I'm Done Looking For A Method To Lower Body Fat Without Caloric Restriction

[ecstatichamster]

In my experience I never found this, although I've read it on the forums many, many times! Sugar never keeps me satiated, so I end up eating again not long after. A decent sized meal with potatoes or rice keeps me fuller for longer, which means I can more comfortably keep calories lower and don't feel the need to keep eating. Have you noticed yourself that sugar benefits fat loss?

Very much so.

But it takes some adaptation to get off starch.

 

[Luann]

Ron J you mentioned you use dry milk in your diet, so I thought I'd mention my experience with dry milk. I actually gained weight and couldn't lose it while using dry non-fat milk as a staple of my diet, but I lost about six pounds when I started using fresh milk and cut down to about half the milk I was using before. I think the milk raised my prolactin. Milk powder also quite the same as fresh, because it has plenty of endotoxin and a different nutrient profile.

 

[Broken man]

I lost about 19 kg with inosine and cypro supplementation.

 

[Hans]

Saturated fat and carbs causes insulin resistance? Huh? Any proof of that?

Im literally doing exactly what Peat recommends, haidut recommends etc. 30 percent max of high saturated fat sources, usually closer to 25 or less. This really isn't extreme. The only thing is LOWER calories than I used to be getting, and lower than my TDEE.

When fats and glucose undergo oxidative phosphorylation, they create NADH and FADH2.
Glycolysis provides 2 NADH and then the TCA cycle provides another 3 NADH and 1 FADH2.
Beta-oxidation provides 1 NADH and 1 FADH2 for each cycle, and then the TCA cycle provides another 3 NADH and 1 FADH2.
Glucose to CO2 provide a 5:1 ratio of NADH:FADH2.
Saturated fats to CO2 provide a 2:1 ratio of NADH:FADH2.

In the electron transport chain, complex I accepts electrons from NADH from the TCA cycle and glutamate dehydrogenase (but this enzyme doesn't contribute significant amounts).
The coenzyme Q10 couple (Q) accepts electrons from complex II (succinic dehydrogenase which provides FADH2), glycerol-3-phosphate dehydrognase (G3Pdh), electron-transferring-flavoprotein dehydrogenase (ETFdh), choline dehydrogenase and dihydroorotate dehydrogenase.
All these electron then run through complex III and IV to CO2. When Q is mostly in the reduced state, electrons from complex I is pushed back, and this is called reverse electron transfer (RET). RET generates lots of superoxides, which will then shut down the enzyme aconitase, and then citrate will leave the mitochondria to create malonyl-CoA via de novo lipogenesis; which will inhibit transport of more fats into the mitochondria. Superoxide will also induce insulin resistance so that glucose cannot further enter the cell. This is good and normal, and is done so that glucose and fats don't flood the mitochondria.
However, when eating in a caloric surplus from saturated fat and glucose, fat gain will ensue, but it will be mostly visceral fat, because the adipose tissue will be more insulin resistant too.
PUFAs, which produce less superoxide than saturated fat, will not induce insulin resistance and glucose and fats will stream into the adipose tissue, and obesity will occur. But this is nothing so say about lipid peroxidation, which causes oxidative stress, diabetes, inflammation, lowers the insulin receptor, destroys the beta-cells of the pancreas, elevates stress hormones, etc. We all know how bad PUFAs are.

What I'm trying to say, is that saturated fat plus glucose will generate more superoxide and insulin resistance from a proton perspective. So you can view PUFAs as more obesogenic than saturated fat, because it makes the adipose tissue more insulin sensitive. Saturated fat is very healthy, I just don't advise to overeat on any macronutrient as to get fat on it. Everyone needs different ratios of macronutrients.
Here is a study to show saturated fat induces insulin resistance: Type of dietary fat and insulin resistance. - PubMed - NCBI

 

[Ron J]

I think he wants to lose fat without cutting calories very low due to a slow metabolism so that it becomes very stressful. If he speeds up his metabolism, he could easily eat 2500+ calories and lose fat without exercise.

Yes, I should have clarified that I wanted to lose weight by not going extremely low calories due to the stress of low calories and fatty acid release/oxidation. I was eating over 4,000 calories, and I recently reduced it to 3,000. As I previously mentioned, I believe that the substances mentioned here that help with weight loss(lowering cortisol, using DHT, NDT, upping dopamine etc.) may have been doing their job, but I must have been eating too much.

