Similarities and differences regarding acute anorexia nervosa and semi-starvation: does behavioral thermoregulation play a central role?

Objective: To clarify the association between acute anorexia nervosa (AN) and semi-starvation (SS) by focusing on similarities and differences in physiology, mood, and behavior. Method: A comparison of published literature between these two groups. Results: Both groups show similar hormonal and metabolic changes in response to caloric restriction and extreme weight loss (~25%). Associated changes result in a reduced body temperature (Tcore-low). Maintenance of body temperature within a specific range is crucial to survival. However, both groups cannot activate autonomic strategies to maintain their Tcore-low, such as increasing metabolic rate, constricting skin blood vessels, or shivering. Furthermore, Tcore-low increases the individuals' "coldness sensations" throughout the body, hence the frequent reports from ANs and SSs of "feeling cold." To eliminate these uncomfortable "coldness sensations" and, importantly, to maintain Tcore-low, ANs, and SSs "select" different thermoregulatory behavioral strategies. It is proposed that the primary differences between AN and SS, based on genetics, now manifest due to the "selection" of different thermo-regulatory behaviors. AN patients (ANs) "select" hyperactive behavior (HyAc), which increases internal metabolic heat and thus assists with maintaining Tcore-low; in harmony with hyperactive behavior is a lively mood. Also related to this elevated arousal pattern, ANs experience disrupted sleep. In contrast, SS individuals "select" a passive thermo-behavioral strategy, "shallow torpor," which includes reduced activity, resulting in energy conservation. In addition, this inactivity aids in the retention of generated metabolic heat. Corresponding to this lethargic behavior, SS individuals display a listless mood and increased sleep. Conclusion: Initial similarities between the two are attributable to physiological changes related to extreme weight loss. Differences are most likely attributable to genetically programmed "selection" of alternate thermoregulatory strategies, primarily to maintain Tcore-low. However, if acute AN is prolonged and evolves into a chronic condition, AN will more closely align with starvation and more precisely reflect SS symptomology.

The Central Role of Hypothermia and Hyperactivity in Anorexia Nervosa: A Hypothesis.

Typically, the development of anorexia nervosa (AN) is attributed to psycho-social causes. Several researchers have recently challenged this view and suggested that hypothermia and hyperactivity (HyAc) are central to AN. The following hypothesis will attempt to clarify their role in AN. Anorexia nervosa patients (ANs) have significantly lower core temperatures (Tcore) compared to healthy controls (HCs). This reduced temperature represents a reset Tcore that needs to be maintained. However, ANs cannot maintain this Tcore due primarily to a reduced basal metabolic rate (BMR); BMR usually supplies heat to sustain Tcore. Therefore, to generate the requisite heat, ANs revert to the behavioral-thermoregulatory strategy of HyAc. The majority of ANs (~89%) are reportedly HyAc. Surprisingly, engagement in HyAc is not motivated by a conscious awareness of low Tcore, but rather by the innocuous sensation of "cold- hands" frequently reported by ANs. That is, local hand-thermoreceptors signal the brain to initiate HyAc, which boosts perfusion of the hands and alters the sensation of "cold-discomfort" to one of "comfort." This "rewarding" consequence encourages repetition/habit formation. Simultaneously, hyperactivity increases the availability of heat to assist with the preservation of Tcore. Additionally, HyAc induces the synthesis of specific brain neuromodulators that suppress food intake and further promote HyAc; this outcome helps preserve low weight and perpetuates this vicious cycle. Based on this hypothesis and supported by rodent research, external heat availability should reduce the compulsion to be HyAc to thermoregulate. A reduction in HyAc should decrease the production of brain neuromodulators that suppress appetite. If verified, hopefully, this hypothesis will assist with the development of novel treatments to aid in the resolution of this intractable condition.

Differing cytokine responses by ethnic groups to a bout of exercise-induced muscle damage: a preliminary report.

BACKGROUND: Strenuous exercise has been shown to alter immune and inflammatory responses potentially predisposing athletes to infection and injury. Ethnic disparities have been demonstrated in athletic performance and in the way individuals respond to exercise as well as in the predisposition towards certain diseases however, the information relating to immune and inflammatory responses to exercise between ethnic groups is still limited. The aim of this study was to investigate whether serum cytokine levels respond differently to eccentrically-biased exercise in African and Caucasian males. METHODS: Seven black and 8 white males (18-22 years), active but untrained, participated in the study. Participants performed a 60-minute downhill run on a treadmill (gradient -13.5%) at a speed eliciting 75% of their VO2peak on a level grade. Venipunctures were performed before, immediately after and then at 3, 6, 9, 12, 24 hours, and 1, 2 and 3 weeks afterwards. The following serum cytokine concentrations were quantified using the Bio-Plex suspension array system: IL-4, IL-6, IL-10, IL-1ra, IL-12p70, IFNγ, IL-7, IL-8, MCP-1, MIP-1ß, eotaxin, IP-10, IL-1ß, TNFα, GM-CSF, G-CSF, FGF basic and VEGF. RESULTS: Significant differences between the two groups were evident from 6 hours postexercise onwards with the African runners maintaining significantly higher relative cytokine concentrations. IL-6 serum concentrations of the African runners, for example, ranged from 8% to 55.1% higher than that of the Caucasian runners from 6 hours to 2 weeks postexercise (P<0.05). CONCLUSIONS: The study demonstrated that the cytokine response to a bout of downhill running differs between African and Caucasian runners indicating that ethnicity may play a role in exercise-induced immune and inflammatory responses.

