The article differs substantively from the actual conclusions of the study. This study shows a minor correlation in some bacterial DNA "signatures" in arterial plaque in about 200 people (~40% had the correlated bacteria). The study only included tissues from people who died of heart disease or had surgery related to heart disease. There does not currently appear to be a strong baseline about how widespread this bacterial signature may exist in a broad population regardless of health.
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.
This study's main contribution was to identify the specific bacteria, which gives insight into the mechanism behind heart attacks (the antibody the researchers developed was one of their central contributions). So the researchers dissected only people who died of heart disease.
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).
Isn’t it obvious that a heart attack could be caused by a myriad of issues? Sure a bacteria could be a cause. So could be genetics, or an excess of cheeseburgers. A heart ceasing to pump blood effectively is not a singular cause
"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.
> Isn’t it obvious that a heart attack could be caused by a myriad of issues?
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.
I might be reading parts of it wrong, but I think that's a different sort of thing to the research in the article.
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".
While you're not technically wrong, I find this whole approach to be not good.
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.
While do do agree with the general premise of your comment, that is, correct the root cause. For some, "eat healthy and exercise", may not be an option, because they are already addicted and overweight. At least, taking anti-biotics could be the very first line of actionable treatment to prevent the bacterial buildup and save their life immediately.
I very strongly disagree. Antibiotics are very dangerous at the individual level in how they mess up the individual's gut bacteria which are crucial for health.
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.
If you atempt that plan at scale I would expect antibiodic restistant bacteria to develop fast and people soon start dieing younger of what we now think of as minor infections.
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.
Minor correlation? P values are small indicating a strong correlation?
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).
This is a super common misconception, but a small p-value does *not* (necessarily) mean a strong correlation. It means high confidence that the correlation is non-zero.
Yes. I understand that. I was questioning the original assertion that there was a “minor” correlation. The p values indicate a correlation. One that is statistically significant.
That’s what it means in the literal sense. As a more practical interpretation, p value is the ”probability that the observed result was due to random chance instead of the suggested hypothesis”
•
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 think the first question to be addressed should be, does the general population have similar prevalence of this bacteria?
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.
another possibility that was floated in the TFA was vaccination. The whole point of the article was to precisely map out a mechanism, beyond that, many possibilities exist for intervention or prevention.
It's not even "here's another way this can happen" - there's no real evidence that the bacteria are causing the heart disease. Just a fact that 40% of the 200 people with the heart disease had the bacteria, and no baseline for whether everyone else normally has those bacteria.
Of course it depends on fractions. You can develop cervical cancer via some other route, but the vast, vast majority of cervical cancers are caused by HPV infection. So knowing that all the plans towards eliminating this disease focus on HPV.
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.
Peptic ulcers are another well-known case, in which most (though not all) instances can be traced to a Helicobacter pylori infection. Other causal factors include NSAID usage, stress, and diet.
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.
> 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.
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).
sure, let's not forget about the brain. Toxoplasma is another that is transmitted from cats to humans. It's pretty creepy and something that cat lovers don't like to hear about. Extremely common, and it lies dormant in the brain for decades.
> You can develop cervical cancer via some other route, but the vast, vast majority of cervical cancers are caused by HPV infection.
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.
Computer programs always fail in predictable — but usually unpredicted — ways.
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).
Spontaneous mutations? Which no matter how much you carve out modifiable risk factors will always be a thing. At least 5% of cervical cancers are HPV negative, so it's not even all the uncommon (not I would call "vast, vast" IMHO)
> Spontaneous mutations? Which no matter how much you carve out modifiable risk factors will always be a thing. At least 5% of cervical cancers are HPV negative
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.
> 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.
Where did you see 5%? I'm not an expert (though I think I know one) but the study I'm looking at says 0.3% - hence my "vast, vast". That's 3 patients out of 1000.
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.
> 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%.
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.
This has nothing to do with "liking" or appeals to emotion. The fact is that paper does not have a control and the methods are not sophisticated enough to determine causation.
"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.
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.
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.
Anecdotally, I had a myocardial infarction at 23, and I was honestly surprised to learn that it wasn’t already well known that infectious diseases could trigger such events.
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.
Can you clarify -- if you're comfortable sharing additional details -- did you have an "occlusion MI" heart attack, involving balloons / stents in the cath lab?
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).
“Dormant bacteria within the biofilm remain[ing] shielded from both the patient’s immune system and antibiotics because they cannot penetrate the biofilm matrix…”
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.
