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Author Topic:   Good Calories, Bad Calories, by Gary Taubes
molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 61 of 451 (465495)
05-07-2008 1:32 PM
Reply to: Message 58 by Percy
05-07-2008 8:53 AM


Re: Balanced Diets are Bunk
This is another citation which doesn't support your position that the liver does not convert glucose to triglycerides as part of any common process of VLDL production
It directly rebuts Taube's claim.
Taube said carbs = glucose spike = insulin spike.
Taube said glucose spike = elevated VLDL production.
Do the math. A = B = C. B = D. Therefore, C = D.
IF carbs = glucose spike AND
IF glucose = insulin spike AND
IF insulin = suppressed VLDL production
THEN carbs do not lead to an increase in VLDL production.
You seem unwilling to try to find other Taube VLDL quotes. Fine. I'll do it myself next week.
If Taube makes no mention of the role insulin plays in VLDL production, then that's an excellent example of how metabolically naive his arguments are.
His argument that glucose = elevated VLDL levels is metabolically impossible. Period.

This message is a reply to:
 Message 58 by Percy, posted 05-07-2008 8:53 AM Percy has replied

Replies to this message:
 Message 63 by Percy, posted 05-07-2008 2:24 PM molbiogirl has replied

Percy
Member
Posts: 22391
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 62 of 451 (465496)
05-07-2008 1:44 PM
Reply to: Message 60 by molbiogirl
05-07-2008 12:39 PM


Re: Balanced Diets are Bunk
molbiogirl writes:
They are not irrelevant. They are on point. And I think you stopped listening 2 days ago.
If I'm mistaken that they don't support your position then all that is probably needed is to explain in your own words at a layperson level how they support your position. The abstracts and excerpts you provided give no such indication to me, but perhaps if you explain the tie-in it will help.
About your previous post, of course Taubes addresses the topic in other places in the book, but that was the only passage I found that describes in any detail that particular process. Maybe he adds more details in other places, but as you say, it's a long book, I don't know. Another pair of eyes on the text would certainly be helpful in ferreting out details.
But I'm curious, given that that passage doesn't mention insulin, and given that you haven't read the book, why are you so certain that Taubes must elsewhere in the book make that particular error? That just seems incredibly, uh, I don't know, weird? You're so sure that Taubes is wrong that you're certain that if you read the book you'll find errors that you made up yourself?
Why don't you just go back to trying to support the point you were originally trying to make, which is that the production of VLDL from glucose by the liver is an incredibly rare process?
But as far as actual weight loss goes, this discussion is becoming academic for me. I'm down 9-1/2 pounds now after about 4 weeks, and I'm going to have to take a link out of my watchband soon because it's getting loose on my wrist.
In other words, concerning weight loss, the problem for you is reality, which is the same problem creationists have. It doesn't matter what arguments you make or research you cite if the evidence from reality is that low carb diets cause weight loss without hunger at higher calorie intake levels than low fat diets.
There is of course still the main question of whether the western diseases of heart disease, metabolic syndrome, diabetes and obesity are caused primarily by fat or carbohydrates, but here reality also runs against you. In the United States, the national health problem with these diseases worsened during the same period that the emphasis on low fat diets increased. This is nearly impossible to fathom if dietary fat is truly the cause.
At one point you said that if you knew the answer to this crisis of western diseases you'd win an "FN Nobel", indicating your belief that the causes remain mysterious or at least unknown. This is again so reminiscent of creationists who when presented the contradictions between their position and reality say that it is a mystery. It's only a mystery because they refuse to follow the evidence where it leads because they believe they already have the answer.
--Percy

This message is a reply to:
 Message 60 by molbiogirl, posted 05-07-2008 12:39 PM molbiogirl has replied

Replies to this message:
 Message 64 by molbiogirl, posted 05-07-2008 3:14 PM Percy has replied

Percy
Member
Posts: 22391
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 63 of 451 (465498)
05-07-2008 2:24 PM
Reply to: Message 61 by molbiogirl
05-07-2008 1:32 PM


Re: Balanced Diets are Bunk
I think you raised this exact point a few days ago. The answer is that the triglycerides that form in the liver while insulin levels are presumably high because of elevated blood sugar levels remain in the liver after insulin levels decline, at which time they can become part of the process of VLDL production.
You actually already accept that this is case, because you've already said that the glucose => triglycerides => VLDL process does indeed exist. The liver converts glucose to triglycerides, but won't produce VLDL at that particular time until the insulin response to the glucose diminishes. The only difference between us is that you believe the process rarely takes place.
I bought a blood sugar test kit a few days ago and for a while I sampled my blood sugar at regular intervals. My blood sugar levels never drop below 90 and never rise above 120, except for one time I hit 141 about 15 minutes after eating a South Beach Diet snack bar that said it contained 18 grams of carbohydrate. Most of the time my blood sugar level is right around 100.
My carbohydrate intake is so low that I'm wondering how my blood sugar level is being maintained. I would guess that the triglycerides in adipose tissue are being converted into FFAs, but are the FFAs used directly for energy, or are they first converted to glucose, or do both processes (and more?) take place. I'm trying to explain my extremely consistent blood sugar levels.
--Percy

