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Author Topic:   Good Calories, Bad Calories, by Gary Taubes
Percy
Member
Posts: 22391
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.2


Message 16 of 451 (465096)
05-02-2008 11:23 PM
Reply to: Message 9 by molbiogirl
04-30-2008 11:38 AM


Re: Balanced Diets are Bunk
molbiogirl writes:
Refined carbohydrates are digested exceptionally quickly and cause blood sugar spikes which in turn cause the liver to release LDLs that initially carry a large payload of cholesterol.
Percy, can you peek at the cites at the back of the book and find a couple of papers I can look up re: this point?
Sure. The original researcher in this area was Ronald Krauss, here's one of the first papers:
Identification of multiple subclasses of plasma low density lipoproteins in normal humans. Ronald M. Krauss and David J. Burke. Journal of Lipid Research, Vol 23, 970194, January, 1982.
Here's a more recent one:
Properties of triglyceride-rich and cholesterol-rich lipoproteins in the remnant-like particle fraction of human blood plasma. Elisa Campos, Leila Kotite, Patricia Blanche, Yasushi Mitsugi, Philip H. Frost, Umesh Masharani, Ronald M. Krauss, and Richard J. Havel. Journal of Lipid Research, Vol 43, 365-374, March, 2002.
I have a feeling that individual papers aren't going to tell the whole story as the process is fairly complicated and probably took time to tease out.
Why are you asking, by the way? Is there something controversial about that characterization of the liver's response to elevated blood sugar levels?
--Percy

This message is a reply to:
 Message 9 by molbiogirl, posted 04-30-2008 11:38 AM molbiogirl has replied

Replies to this message:
 Message 18 by molbiogirl, posted 05-03-2008 1:15 AM Percy has replied

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


Message 17 of 451 (465097)
05-02-2008 11:44 PM
Reply to: Message 15 by molbiogirl
05-01-2008 10:39 AM


Re: Balanced Diets are Bunk
molbiogirl writes:
Stating categorically that refined carbs are very, very bad is just as deceptive as stating categorically that fats are very, very bad.
The problem with refined carbohydrates is that they're rapidly digested and cause blood sugar spikes, which in turn cause an insulin response from the pancreas, which in turn causes the liver to produce LDLs with a high payload of cholesterol. The eventual destiny of these LDLs is to give up their cholestrol and end up as small, dense LDLs which have a greatly heightened ability to leave deposits on blood vessel walls, and they have a deleterious effect generally on cell metabolism.
The cause of obesity is levels of insulin in combination with other hormones and a person's individual metabolism sufficient to encourage fat cells to emphasize the fatty acid=>triglyceride process, rather than the reverse triglyceride=>fatty acid process. Triglyerides are stored in the fat cells for later use as energy. Significantly, this process of storage of triglycerides in fat cells in the presence of insulin will take place at the expense of other demands of the body for energy, for example, hunger and exercise. And most importantly, the presence of fatty acids by themselves is insufficient to cause their net conversion into triglycerides - that takes insulin, whose levels are driven by blood sugar levels, whose levels are in turn driven by carbohydrate intake.
Glycemic index can be a very misleading measure of the goodness/badness of carbohydrates.
Then how does one distinguish between good and bad?
I don't really know. I was only pointing out that the glycemic index is very misleading. Whatever the right way is of "distinguishing between good and bad," that isn't it. Perhaps the presence of fiber is a better determinate of the goodness/badness of carbohydrates.
--Percy

This message is a reply to:
 Message 15 by molbiogirl, posted 05-01-2008 10:39 AM molbiogirl has replied

Replies to this message:
 Message 19 by molbiogirl, posted 05-03-2008 1:33 AM Percy has seen this message but not replied

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


(1)
Message 18 of 451 (465100)
05-03-2008 1:15 AM
Reply to: Message 16 by Percy
05-02-2008 11:23 PM


Re: Balanced Diets are Bunk
I have a feeling that individual papers aren't going to tell the whole story as the process is fairly complicated and probably took time to tease out.
Neither of your cites has anything to do with insulin.
The first talks about different kinds of LDL particles.
The second talks about how to measure LDL levels.
Both cites are open access, so you can read them if you'd like.
Why are you asking, by the way? Is there something controversial about that characterization of the liver's response to elevated blood sugar levels?
Because you (and the author) claim that insulin levels are related to elevated LDL levels.
The problem with refined carbohydrates is that they're rapidly digested and cause blood sugar spikes, which in turn cause an insulin response from the pancreas, which in turn causes the liver to produce LDLs with a high payload of cholesterol. The eventual destiny of these LDLs is to give up their cholestrol and end up as small, dense LDLs which have a greatly heightened ability to leave deposits on blood vessel walls, and they have a deleterious effect generally on cell metabolism.
Insulin spikes are perfectly normal.
It's the link to LDL and CHD that are in question.
I can't find any supporting evidence in the literature.
I did find this:
No consensus has been obtained for the notion that hyperinsulemia or insulin resistance contributes significantly to the risk of coronary heart disease (CHD) similarly to major risk factors, high total and LDL cholesterol, elevated blood pressure, smoking, low HDL cholesterol, diabetes and aging.
Metabolic Syndrome in the 21st Century, Jose Antonio Gutierrez, 2005.
Available here.
I have also found plenty of evidence that insulin suppresses VLDL synthesis (VLDL = the small, dense LDLs you mention).
Durrington PN, Newton RS, Weinstein DB, Steinberg D. 1982 Effects of insulin and glucose on very low density lipoprotein triglyceride secretion by cultured rat hepatocytes. J Clin Invest. 70:63-73.
Patsch W, Franz S, Schonfeld G. 1983 Role of insulin in lipoprotein secretion by cultured rat hepatocytes. J Clin Invest. 71:1161-1174.
Lewis GF, Uffelman KD, Szeto LW, Steiner GP. 1993 Effects of acute hyperinsulinemia on VLDL triglyceride and VLDL apoB production in normal weight and obese individuals. Diabetes. 42:833-842.
Lewis GF, Uffelman KD, Szeto LW, Weller B, Steiner G. 1995 Interaction between free fatty acids and insulin in the acute control of very low density lipoprotein production in humans. J Clin Invest. 95:158-166.
Nor have I found any evidence for the notion that ...
The cause of obesity is levels of insulin ...
If you can find any other cites in the book, that would help. I would love to look at the author's evidence.
I have a feeling that individual papers aren't going to tell the whole story as the process is fairly complicated and probably took time to tease out.
I'd be happy with a paper that gives me just a piece of the puzzle. Something that looks at insulin and LDL levels, for example.
Edited by molbiogirl, : No reason given.

