Cigarette smoking is a risk factor for the onset of fatty liver disease in nondrinkers: A longitudinal cohort study

Okamoto, Masashi; Miyake, Teruki; Kitai, Kohichiro; Furukawa, Shinya; Yamamoto, Shin; Senba, Hidenori; Kanzaki, Sayaka; Deguchi, Akiko; Koizumi, Masaru; Ishihara, Toru; Miyaoka, Hiroaki; Yoshida, Osamu; Hirooka, Masashi; Kumagi, Teru; Abe, Masanori; Matsuura, Bunzo; Hiasa, Yoichi

doi:10.1371/journal.pone.0195147

Cited by 46 publications

(35 citation statements)

References 26 publications

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“…There have been several longitudinal cohort studies on lifestyle habits involved in the development or remission of NAFLD. However, most of these studies assessed lifestyle habits at baseline but not changes in these habits during the study period 14,[16][17][18]26 . We conducted a longitudinal cohort study to investigate the association of the development or remission of NAFLD with favorable changes in the lifestyle habits during follow-up period: weight loss, starting to exercise, quitting smoking, and stopping eating dinner within 2 hours of going to bed.…”

Section: Discussionmentioning

confidence: 99%

Effect of weight change and lifestyle modifications on the development or remission of nonalcoholic fatty liver disease: sex-specific analysis

Yoshioka

Ishigami

Watanabe

et al. 2020

Sci Rep

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The effects of changes in various lifestyle habits on nonalcoholic fatty liver disease (NAFLD) have not been well elucidated. We aimed to clarify how weight change and lifestyle modifications were associated with the development or remission of NAFLD. In this longitudinal cohort study, we reviewed the periodic health checkup data of 1,421 subjects with no causes of liver disease besides NAFLD who had received at least two health checkups between 2009 and 2018. The prevalence of NAFLD at baseline was 34.1% (484/1,421). During follow-up period (4.6 ± 2.8 years), 104 subjects developed NAFLD and 127 subjects demonstrated NAFLD remission. The frequency of NAFLD development or that of NAFLD remission significantly increased as the larger weight gain or weight loss was, respectively (both, p < 0.001). Approximately 40% of the subjects who maintained ≥ 1%/year weight loss achieved NAFLD remission. By multivariate analysis, quitting smoking were independently associated with NAFLD development (adjusted odds ratio [AOR], 2.86; 95% CI, 1.24-6.62). Subjects who quit smoking demonstrated large weight gain (≥1%/year) significantly more frequently than the other subjects (p < 0.001). In sex-specific analysis, starting to exercise was independently associated with NAFLD remission in men (AOR, 2.38; 95% CI, 1.25-4.53). Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases and will become the leading cause of end-stage liver disease in the near future. NAFLD is a global public health concern with a heavy healthcare burden 1. NAFLD encompasses a spectrum of progressive pathological conditions, ranging from nonalcoholic fatty liver (NAFL) to steatohepatitis (NASH) 2. Many clinical trials have shown that weight loss and lifestyle intervention improve markers of liver function and histological features in patients with NAFLD 3-13. Thus, NAFLD is closely related to lifestyle habits, and is often described as the hepatic manifestation of metabolic syndrome. NAFLD is reversible to some extent. There have been several studies on lifestyle habits associated with the development or remission of NAFLD 14-18. However, most of the studies focused only on the lifestyle habits at baseline, but not the changes in lifestyle habits during the study period. Beginning in April 2008, Japan initiated a change in the national health policy in order to prevent metabolic syndrome. This comprehensive preventive policy involves unprecedented nationwide screening and lifestyle intervention for abdominal obesity, and the effectiveness of the nationwide preventive program has been demonstrated 19. In addition, various lifestyle habits can be modified as a result of recently growing health consciousness across Japanese society.

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Section: Discussionmentioning

confidence: 99%

Effect of weight change and lifestyle modifications on the development or remission of nonalcoholic fatty liver disease: sex-specific analysis

Yoshioka

Ishigami

Watanabe

et al. 2020

Sci Rep

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“…However, we believe that these flaws are balanced by the benefits of this large study, and the ability to generalize these results to the population. As the mechanism of the association between NAFLD and smoking remains controversial, future prospective studies should investigate the underlying mechanisms of this association. In addition, future studies are needed to elucidate the effects of active and passive smoking on NAFLD.…”

Section: Discussionmentioning

confidence: 99%

The interaction of nonalcoholic fatty liver disease and smoking on mortality among adults in the United States

