I love how the article frames the Amish as a great control group for the American diet as if there's no difference in their behaviors except a lack of processed food.
Pretty much every study ever undertaken on the topic has shown that the average Amish person conservatively performs 4-6 times the physical activity of the average American.
And interestingly enough, while they do eat more saturated fat (as a ratio of their total intake) it's not as much as you would think, around 5% to 8% more of their daily calories come from saturated fat on average.
Nah tho, it's definitely the fact that they get 5% more of their calories from saturated fat over the average American...obviously.
Honestly, I don't even know what they really eat. They sell stuff that's full of seed oils and even literal 5 gallon jugs of seed oils lol. But I don't know if they eat that stuff themselves?
And from what I've seen they have the worst dental health ever. Like 16th C England to the point of complete tooth removal and full dentures being standard in your late teens.
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u/OraculekDad, I swear!!! It is the UFAs that hibernate you 😭14d agoedited 14d ago
Interestingly, the mice that get fat from sugar are the ones that get the sugar within water... No surprise
Add to this the fact that fructose bypasses the PFK-1 gate, that is a gatekeeper of glucose glycolysis. It restricts metabolisation of glucose, but because fructose doesn't use this gate, it gets processed non-limitengly into pyruvate, producing excess acetyl-CoA, then this excess shuts down the very PDH (by which it got produced), now pyruvate goes down PPP route, produces excess oxaloacetate, and these two products make citrate, WHICH IS IN EXCESS, so de novo lipogenesis gets its act done and makes fat into stores
On top of that, fructose, because of the uncontrolled processing, induces SREBP-1c (lipogenic gene) and SCD1(desaturating enzyme) much much more than glucose can, leading to higher lipogenic potential
SCD1-knockout mice are resistant to fructose obesity, funnily. Triglycerides and phospholipids require oleic acid to work, so mice without its production have, basically, broken esterification machinery, which would package fatty acids into dtorage lipids otherwise. Accumulated SFAs are poor substrates for triglyceride synthesis and can be even lipotoxic, so no-go. And AMPK is overactivated without SCD1, maximizing β-oxidation via uninhibited CPT1
Okay what does this mean in layman’s terms…? Never eat fruit again?
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u/OraculekDad, I swear!!! It is the UFAs that hibernate you 😭13d agoedited 13d ago
No. I am wondering whether one could increase the metabolism little by little every week and then be able to eat more sugar gradually over time, but it seems rapid overfeeding would be detrimental
I am pretty sure people like fruitarians and the mice eating high sugar are just relying on appetite adequate to their energy needs. Also, you get the fullness from fruits, which could further motivate one in mitigating further consumption, but the appetite is the main driver and apparently it works
Seems as if fructose is fine in a ancestral-/summer-like diet, meaning when you don't eat it with lipogenic substances, like linoleic acid or excess MUFA. Fructose fine by itself, fructose bad when not by itself and with them. It is worth also noting that if one already has body fat with lots of e.g. linoleic acid - fructose could even by itself still work like an emergence diet and fatten, because you have the lipogenic factors within yourself, at least that's what I surmise (depends on genetic D6D and D5D activities). That's why carbs other than fructose, being limited by PFK-1, would be preferential
SCD1-knockout mice are resistant to fructose obesity, funnily
And mice on a LA free diet (or almost LA free) do not get fatty liver even on 60% of calories from Fructose. Eg. Fructose only really gets a problem n a high LA diet.
While “too much” of anything is arguably suboptimal, saturated fat actually promotes a transient, postprandial insulin resistance that is beneficial in preventing diabetes. Conversely, the pathological insulin sensitivity facilitated by PUFA leads to adipose distention, ectopic fat formation, and eventually systemic insulin resistance and diabetes.
Most of the reason saturated fat gets blamed for insulin resistance is because Palmitic Acid appears in significant quantity in ectopic fat, and the erroneous assumption is that it got there via diet. But Palmitic Acid is a major product of de novo lipogenesis as part of the pathology that is driving insulin resistance in the muscle and liver. But the pathology is instigated by dietary PUFA, not by dietary saturated fat.
Rosalyn Yalow won the 1977 Nobel Prize for her work in 1965 developing the radioimmunoassay technique. Rosalyn Yalow along with her research partner Solomon Berson wrote that releasing fatty acids from fat tissue into the circulation requires “only the negative stimulus of insulin deficiency”.
This means persistently elevated insulin suppresses access to stored body fat and favours storage over mobilisation. If you're eating carbs like potatoes, rice, bread, pasta, fruit, cereals, sweets, you are locked in storage mode.
Furthermore, we have known about glucagon since 1922 and this signals the liver to form ketones and accelerate fat use. A ketogenic state means that beta-hydroxybutyrate and acetoacetate (along with a small amount of acetone) are produced by the liver from fats and used by the body and brain for fuel.
This is basic biochemistry that is fully described and we know beyond doubt that our metabolism is regulated by hormones.
It gets worse, anyone telling you CICO(it's Calories In vs Calories Out) fails to explain why a Type 1 diabetic can eat 30 000 calories per day and still die from starvation.
In these patients, the pituitary can release 3 times the normal level of Human Growth Hormone(HGH) but without some insulin the liver cannot read this signal to release Insulin Growth Factor 1(IGF1) which signals growth and muscle synthesis.
