Overindulgence In Alcohol Research Articles

The importance of behavioural insights in disease prevention and health promotion

Abstract Issue/problem The need for behavioural insights in disease prevention and health promotion could hardly be over-emphasised. Health behaviours constitute the foundation of good physical and mental health. It is well-know that people acquire a chronic disease because of a poor quality diet, physical inactivity, overindulgence in alcohol and tobacco use, but also because of non-adherence to the treatment regimen and adverse psychosocial influences such as negative affect, depression, or loneliness. Description of the problem Yet, how can we explain the chasm between knowledge about health determinants and action? Why we are not able to close the gap between what we know and what we put into practice to improve people's health? Maybe part of the answer is that we should break the silos and apply knowledge and expertise from also other fields and disciplines; and based on the synergistic use of knowledge from multiple sources to obtain new useful knowledge elements. Results One of the most promising knowledge fusions lie in behavioural insights that combine lessons from behavioural economics, psychology, neuroscience, and social science with empirically-tested results to provide a better understanding of how people behave and make decisions. The opportunities that behavioural insights may offer to fight chronic diseases have recently been acknowledged by several leading public health institutions and organisations. For instance, ‘Healthier choices: Incorporating behavioural insights' is one of the four flagship initiatives of the WHO's European Programme of Work 2020-2025. Lessons The potential benefits of behavioural insights are multiple as they are often very low cost, scalable, and light touch. This is especially relevant within the context of overstretched healthcare systems. What is needed is capacity building in order to broaden our understanding of measures that have originated from behavioural sciences and have a lot to offer to public health.

Diet Quality is Lower and Energy Intake Greater on Weekends than Weekdays: A One‐Year Longitudinal Study of Midlife Women

ObjectiveTo test differences in dietary intake by individual day and on weekends (Friday, Saturday, Sunday) compared to weekdays using energy and macronutrient intake, food groupings and Healthy Eating Index‐2010 diet quality scores.MethodsLongitudinal design; 52 women ages 40–60 y completed online diet recalls approximately every 10 days for one year using the Automated Self‐administered 24‐hour Recall system. Energy (kcal), macronutrient (%en) and food group portions were derived. Healthy Eating Index‐2010 (HEI‐2010) total and component scores were calculated. Differences were tested by mixed model analysis of variance.ResultsWomen completed a total of 1,866 diet recalls. Reported energy intake was greater on weekends than on weekdays (1990 ± 62 kcal vs 1832 ± 53 kcal; P<0.001). Reported %en from protein and carbohydrate was lower and %en from alcohol greater on weekends. There was no difference in the % energy from fat (34.3 ± 0.7 vs 33.4 ± 0.6, respectively; P = 0.07). On weekends, women reported consuming more alcohol, added sugar, fats and oils, eggs, potatoes, meats, and refined grains and less yogurt, whole fruits, orange vegetables, and whole grains than on weekdays. The total HEI‐2010 score was lower on weekends than weekdays (58.5 ± 1.5 vs 62.0 ± 1.4; P <0.001). Component scores were lower for Whole Fruits (P = 0.003), Greens and Beans (P = 0.017), Whole Grains (P = 0.002), and Dairy (P = 0.003). Energy intake was greatest on Saturday (2061 ± 78 kcal) and lowest on Tuesday (1756 ± 52 kcal). The %en from carbohydrate was greatest on weekdays and lowest on Friday. The %en from protein was lowest on Saturday. The %en consumed as alcohol was significantly greater on Friday and Saturday than all other days of the week.ConclusionsIn this population, weekend eating was associated with lower diet quality scores and different dietary patterns than weekdays. Maintaining weekday intakes of yogurt, whole fruits, orange vegetables and whole grains would be beneficial. Avoiding weekend overindulgence in alcohol, added sugars, and fats may help individuals maintain a healthy weight while consuming a variety of nutrient‐rich foods.Support or Funding InformationUSDA‐ARS 3062‐51000‐051‐00D.

Potentiated clinoptilolite reduces signs and symptoms associated with veisalgia.

