Why Is Burning Sugar Better Than Burning Fat?

[lampofred]

I don't understand Peat's fundamental reason for preferring burning sugar over fat, as I'm reading a lot of conflicting evidence online. Below is the background as to why I'm questioning Peat's tenets:

I'm only 20, and I got a A1C test just a few days saying I have very high blood sugars (far above the threshold for diabetes, but I have no symptoms, which is why I just got a glucose tolerance test done and am waiting for the results) because of the Peat way of eating. Before Peat, my blood glucose was perfectly in range even though I had never experimented with low-carb/low-fat/low-anything my entire life, so I attribute this new problem only to my diet change, which involves eating far more sugar than before.

I want to do my best to understand on a fundamental, scientific level what went wrong instead of doing something rash and emotional like doing a 180 and switching to a low-carb/no-carb diet. Most likely, I'm healthy enough to just go back to eating as I used to eat before Peat for my high sugars to go down, but now that I've seen how Peat's principles worked like nothing else for my mood and my hair, I want to understand his theories in more depth and figure out what I hadn't understood before.

Peat's main suggested benefit related to burning sugar seems to be an increase in CO2, which offers multiple benefits. Is this it? Or is there any other concrete reason? The reasons I read for burning fat seem a lot more compelling.

(1) fundamentally, it makes sense that we are meant to burn fat instead of sugar considering how much more fat we store than sugar (assuming that fat's sole purpose is energy storage and not insulation, which I believe is a reasonable assumption to make)

(2) fat provides much more ATP

(3) I read that burning sugar produces a lot more free-radicals

So what am I not understanding about why burning sugar is better?

 

[Westside PUFAs]

You should only do blood tests when you've fasted for at least 12 hours, including sleep time to get accurate readings. We are always burning both sugar and fat for energy and if we don't take in glucose we start burning our own tissue to make glucose. The more lean muscle mass you have the more you'll burn fat directly in your muscle as opposed for waiting for it to be turned into ketones. The problem is that some toxic by products can be produced, depending on many things. We also burn a lot of fat while we sleep. There is a part of the heart that prefers to burn fat for its energy. But your brain, organs, and red blood cells need sugar. They can't just burn fat, they need sugar, it's more important than fat in terms of the first energy substrate. Your brain and red blood cells are more important than your muscles. Only in true ketosis can they use ketones. But that's not a long term solution. If you want to burn fat, do a water only fast and at about day three you'll start to burn through one whole pound of fat tissue every day. That's true fat burning. Homo sapiens are carbohydrate burning machines with the ability to turn fat into ketones for the sole purpose of surviving a famine.

If you have zero glucose in your blood, you die. Glucose is so important that your body will catabolize your muscles to turn them into glucose aka sugar.

What is your height and weight? I know not everyone is comfortable with talking about their weight but I'm simply trying to find a reason as to why you have a high a1c. If you're overweight, that may be why.

 

[tyw]

(1) "Meant to burn fat" doesn't argue for any position

We have lots of fat stores, and can use them well.

That says nothing about the metabolic consequences of using primarily fat or carbs as fuel.

----

(2) It is not clear that Fat provides "much more ATP"

ATP production from beta oxidation depends on fatty acid chain length. We'll take Palmitate as an aggressive estimate -- this has 16 carbons, which is most likely above the "average fatty acid chain length" found in regular foods (which I think is closer to 14 carbons).

In any case, the maximum beta oxidation of Palmitate yields 129 ATP, yields 16 CO2. This is assuming maximum theoretical yield in beta oxidation. In practice, you'll find a yield of 106 ATP.

Ref: Chapter 16 : Oxidation of Fatty Acids

If we take it on a carbon-by-carbon basis, glucose will provide about 30 ATP per molecule. This yields 24 CO2.

On a per-unit-carbon basis, palmitate has a 32.5% ATP advantage:

- Glucose: 30 / 6 = 5 ATP
- Palmitate: 106 / 16 = 6.625 ATP

Comparing oxygen per unit carbon, we find that fat seems to require more oxygen per unit carbon:

- Glucose: 1 O2 per unit carbon
- Palmitate: 1.4375 O2 per unit carbon

Peter @ Hyperlipid did the ATP:O2 calculations here as well (based on ideal values), and the differences are pretty small even at the low level (5.5% difference between glucose and sat fat, and we see this pan out in the example bewlo) -- Hyperlipid: Not really much about swimming underwater

Note: that posts paints glucose use as requiring less oxygen per unit ATP. That is true on the mechanical low-level, but not necessarily true when we observe free-living organisms.​

CO2 production is the same per unit carbon, but it is a 1-to-1 O2-to-CO2 ratio for glucose, and 40+% higher for fatty acids.