 

[raypeatclips]

When fats and glucose undergo oxidative phosphorylation, they create NADH and FADH2.
Glycolysis provides 2 NADH and then the TCA cycle provides another 3 NADH and 1 FADH2.
Beta-oxidation provides 1 NADH and 1 FADH2 for each cycle, and then the TCA cycle provides another 3 NADH and 1 FADH2.
Glucose to CO2 provide a 5:1 ratio of NADH:FADH2.
Saturated fats to CO2 provide a 2:1 ratio of NADH:FADH2.

In the electron transport chain, complex I accepts electrons from NADH from the TCA cycle and glutamate dehydrogenase (but this enzyme doesn't contribute significant amounts).
The coenzyme Q10 couple (Q) accepts electrons from complex II (succinic dehydrogenase which provides FADH2), glycerol-3-phosphate dehydrognase (G3Pdh), electron-transferring-flavoprotein dehydrogenase (ETFdh), choline dehydrogenase and dihydroorotate dehydrogenase.
All these electron then run through complex III and IV to CO2. When Q is mostly in the reduced state, electrons from complex I is pushed back, and this is called reverse electron transfer (RET). RET generates lots of superoxides, which will then shut down the enzyme aconitase, and then citrate will leave the mitochondria to create malonyl-CoA via de novo lipogenesis; which will inhibit transport of more fats into the mitochondria. Superoxide will also induce insulin resistance so that glucose cannot further enter the cell. This is good and normal, and is done so that glucose and fats don't flood the mitochondria.
However, when eating in a caloric surplus from saturated fat and glucose, fat gain will ensue, but it will be mostly visceral fat, because the adipose tissue will be more insulin resistant too.
PUFAs, which produce less superoxide than saturated fat, will not induce insulin resistance and glucose and fats will stream into the adipose tissue, and obesity will occur. But this is nothing so say about lipid peroxidation, which causes oxidative stress, diabetes, inflammation, lowers the insulin receptor, destroys the beta-cells of the pancreas, elevates stress hormones, etc. We all know how bad PUFAs are.

What I'm trying to say, is that saturated fat plus glucose will generate more superoxide and insulin resistance from a proton perspective. So you can view PUFAs as more obesogenic than saturated fat, because it makes the adipose tissue more insulin sensitive. Saturated fat is very healthy, I just don't advise to overeat on any macronutrient as to get fat on it. Everyone needs different ratios of macronutrients.
Here is a study to show saturated fat induces insulin resistance: Type of dietary fat and insulin resistance. - PubMed - NCBI

Why does Peat say that PUFA causes insulin resistance, and saturated fat doesn't, if you're saying the opposite?

Saturated fat is very healthy, I just don't advise to overeat on any macronutrient as to get fat on it.

Who is advising overeating on saturated fat? (Or overeating at all? I mentioned eating below my maintence calories and im losing weight) Im confused as to what point you are trying to make?

 

[Ron J]

@Jem Oz
I'll mostly go by how I look, but I'll update the results on a 3,000 diet.
@Liubo
With the exception of some liver and an oyster, my diet used to be fat free milk powder and sugar. Before milk only, I was also using casein with milk powder. Now I'm only consuming the equivalent of 24 fl oz of fat free milk, and replaced the calcium with limestone(calcium carbonate).

 

[Jon]

Yes, I should have clarified that I wanted to lose weight by not going extremely low calories due to the stress of low calories and fatty acid release/oxidation. I was eating over 4,000 calories, and I recently reduced it to 3,000. As I previously mentioned, I believe that the substances mentioned here that help with weight loss(lowering cortisol, using DHT, NDT, upping dopamine etc.) may have been doing their job, but I must have been eating too much.

What is your maintenance?

 

[Ron J]

I lost about 19 kg with inosine and cypro supplementation.

Cypro is something that I'd like to try, but the weight gain people report is something that I'm not willing to risk for now. Perhaps when I go down to 10-12% body fat.

 

[Ron J]

What is your maintenance?

I don't know if the calculators online are accurate, but I'll find out as I lower calories.

 

[Andman]

I don't know if the calculators online are accurate, but I'll find out as I lower calories.

