Myocardial infarction may be an infectious disease
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tuni.fi
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 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).
One could apply the same flawed logic to claim that propensity for myocardial infarction may cause certain bacterial infections.
"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.
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.
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.
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.
On the other hand most people with "flu" in summer months are not infected with Influenza, so an improved influenza treatment isn't going to make a big difference for them unlike in winter. We know other reasons you might get those symptoms which are more likely in summer.
<https://en.wikipedia.org/wiki/Peptic_ulcer_disease>
<https://en.wikipedia.org/wiki/Timeline_of_peptic_ulcer_disea...>
One of the rare examples of a mental health condition being virtually completely eliminated is that of General paresis of the insane, a symptom of late-stage syphilis.
Successful treatment and elimination of syphilis in patients and populations through antibiotics. As one of the few cases of near-total elimination of a class of mental conditions, this a useful reminder to the psychiatric profession that not all mental conditions have causes limited to the brain and its function, whether through its biochemistry or neural/behavioural processes.
<https://en.wikipedia.org/wiki/General_paresis_of_the_insane>
I think a better example is the very recent (i.e., in the 2000s) discovery of anti-NMDAR encephalitis which can very closely resemble schizophrenia [1].
In syphilis, there were at least other manifestations of disease that can (and were) known, unlike this totally unappreciated mechanism (which better resembles Barry Marshall and H. pylori).
What are these other ways? There's an intuition that bodies are like computer programs that can fail in unpredictable ways, but this is usually false and belies a failure to see links between 'novel' and previously described mechanisms.
Human bodies, not so much, mostly because we lack the capability to monitor, measure and emulate the behaviour of such complex systems. As such, we gain medical knowledge using statistics, usually covering most common "failure modes" first, but we increasingly learn that those are never as clear cut either as our observation technology improves (as it does with science otherwise too — eg. Newtonian mechanics is completely true up to some error bars and constraints achievable in that period).
Random mutations causing cervical cancer essentially does not happen - as a sibling commenter writes, well-studied cases of this are so rare that they’re below our sensitivity of detection/technical error rates.
This is what I mean when I say we try to apply our intuitions to medicine - they’re not reliable and the truth is idiosyncratic.
Because our prior for cervical cancer being caused by HPV is so incredibly high, we would require overwhelming evidence to reject the hypothesis that any new case is due to HPV. There are ways to do this, and, should they be attained, would be published in a reputable journal based on their novelty.
And yet not a single cite in sight. A random commenter on orange site is not evidence
However I know the paper they are referring to - it is from 1999 in J Pathology, famous at the time, and it is woefully out of date.
> they’re below our sensitivity of detection/technical error rates.
Hogwash.
https://www.mdpi.com/2076-0817/14/7/668
> There are ways to do this, and, should they be attained, would be published in a reputable journal based on their novelty.
There are plenty of papers on HPV independent cervical cancer based on actual gene expression methods published in reputable journals in the last 30 years.
> And yet not a single cite in sight. A random commenter on orange site is not evidence
At a certain point, one has to take on the obligation of self-education.
> Hogwash.
From the website link you pasted: "Test-Specific Technical Issues - Standard tests (such as PCR or in situ hybridization) may not detect HPV types not included in the test panel (rare or classic non-oncogenic variants)."
> There are plenty of papers on HPV independent cervical cancer based on actual gene expression methods published in reputable journals in the last 30 years.
You don't understand the field, so you don't know why the gene expression does not establish the presence or absence of HPV but instead can be used as an argument for the absence of HPV.
EDIT: Also, a fundamental point of misunderstanding - cervical cancer is not a 'new' disorder, so unless you have an explanation for why the 1999 article is wrong, we can't simply discard its result and favor a next-generation sequencing article.
In that study they take cancer cells and check for HPV, get about 7% negatives which I'm guessing is what you're describing too, but they take those negatives and PCR them to figure out, well, OK, what was wrong with these cells and when you take the cells to pieces very often your assay goes oh, these instructions are HPV. So, you know, the cancer cells aren't "infected" with HPV but well the genetics are just HPV, the replication has gone haywire and tangled parts of HPV with the human cell instructions and now it's cancer.