This message is a reply to:
 Message 61 by molbiogirl, posted 05-07-2008 1:32 PM molbiogirl has replied

Replies to this message:
 Message 65 by molbiogirl, posted 05-07-2008 5:45 PM Percy has replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 64 of 451 (465499)
05-07-2008 3:14 PM
Reply to: Message 62 by Percy
05-07-2008 1:44 PM


Re: Balanced Diets are Bunk
If I'm mistaken that they don't support your position then all that is probably needed is to explain in your own words at a layperson level how they support your position.
OK.
Chronic calorie restriction = defense of body weight (aka no weight loss) + chronic calorie restriction = lowered metabolic rate.
But I'm curious, given that that passage doesn't mention insulin, and given that you haven't read the book, why are you so certain that Taubes must elsewhere in the book make that particular error?
Either he mentions the link between insulin and VLDL levels or he doesn't.
If he doesn't, I am correct. He is a sloppy researcher and his ideas are painfully naive and metabolically impossible.
If he does, you could easily find the quote instead of posting the same 6 sentences over and over again.
But instead, you shrug your shoulders and say "I don't know if he links the two."
Look in the index. Find "insulin". Make a note of the page numbers. Find "VLDL". Make a note of the page numbers. Find the page numbers they have in common.
It is easy to find the answer. You just don't want to for some reason.
Why don't you just go back to trying to support the point you were originally trying to make, which is that the production of VLDL from glucose by the liver is an incredibly rare process?
I will address this in my next post. I'm at work right now and can't do the necessary research.
In other words, concerning weight loss, the problem for you is reality, which is the same problem creationists have.
I wasn't going to go there, but you opened the door, so I'm going to walk thru it.
It has been patently obvious to me for days now that Taube's arguments are ridiculous on their face. I feel like cavediver facing ICANT. (ABE: I = cavediver and Taube = ICANT.) Taube's whole "I'm being persecuted for my novel theory -- the big bad scientists are ignoring me!" thing reeks of creo too.
It doesn't matter what arguments you make or research you cite if the evidence from reality is that low carb diets cause weight loss without hunger at higher calorie intake levels than low fat diets.
Prove it.
Don't use yourself as an example. Give me evidence.
There is of course still the main question of whether the western diseases of heart disease, metabolic syndrome, diabetes and obesity are caused primarily by fat or carbohydrates...
No. This isn't the question.
The question is "What causes CHD?" or "What causes obesity?" or "What causes metabolic syndrome?" or "What causes diabetes?".
They are all separate questions.
And the answer is NOT either carbs or fat.
The answer is MUCH more complex.
And while CHD/obesity/metabolic syndrome/diabetes may be correlated, there is no ONE answer to all 4 questions.
At one point you said that if you knew the answer to this crisis of western diseases you'd win an "FN Nobel", indicating your belief that the causes remain mysterious or at least unknown. This is again so reminiscent of creationists who when presented the contradictions between their position and reality say that it is a mystery.
Just because the whole picture isn't known doesn't mean we don't have a lot of the pieces.
And because the whole picture is multi-faceted, because the metabolic pathways are so complex and inter-related, yes ... to find a definitive answer to any of those 4 questions mentioned above would merit a Nobel.
It sounds like you are saying: "You don't have the answer to (this question) therefore your whole theory is bullshit." That reeks of creo.
Perhaps you meant to say: "Taube doesn't have the answer. Researchers who disagree with Taube don't have the answer. Nobody has the answer."
It's only a mystery because they refuse to follow the evidence where it leads because they believe they already have the answer.
You haven't managed to refute any of my evidence, tho. There are no contradictions.
I will follow ANY evidence where it leads.
You haven't provided any, tho.
You repeat bald assertions made by Taube, refuse to cite the papers he uses, and claim I'm the one responsible for not "following the evidence"?
Have you bothered to look into the claims he makes?
Have you looked up any of his sources?
I bet the answer is "No.".
You take what he says at face value.
And because you refuse to provide cites, I am faced with refuting Taube's bald assertions. And I have to give the lousy SOB my money to find the cites.
Edited by molbiogirl, : No reason given.