Adding to this: a chief advantage of antibiotics (particularly the early ones) is that they were both broad-spectrum (controlling a vast array of bacteria) and sparing of non-bacterial cells (e.g., those of our own bodies).
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.)
The problem is, you need to gather information about the specific bacterial composition of the biofilm. Unless Star Trek style transporter technology (which, iirc, is also used in their tricorders) is invented, we're stuck with invasive procedures to acquire a sample, and that kind of invasive procedure is pretty dangerous!
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.
> you can't patent phages, so we'll just continue ignoring them
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.
This is a nicely-designed study. For decades, we've known that inflammation is a risk factor for heart attacks.
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).
You should probably disclose that the order link at the end of your post goes to your own company.
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.
Basic LDL cholesterol is often covered by insurance, but ApoB, Lp(a), and hs-CRP are unfortunately usually not. If insurance doesn't end up covering it, sometimes the fee is just ridiculous.
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.)
In our case, we're providing the testing as part of a comprehensive program (including a review of results with a doctor, customized nutrition plans, etc) -- so it's slightly different than companies that only offer the labs in isolation.
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.
1) ApoB itself is more accurate than LDL and triglycerides. The latest evidence is that ApoB and Lp(a) together are more accurate than even LDL, VLDL, non-HDL, triglerycerides, etc combined: https://academic.oup.com/eurheartj/article-abstract/46/27/27...
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 lipids, besides the named tests, HDL, LDL, and triglyceride tests are older but shouldn't be overlooked.
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.
Can you expand more on why you'd want regular CRP over hs-CRP (specifically for cardiovascular risk)?
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.
It is true that hs-CRP is relevant for cardiovascular risk. CRP and ESR are more for broader inflammatory risk, for acute and chronic values respectively.
I live in Canada, despite being free this would be way more complicated to get. I don't want to be political, but just paying for this would be very appealing.
I live in Greece, I can go to a lab, order this, and pay for it. I actually did, the other day, though it was free because the government happens to be running a Lp(a) testing program right now.
I've always thought you need a requisition from a doctor, you can't just go pay for something, that's the only way I've seen it done. At least I've never seen services like the OP advertised, that's why I was stricken by it.
Interesting that you can do this in Greece. In the US, a doctor has the order the labs. (Direct-to-consumer lab testing technically exists, but is always ordered by a doctor.)
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.
Those places are very clear that they have a doctor on board who will order the actual test in your name. That’s why e.g privateMdlabs is promising that you “can avoid the doctors office”, not “no doctor involved”.
To be fair, I don't think anyone actually does it, because who will do their own bloods, but you definitely can. Labs expect to see an order from the doctor, because that's what 99.9% of people have, but they're happy if you just pay out of pocket too.
The reason I would do it, or do it when in the US is just the convenience. Seeing a doctor is complicated and obviously involves at least one extra step. If you just go and get the tests and have the info, it simplifies things, which is presumably the reason why these direct to consumer options exist in the US.
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.
No, the doctor doesn't need to prescribe the test, you can test whatever you want. It's just that the vast majority of people don't test anything unless a doctor tells them to.
In Ontario the doctor gives me a requisition form with the blood tests they want to do. I take that to whatever bloodwork chain is closest to me, they do the test, and get reimbursed by the government.
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.
I'm in the US and our local hospital lab has "test fair" week every year when anyone can roll up and get any test for a nominal payment (basic common tests). No doctor involved.
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
If you check the lab report, did you see a doctor listed somewhere near the top? (Even if you didn't explicitly talk to that doctor, I think it's legally necessary in all US states).
(Agree that ordering and paying the cash price is often cheaper than insurance.)
Every reference lab in the US is required to have a medical director who is legally accountable for quality. That doctor's name will often appear somewhere on the report but that doesn't mean they ordered it. The ordering provider (if any) will be listed on a separate field.
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.
> Direct-to-consumer lab testing technically exists, but is always ordered by a doctor.)
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.
At least for the tests I've gotten in the past, there's always a doctor's name on the lab order. They might not do an appointment with you, but it's still a legal requirement to get the test done.
Yes, what you said was incredibly misleading given the context of the discussion.
> 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.
What is the purpose of running lp(a) testing, if i may ask? Just for knowing the risk factor and dealing with it? As far as i know there is no easy way for dealing with it once and for all times (gene editing...)
