Topic: Gary Taubes argues that sugar is the root cause of obesity

[GodSlayer]

Are you sure about that? Dietary fructose is not the same as fructose phosphates. Dietary fructose is metabolized in the liver, almost exclusively. Not in muscles.

Biochemist here, I have had to memorise glycolysis and Kreb's cycle several times over.

[estockly]

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1136029/

Biochem J. 1995 October 15; 311(Pt 2): 517–521. PMCID: PMC1136029

http://www.ncbi.nlm.nih.gov/pubmed/2262441

J Appl Physiol. 1990 Oct;69(4):1244-51.

Those are interesting studies, but not terribly relevant and don't help that much.

In the first second study, they inject the fructose directly into the blood. But fructose is passed through the liver in humans in the wild, and that situation would never occur.

In the second first study, they measured fructose uptake in vitro.

In the full text of both papers they explain that fructose is handled almost exclusively by the liver (one also mentions the kidneys).

ES

[WeeDavie]

Fructose can also be processed directly by muscle tissue.

My understanding is that fructose can only be directly metabolized in the liver. In the liver it can be converted to fat and/or glucose, which can be metabolized by muscle.

ES

Yet again you have simplified metabolism to the point of absurdity and then use this to understand metabolism. You are described metabolism in terms of a flow cartoon where x does y. This is a compete nonsense. Biological metabolism is simply a set of chemical reactions with each step having reaction rates.  By dropping rate constants as you have done, anything you say is incorrect by definition.

Dietary fructose is subject to first past metabolism by the liver and is metabolised into glucose. As this is a chemical reaction some fructose always is not metabolised and passes the liver unmetabolised and is available for metabolism in muscle, this level is directly proportional to the rate of ingestion. As the rate of ingestion of fructose passes the capacity of the liver to metabolise fructose all further fructose passes the liver unmetabolised.

During non-exercise it takes several passes of circulation for the liver for covert all of the fructose to glucose with little fructose used elsewhere. While this fructose derived glucose effects insulin in exactly the same way as glucose direct from the gut, the multi pass metabolism by the liver dampens down changes in blood glucose concentration independent of insulin.

Fructose is a great example of why the glucose insulin hypothesis is wrong. Namely changing the carb intake from glucose to fructose should according to the hypothesis reduce the development of metabolic syndrome, however all the data indicates that it does the opposite and promotes the development of metabolic syndrome.

Perhaps you can tells us why glucose compared to fructose is protective against obesity in humans if the glucose insulin hypothesis is correct?

In before where does this data come from! - use pubmed or buy a metabolism textbook not designed for beginning students (one without cartoons of metabolic pathways).

[GodSlayer]

My understanding is that fructose can only be directly metabolized in the liver...

Dietary fructose is subject to first past metabolism by the liver and is metabolised into glucose. As this is a chemical reaction some fructose always is not metabolised and passes the liver unmetabolised and is available for metabolism in muscle, this level is directly proportional to the rate of ingestion. As the rate of ingestion of fructose passes the capacity of the liver to metabolise fructose all further fructose passes the liver unmetabolised.

like alcohol?
does this mean ES's understanding can't explain how intoxication happens?

[estockly]

Dietary fructose is subject to first past metabolism by the liver and is metabolised into glucose.

So fructose is converted to glucose in the liver? Not fat?

ES

[GodSlayer]

So fructose is converted to glucose in the liver? Not fat?

even google suggests that if you begin asking about fructose in the liver...

[estockly]

Yet again you have simplified metabolism to the point of absurdity and then use this to understand metabolism. You are described metabolism in terms of a flow cartoon where x does y.

I'm not the one posting links to illustrations of the process.

Fructose is a great example of why the glucose insulin hypothesis is wrong. Namely changing the carb intake from glucose to fructose should according to the hypothesis reduce the development of metabolic syndrome, however all the data indicates that it does the opposite and promotes the development of metabolic syndrome.