This message is a reply to:
 Message 16 by Percy, posted 05-02-2008 11:23 PM Percy has replied

Replies to this message:
 Message 20 by Percy, posted 05-03-2008 8:42 AM molbiogirl has replied

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


Message 19 of 451 (465102)
05-03-2008 1:33 AM
Reply to: Message 17 by Percy
05-02-2008 11:44 PM


Re: Balanced Diets are Bunk
The problem with refined carbohydrates is that they're rapidly digested and cause blood sugar spikes, which in turn cause an insulin response from the pancreas, which in turn causes the liver to produce LDLs with a high payload of cholesterol. The eventual destiny of these LDLs is to give up their cholestrol and end up as small, dense LDLs which have a greatly heightened ability to leave deposits on blood vessel walls, and they have a deleterious effect generally on cell metabolism.
The cause of obesity is levels of insulin in combination with other hormones and a person's individual metabolism sufficient to encourage fat cells to emphasize the fatty acid=>triglyceride process, rather than the reverse triglyceride=>fatty acid process. Triglyerides are stored in the fat cells for later use as energy. Significantly, this process of storage of triglycerides in fat cells in the presence of insulin will take place at the expense of other demands of the body for energy, for example, hunger and exercise. And most importantly, the presence of fatty acids by themselves is insufficient to cause their net conversion into triglycerides - that takes insulin, whose levels are driven by blood sugar levels, whose levels are in turn driven by carbohydrate intake.
I addressed a couple of these points in my previous post, but I'd like to add one more thing.
To jump from "glucose = insulin spike" to "insulin = LDL" to "insulin = CHD risk factor" is way off the deep end.
As is "insulin + hormones/metabolism = obesity".
My point is, the author has jumped the gun big time. His theories aren't supported by the evidence. And if his theories aren't supported by the evidence, what are we to make of them?
His book sounds like it's just another in a long line of scare tactic diet books.
In fact, it sounds an awful lot like Eat Right For Your (Blood) Type.

This message is a reply to:
 Message 17 by Percy, posted 05-02-2008 11:44 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 20 of 451 (465117)
05-03-2008 8:42 AM
Reply to: Message 18 by molbiogirl
05-03-2008 1:15 AM


Re: Balanced Diets are Bunk
molbiogirl writes:
Neither of your cites has anything to do with insulin.
You didn't ask about insulin. This was your original question in Message 9:
molbiogirl in Message 9 writes:
Refined carbohydrates are digested exceptionally quickly and cause blood sugar spikes which in turn cause the liver to release LDLs that initially carry a large payload of cholesterol.
Percy, can you peek at the cites at the back of the book and find a couple of papers I can look up re: this point?
Your inquiry didn't mention insulin, so there should be no surprise that the papers I provided don't mention insulin.
So I guess the real issue is that your questioning this assertion:
Because you (and the author) claim that insulin levels are related to elevated LDL levels.
I don't understand why this is controversial, either. Just a simple Google reveals this in Wikipedia's article on LDL's:
Wikipedia writes:
Dietary Insulin induces HMG-CoA reductase activity, whereas glucagon downregulates it. [7]
I've not heard of "HMG-CoA reductase", but apparently it encourages the production of LDL's.
(VLDL = the small, dense LDLs you mention).
In my early reading I thought this was true myself, but I was never able to establish that this was actually the case, and Wikipedia seems to agree that they are distinct entities, e.g. from the same article:
Wikipedia writes:
LDL is formed as VLDL lipoproteins lose triglyceride through the action of lipoprotein lipase (LPL) and become smaller and denser, containing a higher proportion of cholesterol.
So if LDL is formed from VLDL, VLDL shouldn't really be considered one of the sub-forms of LDL. But maybe it is thought of that way in some circles. There's a degree of ambiguity concerning this in what I've read so far.
But if VLDL is actually small, dense LDLs as you claim, then I think you believe I'm in effect claiming that insulin encourages VLDL synthesis, because you say this:
I have also found plenty of evidence that insulin suppresses VLDL synthesis
But I'm not sure VLDL and small, dense LDLs and the same thing, so I'm not sure I'm making the claim you think I am. I just don't know.
No consensus has been obtained for the notion that hyperinsulemia or insulin resistance contributes significantly to the risk of coronary heart disease (CHD) similarly to major risk factors, high total and LDL cholesterol, elevated blood pressure, smoking, low HDL cholesterol, diabetes and aging.
Metabolic Syndrome in the 21st Century, Jose Antonio Gutierrez, 2005.
One of the complaints in the book is that health research has become specialized to the point where there is little exchange of information between the various disciplines, and one of the many regrettable effects is a lack of consensus, so Taubes certainly agrees that there is no consensus. But he presents the evidence that supports a connection between hyperinsulemia and heart disease.
I'd be happy with a paper that gives me just a piece of the puzzle. Something that looks at insulin and LDL levels, for example.
I'm not a health researcher and would prefer to debate on the basis of arguments offered here about the processes involved, with references to papers provided only for reinforcement, which is what the Forum Guidelines attempt to encourage (see rules 4 and 5). For example, you cite four papers in support of your position but offer no argument in your own words. If you describe what you think is really happening in the body then I'll have something more concrete to go on.
--Percy

This message is a reply to:
 Message 18 by molbiogirl, posted 05-03-2008 1:15 AM molbiogirl has replied

Replies to this message:
 Message 22 by molbiogirl, posted 05-03-2008 3:28 PM Percy has replied