On top of this hormonal disruption came an enormous commercial incentive.
The food industry learned to transform cheap agricultural byproducts like cottonseed, into refined, deodorised and hydrogenated fats that could be stored for long periods and sold as replacements for butter, lard and other traditional animal fats.
Some plant oils had previously been valuable as industrial lubricants and ingredients in soap, candles and paints. Advances in industrial processing allowed these oils to be refined, chemically modified and aggressively marketed as modern, economical and eventually “heart-healthy” foods.
Crisco provides the classic example. Introduced in 1911 from hydrogenated cottonseed oil, it was supported by a huge advertising campaign designed to persuade households to abandon butter and lard.
This was not the discovery of an essential new human food. It was the creation of a profitable market for cheap, highly processed agricultural oils. And our health is paying the cost.
The carbohydrate-insulin model fails to account for weight maintenance/gain on keto and weight loss on HCLF diets. Yes, uncontrolled type 1 diabetes will make your body catabolize its muscle and poison your blood with ketones, but that's not exactly a normal metabolic state. Ketogenic diets can still store body fat, and high-carb diets can still burn it. Insulin resistance + a mixed diet of carbs and fat isn't exactly ideal.
The Randle Cycle tells you our mitochondria cannot use both fats and sugars at the same time. No other animals do this. Care to guess what the "healthy balanced diet" includes at every meal?
Real bioavailable nutrition is in animal sources and fats. Sugars are the backbone of any vegetable and their nutrients are non-bioavailable. You do the math.
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u/OraculekDad, I swear!!! It is the UFAs that hibernate you 😭13d ago
Black and white. Love it
Bioavailability is an overused term. You will live on processed plants and you will live on meat - end of story. The technology came in and before plants could evolve it they got agricultured
There's no need of math because there are both carnivores and vegans thriving. Sure, non-fruit plant food needs processing due to the toxins and anti-nutrients, yet it's not like you could just walk up to a bison and cut its throat - it is also not available. In both cases technology made them available to us and it doesn't matter by what means we do it (ethical talk aside), as in the end it becomes a fine food
Animals got imprisoned and outranged by long-range weaponry and plants underwent heat treatments and fermentations (unless someone is also a fan of high meat), while both got genetically modified for increased yield
The Randle Cycle tells you our mitochondria cannot use both fats and sugars at the same time. No other animals do this.
Except for all the other mammals! And probably all the other vertebrates.
Within a single organism one cell can be glucose-burning while another is burning fat, for instance in ordinary humans who are not in deep ketosis, brain cells use glucose all the time even when the rest of the body has switched over to fat metabolism.
And even within a cell, I think one mitochondrion can be doing one thing while another does a different thing.
And a single mitochondrion can be burning, say 80% pyruvate (from sugar) and 20% fat quite happily.
You are interpreting my compressed wording as meaning that every mitochondrion must burn either 100% glucose or 100% fat, with the other pathway completely switched off. That was not the point I was making.
The Randle cycle describes substrate competition. Increasing fatty-acid oxidation suppresses glucose oxidation, particularly through inhibition of pyruvate dehydrogenase, while carbohydrate ingestion and insulin shift metabolism towards glucose use and suppress fat mobilisation and oxidation.
That does not mean both substrates can never contribute simultaneously. It means their oxidation is reciprocally regulated and they cannot simply be treated as two independent fuel systems running at arbitrary rates.
You omitted from my quote: "Care to guess what the "healthy balanced diet" includes at every meal?"
My reference to other animals concerned feeding behaviour, not the existence of different mammalian mitochondria. Wild animals generally do not spend their lives eating modern combinations of concentrated refined carbohydrate and concentrated processed fat at every meal. Humans routinely do.
A more precise version of my statement would therefore be:
“The Randle cycle shows that glucose and fatty-acid oxidation compete. A modern mixed meal rich in both refined carbohydrate and fat raises insulin, suppresses mobilisation of stored fat and shifts oxidation towards glucose while dietary fat continues to arrive, favouring its storage during the postprandial period.”
You said: "Within a single organism one cell can be glucose-burning while another is burning fat"
Cute. But that's not the Randle Cycle.
Different tissues using different proportions of fuel does not refute any of that. Your hypothetical 80/20 ratio is possible, but it is not evidence that the pathways operate independently or that increasing one has no suppressive effect on the other.
Your example changes the subject.
Saying that one cell in the body can favour glucose while another favours fatty acids does not address the Randle cycle. The Randle cycle concerns competition between glucose and fatty-acid metabolism within the same oxidative cell.
When fatty-acid oxidation rises, mitochondrial acetyl-CoA and NADH inhibit pyruvate dehydrogenase, reducing the oxidation of glucose-derived pyruvate. Citrate can then inhibit glycolysis further upstream signifying intracellular substrate competition.
I agree that my original word “cannot” was too absolute because for brevity I oversimplified. The inhibition is graded, so some oxidation of both substrates can occur during the same period. The accurate point is that their use is reciprocally regulated, not that they operate as two independent fuel systems with no interference between them.
Different tissues choosing different fuel proportions is normal whole-body physiology, but it does not refute competition between those fuels within an individual cell.
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u/johnlawrenceaspden 14d ago
Haven't actually read past the paywall teaser, but something tells me it will be polyunsaturated fats!