Yes, fructose has been linked to insulin resistance. Remember we're talking about chronically high doses over a long period of time. Also, you very rarely find foods with fructose and no glucose. Together they each contribute to fat storage and metabolic syndrome.

Perhaps you can tells us why glucose compared to fructose is protective against obesity in humans if the glucose insulin hypothesis is correct?

I disupute that. Glucose is not protective against obesity. Fructose contributes via production of fat and insulin resistance. Glucose contributes via increased insulin/fat storage. Carbs, in general, contribute through increased appetite, cravings etc.

... use pubmed...

I always do...

Fructose
How bad is fructose?
http://ajcn.nutrition.org/content/86/4/895.full

Fructose is metabolized, primarily in the liver, by phosphorylation on the 1-position, a process that bypasses the rate-limiting phosphofructokinase step (4). Hepatic metabolism of fructose thus favors lipogenesis, and it is not surprising that several studies have found changes in circulating lipids when subjects eat high-fructose diets

Metabolic Effects of Fructose and the Worldwide Increase in Obesity
http://physrev.physiology.org/content/90/1/23.full

Fructose has the same chemical formula as glucose (C6H12O6), but its metabolism differs markedly from that of glucose due to its almost complete hepatic extraction and rapid hepatic conversion into glucose, glycogen, lactate, and fat.

The Effect of High-Fructose Corn Syrup Consumption on Triglycerides and Uric Acid
http://jn.nutrition.org/content/139/6/1242S.full

Fructose metabolism is also known for its lipogenic potential. On entry into the liver, it is broken down into dihydroxyacetone phosphate and glyceraldehyde-3-phosphate. The former ultimately becomes the glycerol backbone of triglycerides, and the latter produces the acetyl-CoA units required for de novo lipogenesis and the synthesis of fatty acids. Thus, hepatic fructose metabolism can produce the 2 required components for triglyceride synthesis. Importantly, this pathway is unaffected by the regulatory step of glycolysis, phosphofructokinase, meaning that when exposed to high levels of fructose, it is metabolized by the liver unabated and thus rapidly increases triglyceride synthesis.

Nutrition & Metabolism | Full text | Fructose, insulin resistance, and metabolic dyslipidemia
http://www.nutritionandmetabolism.com/content/2/1/5

Fructose-induced insulin resistant states are commonly characterized by a profound metabolic dyslipidemia, which appears to result from hepatic and intestinal overproduction of atherogenic lipoprotein particles. Thus, emerging evidence from recent epidemiological and biochemical studies clearly suggests that the high dietary intake of fructose has rapidly become an important causative factor in the development of the metabolic syndrome.

[WeeDavie]

I disupute that. Glucose is not protective against obesity. Fructose contributes via production of fat and insulin resistance. Glucose contributes via increased insulin/fat storage. Carbs, in general, contribute through increased appetite, cravings etc.

Fructose
How bad is fructose?
http://ajcn.nutrition.org/content/86/4/895.full

Fructose is metabolized, primarily in the liver, by phosphorylation on the 1-position, a process that bypasses the rate-limiting phosphofructokinase step (4). Hepatic metabolism of fructose thus favors lipogenesis, and it is not surprising that several studies have found changes in circulating lipids when subjects eat high-fructose diets

Metabolic Effects of Fructose and the Worldwide Increase in Obesity
http://physrev.physiology.org/content/90/1/23.full

Fructose has the same chemical formula as glucose (C6H12O6), but its metabolism differs markedly from that of glucose due to its almost complete hepatic extraction and rapid hepatic conversion into glucose, glycogen, lactate, and fat.

You do realise that you are using references that support the view that fructose promotes obesity, while earlier saying that glucose is not protective against obesity. You can't have both:

either fructose promotes obesity which means that replacing fructose in the diet with glucose will protect against obesity.

Or glucose promotes obesity and hence replacing glucose by fructose will protect against obesity.

So which one of the two mutually exclusive statements that you have made are true?

