Total cholesterol and all-cause mortality – a study among 13M adults
nature.com
nature.com
If they failed to account for statin use, then they will get the wrong answer due to confounding by indication.
https://twitter.com/skathire/status/1110909549811322880
Edit: Found it - they are not accounting for statin use! None of their conclusions seem warranted.
Why would you need to account for it? Trying to understand the logic here.
The study goes to showing the association between high cholesterol and all-cause mortality (which is what we really care about right?) is weak.
This would seem to diminish the benefits of statin use, all other things being equal.
With regard to the point of the study, they start by saying, "It is unclear whether associations between total cholesterol (TC) levels and all-cause mortality and the optimal TC ranges for lowest mortality vary by sex and age."
So, interpreting their statement, I would say that their goal with this study was to investigate whether the relationship between total cholesterol and mortality was consistent across age and sex. That is a different point from assessing the strength of the relationship between cholesterol and mortality.
I do agree, however, that there is no single biomarker aside from age that is a particularly powerful predictor of mortality in the general population.
[Edit] I just read another one of your comments that answers my question, and I think you're right: https://news.ycombinator.com/item?id=20138685
If you mean there are no reliable bio markers, period, it would be more clear to just say that.
We actually can measure the biological age. There are clinical biomarkers for that. It is not commonly done. The best one, epigenetic signature, is yet to be clinically approved or widely available.
Now, in that paper, they use broad range of age as a descriptor, confounding many age-associated phenotype and genotypes, which also translate into risk factors. You can definitely say that the 18-34 cohort is different 45-54, and that the later as more risk factors, the same a specific mutation might be associated with higher or even guaranteed chance of developing a disease, and hence will be use as a biomarker.
That being said, it is not typical to measure the biological age of healthy individuals. Actually, we don't know what an healthy individual is. We know a great deal more about diseased individuals. The current status seems to be that if you are not diseased you are healthy. I don't agree with that. That's how science is done. And that is how we end up with half-baked studies in one of the most impactful journal .
What is the precision and accuracy of the best biomarker? ie. if I gave you the necessary sample, how close can you get to the correct age and what are the error bars?
I didn't get enough from the tweets to understand how that was accounted for in the data. But I have questions.
By "inverts the causal relationship" I assume you threw "causal" in there by mistake. Nobody is going to think mortality causes high cholesterol. More importantly, if ignoring statin use reverses the slope to weaken the relationship "high cholesterol causes mortality" doesn't that suggest a lack of efficacy for statins? We know they lower cholesterol, but if that also reduces mortality the relationship (between cholesterol and mortality) should hold weather they are accounted for or not. Right?
Prevalent cardiovascular disease, or having a high risk for cardiovascular disease, causes low cholesterol. It does so by your doctor recognizing your elevated risk and putting you on statins.
Statins, like all drugs for prevention, do not prevent all subsequent disease. Perhaps most importantly, they only reduce cholesterol from the time you start taking them (as opposed to a genetically-driven low cholesterol throughout life). All of the drugs for chronic disease prevention tend to have a pretty small effect on the disease risk. Therefore, detecting that someone is taking a statin is a great signal that the person is at high risk for disease. They would be at an even higher risk if they weren't on a statin, but the statin does not erase all risk. That is why failing to account for statin use will lead to low cholesterol looking protective, if there are people in the population taking statins.
> First, the use of lipid-lowering medication was unaccounted for. The risk associated with high cholesterol might have been underestimated. However, in Korea, IHD mortality accounted for only approximately 5% of all-cause mortality, and only 10% of people with hypercholesterolemia received lipid-lowering therapy[39]. Therefore, the impact of not considering medication use is likely to be modest, and the TC levels in this study generally reflect levels without lipid-lowering medications
> only 10% of people with hypercholesterolemia received lipid-lowering therapy
Wouldn't this be much higher in the UK cohort? Also,
> The sex- and age- specific levels of TC in the current study of Koreans were lower than those reported in other high-income countries, including Japan, England, and the US
Which would reduce the effect (relative to what was found in the analysis of UK data) even further.