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


Message 21 of 451 (465127)
05-03-2008 11:02 AM


MSG and Obesity
As one might imagine, I've been playing with applying the lessons of Good Calories, Bad Calories by reducing my intake of carbohydrates. I attempt to keep it below 100 grams/day, and I'm probably somewhere in that ballpark.
One of the problems with traditional diets is hunger. As any obesity researcher who accepts the conventional wisdom that obesity is caused by consuming more calories than are used will tell you, diets don't work, primarily because very few can endure hunger for lengthy periods without surrendering to it, and this has been my own experience.
One of the seemingly contradictory qualities of a low carbohydrate diet is that one does not get hungry on it, even when eating very little (it's 10:30 AM, I haven't had breakfast yet because I'm simply not hungry), but I didn't know that going in, so once I decided to reduce my carbohydrate intake, I immediately set out to address the problem of what to snack on to alleviate what I thought would be the inevitable hunger pangs. I hit upon meat snacks, generally very low in carbohydrates and sugar.
Naturally since I was following no diet book the structure of my diet took a while to form itself, and in the early stages I was consuming more vegetables and less meat than I am now, and I was less aware of the carbohydrate contributions of some foods, like sweet pickles that had been a common resort when I needed to hold off hunger. I was also less strict about staying away from rice and potatoes.
What I found was that even small amounts of rice and potatoes are fatal to the diet, and that you have to be careful with some vegetables (still learning which ones), especially starchy vegetables or those low in fiber. I think younger people wouldn't have to be so strict, but the weight is harder to hold off as you grow older.
But it was the meat snacks that gave me the greatest surprise. Despite the low carbohydrate/sugar content on the labels, it quickly became evident that consuming meat snacks was counterproductive. But why?
I had set the meat snacks aside for a while, but a few days ago I had a few (well, it might have been more than a few), and within an hour I was suffering all the effects of MSG that I'm so familiar with.
For me, MSG ingestion is experienced as physical fatigue, drowsiness and brain fogginess. It's unmistakable. I immediately checked the meat snack labels for MSG and found it listed on one of the five. But that one meat snack all by itself, even if full of MSG, would be unlikely to cause such a strong effect, so I began investigating MSG and found that it's a sodium salt of glutamate (hence the name, monosodium glutamate), and that it's the glutamate that is the active element in body metabolism.
Glutamate can find it's way into our diet through more than just MSG, because it is a very common additive that appears in a number of different forms, such as hydrolyzed vegetable proteins and yeast extract, and it can be hidden under completely generic names like "spices" and "natural flavorings". Checking the other meat labels for these kinds of ingredients, I found:
  • Hydrolized soy corn
  • Hydrolized corn protein
  • Hydrolized corn and soy protein
  • Spices and flavorings
  • Flavorings
So potentially the meat snacks I had just consumed contained significant levels of glutamate. But why would glutamate cause physical fatigue, drowsiness and brain fogginess?
One way would be if glutamate caused insulin levels to increase. Insulin would trigger the fat cells to increase their uptake of fatty acids to store them as triglycerides, making less energy available for body metabolism and causing all the symptoms.
But does glutamate cause elevated insulin levels. There isn't much about this on the Internet, but I did find one study: Glutamate ingestion: the plasma and muscle free amino acid pools of resting humans. It found that 150 mg/kg of MSG caused a threefold increase in insulin levels after 15 minutes.
So if MSG elevates insulin levels, then MSG is another factor in obesity.
One obvious question is why I had not experienced the MSG response before this, since this wasn't the first time I had eaten the meat snacks. The answer is that I had always consumed them just before going to bed, and so wouldn't notice the MSG effects as I fall asleep very quickly, and the MSG would only aid the process. But this time my Internet was out and I was waiting for the Internet service person in the middle of the afternoon.
So no more meat snacks, and my favorite sausage patty also lists MSG, so I'm debating that one. But I'm wondering if anyone out there has more information about glutamates in foods and their effects on body metabolism.
--Percy

Replies to this message:
 Message 26 by molbiogirl, posted 05-04-2008 5:50 AM Percy has replied

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


Message 22 of 451 (465145)
05-03-2008 3:28 PM
Reply to: Message 20 by Percy
05-03-2008 8:42 AM