----

As far as I'm concerned, there is no way to measure exact efficiencies of beta oxidation and glucose oxidation in real time.

However, the oxidation of glucose has less potential inefficiency leaks. Beta oxidation on the other hand, has more ways to break (remember than every cycle of beta oxidation is a another cycle of reactions that need to occur, whereas glucose gets a free-fall to pyruvate so long as the needed enzymes are there).

As as sidenote: yes, glucose oxidation has less dependencies, but breakage of those dependencies usually comes hard and fast -- less things to depend on, also means less fallback when things fail.​

-----

Also note that none of this takes into account mitochondrial uncoupling -- which fatty acids, especially saturated fatty acids, are known to do. Uncoupling of metabolism reduces ATP yield, but generates red light (which I've discussed as being useful on multiple occasions).

There is no way of figuring out just how much uncoupling goes on with a high degree of fatty acid use. Comparisons to the uncoupling seen in high-carb "PUFA depleted" states is also impossible.

----

The above are low level calculations. Real world scenarios will differ, and the oxygen consumption under fat oxidation is slightly lower than carbohydrate oxidation, with only a slightly better ATP yield.

Less oxygen is required for beta oxidation, and this can be an advantage at times (eg: breath holding, or extreme endurance event). Peter @ Hyperlipid has done the math, and it's about a 5% lower oxygen requirement when oxidising fat, and a 5% -- Hyperlipid: Endurance and oxygen flux during fatty acid oxidation

Of course, CO2 production with fatty acid oxidation will be lower than carbohydrate.

----

"Sugar" needs to be distinguished from "carbohydrate". Glucose and Fructose have different effects at the mitochondrial level. Peter gives a very nice breakdown here -- Hyperlipid: Protons (38) and ultra low fat once more

But, if you want more details on Reaction Oxygen Species (ROS) production, look to -- How mitochondria produce reactive oxygen species

Therefore, (3) No, oxidising sugar does not necessarily produce more ROS, and likely produces less.

A short summary of the two links:

(a) During pure forward-flow Electron Chain Transport (ECT), ROS is produce at Complex 3. ie: regardless of primarily NADH inputs (glucose) at Complex 1, or FADH2 inputs (from fats) at Complex 2, the net result is exactly the same.

(b) During reverse electron transport from Complex 1, which is required and desirable during a primarily Complex 2 driven metabolism that is dominant during heavy fatty acid use, you get a lot (a LOT) of ROS, and this is desired --- without this transient burst of ROS, you cannot achieve the physiologic insulin resistance in the cell that is required for further fatty acid use.

Repeat: fatty acid use directly leads to a lot of ROS production at Complex 1, shuts down membrane potential, and does not allow insulin to signal to the cell. This is perfectly normal behaviour during heavy fatty acid oxidation. This sort of phenomenon is then used by biology under varying circumstances.​

(c) Beta Oxidation itself provides multiple channels for electron leak. ETFdH is a heavy offender. Quantification of amount of leak, and subsequent ROS formation, is not possible.

(d) Fructose does activate Mitochondrial GAPDH, which is another possible reverse input to Complex 1. This means that fructose can cause the same Reverse Electron Flow that Fatty acid metabolism does. The consequences of Fructose + Fatty acids is a lot (a LOT) of ROS. This is generally not a good thing, since such a case often happens under circumstances where substantial carbohydrates are consumed, and insulin sensitivity needs to be high. (the above explains why this scenario leads to insulin resistance)


-----

Higher level Mechanics

What is listed above are low level mechanics directly targeted at the questions the original poster raised.

There are lots of high level reasons to not want high Free Fatty Acids as well. Haidut has done a much better job than me at stating these effects. Search for "free fatty acids" or "FFA" with the user set as "haidut" to look for his posts.

I personally do not see much utility for high FFAs, unless utility is defined by faster delivery to tissues for oxidation.

----

CO2

This is a factor that I have not looked into enough.

At a high level, it definitely helps deliver oxygen to tissues (Bohr effect).

At a low level, it could mean nothing, or it could be an Electron Withdrawing Cardinal Adsorbent that is on par with importance as ATP.

