Relying on the lay press for medical advice can often lead to incorrect conclusions or misguided directions. The article linked below is a good example of how well-meaning but improperly thought out reporting can lead to conclusions not based on solid experimental design or reasoning.
Drinking More Than 1 Can of Any Soda Daily Linked to Liver Disease
The following is a quotation from the news report: A study of nearly 124,000 people found that drinking just one daily serving of artificially sweetened drinks increased the risk of a liver disease known as nonalcoholic fatty liver disease or metabolic dysfunction-associated steatotic liver disease (MASLD).
It’s from a British study that has not yet gone through peer review. It’s a self-reported study which always adds uncertainty to the data. It also has many uncontrolled variables, at least according to the press report. First, who gets fatty liver disease? The list below shows the major risk factors for the disorder. Who were the control groups for this study? Were they the same, save for their propensity to drink artificially sweetened drinks? Who drinks these beverages? People who are already at risk for fatty liver disease – ie, the obese.
For this study to have any meaning (I’m faulting the reporter who may not have had the full extent of the study, though, I doubt that’s the whole explanation) it would have controlled for all the other variables that predispose to fatty liver disease except for the consumption of artificially sweetened drinks.
Such a study would be very difficult and certainly could not be done by self reporting. Another conclusion to these data could easily be that people at the highest risk for fatty liver disease drink artificially sweetened drinks. It’s even possible that they may be reducing their risk by keeping their weight down. This is pure conjecture on my part, but it’s a possibility no matter how remote.
It’s hard enough to get decisive medical advice from your general physician who may not be well-trained in clinical investigation, epidemiology, and study design. But you certainly won’t get it from the lay press. Aeger medicīnālis, cave!
Obesity – especially central (abdominal) obesity
Type 2 diabetes mellitus
Insulin resistance or metabolic syndrome
Dyslipidemia – high triglycerides and/or low HDL cholesterol
Hypertension
Sedentary lifestyle and poor diet (high in sugar, refined carbs, and saturated fats)
Genetic predisposition (variants in genes like PNPLA3, TM6SF2, MBOAT7)
Age – risk increases with age
Sleep apnea
Polycystic ovary syndrome
Hypothyroidism and hypopituitarism
Medications – e.g., corticosteroids, tamoxifen, methotrexate, amiodarone