I don't think it adds a whole lot to talk about the confounding variables of this nature - it's an observational study, so of course it will have all sorts of confounding variables. If you are going to make a strong case that controlling for a specific confounding variable would reverse the relationship though, you should quantify the impact. It's unclear to me that statin usage would make a large difference, given that the study notes it wasn't a popular treatment.
My general feeling is that these types of studies tend to end up measuring overall health - given that most of the factors that lead to high cholesterol level were controlled for (BMI, physical activity, smoking status, drinking, etc) - and the average person in any population is relatively healthy and well-adjusted to the common diet, any large deviation from the norm in any direction statically makes it likely that the subject has some health issues.
What would be interesting to see in a meta-study is whether the optimal level of cholesterol either was consistent across populations that had very different averages or it tends to be near the median in each population. The former would be evidence that it's an independently meaningful biomarker; the latter would be evidence that it's just measuring how normal you are.
Also, I created those graphs and sent them to him, so (1) he didn't create the graphs or influence how they were created, and (2) and I have no financial interests in that company. His company plans to produce a molecule that disrupts PCSK9 production, thereby reducing LDL-cholesterol.
If you think that the conflict of interest influenced the analysis in a way that you would have done differently, what is the alternative approach by which you suggest analyzing the data?
We have drugs (PKCS9 inhibitors: https://www.nejm.org/doi/full/10.1056/NEJMoa1615664, bile acid sequesterants, CETP Inhibitors: https://www.nejm.org/doi/full/10.1056/NEJMoa1609581) that can lower LDL to 10-20mg/dL — the later even increased HDL. No impact on cardiovascular mortality. The studies all use composite endpoints.
What might cause Atherosclerosis?
- Bacteria
- Bacterial lipid byproducts
- Endothelial damage from toxins (lead, mecury, etc)
- Endothelial glycation from high blood sugar (Diabetics have a lot of CVD)
- Bad genetics resulting in excess hemodynamic stress at coronary branch points (fun fact: CVD only develops in a few specific spots)
- Autoimmune conditions (higher rates of CVD in this population)
What most of these things have in common is they trigger the activation of the immune system.
Have you got a link to some relevant research?
https://www.marksdailyapple.com/the-evidence-continues-to-mo...
The CTT is probably the best summary of these data: https://www.cttcollaboration.org/
Is that a composite endpoint of vascular events AND mortality?
From TheNNT:
"It takes 5 years of daily statin therapy to achieve a 1.6% chance of avoiding a heart attack, and a 0.37% chance of avoiding a stroke. Most disappointing, statins seem unable to prevent death in this group. And most concerning, the drugs may increase diabetes, a serious and life-altering disease." (Primary Prevention)
http://www.thennt.com/nnt/statins-for-heart-disease-preventi...
0 http://www.drjohnm.org/2014/06/growing-doubt-on-statin-drugs...
Additionally, I think you will not find many studies that claim that high HDL is bad for you, whereas you will find many that claim it's good (because it protects from CVD). I can't say I see much of "a mess" here- just ordinary, progressing scientific understanding of a complex system.
Are there really any studies that attribute atherosclerosis to bacteria, or some of the other conditions you describe? If so- are there many of those and are they good quality studies? I am very skeptical of your comment's suggestion that the immune system may be involved in atherosclerosis.
Yes, folks agree high HDL is good, high LDL is bad. However, drug trials to raise HDL didn't work so well.
> "Are there really any studies that attribute atherosclerosis to bacteria, or some of the other conditions you describe?"
Yes! Many!
- "Accelerated Atherosclerosis in Autoimmune Rheumatic Diseases" https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA....
- "Deposition and hydrolysis of serine dipeptide lipids of Bacteroidetes bacteria in human arteries: relationship to atherosclerosis"
- "The immune system in atherosclerosis" https://www.nature.com/articles/ni.2001
- "Is atherosclerosis an autoimmune disease?" https://bmcmedicine.biomedcentral.com/articles/10.1186/1741-...
- "Atherosclerosis and the role of immune cells" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4391004/
I keep getting the impression that using TC as a guide the ratio of number needed to treat vs morbidity reduced is kinda dismal.