This message is a reply to:
 Message 62 by Percy, posted 05-07-2008 1:44 PM Percy has replied

Replies to this message:
 Message 66 by Percy, posted 05-07-2008 8:13 PM molbiogirl has replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 65 of 451 (465503)
05-07-2008 5:45 PM
Reply to: Message 63 by Percy
05-07-2008 2:24 PM


Re: Balanced Diets are Bunk
The answer is that the triglycerides that form in the liver while insulin levels are presumably high because of elevated blood sugar levels remain in the liver after insulin levels decline, at which time they can become part of the process of VLDL production.
I see we are back to the "fat in the liver" thing again. "Temporary storage", right?
Prove it.
Hint: Message 55. "Instead, insulin signaling mediates the return of TAGs to the cytosolic pool, an effect similar to that of MTP inhibition, which is also required for the efcient production of the TAG-rich VLDL precursors but has no effect on TAG synthesis."
TRANSLATION: The TAGs are exported. Not stored.
You actually already accept that this is case, because you've already said that the glucose => triglycerides => VLDL process does indeed exist.
I said in no uncertain terms that TAGs are not stored in the liver.
Yes, carbs can turn into TAGs. No, TAGs are not stored in the liver.
My carbohydrate intake is so low that I'm wondering how my blood sugar level is being maintained.
If your evergy needs exceed your glucose intake, by breaking down the fat you eat. The glycerol is converted into glucose.
If your energy requirements exceed your deitary fat intake, yes, you would be digging into your fat tissue for triacylglycerols. They would be broken apart and the glycerol would be converted to glucose.
Edited by molbiogirl, : No reason given.

This message is a reply to:
 Message 63 by Percy, posted 05-07-2008 2:24 PM Percy has replied

Replies to this message:
 Message 67 by Percy, posted 05-07-2008 8:36 PM molbiogirl has replied

Percy
Member
Posts: 22391
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 66 of 451 (465509)
05-07-2008 8:13 PM
Reply to: Message 64 by molbiogirl
05-07-2008 3:14 PM


Re: Balanced Diets are Bunk
If I'm mistaken that they don't support your position then all that is probably needed is to explain in your own words at a layperson level how they support your position.
OK.
Chronic calorie restriction = defense of body weight (aka no weight loss) + chronic calorie restriction = lowered metabolic rate.
You offered a citation in support of your position that did not actually appear to provide any support, at least to me, so I suggested that it might be more helpful if you explained in layperson's terms how the citation provided that support. But what you've provided is just a restatement of your position. How does your citation support your position?
If he doesn't, I am correct. He is a sloppy researcher and his ideas are painfully naive and metabolically impossible.
...etc...
The difficulty you're having supporting your positions should not serve as an excuse for taking out your frustrations on me and Taubes. It would be more constructive to just focus on the topic. You're not the only human being involved in this discussion, and all human beings have feelings.
It doesn't matter what arguments you make or research you cite if the evidence from reality is that low carb diets cause weight loss without hunger at higher calorie intake levels than low fat diets.
Prove it.
Don't use yourself as an example. Give me evidence.
We've been over these two points before. Concerning the first point, I'm using myself as an example because I'm typical. Most people lose weight on low carb diets without experiencing the hunger associated with low fat diets.
Concerning the second point, the dietary fat crowd concedes that low carb diets are effective but criticizes them for being nutritionally dangerous or being low calorie diets in disguise, and there are probably other criticisms. In other words, they don't share this particular aspect of your skepticism. Your request for evidence is not unreasonable, but it is unexpected as you personally are disputing a characteristic of low carb diets that isn't considered controversial. It might help if you explained why you doubt the consensus view on this particular aspect of low carb diets. Is it that you don't really believe there's a consensus, or is it something else specifically?
And while CHD/obesity/metabolic syndrome/diabetes may be correlated, there is no ONE answer to all 4 questions.
True, but it is widely believed that there is a dominant factor. For advocates of the dietary fat hypothesis, it is believed that the dominant factor is dietary fat. This has become the mainstream view, and it is the cause of all the low fat foods in grocery stores.
For advocates of the carbohydrate hypothesis, it is believed that the dominant factor is refined carbohydrates, but this hypothesis has not found any widespread degree of acceptance and has had little influence on dietary recommendations.
The result is dietary recommendations that over the past half century have caused people to increasingly deemphasize fat while simultaneously increasing carbohydrate intake, and the result is an increasingly fat and diabetic population.
I understand that you would like a discussion that involves more citations, and I encourage you to bring whatever references you like to the discussion, but arguments and explanations should be in your own words with references serving only as pointers to the sources of information.
--Percy

This message is a reply to:
 Message 64 by molbiogirl, posted 05-07-2008 3:14 PM molbiogirl has replied

Replies to this message:
 Message 69 by molbiogirl, posted 05-08-2008 1:02 PM Percy has seen this message but not replied

