> 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?
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.