LDL-c is bad. LDL-p (the particle number), LDL size, and ApoB (which is the protein part of LDL) are all very well correlated with LDL-c. So, while some people prefer one measurement or another, they're all proxies for one another.
We have lifelong exposure to our genetics-and-diet-induced cholesterol levels, whereas clinical trials run for a few years. The long-term follow up of the statin trials show mortality reduction. PCSK9 inhibitors reduce all-cause mortality, and the long-term follow-up of the PCSK9 trials may or may not show the same for cardiovascular specific mortality. However, everyone in the field thinks they will, because those with loss-of-function PCSK9 variants live longer with less cardiovascular disease. Also, adjudicating the cause of death is hard - autopsy, if done, overturns the diagnosis nearly 60% of the time[1].
Cholesterol isn't the only risk factor for cardiovascular disease, so other things (like autoimmune conditions) will contribute to risk as well, but this isn't an either/or phenomenon.
Check the evalocumab trial I posted, ACM was actually slightly worse in the PCSK9 side of the trial.
> "LDL-c is bad. LDL-p (the particle number), LDL size, and ApoB (which is the protein part of LDL) are all very well correlated with LDL-c. So, while some people prefer one measurement or another, they're all proxies for one another."
Yes, this tends to be true, however discordance between them is possible - and generally not a good thing.
> "Cholesterol isn't the only risk factor for cardiovascular disease"
Sure, but I think the whole of the field has rabbit-holed on lipids for too long, ignoring actual causal factors.
LDL cholesterol is by far the best established causal risk factor for coronary artery disease.
> "Check the evalocumab trial I posted, ACM was actually slightly worse in the PCSK9 side of the trial."
All cause mortality was significantly lower in Odyssey: https://www.nejm.org/doi/full/10.1056/NEJMoa1801174
Is it causal, or is it a risk factor? I'd say at best it is "necessary but not sufficient". CVD risk calculators don't even take LDL-C into account, that's how good of a marker it is.
- studies that incorporate statins don’t seem to segregate impact of anti-inflammatory effect of some statins vs cholesterol lowering.
- some docs are prescribing statins to healthy individuals based on only cholesterol scoring, also not taking into account more expensive but better imaging like coronary calcium scoring
- Are there studies that show proactive use of statins on otherwise healthy individuals lead to decreased overall mortality?
- there’s less question in my mind that a subpopulation with cardiovascular disease could benefit from statins but mainstream medical care seems far more aggressive that that, especially when dealing with asymptomatic elderly.
How would you tease that apart? CAD requires some amount of inflammation, since macrophages have to enter the blood vessel wall to become foam cells. So, it may be mechanistic that reducing LDL also reduces some markers of inflammation. If you have a method of testing statins' anti-inflammatory effects in some way that is independent of their LDL lowering effects, by all means someone would do that study.
> "- some docs are prescribing statins to healthy individuals based on only cholesterol scoring, also not taking into account more expensive but better imaging like coronary calcium scoring"
Coronary calcium scoring can be a good tiebreaker when someone's risk factors suggest that they should be on a statin, but they don't want to take a statin.
> "- Are there studies that show proactive use of statins on otherwise healthy individuals lead to decreased overall mortality?"
There are many primary prevention statin trials. They all involve people with at least one risk factor (high blood pressure, etc). I consider them trials in "healthy" people, since they don't yet have coronary artery disease, but if you meant people with zero risk factors, these wouldn't answer your question. Primary prevention trial examples: ASCOT https://www.ncbi.nlm.nih.gov/pubmed/14997313 and Jupiter https://www.ncbi.nlm.nih.gov/pubmed/18997196
This was my point. On one hand, statin supporters use these studies to say "cholesterol lowering" is warranted, but there's no quantification on how much protective effect is from its anti-inflammatory properties vs the cholesterol lowering aspects. The anti-inflammatory effect is also not tied to reducing LDL alone, but has separate mechanisms (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3394171/). Rather than try to isolate the cholesterol lowering aspect, I'd be interested in studies that compared a range of anti-inflammatory drugs (other than just low-dose aspirin) to a variety of statins that also differ in the degree of their anti-inflammatory effects. But as far as I know (and I'm definitely no expert in this field), such studies have not been done.