There are easily accessible direct-to-consumer startups in Canada that do this sort of testing.
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.
Thank this looks interesting though I do see it's a very early stage startup (and inexplicably subscription based which appears to just be a naked cash grab).
It was not a subscription when I did it a year or two ago, but I guess the one-off model may not have worked out. I work in this field and the economics of doing something like this with a D2C model in Canada are not great. People are just not used to exchanging money for healthcare.
I’ve used getmaple.ca for this kinda thing. You end up using web chat to ask a NP for what you want and it gets done. All said, lack of private medical care in general has played a big part in stopping me moving to Canada.
The standard risk model based on SCORE-2 and PREVENT like parameters are very poor as reported in the recently published paper on the their accuracy performance by the Swedish team [1].
>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:
For what it's worth, I did one of these sorts of heart health blood panels, which showed everything as fine except for hs-CRP which was something like 8x what it should be.
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.
Yeah. If you don't have obvious symptoms, they'd likely prescribe you a statin, metformin, or some sort of dietary intervention. But you'd want to discuss it with your doctor in any case...
This particular panel includes a consult with a doctor (who can advise on next steps, prescribe medication, and so on). Or you can take the results to your doctor.
The original title is "Myocardial infarction may be an infectious disease" which appears to be clickbait, with the title posted here being much more accurate.
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.
> bacteria in arterial plaques can cause them to break up and cause the attack
“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.
Not all infarctions are due to infectious disease. The title (even on HN) is incorrect.
"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.
Gaining a ton of body mass working out thickens the heart. It's necessary to push the blood into veins that get constricted, more and more with increased weight. In the epilogue, as you get older, optimal function fades. The thickened tissue isn't as elastic, compounding cardiac problems and sometimes causing infarction (also, not infectious related). Ironically, a thickened heart gives you better odds at surviving surgery, due to the excess tissue and the minimal effect of scarring already-rigid tissue.
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.
For the Listerine part: they are referencing this study: https://pubmed.ncbi.nlm.nih.gov/16373688/ that seems to show a correlation between poor oral health and sudden cardiac death, so it might help indeed, with other good oral health practices.
I only use very dilute Listerine - for the fluoride. A dentist told me that undiluted, alcohol based products can cause tissue damage (which conceivably would result in a vector for oral bacteria infiltrating to the bloodstream?)
Alcohol-free mouthwash is even more likely to cause tissue damage because they almost all contain SLS. Some people are more sensitive to it than others (causing the mucosa to peel) but it causes mild damage to everybody.
Almost all? I just checked and Act, Crest, CloSYS and many others are all SLS-free and alcohol-free. The only one with SLS I could find is Listerine Cool Mint.
Maybe you’re thinking toothpastes? SLS in toothpaste is indeed hard to avoid.
I probably should find sources first but I was always under the impression that the mouth biome is strongly correlated to gut biome which strongly correlated to immune system.
Yes, there are studies where they compared heart attack rates for people who'd taken a course of antibiotics with those who hadn't and there was quite a large effect in some of them.
TFA says the biofilms protect the bacteria from antibiotics. Better approach is probably engineered antibodies or even a phage (engineered virus that attacks the bacteria).
Have always been fascinated with Paul Ewald's arguments (as laid out in his books The New Germ Theory of Disease and Evolution of Infectious Disease) that most chronic illnesses are due to pathogens.
Interesting, I'm noticing this pattern too more and more. The classic case was of course stomach ulcers. Now cardiovascular. Wouldn't be surprised if at least some neuro-degnerative diseases are also possibly caused by infections
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.
In the context of the article, it's inflammation rupturing the 'fibrous cap' on plaque deposits leading to a heart attack, so I presume OP is talking about the inflammatory response to having the 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.
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
"The most unique finding in our study was that viridans streptococci seemed to colonize the lipid core and wall of an atheroma as a biofilm and that this biofilm was not recognized by cells of the innate immune system. "
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.
Streptococcus pyogenes (group A streptococci) are well known for being able to form this kind of biofilm [1] and stay hidden from the immune system.
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.
Titles like this are very confusing. The paper better explains it, but a disease can't be contagious or infectious. The paper describes a link between a potential bacterial infection and myocardial infarctions that may take years or decades to develop.
The disease is only the named group of symptoms. The potential cause of the disease is the bacterial infection. Those are very different concepts.