Re: Balanced Diets are Bunk
Your inquiry didn't mention insulin, so there should be no surprise that the papers I provided don't mention insulin.
I thought it was clear that my question concerned the link between insulin and LDL/CHD.
Here's a brief summary of HDL/LDL/VLDL.
HDL High-density lipoprotein
* Makes up 20%-30% of total cholesterol
* The “good” cholesterol
* Moves cholesterol from arteries to the liver.
LDL Low-density lipoprotein
* Makes up 60%-70% of total cholesterol
* Main form of “bad” cholesterol
* Causes build up of plaque inside arteries.
VLDL Very-low-density lipoprotein
* Makes up 10%-15% of total cholesterol
* With LDL, the main form of “bad” cholesterol
* A precursor of LDL
Making sense of cholesterol tests - Harvard Health
Here's a picture of the pathway.
Please note that VLDL is a precursor of LDL. Therefore, anything that suppresses the biosynthesis of VLDL will necessarily suppress the biosynthesis of LDL.
And insulin suppresses VLDL biosynthesis.
Specifically, the results of studies, both in vitro and in vivo have demonstrated that insulin acutely inhibits hepatic (liver) VLDL secretion.
Hyperinsulinemia and in vivo very-low-density lipoprotein-triglyceride kinetics, Am J Physiol Endocrinol Metab 246: E187-E192, 1984.
Percy writes:
I've not heard of "HMG-CoA reductase", but apparently it encourages the production of LDL's.
HMG coA is part of the mevalonate pathway.
Please note that insulin upregulates the LDL receptor gene, not the synthesis of LDL particles. (The dotted lines on the left refer to insulin's role in the pathway.)
Percy writes:
But I'm not sure VLDL and small, dense LDLs and the same thing, so I'm not sure I'm making the claim you think I am. I just don't know.
It appears that I was wrong. VLDL particles are not the same as small, dense LDL particles.
LDL particles are heterogeneous respective sizes, densities, and lipid compositions. LDL particles have been divided into 2 distinct phenotypes: pattern A, with a higher proportion of large, more buoyant LDL particles, and pattern B, with a predominance of small dense LDL particles.
Small Dense Low-Density Lipoproteins and Other Risks to CHD
However, small, dense LDLs cannot be reliably measured.
There is no standardization of the methods for assessment of small dense LDL, so different assays can give different results, with agreement between methods in only 8% of patients.
So they measure VLDL levels and TG levels.
Samples from the Familial Metabolic Syndrome Study in Saxony were used to assess the determinants of small dense LDL levels. After correction for degree of hyperglycemia, hyperinsulinemia, age, gender and BMI the strongest correlates of particle size were the levels of VLDL triglyceride or plasma triglycerides (TG).
Detection of small dense LDL-cholesterol: is it necessary to determine particle size? http://www.futuremedicine.com/...pdf/10.2217/17460875.3.1.23
But the fact remains. Insulin downregulates VLDL biosynthesis; therefore, it necessarily downregulates LDL biosynthesis.
Percy writes:
But he presents the evidence that supports a connection between hyperinsulemia and heart disease.
Hyperinsulemia is insulin resistance.
wiki writes:
Insulin resistance is the condition in which normal amounts of insulin are inadequate to produce a normal insulin response from fat, muscle and liver cells.
Insulin resistance in fat cells results in elevated hydrolysis of stored triglycerides ... Increased mobilization of stored lipids in these cells elevates free fatty acids in the blood plasma.
Insulin resistance in muscle cells reduces glucose uptake (and therefore increases local storage of glucose as glycogen), whereas insulin resistance in liver cells reduces storage of glycogen, making it unavailable for release into the blood when blood insulin levels fall.
High plasma levels of insulin and glucose due to insulin resistance often lead to metabolic syndrome and type 2 diabetes.
Metabolic syndrome (aka Syndrome X) is a combination of medical disorders that increase the risk of developing cardiovascular disease and diabetes.
A blood sugar spike (and its attendant insulin release) is not the same thing as insulin resistance.
The cause of insulin resistance is largely unknown, but it tends to run in families, suggesting a strong genetic component.
3 mutations are associated with hyperinsulemia: insulin receptor mutations (Donohue Syndrome), LMNA mutations (Familial Partial Lipodystrophy) and mitochondrial mutations.
All 3 are heritable, of course.
Here's a brief summary of the mitochondrial mutations and their link to hyperinsulemia.
To explore the metabolic origin of insulin resistance, Shulman and his colleagues recruited young healthy volunteers who tested positive for insulin resistance and who were the offspring of patients with type 2 diabetes. They also recruited a second, control group of volunteers who exhibited insulin sensitivity who were matched for age, height, weight and physical activity.
According to Shulman, the researchers had to distinguish between two possible causes of the fat accumulation in the muscle that could trigger insulin resistance.
“Either there were defects in the fat cells, called adipocytes, in which there was increased release of fatty acids to muscle cells,” said Shulman.
“And/or, there was a defect in mitochondrial function in the muscle cells which would lead to decreased metabolism of these fatty acids. So, we designed the study to look at both of these possibilities.”
“We found that these lean insulin-resistant offspring”who have a high probability of later developing type 2 diabetes”had muscle insulin resistance, but no detectable abnormalities in their fat cells compared to the insulin-sensitive subjects,” said Shulman.
“Using this method we found that rates of ATP production in the muscles of the insulin-resistant offspring was decreased by thirty percent compared to normal subjects,” said Shulman.
Shulman and his colleagues are now performing muscle biopsy studies to determine whether the mitochondrial impairments are due to defects in the mitochondria themselves, or due to a reduced number of mitochondria in the subjects' cells.
It is important to distinguish between hyperinsulemia and normal insulin response (which is all a blood sugar spike induces -- a perfectly normal insulin response).
If you could post a couple of cites that support the author's assertion that a normal insulin response (not hyperinsulemia) is linked to elevated LDL levels (either form -- A or B), that would be great. Or a cite that supports the author's contention that a blood sugar spike (and its perfectly normal insulin response) is directly linked to CHD.

This message is a reply to:
 Message 20 by Percy, posted 05-03-2008 8:42 AM Percy has replied

Replies to this message:
 Message 23 by Percy, posted 05-03-2008 8:41 PM molbiogirl has replied

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


Message 23 of 451 (465175)
05-03-2008 8:41 PM
Reply to: Message 22 by molbiogirl
05-03-2008 3:28 PM


Re: Balanced Diets are Bunk
molbiogirl writes:
I thought it was clear that my question concerned the link between insulin and LDL/CHD.
Check the message links. I was responding to your inquiry in Message 9, which preceded the first mention of insulin in the thread.
Taubes agrees with you that VLDL is a precursor of LDL, this is from page 175:
Taubes writes:
As for secretion, the key point is that most low-density lipoproteins, LDL, begin their lives as very low-density lipoproteins, VLDL. (This was one implication of the observation that both LDL and VLDL are composed of the same apo B protein, and it was established beyond reasonable doubt in the 1970s.) This is why VLDL is now commonly referred to as a precursor of LDL, and LDL as a remnant of VLDL.
But you're right that I explained it incorrectly. What Taubes is actually saying is that blood sugar spikes encourage the liver to temporarily store fatty acids away as triglycerides, and these are later released into the bloodstream as VLDLs.
If you're saying that the release of VLDLs doesn't occur while insulin levels are high, this is certainly consistent with Taubes' description as he isn't specific on this point. What he does say is that once triglycerides are stored in the liver that their release is inevitable. The more often you spike your blood sugar, the more often the liver will sock away triglycerides, and the more VLDLs the liver will eventually produce.
What insulin does do more directly is influence fat cells to tilt the balance of conversion back and forth between fatty acids and triglycerides toward the production of triglycerides, which means you get fatter independent of any energy demands from the body in terms of hunger or exercise. In other words, even if you're starving, or even if you're in the middle of 5 set tennis match under a hot sun, if you elevate your insulin levels then fat cells will steal from the rest of the body by gobbling up the available fatty acids that other cells (muscle cells, for example) might use for energy.
Probably Taubes' most important point is that the conventional wisdom about obesity, that it is a simple result of too many calories in and too few calories out, that the obese simply eat too much and exercise too little, is wrong. Exercise, hunger and fat storage are not independent variables. If you exercise more you'll eat more. If you eat less you'll exercise less. The willpower necessary to overcome this reality is in limited supply for most people.
--Percy

This message is a reply to:
 Message 22 by molbiogirl, posted 05-03-2008 3:28 PM molbiogirl has replied

Replies to this message:
 Message 24 by molbiogirl, posted 05-03-2008 10:17 PM Percy has replied

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


Message 24 of 451 (465184)
05-03-2008 10:17 PM
Reply to: Message 23 by Percy
05-03-2008 8:41 PM


