Martin Hofmeister

Substances used in wine clarification as potential allergens.

Potential allergens also include proteins and substances used in the clarification of wine: fish gelatin or isinglass, protein from chicken eggs (ovalbumin), milk (casein) products, rubber arabicum, lysozyme, pectinase, cellulose, glucosidase, urease, and aroma enzymes (1). Furthermore, moulds—especially Botrytis cinerea, which is responsible for noble rot in grapes—as well as insect proteins (for example, wasp venom or bee venom), which may have contaminated the mash during the pressing process, play an allergenic part that should not be underestimated (1, 2). Triggers for allergic intolerance reactions such as headaches or migraine after ingestion of red wine may also be the phenolic flavonoids that are present in the skin of the grapes (anthocyanins and catechins), because they inhibit catechol-O-methyltransferase in the intestinal wall as well as the phenol sulfotransferase. Other non-organic ingredients, such as the ethanol metabolite acetaldehyde and acetic acid, also play a part in wine intoleranceoften in the shape of urticaria (1). The intolerance to alcohol in general that was observed by the authors is supported by a representative survey in adults in Copenhagen (4142/6000=70.7% response rate), which showed a prevalence of hypersensitivity reactions after alcohol consumption (especially red wine) of 8% (3, 4). In Bavaria, for example, all superior quality wines have to be examined by the Bavarian Health and Food Safety Agency, in order to ensure that the legally defined upper limits of sulfur dioxide are adhered to. In order to protect consumers from intolerance reactions to sulfites, this type of state controlled wine examination in addition to the official testing number on the label would also be desirable for other German states.

Account for Increased Fat Mass.

With regard to risk factors for osteoporosis, I would like to point out (1) that obesity, while having a positive effect on fractures, such as hip, pelvic and wrist fractures, is associated with an increased risk of ankle, lower leg and proximal humeral fractures in postmenopausal women (2). The pathogenic mechanisms possibly underlying this association between obesity and fracture include, among others, increased production of pro-inflammatory cytokines (interleukin-6, tumor necrosis factor alpha), insulin resistance, an increased tendency to fall, restricted muscular mobility, co-morbidities (such as asthma, diabetes mellitus, metabolic syndrome), hypogonadism, calcium malabsorption, and reduced plasma levels of 25-hydroxy-vitamin D in obese persons (2, 3). Therefore, further data analyses assessing modifiable risk factors of osteoporosis in Germany should include increased fat mass in the study population in addition to underweight.

Validated questionnaire should be used.

The decrease by almost 40% in physical inactivity in their leisure time in 70–81 year olds in Mecklenburg-Western Pomerania in the 10-year comparison is to be welcomed (1). On reading the report of this very interesting population-based study, I was not quite clear whether the data on the very complex and multidimensional behavior of habitual physical activity had been collected by using a single item question or the Baecke questionnaire (2)—as an earlier publication by the authors would lead me to believe (3). For this reason I would ask the authors to clarify this briefly. I would like to add that modified versions of Baeckes original questionnaire have shown greater test-retest reliability in older study populations. In future it would be desirable, depending on the situation and the cases, if the operationalizing instruments were to consider subjective expectations of benefit and needs in relation to physical activity more strongly.

Increased quality of life.

I like to make a small critical point to the excellent systematic review by Dipl.-Psych. Muhlig et al. (1). I cannot agree with the authors’ statement that the evidence currently available only supports short-term improvements in quality of life under conservative weight-loss treatments. As early as 2001, a research team led by Petra Warschburger conducted a randomized controlled long-term study including 197 children and adolescents that showed an increase in health-related quality of life even 12 months after an 8-week period of multimodal cognitive-behavioral treatment for obesity (2). Furthermore, the recent analysis of the German LOGIC study (Long-term effects of lifestyle Intervention and Genetic Influence in Children) demonstrated that the quality of life of overweight/obese children and adolescents remained significantly improved 2 years after the end of the treatment. “Self-esteem“ was the dimension where patients benefited the most from the program (3). I think we should make more use of volitional and awareness-based weight management strategies for obese or overweight patients, including children.

Correspondence (letter to the editor): Mediterranean Diet

Certainly, the information about non-alcoholic fatty liver disease (NAFLD) provided by the authors can only be agreed with (1). Nevertheless, I think that the “Fatty Liver Index“ (FLI), a validated non-invasive diagnostic tool, should also be mentioned as a relevant aid to decision-making in everyday clinical practice. Developed by the working group around Giorgio Bedogni in 2006, the FLI is calculated using an algorithm based on body-mass index, waist circumference, triglycerides, and gamma-glutamyl transferase. An FLI higher than 60 indicates a more than 80% likelihood of hepatic steatosis (2, 3). Implementing the easy-to-use FLI as part of a tight patient monitoring regimen could offer clinical advantages as patients with an FLI above 60 also have an increased incidence of diabetes, develop early atherosclerosis (thicker intima/media, higher plaque burden) and show an increased mortality compared with patients with low FLIs. As a nutritional scientist, I like to point out with regard to the alimentary management of the disease—which plays a critical role in NAFLD patients—that only the Mediterranean diet is supported by some potential evidence (4): plenty of vegetables, fruits, legumes, mainly complex carbohydrates with low glycemic index, fish, olive oil, dairy products, etc. and little processed food, “red meat“, sweets and sugary soft drinks would thus be the primary long-term diet for NAFLD patients.