Arterial plaque is a long standing, foreign body without vessels causing high flows. No surprise it can be infected by bacteria sometime. That is infection can exacerbate the MI, not cause it.
Wild I see only one mention of COVID so far, it has been shown to attack all kinds of organ tissues, the perspectives around "with or from" somehow permanently prevents people from discussing the underlying changes from this continued global cycling of the pathogen.
It's been known for many years that the flu vaccine reduces heart attack incidence. The flu either causes lasting damage to the cardiovascular system or directly causes heart attacks.
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)
Typical of the medical field: one of the most studied diseases in the past several decades and now there is a ground-breaking new study that questions all knowledge.
I blame the corruption from American medical experts and organizations which only object is to sell drugs.
This does not question all knowledge. Bacteremia and cardiac disease have been linked for years (see upvoted comment above), which is why these studies were done in the first place. This study isn't ground breaking, it's extending an already established area of study.
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.
This idea is not supported by the study in question. Even if it were, what you’re describing is just how science works! The cynicism, while understandable, seems widely irrelevant here.
The article differs substantively from the actual conclusions of the study. This study shows a minor correlation in some bacterial DNA "signatures" in arterial plaque in about 200 people (~40% had the correlated bacteria). The study only included tissues from people who died of heart disease or had surgery related to heart disease. There does not currently appear to be a strong baseline about how widespread this bacterial signature may exist in a broad population regardless of health.
In a nutshell there is a slightly interesting idea that deserves further study. That's it.
Interesting.
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.
This study's main contribution was to identify the specific bacteria, which gives insight into the mechanism behind heart attacks (the antibody the researchers developed was one of their central contributions). So the researchers dissected only people who died of heart disease.
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).
> So, one could make a similar article saying "Myocardial infarction may be caused by sugar consumption" (...
One could apply the same flawed logic to claim that propensity for myocardial infarction may cause certain bacterial infections.
Try it and see where you get, since you assume these scientists are so foolish.
Isn’t it obvious that a heart attack could be caused by a myriad of issues? Sure a bacteria could be a cause. So could be genetics, or an excess of cheeseburgers. A heart ceasing to pump blood effectively is not a singular cause
Exactly, it's complex.
"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.
> Isn’t it obvious that a heart attack could be caused by a myriad of issues?
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.
I might be reading parts of it wrong, but I think that's a different sort of thing to the research in the article.
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".
While you're not technically wrong, I find this whole approach to be not good.
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.
While do do agree with the general premise of your comment, that is, correct the root cause. For some, "eat healthy and exercise", may not be an option, because they are already addicted and overweight. At least, taking anti-biotics could be the very first line of actionable treatment to prevent the bacterial buildup and save their life immediately.
I very strongly disagree. Antibiotics are very dangerous at the individual level in how they mess up the individual's gut bacteria which are crucial for health.
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.
If you atempt that plan at scale I would expect antibiodic restistant bacteria to develop fast and people soon start dieing younger of what we now think of as minor infections.
Are there any human randomised control trials that show stuff like vegetable oil cause inflammation? Atleast the ones I've seen show the opposite
https://youtu.be/-xTaAHSFHUU
No, such human rcts haven't been done.
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.
Minor correlation? P values are small indicating a strong correlation?
This is a super common misconception, but a small p-value does *not* (necessarily) mean a strong correlation. It means high confidence that the correlation is non-zero.
Yes. I understand that. I was questioning the original assertion that there was a “minor” correlation. The p values indicate a correlation. One that is statistically significant.
P value means "if the null hypothesis were true, the probability we would have observed what we actually observed."
It's definitely not the strength of correlation. It's not even the probability that the opposite of the null hypothesis is false!
That’s what it means in the literal sense. As a more practical interpretation, p value is the ”probability that the observed result was due to random chance instead of the suggested hypothesis”
.. and only if myriad of other assumptions (many are unstated) hold.
yes from tfa:
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 think the first question to be addressed should be, does the general population have similar prevalence of this bacteria?
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.
another possibility that was floated in the TFA was vaccination. The whole point of the article was to precisely map out a mechanism, beyond that, many possibilities exist for intervention or prevention.
I assume this is a "here's another way this can happen" rather than "actually this is caused only by this and not by what we used to think"?
It's not even "here's another way this can happen" - there's no real evidence that the bacteria are causing the heart disease. Just a fact that 40% of the 200 people with the heart disease had the bacteria, and no baseline for whether everyone else normally has those bacteria.
