Menopause and liver health -
Para a obtenção dos resultados foram realizadas as análises uni e multivariada. A média de idade foi de 56,5 ± 6,7 anos.
A síndrome metabólica também foi mais frequente em mulheres com DHGNA, que não utilizaram a terapia de reposição hormonal. Estes dados sugerem uma elevada prevalência de DHGNA em mulheres na pós-menopausa, e ainda apontam para uma associação negativa da terapia de reposição hormonal com a DHGNA.
Nonalcoholic fatty liver disease NAFLD is characterized by the focal or diffuse accumulation of fat in the liver parenchyma of patients who deny abusive alcohol consumption 12 Karnikowski M, Córdova C, Oliveira RJ, Karnikowski MG, Nóbrega O deT.
Non-alcoholic fatty liver disease and metabolic syndrome in Brazilian middle-aged and older adults. Sao Paulo Med J. Clark JM. The epidemiology of nonalcoholic fatty liver disease in adults. J Clin Gastroenterol. de Moura Almeida A, Cotrim HP, Barbosa DB, de Athayde LG, Santos AS, Bitencourt AG, de Freitas LA, Rios A, Alves E.
Fatty liver disease in severe obese patients: diagnostic value of abdominal ultrasound. World J Gastroenterol. It increases with increasing age 27 Yatsuji S, Hashimoto E, Tobari M, Tokushige K, Shiratori K.
Influence of age and gender in Japanese patients with non-alcoholic steatohepatitis. Hepatol Res. Coral G, de Mattos AA, de Mattos AZ, dos Santos DE. Arq Gastroenterol. NAFLD is frequent in postmenopausal women PMW and it is usually associated with metabolic syndrome.
The influence of hormone replacement therapy HRT in NAFLD development in these women has been discussed 3 3. In menopause occurs a decrease in the liver ability to oxidize fatty acids, and an increased on lipogenesis that causes excessive accumulation of hepatic fat and culminates with inflammation 21 Suzuki A, Abdelmalek MF.
Nonalcoholic fatty liver disease in women. Womens Health ; The estrogen deficiency causes body fat redistribution, with accumulation of visceral fat, which can influence the development and progression of NAFLD 13 Lavoie JM, Pighon A. NAFLD, estrogens, and physical exercise: the Animal Model.
J Nutr Metab. An experimental study with ovariectomized rats showed that the absence of estrogens could stimulate fat accumulation in the liver, and that ovariectomized rats subjected to an endurance program had decreased fat in the liver and abdomen 6 6.
Corriveau P, Paquette A, Brochu M, Prud'homme D, Rabasa-Lhoret R, Lavoie JM. Resistance training prevents liver fat accumulation in ovariectomized rats.
Maturitas ; It was also observed lower levels of ALT in type 2 diabetics undergoing HRT for 6 months 16 McKenzie J, Fisher BM, Jaap AJ, Stanley A, Paterson K, Sattar N. Effects of HRT on liver enzyme levels in women with type 2 diabetes: a randomized placebo-controlled trial. Clin Endocrinol. The present study describes the clinical characteristics of NAFLD in PMW, and investigates the relationship between HRT and this liver disease.
In a sectional study, a total of PMW coming from the National Health System from Northeast of Brazil, who reported the use of HRT G1 or who denied the use G2 , were analyzed.
The use of HRT was defined as the use of estrogen in hysterectomized PMW or estrogen associated with progesterone when the uterus was present, or also the use of tibolone, by oral or transdermal routes for more than 6 months. The sample was calculated by the method of proportions according to Arkin and Colton 1 1.
Arkin H, Colton R. Tables for statisticians. The indication for HRT use was made by the gynecologists who accompanied the PMW based on the clinical features and climacteric symptoms.
The use of HRT was confirmed by patients report during the interview. From April to April , women were included and evaluated. This study was conducted in accordance with the Declaration of Helsinki an the Institutional Ethics Committee from the Federal University of Campina Grande approved the study under the number Written informed consent was obtained before include the participants.
All participants had a complete physical exam and answered a questionnaire that included demographic characteristics age, marital status and family income and physical activity level example: participation in any kind of sport at least three times a week , history of obesity, dyslipidemia and diabetes; history of alcohol intake and other illicit drugs usage.
Laboratory evaluation included: viral hepatitis infection markers for B virus HBsAg and C virus anti HCV , ALT, AST, GGT, ferritin, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglycerides, glucose, insulin, transferrin saturation.
Menopause was defined in woman who has been amenorrhea absence of any menstruation for 12 or more months. The metabolic syndrome MS was defined according to the National Cholesterol Education Program's Adult Treatment Panel III report 14 Marfell-Jones M.
International standards for anthropometric assessment. Potchefstroom, South Africa: International Society for the Advancement of Kinanthropometry. Abdominal ultrasound exam was performed in all patients by a single radiologist in the same institution, and steatosis was classified in grades I, II and III, with the grade I corresponding to the increase of the echogenicity of the liver parenchyma, II hepatic hyperechogenicity associated with attenuation of the sound beam in posteriors planes and III the sum of the above plus the loss of definition in liver vascular structures and the diaphragm.
Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.
Diabetologia ; The hepatic enzymes were considered elevated when their values were at least 1. Data were processed and analyses were performed using Statistical Package for the Social Sciences software SPSS Inc. Continuous variables were summarized with means and standard deviations while categorical variables were presented in frequencies and percentages.
Comparisons between the means of two groups were performed using Student's t -test for independent samples. Chi-square and Fisher's exact tests were used to test associations between categorical variables. One-way analysis of variance was used to compare the means of the four groups.
This was followed by the Bonferroni's post hoc test. All comparisons performed were two-tailed, P values were calculated and significance level was set to equal or less than 0. The mean age of the participants was Further demographic data are shown in Table 1. Fifty-three The prevalence of NAFLD was The time of menopause varied as follows: women Regarding the HRT usage time, 22 women PMW from G2, with and without NAFLD diagnosis, had higher rates of overweight, obesity and insulin resistance when compared with G1.
The frequency of MS in the entire group of PMW was ALT, GGT and ferritin levels were higher in G2 with NAFLD Table 3. ALT and ferritin levels were higher in the PMW with grades II and III steatosis in G2 than in women with equal degrees of steatosis in G1 Table 4.
The use of HRT, type of hormone used, route of administration and the duration of HRT use, did not reveal an association with NAFLD according to our results Table 5. The multivariate logistic regression model showed that prognostic factors for NAFLD were: presence of MS — Odds Ratio: 2.
There is not much information about the NAFLD and HRT in PMW. Some reports are experimental or include patients with chronic hepatitis C CHC and type 2 diabetes. Although the present sample of PMW has revealed a higher frequency of NAFLD, it was lower among those who referred HRT use, similar to the findings described in another study 11 Hamaguchi M, Kojima T, Ohbora A, Takeda N, Fukui M, Kato T.
Aging is a risk factor of nonalcoholic fatty liver disease in premenopausal women. Despite some researchers find no differences between the effects of HRT on hepatic proteins sensitive to estrogen regarding different routes of administration 20 Sitruk-Ware R, Plu-Bureau G, Menard J, Conard J, Kumar S, Thalabard JC, Tokay B, Bouchard P.
Effects of oral and transvaginal ethinyl estradiol on hemostatic factors and hepatic proteins in a randomized, crossover study. J Clin Endocrinol Metab. Rosa-e-Silva AC, Melo AS. A importância da via de administração na terapia hormonal do climatério.