> Coronary calcium scoring can be a good tiebreaker when someone's risk factors suggest that they should be on a statin, but they don't want to take a statin.
I know a healthy guy who has sky high LDL-P, didn't want to take a statin, and then got CAC imaging with a score of zero. If he hadn't talked his cardiologist into that scan, he'd be on a statin with all the side-effects it entails. That to me seems at odds with the "do no harm" mantra, especially when the CAC imaging seems more directly indicative of underlying CVD in asymptomatic individuals. There are many examples of people with low cholesterol (not on statins) who have underlying CVD as well as people with high cholesterol who have no CVD.
> There are many primary prevention statin trials. They all involve people with at least one risk factor (high blood pressure, etc). I consider them trials in "healthy" people, since they don't yet have coronary artery disease
Similar to your critique of the OP research paper, I am troubled with studies that treat all asymptomatic individuals the same and don't assess state of atherosclerosis (i.e., a CAC score) and differentiate types of risks (high blood pressure vs high cholesterol). The question is whether high cholesterol itself _in the absence of underlying pathology_ leads to worse outcome. If we have no idea whether the starting population has underlying pathology to begin with, IMHO there's a problem with extrapolating those results to asymptomatic people with those risk factors. Other risk factors like HBP may actually be causal.
And this is where this is disagreement. What is appropriately elevated risk? In the case of asymptomatic high cholesterol individuals, especially those without additional risk factors beyond cholesterol, (1) there are flawed studies that include people with underlying pathology together with people who have none to assess statin "benefit", and (2) there are flawed studies that show statins might actually be detrimental with regard to overall mortality. Mainstream medicine currently is fine with #1 (your "they keep people alive longer") and disregard #2 ("they are inversely associated with mortality").
I completely disagree with your dismissal of statin side effects and definite overplaying of the radiation dose of CAC scanning. Nobody has complete understanding of the full side-effect profile of long-term statin treatment let alone all the different types of statins. You have a point with expense, but lets not kid ourselves about the relative side effect profile of long-term statins vs a CAC scan. There's also the management advantages knowing CAC score vs just using LDL.
http://imaging.onlinejacc.org/content/10/3/304 "The presence of CAC is both a sensitive and specific indicator of atherosclerosis, while the total CAC score is a strong predictor of both short- and long-term clinical outcomes. A zero CAC score has become the most definitive predictor of low risk, mild CAC score elevations are indicators for initiating optimal prevention strategies, and high CAC scores may indicate the need for more aggressive management and follow-up. Furthermore, the test has become inexpensive and, with current imaging technologies, is associated with radiation exposure that has decreased to 1.0 to 1.5 mSv per study and to even lower radiation exposure with the newer low-dose imaging protocols (34)."
Average person receives about 3 mSv per year from natural sources. The annual dose for flight attendants is 1.5-1.7 mSv. Mammograms and CAC imaging is similar and less than what flight attendants get in a year.
So on one hand, you argue the OP article is fatally flawed because the low-cholesterol group contains high-risk people given statins. On the other hand, you don't concede that the studies lumping all asymptomatic "high risk" individuals together suffer from the same issue. The EISNER study started with "an older population with baseline risk factors" and found 52% had CAC abnormality. I would be interested to see what percentage of asymptomatic high cholesterol people have CAC zero scores and would be treated with statins anyway under current guidelines.
There’s also no consideration of non-CVD mortality and especially morbidity in most of these studies. Despite your unequivocal statement that (all) statins are safe, there’s still a lot we don’t know about long-term use including effects on cognition (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5830056/).
The medical profession is rather vulnerable the promise of miracle cures to offer their patients, and prescribed the new anti-cholesterol drugs with gusto. Later studies have found the benefit of statin therapy to be minuscule: the "number needed to treat" to prevent one fatal cardiac event is rather high, on the order of 217 for low-risk patients [1]. That is, ~216 patients get to experience the side effects of artificially-reduced cholesterol levels while only 1 person avoids the problem the pill was prescribed to prevent.