IntroductionAbundant anecdotal evidence for products claiming to reduce veisalgia after alcohol overindulgence are available on the Internet and as many advertisements in journals. None of these claims are, however, substantiated by research. The aim of this research was to ascertain the validity of such claims for the substance Absorbatox™, a potentiated aluminosilicate (cation exchanger able to bind NH4+, histamine, and other positively charged ions) by investigating the signs and symptoms, as well as blood or breath alcohol levels, in healthy volunteers.MethodsBlood or breath alcohol levels were measured in all volunteers in initial controlled experiments, and symptoms were scored on a diary card for gastrointestinal tract symptoms, as well as other symptoms such as headache and light sensitivity. Eighteen volunteers completed the initial blood alcohol study, which investigated the effect of Absorbatox™ on blood alcohol levels after fasting. The follow-up studies researched the effects of the symptoms and signs of alcohol overindulgence. The “night out” study was completed by ten volunteers in a typical controlled environment, which was followed by the real-life four-leg crossover study. In the crossover study, volunteers (number =25 completers) had to fill matching diary cards to containers of two placebo and two active drugs after a night out where they themselves decided on the container (color coded) to be used and the amount of alcohol to be consumed.ResultsAbsorbatox™ had no effect on blood alcohol levels, but it significantly reduced the symptoms and signs of veisalgia by approximately 40%–50%.ConclusionThis research indicates that Absorbatox™ does not have an effect on blood- or breath-alcohol levels. Furthermore, treatment with Absorbatox™ resulted in an overall significant reduction in central nervous system and gastrointestinal tract symptoms associated with veisalgia, warranting further investigation.

Ethanol induced impairment of glucose metabolism involves alterations of GABAergic signaling in pancreatic β-cells.

Alcohol overindulgence is a risk factor of type 2 diabetes mellitus. However, the mechanisms by which alcohol overindulgence damages glucose metabolism remain unclear. Pancreatic islet β-cells are endowed with type-A γ-aminobutyric acid receptor (GABAAR) mediated autocrine signaling mechanism, which regulates insulin secretion and fine-tunes glucose metabolism. In neurons GABAAR is one of the major targets for alcohol. This study investigated whether ethanol alters glucose metabolism by affecting GABAAR signaling in pancreatic β-cells. Blood glucose level of test mice was measured using a blood glucose meter. Insulin secretion by the pancreatic β-cell line INS-1 cells was examined using a specific insulin ELISA kit. Whole-cell patch-clamp recording was used to evaluate GABA-elicited current in INS-1 cells. Western blot and immunostaining were used to measure the expression of GABAAR subunits in mouse pancreatic tissues or in INS-1 cells. Intraperitoneal (i.p.) administration of ethanol (3.0g/kg body weight) to mice altered glucose metabolism, which was associated with decreased expression of GABAAR α1- and δ- subunits on the surface of pancreatic β-cells. Acute treatment of cultured INS-1cells with ethanol (60mM) decreased the GABA-induced current and reduced insulin secretion. In contrast, treating INS-1 cells with GABA (100μM) largely prevented the ethanol-induced reduction of insulin release. Importantly, pre-treating mice with GABA (i.p., 1.5mg/kg body weight) partially reversed ethanol-induced impairment of glucose homeostasis in mice. Our data suggest a novel role of pancreatic GABA signaling in protecting pancreatic islet β-cells from ethanol-induced dysfunction.

The Prevalence of Cationic Trypsinogen (PRSS1) and Serine Protease Inhibitor, Kazal Type 1 (SPINK1) Gene Mutations in Polish Patients with Alcoholic and Idiopathic Chronic Pancreatitis