Femina ; Walsh BW, Li H, Sacks FM. Effects of postmenopausal hormone replacement with oral and transdermal estrogen on high density lipoprotein metabolism. J Lipid Res. NAFLD was also studied in premenopausal, postmenopausal and polycystic ovary syndrome women by Gutierrez-Grobe et al.
Gutierrez-Grobe Y, Ponciano-Rodríguez G, Ramos MH, Uribe M, Méndez-Sánchez N. Prevalence of non alcoholic fatty liver disease in premenopausal, posmenopausal and polycystic ovary syndrome women: the role of estrogens.
Ann Hepatol. who observed higher index in polycystic ovary syndrome and postmenopausal than those premenopausal ones. The authors suggested that estrogens might have a protective effect against NAFLD in women and this drug protection against liver injury have also been suggested for others studies.
One of them showed that physiological concentration of estrogen inhibits spontaneous secretion of pro-inflammatory cytokines such as interleukins IL -1, IL-6 and tumor necrosis factor alpha. However, after menopause and the decreased of ovarian hormone production these cytokines levels could increase 8 8.
Di Martino V, Lebray P, Myers RP, Pannier E, Paradis V, Charlotte F, Moussalli J, Thabut D, Buffet C, Poynard T. Progression of liver fibrosis in women infected with hepatitis C: long-term benefit of estrogens exposure.
Hepatology ; Villa et al. Villa E, Karampatou A, Cammà C, Di Leo A, Luongo M, Ferrari A, Petta S, Losi L, Taliani G, Trande P, Lei B, Graziosi A, Bernabucci V, Critelli R, Pazienza P, Rendina M, Antonelli A, Francavilla A.
Early menopause is associated with lack of response to antiviral therapy in women with chronic hepatitis C. Gastroenterology ; observed that the estrogens-deprived environment in PMW with chronic hepatitis C virus CHC had influence in progression to fibrosis. There are reports that estrogen inhibits the myofibroblastic transformation of rat stellate cells that are responsible for hyper secretion of collagen and fibrosis, pointing to a possible anti fibrotic effect of this drug 26 Yasuda M, Shimizu I, Shiba M, Ito S.
Suppressive effects of estradiol on dimethylnitrosamine-induced fibrosis of the liver in rats. A hepatic anti fibrogenic effect of HRT has also been referred in menopausal patients using HRT with the diagnosis of chronic hepatitis C 4 4.
Codes L, Asselah T, Cazals-Hatem D, Tubach F, Vidaud D, Paraná R, Bedossa P, Bedossa P, Valla D, Marcellin P. Liver fibrosis in women with chronic hepatitis C: evidence for the negative role of the menopause and steatosis and the potential benefit of hormone replacement therapy.
Gut ; Gervais A, Bacq Y, Bernuau J, Martinot M, Auperin A, Boyer N, Kilani A, Erlinger S, Valla D, Marcellin P. Decrease in serum ALT and increase in serum HCV RNA during pregnancy in women with chronic hepatitis C.
J Hepatol. The relevance of HRT in patients with CHC was also evaluated by Codes et al. Increasing BMI correlated with increased reporting of hypertension, heart disease, hypercholesterolaemia and diabetes. Three hundred twenty five 0. The most common ICD code signaling a first presentation of LRE was K76 Additional file 1 : Table S1.
Only 0. There were 2. Other covariates also demonstrated independent association with liver-related events Table 1. Significant HRs were seen with smoking, hypertension, heart disease, hypercholesterolaemia, diabetes and IMD.
Crude rates of LREs increased with rising BMI. HRs for LRE were significantly higher in both overweight 1. A fully adjusted model is presented incorporating adjustment for confounders with significant HRs Table 2. A fully adjusted model is shown, adjusted for variables with significant HRs for LRE Table 2.
In the group reporting no alcohol consumption the proportion of LREs that were alcohol-related was 3. Participants were grouped according to combinations of BMI and alcohol consumption. Table 3 shows the rates of LRE in each group.
To estimate the effect of cardiovascular disease and diabetes on the morbidity associated with fatty liver disease, HRs were adjusted for confounding factors associated with the metabolic syndrome.
When elements of the metabolic syndrome were controlled for, risk of LRE attributable to heavier drinking increased. This suggests that the risk of liver disease attributable to BMI in patients with, or at risk of, metabolic syndrome is not entirely accounted for by hypertension, heart disease, hypercholesterolemia or diabetes, but may be partly attributable to steatosis itself.
There was no significant interaction between BMI and high alcohol use. Similarly, no interaction was seen with BMI and any alcohol use.
While the association between alcohol consumption and CLD is well established, there is still much to characterise in the natural history of non-alcoholic fatty liver disease NAFLD [ 3 ].
Furthermore the study supports the adverse impact of heavy drinking compounding the effects of overweight and obesity. Strategies for preventing and detecting liver disease should be developed accommodating these findings.
Those that are overweight or obese have an increased risk of liver disease. It is possible, however, that some abstainers had previously been heavy drinkers.
The highest risk is in those who are overweight or obese and drink the most alcohol. After adjustment for confounding due to metabolic risk factors, HRs in the two highest alcohol categories increased in all BMI groups, suggesting that these factors may contribute to the risk of CLD.
It is biologically plausible that diabetes, hypercholesterolaemia and hypertension may contribute to liver disease over and above that caused by fatty liver disease and alcoholic liver toxicity. Strengths of this study include the size and duration of follow-up, the prospective design and the independence of the data capture for outcomes.
This study was also able to adjust for confounding factors, which has not been possible in other cross-sectional studies. In an effort to capture all morbidity and mortality attributable to liver disease, rather than just cirrhosis, we selected ICD codes that encompass a clinically relevant group of diseases including codes for CLD and those relating to the consequences of decompensated liver disease.
This was designed to maximise the ability to detect liver disease. Limitations include reliance on self-reporting of alcohol consumption, co-morbidities, height and weight, which may be a factor in the wide confidence intervals seen for all HR estimates. However, good reliability of self-reporting height and weight [ 20 , 21 , 22 , 23 , 24 ], and alcohol [ 25 , 26 , 27 ], has been demonstrated in other studies.
Height and weight were reported at recruitment, and alcohol consumption reported later, on the follow-up questionnaire. Participants were asked to report current alcohol use, rather than lifetime patterns. We used the convention that one drink is equivalent to 1 unit of alcohol.
However assumptions about alcohol content are difficult to make as measures of volume are likely to vary depending on where the alcohol is consumed, and the alcohol content of drinks continues to change. Reliance on ICD to define events may result in errors due to mis-coding.
We used additional codes to those used to define cirrhosis in order to maximize the capture of cases, but these may also be subject to mis-coding. We attempted to reduce the risk of non-coding of events by using 3 independent sources, and in the case of death certification also used hand searching of key words in the text of death certificates.
Also, the HES database may not capture some areas of healthcare, for example the private sector. The number of LREs that included ICD Z This may be because participants with liver transplants are engaged in hospital care and are easily identified and coded.
The loss to follow up rate in UKCTOCS was very small 0. Although the health section of the follow-up questionnaire did not specifically ask about liver disease, we excluded those who had a code of interest recorded between recruitment to UKCTOCS and the start of this study.
However, exclusion of all participants with known CLD could not be guaranteed. It is unlikely that viral hepatitis made a significant contribution to LRE based on low prevalence in the demographic of women in this study [ 30 ].