Does the extra CO2 (as a ratio with respect to O2) you get with carbohydrate metabolism contribute significantly to metabolism? This is where I have no clue.

----

Philosophy

Everyone confused by the mechanics yet?

And we haven't even touched on major topics like NAD+ pool effects from carbohydrate and fatty acid metabolism (though I am biased to say that carbohydrate metabolism maintains NAD+ pool better), nor have we talked about any of the circadian shifting effects of carbs vs fat.

This is why I maintain that the useful way to go about treating dietary macronutrients is by experimenting with various macronutrient ratios, while using such mechanics as hypotheses generating tools, and not hard facts.

Claiming a particular mechanic as a good reason to do something, is not a useful path when the underlying system is so complex.

On the other hand, claiming a particular mechanics as being clearly harmful, is useful information. ie: we need "Not to Do" heuristics, and then try to fill the void with whatever is left, which in macronutritional terms, ends up being mostly saturated fat and glucose:

Note: protein is usually not a majority of calories, and requires it's own discussion anyway. Fructose I have discussed many times before.​

In the spirit of that, I have said before that I am not opposed to a low PUFA ketogenic diet ...

- What 4000kcal Of Fruit Looks Like
- Troubleshooting Manual, When "RP Diet" Doesn't Seem To Work As Expected?


Therefore, all of the above is a mechanical discussion, but we cannot assume that those mechanics always hold true.

One may not deal with sugar well due to a bad liver. Or one may lack the ability to process large amounts of fat. Or one may lack a gallbladder .... or many other things that contribute to harm being done by taking an approach closer to either of the fat/carb extreme.

I focus on reducing harm from the diet, not necessarily trying to squeeze out benefit. In that sense, I personally view carbohydrates oxidation as having more theoretical benefit, that if not capable of being manifested in an individual, should not be chased at the expense of further harm.


.....

 

[Koveras]

Less oxygen is required for beta oxidation, and this can be an advantage at times (eg: breath holding, or extreme endurance event). Peter @ Hyperlipid has done the math, and it's about a 5% lower oxygen requirement when oxidising fat, and a 5% -- Hyperlipid: Endurance and oxygen flux during fatty acid oxidation

Of course, CO2 production with fatty acid oxidation will be lower than carbohydrate.

[CO2] At a high level, it definitely helps deliver oxygen to tissues (Bohr effect).

Any clue if the increased oxygen delivery to tissues via increased CO2 production with carbohydrates 'makes up' for increased oxygen requirements relative to fats (during endurance exercise)?

ie. Although 5% less oxygen is required with fat oxidation - is the oxygen being delivered to tissues less effectively then would otherwise be possible?

 

[tyw]

Any clue if the increased oxygen delivery to tissues via increased CO2 production with carbohydrates 'makes up' for increased oxygen requirements relative to fats (during endurance exercise)?

ie. Although 5% less oxygen is required with fat oxidation - is the oxygen being delivered to tissues less effectively then would otherwise be possible?

IMO, this is too complex to answer , because there are so many factors that involve CO2 produced from respiration (at the mitochondria, inside cells), to systemic distribution of CO2 in the rest of the body (and those effects of CO2 on the oxygen delivery by hemoglobin).

The short answer is that I think environmental factors matter more in this scenario.

----

I'll talk about altitude, since it related to CO2

I do not agree with some of the effects of altitude that Peat claims (eg: cosmic rays exposure is dependent on so many more factors than altitude). And I definitely do not agree with the uniform "altitude is better for everyone" stance, since we've definitely witnessed some people do really well at altitude, and others do really poorly -- Altitude and Mortality

But those are minor gripes . I'll fully agree with the mechanic that lower oxygen concentrations actually stimulate the ability to metabolise and deal with glucose.

Glucose Homeostasis During Short-term and Prolonged Exposure to High Altitudes

^^ Read that paper. At the least the abstract, and ideally in full, for the observations that we see at altitude.

I am not convinced at this point that a statement like "CO2 stimulates metabolism further" is 100% correct, but we have to admit that slightly lower than 20% oxygen air leads to significant positive impacts on metabolism, and that this is likely CO2 driven.

Are we going to say that being at altitude allows one to leverage carbohydrate metabolism better? It sure seems so, and the effect of a higher Respiratory Quotient (RQ) at lower oxygen tensions may be more pronounced -- ie: more substrate being pushed through mitochondria generates more metabolic end products like ATP and CO2.