Crucially we can assume that if you don't get infected with HPV this wouldn't happen. So HPV was still causal.
Nope. This is literally “correlation does not equal causation” 101. Based on the 0.3% I’m gonna guess you’re (either directly or indirectly) citing a famous, 1999 paper in J Pathology (Walboomers et al). It’s outdated, missing a control *, and it’s pretty well accepted that just finding a bystander HPV DNA fragment around somewhere is not conclusive of causality. We have much more sophisticated assays of gene expression. Try looking for review articles in the last 3 to 4 years rather than 30, the prevalence of truly HPV independent cervical cancer is not precisely characterized but it’s almost certain much greater than 0.3%.
https://www.mdpi.com/2076-0817/14/7/668
https://journals.lww.com/md-journal/fulltext/2024/10110/rese.... (3% to 8%)
One of those cited resources just keeps citing other people for a 5% risk, if they came up with their own number I didn't find it and I wonder why they'd cite somebody else in their own abstract without even mentioning they don't agree if somewhere in their work they do get a different number.
The other citation from the second link seems to be a paper which doesn't say 3% it says, and I'll quote: "The main explanation for HPV-negative cervical cancer was a false diagnosis, followed by cancers associated with non-HR-HPV types, and false-negative HR-HPV results. Truly HPV negative seem to be very rare in Caucasian populations".
If they're to be taken for 3% the only way to get there is by disregarding that conclusion and deciding that false negatives count as true negatives. Reviewers should ideally catch that but didn't here.
As I said, I don't doubt it exists, but 8% seems insane and these citations did not persuade me I was wrong to say 0.3% based on the paper you don't like.
"The other citation from the second link seems to be a paper which doesn't say 3% it say". Yes it does dude. You need to read the actual results from the paper more carefully: "Overall, 340/350 cases of primary cervical cancer confirmed by surgical staging tested HC2 positive (97.2%)." Ie 2.8% (~3%) were considered true HPV negative by this testing.
They're going from 8.8% (in that particular admitted biased dataset) to still 2.8%, the wording of the conclusion is wonky, but the results of the paper are overall consistent. You're taking that quote out of context.
In that same paper it says: "Our results are in accordance with The Cancer Genome Atlas Research Network (CGARN) ‘Integrated Genomic and Molecular Characterization of Cervical Cancer Study’, which used next-generation sequencing to characterize primary cervical cancers. The CGARN study found 95% of primary cervical cancers were HPV-positive and 5% HPV-negative."
Which is one of the primary sources for the 5% figure.
https://pmc.ncbi.nlm.nih.gov/articles/PMC5354998/
In any case these are both order of magnitude more than 0.3%
I'll agree 8% worldwide is high (though since environmental factors and genetics both play a role in both HPV-positive and negative cases), these incidences can vary throughout the world or within certain subgroups, and if you manage those groups that matters.
https://pmc.ncbi.nlm.nih.gov/articles/PMC11075765/
GAS is a clearly known cervical adenocarcinoma not related to HPV, and it accounts for 20% of all cervical adenoca in Japan, which overall places it close to 5% of all cervical cancer diagnoses there, just for this subtype.
That study literally explains each of the ten excess you say are "true negative", and only puts one in that bucket. You've made the same error as the author you cited previously. You're conflating HC2 negative ("it wasn't seen in this common test") with HPV negative ("it wasn't present")
They start with 371 smears and access to the patients, in all 371 cases there was also surgical biopsy.
* 340 of the smears say HPV with HC2. So we're agreed those are HPV positive.
* 21 of the biopsies aren't Cervical cancer. If cancer cells from other nearby tissues spread and and we find that in a cervical biopsy that's extremely bad news but it is NOT cervical cancer.
* 5 have non high-risk HPV. HPV-53, HPV-70, HPV-73
* 4 do have high-risk HPV even though the HC2 assay was negative
* Which leaves just one true negative case.