During the follow-up period in our study, only 21 0. A number of studies have demonstrated a reduced risk of liver disease in patients with NAFLD who consume low or moderate amounts of alcohol [ 31 , 32 , 33 ], and it has been suggested that these levels of alcohol use may be associated with beneficial effects of insulin sensitivity in post-menopausal women [ 34 ].
However, at higher extremes of BMI and alcohol use, data is not conclusive. Previous studies have attributed a lower incidence of CLD to BMI and alcohol, and as expected a lower incidence of CLD when only alcoholic cirrhosis is examined [ 35 ].
However these have relied on cirrhosis codes alone, ignoring complications characterising decompensated cirrhosis that are indicative of CLD and clearly associated with BMI and alcohol included in the present study.
This study is in broad agreement with some other studies including the National Health and Nutrition Examination Survey NHANES [ 6 ] which found increasing risk with both increasing BMI and alcohol, but no excess risk in overweight or obese drinkers or in abstainers.
A Scottish prospective study reported increasing risk with increasing BMI in men, but not in women [ 10 ]. A sub-analysis of men found the lowest risk of CLD in abstainers with normal BMI with a supra-additive interaction between BMI and alcohol [ 36 ].
The UK-based Million Women Study [ 9 ] used a limited range of ICD codes to identify cirrhosis and reported a rate of hospital admission or death from liver disease less than half that found in our study.
However, as in our study, highest risk was in overweight or obese women consuming the most alcohol. In a study of patients with a history of alcohol excess who were admitted to hospital with an alcohol-related problem, risk of cirrhosis was twice as high among the overweight group as those with normal BMI [ 37 ].
A recent prospective study of , middle-aged males used self-reported BMI and alcohol use to assess liver-related mortality ascertained form record linkage, using ICD codes KK76, demonstrating a U-shaped relationship between alcohol and mortality and BMI and mortality.
Although there was evidence of synergy between low BMI and high alcohol, as in our study there was no evidence of interaction between high BMI and high alcohol use [ 38 ]. Our finding of increased risk in abstainers has precedent but is controversial.
Some prospective studies have found that men but not women abstainers were at increased risk [ 9 , 44 ], in contrast to the present study that provides a more comprehensive insight into the effects of weight and alcohol.
Using raised aminotransferase levels to diagnose suspected NAFLD in men and women in NHANES the highest risk was seen in non-drinkers compared to modest drinkers [ 45 ], and in biopsy-proven NAFLD, moderate drinkers had lower risk of steatohepatitis compared to non-drinkers [ 46 ].
The increased risk of alcoholic cirrhosis in abstainers compared to light drinkers may be due, in part, to this group containing previous drinkers who raise the overall risk in the abstainer group, rather than due to a true protective effect of alcohol in the light drinkers.
In a small study of patients with biopsy-proven NAFLD, a comprehensive alcohol history was obtained and found to be higher than the original estimate at diagnosis in some patients, suggesting that some of these patients may have had alcohol-related liver disease rather than NAFLD [ 47 ].
We found alcohol-related LREs in abstainers although at less than half the rate seen in drinkers which, although may partly be a function of miscoding, provides further evidence that this group comprises some ex-drinkers.
Interaction between higher levels of alcohol consumption and NAFLD may result in greater risk of liver disease. A study measuring aminotransferase activity found that increased BMI potentiates the harmful effect of alcohol on the liver [ 48 ].
Increased aminotransferase levels were associated with higher alcohol consumption and BMI. In those with normal BMI there was no association between alcohol and raised aminotransferase levels, but in the overweight and obese groups, alcohol increased risk of elevated aminotransferases.
This group also examined the risk of hepatocellular carcinoma in people with chronic hepatitis B, finding synergism between obesity and alcohol [ 50 , 51 ]. Our results suggest a substantial influence of both elevated BMI and alcohol on risk of CLD.
Although no significant interaction between BMI and alcohol was seen and this lack of synergy is reassuring, the compelling risk in the overweight and obese groups adds to the evidence that rising BMI and increasing alcohol use are risk factors for liver disease among women.
By considering the clinical consequences of liver disease beyond the diagnosis of cirrhosis we revealed a greater burden of disease than previously recognised. Currently much CLD goes undiagnosed until complications of cirrhosis result in serious morbidity and mortality.
Earlier identification of those at risk could avert illness and reduce costs by targeted interventions. While the risks associated with heavy alcohol consumption are frequently publicised these data emphasise the importance of disseminating awareness of the risks of liver disease associated with BMI, particularly in light of the growing prevalence of overweight and obesity throughout the world [ 52 ].
Public health policy and health education and awareness campaigns should take these facts into account. This study of post-menopausal women suggests that elevated BMI and high alcohol intake are independent risk factors for liver disease.
Strategies for detecting liver disease and public health strategy should recognise the importance of BMI as well as alcohol when confronting the growing burden of liver disease. Leon DA, McCambridge J. Liver cirrhosis mortality rates in Britain from to an analysis of routine data.
Article PubMed Google Scholar. Department of Health. Safe, sensible, social — consultation on further action. London: Department of Health; Google Scholar. Williams R, Aspinall R, Bellis M, Camps-Walsh G, Cramp M, Dhawan A, et al.
Addressing liver disease in the UK: a blueprint for attaining excellence in health care and reducing premature mortality from lifestyle issues of excess consumption of alcohol, obesity, and viral hepatitis.
Scaglione S, Kliethermes S, Cao G, Shoham D, Durazo R, Luke A, et al. The epidemiology of cirrhosis in the United States: a population-based study. J Clin Gastroenterol.
Whitlock G, Lewington S, Sherliker P, Clarke R, Emberson J, Halsey J, et al. Body-mass index and cause-specific mortality in adults: collaborative analyses of 57 prospective studies. Ioannou GN, Weiss NS, Kowdley KV, Dominitz JA. Is obesity a risk factor for cirrhosis-related death or hospitalization?
A population-based cohort study. Batty GD, Shipley MJ, Kivimaki M, Barzi F, Smith GD, Mitchell R, et al.
Obesity and overweight in relation to liver disease mortality in men: 38 year follow-up of the original Whitehall study. Int J Obes.
Article CAS Google Scholar. Marchesini G, Brizi M, Bianchi G, Tomassetti S, Bugianesi E, Lenzi M, et al.
Nonalcoholic fatty liver disease: a feature of the metabolic syndrome. Article CAS PubMed Google Scholar. Liu B, Balkwill A, Reeves G, Beral V. Body mass index and risk of liver cirrhosis in middle aged UK women: prospective study. Article PubMed PubMed Central Google Scholar.
Hart CL, Batty GD, Morrison DS, Mitchell RJ, Smith GD. Obesity, overweight and liver disease in the Midspan prospective cohort studies.
Garcia-Tsao G, Friedman S, Iredale J, Pinzani M. Now there are many stages where before there was one: in search of a pathophysiological classification of cirrhosis. Diehl AM. Obesity and alcoholic liver disease. Serfaty L, Poujol-Robert A, Carbonell N, Chazouillères O, Poupon RE, Poupon R.
Am J Gastroenterol. Menon U, Gentry-Maharaj A, Hallett R, Ryan A, Burnell M, Sharma A, et al. Sensitivity and specificity of multimodal and ultrasound screening for ovarian cancer, and stage distribution of detected cancers: results of the prevalence screen of the UK collaborative trial of ovarian cancer screening UKCTOCS.