----

And as a final sidenote, there are people who will claim that improper breathing leads to loss of CO2, and this is a significant factor (more so than metabolic substrate).

I do not know if this is true, but a test using a capnometer with and without various breathing techniques is a way to quantify it.

Or just learn to breathe deep, don't stress over measurements, and accept whatever results that come

....

 

[cats]

And as a final sidenote, there are people who will claim that improper breathing leads to loss of CO2, and this is a significant factor (more so than metabolic substrate).

I do not know if this is true, but a test using a capnometer with and without various breathing techniques is a way to quantify it.

Or just learn to breathe deep, don't stress over measurements, and accept whatever results that come

I believe that, according to this theory, breathing deep would result in CO2 loss

 

[lampofred]

You should only do blood tests when you've fasted for at least 12 hours, including sleep time to get accurate readings. We are always burning both sugar and fat for energy and if we don't take in glucose we start burning our own tissue to make glucose. The more lean muscle mass you have the more you'll burn fat directly in your muscle as opposed for waiting for it to be turned into ketones. The problem is that some toxic by products can be produced, depending on many things. We also burn a lot of fat while we sleep. There is a part of the heart that prefers to burn fat for its energy. But your brain, organs, and red blood cells need sugar. They can't just burn fat, they need sugar, it's more important than fat in terms of the first energy substrate. Your brain and red blood cells are more important than your muscles. Only in true ketosis can they use ketones. But that's not a long term solution. If you want to burn fat, do a water only fast and at about day three you'll start to burn through one whole pound of fat tissue every day. That's true fat burning. Homo sapiens are carbohydrate burning machines with the ability to turn fat into ketones for the sole purpose of surviving a famine.

If you have zero glucose in your blood, you die. Glucose is so important that your body will catabolize your muscles to turn them into glucose aka sugar.

What is your height and weight? I know not everyone is comfortable with talking about their weight but I'm simply trying to find a reason as to why you have a high a1c. If you're overweight, that may be why.

I'm 5'10" and 145 pounds. For a 20 year old guy, I'm probably underweight. I've never been able to put on weight no much how much I ate, but at the same time, I have several hypothyroid, low metabolism symptoms along with pre-diabetes (I waited to respond to this thread until I got a full fasting glucose tolerance test and the endocrinologist confirmed I have a high degree of insulin resistance). I don't understand my body at all.

Peat offers many great ideas, but "sugar is good" doesn't work, at least for me.

 

[Westside PUFAs]

I'm 5'10" and 145 pounds. For a 20 year old guy, I'm probably underweight. I've never been able to put on weight no much how much I ate, but at the same time, I have several hypothyroid, low metabolism symptoms along with pre-diabetes (I waited to respond to this thread until I got a full fasting glucose tolerance test and the endocrinologist confirmed I have a high degree of insulin resistance). I don't understand my body at all.

Peat offers many great ideas, but "sugar is good" doesn't work, at least for me.

You're not underweight. You'd have to be 20 lbs. lighter to be underweight. If you want to put on muscle mass, weight train, eat enough total food, and sleep. If you want to put on fat mass, drink whole milk, eat more cheese, and drink a pint of pure cream daily, on top of your basic diet (though it will make your blood sugar issue worse, it will achieve your goal of "putting on weight"). If you truly are a type two diabetic but are not overweight then you are an extremely rare person. Sugar is good. Without it, you die. Don't fall for the snake oil of the paleo/keto crowd. Study physiology. Any physiologist will tell you that we are sugar burning machines. You're only 20 so you'll see that your views will change as you get older and you will look back and laugh at yourself for the things you used to do. Our frontal lobes aren't fully developed until our late 20's so I'm just now almost finished with mine as I'm 29. Haha. I'm just now becoming a real person. We're not even real people until our brain is fully developed.

 

[Derek]

If you want to put on fat mass, drink whole milk, eat more cheese, and drink a pint of pure cream daily, on top of your basic diet (though it will make your blood sugar issue worse, it will achieve your goal of "putting on weight").

Just because you put on weight eating dairy fat doesn't mean that everyone will. Eating high amounts of dairy fat actually causes me to lose weight and have crazy lean muscle gains. Anytime I try consuming large amounts of ice cream, I lose body fat and have huge gains in lean muscle mass. I have never gained weight eating dairy fat.

