It doesn't give me much confidence bringing it up at all in this convo. As if replacing HFCS with cane sugar (55% vs 50% fructose) changes anything about junk food.
Exercise temporarily raises your heart rate and systolic blood pressure, yet avid exercisers have lower RHRs and SBPs; how do you know it isn't the same with carbohydrates, provided fat (especially saturated) is restricted?
And if sugar is so metabolically harmful, where are the RCTs showing this? All I've seen is that outside of a caloric surplus, it isn't especially metabolically harmful, and ironically, even outside of a surplus, saturated fat is much worse:
> US sugar consumption declined from 2000-2020 to 1970s levels, while its T2D prevalence only increased
Seems like you are cherry picking data and ignoring other data from the chart - sure the total sugars from 2000-2020 are down slightly while what’s being labeled as “corn sweeteners” or HFCS is up 3x.
Since you mention diabetes it’s probably worth noting from 1970-1985 “corn sweeteners” more than 3x and before 1985 T2D was called adult onset diabetes considered an adult disease and 1983 was the first case of pediatric nonalcoholic fatty liver disease.
> Meanwhile tribes of hunter-gatherers in Africa get 15-80% of their daily calories from honey during certain seasons;
The chart shows honey is a nominal source of sugar for Americans. There are other facts about honey, like its low glycemic index compared to other forms so it doesn’t raise blood sugar levels as dramatically as regular sugar and especially HFCS.
The fact is the US government just lumps all forms of sugar together and labels it all genetically as sugar…ignores there are different forms of sugar, each processed by our bodies differently and having different metabolic impacts and harms.
People will spend the next 100 if not 1000 years arguing if sugar is responsible for metabolic diseases like T2D and nonalcoholic fatty liver disease - yet it’s settled now that T2D & NAFLD are both 100% preventable diseases and in some cases T2D can be reversed by minimizing sugars/carbs and increasing fats so your mitochondria is primarily using ketones rather than glucose.
> Seems like you are cherry picking data and ignoring other data from the chart - sure the total sugars from 2000-2020 are down slightly while what’s being labeled as “corn sweeteners” or HFCS is up 3x
HFCS consumption is still higher than it was in 1970, but it has declined since 2000, and its decline has driven the overall decline in sugar consumption, yet obesity and diabetes incidence have only increased.
> some cases T2D can be reversed by minimizing sugars/carbs and increasing fats so your mitochondria is primarily using ketones rather than glucose.
"Reversed" means you can eat carbohydrates normally again. If anything, high-fat, low-carb diets seem to worsen actual insulin sensitivity, which carbohydrate restriction just masks (even then, not always, as many on keto find when they check their BG): https://pmc.ncbi.nlm.nih.gov/articles/PMC5291812/
Severely restricting carbohydrate enough to get an artificially low HbA1c or fasting BG and claiming you "reversed" diabetes is like claiming you "reversed" your lactose intolerance by never drinking milk. But actual weight-loss (however you achieve it) does improve real insulin sensitivity, but low-carb isn't magic when it comes to that either.
>HFCS consumption is still higher than it was in 1970, but it has declined since 2000, and its decline has driven the overall decline in sugar consumption, yet obesity and diabetes incidence have only increased.
Because metabolic diseases are progressive chronic conditions. That’s why T2D & fatty liver were historically adult diseases, it’s not because throughout history people gradually increased sugar consumption as they got older and got the diseases, rather the metabolic damage progressed. In short when you are over consuming sugar for 20 years and see obesity, T2D and fatty liver disease increase you don’t necessarily expect to see it decrease even if sugar use slightly decreases…if you want to decrease or eliminate T2D/fatty liver disease then eliminate the sugar.
>"Reversed" means you can eat carbohydrates normally again.
That’s not what “reversing diabetes” means, it means getting off insulin because you manage your BG through diet and lifestyle.
>Severely restricting carbohydrate enough to get an artificially low HbA1c or fasting BG and claiming you "reversed" diabetes is like claiming you "reversed" your lactose intolerance by never drinking milk.
It’s just not a good metaphor because your definition of “reverse” is returning to eating carbs normally was wrong. Lactose intolerance is an acute reaction related to inability to produce an enzyme to breakdown and digest lactose - it’s managed not treated with medication, though some may take the enzyme lactase. Further, taking lactase because you’re lactose intolerant and want to eat some ice cream tonight is in no way comparable to having T2D and the need to take insulin.