In the holistic way of looking at the role of cholesterol, it is more important to think about why the body is manufacturing excess cholesterol and depositing it where it does. As you indicated above, inflammation is an important consideration. Another line of thinking is that there is a roadblock in the steroidogenesis pathway, and that supporting the body's effort to make steroids takes care of the elevated cholesterol levels too.
But our medical professionals tend to develop tunnel vision as they specialize, and assume their specialty's understandings of their domain is basically correct. The drug companies find it much more profitable to peddle anti-cholesterol drugs than to address patients' actual problems.
At least patients who are harmed by statins have the freedom to discontinue their anti-treatment.
[1] http://www.thennt.com/nnt/statins-persons-low-risk-cardiovas...
Is it really? For example:
Ravnskov, Uffe, Michel de Lorgeril, David M. Diamond, Rokuro Hama, Tomohito Hamazaki, Björn Hammarskjöld, Niamh Hynes, et al. 2018. “LDL-C Does Not Cause Cardiovascular Disease: A Comprehensive Review of the Current Literature.” Expert Review of Clinical Pharmacology 11 (10): 959–70. https://doi.org/10.1080/17512433.2018.1519391.
This review summarized the evidence in a way that most of the rest of the field would not. Fringe views are valuable, but unless they can actually refute the underlying hypothesis or provide a better model, the work is not very impactful. Particularly so with a review article.
Not all mortality risk operates through cholesterol-dependent mechanisms. And even for those that do, decades of exposure to high cholesterol can’t be totally reversed by medications.
Edit: they do decrease your risk of a heart attack a bit, but the increased incidence of cancer and diabetes actually eliminates the benefit for most users. The only people who showed any measurable reduction in mortality were non-elderly patients with a history of cardiovascular disease.
https://www.marksdailyapple.com/the-evidence-continues-to-mo...
Also interesting: Current physician guidelines don't recommend treating to a specific number, like <200. When I trained (<5 years ago) we were taught to check cholesterol levels and if LDL > n then start a statin and increase the dose until LDL < n.
Now, its (almost) entirely risk assessment based: https://www.acc.org/latest-in-cardiology/ten-points-to-remem...
They may lower cholesterol some amount, but in many populations this has almost 0 impact on morality. Watch out for those relative risk ratios.
But, across all fields of medicine, we know that confounding by indication is a problem. Preventive medicines, by and large, are not sufficiently powerful to reduce risk to zero.
Reverse causality has been suggested as an explanation of higher mortality associated with low cholesterol levels. However, a long term follow-up study in a Japanese-American population showed that individuals with low cholesterol levels maintained over a 20-year period had the worst all-cause mortality, and concluded that reverse causality was unlikely to account for the higher mortality associated with low cholesterol entirely14.
My reading of "reverse causality" here is that people with high TC have more cardiovascular disease and take more statins that lower their cholesterol. I haven't read the referenced study.
Considering how complex this system is, measuring TC is like measuring average body temperature in the hospital.
It’s cool that they found a U-shape but this approach just makes patients(and doctors) hack the TC number without understanding how that affects lipoprotein composition and, subsequently, patient’s health.
That is really interesting, do you have a source you can recommend for reading further?
The whole series is a gold mine tbh
https://medlineplus.gov/cholesterollevelswhatyouneedtoknow.h...
It doesn't seem at all strange that there should be an optimum level that is non-zero.
[1] https://www.nytimes.com/2016/09/13/well/eat/how-the-sugar-in...
The body sythesizes sexual hormones from cholesterol.
> U-curve associations were found. In the TC ranges of 50–199 and 200–449 mg/dL, each 39 mg/dL (1 mmol/L) increase in TC was associated with 23% lower (95% CI:23%,24%) and 7% higher (6%,7%) mortality, respectively. In the age groups of 18–34, 35–44, 45–54, 55–64, 65–74, and 75–99 years, each 1 mmol/L higher TC increased mortality by 14%, 13%, 8%, 7%, 6%, and 3%, respectively (P < 0.001 for each age group), for TC ≥ 200 mg/dL, while the corresponding TC changes decreased mortality by 13%, 27%, 34%, 31%, 20%, and 13%, respectively, in the range < 200 mg/dL (P < 0.001 for each age group).
