Batista, M. Desmond, P. Townsend, P.

Caffeine and liver health -

The authors suggest that future research could test the relationship between coffee and liver disease with more rigorous control of the amount of coffee consumed.

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Decaffeinated coffee, or decaf, is similar to regular coffee but contains very little caffeine. Research suggests that drinking decaf is not harmful…. Scientists have conducted a lot of research into the effects of caffeine in people with depression.

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Medical News Today. Health Conditions Health Products Discover Tools Connect. Drinking any coffee reduces the risk of liver disease, study finds. By Robby Berman on June 28, — Fact checked by Zia Sherrell, MPH. Share on Pinterest A new study finds a link between drinking any type of coffee and a lower risk of liver problems.

Liver disease and a welcome study. Reaction to the study. Share this article. Latest news Ovarian tissue freezing may help delay, and even prevent menopause. RSV vaccine errors in babies, pregnant people: Should you be worried? To investigate possible reverse causation, HRs were calculated for each outcome according to coffee consumption after removing all cases occurring within the first 5 years from recruitment.

Finally, subgroup analyses were performed by calculating adjusted HRs of CLD in each BMI category i. All analyses were performed in R Version 4. The Strengthening the Reporting of Observational Studies in Epidemiology STROBE guidelines [ 17 ] were followed in reporting this study.

This work was informed by the results of a patient and public involvement focus group and survey of patients with CLD.

This demonstrated a high level of interest among patients in potential randomised controlled trials evaluating coffee as an intervention in CLD.

A total of , participants with known baseline coffee consumption and without baseline CLD were followed-up for a median of During the follow-up, there were cases of incident CLD, cases of incident CLD or steatosis, cases of incident HCC including 83 deaths and deaths from CLD Fig.

A flow diagram showing the derivation of the cohort used in this study and the sources for identification of cases for each outcome. Non-coffee drinkers were more likely to be non-smokers and teetotal but were more deprived and had a higher prevalence of diabetes and obesity Table 2.

Coffee drinkers in the highest category of consumption i. The baseline characteristics of these participants are shown in supplementary Tables 5 , 6 , 7 , 8.

Decaffeinated coffee drinkers were more likely to be female Drinkers of ground coffee had the highest median weekly alcohol consumption Townsend deprivation quartile, previous or current smoking, diabetes and BMI were associated with increased risk of incident CLD and death from CLD, as shown in supplementary Table 9.

The highest quartile of weekly alcohol units and daily or almost daily alcohol consumption were also associated with increased risk but not the lower categories. There was no association of ethnicity with incident CLD or death from CLD.

The results of the univariate Cox analyses using penalised splines are shown in in supplementary Figs. Thus, these continuous covariates were modelled in the main analysis using splines for BMI and weekly alcohol units and linear terms for age and deprivation.

Coffee drinkers all types combined had lower fully adjusted risks than non-coffee drinkers of incident CLD HR 0. There was a similar, though less statistically significant, association between coffee consumption and incident HCC HR 0.

The reductions in HRs were proportional to the quantity of coffee consumption up to around 3—4 cups each day beyond which further increases in consumption provided no additional benefit. The adjusted HRs were very similar though slightly larger in magnitude compared to the unadjusted HRs.

A forest plot showing the associations between consumption of all coffee, decaffeinated coffee, instant coffee and ground coffee including espresso with incident CLD, incident CLD or steatosis, incident HCC and death from CLD. Schoenfeld residuals from the fully adjusted Cox model indicated that smoking status did not meet the PH assumption p -value 0.

When the Cox model was stratified on smoking, which accounts for violation in the PH assumption, the estimates for the association between coffee and incident CLD were the same as the unstratified analysis i. In addition, the Schoenfeld residuals did not show any evidence of violation when smoking status was re-categorised as smokers vs.

non-smokers, and when this was used in the fully adjusted Cox model the association of coffee consumption with CLD was essentially unchanged. As such, the effect of any violation in the PH assumption on the estimates was negligible.

HRs of incident CLD, incident CLD or steatosis, incident HCC and death from CLD according to consumption of decaffeinated, instant and ground including espresso coffee are shown in Tables 4 , 5 , 6 and Fig. For consumption of each coffee type, there were strong inverse associations with incident CLD, incident CLD or steatosis and death from CLD, though precision was lower due to smaller sample sizes.

There was a weaker inverse association of all coffee types with HCC that did not reach significance in the fully adjusted models. The inverse associations between coffee and CLD were similar in the normal, overweight and obese BMI categories and in participants with and without diabetes supplementary Table During a median follow-up of The maximal protective effect was seen at around 3—4 cups each day.

