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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 31 of 451 (465277)
05-04-2008 5:25 PM
Reply to: Message 30 by molbiogirl
05-04-2008 2:53 PM


Re: Balanced Diets are Bunk
Maybe we need to break this down into smaller pieces. You say in response to Taubes' claim that triglycerides are packaged into VLDL:
Molbiogirl writes:
And triglycerides aren't "packaged" into anything except fat tissue.
The Wikipedia article on triglycerides says:
Wikipedia writes:
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.
Once we figure this one out we can move on to the next item.
--Percy

This message is a reply to:
 Message 30 by molbiogirl, posted 05-04-2008 2:53 PM molbiogirl has replied

Replies to this message:
 Message 32 by molbiogirl, posted 05-04-2008 8:59 PM Percy has replied

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


Message 32 of 451 (465286)
05-04-2008 8:59 PM
Reply to: Message 31 by Percy
05-04-2008 5:25 PM


Re: Balanced Diets are Bunk
Just to be clear. A chylomicron ≠ VLDL particle.
Chylomicron on the right. VLDL/IDL/HDL on the left.
How are chylomicrons formed?
* The triglycerides, phospholipids and cholesteryl esters are combined with an apolipoprotein, known as apolipoprotein (apo) B48, in the enterocyte. The lipoproteins formed in this manner are secreted into the lymph (chyle) and are termed chylomicrons.
* They are large (diameter >75 nm; density
What is the role of lipoprotein lipase?
Lipoprotein lipase is located on the vascular endothelium of tissues that have a high requirement for triglycerides, for example:
* skeletal and cardiac muscle (for energy);
* adipose tissue (for storage); and
* lactating mammary gland (for milk).
Lipoprotein lipase releases triglycerides from the core of the chylomicron by hydrolysing them to fatty acids and monoglycerides, which are taken up by the tissues locally.
In this way, the circulating chylomicron becomes progressively smaller, its triglyceride content decreases and it becomes relatively richer in cholesterol and proteins.
As the core shrinks, its surface materials (phospholipids, free cholesterol and apo Cs) become overcrowded and are transferred to HDL.
The relatively cholesterol ester-enriched, triglyceride-depleted product of chylomicron metabolism is known as the chylomicron remnant.
The apo B48, present from the time of assembly, remains tightly anchored to the core throughout.
http://www.cmglinks.com/asa/lectures/Part_2/lecture/2.htm
VLDL particles, on the other hand, contain 3 sorts of "apo" particles: apoB (100), apoC (I & II) and apoE. These apo particles are made of triglycerides, phospholipids, cholesterol and cholesteryl esters.
VLDL is the body's transport mechanism for these apo particles (which carry the TAGs, P-lipids and cholesterol).
Please note that the triacylglycerides are that yellow thing -- which represents the apo particles. The red thing represents the cholesterol. Don't take that representation of the particles literally. It's just drawn that way to show the proportions of the various components.
Here's another figure.
See the apo particles being added on the right to form the mature VLDL? See that the FFAs are immediately released by lipoprotein lipase?
OK.
Now to the "package" comment.
You will notice that I had no problem with Taube's description of apoB in my last post:
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.
Nor did I have any problem with this statement...
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.
...except to correct the source of the TAGs.
Also.
Take a look at this figure again. See FFAs in the "liver box" at the top? See how the arrow points to VLDL? See how the VLDL arrow points to adipocytes (fat cells)? See how the FFAs are PACKAGED into TAGS in the adipocytes?
One last thing.
Just for future reference, here are the 2 disease processes that Taube keeps talking about as if they were normal responses to carb intake: hypertriglyceremia and dyslipidemia.
Here's a comparison of normal VLDL metabolism and abnormal metabolism aka hypertriglyceridemia (hyper = too much ... triglyceride = TAGs ... emia = disease).
Those yellow and red balls are just to represent the proportions of the particle's components. They shouldn't be taken literally.
Hypertriglyceremia, btw, is what you keep talking about (elevated TAG levels).
The ppt slide also mentions the small, dense LDLs.
Here's a look at another abnormal metabolic cycle that produces the small, dense LDLs.
This is a dyslipidemia.
See the comment down in the lower left corner? "Fatty liver" aka adiposopathy?
If you have fatty liver, you have a disease. A very serious disease, actually.
OK.
Are we all set on VLDL and chylomicrons?
And do you concede that the FFAs that are used to produce the VLDL particles come from dietary fat and not carbs?
Edited by Admin, : Adjust image width.
Edited by Admin, : Typo.

