There’s an important caveat to keep in mind when it comes to food databases, especially those relying on branded or restaurant items:
U.S. law does not require food manufacturers to disclose everything that goes into their products. Under the Code of Federal Regulations (21 CFR § 101.100), there are exemptions to ingredient labeling... An example: flavorings, spices, and incidental additives (like processing aids or anti-caking agents) are not always listed explicitly. Also: proprietary blends and "natural flavors" can legally conceal dozens of chemicals (some synthetic), which consumers have no way of identifying.
Micronutrient data is often estimated or missing from labels and restaurant menus, which limits the accuracy of even the best-intentioned databases. Studies show that the nutritional information provided by restaurants and brands is frequently incomplete or inaccurate, especially when it comes to sodium, sugar, and actual serving sizes.
(Urban et al. "The Energy Content of Restaurant Foods Without Stated Calorie Information" ; Labuza et al., 2008 and others)
IMO Food databases are only as accurate as the source data allows. Until food labeling laws mandate full disclosure and third-party verification, apps like this can support health awareness. Still, they shouldn't be treated as precise medical or dietary guidance—particularly for people with allergies, sensitivities, or chronic health conditions that require strict tracking.
It’s easy to paint with broad strokes, but sweeping generalizations rarely capture the full picture. Not all of us “gatekeep” or overprescribe, we follow evidence-based guidelines and clinical judgment. When a patient presents with nonspecific fatigue and unintended weight loss, for instance, ordering a CBC, CMP, TSH, and A1C isn’t "unnecessary" it’s standard of care to rule out anemia, metabolic derangements, thyroid dysfunction, or early diabetes. That’s not about revenue.. it’s about ruling out high-risk pathology before it escalates.
As for the AMA, it’s far from perfect, but it doesn’t define the ethos of every practicing clinician. Many of us—regardless of where we trained—are here because we care deeply about patient outcomes, not profit. I don’t dismiss international medical graduates; I’ve worked alongside phenomenal ones. What matters to me isn’t where someone studied, but how they think, how they treat, and whether they practice medicine with integrity.
Healthcare needs reform, no doubt—but assuming every U.S. physician is complicit in systemic issues is reductive. Most of us are doing the best we can within a deeply flawed system.
Pharmacies have to have crazy high prices though because PBMs reimburse at such shit rates, based on some percentage of the price given to them. Because if they buy the bottle at $30 and list the price at $60, the PBM contract will only reimburse at the adjusted wholesale price (another made up number), eg: 17% plus a $1.99 dispensing fee. This disgusting math results in getting a loss on the drug.
Even all this leaves out some of the most absurd abuses of PBMs. They set minimum drug copays, have the pharmacy collect a $15 copay for a $5 drug, and have the pharmacy pay the PMB the $10 difference. They make it a breach of contract for the pharmacy to inform the patient this is happening or to charge the $5 and bypass the insurance. The total lack of anything even approaching ethnics is absurd...
This is an extremely politicized question in the US, where a public health insurance option (a solution that's popular in much of the rest of the OECD) is fiercely opposed by a large swath of the population.
At the very least though, in an ideal world, payers, providers, pharmacies, and PBMs should not be allowed to be part of the same company.
Just force price transparency. Force drug makers to advertise the selling prices of their drugs, and enforce price discrimination laws. Force insurance and PBM companies to advertise the drug prices if purchased through insurance or PBM. Everybody should be paying the same price. And if not, everyone should be allowed to find out if they can pay a lower price.
And yes, get rid of PBMs. They are toxic middlemen who want their 'cut' for doing nothing at all.
The most egregious limitation is the absurdly small sample size (n=16), which utterly cripples its statistical power. The authors throw around p-values without any serious correction for multiple comparisons.. Their confidence intervals (CIs) are embarrassingly wide in several places, making many of their so called significant findings borderline meaningless. For example, their pharmacokinetic (PK) values show ranges so broad (eg: Tmax varying from 0.25–5.0h, CL/F spanning 1.6–22 L/h) that any attempt at a reliable dose-response relationship collapses under basic scrutiny; their p-values dance precariously around the threshold of significance. (There are many more)
If this is what’s guiding psychedelic research, we’re in serious trouble.
