Do Carbohydrates Turn Into Fat?

Travis

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The main signal might be ATP phosphorylation of alcoholic sidechains (Tyr, Thr, Ser). Tyrosine phosphorylation seems especially interesting since it is stabilized by resonance. The conjugated π-bond system would be expected to help with signal transduction (e⁻), especially if tyrosine's β-carbon were deprotonated forming another conjugated double bond.

1ReacPhospho.gif


The resonance also stabilizes the phenylate ion making this reaction easily reversible.

In discussions about the evolution of tyrosine phosphorylation, a common question is “Why tyrosine?”. Like Ser/Thr phosphate esters, the P.Tyr phosphate ester linkage has a relatively high bond energy, and the equilibrium constant for most protein kinases is close to 1, meaning that kinases can catalyze the reverse reaction in the presence of ADP and remove phosphate from the phosphorylated residue in a target protein to generate ATP. Perhaps the major reason why P.Tyr was selected is that the SH2 domain binding energy for a P.Tyr residue is higher than that for P.Ser or P.Thr, because of the contribution of contacts that can be made with the phenolic ring in addition to interactions with the phosphate [...] P.Tyr residues have a very short half life, unless protected by binding to SH2/PTP domains.

Tyrosine phosphorylation: thirty years and counting

Phosphate would certainly change the c-value, and may even act as an all-out electron donor.

It is well-known that serine can be phosphorylated too. This is, after all, how organophosphates paralyze. The target for acetylcholine esterase inhibition is serine.

b615227a-f2.gif


Lysine of course can be phosphorylated too.

No high-energy phosphate bonds required. I think ATP works it's magic mainly by phosphorylating proteins, especially tyrosine. Lysine has a long and saturated side-chain that would seem to isolate it from the peptide backbone.

Phosphorylation | Thermo Fisher Scientific



 

Giraffe

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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."

In reply to @schultz post @tyw wrote:
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.


The table below is taken from the study I linked here: Ingestion of sucrose at 70 mg/kg body weight triggered less insulin than 35 mg/kg glucose.

Table 3 -- plasma glucose and insulin.GIF



This table is taken from the study @tyw inked in his post: 50 g sucrose triggered less insulin than 25 g glucose.

table 1 glucose insulin.GIF


Sucrose triggers less insulin than an equal dose of glucose does: the plasma insulin peak is lower, and it returns faster to basal levels. At moderate doses the addition of fructose to glucose seems to blunt some of the insulin response to glucose.
 

tyw

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@Giraffe Yes, the amount of Insulin that is observed with an equal dose of fructose is 0.2-0.25x that of glucose (1/5th to 1/4th). This is acknowledged, but still indicates that eating fructose causes insulin to rise.

Also, insulin release is not the most important factor. I will get to this point later in the post.

----

First, the addition of fructose to glucose does not affect insulin mechanics much, under the lab test conditions used, which often is a comparison of isolated sugars. We can assume sucrose to mean 1/2 glucose and 1/2 fructose. Using the averages of plasma insulin in the image given -- https://raypeatforum.com/community/attachments/table-1-glucose-insulin-gif.5172/

- 25g sucrose (12.5g + 12.5g fructose) vs 25g glucose: 4.7 / 8.1 = 0.58
- 50g sucrose (25g + 25g fructose) vs 50g glucose: 7.4 / 16.3 = 0.45
- 100g sucrose (50g + 50g fructose) vs 100g glucose: 18.9 / 32.0 = 0.59

If fructose were to exert a consistent lowering of insulin effect during addition to glucose, then we should consistently see the sucrose-to-glucose insulin ratio be less than 0.5. Instead, only the one case of 50g sucrose vs 50g glucose showed this effect.

This can then be explained by other factors, which is most likely the accelerated rate of carbohydrate absorption of glucose + fructose versus just glucose (the reader can look up the many studies in many different contexts showing this effect.).

Faster absorption rates means faster access of said substrate to tissues. What we may be seeing with the 50g sucrose case, is faster absorption shunting the fructose component to the liver, where it is immediately used or stored, and not stimulating as much insulin release.

The 25g sucrose vs 25g glucose dose experiences the same effect, but the dose of both are sufficiently small, and the insulin response is also sufficiently small, such that clearance / tissue uptake rates exceed nutrient supply, and not rate-limited by absorption rates.