Re: Balanced Diets are Bunk
What Taubes is actually saying is that blood sugar spikes encourage the liver to temporarily store fatty acids away as triglycerides, and these are later released into the bloodstream as VLDLs.
First. Glucose is stored in the liver as glycogen, not triglycerides. Glycogen is a complex carbohydrate. A triglyceride is a fat, formed from three fatty-acid molecules and one glycerol molecule. Triglycerides are stored in adipose tissue.
Second. There are "triglyceride storage diseases" that result in fatty deposits in the liver. But these are not related to blood sugar spikes. They are metabolic defects.
Third. Blood sugar spikes don't "encourage" anything but an insulin response. If you have evidence to the contrary, I would be interested in hearing it.
Fourth. The release of glycogen as VLDL is not "inevitable". Glycogen is released from the liver as glucose, not VLDL.
Fifth. FFAs are released from adipose tissue (fat), not the liver.
Sixth. FFAs are packaged into VLDL by the liver ... from blood plasma FFAs derived from dietary fat, not carbohydrates.
In the absence of insulin (in other words, when you haven't eaten or you're exercising a lot), the action of its counter hormone glucagon is dominant.
Glucagon stimulates the liver to provide glucose for the rest of the body, initially via glycogenolysis (breaking down glycogen) and later by gluconeogenesis (making new glucose) as liver glycogen supplies are depleted.
To provide the energy (ATP) needed for gluconeogenesis the liver oxidizes fats derived from the adipose tissue.
In the absence of insulin, the adipose hormone sensitive lipase is active, releasing fatty acids (from adipose tissue) to the blood, where they are transported in association with albumen to the liver (and other tissues).
http://www.usd.edu/...ept/biochem/courses/bioc520/b520c6.htm
Here's a picture:
(Note: Acetyl CoA derived from glycogen stores in the liver can be used to synthesize FFAs (box at top of figure). Acetyl CoA is produced when it is needed for fatty acid synthesis, but normally the gene is inactive and has certain transcriptional factors that activate transcription when necessary. Necessary means when there's a shortage of FFAs.)
What insulin does do more directly is influence fat cells to tilt the balance of conversion back and forth between fatty acids and triglycerides toward the production of triglycerides...
Elevated TG levels are correlated to insulin resistance, not normal insulin response. In other words, hyperinsulemia is correlated to elevated TGs, not blood sugar spikes. And, as I said before, the causes of hyperinsulemia are probably genetic, not behavioral (aka carb intake).
In other words, even if you're starving, or even if you're in the middle of 5 set tennis match under a hot sun, if you elevate your insulin levels then fat cells will steal from the rest of the body by gobbling up the available fatty acids that other cells (muscle cells, for example) might use for energy.
When under stress from starvation, the body uses protein and fat as energy. Because no glucose is available.
When under stress from overexertion, the body uses glycogen stores in the liver. That's just plain old glucose.
(Glycogen is also stored in the muscles. It is used up in the first 10 minutes or so of heavy exercise, tho.)
Fat cells (adipose tissue) don't "steal" anything from anywhere. They are storage depots. That is all.
Probably Taubes' most important point is that the conventional wisdom about obesity, that it is a simple result of too many calories in and too few calories out, that the obese simply eat too much and exercise too little, is wrong.
I have yet to see any evidence of that.
If you'd like to post some cites, I'd be happy to read the papers.

This message is a reply to:
 Message 23 by Percy, posted 05-03-2008 8:41 PM Percy has replied

Replies to this message:
 Message 27 by Percy, posted 05-04-2008 9:11 AM molbiogirl has replied

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


Message 25 of 451 (465227)
05-04-2008 5:25 AM
Reply to: Message 1 by Percy
04-17-2008 11:22 AM


NYT review
Good Calories, Bad Calories - Gary Taubes - Books - Review - The New York Times
But the problem with a book like this one, which goes on and on in great detail about experiments new and old in areas ranging from heart disease to cancer to diabetes, is that it can be hard to know what has been left out.
For example, Taubes argues at length that people get fat because carbohydrates in their diet drive up the insulin level in the blood, which in turn encourages the storage of fat. His conclusion: all calories are not alike. A calorie of fat is much less fattening than a calorie of sugar.
It’s known, though, that the body is not so easily fooled.
Taubes ignores what diabetes researchers say is a body of published papers documenting a complex system of metabolic controls that, in the end, assure that a calorie is a calorie is a calorie.
He also ignores definitive studies done in the 1950s and ’60s by Jules Hirsch of Rockefeller University and Rudolph Leibel of Columbia, which tested whether calories from different sources have different effects.
The investigators hospitalized their subjects and gave them controlled diets in which the carbohydrate content varied from zero to 85 percent, and the fat content varied inversely from 85 percent to zero. Protein was held steady at 15 percent.
They asked how many calories of what kind were needed to maintain the subjects’ weight. As it turned out, the composition of the diet made no difference.
My point exactly.
Here's insulin signaling.
KEGG PATHWAY Database
I'm not going to post the carbohydrate diagrams. There are too many.
Here's a list, tho.
1.1 Carbohydrate Metabolism
Glycolysis / Gluconeogenesis
Citrate cycle (TCA cycle)
Pentose phosphate pathway
Pentose and glucuronate interconversions
Fructose and mannose metabolism
Galactose metabolism
Ascorbate and aldarate metabolism
Starch and sucrose metabolism
Aminosugars metabolism
Nucleotide sugars metabolism
Pyruvate metabolism
Glyoxylate and dicarboxylate metabolism
Propanoate metabolism
Butanoate metabolism
C5-Branched dibasic acid metabolism
Inositol metabolism
Inositol phosphate metabolism
Each of those is just as hairy looking as insulin signaling. And they are all interconnected.
Same story for lipid metabolism.
That KEGG site is worth a look.
NYT writes:
Cascades are especially common in medicine as doctors take their cues from others, leading them to overdiagnose some faddish ailments (called bandwagon diseases) and overprescribe certain treatments (like the tonsillectomies once popular for children).
He acknowledges that that hypothesis is unproved, and that the low-carb diet fad could turn out to be another mistaken cascade.
Second NYT article.