That does not make sense statistically. A decrease in total HFCS consumption would lead to a decrease in new diabetes cases if it was the actual root cause.
As far as I can tell, we do not know why it happens, but monitoring sugar intake is a key strategy for managing the disease, which also has no known cure.
Assume type 2 diabetes is actually just a natural phenomenon associated with aging, that hits some people earlier, some later, and some little or not at all. Wouldn’t it stand to reason that careful moderation of sugar intake is still a good idea?
Regarding sugar consumption declining while T2D and NAFLD increase, could it be the case that metabolic effects could translate to genetic mutations that are expressed in later generations?
You perfectly framed why it’s my belief this debate will rage on for 100-1000 years.
People irrationally get agitated and become sugar advocates when you explain the two truths:
1. 100% of T2D cases can be prevented through diet/lifestyle
2. Some T2D cases can be reversed (not a cure but getting off insulin) through diet/lifestyle
As you point out that the diet/lifestyle I am referring to consists of restricting carbs and sugars.
Unfortunately, that’s where people freak out and declare “sugar doesn’t cause diabetes” as if that’s well settled science - it’s not. Maybe sugar causes T2D or maybe it doesn’t, but it is immaterial to the point that it is established that sugar/carb restriction can prevent 100% of cases and is both practical and actionable for nearly everyone.
The study you linked to defines the "high fat diet" as 55 % fat/25 % saturated fat/27 % carbohydrate.
Besides the fact that these figures add up to 107%, 27% of a 2000 kcal/d diet is 540 calories. At 4 calories per gram of carbohydrates, that works out to 135g of carbohydrates. Even if they were only eating 1200 kcal/d, that's still 81g of carbs.
Most ketogenic diets recommend no more than 20g of net carbohydrates per day (net carbs = total carbs - fiber - certain sugar alcohols).
This study may be valid, but I'd bet money there wasn't a single participant actually in a state of ketosis for this study, which makes it moot as a response to the parent comment you're refuting, which specifically mentions ketosis, not just a "high fat diet" that also contains 80g+ of carbs daily.
> The fact is the US government just lumps all forms of sugar together and labels it all genetically as sugar…ignores there are different forms of sugar, each processed by our bodies differently and having different metabolic impacts and harms.
At the same time, these differences can be overstated. E.g. look at how "added sugar" is distinct from other carbohydrates but no "total sugar" metric on nutritional boxes on food products.
> E.g. look at how "added sugar" is distinct from other carbohydrates but no "total sugar" metric on nutritional boxes on food products.
I had to go check a few labels to be sure, but this is absolutely not true in the US—each nutrition label has a "total sugars" category that additionally breaks out the added sugars from the total sugar.
See the example on this page [0], and discussion of the sugars lines here [1]. Also see this PDF showing the differences in the 2018 nutrition facts label from the old one [2], which clearly shows total sugars have been there in at least the last two iterations.
Maybe you're thinking of the fact that there's no daily value listed?
Just for context, total sugar is the only thing shown on European food labels. Makes it somewhat annoying the other way around, it's hard to figure out if it's just the sugars the ingredients contained or if it's stuffed with extra. I prefer this worry over the other option though. In a perfect world we would have both.
If sugar is added, it’s in the ingredients list in the EU. They are sorted by decreasing amount, hence while you won’t be able to tell exactly how much was added, you can narrow it down. But sometimes they add different sugar types and it becomes really difficult to estimate the quantity of added sugar.
Hence I would say it’s easy to know if sugar is added if you know the names it goes by. But it’s difficult to know how much.
It has had total sugars for as long as I've known the labels, and was changed in 2018 to break out added sugars. I'm not at all sure what OP is thinking.
Do you mean oils that have turned rancid before they are consumed? I don’t really get the hate seed oils are getting. In studies they seem to have shown no ill effects. They do certainly use oils in studies that are not rancid, while your average supermarket oil might be (?).
Without a literature review, they'd certainly be a number one suspect.
Consider this statement elsewhere in the thread:
> before 1985 T2D was called adult onset diabetes considered an adult disease and 1983 was the first case of pediatric nonalcoholic fatty liver disease.
We've eaten sugar and saturated fats for ages. Of course, not everyone ate the same amounts that people do today - but we'd expect someone to be feeding their kid enough bacon (which people ate huge amounts of even ~100 years ago relative today) to give them fatty liver disease, if e.g., its saturated fats, or feeding them enough sugar.