Drinkers of decaffeinated, instant and ground coffee including espresso also had lower risks of incident CLD, incident CLD or steatosis, death from CLD and, to a lesser extent, HCC, with ground coffee including espresso having the largest effect.

This study agrees with previous cohort studies that generally report inverse associations between coffee consumption and CLD outcomes, including deranged liver enzymes [ 18 ], fibrosis [ 19 ], cirrhosis [ 7 ] and HCC [ 6 ].

The protective effects of coffee have been observed in different CLD aetiologies, such as ALD [ 7 ], NAFLD [ 20 ] and chronic viral hepatitis [ 21 ]. Previous studies also report a dose-response relationship up to 5 cups each day [ 6 ] but there are limited data above this range.

The inverse association between coffee and HCC was weaker in this study compared to previously reported estimates [ 6 , 22 , 23 ]. This was likely because of low power from a small number of HCC cases and a shorter follow-up time compared to other studies e.

and Lai et al. There may also have been a lower proportion of ground coffee drinkers, which may be more protective than other coffee types see below. The association between coffee consumption and NAFLD was investigated in a recent Mendelian randomisation study [ 24 ].

In that study, lifetime exposure to coffee was estimated using genetic variants, which are fixed before birth and not affected by confounders. While there was an inverse association between coffee and NAFLD, it did not reach statistical significance odds ratio 0.

The lack of significance may have been because the genetic variants used four single nucleotide polymorphisms only explained a small proportion of the variability of actual coffee consumption.

This study is the first, to our knowledge, to directly investigate the effect of different coffee types on CLD outcomes in a single large cohort. There are few reports in the literature about specific coffee types. A small study in France found that filtered ground coffee but not espresso was associated with a reduced risk of fibrosis in obese women with NAFLD [ 25 ].

Indirect conclusions about other coffee types can be inferred from studies in countries where drinking preferences differ. For example, in Finland and Japan instant coffee is the most popular type, and inverse associations with CLD outcomes have been reported in both those countries [ 23 , 26 ].

A meta-analysis of three studies reported inverse associations between decaffeinated coffee and HCC, though smaller in magnitude compared to caffeinated coffee [ 6 ]. A cohort study in the United States reported a lower risk of death from CLD among drinkers of two cups of decaffeinated coffee each day compared to none, even after adjustment for caffeinated coffee intake [ 9 ].

The observation of a protective effect of decaffeinated coffee is highly relevant to the development of a coffee-based intervention for preventing CLD onset or progression.

Caffeine intolerance may limit increases in coffee consumption, and thus decaffeinated coffee may be a preferable alternative. Given its well know safety profile and cheap cost, coffee has potential as widely accessible lifestyle intervention, even in low to middle-income countries.

A limitation is the observational cohort design, which cannot infer causation. There was a single timepoint of coffee consumption, and volumes and preferred types may have changed over the follow-up period. Cup sizes may also have varied.

However, misclassification of coffee consumption would have pushed the effect size towards null and not explain our results. There was also no data on ex-coffee drinkers, which may be relevant to reverse causation, as is discussed below.

In addition, there may have been differences in chemical composition between coffees within the same type e. due to different processes for decaffeination. The risk of confounding was reduced by making adjustments for baseline covariates, but these may have been assessed inaccurately or changed during follow-up.

In relation to alcohol consumption, a key CLD risk factor, the assumptions used to convert drinks into units, such as the volume and alcohol content of each beverage, may have been inaccurate. In addition, imputation of alcohol units was not used for missing data.

The HRs adjusted for weekly units were similar to those adjusted for alcohol consumption frequency. While there may have been some residual confounding from alcohol, it is unlikely that this alone is responsible for the findings of this study. Bias may have been introduced from incomplete adjustment for socio-economic status using Townsend deprivation index scores rather than individual level socioeconomic variables e.

education [ 12 ]. This would have exaggerated the effect sizes because deprivation was associated with CLD and non-coffee drinkers were more deprived than coffee drinkers. There were small differences in proportions of ethnicities in the non-coffee drinking reference group compared to the coffee drinking groups.

Prevalence and aetiology of CLD is known to vary between ethnic groups [ 27 ], and this would have introduced bias if not fully accounted for by binary adjustment for white or other ethnicity.

The results were also not adjusted for waist circumference, which may be related to metabolic syndrome independently of BMI, or prediabetes. Other CLD risk factors not adjusted for included chronic infection with hepatitis B or C, though prevalence of these conditions was likely low in this UK volunteer cohort.