BackgroundThe main cause of chronic pancreatitis (CP) is excessive alcohol consumption. On the other hand, only 5–10% of heavy drinkers develop chronic pancreatitis. We have only limited information regarding the pathogenic mechanism by which alcohol leads to the disease. Mutations of the PRSS1 and SPINK 1 have been mostly implicated in hereditary and idiopathic CP, but their presence in other types of this disease have also been reported.AimsThe aim of the study was to determine the frequency of PRSS1 and SPINK1 mutations in patients with chronic alcoholic (ACP) and idiopathic pancreatitis (ICP) as well as to investigate their relation to the clinical course of the disease.MethodsThe study included 33 ACP and 14 ICP patients as well 46 healthy subjects. The diagnosis of CP was based on clinical data, ultrasound, and computed tomography. After isolation of DNA from peripheral blood two trypsinogen mutations were detected N29I and R122H by allelo-specific amplification polymerase chain reaction (ASA-PCR) and by the PCR-restriction fragment length polymorphism (RFLP). Beside this N34S mutation of SPINK1 was analyzed by PCR restriction fragment length polymorphism (PCR-RFLP).ResultsPRSS1 mutations have been detected in 11 (33%) patients with ACP. The frequency of the PRSS1 mutations was higher in patients with ACP than in controls (4.3%) (p < 0.001). The frequency of PRSS1 mutation was present in 21.4% of ICP patients, which was significantly higher (p < 0.05) than in controls. Overall, six (18%) SPINK1 mutations in ACP group have been detected. Among 14 patients with ICP, in four (28.6%) of them SPINK1 has been detected. The same mutations have also been found in three (6.5%) control subjects. The frequency of the N34S mutation was higher in patients with ICP than in the controls (p < 0.05), but the frequency of N34S mutation did not differ between ACP and the control group. No relations have been detected between PRSS1 and SPINK1 mutations presence and clinical course and complications of CP.ConclusionsThose preliminary data suggest the high prevalence of SPINK1 and PRSS1 mutations in the Polish population, generally, as well as in CP patients. It may be speculated that those mutations contribute to the development of chronic pancreatitis, especially in patients with alcohol overindulgence.

Ask the Expert: Exploring the Clinician's Concern About Unreported Abuse of Alcohol

Ask the Expert: Exploring the Clinician's Concern About Unreported Abuse of Alcohol

FREQUENCY OF CATIONIC TRYPSINOGEN (PRSS1) GENE AND THE SERINE PROTEASE INHIBITOR, KAZAL TYPE 1 (SPINK1) GENE MUTATIONS IN PATIENTS WITH CHRONIC ALCOHOLIC PANCREATITIS (CAP)

Background: We have only limited information regarding the pathogenic mechanism by which alcohol leads to CAP. Aims & Methods: The aim of the study was to determine the frequency of PRSS1 and SPINK1 mutations in patients with chronic alcoholic pancreatitis (CAP) as well as to investigate their relation to the clinical course of the disease. The study included 37 patients with CAP and 46 healthy subjects. After isolated DNA from peripheral blood two trypsinogen mutations N29I and R122H have been detected and N34S mutation of SPINK1 (by ASA-PCR and PCR-RFLP). Results: Overall 9 (24.5%) N34S SPINK1 mutations in CAP group have been detected. The same mutations have also been found in 3 (6.5%) control subjects. N29I mutations of PRSS1 have been detected in 5 (13.5%) patients with CAP and only in those with accompanying SPINK1 mutations. R122H mutations of PRSS1 have been detected in 8 (21.6%) patients with CAP. Both mutations of PRSS1 concerned in 2 (4.3%) controls. In patients with CAP and the presence of SPINK1 mutations, pancreatic calcifications have been detected significantly less frequently (p < 0.05) that in patients with no mutations. In addition complications requiring endoscopic or surgical treatment (p < 0.01) have been also less frequently noted in CAP with detected mutations compared with the remaining CAP group. Compared to the remaining patients with CAP, diabetes was seen significantly more frequent in patients with R122H mutation. Conclusion: Those data suggest the high incidence of SPINK1 and PRSS1 mutations in Polish population generally, as well as in CAP patients. It may be speculated that those mutations contribute to the development of chronic pancreatitis in patients with alcohol overindulgence. On the other hand the clinical course of CAP seems to be more severe in patients with no SPINK1 mutations detected.

Preventing alcohol misuse: The impact of refusal skills and norms.

The purpose of this study was to determine the extent to which refusal skills and norm setting mediated the impact of a school-based prevention program from the Alcohol Misuse Prevention Study (AMPS) on adolescent alcohol overindulgence. The AMPS is a randomized, pre-post, experimental-control study. Respondents in the present study included 6th through 10th graders (ns ranged from 232 to 371). Structural equation modeling analyses using EQS indicated that norm setting mediated the effect of the intervention on alcohol overindulgence at the 7th through the 8th grade and at the 8th through the 10th grade. In contrast, although the prevention program served to increase refusal skills, refusal skills did not mediate the effect of the program on alcohol misuse.