But what people didn't eat, almost at all, was seed oils. Canola oil was not consumed at all before the 1970s - canola is a CANadian scientist created version of rape Oil, with Low Acid - rape oil itself being too poisonous/bitter to eat. Soybean oil was practically unheard of. Cottonseed oil (aka Crisco) was just being invented as a wonderfood, here to solve our problems. Today these oils, particularly soybean and canola, are the second highest source of calories in the average American diet, and the single highest source of fats. We're suddenly beset by major metabolic problems, from heart disease, obesity, fatty liver, T2D, that did not exist or existed in much smaller proportions, even in historical populations where people were eating tons of bacon or sugar. Meanwhile, we have a food source that went from "negligible" to "one of our main sources of calories." It's not proof, there are almost certainly other factors involved as well, but it's really, really suspicious. Making matters worse, what you feed animals also impacts the fat composition of their meat, and we now feed cows and pigs canola and soy.
> before 1985 T2D was called adult onset diabetes considered an adult disease and 1983 was the first case of pediatric nonalcoholic fatty liver disease.
This statement is factually false, though: https://www.sciencedirect.com/science/article/pii/S258955592.... It may not have been explicitly called that, but it was clearly shown to exist. This is not some new phenomenon that first popped up after the introduction of seed oil.
>The term non-alcoholic fatty liver disease entered the hepatology lexicon in 1986, introduced by Fenton Schaffner (American physician and pathologist).
As you acknowledge the disease didn’t even have a name until 1986, or 3 years after the first diagnosis in children.
There is nothing in the study you link suggesting kids were being diagnosed and treated for nonalcoholic fatty liver disease pre-1983 under a different name - they weren’t.
This is easy enough to confirm on google independently [1].
>This is not some new phenomenon
Yes it is, in the ~40 years since the first recorded medical diagnosis it’s become an epidemic effecting 5-10% of kids or ~10M kids in the US. There is no way this is not a new phenomenon and 5-10% of kids had nonalcholic fatty liver disease throughout history and we have no record of it.
[1] Title: Steatohepatitis in Obese Children: A Cause of Chronic Liver Dysfunction.
> Today these oils, particularly soybean and canola, are the second highest source of calories in the average American diet, and the single highest source of fats
Isn't canola oil one of the oils with the fewest saturated fatty acids, typically 7-8g per 100g?
Olive oil has ~twice as much, sunflower oil as well. Palm oil has ~7x more. And coconut oil ~10x more.
Calories-wise, all these oils are pretty much the same, typically in the range of ~800kcal per 100ml. So, I am not sure I understand the arguments against it.
Canola oil is pretty much the best bet if you want to reduce your fatty acids intake.
I didn't say saturated fats, I said fats - obviously, oil is pretty much 100% fat by definition.
Of course, it's also controversial in some circles whether saturated fats are bad, but that's a separate discussion. There is more to a cooking oil than it's saturated/polyunsaturated/monounsaturated fat ratios.
The problem is linoleic acid and our overconsumption of it. It seems to cause way more oxidative stress during metabolism, to which the brain is more sensitive. Plus it also seems to adversely affect metabolism of other kinds of fats. And it plasticizes during cooking.
The idea being in the past the only linoleic acid we would be getting was from whatever seeds we consumed naturally. With the advent of industry it's now a 20B+ business. It was hard for humans to consume so much seed oil in the past.
"Seed oils" are a nonsensical category because the main example is canola oil which doesn't actually have the problems associated with them (bad omega-3:6 ratios).
I thought the problem with seed oils is that seeds don’t want you to eat them and their chemistry may reflect that. Fruit bodies such as olives on the other hand are “designed” to be eaten and so aren’t likely to have such defenses.
Olives are a pretty weird example of something that "wants" to be eaten by us, given the insane amount of processing it takes to make anything remotely palatable from them.
Contrast with, say, sesame or sunflower seeds which can be eaten straight from the plant raw, or pumpkin seeds which just need a simple roast and peel, I'm not sure that your categorical assertion really holds up, as intuitive as it may seem.
It just has to be mammals in general. If e.g. a rape seed doesn’t want to be eaten by squirrels, to take a common seed eating mammal, there’s a decent chance that as mammals we share enough in common that whatever surface is being targeted in squirrels would affect us as well.
If something was specifically targeting birds or reptiles then it may not affect humans, but are the seeds in question in environments without mammals? I don’t think so?
> And if sugar is so metabolically harmful, where are the RCTs showing this?