Percy
Member
Posts: 22391
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 67 of 451 (465510)
05-07-2008 8:36 PM
Reply to: Message 65 by molbiogirl
05-07-2008 5:45 PM


Re: Balanced Diets are Bunk
I think part of the problem is that you're judging Taubes' mass market book using the criteria of a peer reviewer for a technical journal. If that's to be your approach then no doubt you'll be able to write thousands of pages of criticism once you have the book in hand.
Science books written for the mass market have to be written in terms that laypeople unfamiliar with the area can understand. That requires addressing things at a level of detail that apparently drives researchers like yourself crazy.
Taubes doesn't say that the triglycerides are stored in the liver. He says they're produced in the liver for temporary storage, but doesn't say where they're actually stored. Honestly, I would have assumed the liver myself, but from what you say that must not be the case. But you're again putting me in the position of having to say, "No, Taubes isn't saying that," and I'm becoming concerned at the frequency with which this is occurring. A little more focus on accuracy on your part would be appreciated, especially since you're attributing what are actually your own misinterpretations to Taubes and then excoriating him for them. I'm sure Taubes' book has its share of mistakes, but please criticize him for mistakes he actually makes.
The reference information Taubes provides for this is:
  • Mayes and Botham 2004
  • Berneis and Krauss 2002
  • DeFronzo 1992
--Percy

This message is a reply to:
 Message 65 by molbiogirl, posted 05-07-2008 5:45 PM molbiogirl has replied

Replies to this message:
 Message 68 by molbiogirl, posted 05-08-2008 10:40 AM Percy has replied
 Message 70 by molbiogirl, posted 05-08-2008 1:27 PM Percy has replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 68 of 451 (465590)
05-08-2008 10:40 AM
Reply to: Message 67 by Percy
05-07-2008 8:36 PM


Re: Balanced Diets are Bunk
I think part of the problem is that you're judging Taubes' mass market book using the criteria of a peer reviewer for a technical journal.
No. I'm asking you to look at the footnotes.
The reference information Taubes provides for this is:
* Mayes and Botham 2004
* Berneis and Krauss 2002
* DeFronzo 1992
This is useless, Percy. Scholar.google it yourself if you don't believe me.
Later today I will try to track down their academic affiliations and see if they've posted a list of publications on their webpages.
The man doesn't provide cites in the index? If not, how are his "theories" any different from bare assertions?
Taubes doesn't say that the triglycerides are stored in the liver. He says they're produced in the liver for temporary storage, but doesn't say where they're actually stored.
Well, we can't know if they're transformed into VLDLs then. Taube can't just going to wave his hands and say they're "temporarily stored" somewhere.
It makes a huge difference where a metabolite is. It determines its fate.
But you're again putting me in the position of having to say, "No, Taubes isn't saying that...
Taube may not have said that, but you sure did. Now you tell me it's your assumption.
I couldn't have known Taube didn't say that, Percy. I have only your word for what the man does or does not say.

This message is a reply to:
 Message 67 by Percy, posted 05-07-2008 8:36 PM Percy has replied

Replies to this message:
 Message 71 by Percy, posted 05-08-2008 2:27 PM molbiogirl has replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 69 of 451 (465605)
05-08-2008 1:02 PM
Reply to: Message 66 by Percy
05-07-2008 8:13 PM


Re: Balanced Diets are Bunk
The difficulty you're having supporting your positions should not serve as an excuse for taking out your frustrations on me and Taubes.
The reason I am having difficulty is either:
(1) Taube doesn't document his work.
(2) You won't give me the cites.
You don't seem to understand the what Taube is doing.
If, in the text, he says something like, "Jones and Smith showed in 2004 that..." and that is the full extent of his documentation, how is that any different from my saying "Nope. Hannink and Liscum showed in 2007 that that is not the case."
How on earth is one to verify either assertion?
And I am not holding Taube to peer reviewed literature standards. Reputable popsci books use footnotes, references, and/or bibliographies. Just look at Brian Greene's The Elegant Universe.
If Taube does not document his work, how am I to track down the paper he pseudo cites to see if:
(1) he is quote mining
(2) he is misinterpreting the data
(3) the paper is published in a reputable journal
et cetera.
Furthermore, without a paper, I can't check the cites the paper uses to find more information of that specific phenomenon.
We've been over these two points before.
Percy, I guess I'm done with the bare assertions.
Weight loss, yes. I know that because I did the research to confirm it.
At higher caloric levels? With more saiety?
You need to document this.
You can't just assert something is true and fail to support your argument in a debate. And neither can Taube.
I need a starting point. I need a cite.