They usually are suprisingly accurate
bodyweight in lbs x14/15/16 (inactive, moderately active, very active) will save you some time

 

[raypeatclips]

@Ron J Jon sent me this calculator and based on the calories it gave me I've begun losing weight after changing my diet, so I think it's pretty accurate.


https://goodcalculators.com/tdee-bmr-calculator/

 

[Hans]

Why does Peat say that PUFA causes insulin resistance, and saturated fat doesn't, if you're saying the opposite?



Who is advising overeating on saturated fat? (Or overeating at all? I mentioned eating below my maintence calories and im losing weight) Im confused as to what point you are trying to make?

According to the mechanisms I explained to you do saturated fat cause insulin resistance. I did say PUFAs are the guilty one causing diabetes, not saturated fat.

No one is advising to overeat on saturated fat. Some people are just eating lots of saturated fat without knowing how much they actually eat and end up eating more than maintenance. I wasn't pointing any fingers, so sorry if it came across that way. Many people are overeating on a Peat diet without even knowing it, be it from saturated fat or sugar or both.

 

[Ron J]

@Ron J Jon sent me this calculator and based on the calories it gave me I've begun losing weight after changing my diet, so I think it's pretty accurate.


https://goodcalculators.com/tdee-bmr-calculator/

I'll look it up. Thanks.
I think I should stick with 3,000 calories for a while before making any more sudden changes. If I achieve fat loss, I'll stick to it until I stop losing or achieve my body fat percentage goal.

 

[raypeatclips]

Some people are just eating lots of saturated fat without knowing how much they actually eat and end up eating more than maintenance. I wasn't pointing any fingers, so sorry if it came across that way. Many people are overeating on a Peat diet without even knowing it, be it from saturated fat or sugar or both.

+1 This was me. I didn't realise how calorifically dense saturated fat is, so in my mind I was eating much less than I actually was. I wonder if this is the reason for so much weight gain on the Peat diet. I'd advise everyone to track every calorie you eat, at least for a few days, in order to better understand it. Also a few cokes can add excess calories on top of an already good amount of calorie meal.

 

[Jon]

When fats and glucose undergo oxidative phosphorylation, they create NADH and FADH2.
Glycolysis provides 2 NADH and then the TCA cycle provides another 3 NADH and 1 FADH2.
Beta-oxidation provides 1 NADH and 1 FADH2 for each cycle, and then the TCA cycle provides another 3 NADH and 1 FADH2.
Glucose to CO2 provide a 5:1 ratio of NADH:FADH2.
Saturated fats to CO2 provide a 2:1 ratio of NADH:FADH2.

In the electron transport chain, complex I accepts electrons from NADH from the TCA cycle and glutamate dehydrogenase (but this enzyme doesn't contribute significant amounts).
The coenzyme Q10 couple (Q) accepts electrons from complex II (succinic dehydrogenase which provides FADH2), glycerol-3-phosphate dehydrognase (G3Pdh), electron-transferring-flavoprotein dehydrogenase (ETFdh), choline dehydrogenase and dihydroorotate dehydrogenase.
All these electron then run through complex III and IV to CO2. When Q is mostly in the reduced state, electrons from complex I is pushed back, and this is called reverse electron transfer (RET). RET generates lots of superoxides, which will then shut down the enzyme aconitase, and then citrate will leave the mitochondria to create malonyl-CoA via de novo lipogenesis; which will inhibit transport of more fats into the mitochondria. Superoxide will also induce insulin resistance so that glucose cannot further enter the cell. This is good and normal, and is done so that glucose and fats don't flood the mitochondria.
However, when eating in a caloric surplus from saturated fat and glucose, fat gain will ensue, but it will be mostly visceral fat, because the adipose tissue will be more insulin resistant too.
PUFAs, which produce less superoxide than saturated fat, will not induce insulin resistance and glucose and fats will stream into the adipose tissue, and obesity will occur. But this is nothing so say about lipid peroxidation, which causes oxidative stress, diabetes, inflammation, lowers the insulin receptor, destroys the beta-cells of the pancreas, elevates stress hormones, etc. We all know how bad PUFAs are.

