rationale for this review. Glutamate is the brain’s principal excitatory neurotransmitter (NT), a metabolic and synthesis substrate, and an immune mediator. These overlapping roles and multiple glutamate NT receptor types complicate research into glutamate neurotransmission. The glutamate microcircuit comprises excitatory glutamatergic neurons, astrocytes controlling synaptic space levels, through glutamate reuptake, and inhibitory GABA interneurons. Astroglia generate and respond to inflammatory mediators. Glutamatergic microcircuits also act at the brain/body interface via the microbiome, kynurenine pathway, and hypothalamus–pituitary–adrenal axis. Disruption of excitatory/inhibitory homeostasis causing neuro-excitotoxicity, with neuronal impairment, causes depression and cognition symptoms via limbic and prefrontal regions, respectively. Persistent dysfunction reduces neuronal plasticity and growth causing neuronal death and tissue atrophy in neurodegenerative diseases. A conceptual overview of brain glutamatergic activity and peripheral interfacing is presented, including the common mechanisms that diverse diseases share when glutamate homeostasis is disrupted.

Excessive release of inflammatory cytokines and oxidative stress (OS) are triggering factors in the onset of chronic diseases. One of the factors that can ensure health in humans is regular physical activity. This type of activity can enhance immune function and dramatically prevent the spread of the cytokine response and OS. However, if physical activity is done intensely at irregular intervals, it is not only unhealthy but can also lead to muscle damage, OS, and inflammation. In this review, the response of cytokines and OS to exercise is described. In addition, it is focused predominantly on the role of reactive oxygen and nitrogen species (RONS) generated from muscle metabolism and damage during exercise and on the modulatory effects of antioxidant supplements. Furthermore, the influence of factors such as age, sex, and type of exercise protocol (volume, duration, and intensity of training) is analyzed. The effect of antioxidant supplements on improving OS and inflammatory cytokines is somewhat ambiguous. More research is needed to understand this issue, considering in greater detail factors such as level of training, health status, age, sex, disease, and type of exercise protocol.

The main focus of this review is illness among elite athletes, how and why it occurs, and whether any measures can be taken to combat it or to prevent its onset. In particular, there is particular interest in exercise-induced immunodepression, which is a result of the immune system regarding exercise (e.g., prolonged, exhaustive exercise) as a challenge to its function. This promotes the inflammatory response. There is often a high incidence of illness in athletes after undertaking strenuous exercise, particularly among those competing in endurance events, not only mainly in terms of upper respiratory tract illness, but also involving gastrointestinal problems. It may well be that this high incidence is largely due to insufficient recovery time being allowed after, for example, a marathon, a triathlon, or other endurance events. Two examples of the incidence of upper respiratory tract illness in moderate versus endurance exercise are provided. In recent years, increasing numbers of research studies have investigated the origins, symptoms, and incidence of these bouts of illness and have attempted to alleviate the symptoms with supplements, sports foods, or immunonutrition. One aspect of the present review discusses iron deficiency, which has been primarily suggested to have an impact upon cell-mediated immunity. Immunonutrition is also discussed, as are new techniques for investigating links between metabolism and immune function.

Of primary concern is the health of the athlete. Performance issues are secondary and performance will only be helped if optimum health is maintained. The ergogenic effects of many supplements are controversial and good evidence for efficacy is rare.

Growth hormone (GH) has many direct and indirect actions and roles including substrate regulation and priming of some cells of the immune system, and the expected aspects of growth and repair. Different concentrations in human body fluids reflect the exercise-induced growth hormone response (EIGR) after exercise. In populations such as elite athletes, the invasive nature of venous sampling is poorly accepted. Thus, this study examines possible viable alternatives such as urine and saliva samples and the GH concentration. A heterogeneous group of 11 males (age 26.0 ± 5.0 years; body mass 76.5 ± 9.3 kg; VO2peak 57.0 ± 6.0 mL kg−1 min−1) ran for 40 min on a treadmill at 5 % below their individually indentified lactate threshold pace. Samples of urine, saliva and blood were collected immediately pre- and post-test and at 30 and 60 min post-test. Salivary GH was correlated with serum pre- and post-exercise (p < 0.001); urinary GH was correlated with serum (p < 0.05). However, despite being significantly correlated, it is clear from the large differences in absolute concentration in the three media that the appearance of serum GH due to exercise is different from that of the appearance of salivary and urinary GH. This aspect of compartmental exchanges is very difficult to define and to investigate. Differences in any analyte concentration in different compartments are to be expected between different media, and hence the same medium should be used where the same ‘pattern of response’ can be tracked. The results suggest that urinary and saliva sampling cannot substitute for venous sampling with respect to exercise-induced changes in GH concentration. The use of the analyses in these three areas may be appropriate for further investigation.