The 100g sucrose vs 100g glucose case is where tissue uptake rates are limiting, and where absorption rates exceed tissue uptake, and thus reverting back to the same insulin ratio of the 25g dose.

----

Next, to make the comparison more realistic, we need to talk about real-life consumption scenarios. Note how even the GI=100 white bread had a reduced insulin secretion rate to sucrose. At the 100g dose, you had 21.4 / 22.3 = 0.95x the amount of insulin stimulated from 100g sucrose vs 100g of white bread, and note how the differential between sucrose vs white bread became smaller and smaller as the dose increased. Keep in mind that 100g of carbohydrate is only 400kcal, which is less than what most people would consume in a meal.

Once we compare real life foods, we see that so many things impact their insulinogenic ability, with wildly varying values amongst different foods. See Appendix 2 of this paper for a list of Food Insulin Index numbers -- https://ses.library.usyd.edu.au//bitstream/2123/11945/2/Bell_KJ_thesis_2.pdf

One will see that Fibre and Fat content drastically reduces the food insulin index. This will segway well into the next section.

----

We always need to consider tissue uptake / clearance rate of various carbohydrates. Insulin is simply a signal, asking cells to take in / clear nutrients from serum. Moreover, insulin is a signal only of excess nutrients floating around in serum; it does not need to signal as much if nutrient absorption is matched tightly with nutrient uptake into tissues. This is why we see less overall insulin release under the absorption-slowing effects of concurrent fibre or fat intake.

This involves balancing the ability of tissues / cells to use or store nutrients, vs the amount of nutrients being supplied to them. Insulin is just a highway patrolman managing specific types of nutrient trafficking, but cannot determine how well a cell is able to use energy. The secretion of insulin is thus a constant guessing and calibration game, which is sensitive to all nutrients -- protein causes insulin to rise, fructose does so too, ketones do so to, even pure fat can do so .....

The common theme is "there are nutrients being input into the system now, and are being transported in serum. We need to tell cells to take up those nutrients".

SIDENOTE: which is why Bill Lagakos will be adamant about circadian timing of nutrients -- “Afternoon diabetes” and nutrient partitioning . Carbohydrate utilisation is significantly better during daylight hours. It is at this time in which carbohydrate energy inputs can best be met with good energy usage and storage capacity, and which is when high carbohydrate loads are best introduced.​



My caution wrt fructose has been that uptake rate is limited by the liver, thus leading to localised overload. Whether or not insulin has anything to do with this, it is still an overload condition.

Hence why I do not fixate much on insulin in the discussion of fructose. Insulin does not significantly impact fructose mechanics, and because of that, the risk of overload is even higher -- one of the important traffic conductors (insulin) can't do too much about a particular driver (fructose) should they decide to go rogue.

.....
 

Milena

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----

We always need to consider tissue uptake / clearance rate of various carbohydrates. Insulin is simply a signal, asking cells to take in / clear nutrients from serum. Moreover, insulin is a signal only of excess nutrients floating around in serum; it does not need to signal as much if nutrient absorption is matched tightly with nutrient uptake into tissues. This is why we see less overall insulin release under the absorption-slowing effects of concurrent fibre or fat intake.

This involves balancing the ability of tissues / cells to use or store nutrients, vs the amount of nutrients being supplied to them. Insulin is just a highway patrolman managing specific types of nutrient trafficking, but cannot determine how well a cell is able to use energy. The secretion of insulin is thus a constant guessing and calibration game, which is sensitive to all nutrients -- protein causes insulin to rise, fructose does so too, ketones do so to, even pure fat can do so .....

The common theme is "there are nutrients being input into the system now, and are being transported in serum. We need to tell cells to take up those nutrients".

SIDENOTE: which is why Bill Lagakos will be adamant about circadian timing of nutrients -- “Afternoon diabetes” and nutrient partitioning . Carbohydrate utilisation is significantly better during daylight hours. It is at this time in which carbohydrate energy inputs can best be met with good energy usage and storage capacity, and which is when high carbohydrate loads are best introduced.​



My caution wrt fructose has been that uptake rate is limited by the liver, thus leading to localised overload. Whether or not insulin has anything to do with this, it is still an overload condition.

Hence why I do not fixate much on insulin in the discussion of fructose. Insulin does not significantly impact fructose mechanics, and because of that, the risk of overload is even higher -- one of the important traffic conductors (insulin) can't do too much about a particular driver (fructose) should they decide to go rogue.

