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PubMed1993

[Panic disorder and alcoholism: effects of comorbidity].

Both epidemiological and clinical studies have demonstrated a high prevalence of panic disorder among alcoholic patients. In contrast, little attention has been given to studying alcohol abuse and/or dependence in patients suffering from panic disorder. One hundred and fifty-five consecutive referrals for treatment for panic disorder were interviewed using a modified version of the Schedule for Affective Disorders and Schizophrenia--Lifetime Version, modified for the study of anxiety disorders. Thirty-two patients (20.7%) had a lifetime history of alcohol abuse and/or dependence. Although the lifetime comorbidity rate of either agoraphobia and/or social phobia seems without any influence on the risk of alcohol-related disorder, alcoholic patients suffering from panic disorder appear to be more likely to have a history of depression and other addictive disorders. The majority of patients with primary alcoholism were male, and those who became alcoholics after they developed panic disorder were more likely to be female. The comparison between patients with primary and secondary alcoholism did not indicate any difference in the comorbidity rate with other psychiatric disorders nor the severity of panic disorder.

Adult↗
PubMed2006

Neuroprotective and disease-modifying effects of the ketogenic diet.

The ketogenic diet has been in clinical use for over 80 years, primarily for the symptomatic treatment of epilepsy. A recent clinical study has raised the possibility that exposure to the ketogenic diet may confer long-lasting therapeutic benefits for patients with epilepsy. Moreover, there is evidence from uncontrolled clinical trials and studies in animal models that the ketogenic diet can provide symptomatic and disease-modifying activity in a broad range of neurodegenerative disorders including Alzheimer's disease and Parkinson's disease, and may also be protective in traumatic brain injury and stroke. These observations are supported by studies in animal models and isolated cells that show that ketone bodies, especially beta-hydroxybutyrate, confer neuroprotection against diverse types of cellular injury. This review summarizes the experimental, epidemiological and clinical evidence indicating that the ketogenic diet could have beneficial effects in a broad range of brain disorders characterized by the death of neurons. Although the mechanisms are not yet well defined, it is plausible that neuroprotection results from enhanced neuronal energy reserves, which improve the ability of neurons to resist metabolic challenges, and possibly through other actions including antioxidant and anti-inflammatory effects. As the underlying mechanisms become better understood, it will be possible to develop alternative strategies that produce similar or even improved therapeutic effects without the need for exposure to an unpalatable and unhealthy, high-fat diet.

Alzheimer Disease↗
PubMed1992

[Physical activity and blood pressure. An epidemiological brief review of primary preventive effects of physical exercise activities].

The relation between physical exercise and blood pressure as well as the risk of hypertension has been investigated extensively during recent years. Cross-sectional studies on exercising and physically fit subjects have shown that endurance capacity (i. e. maximum aerobic capacity) is inversely related to resting blood pressure. However, not all physical activities are associated with lower blood pressure levels; e.g. swimming, weight lifting and competitive cross-country skiing were found to be related to elevated blood pressure values in some studies. Population-based investigations reveal a trend towards lower blood pressure values in physically habitually active persons, with the difference between active and inactive subjects not exceeding 5 mmHg. Three epidemiological cohort studies have consistently demonstrated that sedentary, unfit persons have a 20 to 50% higher prospective risk of hypertension, as compared to exercising, physically fit persons. Some intervention studies with normotensive subjects show a reduction in resting blood pressure of 5 to 10 mmHg at best after several months of aerobic training, while other studies show no effect. At least two factors could be responsible for these somewhat inconsistent observations: 1. exercise intensity may act as an 'effect modifier', since vigorous to maximally hard exercise rather increases than lowers resting blood pressure, 2. in statistical analysis on the effect of physical training on blood pressure, it is crucial whether concomitant changes in body weight and body composition are taken into account: any adjustment for changes in body composition will substantially reduce the magnitude of 'exercise-induced' reductions in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed2005

Biomonitoring of inhaled complex mixtures--ambient air, diesel exhaust and cigarette smoke.