 

[Bahaa El wazzan]

(1) "Meant to burn fat" doesn't argue for any position

We have lots of fat stores, and can use them well.

That says nothing about the metabolic consequences of using primarily fat or carbs as fuel.

----

(2) It is not clear that Fat provides "much more ATP"

ATP production from beta oxidation depends on fatty acid chain length. We'll take Palmitate as an aggressive estimate -- this has 16 carbons, which is most likely above the "average fatty acid chain length" found in regular foods (which I think is closer to 14 carbons).

In any case, the maximum beta oxidation of Palmitate yields 129 ATP, yields 16 CO2. This is assuming maximum theoretical yield in beta oxidation. In practice, you'll find a yield of 106 ATP.

Ref: Chapter 16 : Oxidation of Fatty Acids

If we take it on a carbon-by-carbon basis, glucose will provide about 30 ATP per molecule. This yields 24 CO2.

On a per-unit-carbon basis, palmitate has a 32.5% ATP advantage:

- Glucose: 30 / 6 = 5 ATP
- Palmitate: 106 / 16 = 6.625 ATP

Comparing oxygen per unit carbon, we find that fat seems to require more oxygen per unit carbon:

- Glucose: 1 O2 per unit carbon
- Palmitate: 1.4375 O2 per unit carbon

Peter @ Hyperlipid did the ATP:O2 calculations here as well (based on ideal values), and the differences are pretty small even at the low level (5.5% difference between glucose and sat fat, and we see this pan out in the example bewlo) -- Hyperlipid: Not really much about swimming underwater

Note: that posts paints glucose use as requiring less oxygen per unit ATP. That is true on the mechanical low-level, but not necessarily true when we observe free-living organisms.​

CO2 production is the same per unit carbon, but it is a 1-to-1 O2-to-CO2 ratio for glucose, and 40+% higher for fatty acids.

----

As far as I'm concerned, there is no way to measure exact efficiencies of beta oxidation and glucose oxidation in real time.

However, the oxidation of glucose has less potential inefficiency leaks. Beta oxidation on the other hand, has more ways to break (remember than every cycle of beta oxidation is a another cycle of reactions that need to occur, whereas glucose gets a free-fall to pyruvate so long as the needed enzymes are there).

As as sidenote: yes, glucose oxidation has less dependencies, but breakage of those dependencies usually comes hard and fast -- less things to depend on, also means less fallback when things fail.​

-----

Also note that none of this takes into account mitochondrial uncoupling -- which fatty acids, especially saturated fatty acids, are known to do. Uncoupling of metabolism reduces ATP yield, but generates red light (which I've discussed as being useful on multiple occasions).

There is no way of figuring out just how much uncoupling goes on with a high degree of fatty acid use. Comparisons to the uncoupling seen in high-carb "PUFA depleted" states is also impossible.

----

The above are low level calculations. Real world scenarios will differ, and the oxygen consumption under fat oxidation is slightly lower than carbohydrate oxidation, with only a slightly better ATP yield.

Less oxygen is required for beta oxidation, and this can be an advantage at times (eg: breath holding, or extreme endurance event). Peter @ Hyperlipid has done the math, and it's about a 5% lower oxygen requirement when oxidising fat, and a 5% -- Hyperlipid: Endurance and oxygen flux during fatty acid oxidation

Of course, CO2 production with fatty acid oxidation will be lower than carbohydrate.

----

"Sugar" needs to be distinguished from "carbohydrate". Glucose and Fructose have different effects at the mitochondrial level. Peter gives a very nice breakdown here -- Hyperlipid: Protons (38) and ultra low fat once more

But, if you want more details on Reaction Oxygen Species (ROS) production, look to -- How mitochondria produce reactive oxygen species

Therefore, (3) No, oxidising sugar does not necessarily produce more ROS, and likely produces less.

A short summary of the two links:

(a) During pure forward-flow Electron Chain Transport (ECT), ROS is produce at Complex 3. ie: regardless of primarily NADH inputs (glucose) at Complex 1, or FADH2 inputs (from fats) at Complex 2, the net result is exactly the same.

(b) During reverse electron transport from Complex 1, which is required and desirable during a primarily Complex 2 driven metabolism that is dominant during heavy fatty acid use, you get a lot (a LOT) of ROS, and this is desired --- without this transient burst of ROS, you cannot achieve the physiologic insulin resistance in the cell that is required for further fatty acid use.