Now the 5 aren't proof of anything, and you can (and doubtless will) argue that it's just a coincidence. Uncleared infections with HPV aren't rare, so we can't rule that out, but equally it is wrong to insist it must be a coincidence. You'd need a mechanism, present only in the high risk variants to explain why these are innocent bystanders or else that's correlation.
The four high risk cases are even more clear cut, that's simply a false negative. Insisting you get to count these as true negative is crazy. HC2 was not adequate to detect the virus here, these patients were HC2-negative but they had high risk HPV anyway, the HC2 assay just didn't see it.
Why so much aggression? I’ll accept those results as presented. I’ll concede a lot of the reviews are junk.
There’s also no argument against aggressive eradication efforts for HPV.
Though it does seem like in some parts of the world the incidence of truly HPV independent adenocarcinoma like GAS is substantially higher than global averages.
That GAS paper was entirely new to me. I am focused on the UK and to some extent Northern Europe because I live here and the pathologist I know who is intensely involved in this stuff works for whatever the mutual self-calibration panels are called in Northern Europe. So, while a Japanese woman's life is worth no less, my friend cares that a lab analysing a smear in Oslo gives consistent results with a lab doing that analysis in Manchester or Paris and Tokyo doesn't enter into it.
Demographically there are a lot of white women in these parts, which I'm sure skew the numbers, so I can well believe what you said in the last sentence. I'd still be sceptical it could be as high as 8% for real population groups.
Up until that point, I’d never had any heart-related issues, nor does anyone in my family. Just two days before being admitted to the hospital with a suspected heart attack, I came down with food poisoning. It wasn’t pleasant, of course, but I thought it was nothing unusual—something a couple of days of rest and hydration would normally resolve.
Since my bloodwork at the hospital matched the expected results for a heart attack, and I underwent surgery, the doctors understandably focused on treating the immediate problem rather than identifying the underlying cause (I’m eternally grateful to the team and staff at St. Vincentius-Kliniken. I truly don’t think I’d be here without them).
That said, I’m glad to see this area receiving more attention. Hopefully, it will lead to further studies and the development of better strategies for prevention and treatment.
Most people assume that "heart attack" is a distinct clinical entity, but the majority (~80%) of elevated troponin levels are not exactly what comes to mind when people say "heart attack," but will often be described to patients as a heart attack (sometimes out of ignorance and others out of convenience, as the actual explanation for what is going on takes a lot more time and effort).
https://www.thelancet.com/journals/laninf/article/PIIS147330...
Hopefully it leads somewhere that brings us new preventative care.
Phages can penetrate biofilms [1]. (They have practice.)
Phages are intensely species specific to bacterial species, so they don't work unless you identify exactly what you're targeting. Also, even if they can penetrate biofilms, that doesn't mean you can successfully deliver them to the biofilm in the human body, since they have to survive the whole blood stream and the normal human immune response to "not self" things.
Evolved resistance is changing at least the first part of that relationship.
Phages as you note are far more tailored, and may (if I understand correctly) need to be targeted to a patient's specific infection's genetic line. It's as if you had to select ammunition based on the specific type of target you were hunting, if not specific individuals. In the early days of antibiotics it was far more a case of "fire and forget" with a single magic bullet. (Not literally always, but for the overwhelming majority of bacterial infections.)
There are countless ways to make medicines and treatments around old technologies and other things that are off-patent, in a way that is novel and able to be patented.
Even boring old generic medicines often find themselves reformulated into new treatments as combinations, variations, or in some cases simply a different dose and indication.
Nope. Plenty of governments fund this sort of research. And chances are there isn’t an off-the-shelf phage that ticks the boxes, which means you need some amount of genetic engineering, in which case Monsanto has your back.
In this study, the researchers designed a custom antibody that binds to oral bacteria. Then they used histological staining to identify specific biofilm structures inside the atherosclerotic tissue. Bacteria released from the biofilm were observed in heart attack cases, which gives us evidence that when the body's immune system responded to these bacteria, it triggered inflammation which ruptured cholesterol-laden plaque. So now we have more insight into the mechanism behind why inflammation is associated with heart attack risk.