Human biomonitoring comprises the determination of biomarkers in body-fluids, cells and tissues. Biomarkers are generally assigned to one of three classes, namely, biomarkers of exposure, effect or susceptibility. Since biomarkers represent steps in an exposure-disease continuum, their application in epidemiological studies ('molecular epidemiology') shows promise. However, to be a predictor of disease, a biomarker has to be validated. Validation criteria for a biomarker include intrinsic qualities such as specificity, sensitivity, knowledge of background in the population, existence of dose-response relationships, degree of inter- and intra-individual variability, knowledge of the kinetics, confounding and modifying factors. In addition, properties of the sampling and analytical procedures are of relevance, including constraints and non-invasiveness of sampling, stability of sample as well as simplicity, high sensitivity, specificity and speed of the analytical method. It is of particular importance to prove by suitable studies that the biomarker of exposure indicates the actual exposure, the biomarker of effect strongly predicts the actual risk of disease and the biomarker of susceptibility actually modifies the risk. Biomonitoring of the exposure to complex mixtures such as polluted ambient air, diesel exhaust or tobacco smoke is a particular challenge since these exposures have many constituents in common and many people were exposed to more than one of these mixtures. Data on the exposure to polycyclic aromatic hydrocarbons (PAH) and benzene from ambient air, diesel exhaust and tobacco smoke will be presented. In addition, some source-specific biomarkers such as nitro-arenes and nicotine metabolites as well as their application in population groups will be discussed. The second part of the presentation addresses the application of biomarkers for assessing so called 'potentially reduced exposure products' (PREPs). According to a recent report of the Institute of Medicine (USA), "reducing risk of disease by reducing exposure to tobacco toxicants is feasible" and "surrogate biological markers that are associated with tobacco-related diseases could be used to offer guidance as to whether or not PREPs are likely to be risk-reducing." In general, the same validation criteria apply as discussed above. In addition, it is suggested that a panel of biomarkers should be used, representing both smoke phases (gas and particulate phase) and the various chemical classes of smoke constituents (e.g., carbonyls, benzene, PAH, tobacco-specific nitrosamines, aromatic amines). Also, a panel of biomarkers of effect should cover the major known adverse effects of smoking (e.g., oxidative stress, inflammatory processes, lipid peroxidation, lipometabolic disorders, mutagenic effects). Biomarkers of nicotine and carbon monoxide uptake are of interest for evaluating the smoking and inhalation behavior, respectively. Finally, suitable study designs for evaluating PREPs are discussed. It is concluded that suitable biomarkers for assessing the exposure to complex mixtures such as ambient air, diesel exhaust and tobacco smoke as well as for evaluating the exposure-reducing properties of PREPs are already available. Future efforts should focus on the development and validation of biomarkers of effect.

Air↗
PubMed1985

Epidemiology, risk factors, and pathophysiology of ischemic heart disease.

Epidemiological studies have identified several risk factors that increase the likelihood of developing ischemic heart disease (IHD). Many of these factors, including hypertension, smoking, elevated blood fats, sedentary life style, and Type A personality, are related to life-style habits and, therefore, are modifiable. Studies indicate that the major risk factors directly influence the basic mechanisms of atherogenesis. Evidence from the primary and secondary prevention trials shows that reducing the risk factors decreases the likelihood of coronary disease progression and coronary morbidity and mortality. Therapeutic exercise programs for primary or secondary prevention clients can lead to significant risk-factor reduction. For therapists to design such programs safely and effectively, they must 1) be knowledgeable in the epidemiology, risk factors, and pathophysiology of IHD and 2) be able to relate this knowledge to a given client.

Adult↗
PubMedDate not supplied

The impact of terrorism on children: a two-year experience.