Ninety percent of house fires have these giant red trucks out in front of them. How do I apply for a grant?
Surely this? The number of ‘oh, it turned out to be more more complicated’ scenarios in medicine is high.
Of course it depends on fractions. You can develop cervical cancer via some other route, but the vast, vast majority of cervical cancers are caused by HPV infection. So knowing that all the plans towards eliminating this disease focus on HPV.
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.
Peptic ulcers are another well-known case, in which most (though not all) instances can be traced to a Helicobacter pylori infection. Other causal factors include NSAID usage, stress, and diet.
<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>
> 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.
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).
1. https://www.ncbi.nlm.nih.gov/books/NBK551672/
sure, let's not forget about the brain. Toxoplasma is another that is transmitted from cats to humans. It's pretty creepy and something that cat lovers don't like to hear about. Extremely common, and it lies dormant in the brain for decades.
> You can develop cervical cancer via some other route, but the vast, vast majority of cervical cancers are caused by HPV infection.
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.
Computer programs always fail in predictable — but usually unpredicted — ways.
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).
Spontaneous mutations? Which no matter how much you carve out modifiable risk factors will always be a thing. At least 5% of cervical cancers are HPV negative, so it's not even all the uncommon (not I would call "vast, vast" IMHO)
> Spontaneous mutations? Which no matter how much you carve out modifiable risk factors will always be a thing. At least 5% of cervical cancers are HPV negative
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.
> as a sibling commenter writes, well-studied cases of this are so rare that
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.
Where did you see 5%? I'm not an expert (though I think I know one) but the study I'm looking at says 0.3% - hence my "vast, vast". That's 3 patients out of 1000.
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.
> 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%)
That 3-8% cites two sources but...
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.
This has nothing to do with "liking" or appeals to emotion. The fact is that paper does not have a control and the methods are not sophisticated enough to determine causation.
"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.
Anecdotally, I had a myocardial infarction at 23, and I was honestly surprised to learn that it wasn’t already well known that infectious diseases could trigger such events.
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.
Can you clarify -- if you're comfortable sharing additional details -- did you have an "occlusion MI" heart attack, involving balloons / stents in the cath lab?
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).
This has been suspected for decades.
https://www.thelancet.com/journals/laninf/article/PIIS147330...
Hopefully it leads somewhere that brings us new preventative care.
Might explain why some have success with carnivore. Less dental plaque.
“Dormant bacteria within the biofilm remain[ing] shielded from both the patient’s immune system and antibiotics because they cannot penetrate the biofilm matrix…”
Phages can penetrate biofilms [1]. (They have practice.)
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC8875263/
But you can't patent phages, so we'll just continue ignoring them
"simple, obvious and wrong".
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.
Adding to this: a chief advantage of antibiotics (particularly the early ones) is that they were both broad-spectrum (controlling a vast array of bacteria) and sparing of non-bacterial cells (e.g., those of our own bodies).
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.)
I guess specific (custom-made) IV phages might work. We „just“ need tech that makes the whole process affordable.
The problem is, you need to gather information about the specific bacterial composition of the biofilm. Unless Star Trek style transporter technology (which, iirc, is also used in their tricorders) is invented, we're stuck with invasive procedures to acquire a sample, and that kind of invasive procedure is pretty dangerous!
This is basically a myth.
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.
> you can't patent phages, so we'll just continue ignoring them
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.
This is a nicely-designed study. For decades, we've known that inflammation is a risk factor for heart attacks.
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...
You should probably disclose that the order link at the end of your post goes to your own company.
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.
Fwiw, since it seems like a number of people on here have Kaiser, my experience asking my Kaiser pcp for these as a mid-30s otherwise healthy person:
-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
Basic LDL cholesterol is often covered by insurance, but ApoB, Lp(a), and hs-CRP are unfortunately usually not. If insurance doesn't end up covering it, sometimes the fee is just ridiculous.
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.)
I'm curious how you managed to get access to testing centers in NYC. I thought there was a law that restricted this last I checked.
In our case, we're providing the testing as part of a comprehensive program (including a review of results with a doctor, customized nutrition plans, etc) -- so it's slightly different than companies that only offer the labs in isolation.
IANAD, but
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.
1) ApoB itself is more accurate than LDL and triglycerides. The latest evidence is that ApoB and Lp(a) together are more accurate than even LDL, VLDL, non-HDL, triglerycerides, etc combined: https://academic.oup.com/eurheartj/article-abstract/46/27/27...