The "pantheon" of risk factors for heart disease are:
* hs-CRP (inflammation): the mechanism studied by this research. High inflammation roughly doubles your risk of heart disease.
* ApoB - 20% of people with normal cholesterol will have abnormal ApoB, and be at risk of heart disease (ApoB is a structural protein in lipoproteins which cause arterial plaque).
* Lp(a) - the strongest hereditary risk factor for heart disease (Lp(a) acts as a multiplier on ApoB, since it camouflages cholesterol particles from your liver)
* HbA1c - insulin resistance /diabetes is a risk factor for just about everything.
* eGFR - estimates the volume of liquid your kidneys can filter, and is an input to the latest heart disease risk models (PREVENT).
All of these risk factors can be measured with a blood test + doctor review. Easy to order online: https://www.empirical.health/product/comprehensive-health-pa...
Basic LDL cholesterol and triglycerides blood panels are still an essential part of heart disease bloodwork, too.
I would suggest most people start by asking your doctor for some of these tests at your next annual checkup, as many of them and the doctor visit are likely covered by insurance. The ACA has special handling for routine annual checkups, so don’t assume it’s going to be expensive until you’ve checked the cost with your insurance. A routine bloodwork panel will also include a number of other important measures that are routine and very cheap. It’s helpful to have all of these on your medical record so trends can be identified over time.
-lp(a) and apob were covered
-ldl is computed on the standard panel, not an actual measurement
-accidentally got lp(a) twice and it varied quite a bit, so they may use different labs that are calibrated differently
-hs-crp is not offered
-doctor didn’t seem particularly aware of the more “niche” tests but was open to putting them in during my yearly physical
For example, one person got billed $1,338 for just an ApoB test when insurance denied coverage: https://www.reddit.com/r/PeterAttia/comments/14a4an1/apob_te...
Part of why we do cash pay (and pre-negotiated pricing with the labs) is that you avoid weird catastrophic scenarios like this. The price is upfront and transparent.
(It's too late to edit the original post, but my affiliation is on my HN profile.)
1) Isn't ApoB measurement pretty much in tandem with LDL, VLDL, and triglycerides? I realize it's being recognized now as the necessary factor for arterial dysfunction, but it seems like a lot of hoopla is being made as if it were some "silent" overlooked factor when for the vast, vast majority of people their ApoB levels are entirely explained by the other 3 lipid panel line items carrying it, and they have been in use for decades and are strongly targeted by the medical establishment
2) Isn't Lp(a) a separate lipoprotein altogether which is an independent risk factor for MACE? I've never heard of it "disguising" other cholesterol in testing.
2) The terminology is confusing, but each Lp(a) particle is "just" a cholesterol particle wrapped with an extra protein, apoprotein (a). So each Lp(a) particle includes one ApoB molecule (the structural protein in atherogenic cholesterol particles) and many cholesterol and triglyceride molecules, but the extra protein makes each Lp(a) particle about 6x more atherogenic than a typical cholesterol particle.
there's a small subset of people with more atherogenic triglycerides that ApoB picks up over and above just tracking with the LDL, but...you probably knew that just looking at them
For measuring inflammation, besides hs-CRP, additional tests are relevant and overlooked: regular CRP, ESR, and homocysteine.
Additionally, a heart attack can result from parasite induced inflammation too, e.g. in chagas disease, which is becoming increasingly common in the US while being very undetected without explicit testing. It is also very difficult to treat, but the gist 4196f31d12a43a95756e792500ff516f has some info on treating it. Lyme disease too can harm the heart permanently. In both cases a pacemaker could help as applicable.
For homocysteine, one proxy is B12 or folate (which are more cost-effective to test). To my knowledge, ESR is used in certain rheumatologic conditions, and was used more often in the past, but isn't currently used for heart disease.
Can you not get private labs in Canada?
(Happy to be corrected)
https://www.discountedlabs.com/
I’ve used both of these in USA with no physician or insurance involved at all. Zero red tape. I believe Canada has some additional rules/barriers against private testing without a physician.