Lancet Oncol. Menon U, Gentry-Maharaj A, Ryan A, Sharma A, Burnell M, Hallett R, et al. Recruitment to multicentre trials--lessons from UKCTOCS: descriptive study. Menon U, Ryan A, Kalsi J, Gentry-Maharaj A, Dawnay A, Habib M, et al.
Risk algorithm using serial biomarker measurements doubles the number of screen-detected cancers compared with a single-threshold rule in the United Kingdom collaborative trial of ovarian cancer screening. J Clin Oncol.
Alcohol unit guidelines. Drinkaware, London. Accessed 21 February Burnell M, Gentry-Maharaj A, Ryan A, Apostolidou S, Habib M, Kalsi J, et al. Impact on mortality and cancer incidence rates of using random invitation from population registers for recruitment to trials.
Day CP, James OFW. Bolton-Smith C, Woodward M, Tunstall-Pedoe H, Morrison C. Accuracy of the estimated prevalence of obesity from self reported height and weight in an adult Scottish population.
J Epidemiol Community Health. Article CAS PubMed PubMed Central Google Scholar. Hill A, Roberts J. Body mass index: a comparison between self-reported and measured height and weight.
J Public Health Med. Nieto-Garcia FJ, Bush TL, Keyl PM. Body mass definitions of obesity: sensitivity and specificity using self-reported weight and height.
Roberts RJ. Can self-reported data accurately describe the prevalence of overweight? Public Health. Kuskowska-Wolk A, Karlsson P, Stolt M, Rössner S. The predictive validity of body mass index based on self-reported weight and height.
CAS PubMed Google Scholar. Midanik L. The validity of self-reported alcohol consumption and alcohol problems: a literature review. Br J Addict.
Romelsjö A, Leifman H, Nyström S. A comparative study of two methods for the measurement of alcohol consumption in the general population.
Int J Epidemiol. Parker DR, Derby CA, Usner DW, Gonzalez S, Lapane KL, Carleton RA. Self-reported alcohol intake using two different question formats in southeastern New England. Goddard E. Estimating alcohol consumption from survey data: updated method of converting volumes to units.
National Statistics methodological series no. Office of National Statistics. London: HMSO; Pinsky PF, Miller A, Kramer BS, Church T, Reding D, Prorok P, et al.
Evidence of a healthy volunteer effect in the prostate, lung, colorectal, and ovarian cancer screening trial. Am J Epidemiol. Hepatitis C in the UK report. London: Public Health England; Ajmera VH, Terrault NA, Harrison SA.
Is moderate alcohol use in non-alcoholic fatty liver disease good or bad? A critical review. Hagström H, Nasr P, Ekstedt M, Kechagias S, Önnerhag K, Nilsson E, et al. Low to moderate lifetime alcohol consumption is associated with less advanced stages of fibrosis in non-alcoholic fatty liver disease.
Scand J Gastroenterol. Sogabe M, Okahisa T, Taniguchi T, Tomonari T, Tanaka T, Tanaka H, et al. Light alcohol consumption plays a protective role against non-alcoholic fatty liver disease in Japanese men with metabolic syndrome.
Liver Int. Davies MJ, Baer DJ, Judd JT, Brown ED, Campbell WS, Taylor PR. Effects of moderate alcohol intake on fasting insulin and glucose concentrations and insulin sensitivity in postmenopausal women: a randomized controlled trial. Askgaard G, Grønbæk M, Kjær MS, Tjønneland A, Tolstrup JS.
Alcohol drinking pattern and risk of alcoholic liver cirrhosis: a prospective cohort study. J Hepatol. Hart CL, Morrison DS, Batty GD, Mitchell RJ, Davey SG. Effect of body mass index and alcohol consumption on liver disease: analysis of data from two prospective cohort studies.
Naveau S, Giraud V, Borotto E, Aubert A, Capron F, Chaput JC. Excess weight risk factor for alcoholic liver disease. Yi S-W, Hong J-S, Yi J-J, Ohrr H.
Impact of alcohol consumption and body mass index on mortality from nonneoplastic liver diseases, upper aerodigestive tract cancers, and alcohol use disorders in Korean older middle-aged men. Medicine Baltimore. Grønbæk M, Deis A, Sørensen TI, Becker U, Schnohr P, Jensen G. Mortality associated with moderate intakes of wine, beer, or spirits.
Klatsky AL, Armstrong MA, Friedman GD. Alcohol and mortality. Ann Intern Med. Shaper AG, Wannamethee G, Walker M.
Alcohol and mortality in British men: explaining the U-shaped curve. Grønbæk M, Deis A, Sørensen TI, Becker U, Borch-Johnsen K, Müller C, et al. Influence of sex, age, body mass index, and smoking on alcohol intake and mortality.
Becker U, Grønbæk M, Johansen D, Sørensen TI. Lower risk for alcohol-induced cirrhosis in wine drinkers. Becker U, Deis A, Sørensen TI, Grønbæk M, Borch-Johnsen K, Müller CF, et al. Prediction of risk of liver disease by alcohol intake, sex, and age: a prospective population study.
Dunn W, Xu R, Schwimmer JB. Modest wine drinking and decreased prevalence of suspected nonalcoholic fatty liver disease.
Findings Post-workout recovery nutrition whether menopause heealth a risk factor for nonalcoholic fatty liver disease NAFLD have been Leafy greens for lactose intolerance, although NAFLD is as prevalent, Leafy greens for lactose intolerance more so, in post-menopausal women Mehopause it is in men Menopuse similar age. A systematic review and meta-analysis by Jaroenlapnopparat et al analyzed all available data to determine the association between the disease and menopause. The meta-analysis of these studies found a significant association between menopause and NAFLD with a pooled odds ratio of 2. This association persisted in a sensitivity meta-analysis of six studies, which factored in age and metabolic factors. The pooled odds ratio here was 2. The meta-analysis found that menopause was associated with a roughly 2.Menopause and liver health -
A média de idade foi de 56,5 ± 6,7 anos. A síndrome metabólica também foi mais frequente em mulheres com DHGNA, que não utilizaram a terapia de reposição hormonal.
Estes dados sugerem uma elevada prevalência de DHGNA em mulheres na pós-menopausa, e ainda apontam para uma associação negativa da terapia de reposição hormonal com a DHGNA. Nonalcoholic fatty liver disease NAFLD is characterized by the focal or diffuse accumulation of fat in the liver parenchyma of patients who deny abusive alcohol consumption 12 Karnikowski M, Córdova C, Oliveira RJ, Karnikowski MG, Nóbrega O deT.
Non-alcoholic fatty liver disease and metabolic syndrome in Brazilian middle-aged and older adults. Sao Paulo Med J. Clark JM. The epidemiology of nonalcoholic fatty liver disease in adults. J Clin Gastroenterol. de Moura Almeida A, Cotrim HP, Barbosa DB, de Athayde LG, Santos AS, Bitencourt AG, de Freitas LA, Rios A, Alves E.
Fatty liver disease in severe obese patients: diagnostic value of abdominal ultrasound. World J Gastroenterol. It increases with increasing age 27 Yatsuji S, Hashimoto E, Tobari M, Tokushige K, Shiratori K.
Influence of age and gender in Japanese patients with non-alcoholic steatohepatitis. Hepatol Res. Coral G, de Mattos AA, de Mattos AZ, dos Santos DE. Arq Gastroenterol. NAFLD is frequent in postmenopausal women PMW and it is usually associated with metabolic syndrome.
The influence of hormone replacement therapy HRT in NAFLD development in these women has been discussed 3 3.