.....
Thanks, Tyw. Understand :)
 

Wagner83

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Next, to make the comparison more realistic, we need to talk about real-life consumption scenarios. Note how even the GI=100 white bread had a reduced insulin secretion rate to sucrose. At the 100g dose, you had 21.4 / 22.3 = 0.95x the amount of insulin stimulated from 100g sucrose vs 100g of white bread, and note how the differential between sucrose vs white bread became smaller and smaller as the dose increased. Keep in mind that 100g of carbohydrate is only 400kcal, which is less than what most people would consume in a meal.

Once we compare real life foods, we see that so many things impact their insulinogenic ability, with wildly varying values amongst different foods. See Appendix 2 of this paper for a list of Food Insulin Index numbers -- https://ses.library.usyd.edu.au//bitstream/2123/11945/2/Bell_KJ_thesis_2.pdf

One will see that Fibre and Fat content drastically reduces the food insulin index. This will segway well into the next section.

----



My caution wrt fructose has been that uptake rate is limited by the liver, thus leading to localised overload. Whether or not insulin has anything to do with this, it is still an overload condition.
Ok but 100 g of white bread has only 50 grams of carbs and about 10 grams of proteins, hard to compare this with 100g of carbs.

I'm curious what are your thoughts on dairy products and their various insulinogenicity (low fat, high fat, cheese vs milk) compared to other sources of proteins like chicken breast or cod and how they may impact general health?
Given your diet (very low in fat and high in refined carbs) and what you just wrote it is clear you do not see insulin secretion after a meal as a major clue towards future issues with diabetes /insulin resistance.



But this is based on the assumption that fructose is converted to triglycerides in the liver right? @WestsidePUFAS has suggested a few times that the higher triglycerides is just fat being excreted. Also studies have shown that switching from a high fat low carb diet to a high carb low fat diet overnight results in hypertryglyceridemia (it was not refined sugar either) while a gradual transition did not lead to these issues.
From this post and a study that @ShirtTieFitness posted:
"Studies in humans examining the ability of dietary sucrose to produce insulin resistance have not been nearly as convincing (3). Studies in both normal adults and adults with type 2 diabetes have fairly consistently shown no effect on insulin sensitivity of isoenergetic substitution of sucrose or fructose for starch. Many of these studies had relatively few subjects and were of short duration. Isolated studies have shown adverse effects of dietary sucrose, but these are the exception rather than the rule. Both fructose and sucrose are associated with lower glucose excursions after ingestion, and some recommendations have even advocated the use of fructose as a beneficial sweetener for individuals with type 2 diabetes. The most recent nutritional recommendations of the American Diabetes Association do not advocate or discourage the use of these sweeteners on the basis of available data. They do caution about the development of hypertriglyceridemia with high fructose diets. Epidemiologic studies have also failed to show a relationship between fructose or sucrose consumption and the development of type 2 diabetes.

How can the discrepant results in animals and humans be reconciled? The studies done in rats suggest that if a low dose of sucrose or fructose is used, prolonged exposure is necessary to produce insulin resistance. In addition, the animal studies suggest that if adult animals or animals with preexisting insulin resistance are examined, the effects of these nutrients are reduced. Because most studies in humans have been done in older adult populations and many of the studies have been done in subjects with type 2 diabetes whose liver glucose production is already markedly elevated, it is perhaps not surprising that no effects of these nutrients has been seen.

In summary then, if sucrose has deleterious effects in humans, they are most likely to be produced in younger individuals with moderate-to-high sucrose and fructose intakes over a prolonged period. Information from human studies is not sufficient to conclusively demonstrate any adverse affects of sucrose or fructose in the diet. However, studies adequate to test this idea in younger individuals have not been done."
 

Giraffe

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First, the addition of fructose to glucose does not affect insulin mechanics much [...]

- 25g sucrose (12.5g + 12.5g fructose) vs 25g glucose: 4.7 / 8.1 = 0.58
- 50g sucrose (25g + 25g fructose) vs 50g glucose: 7.4 / 16.3 = 0.45
- 100g sucrose (50g + 50g fructose) vs 100g glucose: 18.9 / 32.0 = 0.59

If fructose were to exert a consistent lowering of insulin effect during addition to glucose, then we should consistently see the sucrose-to-glucose insulin ratio be less than 0.5. Instead, only the one case of 50g sucrose vs 50g glucose showed this effect.
This doesn't make sense to me. See my post above.