OBJECTIVES: To review and analyze the cumulative two-year, Israeli experience with medical care for children victims of terrorism during the prehospital and hospital phases. METHODS: Data were collected from the: (1) Magen David Adom National Emergency Medical System Registry (prehospital phase); (2) medical records from the authors' institutions (pediatric triage); and (3) Israel Trauma Registry (injury characteristics and utilization of in-hospital resources). Statistical analyses were performed as appropriate. INTRODUCTION: During the recent wave of violence in Israel and the surrounding region, hundreds of children have been exposed to and injured by terrorist attacks. There is a paucity of data on the epidemiology and management of terror-related trauma in the pediatric population and its effects on the healthcare system. This study focuses on four aspects of terrorism-related injuries: (1) tending to victims in the prehospital phase; (2) triage, with a description of a modified, pediatric triage algorithm; (3) characteristics of trauma-related injuries in children; and (4) utilization of in-hospital resources. RESULTS: During the study period, 41 mass-casualty events (MCEs) were managed by Magen David Adom. Each event involved on average, 32 regular and nine mobile intensive care unit ambulances with 93 medics, 19 paramedics, and four physicians. Evacuation time was 5-10 minutes in urban areas and 15-20 minutes in rural areas. In most cases, victims were evacuated to multiple facilities. To improve efficiency and speed, the Magen David Adom introduced the use of well-trained "first-responders" and volunteer, off-duty professionals, in addition to "scoop and run" on-the-scene management. Because of differences in physiology and response between children and adults, a pediatric triage algorithm was developed using four categories instead of the usual three. Analysis of the injuries sustained by the 160 children hospitalized after these events indicates that most were caused by blasts and penetration by foreign objects. Sixty-five percent of the children had multiple injuries, and the proportion of critical to fatal injuries was high (18%). Compared to children with non-terrorism-related injuries, the terrorism-related group had a higher rate of surgical interventions, longer hospital stays, and greater needs for rehabilitation services. CONCLUSION: Terrorism-related injuries in children are severe and increase the demand for acute care. The modifications in the management of pediatric casualties from terrorism in Israel may contribute to the level of preparedness of medical and paramedical personnel to cope with future events. Further studies of other aspects of traumatic injuries, such as its short- and long-term psychological consequences, will provide a more comprehensive picture of the damage inflicted on children by acts of terrorism.

Algorithms↗
PubMed2005

Gene-environment interactions in human diseases.

Studies of gene-environment interactions aim to describe how genetic and environmental factors jointly influence the risk of developing a human disease. Gene-environment interactions can be described by using several models, which take into account the various ways in which genetic effects can be modified by environmental exposures, the number of levels of these exposures and the model on which the genetic effects are based. Choice of study design, sample size and genotyping technology influence the analysis and interpretation of observed gene-environment interactions. Current systems for reporting epidemiological studies make it difficult to assess whether the observed interactions are reproducible, so suggestions are made for improvements in this area.

Environment↗
PubMed1991

Implications for cancer epidemiology of differences in dietary intake associated with alcohol consumption.

Several dietary factors are thought to modify risk for cancers that are known to be associated with alcohol intake. In this study, we sought to identify and describe alcohol-related differences in dietary and nutritional factors that are potential independent predictors of cancer risk or effect modifiers or confounders of alcohol-cancer relationships. Data were obtained from a large hospital-based case-control study that was designed to estimate the cancer risk from various tobacco products. Study subjects consisted of 465 male and 300 female incident lung cancer cases and 870 male and 556 female hospitalized patient controls matched on age (+/- 5 yrs). Nutritional data were analyzed as log-transformed frequencies of 30 food items, 9 factor scores generated to describe overall patterns of dietary intake, and nutrient scores estimating daily intake of fat, vitamin A, fiber, and cholesterol. We observed many more significant differences in nutritional exposures by alcoholic beverage intake than would be expected merely by chance. For males, the most striking relationships included increased meat and egg consumption with increasing alcohol consumption and higher intake of cantaloupe and cold cereal among lighter drinkers. For females, we observed strong inverse relationships between alcohol consumption and reported intake of fruit, cold cereal, and ice cream. We also observed a direct association between alcohol and meat consumption, though it was weaker than that found among men. Findings based on factors and nutrients followed the pattern observed for the individual food items, with highest fat scores and lowest fruit scores among the heaviest drinkers. Implications for nutrient-alcohol interactions and statistical considerations are discussed.