Some cases and non-cases may have been misclassified because of inaccuracies in the coded data used to ascertain outcomes. Participants with an associated ICD code K nonalcoholic steatohepatitis, which corresponds to K While this assumption may have led to under-ascertainment of CLD cases, the risk of bias was likely small given the similar associations of all coffee types with CLD and CLD or steatosis.

Reverse causation was addressed by excluding diagnosed CLD at baseline. The presence of undiagnosed cases might have exaggerated the effect sizes if CLD resulted in coffee intolerance, and it was not possible to identify previous coffee drinkers in our non-coffee drinker category.

However, the protective effect of coffee was robust to exclusion of CLD outcomes in the first five years of follow-up, suggesting that any effect of reverse causation was small. It was not possible to fully assess the effects of very high levels of coffee consumption as the numbers of events in these categories were low.

Dose-response meta-analyses report protective effects up to around 5 cups each day with increasing uncertainty thereafter [ 6 , 7 ]. The results of this study may be limited by the demographics of the voluntary UK Biobank Cohort, who were predominantly white and likely over-representative of those from higher socio-economic groups.

As such, the findings may not generalise to populations with a very different ethnic and socio-economic composition. Confidence in the veracity of the observed inverse associations of coffee consumption with CLD outcomes is increased by several factors.

These include the magnitude and significance of the effect sizes and the presence of a dose response. In addition, residual confounding was likely to have led to underestimation of the effect sizes given that the adjusted HRs were generally larger in magnitude and significance than the unadjusted HRs, indicating coffee drinkers had a greater overall burden of known CLD risk factors.

There is biological plausibility of a protective effect of coffee against CLD outcomes. Caffeine is a non-selective antagonist of the A2aA receptor, activation of which stimulates collagen production by hepatic stellate cells, the primary mediators of fibrosis [ 28 , 29 ].

However, in the present study as well as in previous studies [ 6 ] decaffeinated coffee was also protective. Alternative active ingredients in coffee may include chlorogenic acid, kahweol and cafestol, which protect against liver fibrosis in animal studies [ 30 , 31 ].

Kahweol and cafestol are present in highest concentrations in ground coffee, which was most protective. Given the protective effects of the different coffee types with varying composition, there may be a complex relationship involving more than one active ingredient. This study provides evidence of a protective effect of all types of coffee including decaffeinated against CLD outcomes.

These findings are significant given the paucity of effective preventative and treatment strategies for CLD, especially in low to medium income countries, where the burden of CLD is highest. Further work is now needed to replicate these findings using more robust methods, including Mendelian randomisation with a more powerful set of genetic variants to estimate coffee consumption than available previously.

Randomised trials should then investigate the efficacy of a coffee-based intervention in those at risk of CLD or its complications. Sepanlou SG, Safiri S, Bisignano C, Ikuta KS, Merat S, Saberifiroozi M, et al.

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Coffee, including caffeinated and decaffeinated coffee, and the risk of hepatocellular carcinoma: a systematic review and dose-response meta-analysis.

For many, coffee is Cafeine favorite — some might say Caffdine — heakth of each day. A Caffeine and liver health Caffeije study has now Caffeine and liver health that coffee of Sports-specific meal planning kinds Collagen in Traditional Chinese Medicine the risk of chronic Collagen in Traditional Chinese Medicine hwalthfatty Caffeine and liver health diseaseliver cancerand death from chronic liver disease. The greatest benefit is derived from drinking 3—4 cups of coffee, even decaffeinated, per day. Coffee from grounds is slightly more beneficial than instant coffee. The study, from researchers at the Universities of Southampton and Edinburgh in the United Kingdom, appears in the journal BMC Public Health. Worldwide, liver disease causes 2 million deaths annually, with 1 million people dying from complications of cirrhosis and another from viral hepatitis and hepatocellular carcinoma. According to the study, the area most profoundly affected by liver disease is sub-Saharan Africa. Drinking coffee that is caffeinated ground Cafeine instant healtj decaffeinated Cafefine associated with a reduced risk of Energizing botanical blend chronic liver disease and related Almond industry trends conditions, new study published in the open access journal BMC Healty Health suggests. Researchers at the Fall prevention for seniors of Southampton and Lover, UK, Caffeinf that hfalth any type Heslth coffee was associated with a reduced risk of developing and dying from chronic liver disease compared to not drinking coffee, with the benefit peaking at three to four cups per day. The authors studied UK Biobank data onparticipants with known coffee consumption, who were followed over a median of During the study period, there were 3, cases of chronic liver disease, including deaths. Additionally, there were 5, cases of chronic liver disease or steatosis a build of up fat in the liver also known as fatty liver diseaseand cases of Hepatocellular carcinoma, a type of liver cancer.