Do Carbohydrates Turn Into Fat?

[Ahanu]

Yes, and often I simply get too lazy to eat. The problem is that I can't really have big separated meals because of past issues with gastritis and reflux which have left me with a bit of a sensitive stomach.

I understand, 180 cm with 2300 kcal would leave me very hungry. Why do you think you gained weight with no Fat and why did you do it in the first place?

 

[Such_Saturation]

I understand, 180 cm with 2300 kcal would leave me very hungry. Why do you think you gained weight with no Fat and why did you do it in the first place?

I did it because it gives you lots of energy (and was hoping to lose fat but no chance). The fat could come just from the carbs to be honest, I basically would go over 500 grams of sugars every day which I think @haidut said is the threshold. But there are also those 10-15 grams a day of fat that come from skim milk and some coconut oil and you could be storing those, and then I had one "cheat" day a week where I would have maybe some macadamia nuts and some butter to ensure I would absorb vitamins from the calf liver.

 

[PhilParma]

I basically would go over 500 grams of sugars every day which I think @haidut said is the threshold.

The threshold for what?

 

[Such_Saturation]

The threshold for what?

Threshold for making fat from carbs I guess... also I think for a given body size, there's a certain amount of sugar that can enter the cells in a given time, no matter how "insulin sensitive" you are. So basically you will always be above "fasting blood sugar" except maybe at night, so almost 100% of the fat you eat, even if it's just a few grams, it will be stored and not burned. That's just my take on it, but indeed I felt like there was constantly sugar entering my blood. Any breaks in eating would mean not reaching my target calories.

 

[Mito]

This is significant DNL, and basically its mostly SFA (and maybe some n-9 unsaturated fats). Again, whether or not this DNL leads to fat accumulation is contingent upon overall energetic factors. As usual, context matters. Each person should be examined for the factors listed above to determine their own risk of excessive DNL.

So do you believe Chris Masterjohn is incorrect when he says "So this process of converting sugar to fat is called de novo lipogenesis. And putting these animal experiments aside, there are quite a number of studies where investigators have looked at humans and said, okay, on this diet or that diet, in this condition or that condition, what is the net rate of de novo lipogenesis, of converting sugar to fat. And what those studies show is that if you take healthy men on a standard Western diet, net de novo lipogenesis is 1 to 2 grams per day. If you take healthy women on a standard Western diet, it’s 1 to 2 grams per day in the luteal phase of their menstrual cycle, and it raises 3 to 6 grams per day in the follicular phase. If you have men with conditions like a obesity, diabetes, infection or inflammatory disease, you see a 3-fold increase over the standard rate for healthy men, from 1 to 2 grams per day to 3 to 6 grams per day.......Now if you take something like the American diet, and you look at 1 to 2 grams per day of fat made from carbohydrate, compared to the that amount of fat that is eaten on a typical American diet, then, you know, even more so we would say that de novo lipogenesis is a minor pathway in humans, it’s a minor way of disposing of carbohydrate, and it’s a minor way of generating fat compared to eating fat in the diet." https://chrismasterjohnphd.com/2016/04/26/im-excited-to-announce-that-with-this/

 

[tyw]

So do you believe Chris Masterjohn is incorrect when he says "So this process of converting sugar to fat is called de novo lipogenesis. And putting these animal experiments aside, there are quite a number of studies where investigators have looked at humans and said, okay, on this diet or that diet, in this condition or that condition, what is the net rate of de novo lipogenesis, of converting sugar to fat. And what those studies show is that if you take healthy men on a standard Western diet, net de novo lipogenesis is 1 to 2 grams per day. If you take healthy women on a standard Western diet, it’s 1 to 2 grams per day in the luteal phase of their menstrual cycle, and it raises 3 to 6 grams per day in the follicular phase. If you have men with conditions like a obesity, diabetes, infection or inflammatory disease, you see a 3-fold increase over the standard rate for healthy men, from 1 to 2 grams per day to 3 to 6 grams per day.......Now if you take something like the American diet, and you look at 1 to 2 grams per day of fat made from carbohydrate, compared to the that amount of fat that is eaten on a typical American diet, then, you know, even more so we would say that de novo lipogenesis is a minor pathway in humans, it’s a minor way of disposing of carbohydrate, and it’s a minor way of generating fat compared to eating fat in the diet." https://chrismasterjohnphd.com/2016/04/26/im-excited-to-announce-that-with-this/

Context needs to be qualified. Masterjohn doesn't assume the very low fat context, and didn't specify where DNL is occurring. Based on his work, I'm sure he wouldn't recommend very low fat, and wouldn't recommend high fructose intake either.

The main distinction of context is that between adipose tissue DNL, and hepatic DNL.

Adipose tissue DNL just makes you store more fat in a tissue that is designed to store fat relatively harmlessly. This is not too much of an issue, unless one is already too fat, whereby adipose tissue DNL may mean further accumulation of visceral fat.

Still, so what if you store 3 grams of extra visceral fat a day? This is where the problem is minor -- visceral fat has good blood flow, is very prone to be mobilised, and those 3 grams a day would easily be turned over.

Now we get to hepatic DNL, and things become more complicated.

The liver seems to prefer using carbohydrate first (for details, see -- The Randle cycle revisited: a new head for an old hat), which means that the chance of fatty acid sticking around in liver parenchymal tissue increases, especially if the liver is constantly getting an energetic surplus (as is the case with high fructose consumption).