Look at the details of this study. The reason there are no RCTs is, at least for what this study looked at regarding very early childhood, they are impossible because they would be highly unethical. You can't take two groups of babies and randomly assign them to control group vs high-sugar group and test for the outcomes.
What this study is arguing is that the lifting of sugar rationing acted as a "best possible" form of a natural RCT as babies born relative to that lifting date had vastly different levels of sugar consumption in the first 1000 days. Note you see these types of "natural cohort" studies in a bunch of areas. E.g. it's not ethical to say group a is the "high levels of lead" group and group b is the control, but by looking at neighboring states that restricted leaded gasoline at different times you can try to tease out cause and effect.
I see tons of comments here arguing "how can they say it's just sugar!" I had a similar initial reaction, but I see very few comments that are arguing about the specifics of the study itself, and I'd argue the study is quite interesting and, at least from my layman's perspective, well done.
>US sugar consumption declined from 2000-2020 to 1970s levels, while its T2D prevalence only increased
obesity did not decline
>And if sugar is so metabolically harmful, where are the RCTs showing this? All I've seen is that outside of a caloric surplus, it isn't especially metabolically harmful
>Meanwhile tribes of hunter-gatherers in Africa get 15-80% of their daily calories from honey during certain seasons; why aren't they obese and diabetic?
if you are are physically active and don't overeat, you can eat whatever the fuck you want and never get obese. if you are not obese, you will (most likely) never develop T2D
Just one cheeseburger is three miles of running. Not only is it very easy to shop and overeat, your body continually encourages it. The only way out is determination not to eat whatever you want.
I find this is the difficult part. I find it much easier to not eat hyper-palatable foods at all than to eat "just a little".
Sure, I probably won't eat two hamburgers in a sitting, but eating one greatly reduces the calories I can eat during the other meals of the day if I don't want to slowly gain weight.
If you eat a normal burger with high quality meat and traditionally made roll and fresh vegetables on top the overeating thing isn’t as much of an issue. I have a hard time finishing a single one let alone eating more.
The jogging might not be necessary for the calorie burn, but humans evolved based on movement / activity. Our great great great great...n ancestors didn't have desk jobs starring at screens.
I find it way easier not to eat whenever I want. I'm doing 24h break from eating every 24h. Basically one day I'm eating just till 4PM and the next one only after 4PM. I've lost about 6kg (from being slightly overweight) in two months eating whatever I want. Just not whenever I want.
Nobody is implying it’s so simple that you can “eat whatever you want” and be at a healthy weight. This is true if you’re underweight as well. If you’re trying to gain weight, you need to eat more than you want.
> Meanwhile tribes of hunter-gatherers in Africa get 15-80% of their daily calories from honey during certain seasons; why aren't they obese and diabetic?
The fact you even have to ask this question is telling.
Specifically you're talking about Hadza tribe that spends pretty much all of their waking hours outdoors hunting and tracking pray, day in and day out.
They quite literally track honeyguide birds, climb tall baobab trees, get stung repeatedly and then they eat freshest highest quality honeycombs whole, including larva, and not just extracted, industrially processed honey.
Westeners that show up to film hadza can barely keep up to them because just how fast, long and exhausting their hunts are.
This is akin to asking why do long-distance cyclists who spend 10-16hrs a day on bike on long cross country rides can drink liters of cola every day and be skinny like a fig.
I'm getting second hand embarrassment from just reading the question.
> The fact you even have to ask this question is telling. Specifically you're talking about Hadza tribe that spends pretty much all of their waking hours outdoors hunting and tracking pray, day in and day out.
Look up Pontzer's Constrained Total Energy Expenditure Model. His doubly-labeled water experiments show that Hadza and other hunter-gathers have--contrary to his (and your) initial expectations--roughly comparable TDEEs to sedentary western counterparts (controlling for lean body mass) due to metabolic compensation (i.e., the more they exercise, the more their bodies compensate by expending less energy elsewhere, on things like inflammation and thyroid/sex hormones): :
https://pmc.ncbi.nlm.nih.gov/articles/PMC4803033/
Regardless, they're in energy balance, meaning they aren't gaining or losing weight, and despite their high-sugar diets, they aren't presenting any of the metabolic maladies that Lustig ascribes to sugar specifically, and not to weight gain--maladies that saturated fat seems to cause with no weight gain.
> This is akin to asking why do long-distance cyclists who spend 10-16hrs a day on bike on long cross country rides can drink liters of cola every day and be skinny like a fig.