Next, to make the comparison more realistic, we need to talk about real-life consumption scenarios. Note how even the GI=100 white bread had a reduced insulin secretion rate to sucrose. At the 100g dose, you had 21.4 / 22.3 = 0.95x the amount of insulin stimulated from 100g sucrose vs 100g of white bread, and note how the differential between sucrose vs white bread became smaller and smaller as the dose increased. Keep in mind that 100g of carbohydrate is only 400kcal, which is less than what most people would consume in a meal.
The taste buds tell you when you had enough sugar. In real life most people would not ingest 100 g sugar in ten minutes as in those studies, and in real life people eat mixed meals.


"Note how even the GI=100 white bread had a reduced insulin secretion rate to sucrose."

The peak is a little lower with white bread compared to sucrose, but both plasma glucose and insulin stay elevated much longer (see figure 1).


"note how the differential between sucrose vs white bread became smaller and smaller as the dose increased."

Not sure what you are trying to say. If you compare 25 g (4.7 vs 7.0) with 50 g (7.4 vs 13.3) the difference becomes larger not smaller. At 100 g absorption from the intestine becomes a rate limiting factor, and they checked the blood levels only for two hours. At two hours the blood glucose and insulin levels where still quite elevated for bread and glucose (see figure 1).


Hence why I do not fixate much on insulin in the discussion of fructose. Insulin does not significantly impact fructose mechanics, and because of that, the risk of overload is even higher -- one of the important traffic conductors (insulin) can't do too much about a particular driver (fructose) should they decide to go rogue.
There is no food that contains fructose, but no glucose or starch. There will always be a little insulin.

The parts of the body that need a constant supply of glucose get it independent of insulin, while resting skeletal muscle and adipose tissue require insulin for glucose uptake. Hepatic glucose uptake is independent of insulin, but activation of existing enzymes and enzyme synthesis require insuling. In the post-exercise muscle, insulin has a permissive role only, not a direct regulatory effect. (See here.)

I don't know many details about the adipose tissue, I haven't found yet information about a dose-dependent action (vs. permissive role) of insulin on liver glycogen synthesis either.
 

Travis

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I think it's worth mentioning that after isocaloric doses of fructose or glucose, the concentration in the blood was lower for fructose.
Bolus or divided doses of 50–150 g fructose produce plasma concentrations of 3–11 mg/dl of this sugar [47-52], while glucose can spike upwards of 150 mg/dl and more. Although little dietary fructose appears in the circulation, it can influence plasma glucose concentrations via sugar inter-conversion.

So it could be more a function of concentration than it's inherent ability to stimulate insulin.

Fructose is cleaved into the liver into 3-carbon units (half sugars) to be used peripherally in the Kreb's Cycle. These are what is found in the blood, not much free fructose.
Lactate discharge is also a means for fructose carbons to escape the liver and be transported to peripheral tissues. Fructose cleavage to glyceraldehyde can result in the production of glycerol via reduction. It was observed that blood glycerol concentration increased after fructose ingestion in exercise subjects

The authors averaged the oxidation rates across 19 ¹³C or ¹⁴C-labeled fructose and glucose studies. They found that glucose is oxidized slightly faster (Table 1 and Figure 2) but fructose converts into glucose. Six studies on fructose➝glucose conversion are listed in Table 2. The average conversion across all studies was 41%.

Another notable finding:
A very interesting phenomenon noted is that when fructose and glucose are ingested together (including fructose-containing sucrose), the oxidation rates of the mixed sugars were faster than that of either one of them ingested alone at the same dosage.

The radioactive de novo lipogenesis studies are small in number are more difficult to draw conclusions from. The authors admit that a very small fraction of fructose becomes acyl chains, but they attribute higher fat concentrations among fructose drinkers (no fiber) to the energy-sparing effect. When free fructose is available, it will be oxidized before stored and plasma lipids.

Fructose metabolism in humans – what isotopic tracer studies tell us

I think our bodies prefer sucrose, a mix of both glucose and fructose bound together. Fructose converts into glucose and glucose converts into a diphosphorylated fructose during glycolysis. They are very similar molecules.