This message is a reply to:
 Message 66 by Percy, posted 05-07-2008 8:13 PM Percy has seen this message but not replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 70 of 451 (465607)
05-08-2008 1:27 PM
Reply to: Message 67 by Percy
05-07-2008 8:36 PM


Re: Balanced Diets are Bunk
Mayes and Botham 2004
Pubmed has no 2004 paper for either of these authors.
There is a 2000 paper, but it has nothing to do with carbs, TAG biosynthesis from carbs, insulin levels in the liver, or temporary storage of carb-derived TAGs.
The consumption of fat-enriched diets may alter the uptake and metabolism of chylomicron remnant cholesterol by the liver. To test this hypothesis, [3H]cholesterol-labelled chylomicron remnants derived from different dietary fats were studied in perfused livers both from rats fed on diets enriched in the corresponding fats and from rats fed on a low-fat diet. Livers from rats fed on each of the fat-enriched diets removed similar amounts (34-40%) of the [3H]cholesterol-labelled remnants added, whereas livers from rats fed on the low-fat diet removed significantly more labelled fish-oil and butter-fat remnants than olive-, maize- or palm-oil remnants. Significantly more remnant [3H]cholesterol was secreted into the perfusate HDL by livers from rats fed on the olive-oil, fish-oil and butter-fat diets when compared with those from rats fed on the low-fat diet or the maize-oil diet. Furthermore, the excretion of remnant [3H]cholesterol via the bile acid was increased by the olive-, maize-, palm- or fish-oil diets, and decreased by the butter-fat diet when compared with the low-fat diet, although the [3H]bile acid excreted remained less on saturated fat diets. This investigation shows that the hepatic uptake and subsequent metabolism of cholesterol from chylomicron remnants is influenced by the type of fat in the diet as well as the fatty acid composition of the particles themselves, and may help to explain some of the hyper- and hypocholesterolaemic effects of saturated and unsaturated fatty acids.
Paper.
There is a 1995 paper, but it has nothing to do with carbs, TAG biosynthesis from carbs, insulin levels in the liver, or temporary storage of carb-derived TAGs.
The hepatic metabolism of [1-14C]oleate- and [1,2-3H]cholesterol-dual-labelled chylomicron remnants derived from olive, corn, palm and fish oil and butter fat was compared by adding each lipoprotein separately to the perfusate of isolated livers from rats fed on a normal diet. Labelled remnants from butter fat and fish oil were removed more rapidly from the perfusate than remnants derived from olive, corn and palm oil. The oxidation of labelled remnant fatty acid from olive oil, fish oil or butter fat was four to seven times greater than that from corn and palm oil. Labelled fatty acid in fish oil remnants was incorporated into phospholipid significantly more efficiently than the labelled fatty acid in olive, corn or palm oil remnants, with butter fat giving an intermediate value. For all the remnants, there was a significant amount of hydrolysis of labelled esterified cholesterol by the liver which was dependent on the magnitude of hepatic uptake of each type of remnant. The recovery of remnant [3H]cholesterol label in the bile was 50% less with palm oil remnants than with all the other remnants studied. The results indicate that the fatty acid composition of chylomicron remnants has a major impact on their uptake and metabolism by the liver.
Paper.
Ditto for 1992, 1993, 1994, 1996, 1997, 1998 papers by these authors. Nothing to do with carbs, TAG biosynthesis from carbs, insulin levels in the liver, or temporary storage of carb-derived TAGs.
Berneis and Krauss 2002
Found it.
LDLs in humans comprise multiple distinct subspecies that differ in their metabolic behavior and pathologic roles. Metabolic turnover studies suggest that this heterogeneity results from multiple pathways, including catabolism of different VLDL and IDL precursors, metabolic remodeling, and direct production. A common lipoprotein profile designated atherogenic lipoprotein phenotype is characterized by a predominance of small dense LDL particles. Multiple features of this phenotype, including increased levels of triglyceride rich lipoprotein remnants and IDLs, reduced levels of HDL and an association with insulin resistance, contribute to increased risk for coronary heart disease compared with individuals with a predominance of larger LDL. Increased atherogenic potential of small dense LDL is suggested by greater propensity for transport into the subendothelial space, increased binding to arterial proteoglycans, and susceptibility to oxidative modification. Large LDL particles also can be associated with increased coronary disease risk, particularly in the setting of normal or low triglyceride levels. Like small LDL, large LDL exhibits reduced LDL receptor affinity compared with intermediate sized LDL. Future delineation of the determinants of heterogeneity of LDL and other apoB-containing lipoproteins may contribute to improved identification and management of patients at high risk for atherosclerotic disease.
Paper.
Nothing to do with carbs, TAG biosynthesis from carbs, insulin levels in the liver, or temporary storage of carb-derived TAGs.
DeFronzo 1992
Found it.
Non-insulin-dependent diabetes mellitus (NIDDM) results from an imbalance between insulin sensitivity and insulin secretion. Both longitudinal and cross-sectional studies have demonstrated that the earliest detectable abnormality in NIDDM is an impairment in the body's ability to respond to insulin. Because the pancreas is able to appropriately augment its secretion of insulin to offset the insulin resistance, glucose tolerance remains normal. With time, however, the beta-cell fails to maintain its high rate of insulin secretion and the relative insulinopenia (i.e., relative to the degree of insulin resistance) leads to the development of impaired glucose tolerance and eventually overt diabetes mellitus. The cause of pancreatic "exhaustion" remains unknown but may be related to the effect of glucose toxicity in a genetically predisposed beta-cell. Information concerning the loss of first-phase insulin secretion, altered pulsatility of insulin release, and enhanced proinsulin-insulin secretory ratio is discussed as it pertains to altered beta-cell function in NIDDM. Insulin resistance in NIDDM involves both hepatic and peripheral, muscle, tissues. In the postabsorptive state hepatic glucose output is normal or increased, despite the presence of fasting hyperinsulinemia, whereas the efficiency of tissue glucose uptake is reduced. In response to both endogenously secreted or exogenously administered insulin, hepatic glucose production fails to suppress normally and muscle glucose uptake is diminished. The accelerated rate of hepatic glucose output is due entirely to augmented gluconeogenesis. In muscle many cellular defects in insulin action have been described including impaired insulin-receptor tyrosine kinase activity, diminished glucose transport, and reduced glycogen synthase and pyruvate dehydrogenase. The abnormalities account for disturbances in the two major intracellular pathways of glucose disposal, glycogen synthesis, and glucose oxidation. In the earliest stages of NIDDM, the major defect involves the inability of insulin to promote glucose uptake and storage as glycogen. Other potential mechanisms that have been put forward to explain the insulin resistance, include increased lipid oxidation, altered skeletal muscle capillary density/fiber type/blood flow, impaired insulin transport across the vascular endothelium, increased amylin, calcitonin gene-related peptide levels, and glucose toxicity.
Paper.
Nothing to do with carbs, TAG biosynthesis from carbs, insulin levels in the liver, or temporary storage of carb-derived TAGs.
(I haven't access to this paper online -- I have only the abstract to rely on.)