Wijarnpreecha

Scribani

Kim

et al. 2019

Liver International

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Background & Aims Nonalcoholic fatty liver disease (NAFLD) has become the most common liver disease in Western countries. Smoking and diabetes mellitus (DM) have been shown to increase mortality; however, whether NAFLD adds to the detrimental effect of smoking in DM and non‐DM patients is unknown. We evaluated the possible interactive effect of NAFLD and smoking on mortality risk in a US population‐based sample. Methods Cross‐sectional data from 11 205 participants in the third National Health and Nutrition Examination Survey were analysed. NAFLD was defined as ultrasonographic hepatic steatosis without evidence of other liver diseases. Proportional hazards regression modelling was used to test for the multiplicative interaction of NAFLD and smoking on overall mortality, controlling for DM. Results 36.5% of the participants had NAFLD of whom 21.1% were current smokers, while among non‐NAFLD subjects, 26.2% reported current smoking. Smoking was associated with a hazard ratio (HR) of 2.23 (95% confidence interval (CI): 1.87‐2.65) among non‐NAFLD subjects, and 2.31 (95% CI: 1.33‐2.92, P < 0.01) among NAFLD patients. In contrast, the HR for NAFLD was 1.01 (95% CI: 0.78‐1.31, P = 0.96) among smokers and 0.98 (95% CI: 0.87‐1.10, P = 0.73) among non‐smokers. There was no evidence of interaction between NAFLD and smoking (HR = 1.01, 95% CI: 0.74‐1.38, P = 0.94) in the combined model. Conclusion We found that smoking increased mortality by two‐fold among the US population. Although the magnitude of the increase in mortality did not differ from that in non‐NAFLD subjects, smoking represents a modifiable determinant of long‐term outcomes in NAFLD patients.

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“…Accumulating evidence shows that exposure to environmental toxicants, including secondhand smoke (SHS), contributes to the development of NAFLD by promoting mitochondrial dysfunction and oxidative stress within the hepatocytes [9][10][11][12]. Several studies have shown that cigarette smoking is an independent risk factor for the onset of NAFLD [13][14][15][16], and significantly associated with increased intrahepatic fat [17] and advanced liver fibrosis [18,19]. Survey based reports have also shown an association between exposure to SHS and development of NAFLD in children [20,21] and in never-smoking women [22].…”

Section: Introductionmentioning

confidence: 99%

Secondhand Smoke Induces Liver Steatosis through Deregulation of Genes Involved in Hepatic Lipid Metabolism

Tommasi

Yoon

Besaratinia

2020

IJMS

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We investigated the role of secondhand smoke (SHS) exposure, independently of diet, in the development of chronic liver disease. Standard diet-fed mice were exposed to SHS (5 h/day, 5 days/week for 4 months). Genome-wide gene expression analysis, together with molecular pathways and gene network analyses, and histological examination for lipid accumulation, inflammation, fibrosis, and glycogen deposition were performed on the liver of SHS-exposed mice and controls, upon termination of exposure and after one-month recovery in clean air. Aberrantly expressed transcripts were found in the liver of SHS-exposed mice both pre- and post-recovery in clean air (n = 473 vs. 222). The persistent deregulated transcripts (n = 210) predominantly affected genes and functional networks involved in lipid metabolism as well as in the regulation of the endoplasmic reticulum where manufacturing of lipids occurs. Significant hepatic fat accumulation (steatosis) was observed in the SHS-exposed mice, which progressively increased as the animals underwent recovery in clean air. Moderate increases in lobular inflammation infiltrates and collagen deposition as well as loss of glycogen were also detectable in the liver of SHS-exposed mice. A more pronounced phenotype, manifested as a disrupted cord-like architecture with foci of necrosis, apoptosis, inflammation, and macrovesicular steatosis, was observed in the liver of SHS-exposed mice post-recovery. The progressive accumulation of hepatic fat and other adverse histological changes in the SHS-exposed mice are highly consistent with the perturbation of key lipid genes and associated pathways in the corresponding animals. Our data support a role for SHS in the genesis and progression of metabolic liver disease through deregulation of genes and molecular pathways and functional networks involved in lipid homeostasis.

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Cigarette smoking is a risk factor for the onset of fatty liver disease in nondrinkers: A longitudinal cohort study

Cited by 46 publications

References 26 publications

Effect of weight change and lifestyle modifications on the development or remission of nonalcoholic fatty liver disease: sex-specific analysis

Effect of weight change and lifestyle modifications on the development or remission of nonalcoholic fatty liver disease: sex-specific analysis

The interaction of nonalcoholic fatty liver disease and smoking on mortality among adults in the United States

Secondhand Smoke Induces Liver Steatosis through Deregulation of Genes Involved in Hepatic Lipid Metabolism

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