Repeat: fatty acid use directly leads to a lot of ROS production at Complex 1, shuts down membrane potential, and does not allow insulin to signal to the cell. This is perfectly normal behaviour during heavy fatty acid oxidation. This sort of phenomenon is then used by biology under varying circumstances.​

(c) Beta Oxidation itself provides multiple channels for electron leak. ETFdH is a heavy offender. Quantification of amount of leak, and subsequent ROS formation, is not possible.

(d) Fructose does activate Mitochondrial GAPDH, which is another possible reverse input to Complex 1. This means that fructose can cause the same Reverse Electron Flow that Fatty acid metabolism does. The consequences of Fructose + Fatty acids is a lot (a LOT) of ROS. This is generally not a good thing, since such a case often happens under circumstances where substantial carbohydrates are consumed, and insulin sensitivity needs to be high. (the above explains why this scenario leads to insulin resistance)


-----

Higher level Mechanics

What is listed above are low level mechanics directly targeted at the questions the original poster raised.

There are lots of high level reasons to not want high Free Fatty Acids as well. Haidut has done a much better job than me at stating these effects. Search for "free fatty acids" or "FFA" with the user set as "haidut" to look for his posts.

I personally do not see much utility for high FFAs, unless utility is defined by faster delivery to tissues for oxidation.

----

CO2

This is a factor that I have not looked into enough.

At a high level, it definitely helps deliver oxygen to tissues (Bohr effect).

At a low level, it could mean nothing, or it could be an Electron Withdrawing Cardinal Adsorbent that is on par with importance as ATP.

Does the extra CO2 (as a ratio with respect to O2) you get with carbohydrate metabolism contribute significantly to metabolism? This is where I have no clue.

----

Philosophy

Everyone confused by the mechanics yet?

And we haven't even touched on major topics like NAD+ pool effects from carbohydrate and fatty acid metabolism (though I am biased to say that carbohydrate metabolism maintains NAD+ pool better), nor have we talked about any of the circadian shifting effects of carbs vs fat.

This is why I maintain that the useful way to go about treating dietary macronutrients is by experimenting with various macronutrient ratios, while using such mechanics as hypotheses generating tools, and not hard facts.

Claiming a particular mechanic as a good reason to do something, is not a useful path when the underlying system is so complex.

On the other hand, claiming a particular mechanics as being clearly harmful, is useful information. ie: we need "Not to Do" heuristics, and then try to fill the void with whatever is left, which in macronutritional terms, ends up being mostly saturated fat and glucose:

Note: protein is usually not a majority of calories, and requires it's own discussion anyway. Fructose I have discussed many times before.​

In the spirit of that, I have said before that I am not opposed to a low PUFA ketogenic diet ...

- What 4000kcal Of Fruit Looks Like
- Troubleshooting Manual, When "RP Diet" Doesn't Seem To Work As Expected?


Therefore, all of the above is a mechanical discussion, but we cannot assume that those mechanics always hold true.

One may not deal with sugar well due to a bad liver. Or one may lack the ability to process large amounts of fat. Or one may lack a gallbladder .... or many other things that contribute to harm being done by taking an approach closer to either of the fat/carb extreme.

I focus on reducing harm from the diet, not necessarily trying to squeeze out benefit. In that sense, I personally view carbohydrates oxidation as having more theoretical benefit, that if not capable of being manifested in an individual, should not be chased at the expense of further harm.


.....

oh myyyy god ... i didnt understand any thingggg

 

[Bahaa El wazzan]

You're not underweight. You'd have to be 20 lbs. lighter to be underweight. If you want to put on muscle mass, weight train, eat enough total food, and sleep. If you want to put on fat mass, drink whole milk, eat more cheese, and drink a pint of pure cream daily, on top of your basic diet (though it will make your blood sugar issue worse, it will achieve your goal of "putting on weight"). If you truly are a type two diabetic but are not overweight then you are an extremely rare person. Sugar is good. Without it, you die. Don't fall for the snake oil of the paleo/keto crowd. Study physiology. Any physiologist will tell you that we are sugar burning machines. You're only 20 so you'll see that your views will change as you get older and you will look back and laugh at yourself for the things you used to do. Our frontal lobes aren't fully developed until our late 20's so I'm just now almost finished with mine as I'm 29. Haha. I'm just now becoming a real person. We're not even real people until our brain is fully developed.

i loveeee what you said