Alcohol Drinking↗
PubMed1999

Using pooled exposure assessment to improve efficiency in case-control studies.

Assays can be so expensive that interesting hypotheses become impractical to study epidemiologically. One need not, however, perform an assay for everyone providing a biological specimen. We propose pooling equal-volume aliquots from randomly grouped sets of cases and randomly grouped sets of controls, and then assaying the smaller number of pooled samples. If an effect modifier is of concern, the pooling can be done within strata defined by that variable. For covariates assessed on individuals (e.g., questionnaire data), set-based counterparts are calculated by adding the values for the individuals in each set. The pooling set then becomes the unit of statistical analysis. We show that, with appropriate specification of a set-based logistic model, standard software yields a valid estimated exposure odds ratio, provided the multiplicative formulation is correct. Pooling minimizes the depletion of irreplaceable biological specimens and can enable additional exposures to be studied economically. Statistical power suffers very little compared with the usual, individual-based analysis. In settings where high assay costs constrain the number of people an investigator can afford to study, specimen pooling can make it possible to study more people and hence improve the study's statistical power with no increase in cost.

Animals↗
PubMed2006

Genetic predictors of acute toxicities related to radiation therapy following lumpectomy for breast cancer: a case-series study.

INTRODUCTION: The cytotoxic effects of radiation therapy are mediated primarily through increased formation of hydroxyl radicals and reactive oxygen species, which can damage cells, proteins and DNA; the glutathione S-transferases (GSTs) function to protect against oxidative stress. We hypothesized that polymorphisms encoding reduced or absent activity in the GSTs might result in greater risk for radiation-associated toxicity. METHODS: Women receiving therapy in radiation units in Germany following lumpectomy for breast cancer (1998-2001) provided a blood sample and completed an epidemiological questionnaire (n = 446). Genotypes were determined using Sequonom MALDI-TOF (GSTA1, GSTP1) and Masscode (GSTM1, GSTT1). Biologically effective radiotherapy dose (BED) was calculated, accounting for differences in fractionation and overall treatment time. Side effects considered were grade 2c and above, as classified using the modified Common Toxicity Criteria. Predictors of toxicity were modelled using Cox regression models in relation to BED, with adjustment for treating clinic, photon field, beam energy and boost method, and potential confounding variables. RESULTS: Low activity GSTP1 genotypes were associated with a greater than twofold increase in risk for acute skin toxicities (adjusted hazard ratio 2.28, 95% confidence interval 1.04-4.99). No associations were noted for the other GST genotypes. CONCLUSION: These data indicate that GSTP1 plays an important role in protecting normal cells from damage associated with radiation therapy. Studies examining the effects of GSTP1 polymorphisms on toxicity, recurrence and survival will further inform individualized therapeutics based on genotypes.

Adult↗
PubMed2006

Treating asthma in the older patient: is there a place for leukotriene modifiers?

Asthma is a common airway disease found in people of all ages, although most studies of asthma therapies are focused on adolescent and young adults. Little information exists on the use of asthma therapeutics in the older patient (>65 years of age). The newest therapeutic class to be released in the US for the treatment of asthma is the leukotriene modifiers. These medications (either receptor antagonists or enzyme inhibitors) have been found to be beneficial in younger patients with asthma, but their potential role in older patients is less clear. In this review, the data regarding the use of these medications in older patients are examined, as are the epidemiological and pathophysiological issues regarding asthma in this growing patient population. On the basis of the two published reports of leukotriene modifiers in the older patient, we conclude that leukotriene modifiers are useful in this population, but like other controller therapies for asthma, they are less effective in the older population.