Glucose and fructose are in equilibrium between their cyclic ether and straight-chain forms. While in the straight chain form, glucose to fructose isomerization is simple:

rxn1.gif


Once fructose is phosphorylated (and maybe even before that), this conversion can occur nonenzymatically:
Non-enzymatic isomerization reactions are frequently observed, for instance between glycolytic intermediates fructose-6-phosphate, glucose-6-phosphate or mannose-6-phosphate [...]

The widespread role of non-enzymatic reactions in cellular metabolism

Since this happens spontaneously, the very difference between glucose and fructose is somewhat blurry.

My vote goes towards limiting free sugars of any kind, whether it be sucrose, fructose, or glucose makes little difference. Fiber slows down insulin spikes and B-vitamins found in fruit provide the coenzymes necessary for efficient metabolism. I think the anti-fructose movement was sponsored by the meat industry, a blame-shifting technique. People can get the wrong impression and think fruit will make you fat and give you liver damage. This is certainly not the case. Retinol is the biggest dietary factor associated with liver damage and fruitarians are never fat.

 
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tyw

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@Wagner83 and @Giraffe

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

PDF found here: https://www.nature.com/ejcn/journal/v52/n12/pdf/1600666a.pdf?origin=publication_detail

They did compare equal carbohydrate-matched doses of various sources. The 100g bread category means "100g of carbohydrates from bread". The response in the Figure 1 graph is as follows, and basically follows what I described in my last post.

Screen Shot 2017-04-23 at 6.37.24 am.png


Fructose stimulated some small amount of insulin (as expected), and all the others gave significant insulin secretion, and again as expected, glucose is the most insulinogenic.

When I say that the "difference became smaller the larger the dose got", it is clear that the 100g sucrose dose had peak insulin concentrations higher than bread, and similar Area-under-the-curve. The uptick of insulin at 120min is greater for bread and glucose than in sucrose, but is present in all three.

This is a reflection of absorption kinetics more than anything else, which is why I bring up the wildly varying values in food insulin index, even from isolated food done under fasted conditions. In the real world, we are going to be seeing mechanics more alike the 100g case seen in this experiment, whereby digestion is a process that continues through a lot of the day, and meals overlap and interfere with their digestion.

My point is that the important factor in actual real-life practical outcomes, is matching nutrient inputs to ability to use or store those inputs, and not necessarily a focus on insulin, and definitely not in the case of fructose (which bypasses most insulin signalling).

I shall address this statement by @Giraffe to make the above point clear:

The parts of the body that need a constant supply of glucose get it independent of insulin, while resting skeletal muscle and adipose tissue require insulin for glucose uptake. Hepatic glucose uptake is independent of insulin, but activation of existing enzymes and enzyme synthesis require insuling. In the post-exercise muscle, insulin has a permissive role only, not a direct regulatory effect. (See here.)

We should not view insulin from the perspective of the tissues that use energy in this case. We view it from the perspective of systemic regulation of free nutrients.

Like I said before, Insulin is a trafficker of excess free nutrients floating around in the serum. You have a systemic process using insulin to Request any responsive tissue to use the excess of free nutrients. Whether those tissues want or need the extra nutrients doesn't matter ... the pancreas is still going be asked to secrete insulin.

It is helpful to step back and ask why slower absorbing foods have lesser total insulin release. It is because the rate of absorption of nutrients is matched to the rate of utilisation or storage of those nutrients. There isn't a a lot of insulin required to signal excess free nutrients. Again, "excess free nutrients" is what insulin is signalling, and that signalling is done by a larger systemic process that involves the brain as controller, and peripheral tissues.

As an aside, I like Dr Gershom Zijacek's description of diabetes as a condition of vascular disease, in which the brain perceives normal levels of glucose to be insufficient, and drives systemic regulation for increased glucose to meet its needs.​

In that sense, an insulin spike is perfectly accurate in the case of large glucose consumption. "Get rid of the free glucose now!" is the signal being broadcast to cells that are able to respond to the insulin signal. If this eager signal can be met with an eager response, there is nothing inherently wrong with the signal, and no pathogenesis is going to occur, even in the long run.

Again, the important factor is matching nutrient intake to nutrient utilisation and storage. Insulin mechanics are relevant in signalling excesses of particular nutrients that demand fast utilisation (carbs and protein), but total nutrient load vs use over the course of long periods, is the more important factor.