In menopause occurs a decrease in the liver ability to oxidize fatty acids, and an increased on lipogenesis that causes excessive accumulation of hepatic fat and culminates with inflammation 21 Suzuki A, Abdelmalek MF.
Nonalcoholic fatty liver disease in women. Womens Health ; The estrogen deficiency causes body fat redistribution, with accumulation of visceral fat, which can influence the development and progression of NAFLD 13 Lavoie JM, Pighon A.
NAFLD, estrogens, and physical exercise: the Animal Model. J Nutr Metab. An experimental study with ovariectomized rats showed that the absence of estrogens could stimulate fat accumulation in the liver, and that ovariectomized rats subjected to an endurance program had decreased fat in the liver and abdomen 6 6.
Corriveau P, Paquette A, Brochu M, Prud'homme D, Rabasa-Lhoret R, Lavoie JM. Resistance training prevents liver fat accumulation in ovariectomized rats.
Maturitas ; It was also observed lower levels of ALT in type 2 diabetics undergoing HRT for 6 months 16 McKenzie J, Fisher BM, Jaap AJ, Stanley A, Paterson K, Sattar N. Effects of HRT on liver enzyme levels in women with type 2 diabetes: a randomized placebo-controlled trial.
Clin Endocrinol. The present study describes the clinical characteristics of NAFLD in PMW, and investigates the relationship between HRT and this liver disease.
In a sectional study, a total of PMW coming from the National Health System from Northeast of Brazil, who reported the use of HRT G1 or who denied the use G2 , were analyzed. The use of HRT was defined as the use of estrogen in hysterectomized PMW or estrogen associated with progesterone when the uterus was present, or also the use of tibolone, by oral or transdermal routes for more than 6 months.
The sample was calculated by the method of proportions according to Arkin and Colton 1 1. Arkin H, Colton R. Tables for statisticians. The indication for HRT use was made by the gynecologists who accompanied the PMW based on the clinical features and climacteric symptoms.
The use of HRT was confirmed by patients report during the interview. From April to April , women were included and evaluated.
This study was conducted in accordance with the Declaration of Helsinki an the Institutional Ethics Committee from the Federal University of Campina Grande approved the study under the number Written informed consent was obtained before include the participants.
All participants had a complete physical exam and answered a questionnaire that included demographic characteristics age, marital status and family income and physical activity level example: participation in any kind of sport at least three times a week , history of obesity, dyslipidemia and diabetes; history of alcohol intake and other illicit drugs usage.
Laboratory evaluation included: viral hepatitis infection markers for B virus HBsAg and C virus anti HCV , ALT, AST, GGT, ferritin, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglycerides, glucose, insulin, transferrin saturation.
Menopause was defined in woman who has been amenorrhea absence of any menstruation for 12 or more months. The metabolic syndrome MS was defined according to the National Cholesterol Education Program's Adult Treatment Panel III report 14 Marfell-Jones M.
International standards for anthropometric assessment. Potchefstroom, South Africa: International Society for the Advancement of Kinanthropometry. Abdominal ultrasound exam was performed in all patients by a single radiologist in the same institution, and steatosis was classified in grades I, II and III, with the grade I corresponding to the increase of the echogenicity of the liver parenchyma, II hepatic hyperechogenicity associated with attenuation of the sound beam in posteriors planes and III the sum of the above plus the loss of definition in liver vascular structures and the diaphragm.
Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia ; The hepatic enzymes were considered elevated when their values were at least 1.
Data were processed and analyses were performed using Statistical Package for the Social Sciences software SPSS Inc.
Continuous variables were summarized with means and standard deviations while categorical variables were presented in frequencies and percentages.
Comparisons between the means of two groups were performed using Student's t -test for independent samples. Chi-square and Fisher's exact tests were used to test associations between categorical variables. One-way analysis of variance was used to compare the means of the four groups.
This was followed by the Bonferroni's post hoc test. All comparisons performed were two-tailed, P values were calculated and significance level was set to equal or less than 0. The mean age of the participants was Further demographic data are shown in Table 1.
Fifty-three The prevalence of NAFLD was The time of menopause varied as follows: women Regarding the HRT usage time, 22 women PMW from G2, with and without NAFLD diagnosis, had higher rates of overweight, obesity and insulin resistance when compared with G1.
The frequency of MS in the entire group of PMW was ALT, GGT and ferritin levels were higher in G2 with NAFLD Table 3.
ALT and ferritin levels were higher in the PMW with grades II and III steatosis in G2 than in women with equal degrees of steatosis in G1 Table 4. The use of HRT, type of hormone used, route of administration and the duration of HRT use, did not reveal an association with NAFLD according to our results Table 5.
The multivariate logistic regression model showed that prognostic factors for NAFLD were: presence of MS — Odds Ratio: 2. There is not much information about the NAFLD and HRT in PMW. Some reports are experimental or include patients with chronic hepatitis C CHC and type 2 diabetes.
Facebook Twitter Pinterest LinkedIN Email. FULL STORY. RELATED TERMS Cirrhosis Liver transplantation Hepatitis C Trans fat Hepatitis E Liver Saturated fat Alcoholism. Story Source: Materials provided by The Translational Genomics Research Institute. Journal Reference : Johanna K DiStefano.
NAFLD and NASH in postmenopausal women: implications for diagnosis and treatment. Endocrinology , ; DOI: Cite This Page : MLA APA Chicago The Translational Genomics Research Institute.
ScienceDaily, 17 August The Translational Genomics Research Institute. Postmenopausal women at risk for nonalcoholic fatty liver disease, review suggests.
Retrieved February 13, from www. htm accessed February 13, Explore More. Blood Test Developed to Predict Liver Cancer Risk.
June 22, An estimated one-quarter of adults in the U. have nonalcoholic fatty liver disease NAFLD , an excess of fat in liver cells that can cause chronic inflammation and liver damage, increasing the risk About 1 in 4 Adults Has an Often-Missed Liver Disorder Linked to Higher Heart Disease Risk.
NAFLD can lead to permanent liver damage, and Scientists Discover Why Women Are More Resistant to Nonalcoholic Fatty Liver Disease Than Men. However, why premenopausal women are more resistant to NAFLD than men is currently unknown.
Now, scientists Alcohol-Producing Gut Bacteria Could Cause Liver Damage Even in People Who Don't Drink. Now, researchers have linked NAFLD to gut bacteria that All of my clothes felt tight. It was depressing.
But my angst about my weight paled in comparison to the arrival of a new worry — heart palpitations, high blood pressure and cholesterol levels that were climbing through the roof. Not only due to my family history, but because of what I was learning in my doctoral studies.
But acquainting myself with this research was my saving grace. It allowed me to better understand how to turn around my health at a time of life, when our changing hormonal environment makes us more vulnerable to weight gain and the various co-morbities such as heart disease and Type 2 diabetes.
Professor Carla Brady has researched the liver in menopause. Her work helped me understand the importance of our liver and gallbladder as we age. What I discovered was how the liver and gall-bladder both change in structure and function as we move towards post-menopause.
My increasing fatigue also made sense. On oral HRT at the time, I also learnt that HRT places an additional burden on the liver, as do all medications that many women take as we move through menopause.
Our health chaos arrives slowly. Not sleeping, poor temperature regulation, changing weight, high total and LDL cholesterol, bloating and joint pain may send us into further health chaos as we move through menopause.
Whilst the focus is usually on cardiac health when we visit our Doctor with changing cholesterol and weight during menopause which it should be , how many of us are being told that our liver health matters too?