"Fatty Liver" is said to be when 5-10% of liver mass is fatty acids. Take an average liver to be 1,500g (which is on the high side). Take 10% of that, and we have 150 grams. 3 grams a day of extra fat suddenly becomes a significant contribution ..... even 1 gram of accumulation a day will get you into problematic territory after only about 100 days. In reality, accumulation seems to be slower though, and hints at a combination of chronic liver energetic overload plus compromise in fatty acid clearance. Add further liver stressors, and this situation can be made worse.

SIDENOTE: we know that in cases of Non-alcoholic fatty liver disease (NAFLD), DNL contributes about 14.9% ± 7.0% to liver triglycerides -- Sources of fatty acids stored in liver and secreted via lipoproteins in patients with nonalcoholic fatty liver disease

​

Put that together with the other study I cited, 'Hepatic de novo lipogenesis in normoinsulinemic and hyperinsulinemic subjects consuming high-fat, low-carbohydrate and low-fat, high-carbohydrate isoenergetic diets' -- Hepatic de novo lipogenesis in normoinsulinemic and hyperinsulinemic subjects consuming high-fat, low-carbohydrate and low-fat, high-carbohydrate isoenergetic diets

Furthermore, to enroll in the study, subjects had to be weight-stable during the 6 mo preceding the study. Therefore, in this study, overeating could not be responsible for the observed changes in DNL.

In view of this striking difference in fractional hepatic DNL between a high-fat, low-carbohydrate diet (DNL < 3%) and a low-fat, high-carbohydrate diet (DNL > 12%) in lean subjects (Figure 1)

Hepatic DNL may increase VLDL-triacylglycerol secretion by way of 2 processes. The first is a direct effect of the synthesis of new fatty acids made available for triacylglycerol production. The second is an indirect effect of the lipogenic mode of the liver, causing inhibition of fatty acid oxidation and consequently increasing reesterification of circulating fatty acids.

TYW NOTE: see the Randle Effect paper for Malonyl-CoA mechanics. But essentially, we are saying that high carbohydrate influx to the liver can cause fatty acid accumulation. This behaviour is specific to the liver.​

Keep in mind that this was a low fat (16% fat), high sugar diet, and we see a 4x elevation in hepatic DNL. However, we honestly do not know how much of this is stored, for how long this rate of DNL is elevated, how much this translates to absolute liver fatty acid mass, and how it would impact stored liver triglycerides when such a diet is maintained for a longer period of time -- this study was only 5 days, and yet DNL was already elevated that much. What we can say is that there is elevated risk for liver fat storage during such a state.

We also do not know if the elevated DNL seen in NAFLD came about before the disease, or after. Though I personally think it is partly causative, since people have seemed to reverse fatty liver using strategies that limit DNL.

We are left with a decision of risk management, and given the propensity of fructose to energetically overload the liver, we can say that limiting fructose consumption to a threshold below energetic overload will reduce the risk of liver fat accumulation. The oft quoted number is 50 grams of fructose a day, which is what an average liver uses a day.

Interventions like high caffeine intake may increase this threshold slightly, but we do not know how much added risk tolerance this gives to a particular person. We also do not know how well a person will be able to handle the side effects of such interventions (many report issues with both coffee and caffeine for example).

....

 

[ATP]

@tyw Considering context is needed, I am interested in what your daily macro nutrient ratio is?

 

[Mito]

We are left with a decision of risk management, and given the propensity of fructose to energetically overload the liver, we can say that limiting fructose consumption to a threshold below energetic overload will reduce the risk of liver fat accumulation. The oft quoted number is 50 grams of fructose a day, which is what an average liver uses a day...

In this article, Brad Dieter suggests the fructose limit (to prevent liver fat accumulation) is higher than 50g/day. In fact probably twice that amount. Do you not agree with his conclusions?

"Essentially this data suggests that if you were to feed me (85kg male) 255 grams of straight glucose, 255 grams of straight fructose, or 340 grams of straight fructose per day and not really exercise that I would see decreases in insulin sensitivity and have some liver fat accumulation, but it would not occur if you fed me 127.5 grams of fructose. Keep this data in your mind to refer to in our discussion below (8)."

"Now for the most controversial one. When consumed, some fructose is indeed converted into VLDL triglycerides. By nature, this metabolic process presents limitations in methodology so only two studies have been done with isotopic tracers that allow us to get a good picture of what is going on. In one study, the authors showed that lipogenic potential of fructose seems to be small, since only 0.05% and 0.15% of fructose were converted to de novo fatty acids and TG-glycerol at 4 hour, respectively (7). Fructose actually appears to alter current lipid metabolism by favoring esterfication but does not itself contribute to fatty acid synthesis to any meaningful extent. I.e. the conversion of fructose to any lipid is almost meaningless at normal to slightly high intakes (0.75 g/kg)

Fructose: Burying the Boogeyman - Science Driven Nutrition

 

[tyw]

In this article, Brad Dieter suggests the fructose limit (to prevent liver fat accumulation) is higher than 50g/day. In fact probably twice that amount. Do you not agree with his conclusions?

"Essentially this data suggests that if you were to feed me (85kg male) 255 grams of straight glucose, 255 grams of straight fructose, or 340 grams of straight fructose per day and not really exercise that I would see decreases in insulin sensitivity and have some liver fat accumulation, but it would not occur if you fed me 127.5 grams of fructose. Keep this data in your mind to refer to in our discussion below (8)."