Also @Wagner83, note that the cases of "Carbosis" (as coined by Denise Minger) has not been studied well, but it is clear that some switch happens at very low fat that suddenly makes a person much more carbohydrate tolerant. As Peter @ Hyperlipid as speculated, this could very well be a case where fat intake, and all the associated insulin de-sensitising behaviour that it has cause, is low enough such that many tissues rapidly and suddenly improve their ability to utilise carbohydrate -- Hyperlipid: Protons (38) and ultra low fat once more

Note how we are still looking at nutrient intake vs ability to use or store those nutrients. "Carbosis" is simply a state where carbohydrate utilisation and storage is at maximal levels. What happens then is that build-up of excess nutrients (which are going to be carbohydrates in this case) is minimised, as tissues are constantly able to take on those nutrients. Therefore not a lot of insulin signalling is required.

Based on observations, I do not believe that everyone can enter this state of carbosis / extreme insulin sensitivity (and thus relatively lower total insulin than you would expect from lab measurements of insulin). Based on my results, it seems like I am one of the people who can do so.

Generically speaking, we are just looking at how efficiently and effectively our tissues can metabolise a various food stuff. 50g of sucrose taken in as a midnight snack after already having had dinner at 8pm (insulin galore), versus 50g of sucrose taken in the morning after an overnight fast (controlled insulin response), versus 50g of sucrose taken in the morning after an overnight fast and a 30min run (not much insulin), are three completely different scenarios representing three different utilisation and storage capacities.

So when @Wagner83 mentioned dairy vs other protein sources, it has to be framed from the perspective of being able to utilise said protein. Is the person eating too little protein? Too much? What about the rest of their diet (eg: reduced calories will increase nitrogen turnover)? What existing disease burden do they have (eg: kidney disease)? Those I think are much more important questions than "what is the insulin response of X protein source", and I'd just say, "eat enough protein, not too much -- 1g protein / kg bodyweight a day is more than enough -- and don't worry about insulin response".


Finally, I have already stated in prior posts that this energetic overload by fructose isn't just about making more triglycerides. It is about putting excess burden on the liver to deal with excess substrate.

...
 

Giraffe

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It is helpful to step back and ask why slower absorbing foods have lesser total insulin release. It is because the rate of absorption of nutrients is matched to the rate of utilisation or storage of those nutrients.
Agreed that insulin is released when the nutrients (glucose or certain amino acids) are available. It's not true that total insulin release is lower when foods are absorpted slower.
 

tyw

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Agreed that insulin is released when the nutrients (glucose or certain amino acids) are available. It's not true that total insulin release is lower when foods are absorpted slower.

Insulin Index is measured by area under the curve (AUC) for all insulin measurements taken during a period after carbohydrate consumption. This represents "total secreted insulin" in response to a particular food.

There are foods with exactly the same amount of carbohydrates, but very different Insulin Index scores. Usually, the pattern is that those which are higher fibre, or which contain some fat, have a lower Insulin Index Score.

Also, the studies of adding fat to carbohydrates, which slows gastric emptying, show significant (like 20%) decreases in total Insulin AUC.

We must conclude from the existing data that less total insulin is secreted in response to the same carbohydrate load under certain scenarios. Slowing of carbohydrate absorption rate is one of those scenarios.

....
 
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I've had no success losing weight since starting Peating in December 2015. I drink a lot of juice. I am going to cut back on the size of the glasses of juice and similar sugar and see if more even, lower amounts more often can help.
 

Giraffe

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Insulin Index is measured by area under the curve (AUC) for all insulin measurements taken during a period after carbohydrate consumption. This represents "total secreted insulin" in response to a particular food.

There are foods with exactly the same amount of carbohydrates, but very different Insulin Index scores. Usually, the pattern is that those which are higher fibre, or which contain some fat, have a lower Insulin Index Score.

A flaw in many studies is that the observation time is limited to 120 minutes. This is also one of the flaws of the glycemic index. I looked for a study with longer observaton time. The participants here are type 2 diabetics.

Effect of Added Fat on Plasma Glucose and Insulin Response to Ingested Potato in Individuals With NIDDM


After ingestion of potato alone or potato plus different amounts of butter, insulin concentrations peaked at 60 min (120 min when 30 or 50 g fat was added). The insulin concentrations where near initial values after 300 min. After ingestion of 50 g glucose, the glucose concentration was below the initial value by 300 min. The insulin concentration was near initial value, but still elevated at 300 min.