Aged↗
PubMed2006

Genetic polymorphism of xenobiotic metabolising enzymes, diet and cancer susceptibility.

There is increasing evidence identifying the crucial role of numerous dietary components in modifying the process of carcinogenesis. The varied effects exerted by nutrient and non-nutrient dietary compounds on human health and cancer risk are one of the new challenges for nutritional sciences. In the present paper, an attempt is made to review the most recent epidemiological data on interactions between dietary factors and metabolic gene variants in terms of cancer risk. The majority of case-control studies indicate the significant relationship between cancer risk and polymorphic xenobiotic metabolising enzymes in relation to dietary components. The risk of colorectal cancer is associated not only with CYP2E1 high-activity alleles, but also GSTA1 low-activity alleles, among consumers of red or processed meat. Genetic polymorphisms of NAT1 and NAT2 may be also a breast-cancer susceptibility factor among postmenopausal women with a high intake of well-done meat. On the other hand, phytochemicals, especially isothiocyanates, have a protective effect against colorectal and lung cancers in individuals lacking GST genes. Moreover, polymorphism of GSTM1 seems to be involved in the dietary regulation of DNA damage. The European Prospective Investigation into Cancer and Nutrition study shows a significant inverse association between the polycyclic aromatic hydrocarbon-DNA adduct level and dietary antioxidants only among GSTM1-null individuals. However, the absence of a modulatory effect of polymorphic xenobiotic metabolising enzymes and diet on the development of cancer has been indicated by some epidemiological investigations. Studies of interactions between nutrients and genes may have great potential for exploring mechanisms, identifying susceptible populations/individuals and making practical use of study results to develop preventive strategies beneficial to human health.

Acyltransferases↗
PubMedDate not supplied

[The physiology and physiopathology of the venous system in the obese].

The question of knowing to what extent varices occur more frequently in obese, rather than in non-obese, patients is answered variously in the epidemiological studies carried out. But if pathological venous conditions originate in, or are aggravated by, obesity, the question is raised: to what extent is the venous circulation modified by obesity? The authors discuss the factors at play in venous circulation in the obese patient. The effect of super alimentation on the venous system is demonstrated in the autopsy statistics on the occurrence of fatal pulmonary embolism, compared with the general nutrition index.

Humans↗
PubMed1994

Censored survival models for genetic epidemiology: a Gibbs sampling approach.

Methods are proposed for the analysis of diseases with variable age at onset. The Cox proportional hazards model, widely used for epidemiologic analysis, is modified to include both measured (environmental) covariates and latent (genetic) variables, as well as their interactions. A Monte Carlo technique known as Gibbs sampling is utilized to generate observations from the posterior distributions of all model parameters. A correction to account for single ascertainment of pedigrees is also described. Simulation studies show that parameter estimation is nearly unbiased for a wide variety of models, and that moderate gene-environment interaction effects can be detected.

Age of Onset↗
PubMed1986

Current hypotheses on the etiology of colorectal cancer. Critical review of the epidemiological evidence.

The epidemiological evidence supporting hypotheses concerning colorectal carcinogenesis presents conflicting findings. Even the detrimental role of high fat intake and the protective effect of fibre have to be qualified. In order to improve knowledge on the etiopathogenesis of colorectal cancer, more attention should be directed to the modifiers of the action of carcinogenic or anticarcinogenic substances. Sex, age, hormonal and metabolic status should be precisely accounted for, as should the exact anatomical subsite of the cancer.

Adult↗
PubMed2004

ApoAI deficiency results in marked reductions in plasma cholesterol but no alterations in amyloid-beta pathology in a mouse model of Alzheimer's disease-like cerebral amyloidosis.