Sugar has 4 calories per gram. Fat has 9. Are you arguing that sugar calories are more fattening than fat calories?
> I'm getting second hand embarrassment from just reading the question.
Problem with sugar isn’t that is so bad chemically from my experience, it is super mega addicting, it is way more addicting than nicotine for me for example. I don’t crave some eggs and sausage but crave sugar like crazy. So I am very likely to over consume sugar compared to other things. This is what makes is very harmful to me at least
The depressing part is that there's a large subset of people that can't even begin to grasp just how extremely embarassing it is to attach accelerometers to tribesmen and then think it becomes a steam engine and can be modeled as such.
> Sugar has 4 calories per gram. Fat has 9. Are you arguing that sugar calories are more fattening than fat calories?
Show me a molecule called "calory". Make a blood test - or any other measurement involving actual human body and show me exactly where this "calory" is. Obviously that is a rhetorical question, as human body does not operate on "calories", in fact, they are nowhere to be found in the human body.
Human body however does recognize glucose - C6H12O6 - and when your glycogen stores are depleted (such as by running in the jungle whole day, climbing a tall baobab tree or doing long distance cycling sessions) - the monosaccharides you consume will first go directly to replenish glycogen stores in muscles and liver and other organs.
If however, you're big fat couch potato with minimal lean muscle mass and a low basal metabolic rate, your glycogen stores are maxed out easily and continued consumption of sugar will directly lead to insulin spikes that will directly trigger lipogenesis (fat storage) as the fat cells will convert excess blood glucose into triglycerides. Eventually you develop insulin insensitity and eventually diabetes. Which is a very natural progression.
Consuming fat however does not notably spike insulin and does not trigger lipogenesis in the same fasion, quite the opposite - breaking down stored body fat can only happen if you stop constantly spiking insulin and enter a catabolic state. And thus - yes - even though fat is more energy dense on paper, it is way less fattening that sugar. And most important of all - consuming fat and proteins increases satiety via peptide hormones such as cholecystokinin which is released when the gut has to digest proteins and fat.
Embarassment really is the only polite way to express myself when confronted with people that compare hunter-gatherers that eat everything that moves, animals, their guts and organs whole, beas, larva, beawax and honeycombs in their entirity - to sedentary cookie muncher diets and claim that not only are those diets comparable (both being "high sugar" diets allegedly), but have similar daily energy expendiatures.
I suppose - to reach parity - couch potatoes expand all their energy producing... sex hormones? This is some truly fascinating stuff.
Readers here probably aren't hunter gatherers in Africa though. If you live sedentary lifestyle with an abundance of food you may need to take a different approach to nutrition. Sure it would be ideal if we were all hyper athletes, but the reality is that probably isn't going to happen and I am not sure it's even better holistically.
The reason to do RCTs and establish causality isn't to generate excuses for a sugar diet, it's to head off bullshit alternatives that don't fix the problem but advertise like they do.
Almost no RCTs are done when it comes to diet. They are outrageously expensive to do for any length of time, and nobody will fund them. Don't expect to see definitive studies done within your lifetime.
What's your point? The article implied that sugar magically causes obesity and diabetes, all calories being equal, when the weight of the evidence supports neither assertion, and ironically implicates saturated fat as being worse, showing an ability to cause an increase in visceral fat and worsened insulin sensitivity (measured with oral glucose tolerance tests), even in weight-stable subjects.
> different approach to nutrition
The "different approach" HNers gravitate towards is eating bacon and butter (i.e., keto/low-carb) and denying all of the evidence linking these foods to CVD, probably because fat and sodium are so addictive, much more so than sugar: https://news.ycombinator.com/item?id=42028432
> Early-life sugar could drive later-life disease in various ways, Gracner says. Exposure in the womb might affect fetal development in a way that predisposes someone to metabolic diseases. Infants eating a sugary diet might also develop a taste for sweet foods, causing them to eat more sugar as adults—an outcome for which her team has some preliminary evidence.
If there's a significant lag between early-life exposure and disease outcomes, then it seems reasonable that the effects of the 2000-2020 drop won't be seen for some time.
If sugar is not part of the problem, why did the sugar companies pay to suppress studies and promote fat as harmful? No company is going to spend money to suppress results that would show their products in a positive light…
Also, just speculation on my part, but their daily caloric intake may be less than that consumed by a Westerner. Combined with their (presumably) greater expenditure of calories than Westerners, that sugar is not going to result in any significant health issues.