I will let you reflect on that. Once we understand the metabolic pathways that help to rejuvenate our liver, we have the ability to turn around our energy, weight, cholesterol and bloating at this time of life. As I discovered myself, if we are going to change our health and manage our weight as we age, then the liver is the organ to focus on first.
It allowed me to better understand how our body is adjusting to our changing hormones in menopause — some of these changes have a lot to do with how the liver and gallbladder change as we get older.
And for those of you who have had your gallbladder removed over the years, there are changes to your fat intake that you may need to adjust as well because not having a gall-bladder impacts the dumping of emulsified fats directly into your small intestine. Understanding that the liver is the hero in the story of your mid-life weight loss, energy and health as you age is important.
The liver plays a central role in all metabolic processes in the body, especially in fat metabolism. In fat metabolism the liver cells break down fats and produce energy. These cells also produce about to 1, ml of bile per day.
This yellow, brownish or olive green liquid is collected in small ducts and then passed on to the main bile duct, which carries the bile to a part of the small intestine called the duodenum.
Bile is important for the breakdown and absorption of fats. As we age our liver is changing. It shrinks in size and the gall-bladder produces less bile.
Bile is the substance that helps to emulsify or break down fats. If our diet is high in fats including animal fats , then our gallbladder cannot cope with the volume of fats that it has to emulsify.
Our gall-bladder, which stores bile, where fats are broken down further, also changes. Changes in diet and lifestyle have led to a dramatic increase in the prevalence of obesity and metabolic syndrome in Western countries and many Asian countries.
This has resulted in a significant increase in the incidence of non-alcoholic fatty liver disease NAFLD , [Watanabe, et al, Non-alcoholic Fatty Liver Disease NAFLD doubles in incidence in women as they move through menopause.
This condition increases inflammation in the liver. I have no idea if you have an over-burdened liver or not — only you and your Doctor do. But if you are putting on weight and feeling bloated and you are on oral tablets of Menopause-HRT and your cholesterol levels are changing, then please get your liver health checked.
We are a generation of women who have had over 40 years of living in a fast-changing society, with lots of emphasis on changing food production and chemical consumption and toxins that are harmful to our liver health.
Hence, we must understand that if we want to lose weight and improve our health as we age, then our liver matters. Current research supports the effect of inflammation gathered over our lifetime on our changing health as we age.
Liver tissue is made up of lots of smaller units of liver cells called lobules. Many canals carrying blood and bile run between the liver cells.
Blood coming from the digestive organs flows through the portal vein to the liver, carrying nutrients, medication and also toxic substances.
BMC Public Health volume 17Article number: Anc this haelth. Metrics details. We investigated the Leafy greens for lactose intolerance Mejopause Menopause and liver health liver disease Oiver due to alcohol consumption and body mass index BMI and the effects of their interaction in a prospective cohort study of women recruited to the UKCTOCS trial. Hazard ratios HR were calculated for incident liver-related events LRE. First LREs were reported in 0. We found no significant interaction between BMI and alcohol. High BMI and alcohol consumption and abstinence are risk factors for CLD in post-menopausal women.Once upon a time, liver Isotonic drink for hydration was a rare occurrence, mostly affecting alcoholics. But not anymore. Recently, fatty liver disease andd become the most widespread chronic liver disease in Menopauae United States.
And doctors Leafy greens for lactose intolerance miss the early signs and symptoms. Wondering if your liver is at risk? Lievr, there are some Overcoming stress and anxiety signals that you should check ahd whenever they appear.
Leafy greens for lactose intolerance extra fat also ljver inflammation. This is so luver to your health because your liver is a powerhouse organ. Your liver Menopsuse plays a key role in controlling the Menopausd of energy in your body. Menopauwe sugar livdr in your blood is carried into cells by insulin, Menopausf be Menopause and liver health for energy.
The same process hwalth in people Menopquse drink too much alcohol. Leafy greens for lactose intolerance starts out as too Menopauuse fat deposited in the liver can progress to inflammation, Enhances nutrient absorption cell Anti-aging tips and tricks, and eventually scarring.
Various Mnopause risks eMnopause through the stages of fatty liver disease:. The underlying causes of fatty liver hezlth still being studied and debated. Menopause and liver health live you catch anr early Leafy greens for lactose intolerance signs, the remedies are Leafy greens for lactose intolerance.
Especially Anti-angiogenesis and liver cancer its heqlth stages, livef of fatty liver can healyh either non-existent or Menopausee, such as fatigue, fuzzy thinking, mild Menopayse discomfort or swelling, and possible irritable amd syndrome symptoms.
But healt are a few well-recognized indicators of possible fatty liver. If any of the following are true for you, it may be time to take steps to protect your liver:.
Extra weight being overweight or obese 2. High fasting blood triglycerides 3. High or high-normal fasting blood glucose 4. Pre-diabetes metabolic syndrome 5.
Type 2 diabetes. What do all of these conditions have in common? Nutrition and lifestyle. Research shows that, above all, obesity is a clear risk factor.
Around 70 percent of obese people have fatty liver disease, while only 10 to 15 percent of people with a normal weight have it. Importantly, though, fatty liver disease also develops in many lean individuals. This makes it easy to miss.
Although percent of Americans are thought to have fatty liver, this number rises to percent among people with type 2 diabetes or metabolic syndrome prediabetes. Menopause can also increase your risk of developing fatty liver, since estrogen naturally protects the liver and supports insulin sensitivity.
An expanding waist, weight gain and lower energy that causes you to move less all increase the chances of depositing more fat in your liver. Not surprisingly, more postmenopausal women than premenopausal women have been found to have fatty liver disease. Taking steps in your daily life to eat well and maintain a healthy weight can make all the difference.
Exercise and increasing your muscle mass also both help your body to use glucose more effectively. Your call is free. CALL M-F 9AM-6PM EST. Take A QUIZ Main menu Take A QUIZ.
Hormonal imbalance. Bone health. Brain health. Digestive health. Immune System. Weight loss. Understand YOUR SYMPTOMS. Explore WOMEN'S HEALTH Main menu Explore WOMEN'S HEALTH. Blood sugar. Breast health. Brain health and memory.
Heart health. Immune health. Joint health. Sexual health. Skin and beauty. Thyroid health. All health conditions. Shop OUR SOLUTIONS Main menu Shop OUR SOLUTIONS.
Products A to Z. Suggested combos. Daily wellness. Emotional wellness. Hormonal Imbalance. Immune support. Sleep support. Learn ABOUT US. Login to My Account. Contact Us. Link copied. Overcoming the challenges of making a lifestyle change By Caroline Morin, NBC-HWC Embarking on a journey of change,… Read more.
I want to start exercising! How do I begin? Next to… Read more. The Little Mo Effect: The inspiring book we all need right now After a 7. Pier… Read more. Pier Boutin, MD Recovering from surgery is part… Read more.
Call us at Copyright © Women's Health Network. Dev by Digitaliz Designed by Echo Interactive. Support your liver by losing weight with these natural weight loss tips.