This message is a reply to:
 Message 31 by Percy, posted 05-04-2008 5:25 PM Percy has replied

Replies to this message:
 Message 33 by Percy, posted 05-04-2008 9:21 PM molbiogirl has replied

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


Message 33 of 451 (465290)
05-04-2008 9:21 PM
Reply to: Message 32 by molbiogirl
05-04-2008 8:59 PM


Re: Balanced Diets are Bunk
I appreciate that you're going to a great deal of effort to make this clear for me, but I think the very long posts work against clarity. In addition, some of the things you're addressing have nothing to do with anything I or Taubes have said. I never mentioned chylomicron, that was just mentioned in passing in a paragraph of explanation about triglycerides from Wikipedia. And neither I nor Taubes ever claimed that (to use your words) "the FFAs that are used to produce the VLDL particles come from...carbs."
If you can just respond to Message 31 so we can resolve that issue then we can move on to the next item.
--Percy

This message is a reply to:
 Message 32 by molbiogirl, posted 05-04-2008 8:59 PM molbiogirl has replied

Replies to this message:
 Message 34 by molbiogirl, posted 05-04-2008 9:58 PM Percy has replied

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


Message 34 of 451 (465294)
05-04-2008 9:58 PM
Reply to: Message 33 by Percy
05-04-2008 9:21 PM


Re: Balanced Diets are Bunk
And neither I nor Taubes ever claimed that (to use your words) "the FFAs that are used to produce the VLDL particles come from...carbs."
I'm sorry, Percy, but yes you did.
Message 27.
The Taube quote.
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--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.
Here is what Taube said:
Carbs ’ TAGs ’ apoB (which is later incorporated into the mature VLDL -- see figure above)
Here is what really happens:
Fatty acids are usually ingested as triglycerides. They are broken down in the intestine into free fatty acids and monoglycerides by pancreatic lipase.
The short and medium chain fatty acids are then absorbed directly into the blood via intestinal capillaries. They then travel to a lot places -- one of which is the liver.
However, long chain fatty acids are too large to be directly absorbed by the tiny intestinal capillaries. Instead they are absorbed into the walls of the intestinal villi and reassembled again into triglycerides.
Once across the intestinal barrier, chylomicrons and VLDL particles are synthesized by the liver from the dietary fatty acids.
In summary.
Short and medium chain dietary fats: TAGs ’ FFAs ’ chylomicrons and VLDLs.
Long chain dietary fats: TAGs ’ FFAs ’ TAGs ’ chylomicrons and VLDLs.
Is that better?

This message is a reply to:
 Message 33 by Percy, posted 05-04-2008 9:21 PM Percy has replied

Replies to this message:
 Message 35 by Percy, posted 05-05-2008 1:36 AM molbiogirl has replied

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


Message 35 of 451 (465309)
05-05-2008 1:36 AM
Reply to: Message 34 by molbiogirl
05-04-2008 9:58 PM