McArdle disease: another systemic low-inflammation disorder?

McArdle disease is caused by inherited deficit of human muscle glycogen phosphorylase with subsequent blockade in muscle glycogenolysis. Patients usually experience severe exercise intolerance and 'chronic' skeletal muscle damage. We determined circulating levels of 27 cytokines in a group of 31 adult McArdle patients (15 male 16 female; mean (+/-S.E.M.) age: 39+/-3 years) and 29 healthy sedentary controls (14 male, 15 female) before and after an acute exercise bout involving no muscle damage (cycling). Patients had an ongoing state of muscle breakdown even when following a sedentary lifestyle (serum creatine kinase activity at baseline of 2590+/-461 Ul(-1) vs. 97+/-5 Ul(-1) in controls). Under resting conditions, neutrophil count (+20%) and circulating levels of several cytokines were significantly higher (P

Changes in serum cytokines after repeated bouts of downhill running.

The purpose of this study was to examine changes in serum cytokines after repeated bouts of aerobically biased eccentric exercise. Six untrained males ran down a -13.5% treadmill grade for 60 min on two occasions (RUN1 and RUN2) at a speed equal to 75% of their VO2 peak on a level grade; runs were spaced 14 d apart. Serum was collected before, after, and every hour for 12 h, and every 24 h for 6 d. Cytokines were assessed using 17 multiplex bead technology (Bio-Rad). Creatine kinase (CK) and delayed-onset muscle soreness (DOMS) were assessed before and 24-120 h after. Results were analyzed using a repeated measures analysis of variance (p

Perspectives from the front lines of tobacco control.

This research is designed to share valuable experiences and transferable principles from program staff of the Legacy/Community Voices initiative who have been involved in planning, implementing, evaluating, and sustaining tobacco control activities in underserved communities. Interviews were conducted with 13 front line staff from 9 sites: Alameda County, California; Detroit, Michigan; El Paso, Texas; Ingham County, Michigan; Miami, Florida; New Mexico; North Carolina; Northern Manhattan; and West Virginia. A model emerged from these interviews that places the life cycle of a program in a central position, with many of the identified themes (working with local champions, obtaining support from multiple partners, increasing organizational capacity) repeated throughout, albeit in different forms at different stages. Reflecting upon wisdom gained and identifying best processes for such work may help ensure that tobacco control programs are developed that are culturally safe and effective in meeting the needs of diverse communities throughout the United States.

Tissue trauma: the underlying cause of overtraining syndrome?

An athlete who trains intensely, yet consistently underperforms, is considered to be suffering from overtraining syndrome (OTS). OTS is a complex state that involves a large variety of signs and symptoms. Symptoms include changes in mood or behaviour, decreases or increases in concentration of different blood molecules, and alterations in immune function. Although several hypotheses have been proposed, each only explains a selective aspect of OTS. Presently, the sole agreement is that OTS is associated with excessive training and insufficient rest and recovery. The hypothesis proposed in this paper suggests that excessive training/competing causes repetitive tissue trauma, either to muscle and/or connective tissue and/or to bony structures, and that this results in chronic inflammation. It is further proposed that traumatized tissue synthesizes a group of inflammatory molecules, cytokines. Cytokines have been shown to coordinate the different systems of the body to promote recovery. Suggestions are made to detect, prevent, and rehabilitate the overtrained athlete.

Overtraining, excessive exercise, and altered immunity: is this a T helper-1 versus T helper-2 lymphocyte response?

Overtraining syndrome (OTS) occurs where an athlete is training vigorously, yet performance deteriorates. One sign of OTS is suppressed immune function, with an increased incidence of upper respiratory tract infection (URTI). An increased incidence of URTIs is also associated with high volume/intensity training, as well as with excessive exercise (EE), such as a marathon, manifesting between 3-72 hours post-race. Presently, there is no encompassing theory to explain EE and altered immune competence. Recently, it has been conclusively established that T helper lymphocytes (T(H)), a crucial aspect of immune function, represent two distinct functional subsets: T(H)1 and T(H)2 lymphocytes. T(H)1 lymphocytes are associated with cell-mediated immunity (CMI) and the killing of intracellular pathogens, while T(H)2 lymphocytes are associated with humoral immunity and antibody production. When T(H)-precursor cells are activated, the balance is tipped in favour of one or the other. Furthermore, the most appropriate means of determining the T(H)-subset, is by the prevailing cytokine 'pattern'. This paper hypothesises that exercise-related immunosuppression is due to tissue trauma sustained during intense exercise, producing cytokines, which drive the development of a T(H)2 lymphocyte profile. A T(H)2 cell response results in simultaneous suppression of CMI, rendering the athlete susceptible to infection. Additionally, increased levels of circulating stress hormones (cortisol and catecholamines), as well as prostaglandin E(2), support up-regulation of T(H)2 lymphocytes. Marathon-related data are presented to support this hypothesis. It is concluded that an increased incidence of illness associated with OTS and in response to EE is not due to immunosuppression per se, but rather to an altered focus of immune function, with an up-regulation of humoral immunity and suppression of CMI.