Epidemiological studies suggest links between cholesterol metabolism and Alzheimer's disease (AD), with hypercholesterolemia associated with increased AD risk, and use of cholesterol-lowering drugs associated with decreased risk. Animal models using cholesterol-modifying dietary or pharmacological interventions demonstrate similar findings. Proposed mechanisms include effects of cholesterol on the metabolism of amyloid-beta (Abeta), the protein that deposits in AD brain. To investigate the effect of genetic alterations in plasma cholesterol on Abeta pathology, we crossed the PDAPP transgenic mouse model of AD-like cerebral amyloidosis to apolipoprotein AI-null mice that have markedly reduced plasma cholesterol levels due to a virtual absence of high density lipoproteins, the primary lipoprotein in mice. Interestingly and in contrast to models using non-physiological high fat diets or cholesterol-lowering drugs to modify plasma cholesterol, we observed no differences in Abeta pathology in PDAPP mice of the various apoAI genotypes despite robust differences in plasma cholesterol levels between the groups. Absence of apoAI also resulted in reductions in brain but not cerebrospinal fluid cholesterol, but had no effect on brain apolipoprotein E levels. These and other data suggest that it is perhaps the level of brain apolipoprotein E, not cholesterol per se, that plays a primary role in brain Abeta metabolism.

Alzheimer Disease↗
PubMed1996

Destruction of tocopherols, carotenoids, and retinol in human plasma by cigarette smoke.

The mechanisms by which exposure to cigarette smoke dramatically increase the incidence and severity of atherosclerosis and the incidence of lung cancer, chronic obstructive airways disease, and emphysema are incompletely understood. Epidemiologic evidence has suggested a modifying role for antioxidant micronutrients, including tocopherols and carotenoids, in these disease processes. It has been suggested that oxidants in cigarette smoke could be involved. We exposed freshly obtained human plasma to the gas phase of cigarette smoke to assess its effects on tocopherols, carotenoids, and retinol. Exposure to cigarette smoke led to the depletion of most of the lipophilic antioxidants in 20 mL human plasma. The order of disappearance was lycopene > alpha-tocopherol > trans-beta-carotene++ > (lutein + zeaxanthin) = cryptoxanthin > gamma-tocopherol = retinol. However, despite a substantial loss of alpha-tocopherol, there was very little peroxidative damage to lipids, and no detectable change in the content of polyunsaturated fatty acid-rich cholesterol esters. We conclude that a wide spectrum of lipophilic micronutrients undergo degradation when exposed to gas-phase cigarette smoke. The relevance of these in vitro findings to possible cigarette smoke-induced depletions of respiratory tract lipophilic antioxidants remains to be clarified.

Adult↗
PubMed2005

Systematic review of studies of productivity loss due to rheumatoid arthritis.

BACKGROUND: Rheumatoid arthritis (RA) is a chronic, debilitating disease with a significant impact on workplace productivity. AIM: To perform a systematic review of studies of the relationship between RA and reduced workplace productivity. METHODS: Screening of 307 titles identified in bibliographic database searches resulted in 38 articles subject to systematic review. Productivity loss was expressed by three different measures: work disability, work loss (synonymous with absenteeism or short-term sick leave) and work limitation (reduction in productivity while present at work). RESULTS: A median of 66% (range 36-84%) of employed RA subjects experienced work loss due to RA in the previous 12 months, for a median duration of 39 days (range 7-84 days). The times from RA diagnosis until a 50% probability of being work disabled varied from 4.5 to 22 years. In inception cohort studies, the baseline variables consistently predictive of subsequent work disability were a physically demanding work type, more severe RA and older age. CONCLUSIONS: RA-related work-disability rates were similar in the USA and European countries. An apparent decrease in the prevalence of RA-related work disability since the 1970s may be related to a decrease in physically demanding work rather than to epidemiologic changes in RA. The majority of the literature addresses permanent disability and temporary work loss; none of the studies reviewed reported the effect of RA on presenteeism, i.e. work limitation from the employer perspective, and there are few published studies of the effectiveness of disease-modifying anti-rheumatic drugs in reducing work-related productivity loss.

Absenteeism↗