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 Message 1 by Percy, posted 04-17-2008 11:22 AM Percy has replied

Replies to this message:
 Message 28 by Percy, posted 05-04-2008 9:36 AM molbiogirl has not replied

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


Message 26 of 451 (465228)
05-04-2008 5:50 AM
Reply to: Message 21 by Percy
05-03-2008 11:02 AM


Re: MSG and Obesity
Here's the glutamate pathway.
Each of those numbers refers to another metabolic pathway. For a more realistic picture, check this out:
Object not found!
It's truly stunning.
Glutamate is used for a lot of things.
A metabolite isn't an on/off switch. It just isn't.
If you'd like to browse scholar.google, "glutamate metabolism review" produced a lot of useful articles. So did "monosodium glutamate metabolism review".
Edited by Admin, : Fix image width.

This message is a reply to:
 Message 21 by Percy, posted 05-03-2008 11:02 AM Percy has replied

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 Message 29 by Percy, posted 05-04-2008 9:44 AM molbiogirl has not replied

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


Message 27 of 451 (465236)
05-04-2008 9:11 AM
Reply to: Message 24 by molbiogirl
05-03-2008 10:17 PM


Re: Balanced Diets are Bunk
molbiogirl writes:
First. Glucose is stored in the liver as glycogen, not triglycerides. Glycogen is a complex carbohydrate. A triglyceride is a fat, formed from three fatty-acid molecules and one glycerol molecule. Triglycerides are stored in adipose tissue.
It might be best to quote Taubes again. This is from page 175 again:
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.
So you're disputing that the liver converts glucose into triglycerides, so we can look into that. Do you agree with the other portions of the described process, i.e., that the liver does store triglycerides that are later released as VLDLs? In other words, is it just the production of triglycerides from "some glucose" that you dispute, or the entire process?
Third. Blood sugar spikes don't "encourage" anything but an insulin response. If you have evidence to the contrary, I would be interested in hearing it.
Taubes says, "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." He appears to be saying that the presence of a great deal of glucose influences the liver to use some of it for triglyceride production and storage. In conjunction with your earlier point, you seem to not only disagree that the liver creates triglycerides from glucose, but that that point aside, blood sugar spikes don't cause any response anywhere except the pancreas, which produces insulin.
Fourth. The release of glycogen as VLDL is not "inevitable". Glycogen is released from the liver as glucose, not VLDL.
This is one point that I didn't manage to garble. Both mine and Taubes' descriptions said that triglycerides, not glycogen, are released in VLDL.
Fifth. FFAs are released from adipose tissue (fat), not the liver.
This is another point upon which both I and Taubes were clear. Neither of us said that free fatty acids are released from the liver.
Sixth. FFAs are packaged into VLDL by the liver ... from blood plasma FFAs derived from dietary fat, not carbohydrates.
Taubes says that it is triglycerides that are packaged into VLDL, not FFAs. I'm poking around in Wikipedia trying to understand this stuff better, and in the Wikipedia article on triglycerides it says, "Fat and liver cells can synthesize and store triglycerides."
So I presume that the formation of triglycerides in the liver is not controversial, so I guess what you're disputing is that it is actually FFAs that are packaged into VLDLs, not triglycerides. But the same Wikipedia article also says, "Triglycerides, as major components of very low density lipoprotein (VLDL) and chylomicrons, play an important role in metabolism as energy sources and transporters of dietary fat."
Did you really mean to say FFAs? Did you instead mean trigylcerides (for any lurkers, triglycerides are formed from binding together three FFAs (Free Fatty Acids))?
As far as I can see, the description about the liver, insulin and glucagon that you took from GLYCOGEN, GLUCONEOGENESIS, FATTY ACID METABOLISM AND HORMONAL CONTROL OF LIPID AND CARBOHYDRATE METABOLISM is orthogonal to the discussion. If there's a relationship between this and our discussion about the production of VLDL by the liver it is not apparent to me.
I took a look at your diagram, here it is again for reference:
The top box in the diagram labeled "Liver" seems consistent with Taubes description of glucose having a role in the production of VLDL. While it doesn't describe the fatty acids as triglycerides, it doesn't describe them as free fatty acids, either, so since the diagram isn't specific on this point it is again consistent with Taubes description, and if Wikipedia is correct, the liver can synthesize and store triglycerides.
What insulin does do more directly is influence fat cells to tilt the balance of conversion back and forth between fatty acids and triglycerides toward the production of triglycerides...
Elevated TG levels are correlated to insulin resistance, not normal insulin response. In other words, hyperinsulemia is correlated to elevated TGs, not blood sugar spikes. And, as I said before, the causes of hyperinsulemia are probably genetic, not behavioral (aka carb intake).
Are you talking about elevated TG levels in the bloodstream? I don't believe Taubes makes any claims about insulin's influence on triglyceride levels in the bloodstream, and if he does then I missed them. I certainly wasn't trying to say anything about insulin's influence on TG levels in the bloodstream.
What I was saying, in shorthand form since I had said the same thing at greater length and with more clarity in prior posts, is that insulin influences fat cells to tilt the balance of their continual conversion back and forth between FFAs and triglycerides toward the FFA=>triglyceride process, resulting in the fat cell making a net drain upon FFAs in the bloodstream.
When under stress from starvation, the body uses protein and fat as energy. Because no glucose is available.
You can prove to yourself that the absence of intake of glucose in the form of carbohydrates isn't stress or starvation with a simple personal experiment: Eat only meat for an entire week.
When under stress from overexertion, the body uses glycogen stores in the liver. That's just plain old glucose.
The body can draw upon glucose, fatty acids and protein for energy. In the absence of insulin the fat cells in the body will tilt the balance of the FFA/triglyceride conversion process toward the production of FFAs which are released into the bloodstream for use as energy.
Later today I'll be playing tennis for a couple hours and will be experiencing no physical duress after having consumed less than 100 grams/day of carbohydrates for the past few weeks.
Fat cells (adipose tissue) don't "steal" anything from anywhere. They are storage depots. That is all.
In the presence of insulin, fat cells are a net drain upon fatty acids in the blood stream as they convert it to stored triglycerides.
Probably Taubes' most important point is that the conventional wisdom about obesity, that it is a simple result of too many calories in and too few calories out, that the obese simply eat too much and exercise too little, is wrong.
I have yet to see any evidence of that.
So in light of the national experience over the past century with obesity, diabetes and heart disease, how's your theory that it's primarily due to dietary fat working out for you?
--Percy

This message is a reply to:
 Message 24 by molbiogirl, posted 05-03-2008 10:17 PM molbiogirl has replied

