In this guest post Dr Gautam Mehta, a Honorary Consultant and Senior Lecturer in Hepatology at UCL, writes about a recent study exploring the effect of an abstinence period on certain risk factors. He has research interests in alcohol-related liver disease, digital health and liver cirrhosis.
Dry January is an increasingly popular public health campaign, with over 3.1 million individuals participating in the UK in 2018 according to Alcohol Concern. For most, it is seen as an opportunity for a ‘detox’ at the start of the New Year. However, for us it was also a perfect opportunity to study the biological effects of short-term abstinence from alcohol in a group of healthy individuals, with a control group of individuals continuing regular alcohol consumption.
The primary aim of the study was to look for changes in insulin resistance (HOMA score), a marker of risk of diabetes mellitus. This was chosen as we had found an indication of change in insulin resistance in small pilot study a few years earlier, conducted with the help of some New Scientist journalists. We also looked for changes in other cardiovascular risk factors, such as body weight and blood pressure. Additionally, because of the recent interest in alcohol and cancer risk, we looked at the cancer-related growth factors vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF).
Both groups were drinking at similar levels at baseline, around 30 units/week (men 33 units/week, women 28 units/week). Due to the possible ‘confounding’ effect of individuals making many lifestyle changes at the same time, we rigorously assessed for changes in pattern of diet, exercise, smoking and mood. We then statistically adjusted our findings for any change in these lifestyle factors.
Significant benefits?
Our findings were striking. The marker of insulin resistance, HOMA score, fell by almost one-third in the abstinence group, no change in the control group. This implies a similar degree of decrease in risk of diabetes. Blood pressure decreased by around 10mmHg, which is the response you would expect from a drug for hypertension (high blood pressure), and weight decreased by almost 2kg. Again, neither of these changed in the control group, and the all the improvements persisted after adjusting for other lifestyle changes.
The cancer-related growth factors also fell dramatically, in over 90% of the abstinent participants, with no change in the control group. These cancer markers are not routinely measured in healthy individuals, so we can’t be exactly sure what these changes mean, but we do know that these molecules drive the progression of cancer so elevated levels may increase cancer risk.
Our study is among the first to show a direct interaction of alcohol use at this level with diabetes risk. This interaction, and the association with other cardiovascular risk factors, has implications for how we address the rising tide of liver disease in the UK. The majority of deaths attributable to alcohol in the UK are liver-related, and liver disease is now the 3rd commonest cause of preventable death in the UK. Alcohol is the most common cause of liver disease in the UK, but the second most common is non-alcoholic fatty liver disease (NAFLD) which is due to cardiovascular risk factors. However, our results suggest there is a synergistic effect between alcohol and NAFLD risk factors, and therefore there is likely to be a high-risk population with both these risk profiles. Other large registry studies have reported similar findings.
This has implications for the screening of liver disease. A recent NICE Quality Standard document suggests a ‘liver scan’ in all heavy drinkers (males >50 units/week, females >35 units/week). However, since around 4% of the population, over 1.5 million individuals, drink at these levels, we do not currently have the capacity or resource to implement this policy. A better approach may be to identify the high-risk population with both alcohol and NAFLD risk factors, who are likely to have accelerated liver disease. This approach merits testing, but work needs to be done to identify the specific cardiovascular markers to test for, and the cost-effectiveness of this strategy.
Another key question is to what extent these risks vary by baseline level of consumption. Since the average consumption in our study group was just over double the weekly recommended guidelines, it is important to know if these benefits are also seen with lower levels of consumption. However, it is certainly fair to say that our study adds weight to the evidence for health benefits of even short-term abstinence amongst those drinking at risky levels.
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