"Now for the most controversial one. When consumed, some fructose is indeed converted into VLDL triglycerides. By nature, this metabolic process presents limitations in methodology so only two studies have been done with isotopic tracers that allow us to get a good picture of what is going on. In one study, the authors showed that lipogenic potential of fructose seems to be small, since only 0.05% and 0.15% of fructose were converted to de novo fatty acids and TG-glycerol at 4 hour, respectively (7). Fructose actually appears to alter current lipid metabolism by favoring esterfication but does not itself contribute to fatty acid synthesis to any meaningful extent. I.e. the conversion of fructose to any lipid is almost meaningless at normal to slightly high intakes (0.75 g/kg)

Fructose: Burying the Boogeyman - Science Driven Nutrition

Again, context of studies matter. We cannot generalise mechanics without qualification of context.

Example, the study which claimed "0.05% conversion to fatty acids" -- Mechanisms for the acute effect of fructose on postprandial lipemia

Subjects were given instructions to avoid vigorous exercise and alcohol and to have a low-fat evening meal the day before each study.

After an overnight fast and before the subject was given a test meal, 2 baseline blood samples were taken through an antecubital venous cannula. Each test meal consisted of an emulsified chocolate drink and a lemon-flavored sugar drink, which together contained 0.75 g sugar (fructose or glucose)/kg body wt and 0.5 g oil (85% palm oil and 15% safflower oil)/kg body wt.​

For a 70kg person, this would be 52.5g of a carbohydrate (40% carb), and 35g fat (60%), for a total of 525kcal. This is a high fat meal, administered after a fast, without controlling for the rest of the intake through the day.

This is not a representation of an energetic overload state, neither locally in the liver, nor systemic to the whole body. The studies which I've cited specifically highlight the problem with either localised or systemic energetic overload, and that it is the main factor to lipid accumulation of any form.

Next, if you look at the study mentioned as reference (8) -- Effects of fructose and glucose overfeeding on hepatic insulin sensitivity and intrahepatic lipids in healthy humans

Fifty-five healthy young males, (mean age: 22.5 ± 1.6, weight: 71.8 ± 6.4 (SD), height: 1.79 ± 0.06, mean body mass index; 22.4 ± 1.6 kg/m2), with no family history of diabetes were included

Each subject was studied on two occasions, once after 6-7 days on a balanced, weight maintenance diet (control diet; C).

And another time after overfeeding for 6-7 days with the same weight maintenance diet supplemented with one of the following:

- 1.5 g (F1.5; n = 7), 3.0 g (F3; n = 17), or 4.0 g fructose/kg/day (F4; n = 10)
- 3.0 g/kg/day glucose (G3; n = 11),
- or 30% total energy as saturated fat (fat30%; n = 10).

Fructose and glucose were provided as 20% drinks to be consumed with main meals.

Intrahepatocellular lipid (IHCL) concentrations remained unchanged after F1.5, but were nearly doubled with F3 (P < 0.01) and F4 (P < 0.001)​

This is a major overfeeding scenario, and if you look at Table 1, these people were eating way too much food. Also, look at the actual increase in intrahepatocellular lipids (IHCL). The listing is given as `dose of substrate | start concentration of IHCL in mmol/kg | end concentration of IHCL | percentage of end vs start concentration`

1.5g/kg fructose | 6.0 ± 3.0 | 5.7 ± 2.5 | 114.3 ± 64.5
3.0g/kg fructose | 9.0 ± 8.0 | 18.5 ± 15.8 | 213.3 ± 86.4
4.0kg/kg fructose | 13.1 ± 7.9 | 23.7 ± 15.2 | 202.3 ± 114.7
3.0g/kg glucose | 12.9 ± 15.0 | 16.1 ± 15.1 | 158.7 ± 92.2
30% fat | 11.6 ± 8.0 | 21.9 ± 17.2 | 190.4 ± 74.3​

Clearly, this was done with young healthy males who were not obese, for whom 1.5g/kg fructose was about 71 * 1.5 = 106 grams of fructose, in which overfeeding was the primary driven of liver fat accumulation (regardless if the overfeeding was fat or carb), and to which more fructose led to more liver fat accumulation.

If you look at some of the studies highlighting overfeeding in the Science Driven nutrition article, it shows similar rates of DNL when you get into ranges of 20+% overfeeding, regardless of whether the overfeeding was done with glucose or fructose. Again, overfeeding is the main factor; this does not say anything regarding whether or not fructose is going to overload a certain component in the system. All it is says is "energetic substrate overload is not good".

The article you mention shows the large difference in liver carbohydrate clearance given different levels of exercise. This is a big factor, and obviously more active people will have a larger threshold of fructose tolerance.

And ultimately, I quote from the Science Driven Nutrition article:

Based on the current data, there is no real evidence demonstrating that ingestion of up to approximately 100 g/day fructose instead of glucose or sucrose is associated with an increase in food intake or body weight and that despite relatively high levels of fructose you can lose body weight in a hypocaloric state. So it appears that moderate amounts of fructose don’t alter the metabolic milieu enough to make it “obsegenic” per se. Additionally, in both healthy and obese subjects, moderate intakes of fructose don’t appear to result in changes in fasting serum TG. (TYW caveat: given a controlled caloric environment)

Obscenely high levels of intake (>150 grams per day) may have undesirable health effects. Together, these two concepts essentially tell us: 1) that we can consume 3-4 servings of fruit a day, if we so desire, with no health consequences, and 2) that we should not mainline 2 liters of Mountain Dew or consume large amounts of fructose or HFCS.​

To which I agree.

Once again, total energetic substrate intake is going to be a huge factor. Then, in the context of eucaloric intakes, I have provided evidence that fructose can lead to more hepatic DNL.