Try eating mostly honey and roots and see how much you can over consume. The problem in US is the variety of food and how engineered they are to be hyper palatable. Snacks are designed to pump sugar into the blood stream, with just enough salt, fat, or carbonation (in drinks) to mask just how much sugar is in everything. That's the reason why warm flat soda tastes disgustingly sweet.
It's not just sugar, but the amount of it, and how fast it is consumed, and how and when do we expend energy (walking after meals directly consume blood glucose b/c calve muscles don't have a glycogen store) impacts fat buildup and T2D. Check out books by Robert Lustig on the subject.
> The HPF criteria identified 62% (4,795/7,757) of foods in the FNDDS that met criteria for at least one cluster. Most HPF items (70%; 3,351/4,795) met criteria for the FSOD cluster. Twenty-five percent of items (1,176/4,795) met criteria for the FS cluster, and 16% (747/4,795) met criteria for the CSOD cluster. The clusters were largely distinct from each other, and < 10% of all HPF items met criteria for more than one cluster.
(CSOD, carbohydrates and sodium; FS, fat and simple sugars; FSOD, fat and sodium; HPF, hyper-palatable foods.)
> Check out books by Robert Lustig on the subject
Lustig is a crackpot who relies on animal studies and mechanistic speculation, because the highest-quality RCTs (like the ones I cited) don't support his theory.
>The best study done to date on hyperpalatable foods found that fat and sodium were the most common drivers of hyperpalatability...
No, that was not the conclusion from this study and it's absolutely not true. The only goal of this study was to "..develop a quantitative definition of HPF".
Yes, there are more "types" of foods that are high in fat and sodium, but that does not mean that these foods are more popular or more hyper-palatable than the ones with sugar. We would need another, different study to resolve this.
Fizzino's HPF study, while not an RCT, is the most comprehensive study to date done on HPFs. She's also identified links between HPF proliferation and tobacco companies: https://onlinelibrary.wiley.com/doi/10.1111/add.16332
I cited RCTs in other comments pertaining to macronutrient intake and metabolic health. Lustig instead relies on mouse models and mechanistic speculation to make his case, because the RCTs in humans haven't shown sugar to cause all the ills he claims, without associated weight gain. Meanwhile saturated fat (given the available literature) ironically seems to be able to do much of what Lustig claims (impair insulin sensitivity, increase visceral fat), even without weight gain.
>Meanwhile tribes of hunter-gatherers in Africa get 15-80% of their daily calories from honey during certain seasons; why aren't they obese and diabetic?
I'd be willing to entertain a hypothesis that the demographic cohort of T2D Americans aren't getting most of their sugar in the form of organic, unprocessed honey taken directly from the hive.
I don't quite understand the details but diet plays a role in epigenetics. The effects a diet (in this case sugar) can imprint itself across multiple generations.
> US sugar consumption declined from 2000-2020 to 1970s levels
I think this is added sugar only. It wouldn't surprise me if actual sugar consumption reduction were tempered compared to the linked graph. Hell, actual sugar consumption may have even increased. It's certainly far easier to get (fairly high-sugar) juice now than when I was a child.
>It's certainly far easier to get (fairly high-sugar) juice now than when I was a child.
What? Excuse me!?? This comment is just flooring me.
I am on my 40s, so I was born in the early 80s. Back in the 80s children were expected to drink juice, and LOTS of it. It was considered a health food for kids.
Juice came in frozen concentrate and WIC paid for it. Every family had juice, every younger (1-12 yr old) kid was expected to consume juice every single day. Grocery store freezer sections were PACKED with it, I remember being memorized by all the colors of the packaging.
I don't know anyone who feeds their children juice like I was fed it growing up. Even when people allow their kids juice now it's "eh, it's not healthy but at least it's better than soda."
So what is your point, you think sugar is not such a big problem and we're not eating too much of it? Then what is according to you the major cause of diabetes and obesity?
To me it sounds logical that nutrition plays a major role in our health, and that sugar is a kind of food our bodies aren't made to process in such high quantities.
Sugar consumption peaked in 2000 and has been in steady decline since, and not only that, but the decline has been led by a decline in HFCS consumption: https://news.ycombinator.com/item?id=38094768
30% of the US was obese in 2000, now it's over 40%, despite per capita sugar consumption reverting to what it was pre-1975.
> The US needs, and has needed, to offset the corn subsidies that get turned into HFCS by adding a "sugar tax" at the consumer side.