The blinding? Functionally useless UNLESS the researchers genuinely believe subjects couldn't tell whether they were in a psychedelic fugue state or on a placebo. The ketanserin condition? A self-congratulatory exercise in proving that a known 5-HT2A antagonist blocks 5-HT2A-mediated effects. Stunning. rolls eyes
Then there’s the pharmacokinetics section, breathlessly confirming that LSD is absorbed, peaks, and is metabolized..just like every other small-molecule drug with hepatic clearance. The BDNF findings? A biochemical footnote with no functional correlation (tossed in for faux mechanistic depth)
FQ toxicity is likey caused by SNP in a specific gene related to pharmaceutical metabolism (one of the CYP450s). I believe this was published in the literature.
Another possibility is that FQ toxicity is caused by certain genes relating to detoxifying (GSH, COMT, etc) - where the body incorrectly metabolises it, leading to toxicity against cells.
It's unfortunate that there's an insanely high number of folks in the population that are taking FQs and running into toxicity without any hope of figuring out what is going on with their bodies.
It seems that it would behoove folks to be able to take the test and know whether they are safe candidates to take FQ antibiotics.
Similarly rare is the "traditional" EDS phenotype with stretchy skin and hypermobile joints. Usually seeing them for shoulder dislocations or other orthopedic injuries.
By far the most common (and massively increased over the past few years) is the crowd that attracts all the eye rolls. These are almost exclusively women, usually white, age 16-35, presenting with a constellation of nonspecific chronic complaints including myalgias/arthralgias, fatigue, GI symptoms, etc. None of them have stretchy skin or abnormally hypermobile joints. Very high rate of fibromyalgia/POTS/CFS in this group. They're usually coming to the ED for diffuse pains, dizziness, or something else I really can't fix. Maybe there is some underlying organic disorder we haven't sorted out yet, maybe these are somatic manifestations of untreated anxiety/depression.
One thing about the hEDS diagnosis is the explosion of self-dx from social media (TikTok) which makes physicians cringe.
There's no good genetic test, and even if there was there is not much to be done other than supportive measures.
I believe that you're a doctor because your response is exactly typical for a doctor. Have you considered for a second that all these people are right and that you might be wrong? I am similarly self diagnosed. 30 years of not being able to get a diagnosis despite having hypermobility so severe I can subluxate either shoulder on demand, I also had all of those other issues you mention - it's a cluster for a reason.
Hear me out, what if hEDS was 1/50 and not 1/50K or 1/15K or 1/5K or 1/500 or whatever the current literature has it at - which as a data science person is some rather large order of magnitude error bars for a figure. The 1/50 would include those diagnosed with generalized joint hypermobility, this would allow for the more common TNXB SNPs to be causal for hEDS.
And yeah, I've been told by many doctors that it's not worth even testing for because there is no treatment. Also consider the second order effects of not testing - how would you validate the original % numbers if people keep being talked out of getting tested, would subsequent surveys of population include those being talked out of the test? It's a good thing I don't rely on people who can't detect a condition to treat the condition. It is indeed very treatable - the dysautonomia aspect especially so.
There is clearly an entity of hEDS with a yet-to-be-discovered gene. However, the clinical criteria are not very specific and the diagnosis has been given out both for people who don’t fit the criteria and for people who do but are unlikely to have the originally intended underlying disease process. This is driven by several factors including physicians who aren’t strict about diagnosis, supplement companies that use this to push whatever they are peddling, and patients who want a diagnosis for the sake of having one or other reasons mentioned here.
There is a sub group of hEDS which are not that flexible, understand that someone like me who is extremely hypermobile could not get a diagnosis in any amount of time and the implication that has for people who are much less hypermobile yet clearly have the cluster of comorbidities of hEDS. The core problem is that doctors simply are not good at statistics, like unbelievably bad at it. It is a an essential component of their job and in my view being so bad at statistics is malpractice. When you’re good at statistics this stuff sticks out like a sore thumb - you can’t miss it.
Being 'bad statistics is malpractice' is just wrong on so many levels.
Medical malpractice requires a deviation from evidence-based practice that results in harm.. hEDS is diagnosed based on guidelines, not just "obvious statistical patterns.".. If diagnostic criteria exclude certain patients, that reflects the current medical consensus, not physician incompetence.