[estockly]

You do realise that you are using references that support the view that fructose promotes obesity, while earlier saying that glucose is not protective against obesity. You can't have both:

How are they mutually exclusive? Why can't both promote obesity?

Fructose causes insulin resistance, or at least makes it worse. Insulin resistance makes one more prone to obesity.

Glucose stimulates insulin production which directly causes excess fat storage, which is exactly what obesity is.

Fructose also increases production of triglycerides, which is part of metabolic syndrome, and causes non-alcoholic fatty liver disease.

They are bad enough, separately, but together they are worse.

I'm guessing that you're suggesting that when isolated there is evidence that fructose does more to cause obesity than glucose, but to stretch that to say glucose is protective is not valid.

Fructose, by itself, lowers insulin, but that effect on insulin is negligible compared to the influence of glucose.

ES

[lonely moa]

Gary Taubes explains his take on the laws of thermodynamics as regards to weight gain.

http://www.meandmydiabetes.com/2013/05/20/gary-taubes-explains-thermodynamics-to-jillian-michaels/

[GodSlayer]

his take on the laws of thermodynamics

sounds like something Deebag Chopra would do.

[fred.slota]

his take on the laws of thermodynamics

sounds like something Deebag Chopra would do.

My brain hurts thinking about that.

People can decide to enter the room or not, subject to a variety of conditions and the personal volition of individuals.  Is he suggesting that calories can have agency, and decide whether or not they want to go on our plate, or in our mouth, as a personal choice that each calorie makes?

Regardless, he explicitly acknowledges calorie differential producing weight differential.  So, if you reverse his statements, I think he should agree that:

It doesn't matter why you eat more or less, or why you burn more or less, or what the source of the calories are, but if you have red in your ledger, you lose weight, and if you have black in your ledger you gain weight, all at the appropriate exchange.

Have I got that right?

[lonely moa]

his take on the laws of thermodynamics

sounds like something Deebag Chopra would do.

My brain hurts thinking about that.

People can decide to enter the room or not, subject to a variety of conditions and the personal volition of individuals.  Is he suggesting that calories can have agency, and decide whether or not they want to go on our plate, or in our mouth, as a personal choice that each calorie makes?

Regardless, he explicitly acknowledges calorie differential producing weight differential.  So, if you reverse his statements, I think he should agree that:

It doesn't matter why you eat more or less, or why you burn more or less, or what the source of the calories are, but if you have red in your ledger, you lose weight, and if you have black in your ledger you gain weight, all at the appropriate exchange.

Have I got that right?

I don't think so.  The point is why a person would take in more energy than they would expend, or expend less energy than they intake.  He argues that it is hormonally  based.  He thinks insulin is the prime hormone, others, leptin.  If the reason isn't addressed, well, you see how well dieting by calorie restriction works in the real world.

[MurphDogg]

his take on the laws of thermodynamics

sounds like something Deebag Chopra would do.

My brain hurts thinking about that.

People can decide to enter the room or not, subject to a variety of conditions and the personal volition of individuals.  Is he suggesting that calories can have agency, and decide whether or not they want to go on our plate, or in our mouth, as a personal choice that each calorie makes?

Regardless, he explicitly acknowledges calorie differential producing weight differential.  So, if you reverse his statements, I think he should agree that:

It doesn't matter why you eat more or less, or why you burn more or less, or what the source of the calories are, but if you have red in your ledger, you lose weight, and if you have black in your ledger you gain weight, all at the appropriate exchange.

Have I got that right?

I don't think so.  The point is why a person would take in more energy than they would expend, or expend less energy than they intake.  He argues that it is hormonally  based.  He thinks insulin is the prime hormone, others, leptin.  If the reason isn't addressed, well, you see how well dieting by calorie restriction works in the real world.

He never addresses it at all.  He sets up a straw man and says it is obvious and we must never address it again.  It feels "cultish".

[GodSlayer]

If the reason isn't addressed, well, you see how well dieting by calorie restriction works in the real world.

a course of antibiotics doesn't work well in the real world, if the real world is lazy people not following instructions.