Replies to this message:
 Message 30 by molbiogirl, posted 05-04-2008 2:53 PM Percy has replied

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


Message 28 of 451 (465238)
05-04-2008 9:36 AM
Reply to: Message 25 by molbiogirl
05-04-2008 5:25 AM


Re: NYT review
Hi Molbiogirl,
I'm not going to debate a book review. If you'd like to state your objections in your own words I'd be glad to address them, as I have been. But I will say a couple things about the book review.
Taubes' book is lengthy and detailed, but even a book of 10,000 pages couldn't mention everything, so criticizing it because "it can be hard to know what has been left out" is a criticism without merit because it can be leveled at literally anything written.
Along the same lines, criticizing Taubes for not mentioning a specific series of studies by Jules Hirsch in the 1950s and '60's when Taubes mentions Hirsch and his views (very antagonistic toward the carbohydrate hypothesis, of course) copiously throughout the book is pretty misleading. Taubes' index for "Hirsch, Jules" lists these pages: 245-6, 256-7, 270-1, 282, 299, 398, 415, 420-1, 422. He by no means ignores Hirsch or his views.
I'm afraid that your description involving insulin signaling was so sketchy, really non-existent being primarily just a diagram and a list of processes, that I can't tell what point you were trying to make.
--Percy

This message is a reply to:
 Message 25 by molbiogirl, posted 05-04-2008 5:25 AM molbiogirl has not replied

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


Message 29 of 451 (465240)
05-04-2008 9:44 AM
Reply to: Message 26 by molbiogirl
05-04-2008 5:50 AM


Re: MSG and Obesity
Thanks for the information and research suggestions, but I'm just a layperson in this area. I don't think I could muster the time, and certainly not the expertise, to understand this area at the same level of detail as the researchers.
I understand that glutamate is a key part of many metabolic processes, and I know there is widespread doubt in the research community that MSG reactions are real, but something significant is definitely going on. I'm willing to accept any number of explanations, but "it's all in your imagination" is not one of them.
--Percy
Edited by Percy, : Grammar.
Edited by Percy, : Grammar again.

This message is a reply to:
 Message 26 by molbiogirl, posted 05-04-2008 5:50 AM molbiogirl has not replied

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


(1)
Message 30 of 451 (465263)
05-04-2008 2:53 PM
Reply to: Message 27 by Percy
05-04-2008 9:11 AM