Med schools teach Bayesian reasoning and differential diagnoses, not just pattern matching.
If I incorrectly diagnosed a patient with hEDS without ruling out vascular EDS (vEDS) and the patient suffered an undiagnosed arterial rupture, that would be actual malpractice.
If a subgroup of less hypermobile hEDS patients exists, the solution is research, not accusing physicians of malpractice for following evidence-based guidelines.
'Medical malpractice' is different to 'malpractice' in general. The first is deviations from standard care the second is a dereliction of duty. I think it is every doctors duty to get good at statistics. Clearly the Bayesian statistics classes have not been sufficient.
If you consider the role of doctors to be finite state automata that execute instructions handed to them from standards bodies then we wouldn't need anything nearly as sophisticated as a LLM to replace them, a collection of decision trees would be sufficient.
Your input on the topic has not dissuaded me from my belief that doctors in general are bad at stats and therefore bad at their jobs.
I don't care to dissuade you from anything - you are flat-out wrong on things.
In my opinion, hEDS is a real condition, but sick-tok is causing patients to demand from physicians a dx - regardless if they meet the clinical criteria for it or not.
That you're not thinking the implications of this through to their obvious conclusions demonstrates for all to see why statistics and logic skills are important. If you were to tell me that doctors are actually good at statistics then maybe we could have some sort of discussion - but you know that they are not.
I would hazard a guess that I've read far more books and scientific literature on hEDS than you have - and I have the statistical background to understand it. It's a condition that is important to me. I think you're the one who should get out of the lane - you clearly don't know what you're talking about. My reference to the error bars on published figures of propensity of hEDS over time should have been an obvious clue.
>It is indeed very treatable - the dysautonomia aspect especially so.
What is the treatment for the condition itself?
As far as I can tell, the recommended options treat the symptoms, but not the conditions.
It was suggested that a family member of mine has EDS, but if they do, it’s not acute and there would really be nothing to do. The doctor even suggested getting tested for it, but it would not be covered so they didn’t do it.
By my math the test for hEDS has a very high false negative rate and it will cause issues with future insurance so not only would I not bother with it I would recommend against it. This is how bad math in medicine flows on to create more bad math.
It's generally not the hypermobility that is the problem, it's all the autoimmune conditions that come with it. Here is a list of the most common ones, https://ohtwist.com/about-eds/comorbidities. The comorbidities often have specific treatments and it helps to know the name of the things when looking for the treatments. The one that I think limits people the most if they have it is the ME/CFS that is very common in people with hEDS. I'm of the opinion that ME/CFS is downstream from dysautonomia. Low Dose Naltrexone should be step one for dysautonomia, after that weak ligands such as modafinil in the morning and amitriptyline at night - these medications seem compliment each other rather nicely. Modafinil can cause gut issues though so if that's already a problem modafinil can make things worse. A very strict zero sugar diet as well, dopamine dysregulation can cause strong sugar cravings which does make this rather difficult. I think semaglutide will likely be shown to be effective for auto-immune conditions and is probably the best medication I've taken for mine - but I am extremely sensitive to it and had to start at 1/20th the normal starting dose and still had pretty bad side effects. I'm basically 100% except that I have to still be careful with PEM - I'm in the process of building up a tolerance to PEM with the hope to eventually fix it. For the actual hypermobility I think weightlifting is the most effective. I was getting Craniocervical instability for a while and did a year long course of hGH peptides and Test Cypionate and that seemed to resolve it - but I have a severe form of hEDS and was worried about it putting me in a wheelchair. I was willing to take some risks to avoid that.
I switched out the 'TOSLINK' over to a standard coax and the sound is much better - not on par with the Recon 3D card, but it's an improvement. I am using some Logitech speakers and not headphones.
That is surprising. If anything, I would expect the toslink signal to be superior as it is completely galvanically isolated. Is it possible that there is dirt affecting the signal, either in the sockets or on the plugs?
Possibly. Another thing that could be is that I damaged the cable (somehow) when disconnecting it. Or, the Realtek TOSLINK has some design/implementation flaws.