====

Again, this is an exercise in risk management. Put another way, what is the benefit of eating more fructose? (when glucose can also be consumed) Regardless of context, once liver stores are adequately topped off, which is easily achieved with adequate carbohydrate intake (even without any fructose intake), there is essentially no advantage to fructose, especially once you get to the context of disease states where overload becomes more likely.

The conservative approach is to not consume more than 50 grams of fructose a day, since 50-75g is what an average liver of a not-so-active person uses a day. This is not to say that more cannot be tolerated by more active people. Again, it is a conservative approach aimed at reducing risk, and given that glucose can also replenish liver glycogen, there is little downside to this approach.

----

@tyw Considering context is needed, I am interested in what your daily macro nutrient ratio is?

Most days maybe 50-70 grams protein, 10-15 grams fat, 2400-2600kcal (and therefore around 500-600g carb), maybe 30-50g sucrose at most.

Recently, once every 5-7 days I do a day with <150g carbs, mostly fat and protein, typically decently hypocaloric (1600-1900kcal).

This is at a bodyweight of around 70kg / 154lbs. Decently lean, 26-yo male.

....

 

[Mito]

Put another way, what is the benefit of eating more fructose? (when glucose can also be consumed)

For me the benefit is the sweet taste of fructose. I prefer to get minerals such as potassium and polyphenols such as hesperetin and naringenin from OJ and other fruits because I enjoy the taste.

BTW...Thanks for your reply posts. They are extremely informative.

 

[Wagner83]

For me the benefit is the sweet taste of fructose. I prefer to get minerals such as potassium and polyphenols such as hesperetin and naringenin from OJ and other fruits because I enjoy the taste.

BTW...Thanks for your reply posts. They are extremely informative.

This site states that 5g of mexican oregano has as much naringenin as 1L of citrus/fruit juices Phenol-Explorer: Showing all foods in which the polyphenol Naringenin is found . It might be worse using on some foods (steak, potatoes, tomato sauce etc..)

 

[Wagner83]

@tyw what are your thoughts on using glucose powder and syrup instead of some of the starch for people who have issues with them? It does not sound like rice has other benefits than being a source of glucose.

 

[tyw]

@tyw what are your thoughts on using glucose powder and syrup instead of some of the starch for people who have issues with them? It does not sound like rice has other benefits than being a source of glucose.

Rice will have some small degree of other minerals and vitamins, some protein, is arguably more palatable, has a more controlled GI response, can be paired better with other foods, etc ...

In general, whole foods over isolates for energetic needs. There are plenty of starch sources out there beyond rice. See which is suitable.

Pure Glucose IMO should be used only as a primary source of fuel in the situations where it is needed, eg: athletic scenarios, bedridden and unable to tolerate solid food, etc ...

If all starch sources are not tolerable, then one should question whether or not they should be eating as much carbohydrates as they think they need, and experiment with different macronutrients. I still stand by the recommendation to start at high carb, very low fat, and then add fat until a suitable situation is reached, or the opposite -- very low carb, high fat, add carbs until suitable.

Finally, it is not uncommon for someone to:
- not do well with plain potatoes (ie: no fat)
- but be fine with potatoes with some olive oil or duck fat (ie: more unsaturated fats)
- and do poorly with potatoes plus butter (ie: more saturated fats)
- do poorly with more than 30g of fat with the potatoes, but be fine with just a tablespoon (15g) of fat (enough to slow gastric empty by a little)

Or have any permutation of the 4 given scenarios, or not ever tolerate potatoes at all.

....

 

[schultz]

Note again the interplay of insulin signalling and DNL, with the hyperinsulinemic (usually insulin resistant) condition causing more DNL to occur.

"Hyperinsulinemic" is the key word. In population studies, more fat mass is correlated with more insulin, but there are insulin sensitive fat people, and insulin resistant lean people. There is huge genetic variance here, and the "10x difference in insulin sensitivity" is often thrown around -- Genetics of insulin resistance. - PubMed - NCBI

Regardless of how big it is, this variance is observed to be true and significant, and would mean that people who are naturally more insulin resistant may be more predisposed to DNL in the face of higher carbohydrate intakes.

Put another way, what is the benefit of eating more fructose? (when glucose can also be consumed) Regardless of context, once liver stores are adequately topped off, which is easily achieved with adequate carbohydrate intake (even without any fructose intake), there is essentially no advantage to fructose, especially once you get to the context of disease states where overload becomes more likely.

Ray argues that the benefit is "...fructose inhibits the stimulation of insulin by glucose"

Like you said, more DNL can occur when someone is hyperinsulinemic. Fructose would help prevent this.

(his bold, not mine)
http://raypeat.com/articles/articles/glycemia.shtml
"Starch and glucose efficiently stimulate insulin secretion, and that accelerates the disposition of glucose, activating its conversion to glycogen and fat, as well as its oxidation. Fructose inhibits the stimulation of insulin by glucose, so this means that eating ordinary sugar, sucrose (a disaccharide, consisting of glucose and fructose), in place of starch, will reduce the tendency to store fat. Eating “complex carbohydrates,” rather than sugars, is a reasonable way to promote obesity. Eating starch, by increasing insulin and lowering the blood sugar, stimulates the appetite, causing a person to eat more, so the effect on fat production becomes much larger than when equal amounts of sugar and starch are eaten."

========

Regarding the issue of fat accumulation in the liver. Low dose DNP.

Loved your posts in this thread btw! Great topic.