This message is a reply to:
 Message 67 by Percy, posted 05-07-2008 8:36 PM Percy has replied

Replies to this message:
 Message 72 by Percy, posted 05-08-2008 3:24 PM molbiogirl has replied
 Message 74 by Percy, posted 05-08-2008 4:27 PM molbiogirl has replied

Percy
Member
Posts: 22391
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 71 of 451 (465609)
05-08-2008 2:27 PM
Reply to: Message 68 by molbiogirl
05-08-2008 10:40 AM


Re: Balanced Diets are Bunk
molbiogirl writes:
Taube may not have said that, but you sure did. Now you tell me it's your assumption.
I couldn't have known Taube didn't say that, Percy. I have only your word for what the man does or does not say.
I quoted Taubes' own words.
Much of your recent criticism has left the realm of dispassionate and objective topical discourse. It would really help keep the discussion on a constructive footing if you could just focus on the topic, and if you could think of us as partners on an adventure of exploration instead of as enemies on opposite sides of a battle line. The road you're marching down just leads to acrimony and accusations where nothing will be learned. Many aspects of this discussion seem to upset you into caustic responses, and that's just not helpful. If you're just here to yell at people, if you're just here for thunder instead of light, then please let me know now so I can stop wasting my time.
When we started we hoped to explore two separate issues:
  • The current issue, which is whether blood sugar spikes encourage the production of small, dense LDLs, which play a role in heart disease.
  • The next issue, which is whether it is really true that low carbohydrate diets produce weight loss without hunger and at higher calorie levels than low fat diets, and if so, the mechanisms behind that ability.
Excoriating me and Taubes isn't going to help get answers to these questions.
--Percy
Edited by Percy, : Restore version of message that was lost when site went down.

This message is a reply to:
 Message 68 by molbiogirl, posted 05-08-2008 10:40 AM molbiogirl has replied

Replies to this message:
 Message 75 by molbiogirl, posted 05-08-2008 4:40 PM Percy has replied

Percy
Member
Posts: 22391
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 72 of 451 (465611)
05-08-2008 3:24 PM
Reply to: Message 70 by molbiogirl
05-08-2008 1:27 PM