The CEO of PrivateMD labs is on HN: https://news.ycombinator.com/user?id=JeanPierreK
It's interesting to hear that notionally they have the same model as us of a doctor needing to prescribe the test. The difference in Canada is that private healthcare is not available so you are forced to deal with the public system and the pace and inconvenience that entails.
I don't think any of those chains have the credit card readers or cash registers to take payment from me even if they wanted to.
If there is a doctor involved, it’s invisible to the consumer.
I believe there are 2-3 states where the rules are different (one being New York) where you can’t self-order tests, but every other state is unrestricted.
Even in New York where you can’t order via the typical websites, you can still go directly to Quest or Labcorp and buy your labs directly from them (without talking to a doctor).
Source: I regularly get blood panels without seeing doctors. I highly recommend direct labs, or Quest Direct if you live in NY.
Fun fact… my primary care provider ordered a Vitamin D and lipid panel for me last year. The cost of the labs after insurance was 3x more expensive than buying the labs myself without insurance. Insanity.
Edit: states with self-testing restrictions: AZ, NJ, NY, RI
(Agree that ordering and paying the cash price is often cheaper than insurance.)
The parent commenter we're both responding to said "I can go to a lab, order this, and pay for it." -- the point I'm trying to make is that the system in the US is basically the same, since the ordering physician is employed by the lab testing company and you never interact with them, so it's as if they don't exist for the purposes of comparing to Greece.
Edit: I see you own a blood testing startup! Now I understand why you were surprised about the ordering physician detail. I thought you were implying that the process is difficult in some way because a doctor is involved.
More like rubber-stamped by a doctor. There are numerous websites where you can buy the labs you want and the requisition will appear in your inbox shortly afterward after being “reviewed” by a doctor.
It’s really not an impediment at all.
> They might not do an appointment with you
That's the crucial detail missing from your comment. Without, it suggested that you had to go and actually talk to a doctor. But you don't. You can order labs as if there were no doctor involvement at all.
Concierge doctors will do this with a text. It’s dumb. So dumb. But doable.
I did mine a while back with Nia Health. Every marker on the OP’s list was included. You will have to pay out of pocket, but the cost was not unreasonable when i did it.
if you're doing a one-off, it's almost certainly part of a checkup or otherwise ordered by a doctor. any followups will be under their care too
if you're like me, with a longer term health condition that requires periodic measurement, then this actually makes a ton of sense
>All of these risk factors can be measured with a blood test + doctor review
As all CVD risk stratification with cardiologist review, the most important accuracy is sensivity (avoiding false negative that will escape review) of SCORE-2 and PREVENT, 48% and 26%, respectively [1].
The paper alternative proposal increased the sensitivity to 58% by performing clustering instead of conventional regression models as practiced in the standard SCORE-2 (Europe) and PREVENT (US).
These type of models including the latest proposal performed very poorly as indicated by their otherwise excellent and intuitive display of graphical abstract results [1].
[1] Risk stratification for cardiovascular disease: a comparative analysis of cluster analysis and traditional prediction models:
https://academic.oup.com/eurjpc/advance-article/doi/10.1093/...
I took it to the doctor, doctor just shrugged it off and said it's probably fine and I might have just been fighting off a cold.
FYI the person who posted the link is cofounder of the company he linked to.
You can ask your doctor to order these tests at your annual checkup, too.
Major League Eating (MLE): a professional organization focused on competitive eating contests.
Mister Leather Europe (MLE): an event within the European leather subculture.
Immune response to bacteria in arterial plaques can cause them to break up and cause the attack (my lay-interpretation) so the bacteria is a trigger, but "infectious disease" is a bit of hyperbole.
“Dormant bacteria within the biofilm remain[ing] shielded from both the patient’s immune system and antibiotics because they cannot penetrate the biofilm matrix” whose rupture “result[s] in thrombus formation and ultimately myocardial infarction” sounds like infection more than careless bacteria kicking up muck.