Re: Balanced Diets are Bunk
molbiogirl writes:
And neither I nor Taubes ever claimed that (to use your words) "the FFAs that are used to produce the VLDL particles come from...carbs."
I'm sorry, Percy, but yes you did.
No, I didn't, and neither did Taubes. You actually quoted Taubes not saying this, and I'm just echoing Taubes. Read the quote again. Taubes says triglycerides, not FFAs, are in VLDLs.
And this is the question I asked in Message 31, concerning whether it is triglycerides or FFAs that are placed in VLDLs. You're disputing almost everything that Taubes says, and you're even rebutting things he didn't say, often at great length, and this is becoming such a big tangle that I think we need to start finding some common points of agreement. So if we can figure out the answer to this one issue then we can move on to the next item, which, if you like, can be whether glucose is involved at all in VLDL production.
Note that what we're discussing now is related far more to heart disease than to obesity, but once we finish the heart disease issues we can move on to the obesity issues.
--Percy

This message is a reply to:
 Message 34 by molbiogirl, posted 05-04-2008 9:58 PM molbiogirl has replied

Replies to this message:
 Message 36 by molbiogirl, posted 05-05-2008 2:59 AM Percy has replied
 Message 37 by molbiogirl, posted 05-05-2008 3:16 AM Percy has seen this message but not replied

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


Message 36 of 451 (465319)
05-05-2008 2:59 AM
Reply to: Message 35 by Percy
05-05-2008 1:36 AM


Re: Balanced Diets are Bunk
And this is the question I asked in Message 31, concerning whether it is triglycerides or FFAs that are placed in VLDLs.
TAGs are in apo particles. Apo particles are in mature VLDLs.
And Taube is claiming that the TAGs come from carbs.
So if we can figure out the answer to this one issue then we can move on to the next item, which, if you like, can be whether glucose is involved at all in VLDL production.
Carbs can be converted into TAGs. That is not in dispute.
It is not the normal procedure. It only happens when one consumes excess carbs (in excess of the body's need for glycogen and energy, that is).
It is my impression that Taube thinks that every blood sugar spike = carbs into TAGs. And that this inevitably leads to the TAGs being incorporated into apo B particles.
IOW ... Carbs ’ TAGs ’ apoB.
Is that true? Or is he talking about excess carbs?
You're disputing almost everything that Taubes says ...
It's frustrating to see someone distort and/or misrepresent well-established science.
Like I said. The guy is idea-mining. With no regard for the metabolic realities.

This message is a reply to:
 Message 35 by Percy, posted 05-05-2008 1:36 AM Percy has replied

Replies to this message:
 Message 38 by Percy, posted 05-05-2008 9:03 AM molbiogirl has replied

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


(1)
Message 37 of 451 (465323)
05-05-2008 3:16 AM
Reply to: Message 35 by Percy
05-05-2008 1:36 AM


Taube's NYT article
You might want to take a look at this:
Big Fat Fake
It details how Taube pissed off the scientists he quoted in a NYT Magazine article he wrote (published in 2003 -- a trial balloon before his book).
It details how he distorted their findings.
It details how he rejected out of hand literally hundreds upon hundreds of studies that don't support his theory.
Taubes presented University of Washington endocrinologist Michael Schwartz, whom he had interviewed, as a proponent of the idea that blood insulin levels as altered by carbohydrates could be a significant contributor to weight gain.
But a commentary in the same magazine Taubes writes for, Science, sharply contradicted that position.
"Although the concept that insulin triggers weight gain has little scientific merit, it remains a key selling point for advocates of diets that are low in carbohydrate and high in protein and fat," it read. "If hyperinsulinemia has adverse consequences, obesity does not appear to be among them," it concluded. Who wrote that? Michael Schwartz.
Since the publication of Taubes' article, numerous doctors, scientists, and health writers have picked apart various pieces of his argument.
A fatlash has formed against Taubes, The New York Times Magazine, and Knopf. Originally riding an adulatory wave, Taubes complained bitterly to the weekly New York Observer in November that he was "being attacked by sleazebags."
The guy is just up to his same old tricks.