Re: Balanced Diets are Bunk
I thought that Taubes' offered those references in support of this paragraph from page 175:
Taubes writes:
After we eat a carbohydrate-rich meal, the bloodstream is flooded with glucose, and the liver takes some of this glucose and transforms it into fat”i.e., triglycerides”for temporary storage. These triglycerides are no more than droplets of oil. In the liver, the oil droplets are fused to the apo B protein and to the cholesterol that forms the outer membrane of the balloon. The triglycerides constitute the cargo that the lipo-proteins drop off at tissues throughout the body. The combination of cholesterol and apo B is the delivery vehicle. The resulting lipoprotein has a very low density and so is a VLDL particle, because the triglycerides are lighter than either the cholesterol of the apo B. For this reason, the larger the initial oil droplet, the more triglycerides packaged in the lipoprotein, the lower its density.
But evidently he was instead offering them in support of the overall hypothesis that blood sugar spikes encourage the production of small, dense LDLs that in turn lead to heart disease.
So what you're looking for is citations to research supporting the view that elevated glucose levels encourage the production of triglycerides. I don't think that possibility is considered controversial, so it wouldn't be expected that Taubes would offer citations for it. You yourself have offered diagrams that include this possibility, e.g., this one, the box at the top shows glucose being converted to fatty acids, which it does not specify are free or bound up in triglycerides, but we already know from statements elsewhere like Wikipedia that the liver can produce triglycerides:
But you've maintained that this is a very uncommon process, and so I was hoping we could seek evidence of whether that is so or not.
--Percy

This message is a reply to:
 Message 70 by molbiogirl, posted 05-08-2008 1:27 PM molbiogirl has replied

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 Message 73 by molbiogirl, posted 05-08-2008 4:07 PM Percy has seen this message but not replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 73 of 451 (465614)
05-08-2008 4:07 PM
Reply to: Message 72 by Percy
05-08-2008 3:24 PM


Re: Balanced Diets are Bunk
So what you're looking for is citations to research supporting the view that elevated glucose levels encourage the production of triglycerides.
Yes. Taube has no documentation of his claim, then?
Well. If you'd like to look for it, here's the procedure I've been using.
Scholar.google the key terms: glucose, carbohydrates, TAGs, VLDL.
Monkey with the combinations of the terms to see what you get.
Monkey with the publication date (under "Advanced Scholar Google" ... link on upper right). I look for really recent stuff because this is a very active area of research.
See if any of the abstracts look promising.
Find the paper online.
Do a "find" for the terms you're looking for.
See if it's relevant.
I've also had some luck with the key terms: hyperglycemia, hyperinsulinemia, impaired glucose tolerance, dyslipidemia, insulin resistance, metabolic syndrome.
I have yet to find a paper that addresses this point directly.
Insulin and their link to TAGs/VLDL, yes.
Glucose and its link to TAGs/VLDL, no.
And I have dedicated several hours of poking around scholar.google looking.
Hey! Sounds like an NIH grant proposal topic. Pity I work on RNA.
...this one, the box at the top shows glucose being converted to fatty acids, which it does not specify are free or bound up in triglycerides...
The arrow to the left points to VLDL. FFAs are converted to TAGs before they are incorporated into the mature VLDL particle.
btw. Don't forget. That is a chart that shows the negative regulation of this metabolic pathway by insulin.
But that cite I posted a couple of days ago re: VLDL and insulin was much clearer, I thought.

This message is a reply to:
 Message 72 by Percy, posted 05-08-2008 3:24 PM Percy has seen this message but not replied

Percy
Member
Posts: 22391
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 74 of 451 (465615)
05-08-2008 4:27 PM
Reply to: Message 70 by molbiogirl
05-08-2008 1:27 PM


Re: Balanced Diets are Bunk
I think this study is in the general neighborhood of the initial part of the process that Taubes describes, that elevated glucose levels cause increased triglyceride output from the liver: Effects of dietary fructose or glucose on triglyceride production and lipogenic enzyme activities in the liver of Wistar fatty rats, an animal model of NIDDM
The abstract concludes:
These results show that in genetically obese, diabetic rats feeding fructose and glucose is associated with an increase in hepatic lipogenic enzyme activities and triglyceride production, and suggest that fructose stimulates triglyceride production but impairs triglyceride removal, whereas glucose stimulates both of them.
This is consistent with Taubes premise, which is that repeatedly abusing the body's metabolic processes with blood sugar spikes causes insulin resistance and obesity, creating an environment where elevated blood sugar levels cause increased triglyceride production by the liver. This is the part that I've been saying is not controversial, and it doesn't appear to be an incredibly rare process as you've been claiming.
I think we should next focus on what Taubes means by "temporary storage" of triglycerides. I can't answer that question. Do you have any guesses? Is adipose tissue really the only place that triglycerides are stored? They're never stored elsewhere for use by the liver in VLDL production?
--Percy

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 Message 70 by molbiogirl, posted 05-08-2008 1:27 PM molbiogirl has replied

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molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 75 of 451 (465616)
05-08-2008 4:40 PM
Reply to: Message 71 by Percy
05-08-2008 2:27 PM