 

[JRB22]

Again, context of studies matter. We cannot generalise mechanics without qualification of context.

Example, the study which claimed "0.05% conversion to fatty acids" -- Mechanisms for the acute effect of fructose on postprandial lipemia

Subjects were given instructions to avoid vigorous exercise and alcohol and to have a low-fat evening meal the day before each study.

After an overnight fast and before the subject was given a test meal, 2 baseline blood samples were taken through an antecubital venous cannula. Each test meal consisted of an emulsified chocolate drink and a lemon-flavored sugar drink, which together contained 0.75 g sugar (fructose or glucose)/kg body wt and 0.5 g oil (85% palm oil and 15% safflower oil)/kg body wt.​

For a 70kg person, this would be 52.5g of a carbohydrate (40% carb), and 35g fat (60%), for a total of 525kcal. This is a high fat meal, administered after a fast, without controlling for the rest of the intake through the day.

This is not a representation of an energetic overload state, neither locally in the liver, nor systemic to the whole body. The studies which I've cited specifically highlight the problem with either localised or systemic energetic overload, and that it is the main factor to lipid accumulation of any form.

Next, if you look at the study mentioned as reference (8) -- Effects of fructose and glucose overfeeding on hepatic insulin sensitivity and intrahepatic lipids in healthy humans

Fifty-five healthy young males, (mean age: 22.5 ± 1.6, weight: 71.8 ± 6.4 (SD), height: 1.79 ± 0.06, mean body mass index; 22.4 ± 1.6 kg/m2), with no family history of diabetes were included

Each subject was studied on two occasions, once after 6-7 days on a balanced, weight maintenance diet (control diet; C).

And another time after overfeeding for 6-7 days with the same weight maintenance diet supplemented with one of the following:

- 1.5 g (F1.5; n = 7), 3.0 g (F3; n = 17), or 4.0 g fructose/kg/day (F4; n = 10)
- 3.0 g/kg/day glucose (G3; n = 11),
- or 30% total energy as saturated fat (fat30%; n = 10).

Fructose and glucose were provided as 20% drinks to be consumed with main meals.

Intrahepatocellular lipid (IHCL) concentrations remained unchanged after F1.5, but were nearly doubled with F3 (P < 0.01) and F4 (P < 0.001)​

This is a major overfeeding scenario, and if you look at Table 1, these people were eating way too much food. Also, look at the actual increase in intrahepatocellular lipids (IHCL). The listing is given as `dose of substrate | start concentration of IHCL in mmol/kg | end concentration of IHCL | percentage of end vs start concentration`

1.5g/kg fructose | 6.0 ± 3.0 | 5.7 ± 2.5 | 114.3 ± 64.5
3.0g/kg fructose | 9.0 ± 8.0 | 18.5 ± 15.8 | 213.3 ± 86.4
4.0kg/kg fructose | 13.1 ± 7.9 | 23.7 ± 15.2 | 202.3 ± 114.7
3.0g/kg glucose | 12.9 ± 15.0 | 16.1 ± 15.1 | 158.7 ± 92.2
30% fat | 11.6 ± 8.0 | 21.9 ± 17.2 | 190.4 ± 74.3​

Clearly, this was done with young healthy males who were not obese, for whom 1.5g/kg fructose was about 71 * 1.5 = 106 grams of fructose, in which overfeeding was the primary driven of liver fat accumulation (regardless if the overfeeding was fat or carb), and to which more fructose led to more liver fat accumulation.

If you look at some of the studies highlighting overfeeding in the Science Driven nutrition article, it shows similar rates of DNL when you get into ranges of 20+% overfeeding, regardless of whether the overfeeding was done with glucose or fructose. Again, overfeeding is the main factor; this does not say anything regarding whether or not fructose is going to overload a certain component in the system. All it is says is "energetic substrate overload is not good".

The article you mention shows the large difference in liver carbohydrate clearance given different levels of exercise. This is a big factor, and obviously more active people will have a larger threshold of fructose tolerance.

And ultimately, I quote from the Science Driven Nutrition article:

Based on the current data, there is no real evidence demonstrating that ingestion of up to approximately 100 g/day fructose instead of glucose or sucrose is associated with an increase in food intake or body weight and that despite relatively high levels of fructose you can lose body weight in a hypocaloric state. So it appears that moderate amounts of fructose don’t alter the metabolic milieu enough to make it “obsegenic” per se. Additionally, in both healthy and obese subjects, moderate intakes of fructose don’t appear to result in changes in fasting serum TG. (TYW caveat: given a controlled caloric environment)

Obscenely high levels of intake (>150 grams per day) may have undesirable health effects. Together, these two concepts essentially tell us: 1) that we can consume 3-4 servings of fruit a day, if we so desire, with no health consequences, and 2) that we should not mainline 2 liters of Mountain Dew or consume large amounts of fructose or HFCS.​

To which I agree.

Once again, total energetic substrate intake is going to be a huge factor. Then, in the context of eucaloric intakes, I have provided evidence that fructose can lead to more hepatic DNL.

====

Again, this is an exercise in risk management. Put another way, what is the benefit of eating more fructose? (when glucose can also be consumed) Regardless of context, once liver stores are adequately topped off, which is easily achieved with adequate carbohydrate intake (even without any fructose intake), there is essentially no advantage to fructose, especially once you get to the context of disease states where overload becomes more likely.

The conservative approach is to not consume more than 50 grams of fructose a day, since 50-75g is what an average liver of a not-so-active person uses a day. This is not to say that more cannot be tolerated by more active people. Again, it is a conservative approach aimed at reducing risk, and given that glucose can also replenish liver glycogen, there is little downside to this approach.