Nothing. Absolutely nothing. Doubly so if you aren't eating animal products.
I'll add that avoiding all animal products has its own perils, namely the sort that results in vitamin deficiencies. And while a diet filled with whole grains and mostly plant-based foods is considered healthy, we simply don't know enough about nutrition to have one way or another. Or even to get vitamin doses right. I say all this while eating mostly vegetarian myself. I eat fish about once a week. I don't like it so much, but it is healthy.
wheat contains Phytic acid for example: https://en.wikipedia.org/wiki/Phytic_acid which can be reduced with the correct dough process.
The beta-carotene in carrots is fat soluble and the cells are pretty robust, so you get more out of them if you cook them in fat.
Champignons contain a mild poison, which is not deadly for humans but destroyed when heated, digestibility increases too.
There are even suggestions that it was cooking by opening untapped sources of calories that allowed for a bigger brain to evolve.
Are you part of a proper subculture that engages with this? If so, where do you all hang out, what do you read?
https://youtube.com/watch?v=MqmSMunAtss
Also, lose weight. The body induces some beneficial activity while fasting.
eg see https://www.aplaceformom.com/blog/2013-03-29-where-people-li...
Eat a varied diet, leaning towards plant-based foods. Whole grains if you can. Don't unreasonably cut out whole categories of food. Being vegan is HARD, vegetarian (or mostly so), not so much. Watch the sugar, including the fake type. Eat your calories instead of drink them.
Also, get some activity. Walking for 15 minutes daily is better than nothing, but try to get more than that most days. IF you can have fun doing it, great! If you lack motivation, do something on the easy side as it is easier to talk yourself into. It is better to this half-assed than not at all, after all, because it still counts.
Keep an eye on stress as much as possible. If you smoke, try quitting (I suggest a vape or e-cig). Drink in moderation, but do have some coffee.
Once you get these general things done, you are well on your way.
Perhaps the topic is complex and nuanced but the advise in the comment seems fairly good in the general healthy spectrum.
Besides some opinion being thrown in, what do you disagree with?
It's not, it's mildly tricky, and there's not much evidence that people following a vegan diet are nutritionally worse off than the people who don't think about their food at all, many of whom don't eat any fresh fruit or veg across a week.
I might be mostly vegetarian and eat eggs and cheese and fish once a week, but I usually tell folks to reduce their eat. Sometimes I say instead to make sure they eat enough fruit and veg and whole grain. I say this stuff because it is easier for most folks to concentrate on things like this to improve overall diet without feeling like they have to spend days figuring things out.
Also, it's worth noting that the difficulty of going vegan varies greatly with your location. For example, eating vegan in Japan is a legitimate pain in the ass.
There are lots of reasons a person can not have a period. Sure, you can be malnourished, but I'm guessing the more likely contributor was not having enough body fat. IF a woman's body fat is too low, she stops having periods. It happens in a broad cross section of people. A person with an eating disorder will do it as will a woman that works out a lot and eats healthily. Coincidentally, weighing too much can do it as well.
I'm guessing a nutrient deficiency can do it, but I'm unsure on that one. It can be a hormonal imbalance too!
And there are a bunch of other reasons as well. It isn't even necessarily harmful - after all, people quit having periods when they are on birth control with no ill effects.
You also seem to believe that eating meat, not only fruits/veggies/vegan, is good.
Wouldn’t that make you in agreement with the current system of balanced intake?
Public health organisations are staffed by experts who have spent most of their lives studying the relevant subjects. How likely is it that you, or anyone who hasn't dedicated that much time and effort in studying those subjects, will know better than those who have?
I'm not saying it's impossible, mind. But just what are the chances that your opinion is right and that of thousands of experts is wrong?
There have been some successes, we are now very good at catching CVD early, and should you have a heart attack you are now much more likely to survive than before. But on the food front, what we’re talking about here, it has been a complete and unmitigated disaster.