If anything, we need a tax on added fat and sodium, the two biggest drivers of food hyperpalatability, when added in excess of the thresholds identified in this paper (> 25% kcal from fat and ≥ 0.30% sodium by weight):
> The HPF criteria identified 62% (4,795/7,757) of foods in the FNDDS that met criteria for at least one cluster. Most HPF items (70%; 3,351/4,795) met criteria for the FSOD cluster. Twenty-five percent of items (1,176/4,795) met criteria for the FS cluster, and 16% (747/4,795) met criteria for the CSOD cluster. The clusters were largely distinct from each other, and < 10% of all HPF items met criteria for more than one cluster.
(CSOD, carbohydrates and sodium; FS, fat and simple sugars; FSOD, fat and sodium; HPF, hyper-palatable foods.)
Because adding fat (usually in the form of vegetable oil) and sodium is the cheapest, easiest way to make food hyperpalatable, and the share of the grocery store shelf space occupied by these products has exploded in the last 40 years, greatly contributing to the obesity epidemic. Ominously, this a trend that the researcher behind that paper I linked to attributes in large measure to the tobacco companies entering the packaged food business:
https://onlinelibrary.wiley.com/doi/10.1111/add.16332
People are eating about as much sugar per capita now as they were in the early 70s, yet they're fatter and more diabetic than ever, even than when they were consuming significantly more sugar 24 years ago. A tax on added fats (oils, butter, lard) and excessive sodium makes much more sense, but good luck getting such a measure enacted given how effective the propaganda from Big Fat (the dairy and beef industries and people promoting high-fat diets like keto and Atkins) has been.
> Stuff like this tells me the privacy fight is just completely unwinnable
Mozilla has done so many things to weaken users' trust in it (like this: https://news.ycombinator.com/item?id=39166801) that at this point many regard them as the least worst (rather than best) alternative to the competition when it comes to privacy and the open web.
I'd like to hope that Ladybird will give us a genuine alternative, but Google has ensured that current web standards are so complex that even MSFT (another megacap tech company) threw in the towel on maintaining their own browser engine.
I don't agree. This is something so basic that there isn't, from a Q&A standpoint, a justification for it ending up broken for 2/3rds of a year, and where the kind of hard-line stance Linus takes against certain kinds of regressions is warranted. Also consider that a lot of users have been unhappy for years with how the foundation is running and spending money (e.g., more and more on things unrelated to FF, like this: https://blog.mozilla.org/en/mozilla/introducing-mozilla-ai-i...).
I use Linux, so initially I assumed it was some weird Linux thing. Until it happened on my father's brand-new Win-11 notebook. This is embarrassing and disappointing. I'm old enough to have used the Mozilla Suite (now SeaMonkey) betas in 2001 and had no reservations recommending early stable versions to friends and family members over IE. Same with Firefox ten years ago. Now? If asked what I'd recommend, I'd honestly tell them idk.
Funny thing is I use Firefox beta and developer editions a lot in Mac and Linux devices and haven't had a problem yet with this bug... (Also my dad is a bit messy with computers sometimes, that didn't go in favor of his credibility)
Specifically the right-click menu option, which is often greyed out for no apparent reason. This happens on both Windows and Linux. Ctrl+C still works, but how does Firefox break something as basic as the right-click menu and copy in 2024?
Because the bug involves sending and receiving messages to multiple other processes. Each webpage you visit is potentially in a different process, and each of those processes maintains its own selection state (that state is visible to javascript running in the page, and you don't want to leak what you copy on this page to any other, so it would be hard to put it anywhere else). There is only one context menu though (in the main process), so it has to send a message to the content process to find out if anything is selected or not. It seems that somehow the message is going to the wrong content process, to a page where nothing is selected. The context menu itself then displays exactly the right thing, based on the data it got back.
I hear what you are saying but the entire architecture is build around IPC message passing. A lot of user interaction will work the same way. There is nothing inherently more difficult about this scenario than many others within Firefox.
If it has such a convoluted code path that it cannot even be debugged then that’s an issue with the architecture, not that the user has a crazy difficult edge case which every other browser seems to manage.
Judging by the comments a lot of people in this thread have been affected by this issue.
Sometimes people gotta jerk, and that leaves only one hand free, which means. Mouse for interaction, Obviously.
But more seriously - FF isn't vim and no I'm not installing vim keybindings.
And I do use the keyboard a lot (I've had to teach coworkers the tips for tab navigation for example), when in "type/entry" mode (oh maybe VIM is the right metaphor hmm).