----



Most days maybe 50-70 grams protein, 10-15 grams fat, 2400-2600kcal (and therefore around 500-600g carb), maybe 30-50g sucrose at most.

Recently, once every 5-7 days I do a day with <150g carbs, mostly fat and protein, typically decently hypocaloric (1600-1900kcal).

This is at a bodyweight of around 70kg / 154lbs. Decently lean, 26-yo male.

....

Thanks for this thought out response TYW!

Re: your Macros, would you mind sharing your rationale on cycling between fat and carb intake? I have been challenged to find a correct ratio as well as appropriate timing for fat/ carbs in the diet. I seem to do best on a mixed diet. When restricting one or the other libido tanks, sleep is disrupted, etc. Does this 1/1.5 day per week of fat intake in lieu of carbs allow fir some of the supposed benefits of fat consumption (e.g., fat soluble Vit absorption, bile production, fat-burning state), while allowing you to retain the benefits of "carbosis" the other days?

Do enzymes/processes that regulate metabolism of both macros readily adapt over the short-term? I always read about needing a week or more to adapt to either a fat- or carb-centric diet.

Thanks in advance for your thoughts!

 

[tyw]

The

Ray argues that the benefit is "...fructose inhibits the stimulation of insulin by glucose"

Like you said, more DNL can occur when someone is hyperinsulinemic. Fructose would help prevent this.

(his bold, not mine)
Glycemia, starch, and sugar in context
"Starch and glucose efficiently stimulate insulin secretion, and that accelerates the disposition of glucose, activating its conversion to glycogen and fat, as well as its oxidation. Fructose inhibits the stimulation of insulin by glucose, so this means that eating ordinary sugar, sucrose (a disaccharide, consisting of glucose and fructose), in place of starch, will reduce the tendency to store fat. Eating “complex carbohydrates,” rather than sugars, is a reasonable way to promote obesity. Eating starch, by increasing insulin and lowering the blood sugar, stimulates the appetite, causing a person to eat more, so the effect on fat production becomes much larger than when equal amounts of sugar and starch are eaten."

========

Regarding the issue of fat accumulation in the liver. Low dose DNP.

Loved your posts in this thread btw! Great topic.

Hehehe, no to DNP . One dangerous substance there, with the difference between "low dose" and "high dose" being so minuscule in terms of absolute mass.

----

Fructose still stimulates insulin.

Since I brought it up, I will address this idea that fructose "doesn't require insulin for transport". This is false. Fructose stimulates much less insulin release, but does so anyway.

Example -- Effect of glucose, sucrose and fructose on plasma glucose and insulin responses in normal humans: comparison with white bread. - PubMed - NCBI

Test meals consisted of 500 ml of tea or water to which was added either nothing, 25, 50, or 100 g of glucose or sucrose, 25 or 50 g fructose, 50 g glucose plus 50 g fructose, or a 25, 50 or 100 g carbohydrate portion of white bread.

Lean, normal subjects (4 male, 4 female) 21-33 y of age.​

That is good. Isolated carbohydrate testing on non-metabolically deranged subjects. The results were:

The GI and II values of glucose, 149+/-16 and 147+/-18, respectively, were significantly greater than those of bread (100)

he values for fructose, 16+/-4 and 22+/-3 were significantly less than those of bread.

GI values did not differ significantly from II values.​

The II (Insulin Index) is going to be a measure of total insulin secretion in response to a particular food stimulus. Their claim that the Glycemic Index approximates the II is generally true. See this series of posts -- Tyw. Said Something That Makes Alot Of Sense!

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Fructose also doesn't "inhibit insulin secretion by glucose". It simply requires less insulin, and when you substitute glucose with fructose, obviously less insulin is secreted.

By that logic, people also claim that adding fat to a carbohydrate meal, which drastically decreases the total amount of insulin in the meal (see the potato thread here -- Tyw. Said Something That Makes Alot Of Sense!).

This is true, but why reduce insulin for the sake of reducing insulin? Why is a "lesser acute insulin spike" a good thing? How about the populations with up to 80-90% carbohydrate intake, and yet with faster insulin levels way below what we normally see?

What does "Hyperinsulemia" mean? Obviously it doesn't refer to an absolute amount of acute insulin secretion in response to a particular meal.

eg: take a lean and metabolically healthy person, give them a ton of white bread, cause their insulin levels to spike to insane levels for 3 hours, but then because of good pancreatic function, and good glucose clearance, after that spike, everything is back to normal. Insulin is simply a signalling tool to uptake energy. The ability to uptake energy is dependent on the worker processes (ie: cells consuming glucose), and not the signalling agent.

eg: take an obese person with measured high fasting insulin, feed them the same amount of bread, and watch insulin stay elevated for 5 hours while their worker processes struggle to deal with the glucose influx, and the next day, insulin is still elevated, and cellular insulin response becomes more and more confused.

Why I do not like Fructose is because it uniquely creates this overload condition on the liver, and causes this massive mismatch between hepatic and peripheral energy sensing and homeostasis. See the next section for elaboration.

In any case, systemic Hyperinsulemia cannot be inferred from isolated tests of insulin secretion. It must be discussed in the context of long term energy balance and metabolic health. Excess fructose (and excess energy intake of any form) can damage both.