Because of that, I don’t trust public health officials one iota when it comes to food and diet. That doesn’t mean I’m right, but I know that they have a track record of failure and unintended consequences.
Also, as far as I know, public vaccination programmes have greatly reduced, and almost eliminated many diseases like measles, tetanus and typhoid, not just in the US but the world over, although of course measles is making a comeback.
Are you perhaps drawing a conclusion about public health bodies in western countries in general, from an experience with health services in the US? The US seems to be very peculiar in how it treats public health. I live in the UK and I wouldn't say that the national health service (the NHS) has collapsed. It has its problems and it's being attacked constantly but for the time being, it's working fine. The same is true for most central European countries.
Americans have actually followed the recommendations of the USDA for years. They replaced saturated fat with “heart healthy” seed oils, and they diligently consumed low fat diets.
Keep in mind that official recommendations will affect what foods are available for sale too.
> My understanding is that processed foods and sugary drinks are consumed in great numbers, but that is certainly not in accordance with the recommendation of any public health organisations that I know of.
In the United States nutrition labels have a maximum daily amount of most nutrients, except sugar. The official line has been that saturated fat causes heart disease, and that replacing fat in packaged goods with sugar was ok. This is why we have candy in the United States proudly labeling itself as a “fat free food”, and we used to have marketing campaigns touting the weight loss benefit of sugar.
This is finally starting to turn around, but the public health agencies have been laggards when it comes to the realization of how bad sugar is, not at the forefront.
And that’s not even getting into the whole bailiwick about how they process foods, which has changed in accordance with public health recommendations. They used to at least use natural fats in the few processed foods we used to eat, such as lard, but all of those were changed years ago to seed oils that were nominally less bad.
> Also, as far as I know, public vaccination programmes have greatly reduced, and almost eliminated many diseases like measles, tetanus and typhoid, not just in the US but the world over, although of course measles is making a comeback.
As I clearly stated, all public health programs should be judged by their outcomes, and the results of public vaccination have been an unqualified success.
But just because the official recommendations on vaccinations have worked, it doesn’t follow that the official recommendations on diet will too.
> Are you perhaps drawing a conclusion about public health bodies in western countries in general, from an experience with health services in the US?
Yes, that’s a fair criticism.
> I live in the UK and I wouldn't say that the national health service (the NHS) has collapsed.
That’s not what I said. I said that our health has collapsed, i.e. we’re fat and sick.
Did US public health organisations actually recommend replacing fat with sugars? I find this very surprising, if it is the case. I wouldn't be surprised if that was instead a practice adopted by industry, despite and against official recommendations.
For example, Wikipedia tells me that diet Coke was first sold in 1982. That must mean that there was, already, a clear awareness of the detrimental effect of sugar, and sugary drinks in particular, on health. That awareness can't have come from the soft drinks industry itself so it must have come from public health officials.
In 2015 they finally released a recommendation that sugar make up no more than 10% of an American’s daily calories, which is insane.
Also at a practical level, a recommendation to remove fat from diets is a recommendation to add sugar. A wide variety of foods are just absolutely disgusting if you have neither fat nor sugar, and if you declare that the reduction of dietary fat is the main goal for Americans, the result will necessarily be more added sugar. The dietary guidelines still recommend that Americans eat leaner cuts of meat and switch to 1% milk, as if they haven’t already done that.
Because HN is full of people who subscribe to fad diets like keto, carnivore, gluten-free, etc.
If anyone wants to have a healthy life, I recommend you to read the book Nutrition and Physical Degeneration from Weston Price. Basically, eat animal products, the more local based, the best. Grass feed cattle will be the best food source for your body. Cut all carbs (sugar), fruits (man made).
There are 15 nutrients that you can only get from animal products. You can get all minerals and vitamins from animal products you don't need plants at all.
The worst offenders for weight gain are foods that don’t trigger a satiation response, like chips and dip or French fries. Foods where the fat to carbohydrate ratio is nearing 1:1 will cause people to overeat. Processed foods tend to have these ratios.
I finally decided to stop taking them as they have annoying side effects and the cynic in me believes the science may have been pushed a bit off center by monetary incentives to the makers of these patented treatments.