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.
you're correct
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 lipids, besides the named tests, HDL, LDL, and triglyceride tests are older but shouldn't be overlooked.
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.
Can you expand more on why you'd want regular CRP over hs-CRP (specifically for cardiovascular risk)?
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.
It is true that hs-CRP is relevant for cardiovascular risk. CRP and ESR are more for broader inflammatory risk, for acute and chronic values respectively.
Understanding this is a shameless plug, it's very cool this exists.
You don't need to use this specific blood test, by the way. Any lab near you will test these biomarkers for you.
I live in Canada, despite being free this would be way more complicated to get. I don't want to be political, but just paying for this would be very appealing.
I live in Greece, I can go to a lab, order this, and pay for it. I actually did, the other day, though it was free because the government happens to be running a Lp(a) testing program right now.
Can you not get private labs in Canada?
I've always thought you need a requisition from a doctor, you can't just go pay for something, that's the only way I've seen it done. At least I've never seen services like the OP advertised, that's why I was stricken by it.
(Happy to be corrected)
Hm, over here you need a prescription for medication, but you can do whatever test you want to pay for. I don't know about Canada, though.
Interesting that you can do this in Greece. In the US, a doctor has the order the labs. (Direct-to-consumer lab testing technically exists, but is always ordered by a doctor.)
https://www.privatemdlabs.com/
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
Those places are very clear that they have a doctor on board who will order the actual test in your name. That’s why e.g privateMdlabs is promising that you “can avoid the doctors office”, not “no doctor involved”.
Ah - good info! It's very transparent to the customer, I never noticed that there was any doctor involved.
To be fair, I don't think anyone actually does it, because who will do their own bloods, but you definitely can. Labs expect to see an order from the doctor, because that's what 99.9% of people have, but they're happy if you just pay out of pocket too.
In the US you can buy 100+ tests from Quest Labs directly, the price even includes a discussion with MD about the results.
The reason I would do it, or do it when in the US is just the convenience. Seeing a doctor is complicated and obviously involves at least one extra step. If you just go and get the tests and have the info, it simplifies things, which is presumably the reason why these direct to consumer options exist in the US.
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.
No, the doctor doesn't need to prescribe the test, you can test whatever you want. It's just that the vast majority of people don't test anything unless a doctor tells them to.
There are places like 'Any Lab Test Now' in the US that are cash/card and do a large number of tests like this without a prescription.
In Ontario the doctor gives me a requisition form with the blood tests they want to do. I take that to whatever bloodwork chain is closest to me, they do the test, and get reimbursed by the government.
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.
I'm in the US and our local hospital lab has "test fair" week every year when anyone can roll up and get any test for a nominal payment (basic common tests). No doctor involved.
Anyone can order labs via websites like https://directlabs.com/
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
If you check the lab report, did you see a doctor listed somewhere near the top? (Even if you didn't explicitly talk to that doctor, I think it's legally necessary in all US states).
(Agree that ordering and paying the cash price is often cheaper than insurance.)
Every reference lab in the US is required to have a medical director who is legally accountable for quality. That doctor's name will often appear somewhere on the report but that doesn't mean they ordered it. The ordering provider (if any) will be listed on a separate field.
Yes, there is an ordering physician.
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.
> Direct-to-consumer lab testing technically exists, but is always ordered by a doctor.)
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.
This is very much not true. I just paid $12 to have a lipid test done. No doctor order or involvement at all.
At least for the tests I've gotten in the past, there's always a doctor's name on the lab order. They might not do an appointment with you, but it's still a legal requirement to get the test done.
Yes, what you said was incredibly misleading given the context of the discussion.
> 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.
I believe it depends on the state.
> In the US, a doctor has the order the labs
Concierge doctors will do this with a text. It’s dumb. So dumb. But doable.
What is the purpose of running lp(a) testing, if i may ask? Just for knowing the risk factor and dealing with it? As far as i know there is no easy way for dealing with it once and for all times (gene editing...)
There are easily accessible direct-to-consumer startups in Canada that do this sort of testing.
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.
Thank this looks interesting though I do see it's a very early stage startup (and inexplicably subscription based which appears to just be a naked cash grab).