Even then, when you integrate all the studies of fructose, both in the context of isolated bolus and mixed meals, there is basically no impact on metabolism at moderate consumption, and likely a depressing effect on Basal Metabolic Rate -- Effects of fructose-containing caloric sweeteners on resting energy expenditure and energy efficiency: a review of human trials

SIDENOTE: I like how the authors of this study claim "no effect on Energy Expenditure" in the conclusion, but in discussion, continually talk about studies which show Fructose-interventions causing lowered BMR. At least they spelled out their conflict of interest well (pro-fructose Nestle affliation).​

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Fructose overloads the liver. Hepatic DNL is likely

Peat claims in this article -- Glucose and sucrose for diabetes.

Brundin, et al. (1993) compared the effects of glucose and fructose in healthy people, and saw a greater oxygen consumption with fructose, and also an increase in the temperature of the blood, and a greater increase in carbon dioxide production.​

OK, so I dug up that study, 'Whole body and splanchnic oxygen consumption and blood flow after oral ingestion of fructose or glucose.' -- Whole body and splanchnic oxygen consumption and blood flow after oral ingestion of fructose or glucose | Endocrinology and Metabolism . It is also attached to this post, as filename '[email protected]@content@264@[email protected]'

This study, was used to support the idea that fructose causes increase in CO2. So what? What do CO2 magically do?

And more importantly, what was the context and stimulus that led to this observation, and what does "more CO2" in that context?

Breaking it down, first, this is FASTED study with 75g glucose or fructose. The fasted part makes a difference, and nobody eats 75g of pure fructose, and sucrose is metabolised differently to pure fructose. In any case, this being fasted makes for a good comparison of isolated substrate.

Regarding Insulin:

Substrate and Insulin Balance

After fructose: The arterial insulin level rose four-fold above basal after fructose ingestion. Insulin release from the splanchnic region showed a small increase from a basal value of 5 +- 2 to a maximum of 10 +- 2 mU/min at 30 min after the fructose meal.

(TYW note: pure glucose increased insulin 10-fold, which is to be expected. The point of bringing this up is again, to counter the idea that fructose doesn't stimulate insulin)​

Regarding CO2, see the Table 2 (click to expand).

Average 2-h postprandial increase in CO2 production was 50 +- 2 ml/min in the fructose group and 29 +- 2 ml/min in the glucose group (P < 0.02)​

This is somehow used to support the idea that fructose caused more CO2 production, which was assumed to be a good thing, even before interpretation of this context.

If you look at the RQ, it climbed to 0.97 in the fructose group. This is almost entirely carbohydrate based metabolism .... In the glucose group, it hit at most 0.85. This is still a mixed fuel metabolism.

The CO2 production is purely an artefact of more carbohydrate over fatty acid metabolism. In fact, it is a sign that the liver is overloaded, and that the body is rapidly trying to get rid said fructose.

We know this when we look at the tables showing Lactate concentrations. See the tables 4 and 5 (click to expand). The first is for fructose, and the second for glucose.

​

With glucose, hepatic and arterial lactate peaked in the 600 - 800 umol/L range, about 2x basal levels. With fructose, the same lactate measurements peaked in the 2,200 - 3,500 umol/L range, anywhere from 5x to 8x basal levels (depending on whether you're referring to arterial or hepatic measurements)

I do not argue that lactate is always bad. Again, context must be qualified, and then results interpreted in that context. The mechanical fact those, is that:
(a) Lactate production is energetically favourable (in terms of reaction enthalpy) wrt other carbohydrate metabolites
(b) Lactate production doesn't require Oxygen

Therefore, when we see large amounts of lactate accumulating like this, we must conclude that either:
(a) too much carbohydrate substrate is being supplied to the tissue => "spillover" is easily metabolised to lactate
(b) the amount of oxygen available to that tissue is not enough to deal with incoming substrate

SIDENOTE: the brain is the about the only exception to this, since lactate mechanics there are particularly unique.​

Clearly, this is a case of liver overload, and this is just one of many many studies showing precisely this effect. 75g of fructose is definitely above the limit of what an average liver can contain, and here we see that bolus being given all at once, with the appropriate consequence.

Regarding body heat, it is completely expected that it is increased, as a method to get rid of excess energy:

The arterial blood temperatures, in the basal state were 36.4-36.5 in all groups. In the fructose group the arterial temperature rose significantly, especially during the second postprandial hour, and had at the end of the study period risen by 0.205 +- 0.039 C, indicating a significant heat accumulation in the body. In the glucose group the arterial blood temperature showed only a slight tendency to rise during the last 10 min of the postprandial study period (Fig 6).

The hepatic venous blood temperature in the basal state was 36.5-36.6 C in all groups. After ingestion of fructose, it rose in parallel with the arterial temperature, whereas, after glucose, it only tended to rise at the end of the postprandial period.
​

All I see in this study, is the body trying its hardest to get rid of too much energy being supplied to the liver. All the increased heat and CO2 comes from this dumping of energy.

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Now if we put this together with the mechanics I wrote about in post #49 above, we can see how fructose uniquely overloads the liver, and how DNL is likely at that particular site, and how DNL in adipose tissue is not a concern.

Fructose will make Hepatic DNL worse.

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[tyw]

Thanks for this thought out response TYW!

Re: your Macros, would you mind sharing your rationale on cycling between fat and carb intake? I have been challenged to find a correct ratio as well as appropriate timing for fat/ carbs in the diet. I seem to do best on a mixed diet. When restricting one or the other libido tanks, sleep is disrupted, etc. Does this 1/1.5 day per week of fat intake in lieu of carbs allow fir some of the supposed benefits of fat consumption (e.g., fat soluble Vit absorption, bile production, fat-burning state), while allowing you to retain the benefits of "carbosis" the other days?