What I'm trying to say, is that saturated fat plus glucose will generate more superoxide and insulin resistance from a proton perspective. So you can view PUFAs as more obesogenic than saturated fat, because it makes the adipose tissue more insulin sensitive. Saturated fat is very healthy, I just don't advise to overeat on any macronutrient as to get fat on it. Everyone needs different ratios of macronutrients.
Here is a study to show saturated fat induces insulin resistance: Type of dietary fat and insulin resistance. - PubMed - NCBI

Nice write up man, very explanatory. It's understandable that overeating in saturated fat with carbs will make you sick, no arguement here. I've read that there's also I likelyhood saturated fat will raise endotoxins rapidly upon ingestion:
Differential Effects of Cream, Glucose, and Orange Juice on Inflammation, Endotoxin, and the Expression of Toll-Like Receptor-4 and Suppressor of Cytokine Signaling-3

The study also showed a big upside to orange juice and corroborates your explanation of glucose+saturated fat inducing insulin resistance and raising ROS.

The only thing I will say about losing fat is that reguardless of what you're eating, losing bodyfat is going to cause stresses like insulin resistance (this is a transient effect of elevated ffa's as fat is mobilized to the blood stream for energy utilization and severity is dependent upon how deep into ketosis your deficit takes you ). Eating a more balanced diet while in a deficit makes more sense to me because too low of dietary fat (anything under 0.3g of fat per lb of lean mass) seems to slow bile output (thus myself and others I've spoken with becoming very constipated on vlf) and so stress is being caused by that as well. Eating more balanced also offers you the ability to eat enough diversified foods to represent all your micronutrient needs without having to supplement which I think has exponential benefits to health. Some of the lower fat high micronutrient foods (liver, oysters) that are lean enough to accommodate vlf are too high in certain micronutrients and amino acids like b12, iron, copper, methionine, and d-asparic acid to be eaten often enough to keep a baseline of adequate micronutrients and not start to cause issues from over dosing on others. This is why I like eggs a lot (1-2 Whole a day) is they offer enough nutrition to create a daily foundation of micronutrients you can complete with other foods throughout the day but not SO much that you are at risk of over doing it for any one micronutrient. I've also noticed large cravings for fat on vlf which I suppose could indicate I hightened turnover of bodyfat but I'm also wondering if this is also a product of hindering hormone synthesis as this feeling is usually accompanied by a STRONG loss of libido. I don't get those feelings eating more balanced macros while dieting. Also I haven't seen much on the efficacy of vlf improving hormonal profiles, the only thing I was ever able to find was the rat study with soda and they definitely didn't gain fat but they also developed cancer and died lol (though living off just soda is not a fair representation of vlf because it's also not based on Whole Foods making up carbohydrates).

You also mentioned you're in a very low deficit as you're eating vlf. Severity of deficit is a large dictator of how stressful a diet is pertaining to hormonal status. Level of leanness and duration of a diet are also dictators of stress during fat loss as starting from a leaner point means leptin levels are easier to disrupt, and because stress and fatigue are cummilative the longer catabolism of adipose continues without a break, the more stress your body will accumulate, making it harder and harder to keep losing weight.

I do think your explanation of phosphorylation is a great commentary on staying lower fat all the time but not LOW fat.

There's so much more I'd like to bring up but I don't have the time right now lol thanks for the discussion though. I always appreciate this sort of thing.

 

[raypeatclips]

Nice write up man, very explanatory. It's understandable that overeating in saturated fat with carbs will make you sick, no arguement here. I've read that there's also I likelyhood saturated fat will raise endotoxins rapidly upon ingestion:
Differential Effects of Cream, Glucose, and Orange Juice on Inflammation, Endotoxin, and the Expression of Toll-Like Receptor-4 and Suppressor of Cytokine Signaling-3

The study also showed a big upside to orange juice and corroborates your explanation of glucose+saturated fat inducing insulin resistance and raising ROS.

