In a nutshell there is a slightly interesting idea that deserves further study. That's it.
In a nutshell there is a slightly interesting idea that deserves further study. That's it.
So, one could make a similar article saying "Myocardial infarction may be caused by sugar consumption" and support it by analyzing the recent diet of 200 people who died of heart disease and finding that 95% of them recently consumed a lot of sugar.
I think you not only missed the point but also are doubling down on your mistake by conflating correlation with causality. You don't conclude that burger craving is caused by owning a car by observing drive-through restaurants.
"we found some bacteria in people with heart disease, let's try killing the bacteria" is really bad logic.
Like another commenter posted it's similar to saying a lot of house fires had fire trucks in front of them, let's do some trials where we destroy some of the fire trucks to see if that helps.
Sugar is a very indirect cause of heart attacks, everyone knows that most heart attacks are a culmination of decades of diet and exercise habits. It's still worth researching everything to do with that, but it's pretty low value research because it's hard to draw any actionable conclusions from it other than "eat healthier and exercise", which is already well known.
The research in the article is talking about a direct cause. Bacteria exists on arterial plaque, viral infection triggers bacteria to multiply, something about that process causes the plaque to detach and cause a heart attack. If that ends up being a rock solid cause and effect, even for a subset of heart attacks, that could lead to things like direct prevention (anti-virals before the heart attack happens) or changes in patient management (everyone with artery disease gets put far away from sick patients) that could directly and immediately save a lot of lives.
The post you replied to was saying that the data from the study isn't as strong as the article and headline make it out to be, which is usually the case. For this one though I'm reading that less as "it's a nothingburger" and more as "it's a small interesting result that needs a lot of follow up".
And actually, if as a lot of science is now suggesting, inflammation and damage due to eating oxidization-prone lipids (aka refined oils) in combination with refined sugar is a big part of the cause of arterial damage and heart disease, that could be easily be the biggest root cause in most of these cases. The bacteria if they even play a causal role at any point, could be a result of previous damage due to diet (and lack of exercise).
The paper's idea of treating heart disease by giving patients antibiotics seems really problematic to me. Destroy your health with poor diet and lack of exercise, and then once you start to feel the effect of this, take antibiotics and destroy your gut health too.
Furthermore giving everyone antibiotics as a preventative measure for heart disease complications, given that most Americans are on the spectrum of heart disease (i.e. have hypertension) is a recipe for bacterial resistance and other population problems.
The mechanism for how refined linoleic acid if heated would create higher amounts of free radicals that are known to cause oxidative stress / inflammation is well understood.
I agree a large scale rct for this would be great, but I doubt anyone would fund it and if it does get done I'd be surprised if it wasn't designed to meet the biases of the side that funds it.
One could apply the same flawed logic to claim that propensity for myocardial infarction may cause certain bacterial infections.
I think a population study to assess the odds ratios of a risk factor on people who die of heart disease vs not would be valuable (but is a very different beast).
Quote: Of the bacteria detected, oral viridans group streptococcal DNA was the most common, being found in 42.1% of coronary plaques and 42.9% of endarterectomies. Immunopositivity for viridans streptococci correlated with severe atherosclerosis (P<0.0001) in both series and death from coronary heart disease (P=0.021) or myocardial infarction (P=0.042).Imagine, for the sake of argument, that being left-handed is correlated with a 0.001% higher likelihood of accidentally dropping your car keys every time you pick them up. An experiment studying a small sample of people for a month probably wouldn't detect this correlation at all. If you ran the same experiment but carefully monitored every single person in the US around the clock, you would be able to reliably detect it with an extremely small p-value. And yet it's still fair to describe it as an extremely minor correlation.
It's definitely not the strength of correlation. It's not even the probability that the opposite of the null hypothesis is false!
What Question Should Be Addressed Next?
• Could a short‐term antibiotics treatment given at the acute phase affect the outcome of myocardial infarction, and would it be possible to develop new diagnostic imaging and prevention methods for bacterial biofilm?
I didn't read the article but just based on the parent comment, it sounds like this baseline hasn't yet been established. It seems very wrong to start testing antibiotics without first establishing the baseline of whether everyone has this bacteria.