"Some myocardial infarctions attributed to an infectious disease."
"A myocardial infarction may be due to infectious disease."
My maternal grandfather died of an aortic separation. This caused a myocradial infarction, which was not due to infectious disease. I had my aortic valve replaced with a mechanical when I was 2, and 9, and 31, so I'll have a more nuanced kind of heart failure.
Some people see heart walls thinning at a very ripe age (90s+) but for most early heart patients, they don't make it that far.
- Does this suggest that courses of antibiotics might reduce heart attack risk?
- Does this suggest that regular use of, e.g., Listerine might reduce heart attack risk? (While, perhaps, slightly increasing esophageal cancer risk.)
It would be interesting to run an epidemiological study to see if current interventions move the needle in a meaningful way.
Don't use "antiseptic" mouthwash; it kills beneficial bacteria in the mouth, causing bad bacteria to multiply.
I have personal experience of this.
Maybe you’re thinking toothpastes? SLS in toothpaste is indeed hard to avoid.
eg. https://www.science.org/content/article/antibiotics-cut-hear...
https://www.nejm.org/doi/full/10.1056/NEJMoa043526
still hasn't really panned out
How does flu affect the heart? The virus only rarely infects the heart directly. Instead, the adverse effects of the virus on the heart are due to atherosclerosis of the arteries of the heart. Many people over age 50 have atherosclerosis — and in some people it has not yet been diagnosed. Because atherosclerosis narrows the arteries and reduces the flow of blood, less oxygen reaches the heart muscle. When the effect of the flu on the lungs lowers the amount of oxygen in the blood, this further reduces the supply of oxygen to the heart. This can lead to a heart attack or cardiac arrest (sudden death).
Is this risk more than theoretical? Many careful studies have shown there is an increased risk of heart disease following a bout of flu. In one study of 80,000 adults with influenza, nearly 12% had a serious cardiac event, such as a heart attack, during or in the weeks after getting the flu.
Even temporary stress on the respiratory system can cause long-term damage to the brain, lungs, and heart. Because of Covid, we started to learn that an acute, severe infection can affect people much later.
That research led to the beginning of an understanding that repeated flu infections can contribute to premature death even many decades later.
That sounds really high
Okay I just looked it up and this was only among hospitalized individuals which makes a lot more sense because most people just stay home unless it's very bad but that is still surprising to me
This is a pretty cool finding. Biofilms are also beyond reach of antibacterials usually. And seing a commensal become a problem due to "location, location, location" is also cool.
Nice article. Cool leads
Chronic strep throat (sometimes leading to guttate psoriasis) are thought to be due to this feature. The bacteria can form these biofilms in many places, including the tonsils. It's implicated in things like periodontitis. (Another streptococcus, S. mutans, causes cavities.)
They're very sneaky bacteria, due to what's called molecular mimicry. The bacterial surface has a protein called M protein, and some of this protein's epitopes (stretches of amino acids) are the same or similar to human proteins like myosin, similar enough that antibodies cause cross-reactivity with human tissue. This is why strep bacteria can cause rheumatic fever and some other diseases.
Strep has also been implicated in psoriasis; we have good evidence that the cross-reactivity is what kick-starts the disease and is in some way responsible for why it's chronic.
The disease is only the named group of symptoms. The potential cause of the disease is the bacterial infection. Those are very different concepts.
I think I'll go floss.
This is perfectly well known and absolutely nothing new.
This study merely expands research on the topic (focus on bacteria+biofilm instead of flu).
So "Myocardial infarction may be an infectious disease" is a weird clickbait title. We know. We knew for a long time.
We also have quite a few of anti biofilm agents in IV formulations that could have an effect inside of the cardiovascular system if used in high dosages, but the molecules are old, cheap and unsexy, so no one will try. (ambroxol and NAC come to mind)
Furthermore, while there are issues of misaligned incentives across the industry, of the top 10 pharma companies: Roche, AstraZeneca, Bayer, Novartis, Sanofi, Novo Nordisk, GSK, are all based in Europe, so your assertion further down makes no sense.