CARDIOVASCULAR RISK FACTOR CLUSTERING AND CORONARY ARTERY DISEASE : A 4-YEAR FOLLOW UP STUDY OF 257 SERVICE PERSONNEL

Two hundred and fifty seven service personnel with established diagnosis of (a) silent ischaemia (40.47%) (b) Q-infarction (25.68%) and (c) non-Q-infarction (33.85%) along with 50 age-matched controls were subjected to stress tests before and after identification and control of risk factors. Lack of exercise (63.0%), dietetic indiscretion (47.4%) and cigarette smoking (40.4%) were the main risk factors. Hypercholesterolaemia (22.1%), alcohol over-indulgence (17.1%), positive family history (16.3%), diabetes mellitus (9.7%) and hypertension (6.2%) were other contributing factors. Clustering or multiplicity of risk factors was seen in 61.1% cases. All patients were advised for control of risk factors along with necessary specific therapy wherever indicated. Initial stress test was positive in 83.3% of the total and on repetition, after 4 years, the positivity dropped to 45.9% with a rate of improvement of 44.9%. Patients with silent ischaemia showed the maximum improvement (57.8%) following the risk factor intervention. Only 4 cases (1.56%) showed deterioration with reinfarction during the 4-year follow up.

Alcohol Consumption and Diseases of the Liver

Alcoholic liver damage is only produced by constant alcohol intake. Close dose and time relationships are apparent. For many years, alcoholic fatty liver is the only noticeable alteration. It is completely reversible in 2-4 weeks when ethanol intake is stopped. After about 6 years of chronic abuse alcoholic hepatitis may develop. Once established it progresses within weeks or months to cirrhosis if ethanol intake is not discontinued. On the other hand, alcoholic hepatitis heals under complete abstenence from alcohol with unimportant fibrosis. After over-indulgence in alcohol over a period of 22 years, there is a 50% probability of cirrhosis. This shows clearly that the resistance of the liver to alcohol varies considerably in different individuals. Even in early stages of alcoholic cirrhosis the prognosis is reasonable. If these patients observe complete abstenence from ethanol, their life expectation is only slightly different from the average of the population. The extent of the consumption of alcohol is of decisive importance for the development of cirrhosis. New and very careful investigations reveal that the susceptibility to alcohol is different in both sexes. For men the danger level would thus appear to be around 60 g and for women around 20 g of pure alcohol a day. Beyond these critical levels the morbidity of cirrhosis multiplies almost in geometric progression with increasing amounts of ethanol.

Actions of Alcohol, vol 1 &amp;amp; 2.

Alcoholism is a serious disease. In many respects, overindulgence in alcohol is more serious than self-administered overdosage of, say, adrenal corticosteroids. In the latter case, overuse destroys the user, but in the case of alcohol it destroys those around him as well. Over indulgence in alcohol is a euphemism—alcohol poisoning is more descriptive. Before one considers alcoholism one must first consider alcohol, because in all probability it has the broadest ramifications of any drug. For example, one aspect is political. The huge excise taxes collected by the government are a consideration of profound influence should a question of control come up—assuming that control is desired. Another ramification is societal—alcohol is a sort of pot or marijuana of which society heartily approves. This virtually encourages alcoholism. It is only when the alcoholic is on the skids—for drunken driving, arrests, loss of job, or splintering of the immediate family—that society invokes its

Staff attitudes toward the alcoholic patient.

ALTHOUGH countless writers have observed that the personal views of staff members toward the alcoholic is an important factor in treatment, the problem has seldom been explored systematically. It is well known that overindulgence in alcohol often elicits strong negative reactions from hospital staff. In December 1964, the Alcoholism Study Group at Mendocino State Hospital noted in their report that, Within the hospital system, we have failed to identify the built-in attitudes and policies that defeat creative treatment approaches. Similarly, Moore and Ramseur 1 observed that this uncontrolled hedonism evokes various responses, from envy to repugnance, which have decided effect on the alcoholic patient. In addition to expressed attitudes, unconscious reactions by staff members to acting-out forms of disturbance may actually encourage the deviant behavior or force its suppression. In either case, the result is antitherapeutic. With the exception of Selzer's 2 observational study of the relationship between negative attitudes