Re: Balanced Diets are Bunk
It would really help keep the discussion on a constructive footing if you could just focus on the topic, and if you could think of us as partners on an adventure of exploration instead of as enemies on opposite sides of a battle line.
Good. You can help by digging around in the book and finding the documentation. As I just posted, I have spent hours on this topic (I find it interesting ... probably why I'm a grad student at 42). Finding an answer to a very specific question like these 2 we are working on is not easy unless someone has addressed that very specific question with a paper, and that doesn't appear that that is the case. I keep digging around in the intros of very closely related papers hoping to stumble on the answer.
If Taubes documented this claim in any way, shape or form, that paper would at least be a jumping off point -- I can data mine the references in his cite.
About your two questions.
I have 3 separate documents filled with cites and quotes so far (which I am saving until we get these 2 questions answered), but none of them are on point re: this question:
The current issue, which is whether blood sugar spikes encourage the production of small, dense LDLs, which play a role in heart disease.
You have to understand, tho.
We can't just jump from glucose to LDL.
We have to take this one tiny metabolic step at a time.
First we have to establish that elevated glucose levels lead to elevated VLDL levels.
Then we have to see if there is a link between these extra VLDL particles and sdLDLs.
Then we have to see if there is a link between sdLDLs and CHD.
I did, however, stumble across a partial answer to this question last night:
The next issue, which is whether it is really true that low carbohydrate diets produce weight loss without hunger and at higher calorie levels than low fat diets, and if so, the mechanisms behind that ability.
The present review summarises the effects of different carbohydrate and fat structures on food intake and appetite and the differences in response at various levels of processing of macronutrients. Several physico-chemical properties of carbohydrate and fat molecules appear to influence the short-term satiating properties.
However, long-term substantiation of these findings expressed in terms of food intake or body weight is not currently available.
Such studies will be required to make clear recommendations regarding dietary composition to aid satiety.
Three major areas associated with fat structure have been investigated with regard to their satiating effectiveness.
Chain length and degree of saturation of fats have a large impact on their physico-chemical properties and several studies have investigated the role of these factors on appetite and eating behaviour.
The final area that has received some attention relates to the functionality of specific fat molecules, particularly conjugated linoleic acid (CLA), mainly in terms of weight regulation and metabolism, but also recently on food intake and appetite.
A number of studies have shown MCT (medium chain length TAGs) to be more satiating than long-chain triacylglycerols in both animals and S24 S. French human subjects (Stubbs & Harbron 1996; Wymelbeke et al. 1998). Furthermore, MCT added to a very-low energy diet have been shown to speed the rate of weight loss and enhance satiety in the first 2 weeks of weight loss (Krotkiewski, 2001).
Within the C18 fatty acids, linoleic acid was found to be more satiating when infused into the upper small intestine in human subjects than oleic or stearic acids (French et al. 2000). Similar findings have been noted when oils are incorporated into foods (Lawton et al. 2000).
These studies have shown that daily intake of CLA (conjugated linoleic acid) can reduce total body fat (Blankson et al. 2000) or abdominal fat (Riserus et al. 2001). In addition, two studies have also shown significant reductions (Medina et al. 2000) or inverse associations (Belury et al. 2003) with circulating leptin levels.
Of these studies, however, only one has attempted to assess appetite effects of CLA in human subjects without significant findings (Medina et al. 2000).
In a recent review (Raben, 2002) of thirty-one short-term studies, fifteen studies demonstrated that low-GI foods reduce hunger or increase satiety, fourteen found no effect and two actually found lower satiety following the low-GI test compared with the high-GI test.
As with many areas of research, a wide variety of methodologies have been employed, making a systematic analysis of the key factors potentially accounting for differences difficult.
Certainly, the physiological profile of low-GI diets (slower gastric emptying, digestion and absorption, lower peak insulin and glucose followed by slower declines and less severe nadirs in glucose levels) would fit with scientific knowledge concerning appetite suppression (Pawlak et al. 2002).
Further well-controlled, appropriately powered, randomised intervention trials are needed to critically address this question (Astrup, 2002).
Effects of dietary fat and carbohydrate on appetite vary depending upon site and structure
British Journal of Nutrition (2004), 92, Suppl. 1, S23-S26
Nothing on "higher caloric levels", tho. Nor on the metabolic pathway or molecular mechanisms.
I haven't looked into it yet. My plate is full with this carb derived TAG thing.
I asked one of my profs today about carb derived TAGs but he didn't know either (re: temporary storage or VLDL particles).
If I can't find anything in the next day or two, I will try to track down a faculty member who works in this area and ask him/her.

This message is a reply to:
 Message 71 by Percy, posted 05-08-2008 2:27 PM Percy has replied

Replies to this message:
 Message 80 by Percy, posted 05-09-2008 8:53 AM molbiogirl has replied

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