The only thing I will say about losing fat is that reguardless of what you're eating, losing bodyfat is going to cause stresses like insulin resistance (this is a transient effect of elevated ffa's as fat is mobilized to the blood stream for energy utilization and severity is dependent upon how deep into ketosis your deficit takes you ). Eating a more balanced diet while in a deficit makes more sense to me because too low of dietary fat (anything under 0.3g of fat per lb of lean mass) seems to slow bile output (thus myself and others I've spoken with becoming very constipated on vlf) and so stress is being caused by that as well. Eating more balanced also offers you the ability to eat enough diversified foods to represent all your micronutrient needs without having to supplement which I think has exponential benefits to health. Some of the lower fat high micronutrient foods (liver, oysters) that are lean enough to accommodate vlf are too high in certain micronutrients and amino acids like b12, iron, copper, methionine, and d-asparic acid to be eaten often enough to keep a baseline of adequate micronutrients and not start to cause issues from over dosing on others. This is why I like eggs a lot (1-2 Whole a day) is they offer enough nutrition to create a daily foundation of micronutrients you can complete with other foods throughout the day but not SO much that you are at risk of over doing it for any one micronutrient. I've also noticed large cravings for fat on vlf which I suppose could indicate I hightened turnover of bodyfat but I'm also wondering if this is also a product of hindering hormone synthesis as this feeling is usually accompanied by a STRONG loss of libido. I don't get those feelings eating more balanced macros while dieting. Also I haven't seen much on the efficacy of vlf improving hormonal profiles, the only thing I was ever able to find was the rat study with soda and they definitely didn't gain fat but they also developed cancer and died lol (though living off just soda is not a fair representation of vlf because it's also not based on Whole Foods making up carbohydrates).

You also mentioned you're in a very low deficit as you're eating vlf. Severity of deficit is a large dictator of how stressful a diet is pertaining to hormonal status. Level of leanness and duration of a diet are also dictators of stress during fat loss as starting from a leaner point means leptin levels are easier to disrupt, and because stress and fatigue are cummilative the longer catabolism of adipose continues without a break, the more stress your body will accumulate, making it harder and harder to keep losing weight.

I do think your explanation of phosphorylation is a great commentary on staying lower fat all the time but not LOW fat.

There's so much more I'd like to bring up but I don't have the time right now lol thanks for the discussion though. I always appreciate this sort of thing.

That study you posted, the cream is store bought and contains carageenan, a potent gut disruptor/inflammatory agent, according to Peat. I'd really be interested in the study if they could have used a 100% cream cream, but unfortunately I believe the study is tainted because of the brand they used .

It also contains polysorbate 80

Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome. - PubMed - NCBI

 

[Jon]

That study you posted, the cream is store bought and contains carageenan, a potent gut disruptor/inflammatory agent, according to Peat. I'd really be interested in the study if they could have used a 100% cream cream, but unfortunately I believe the study is tainted because of the brand they used .

It also contains polysorbate 80

Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome. - PubMed - NCBI

Good catch! How interesting :)

 

[brix]

I lost about 19 kg with inosine and cypro supplementation.

I am noticing fat loss with cypro (1-2mg x2 a day). Stomach is flatter and can see abs coming through. Only exercise lightly 2-3x week.

 

[Hans]

I've read that there's also I likelyhood saturated fat will raise endotoxins rapidly upon ingestion:

Yes, it's true. @raypeatclips Endotoxin absorption increase with saturated fat and decrease with unsaturation. This is normal, because the saturated fat is transporting the endotoxin via chylomicrons to the liver for detoxification. Fats that don't stimulate chylomicrons, such as medium chain fats, won't increase the absorption of endotoxins. It's just that some peoples immune systems can't handle the endotoxins and reacts badly to it. In general I think it's best to eat the least gut irritating and endotoxin producing food, even if you eat lots of saturated fat or not. Like you probably know, endotoxin increases gut permeability, contributes to insulin resistance, diabetes, weight gain, organ inflammation and damage, increase in serotonin, etc.

The only thing I will say about losing fat is that reguardless of what you're eating, losing bodyfat is going to cause stresses like insulin resistance (this is a transient effect of elevated ffa's as fat is mobilized to the blood stream for energy utilization and severity is dependent upon how deep into ketosis your deficit takes you ). Eating a more balanced diet while in a deficit makes more sense to me because too low of dietary fat (anything under 0.3g of fat per lb of lean mass) seems to slow bile output (thus myself and others I've spoken with becoming very constipated on vlf) and so stress is being caused by that as well. Eating more balanced also offers you the ability to eat enough diversified foods to represent all your micronutrient needs without having to supplement which I think has exponential benefits to health. Some of the lower fat high micronutrient foods (liver, oysters) that are lean enough to accommodate vlf are too high in certain micronutrients and amino acids like b12, iron, copper, methionine, and d-asparic acid to be eaten often enough to keep a baseline of adequate micronutrients and not start to cause issues from over dosing on others. This is why I like eggs a lot (1-2 Whole a day) is they offer enough nutrition to create a daily foundation of micronutrients you can complete with other foods throughout the day but not SO much that you are at risk of over doing it for any one micronutrient. I've also noticed large cravings for fat on vlf which I suppose could indicate I hightened turnover of bodyfat but I'm also wondering if this is also a product of hindering hormone synthesis as this feeling is usually accompanied by a STRONG loss of libido. I don't get those feelings eating more balanced macros while dieting. Also I haven't seen much on the efficacy of vlf improving hormonal profiles, the only thing I was ever able to find was the rat study with soda and they definitely didn't gain fat but they also developed cancer and died lol (though living off just soda is not a fair representation of vlf because it's also not based on Whole Foods making up carbohydrates).