Liver Damage in Addictive Alcoholics

Almost 125 years ago Addison (1836) suggested the existence of a causal relationship between alcoholism and cirrhosis of the liver and more than 100 years ago Rokitansky noted accumulation of fat as the earliest effect on the liver of over-indulgence in alcohol (cited from Connor, 1938). Though the relative importance of infective hepatitis and alcoholism as aetiological agents in liver cirrhosis may vary a great deal in different countries, “alcohol and infective hepatitis are at present the only two unequivocal aetiological factors” (Annotation,Brit. Med. J., 1957). It is usually accepted that over-indulgence in alcoholic drinks often produces liver dysfunction—maybe in an indirect manner—which though reversible at first, tends to become irreversible as over-indulgence is continued and prolonged (Leevy, Cunniff, Walton and Healey, 1954). The terminal phases are characterized by cirrhosis, hypertrophic at first and then contracted, with ascites and eventual death. When individuals whose drinking habits lead them to this state need hospital treatment, they seem to find their way into general hospitals rather than into mental hospitals. Among them may be alcoholics of the type described by a World Health Organization Expert Committee as “habitual symptomatic excessive drinkers” (W.H.O. Rep., 1952) or “non-addictive alcoholics”, and those excessive drinkers whose alcoholism manifests itself in their “inability to stop” continual daily drinking in the face of dangerous consequences (W.H.O. Rep., 1955).

VITAMIN B THERAPY IN PARALYSIS AGITANS

Article1 September 1942VITAMIN B THERAPY IN PARALYSIS AGITANSWINIFRED C. LOUGHLIN, M.D., H. ARNOLD MYERSBURG, M.D., HERMAN WORTIS, M.D.WINIFRED C. LOUGHLIN, M.D.Search for more papers by this author, H. ARNOLD MYERSBURG, M.D.Search for more papers by this author, HERMAN WORTIS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-17-3-423 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe numerous therapeutic approaches to the problem of paralysis agitans indicate clearly the inherent difficulties in this problem. It is, therefore, only natural that several investigators have recently turned to vitamin therapy in the hope of finding a more effective weapon for attacking this apparently incurable disease.It is noteworthy that of the six cases reported by Parkinson in his original essay on the shaking palsy one patient attributed his symptoms to over-indulgence in alcohol and another to a long period of neglect in a Spanish prison.1Furthermore, Kikuchi states that monkeys with experimental B-avitaminosis develop mask-like facies, propulsory movements...Bibliography1. PARKINSON J: An essay on the shaking palsy, 1817, Sherwood, Neely and Jones, London. Google Scholar2. KIKUCHI T: Ueber die Avitaminose bei Affen, Japanese Jr. Med. Sci. Trans., 1927, viii, 265. Google Scholar3. LEWYSPIESARING FHTDCD: The incidence of neuropathy in pellagra, Am. Jr. Med. Sci., 1940, cic, 840. Google Scholar4. JOLLIFFE N: The clinical aspects of vitamin B deficiencies, Minnesota Med., 1940, xxiii, 542. Google Scholar5. JOLLIFFE N: Effects of vitamin B6 in paralysis agitans, Trans. Am. Neurol. Assoc., 1940, lx, 54-59. Google Scholar6. SPIESHIGHTOWERHUBBARD TDDPLH: Some recent advances in vitamin therapy, Jr. Am. Med. Assoc., 1940, cxv, 292. CrossrefGoogle Scholar7. JOLLIFFE N: Further results of vitamin B6 therapy in paralysis agitans, presented before the Section of Neurology and Psychiatry, New York Acad. Med., December 10, 1940. Google Scholar8. BEAN WB: Personal communication to the author. Google Scholar9. SPIES TD: The vitamin B deficiencies, Trans. and Stud. Coll. Phys. Philadelphia, 1940, viii, 12. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York, N. Y.*Received for publication August 8, 1941.From the Neuropsychiatric Service of the Third (New York University) Division of the Welfare Hospital, New York City, and the Department of Psychiatry, New York University College of Medicine. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byNutritional Aspects of Pyrldoxal as a Coenzyme 1 September 1942Volume 17, Issue 3Page: 423-426KeywordsAlcoholsHospital medicineParalysisParkinson disease ePublished: 1 December 2008 Issue Published: 1 September 1942 PDF downloadLoading ...