Cortisol levels are key.

I would like to add three aspects to the most welcome review on postoperative cognitive dysfunction (POCD) by PD Dr. med. Ingrid Rundshagen (1). Because of the significant association between increased interleukin-6 and S100β protein levels and the development of POCD (2), these basic pro-inflammatory markers could be used for POCD screening in a clinical setting. Likewise, the pre-operative ratio of the Alzheimer biomarkers beta-amyloid (1–42) and tau protein in the cerebrospinal fluid (CSF) appears to be of relevant predictive value as it is associated with the incidence of POCD (3). Cortisol levels should be measured pre- and post-operatively to determine the direct pathogenic effect of stress on cognitive performance, as it has been shown that immediately after surgery, patients with POCD have significantly increased cortisol levels compared to patients without post-operative deficits (4). Future research should also explore other factors which may play a role in POCD, such as ubiquitin C-terminal hydrolase L1, body weight or the number of units of blood transfused perioperatively.

Correspondence (letter to the editor): Higher Risk of Obesity

Regarding somatic symptoms in the long-term unemployed, I wish to add from an ecotrophological perspective (1) that longer-term unemployment is also associated with a higher risk of obesity (2, 3). In the targeted health promotion for the long-term unemployed rightly proposed by Dr Herbig et al., the documented increased physical inactivity compared with people in employment should be considered (1, 3). For example, a three-month exercise intervention improved physical performance in long-term unemployed persons and lowered their blood pressure readings, percentage of body fat, backache, and depression (4). In this setting, using pedometers could be a simple but extremely effective aid in motivating long-term unemployed persons to exercise more.

Correspondence (letter to the editor): Regular Muscle Activity

In treating generalized anxiety disorder (GAD) it should not remain unmentioned (1) that individually tailored endurance and strength training as a firm component of the overall treatment plan should be implemented increasingly, including in the outpatient setting (2). Regular muscle exercise has an anxiolytic effect in the acute and chronic settings. Movement related neurobiological adaptation processes seem to have a key part in this, including the increased expression of brain derived neurotrophic factor, vascular endothelial growth factor, insulin-like growth factor 1, sxxx-endorphin, atrial natriuretic peptide, and serotonin, as do psychological factors such as self-efficacy and exposure (3). Patients with GAD are very likely to benefit even from simple, whole-body exercises, such as rising from a chair and sitting back down again, without using their arms to support them (10–15 repetitions, twice a day).

Correspondence (letter to the editor): To be interpreted with caution.

I welcome the survey on health and lifestyle in north-eastern Germany, over a lengthy period of time, which Elkeles and colleagues reported. I wish to add two aspects (1). The more than fourfold increase of the population exercising actively to a total of 56.3% in 2008 compared with 1994 should be interpreted cautiously or put into perspective. Studies that specify criteria about exercise behavior to a measure from which health effects can be expected have shown poignantly lower rates. This means that a classification of physical activity and exercise on the basis of energy consumption can be classed as more meaningful than individual information about exercise activity (2). Furthermore, from the perspective of ecotrophology, the reduction in the proportion of people with enough time to eat and consume their main meal that was observed over the study period may be partly responsible for the slight increase in the prevalence of obesity, since significant evidence exists for the association of a high eating speed and the development of overweight for children as well as adults (3).

Cognitive conscious stimuli with movement.

Etgen et al. explicitly point out that mild cognitive impairment and dementia can be modified by protectively by physical activity (1). This again reinforces old, timeless sayings such as that from the German physician Friedrich Hoffmann (1660–1742): “Physical exercise surpasses all drugs and is the universal medicine.”Neurobiological adaptations to motion include increased cerebral blood flow, new formation of spine, nerve cells, and capillaries, and synapsis hypertrophy, as well as increased gene expression of neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), insulin-like growth factor 1 (IGF-1), and nerve growth factor (NGF); these responses play key roles in structural and functional brain changes (2). It appears that people with mild to moderate dementia can benefit from a progressive strength, balance, and functional exercise training several times a week, especially if this is combined with an individual dual-task training (3). Finally, I would like to point out that there is a negative association between the well-validated “five-times-sit-to-stand test” and global cognitive performance. Using this simple stand-up muscle test in general practices as a screening tool for cognitive impairment would be desirable (4).