The mean plasma glucose area response after ingestion of potato with or without the various amounts of butter were all similar and were 82% of that observed after ingestion of 50 g glucose. The mean insulin area response to potato alone was 532 pmol · h · L−1. The mean insulin area responses to potato plus 5,15,30, and 50 g of fat meals were 660,774,750, and 756 pmol · h · L−1, respectively. Thus, the mean insulin areas were all greater than for ingestion of potato alone, and a maximal response was observed with addition of 15 g fat (1.4-fold).
 
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James IV

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I just have to say this is a wonderful thread. I hope anyone that come across it reads it, particularly @tyw 's post, thoroughly. Tyw definitely has a thorough understanding of energy balance and pathways.
It's all about fuel tanks. Different individuals will use/fill different fuel tanks more/less efficiently based on lifestyle, history, age, activity, etc. Learning to keep the tanks close to full, without constant overfilling is the path to abundant energy at the healthiest level of body fat and musculature. searching for a perfect set calorie intake or macronutrient partition is probably futile. A dynamic organism will never have static energy needs.
 

Milena

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... ...Learning to keep the tanks close to full, without constant overfilling is the path to abundant energy at the healthiest level of body fat and musculature. ... ...A dynamic organism will never have static energy needs.
Thanks for the analysis, peeps!

I seem to easily 'spill-over'. My ability to produce fat from excess calories is pretty perky.
Off to read this info in more detail :bookworm:
 

Wagner83

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Thanks @tyw, a last question, I have seen you talk about the proteins found in starchy foods or legumes not being relevant and usable proteins (or something along those lines) compared to animal foods , do you think the same is true for steamed potatoes? Of course Peat has talked repeatedly about the quality of those proteins and the ones in mushrooms but I'm curious how valuable this information is in the context of regular cooking ( =/= potatoe juice).
I've had no success losing weight since starting Peating in December 2015. I drink a lot of juice. I am going to cut back on the size of the glasses of juice and similar sugar and see if more even, lower amounts more often can help.
Did you see the study I posted on high sucrose diet not leading to weight loss while high starch/ glucose diet did?
 

Mito

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I also drink pear juice and OJ to taste. Like I said before, I don't count calories or liquid, I eat and drink to taste. But I probably average about 2-3 Pepsi bottles per day and the rest is high-mineral carbonated spring water.
@haidut From some of your recent posts it appears that you personally make no attempt to limit fructose consumption. For example 2-3 bottles (assuming 20 oz bottles) of Pepsi alone is around 80-100g of fructose (http://www.sciencedirect.com/science/article/pii/S0899900714001920). It was suggested in this thread (quote below) that a limit of 50g/day of fructose is a conservative target to decrease the likelihood of liver fat accumulation. Since your daily diet includes at least 2x (and maybe even more) that recommendation, I am curious as to your thoughts on the risk of liver fat accumulation considering the amount of fructose in your diet.

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........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.
 

Strongbad

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Feb 12, 2015
Messages
291
The taste buds tell you when you had enough sugar. In real life most people would not ingest 100 g sugar in ten minutes as in those studies, and in real life people eat mixed meals.

Except for hardcore Peaters and fruitians. With all the recommendations in this forum to drink lots of OJ & milk, eat lots of ice cream while avoiding starch (due to endotoxin), it's easy to hit over 100% of sugar within 10 minutes. Since starch is out of question, sucrose / fructore is the primary source of carbs.

I remember when I was 100% Peating and following the recommendations here 2 years ago, 100g of sugar per meal was minimum. Boy, my health hit rock bottom...

I've had no success losing weight since starting Peating in December 2015. I drink a lot of juice. I am going to cut back on the size of the glasses of juice and similar sugar and see if more even, lower amounts more often can help.

I followed tyw's advice and replaced sugar with white rice. Now my weight hovers around 160-170lbs-ish. And I feel way better, like a normal, healthy dude. It's been awhile.
 
B

Braveheart

Guest
Thanks @tyw, a last question, I have seen you talk about the proteins found in starchy foods or legumes not being relevant and usable proteins (or something along those lines) compared to animal foods , do you think the same is true for steamed potatoes? Of course Peat has talked repeatedly about the quality of those proteins and the ones in mushrooms but I'm curious how valuable this information is in the context of regular cooking ( =/= potatoe juice).

Did you see the study I posted on high sucrose diet not leading to weight loss while high starch/ glucose diet did?
?
 

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