: Menopause and liver health| Women with Menopause at Significantly Higher Risk of Developing NAFLD | So, how can you detox your Meno;ause Menopause and liver health Quiz. Open menu. Clin Endocrinol. Menlpause CAS PubMed Google Scholar Kuskowska-Wolk A, Karlsson P, Stolt M, Rössner S. Women were included in the study from the point of return of questionnaire. |
| Today's topic | Jan Leafy greens for lactose intolerance, The healtn of Refillable snack containers seems to be higher in postmenopausal compared with aand women. This can then affect our hormonal balance quite dramatically. The group without NAFLD on HRT also had a higher proportion of women with a normal body mass index. com for assistance. |
| menopause and high liver enzymes | What you can do: Speak up. Many women delay treatment because they're confused and embarrassed, says Ridgeway. If you feel a bulge between your legs or have trouble emptying your bladder or bowels completely, see your doctor, stat. For the best care, seek out a urogynecologist who specializes in pelvic floor disorders. For a mild case, your doctor may simply recommend pelvic floor exercises like Kegels. More advanced cases may merit surgery or a pessary, a device that you wear internally to support your pelvic organs. MORE: 5 Reasons It Hurts Down There. Liver Disease. When you're young and healthy, the liver tends to easily repair damage from things like alcohol, infections, or excess fat. However, sometimes the organ lays down scar tissue instead of healthy cells. Estrogen seems to interfere with this process, so when this hormone drops at menopause, scar tissue can start building up. Estrogen may also protect the mitochondria, or your cells' powerhouses, in your liver cells. As levels of this hormone decline, damage can ensue, further accelerating liver aging. What you can do: The next time your doctor orders a routine blood screen, ask him or her to check the box for a liver enzyme test. Elevated levels are often the first sign that something's wrong in this critical organ. Try the day liver detox for total body health with Heal Your Whole Body. If you were born between and , you should also ask to be tested for hepatitis C , a virus that can wreak havoc on the liver. Autoimmune Disorders Feeling tired , moody, or experiencing hot flashes? Those are all normal menopausal symptoms —but they could also be signs of an autoimmune disorder such as multiple sclerosis, lupus, or rheumatoid arthritis , says Mindy S. Christianson, MD, an assistant professor of reproductive endocrinology and infertility at Johns Hopkins University School of Medicine. It could be a new immune problem cropping up at menopause, or the change of life might very well cause a condition you already had to worsen. Again, blame estrogen: Shifts in this hormone may lead to excess inflammation in your body and cause certain body systems to turn on themselves. What you can do: Keep track of any symptoms you experience during menopause and discuss them with your doctor. They can help you keep tabs on your disease and tweak your treatment as necessary. MORE: 3 Signs You Have Chronic Inflammation. Dry Eye. Estrogen isn't the only hormone that's going awry. Levels of testosterone—yes, women make it, too—also fall during menopause, and that can mess with your eyes. Metabolism Open May 21; National Institutes of Health. Office of Dietary Supplements. Qin X et al. Effect of folic acid intervention on ALT concentration in hypertensives without known hepatic disease: a randomized, double-blind, controlled trial. European Journal of Clinical Nutrition ; Get weekly tips, tools, and a dose of humor for your menopause journey. Because some days, you just gotta laugh about it. Got fellow pausers in your life who are looking for guidance? Invite them to join our judgment-free community. Digestive Health. What are high liver enzymes? Read about the importance of a healthy liver The more common liver enzymes are: Alkaline phosphatase ALP is important for breaking down proteins. Alanine transaminase ALT is necessary for converting proteins into energy for liver cells, removing toxins from the blood, and making bile. Aspartate transaminase AST is an important enzyme for the metabolism of amino acids. Gamma-glutamyl transferase GGT helps metabolize drugs and other toxins. How high liver enzymes are associated with menopause Declining estrogen, along with aging, can be a challenging situation. Thank you. We received your request to join. all symptoms. Hepatology Aug 27 Brady CW. Mayo Clinic Matsui S et al. Office of Dietary Supplements Qin X et al. com—a multiple award-winning website. LATEST ARTICLES. Valentine's Day is the perfect time to give your family and friends some keto dessert love! Medicine Baltimore. Grønbæk M, Deis A, Sørensen TI, Becker U, Schnohr P, Jensen G. Mortality associated with moderate intakes of wine, beer, or spirits. Klatsky AL, Armstrong MA, Friedman GD. Alcohol and mortality. Ann Intern Med. Shaper AG, Wannamethee G, Walker M. Alcohol and mortality in British men: explaining the U-shaped curve. Grønbæk M, Deis A, Sørensen TI, Becker U, Borch-Johnsen K, Müller C, et al. Influence of sex, age, body mass index, and smoking on alcohol intake and mortality. Becker U, Grønbæk M, Johansen D, Sørensen TI. Lower risk for alcohol-induced cirrhosis in wine drinkers. Becker U, Deis A, Sørensen TI, Grønbæk M, Borch-Johnsen K, Müller CF, et al. Prediction of risk of liver disease by alcohol intake, sex, and age: a prospective population study. Dunn W, Xu R, Schwimmer JB. Modest wine drinking and decreased prevalence of suspected nonalcoholic fatty liver disease. Dunn W, Sanyal AJ, Brunt EM, Unalp-Arida A, Donohue M, McCullough AJ, et al. Modest alcohol consumption is associated with decreased prevalence of steatohepatitis in patients with non-alcoholic fatty liver disease NAFLD. Hayashi PH, Harrison SA, Torgerson S, Perez TA, Nochajski T, Russell M. Cognitive lifetime drinking history in nonalcoholic fatty liver disease: some cases may be alcohol related. Ruhl CE, Everhart JE. Joint effects of body weight and alcohol on elevated serum alanine aminotransferase in the United States population. Clin Gastroenterol Hepatol. Loomba R, Bettencourt R, Barrett-Connor E. Synergistic association between alcohol intake and body mass index with serum alanine and aspartate aminotransferase levels in older adults: the rancho Bernardo study. Aliment Pharmacol Ther. Loomba R, Yang HI, Su J, Brenner D, Iloeje U, Chen CJ. Obesity and alcohol synergize to increase the risk of incident hepatocellular carcinoma in men. Loomba R, Yang HI, Su J, Brenner D, Barrett-Connor E, Iloeje U, et al. Synergism between obesity and alcohol in increasing the risk of hepatocellular carcinoma: a prospective cohort study. James PT, Leach R, Kalamara E, Shayeghi M. The worldwide obesity epidemic. Obes Res. Download references. We are grateful to the women who participated in the trial and to the entire medical, nursing, and administrative staff who contributed to the implementation of UKCTOCS. Institute for Liver and Digestive Health, Division of Medicine, University College London, Royal Free Hospital, Rowland Hill Street, London, NW3 2PF, UK. Public Health Sciences and Medical Statistics, Faculty of Medicine, University of Southampton, Southampton, UK. Office of the President and Vice-Chancellor, The University of New South Wales, UNSW Sydney, Sydney, Australia. You can also search for this author in PubMed Google Scholar. All authors were involved in study design. PT, SA, AGM, UM and WR were involved in data collection. PT, UM and WR drafted the manuscript and figs. PT undertook the literature search. PT, JP, ST, UM, WR and MB performed the statistical analysis. All authors critically revised the manuscript and approved the final version. Correspondence to Paul M Trembling. UM and IJ have a financial interest through Abcodia Ltd. in the third party exploitation of the trial biobank. During part of the UKCTOCS trial IJ had a consultancy arrangement with Becton Dickinson in the field of tumour markers. None of the other authors declared any conflicts of interest. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Crude rates of first liver-related events per person years according to a BMI category and b alcohol consumption category over mean follow-up of 5. Table S1. ICD codes and death certificate text of first LREs. DOCX kb. Open Access This article is distributed under the terms of the Creative Commons Attribution 4. Reprints and permissions. Trembling, P. et al. Risk of chronic liver disease in post-menopausal women due to body mass index, alcohol and their interaction: a prospective nested cohort study within the United Kingdom Collaborative Trial of Ovarian Cancer Screening UKCTOCS. BMC Public Health 17 , Download citation. Received : 19 October Accepted : 20 June Published : 28 June Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Rosenberg 1 Show authors BMC Public Health volume 17 , Article number: Cite this article Accesses 10 Citations 2 Altmetric Metrics details. Abstract Background We investigated the risk of chronic liver disease CLD due to alcohol consumption and body mass index BMI and the effects of their interaction in a prospective cohort study of women recruited to the UKCTOCS trial. Results First LREs were reported in 0. Conclusion High BMI and alcohol consumption and abstinence are risk factors for CLD in post-menopausal women. Trial registration UKCTOCS is registered as an International Standard Randomised Controlled Trial, number ISRCTN Background Chronic liver disease CLD is the 5th commonest cause of death in the UK, and the only rising major cause of mortality and morbidity. Methods Study population This prospective cohort study was nested in the United Kingdom Collaborative Trial of Ovarian Cancer Screening UKCTOCS [ 14 ]. Exposures The exposures of interest were BMI and current weekly alcohol consumption. Outcome The main outcome measure was first liver-related event LRE , defined as first presentation of either a hospital admission, outpatient appointment, cancer registration with, or death from, an ICD code of interest. Separate influences of BMI and of alcohol on incident liver disease Cox proportional hazards models were used to calculate hazard ratios HRs of first LRE in three categories of BMI using normal BMI as the reference. Interaction between alcohol and BMI Interaction between alcohol using several thresholds and BMI as a continuous variable was analysed by calculating the interaction term from the Cox regression models. The composition of the final study cohort and its derivation from the UKCTOCS cohort. Full size image. Table 1 Baseline characteristics, number of first events according to BMI category and in all participants, and hazard ratios for LRE for potential confounders continuous a and categorical b variables Full size table. Table 2 Event rates and adjusted hazard ratios of first liver-related events, according to BMI category and according to alcohol category Full size table. Table 3 Event rates and hazard ratios of first liver-related event according to various BMI and alcohol combinations Full size table. Strengths and limitations Strengths of this study include the size and duration of follow-up, the prospective design and the independence of the data capture for outcomes. Other studies A number of studies have demonstrated a reduced risk of liver disease in patients with NAFLD who consume low or moderate amounts of alcohol [ 31 , 32 , 33 ], and it has been suggested that these levels of alcohol use may be associated with beneficial effects of insulin sensitivity in post-menopausal women [ 34 ]. Implications Our results suggest a substantial influence of both elevated BMI and alcohol on risk of CLD. Conclusion This study of post-menopausal women suggests that elevated BMI and high alcohol intake are independent risk factors for liver disease. Abbreviations BMI: Body mass index CLD: Chronic liver disease HES: Hospital episode statistics HR: Hazard ratio ICD International classification of disease 10th revision IMD: Index of multiple deprivation LRE: Liver-related event NAFLD: Non-alcoholic fatty liver disease NHANES: National health and nutrition examination survey UKCTOCS: United Kingdom Collaborative Trial of Ovarian Cancer Screening. References Leon DA, McCambridge J. Article PubMed Google Scholar Department of Health. Google Scholar Williams R, Aspinall R, Bellis M, Camps-Walsh G, Cramp M, Dhawan A, et al. Article PubMed Google Scholar Scaglione S, Kliethermes S, Cao G, Shoham D, Durazo R, Luke A, et al. Article PubMed Google Scholar Whitlock G, Lewington S, Sherliker P, Clarke R, Emberson J, Halsey J, et al. Article PubMed Google Scholar Ioannou GN, Weiss NS, Kowdley KV, Dominitz JA. Article PubMed Google Scholar Batty GD, Shipley MJ, Kivimaki M, Barzi F, Smith GD, Mitchell R, et al. Article CAS Google Scholar Marchesini G, Brizi M, Bianchi G, Tomassetti S, Bugianesi E, Lenzi M, et al. Article CAS PubMed Google Scholar Liu B, Balkwill A, Reeves G, Beral V. Article PubMed PubMed Central Google Scholar Hart CL, Batty GD, Morrison DS, Mitchell RJ, Smith GD. Article CAS Google Scholar Garcia-Tsao G, Friedman S, Iredale J, Pinzani M. Article PubMed PubMed Central Google Scholar Diehl AM. Article CAS PubMed Google Scholar Serfaty L, Poujol-Robert A, Carbonell N, Chazouillères O, Poupon RE, Poupon R. Article CAS PubMed Google Scholar Menon U, Gentry-Maharaj A, Hallett R, Ryan A, Burnell M, Sharma A, et al. Article PubMed Google Scholar Menon U, Gentry-Maharaj A, Ryan A, Sharma A, Burnell M, Hallett R, et al. Article PubMed PubMed Central Google Scholar Menon U, Ryan A, Kalsi J, Gentry-Maharaj A, Dawnay A, Habib M, et al. Article PubMed PubMed Central Google Scholar Drinkaware. Article PubMed PubMed Central Google Scholar Day CP, James OFW. Article CAS PubMed Google Scholar Bolton-Smith C, Woodward M, Tunstall-Pedoe H, Morrison C. Article CAS PubMed PubMed Central Google Scholar Hill A, Roberts J. Article CAS PubMed Google Scholar Nieto-Garcia FJ, Bush TL, Keyl PM. Article CAS PubMed Google Scholar Roberts RJ. Article CAS PubMed Google Scholar Kuskowska-Wolk A, Karlsson P, Stolt M, Rössner S. CAS PubMed Google Scholar Midanik L. Article CAS PubMed Google Scholar Romelsjö A, Leifman H, Nyström S. Article PubMed Google Scholar Parker DR, Derby CA, Usner DW, Gonzalez S, Lapane KL, Carleton RA. Article CAS PubMed Google Scholar Goddard E. Google Scholar Pinsky PF, Miller A, Kramer BS, Church T, Reding D, Prorok P, et al. Article CAS PubMed Google Scholar Hepatitis C in the UK report. Article PubMed Google Scholar Sogabe M, Okahisa T, Taniguchi T, Tomonari T, Tanaka T, Tanaka H, et al. Article CAS PubMed Google Scholar Davies MJ, Baer DJ, Judd JT, Brown ED, Campbell WS, Taylor PR. Article CAS PubMed Google Scholar Askgaard G, Grønbæk M, Kjær MS, Tjønneland A, Tolstrup JS. Article PubMed Google Scholar Hart CL, Morrison DS, Batty GD, Mitchell RJ, Davey SG. Article PubMed PubMed Central Google Scholar Naveau S, Giraud V, Borotto E, Aubert A, Capron F, Chaput JC. Article CAS PubMed Google Scholar Yi S-W, Hong J-S, Yi J-J, Ohrr H. Article PubMed PubMed Central Google Scholar Klatsky AL, Armstrong MA, Friedman GD. Article CAS PubMed Google Scholar Shaper AG, Wannamethee G, Walker M. Article CAS PubMed Google Scholar Grønbæk M, Deis A, Sørensen TI, Becker U, Borch-Johnsen K, Müller C, et al. Article PubMed PubMed Central Google Scholar Becker U, Grønbæk M, Johansen D, Sørensen TI. Article PubMed Google Scholar Becker U, Deis A, Sørensen TI, Grønbæk M, Borch-Johnsen K, Müller CF, et al. |
Welche anmutige Mitteilung