It was not a subscription when I did it a year or two ago, but I guess the one-off model may not have worked out. I work in this field and the economics of doing something like this with a D2C model in Canada are not great. People are just not used to exchanging money for healthcare.
subscription model makes sense, unfortunately
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
I’ve used getmaple.ca for this kinda thing. You end up using web chat to ask a NP for what you want and it gets done. All said, lack of private medical care in general has played a big part in stopping me moving to Canada.
I live in Romania. You can have whatever test you want if they can do it. Mostly they can at least in our central area. No doctor's note needed.
Lots of Canadians come to the USA as medical tourists and pay out of pocket for treatments they can't get (or have to wait for) at home.
Seriously. It's infuriating how hard it is to get "non-essential" diagnostics.
It being an ad casts suspicion on the entire post.
There’s plenty of incorrect information on the internet. We should all be skeptical of claims like this regardless of who makes them.
It still casts suspicion? That doesn't change anything.
The standard risk model based on SCORE-2 and PREVENT like parameters are very poor as reported in the recently published paper on the their accuracy performance by the Swedish team [1].
>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/...
For what it's worth, I did one of these sorts of heart health blood panels, which showed everything as fine except for hs-CRP which was something like 8x what it should be.
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.
Is the fat rapture because the body wants fat to release vitamins and other stuff to help power itself to fight off the bacteria?
Do you happen to know how much that test costs? (Clicking a link to try to find out brought me to a page that asks for my zip code.)
> Do you happen to know how much that test costs?
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.
That panel is $190.
in the US? There was a question from Canada
Yes -- in the US. I'm not super familiar with the options in Canada, unfortunately!
What's the recommendation for someone with a hilariously high Lp(a)? Just pin LDL as low as possible?
Currently yes. There are some really promising drugs in the pipeline that are doing well in trials, though.
So is poor oral hygiene a risk factor?
It's been known for years that bad oral health leads to heart disease.
What do you do next if one is high? See your Doctor?
Yeah. If you don't have obvious symptoms, they'd likely prescribe you a statin, metformin, or some sort of dietary intervention. But you'd want to discuss it with your doctor in any case...
This particular panel includes a consult with a doctor (who can advise on next steps, prescribe medication, and so on). Or you can take the results to your doctor.
are you a cardiologist? Excellent points, thanks
Not a cardiologist, but adjacent to this type of research. I'm an MLE but have published research in cardiology.
TIL MLE = Machine Language Engineer. It wasn't listed in Google's AI overview, although I did get
Major League Eating (MLE): a professional organization focused on competitive eating contests.
Mister Leather Europe (MLE): an event within the European leather subculture.
I've never heard of machine language engineers. Machine learning engineer, on the other hand, is a fairly common title nowadays.
Oops, that's what I meant to type. Too late to change it now, unfortunately.
Really any of the three would be qualified.
thanks for your input on this
The original title is "Myocardial infarction may be an infectious disease" which appears to be clickbait, with the title posted here being much more accurate.
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.
> bacteria in arterial plaques can cause them to break up and cause the attack
“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.
Not all infarctions are due to infectious disease. The title (even on HN) is incorrect.
"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.
Arnold Schwatzenegger also has a congenital history, a few heart surgeries..
Gaining a ton of body mass working out thickens the heart. It's necessary to push the blood into veins that get constricted, more and more with increased weight. In the epilogue, as you get older, optimal function fades. The thickened tissue isn't as elastic, compounding cardiac problems and sometimes causing infarction (also, not infectious related). Ironically, a thickened heart gives you better odds at surviving surgery, due to the excess tissue and the minimal effect of scarring already-rigid tissue.
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.
This raises two questions.
- 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.
Listerine would make it worse for sure.
Don't use "antiseptic" mouthwash; it kills beneficial bacteria in the mouth, causing bad bacteria to multiply.
I have personal experience of this.
agreed, after much research the only mouth wash i use is therasol
For the Listerine part: they are referencing this study: https://pubmed.ncbi.nlm.nih.gov/16373688/ that seems to show a correlation between poor oral health and sudden cardiac death, so it might help indeed, with other good oral health practices.
I only use very dilute Listerine - for the fluoride. A dentist told me that undiluted, alcohol based products can cause tissue damage (which conceivably would result in a vector for oral bacteria infiltrating to the bloodstream?)
Most Listerine products do not contain fluoride. Additionally, there are a variety of readily available alcohol-free mouthwashes that have fluoride.
Alcohol-free mouthwash is even more likely to cause tissue damage because they almost all contain SLS. Some people are more sensitive to it than others (causing the mucosa to peel) but it causes mild damage to everybody.