Yes a very low fat diet will not work for everyone, and might just work for the minority. It depends on what kind of fat you have in your adipose tissue. Most people have mostly unsaturated fat, so it will make the deficit even more stressful (lipid peroxidation, etc.). The lower I take my fat, the better I generally feel. More energy, satiety, glucose tolerance, no sleepiness after a carb meal, etc. I might experiment with higher fat intake later on because fat do make food taste better and stuff like eggs are a great source of nutrients as you say. I actually notice, when going very low fat that my muscle are harder, more vascular and I'm rarely hungry. My bodyfat drops pretty quick (not lbs quick, but to the eye) even though my deficit is not that big. I also notice that my libido isn't reduced, but might actually be increasing.
Fat free rats are actually immune to diabetes, many cancers and are extremely resilient to many stressors. PUFAs are really the driving force for disease and aging.
I don't think mobilizing lots of fats are stressful, because it's excessive beta-oxidation that are, dare I say causing, diabetes, and not excessive lipolysis (but it obviously contributes). When fats flood the mitochondria, most fats only undergo semi beta-oxidation because the TCA and electron transport chain cannot keep up. This leads to a buildup of lots of semi oxidized lipid fragments, which are most likely prone to oxidation by the ROS. These fats accumulate in the cell leading to an increase in intracellular fat, which further interfere with normal cellular function. So I think as long as the body is able to completely oxidize and/or excrete the fats via glucuronidation, and neutralize the ROS, it won't be as stressful. It's the excessive beta-oxidation that mainly leads to problems. Researchers found that when blocking beta-oxidation, it restored insulin function and glucose oxidation, even in the presence of lots of intracellular fat (which are linked to insulin resistance and diabetes).

You also mentioned you're in a very low deficit as you're eating vlf. Severity of deficit is a large dictator of how stressful a diet is pertaining to hormonal status. Level of leanness and duration of a diet are also dictators of stress during fat loss as starting from a leaner point means leptin levels are easier to disrupt, and because stress and fatigue are cummilative the longer catabolism of adipose continues without a break, the more stress your body will accumulate, making it harder and harder to keep losing weight.

True. I guess I was just initially surprised that I am losing fat at 2500 calories without much exercise, because in the past I cut on 2000 calories and weight trained like 5-6 times a week, plus extra cardio lol. Fat loss was fast then, but I won't say that it's slower now. Maybe I was putting myself in such a stress state back then that my weight loss was actually slowed down.
I feel that at 2500 calories the stress isn't accumulating yet, but might if I increase my activity level.
William Brown ate 2500 calories with 2g of fat for 6 months, and his weight dropped from 69kg to 62kg in three months, after which his weight remained stable. He wasn't even active as far as I know. So low fat will definitely speed up the metabolism, if someone can tolerate it.

I want to add that, the more PUFAs someone eats, the more their cardiolipin will become unsaturated with linoleic acid, which is very easily damaged by the free radicals from complex I and III. The linoleic acid creates HNE, which is about 1000 times more reactive than superoxide, and can actually leave the cells and do damage systematically. This leads to a rapid loss in cardiolipin, degradation of electron transfer chain complexes and reduction of mitochiondrial function. The electron transport chain can literally not work without cardiolipin. Replacing the linoleic with oleic acid (made from de novo lipogenesis) in the cardiolipin, protects it from oxidative stress, and so also mitochondrial function. So although saturated fats create more ROS and thus insulin resistance than PUFAs, it will not contribute to lipid peroxidation, mitochondrial destruction, and diabetes as PUFAs would. So many reasons to avoid PUFAs.