Anyways, sometimes you're just chilling with a few tabs and wanna pop back and forth between a few, and not be in type mode... So mouse it is. And if you're using mouse and hand off the keyboard it's far easier to just use the right click (I've only started doing this the past year or two... likewise I've taken to right click, back from the popup menu instead of dragging mouse across to the back arrow. (but if on keyboard yeah I alt-arrow it).
What i love is how everyone just demands everyone use the interface the exact same way for all purposes and times.
I do get frustrated at my roomie who won't just do it my way, when I ask her to search for something or I'm trying to help with something technical and she's in control of her laptop... though, and in those times I'm 100% right and legit. That's the only exception to my paragraph above.
Probably related to how if you go to google, leave the browser for terminal or ide, you still get a google hover text that brands everything else on your desktop depending on where your mouse was when you left the browser.
For one thing, the selection state is visible to the webpage. For another thing, the webpage is where the text lives. Put that way it sounds funny, but think about it. You have a bunch of content processes, each of which is in charge of loading some number of webpages that the user wants to have open. There is a single UI process that the user can interact with. When the user actually initiates a copy, the UI process doesn’t know what text to put into the clipboard. The text is all in the content process! The UI process merely has to figure out which content process to send the messages to, so that the right text ends up in the clipboard. And that's more complicated than it looks because any given page you are looking at might be stored in multiple processes. A page on domain A with a frame that has content from domain B will often have a different content process for both domains, to ensure maximum separation of state between them.
The bug appears to be a race condition in how the state of which content process has the most recent selection is synchronized with the UI process. The patch at the end of the bug report changes it so that when the user unloads a page no message is sent to delete that state. Instead, only whatever page gets loaded or switched to next will send a message to replace the state. This should eliminate the problem.
Left–over tooltips are a completely different kind of problem.
I have been affected by this one on my Ubuntu desktop for months. It is very annoying! Ctrl+C also works for me, but I am so used to right clicking it really throws me off.
I'm pretty sure that merely tab-switching hasn't fixed it for me. I've done both mouse and alt-tab, i've ctrl-w'd the tab and ctrl-shift-T'd it. I've opened the same site in a new tab and it still wouldn't work. I've had to completely shut the browser down. Maybe it's different between Windows and Linux, perhaps (I'm using Windows for this).
Maybe there's more than one cause, but the reason I hate this bug so much is because simple fixes like just alt-tabbing or even closing and re-opening or full-reload doesn't work. I'm like 99% certain that's the case. I'll have to verify next time this happens. It seems to happen at least a couple times a month.
Or just hold down shift, at least in Firefox. This avoids sending the events to the javascript on the page so that the user can act on the page without being blocked, while still using a page’s own context menu if it really does provide a useful one (Google Docs, for example, has one with actual editing actions in it).
It's the duty and responsibility of a properly implemented browser to not allow a "website" to break basic UI functionality because it pushes some javascript. I don't care about how Safari and chrome and edge do it. Firefox should not follow their lead.
This is a fine example of why people install plugins like ublock origin and similar.
Exactly. There are legitimate use cases for hijacking the right-click menu to make it better. For example, Google docs, GMail, etc. The best solution IMHO is the shift key to get the normal menu. It's the best of both worlds.
> Many vegetable oils (and particularly seed oils) are high in linoleic acid. And guess what’s making up a rapidly increasing fraction of body fat? (figure from Stephan Guyunet):
No, this can't be true, since HN has repeatedly told me that the body preferentially stores sugar as fat (presumably via de novo lipogenesis, which studies like [1] show to be only a minor contributor to fat balance, but that's probably just more Big Sugar propaganda, right?), that dietary fat doesn't become body fat, and even that you can eat all the fat you want without getting fat because ketones are magic.
I don’t know which HNers you’re thinking about. But the only supposed mechanism I’ve heard of why sugar makes you fat is that it affects insulin, and insulin is the mechanism that signals fat cells to store fat. I haven’t heard/read anything from the keto community that argues that sugar being converted to fat is the primary mechanism of weight gain.
I may have read theories that it contributes more to visceral fat, which is really bad for your health? But that won’t be the majority of weight gained I think.
Feels to me like you’re arguing against a pretty big straw man.
> I may have read theories that it contributes more to visceral fat, which is really bad for your health? But that won’t be the majority of weight gained I think.
HFCS consumption (along with added sugar consumption in general) peaked in 2000 and declined steadily until 2020: https://news.ycombinator.com/item?id=38094768