Do enzymes/processes that regulate metabolism of both macros readily adapt over the short-term? I always read about needing a week or more to adapt to either a fat- or carb-centric diet.

Thanks in advance for your thoughts!

As for my personal reasons for cycling both calories and fat intake, it is purely for reasons of taste, and maintaining / improving body composition.

Calorie cycling is nothing new wrt body recomposition, and fat-intake-dominant deficit days vs carb-intake-doninant slight surplus days are not uncommon.

Fatty foods can taste good and I found that incorporating them on days where I was already eating less, also led to lack of any side effects. That is to say, eating tim tams and corn chips on a day that is already a 400kcal deficit, does me barely any harm.

I honestly do not bother with the whole "eat fat with fat soluble vitamins" line of thinking ..... I just go eat my fatty seafood and eggs when I like.

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In general, fatty acids are always used to some degree, and will be held at similar levels during non-exercise-induced energy deficits, regardless of body composition. This was discussed here -- Tyw. Said Something That Makes Alot Of Sense!

In a sense, fatty acids are the "default fuel", since everyone has body fat that is always available for mobilisation and use. Also in that sense, high glucose use (and alcohol) should be viewed as a deviation from the default, and one's ability to respond to large deviations is determined by the ability to acutely use glucose.

It is true that adaptation to a huge change in macronutrient intakes requires an adaptation period. This is most common with reducing carbohydrate intake of course, but excess carbohydrate is also a metabolic challenge, and IMO, some people can never adapt to the "carbosis" state.

Personally, I've done the adaptation both ways, have spent prolonged periods in the past on ketosis as well as other schemes, and it seems like I've never lost the ability to metabolise either fatty acids or glucose for fuel when either is given. That is to say, I can reliably drop into ketosis within a day (morning BHOB >0.5mM), and then go back to eating carbohydrates just fine. Call it "metabolic flexibility" or whatever, but I'm not really bothered too much with these 2 macronutrients.

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[tca300]

@tyw If you have time to respond, and haven't addressed it elsewhere, what do you think about fructose being able to help with cholesterol production? Glucose doesnt seem to have that effect. Isnt cholesterol important for a multitude of things? I dont eat hardly any fat and have been relying on fructose for cholesterol production.
Also what do you think about Ray Peats claim of fructose being able to help retain minerals ( gave example of vitamin D deficient mice on a sucrose diet having superior bone development in comparison to starch fed mice ).
Thank you!

 

[tyw]

@tyw If you have time to respond, and haven't addressed it elsewhere, what do you think about fructose being able to help with cholesterol production? Glucose doesnt seem to have that effect. Isnt cholesterol important for a multitude of things? I dont eat hardly any fat and have been relying on fructose for cholesterol production.
Also what do you think about Ray Peats claim of fructose being able to help retain minerals ( gave example of vitamin D deficient mice on a sucrose diet having superior bone development in comparison to starch fed mice ).
Thank you!

The first question is: Why do we want more cholesterol production, and where do we want that production to occur?

The answer to the first part, is that cholesterol is an important membrane building block, and is required for the synthesis of many important hormones.

The answer to the second part, is that we want cholesterol to be available to the tissues where it is used the most -- the adrenals, the testes, etc ... These tissues tend to make the cholesterol which they need, so long as they have adequate resources to do so.

SIDENOTE: wikipedia article on cholesterol biosynthesis is a good enough overview of the many steps required -- Cholesterol - Wikipedia

The starting material, Acetyl-CoA, is basically going to be available from the metabolism of any energetic substrate (any carbohydrate and fatty acid). Then we see a huge number of steps required sufficient O2 and NADPH. NADPH is synthesised via the PPP (pentose phosphate pathway), which requires enough Glucose 6-phosphate -- Pentose phosphate pathway - Wikipedia

Glucose 6-phosphate is basically available through any of the monosaccharides, all of glucose, fructose, and galactose. (SIDENOTE: while galactose forms glucose 1-phosphate as an end product, that can be converted to glucose 6-phosphate by phosphoglucomutase)​

Adequate energetic input to these various tissues will ensure adequate cholesterol synthesis. I do not view fructose as uniquely helping this process.

We must also view this in comparison in terms of fructose vs glucose vs galactose. I see the potential for liver overload with relatively small amounts of fructose, but not so the case with glucose or galactose (and hence I am not opposed to milk consumption in those people who do not have issues with lactose or casein).

Again, fructose can lead to increased cholesterol synthesis in the liver:
- Cholesterol Synthesis Is Associated with Hepatic Lipid Content and Dependent on Fructose/Glucose Intake in Healthy Humans
- Dietary Fructose and Glucose Differentially Affect Lipid and Glucose Homeostasis

Is this a beneficial thing? Personally, I do not think so. It is liver-localised cholesterol production that has to be dealt with, either through oxidation, storage in the liver (not good), or transport out of the liver. Adequate nutrition from any other carbohydrate source can achieve this as well.

I'd rather measure the end points of cholesterol synthesis (eg: measures of serum hormone levels), rather than focus on cholesterol.

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Regarding fructose and mineral retention, again, I tend to compare fructose vs other monosaccharides, and ask, "what is the benefit of more fructose if there is enough glucose or galactose already being supplied?". What if we compared adequate nutrition status, with at least 150g of carbohydrate a day? I have not seen any particular benefit to fructose in this case.

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[tca300]

@tyw Thank you for your time!