Almost all? I just checked and Act, Crest, CloSYS and many others are all SLS-free and alcohol-free. The only one with SLS I could find is Listerine Cool Mint.
Maybe you’re thinking toothpastes? SLS in toothpaste is indeed hard to avoid.
the purple one does. That's what the dentist recommended
I probably should find sources first but I was always under the impression that the mouth biome is strongly correlated to gut biome which strongly correlated to immune system.
Yes, there are studies where they compared heart attack rates for people who'd taken a course of antibiotics with those who hadn't and there was quite a large effect in some of them.
eg. https://www.science.org/content/article/antibiotics-cut-hear...
TFA says the biofilms protect the bacteria from antibiotics. Better approach is probably engineered antibodies or even a phage (engineered virus that attacks the bacteria).
The bacterial contribution to MACE has been an ongoing subject of investigation for decades
https://www.nejm.org/doi/full/10.1056/NEJMoa043526
still hasn't really panned out
Have always been fascinated with Paul Ewald's arguments (as laid out in his books The New Germ Theory of Disease and Evolution of Infectious Disease) that most chronic illnesses are due to pathogens.
Interesting, I'm noticing this pattern too more and more. The classic case was of course stomach ulcers. Now cardiovascular. Wouldn't be surprised if at least some neuro-degnerative diseases are also possibly caused by infections
This seems like a good explanation of how my father died. He had the flu, and died overnight from a massive heart attack.
https://www.health.harvard.edu/heart-health/what-does-the-fl...
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.
> How does flu affect the heart?
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.
In the context of the article, it's inflammation rupturing the 'fibrous cap' on plaque deposits leading to a heart attack, so I presume OP is talking about the inflammatory response to having the 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.
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
For sure it exacerbated an existing cardiovascular system. Once the system is weakened things cause big problems quickly.
sure does. chain of events. The epidemiologists should be able to validate these claims.
"The most unique finding in our study was that viridans streptococci seemed to colonize the lipid core and wall of an atheroma as a biofilm and that this biofilm was not recognized by cells of the innate immune system. "
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
Streptococcus pyogenes (group A streptococci) are well known for being able to form this kind of biofilm [1] and stay hidden from the immune system.
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.
[1] https://www.ncbi.nlm.nih.gov/books/NBK587105/
Titles like this are very confusing. The paper better explains it, but a disease can't be contagious or infectious. The paper describes a link between a potential bacterial infection and myocardial infarctions that may take years or decades to develop.
The disease is only the named group of symptoms. The potential cause of the disease is the bacterial infection. Those are very different concepts.
There are already pretty serious blood disorders linked directly to oral health (https://en.wikipedia.org/wiki/Actinomycosis almost took down slackware linux)
I think I'll go floss.
yeah and dehydration is not good, saliva flow is protective
Wasn't that a plot in DBZ where a virus weakens Goku's heart?
https://dragonball.fandom.com/wiki/Heart_Virus Indeed!
Arterial plaque is a long standing, foreign body without vessels causing high flows. No surprise it can be infected by bacteria sometime. That is infection can exacerbate the MI, not cause it.
see https://pubmed.ncbi.nlm.nih.gov/17420199/
This has been known for at least 5 years though, but good to see this topic resurface
Great concept..
Wild I see only one mention of COVID so far, it has been shown to attack all kinds of organ tissues, the perspectives around "with or from" somehow permanently prevents people from discussing the underlying changes from this continued global cycling of the pathogen.
It's been known for many years that the flu vaccine reduces heart attack incidence. The flu either causes lasting damage to the cardiovascular system or directly causes heart attacks.
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)
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Typical of the medical field: one of the most studied diseases in the past several decades and now there is a ground-breaking new study that questions all knowledge. I blame the corruption from American medical experts and organizations which only object is to sell drugs.
This does not question all knowledge. Bacteremia and cardiac disease have been linked for years (see upvoted comment above), which is why these studies were done in the first place. This study isn't ground breaking, it's extending an already established area of study.
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.
This idea is not supported by the study in question. Even if it were, what you’re describing is just how science works! The cynicism, while understandable, seems widely irrelevant here.
How science works in America perhaps. Not in Europe. Your "conclusion" about the study is ludicrous, please read it again.
Can you elaborate on what this has to do with America or Europe? Aren't half the big pharmaceutical companies European?
In what sense does it “question all knowledge”?