Do Your Patients Consume Enough Caffeine?
Do Your Patients Consume Enough Caffeine?
It is clear from the DGAC that caffeine consumption through coffee intake is associated with at least one other behavior: tobacco use. Before tobacco use was controlled for in research, it appeared that coffee consumption actually increased the risk for lung cancer. After adjustment, however, it lowered that same risk. Are there other behaviors associated with coffee consumption that weren't measured? I bet there are. Without knowing, it is impossible to know whether coffee/caffeine consumption is simply a marker for other healthy behaviors.
Short of an RCT, what else can we do to establish a link between caffeine consumption and beneficial health effects? For observational data, evidence of dose-response and biological plausibility both help. Caffeine consumption certainly shows evidence of the former, particularly for type 2 diabetes and cardiovascular disease. Some studies of endometrial cancer, Parkinson disease, and colorectal cancer also show evidence of a dose-response in risk reduction with coffee or caffeine intake. For many other outcomes, the response is nonlinear, with no change in disease risk for doses greater than four cups of coffee (300 mg caffeine) daily.
Establishing biologic plausibility is messy. To start, the sheer number of outcomes studied makes this difficult. The DGAC reports on associations with cardiovascular disease, all-cause mortality, type 2 diabetes, neurodegenerative disease, and any number of common and uncommon cancers. If there is a true biologic pathway that links coffee or caffeine consumption to disease risk, it's likely to be different depending on the outcome assessed. For example, it seems unlikely that coffee or caffeine reduces prostate cancer and Parkinson disease through the same biologic pathway.
Furthermore, it remains unclear what the active substance in coffee actually is. Is caffeine mediating the beneficial effects, or is it one of the many compounds present in coffee beans?
According to the studies cited in the DGAC, decaffeinated coffee reduced the risk for lung cancer, breast cancer, and type 2 diabetes. Decaffeinated coffee did not reduce cardiovascular-related mortality (although caffeinated coffee did), and caffeinated products other than coffee were associated with improvements in cognitive function. In short, there is evidence that both caffeine and coffee reduce adverse outcomes and improve health.
The Role of Healthy and Unhealthy Behaviors
It is clear from the DGAC that caffeine consumption through coffee intake is associated with at least one other behavior: tobacco use. Before tobacco use was controlled for in research, it appeared that coffee consumption actually increased the risk for lung cancer. After adjustment, however, it lowered that same risk. Are there other behaviors associated with coffee consumption that weren't measured? I bet there are. Without knowing, it is impossible to know whether coffee/caffeine consumption is simply a marker for other healthy behaviors.
Short of an RCT, what else can we do to establish a link between caffeine consumption and beneficial health effects? For observational data, evidence of dose-response and biological plausibility both help. Caffeine consumption certainly shows evidence of the former, particularly for type 2 diabetes and cardiovascular disease. Some studies of endometrial cancer, Parkinson disease, and colorectal cancer also show evidence of a dose-response in risk reduction with coffee or caffeine intake. For many other outcomes, the response is nonlinear, with no change in disease risk for doses greater than four cups of coffee (300 mg caffeine) daily.
Establishing biologic plausibility is messy. To start, the sheer number of outcomes studied makes this difficult. The DGAC reports on associations with cardiovascular disease, all-cause mortality, type 2 diabetes, neurodegenerative disease, and any number of common and uncommon cancers. If there is a true biologic pathway that links coffee or caffeine consumption to disease risk, it's likely to be different depending on the outcome assessed. For example, it seems unlikely that coffee or caffeine reduces prostate cancer and Parkinson disease through the same biologic pathway.
Furthermore, it remains unclear what the active substance in coffee actually is. Is caffeine mediating the beneficial effects, or is it one of the many compounds present in coffee beans?
According to the studies cited in the DGAC, decaffeinated coffee reduced the risk for lung cancer, breast cancer, and type 2 diabetes. Decaffeinated coffee did not reduce cardiovascular-related mortality (although caffeinated coffee did), and caffeinated products other than coffee were associated with improvements in cognitive function. In short, there is evidence that both caffeine and coffee reduce adverse outcomes and improve health.
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