Re: Balanced Diets are Bunk
So you're disputing that the liver converts glucose into triglycerides, so we can look into that.
The top box in the diagram labeled "Liver" seems consistent with Taubes description of glucose having a role in the production of VLDL.
No. I am not disputing that the liver can biosynthesize triglycerides from glucose. If you will recall ...
(Note: Acetyl CoA derived from glycogen stores in the liver can be used to synthesize FFAs (box at top of figure). Acetyl CoA is produced when it is needed for fatty acid synthesis, but normally the gene is inactive and has certain transcriptional factors that activate transcription when necessary. Necessary means when there's a shortage of FFAs.)
That is the "liver box at the top".
I need to rearrange your post a bit to try and untangle all this.
Taubes says that it is triglycerides that are packaged into VLDL, not FFAs.
An FFA is a part of a triglyceride. (The proper name of triglyceride is triacylglycerol.)
Free fatty acid = "Fatty acids can be bound or attached to other molecules, such as in triglycerides or phospholipids. When they are not attached to other molecules, they are known as "free" fatty acids.
The uncombined fatty acids or free fatty acids may come from the breakdown of a triglyceride into its components (fatty acids and glycerol)." (Wiki)
A triglycerides with its glycerol removed = 3 "free" fatty acids.
And triglycerides aren't "packaged" into anything except fat tissue.
FFAs are used in the packaging of VLDLs.
Percy quoting Taube 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."
Temporary storage, yes. In your adipose tissue (aka your butt and thighs). BUT THEY ARE NOT SYNTHESIZED FROM GLUCOSE. Not under ordinary conditions. Take a closer look at the wiki graf you quoted.
Here is the text in its entirety (broken into chunks and capped for clarity).
Triglycerides, as major components of very low density lipoprotein (VLDL) and chylomicrons, play an important role in metabolism as energy sources and transporters of DIETARY FAT.
Right off the bat it says: From dietary fat. Not from carbs.
They contain more than twice as much energy (9 kcal/g) as carbohydrates and proteins.
In the intestine, triglycerides (FROM DIETARY FAT) are split into glycerol and fatty acids (this process is called lipolysis) (with the help of lipases and bile secretions), which are then moved into the cells lining the intestines (absorptive enterocytes).
The triglycerides are rebuilt in the enterocytes from their fragments and packaged together with cholesterol and proteins to form chylomicrons. (IN THE LIVER).
These are excreted from the cells and collected by the lymph system and transported to the large vessels near the heart before being mixed into the blood.
Various tissues can capture the chylomicrons, releasing the triglycerides to be used as a source of energy.
Fat and liver cells can synthesize and store triglycerides.
Yes. Can synthesize. Not does synthesize as a normal part of carb metabolism. As I pointed out earlier, the genes for this process are INACTIVE (aka downregulated) and require a host of transcriptions factors (a cascade of signals from the body telling it to turn the gene on).
When the body requires fatty acids as an energy source, the hormone glucagon signals the breakdown of the triglycerides by hormone-sensitive lipase to release free fatty acids (FROM THE ADIPOSE TISSUE).
As the brain can not utilize fatty acids as an energy source, the glycerol component of triglycerides can be converted into glucose, via gluconeogenesis, for brain fuel when it is broken down. Fat cells may also be broken down for that reason, if the brain's needs ever outweigh the body's.
The brain runs on glucose and glucose alone. And the brain is the body's number one priority.
When the body is under stress (usually starvation), the adipose tissue is broken down into its component parts: FFAs and glycerol. The liver then takes the glycerol and manufactures glucose to send to the brain.
Here's a picture of glycolysis (breaking down glucose) and gluconeogenesis (making glucose).
Please note that they are simply the reverse of one another for the most part.
Glycolysis is the normal breakdown of glucose.
Gluconeogenesis happens only under starvation/overexertion conditions.
The body doesn't like to make sugar from fat. It is very metabolically expensive and it has as "side products" some pretty nasty things called ketone bodies.
Please also note that to make sugar, you have to start with pyruvate (at the bottom of the figure).
Please note that the glycerol from the triglyceride is converted into pyruvate.
OK.
Now that we have all that sorted out, let's unpack your Taube quote.
Taube 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.
No. It doesn't.
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 source of these triacylglycerols is dietary fat.
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.
This is perfectly normal. In fact, it is vital. Your body uses cholesterol in its cell membranes and to manufacture hormones.
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.
This is gobbledygook. There is no "for this reason". The name VLDL just describes the particle. That's all.
And a VLDL particle is perfectly normal. Like I said, your body needs cholesterol and VLDL/IDL/LDL/HDL is the way it moves cholesterol around the body so that it can be used in lots of very important metabolic processes.
Back to your post.
This is one point that I didn't manage to garble. Both mine and Taubes' descriptions said that triglycerides, not glycogen, are released in VLDL.
Triacylglycerols are not packaged into VLDL particles. FFAs are. And they come from dietary fat.
Here is your original quote.
What he does say is that once triglycerides are stored in the liver that their release is inevitable. The more often you spike your blood sugar, the more often the liver will sock away triglycerides, and the more VLDLs the liver will eventually produce.
No. Triacylglycerol is not stored in the liver.
If it is, you have liver disease.
Glycogen (which is just a complex carb made from glucose) is stored in the liver.
This is perfectly normal.
And, one more time, VLDLs are packaged by the liver from dietary fat.
You couldn't function without either glycogen in your iver or VLDL in your bloodstream.
Triacylglycerols, when released from adipose tissue, are used to manufacture sugar (from the glycerol) and as evergy (from the FFAs).
They are not packaged into VLDLs.
And their release is not inevitable. My big butt is evidence of that.
This is another point upon which both I and Taubes were clear. Neither of us said that free fatty acids are released from the liver.
FFAs are part of triacylglycerols.
What insulin does do more directly is influence fat cells to tilt the balance of conversion back and forth between fatty acids and triglycerides toward the production of triglycerides...
MBG writes:
Elevated TG levels are correlated to insulin resistance, not normal insulin response. In other words, hyperinsulemia is correlated to elevated TGs, not blood sugar spikes. And, as I said before, the causes of hyperinsulemia are probably genetic, not behavioral (aka carb intake).
Percy writes:
Are you talking about elevated TG levels in the bloodstream? I don't believe Taubes makes any claims about insulin's influence on triglyceride levels in the bloodstream, and if he does then I missed them. I certainly wasn't trying to say anything about insulin's influence on TG levels in the bloodstream.
You said that Taube said "insulin influences" adipose tissue to push toward a greater release of TAGs. This means "elevated TAGs". If the metabolic process is "pushed" toward one end, it is abnormal and TAG levels are increased above and beyond normal conditions.
And, as I said before, that is a marker of disease.
And insulin does not do that.
You can prove to yourself that the absence of intake of glucose in the form of carbohydrates isn't stress or starvation with a simple personal experiment: Eat only meat for an entire week.
Yes. To the body, it is starvation.
The brain runs only on glucose. (See above.) If you don't eat carbs, your body is under stress. It needs a heckuva lot of glucose to run your brain.
And by manufacturing glucose from fat (and by using only protein for energy for the other vital metabolic processes), you produce those nasty ketone bodies I mentioned earlier.
I'm sure you've heard of ketoacidosis. It's what killed Madeline Neumann.
wiki writes:
This happens in untreated Type I diabetes (see diabetic ketoacidosis), and also in alcoholics after binge drinking, subsequent starvation, and the alcohol-induced impairment of the liver's ability to generate glucose (see alcoholic ketoacidosis).
Percy writes:
The body can draw upon glucose, fatty acids and protein for energy.
Under normal conditions, only glucose and FFAs.
If you are using protein, you are starving.
wiki writes:
During starvation or a prolonged fasting state, the glycogen storage is used up and the level of insulin in the circulation is LOW and the level of glucagon is very high.
The main means of energy production is lipolysis (fat breakdown).
Gluconeogenesis (glucose manufacture -- above) converts glycerol and fatty acids via the TCA cycle via acetyl CoA to produce energy.
Proteolysis (protein breakdown -- the source is your muscles) provides alanine which also enters gluconeogenesis.
Lactate produced from pyruvate enters the gluconeogenesis pathway too.
Too much Acetyl CoA produces ketone bodies which can be detected in a urine exam. The brain starts to use ketone bodies as source of energy.
Percy writes:
In the absence of insulin the fat cells in the body will tilt the balance of the FFA/triglyceride conversion process toward the production of FFAs which are released into the bloodstream for use as energy.
See? You said it again. "Tilt toward TAGs". No, it does not. Not not not. Elevated TAGs = a disease condition, like hyperinsulemia.
Also. The body can manufacture lipids (not FFAs -- there's a difference). That's known as lipogenesis. But it does so in order to manufacture things like cell membranes. Again. A perfectly normal process.
The body DOES NOT manufacture FFAs from the dietary intake OF ANYTHING.
It digests dietary fat and RELEASES FFAs.
In the presence of insulin, fat cells are a net drain upon fatty acids in the blood stream as they convert it to stored triglycerides.
Percy, this just isn't true. Adipose tissue is just storage. Your body uses all the FFAs it needs then it socks away the excess.
Percy writes:
So in light of the national experience over the past century with obesity, diabetes and heart disease, how's your theory that it's primarily due to dietary fat working out for you?
Hey. If I could untangle the root cause(s) of the national obesity epidemic (by uncovering some heretofore unknown metabolic link or some such), I'd get the FN Nobel.
That doesn't mean that Taube isn't "idea-mining" legit scientific papers. He's ripping stuff out of context and completely distorting it.
And I'd like to remind you of something, Percy.
The French have historically had very low obesity rates and very low CHD rates. In fact, Taube mentions it in the book.
"The French Paradox".
The French have historically eaten LOADS of fat and LOADS of refined carbs. Just LOADS.
So.
Why, in the past year and a half, have French obesity rates doubled?

This message is a reply to:
 Message 27 by Percy, posted 05-04-2008 9:11 AM Percy has replied

Replies to this message:
 Message 31 by Percy, posted 05-04-2008 5:25 PM molbiogirl has replied
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