This message is a reply to:
 Message 35 by Percy, posted 05-05-2008 1:36 AM Percy has seen this message but not replied

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


Message 38 of 451 (465337)
05-05-2008 9:03 AM
Reply to: Message 36 by molbiogirl
05-05-2008 2:59 AM


Re: Balanced Diets are Bunk
molbiogirl writes:
And this is the question I asked in Message 31, concerning whether it is triglycerides or FFAs that are placed in VLDLs.
TAGs are in apo particles. Apo particles are in mature VLDLs.
And Taube is claiming that the TAGs come from carbs.
I'm sorry, Molbiogirl, but I cannot connect your answer to the question. I raised an issue concerning triglycerides, FFAs and VHDL, and your answer mentions none of those things.
It's frustrating to see someone distort and/or misrepresent well-established science.
I will refrain from taking potshots at the people involved during what should be a technical discussion to the extent that you do the same, holding fast to my belief that the slowness with which this technical discussion is proceeding is due to its complexity and my unfamiliarity with the area, and ignoring hints that what might be going on is an attempt force concession by way of evasive answers and gallops through data.
In other words, when it isn't easy sledding on either side there is a tendency to ascribe base motives to the other side, and participants in a discussion must resist giving expression to these feelings in order to maintain constructive and open communication.
I'm looking for correct information, but I cannot accede to information I do not understand or that does not make sense to me. Independent of Taubes' accuracy in describing various facets of body metabolism, the evidence strongly suggests that the dietary fat hypothesis of heart disease, diabetes and obesity that has turned our grocery stores into huge repositories of specially produced low fat food while simultaneously in the general population heart disease hasn't abated while diabetes and obesity have reached epidemic proportions, indicates that the dietary fat hypothesis is not the answer, or at a minimum is not even close to being the full answer.
The carbohydrate hypothesis may also be wrong, but Taubes makes a strong case that it has not been properly studied because of the hostility against it within the scientific community, of which you are currently providing a copious example.
I'm only trying to learn what's actually so after years of frustration trying to lose weight through traditional diets. My doctor doesn't believe me when I tell him I can't lose weight on a diet of 1200 calories/day - he says I must be cheating, that I should be able to lose weight on 1600 calories/day. But I'm your traditional obsessive/compulsive engineer. This personality likes to be in control and tends to keep close track of everything. So when I say I'm consuming only 1200 calories/day (and am enormously hungry to the point of waking in the night with hunger pains) then you can take that to the bank.
During the last decade or so, every 3 years or so I decide I've got to lose weight, so I've been on 3 diets in the last decade, the only 3 diets of my life. On the first one I lost the weight easily on 1400 calories/day. On the second one I lost the weight more slowly, but again on 1400 calories/day. On the latest one I did not lose any weight in over a year on 1200 calories/day. I'm obviously experiencing the common problem of finding it harder to keep weight off as I get older. But three weeks after cutting down on carbs I'm suddenly down 8 pounds, and I'm never hungry.
So what explains not being able to lose weight on 1200 calories/day? Taubes explanation is that hunger, exercise and calorie intake/outgo are not independent variables. If you eat more you'll exercise more and maintain your weight. If you eat less you'll exercise less and maintain your weight. Certainly while I was eating only 1200 calories/day I was experiencing severe energy problems, especially in the afternoon, and this problem has suddenly completely disappeared. I used to roll into bed at the end of the day completely exhausted and would be asleep literally in less than a minute. Now I'm suddenly reading for a good hour before turning out the light, a habit I had kept up for years that I abandoned only in the past year when I couldn't keep my eyes open.
My dietary experience is probably nearly the identical one that all older people have, and the dietary fat, calorie intake/outgo hypothesis of obesity completely fails to explain this experience. That it still survives is utterly amazing, but you and my own doctor are my personal evidence that is very much alive and kicking.
The problem is that when anyone thinks they already have the answer they stop looking for the answer, and Taubes main point is that we have all the evidence we need to tell us that the dietary fat hypothesis is not the answer and that we should still be looking. It is true that there is much ongoing health research, but one of the answers that researchers already think they have is that the carbohydrate hypothesis has been disproven, but there is strong evidence that they're mistaken, that at a minimum it is a significant part of the equation.
--Percy

This message is a reply to:
 Message 36 by molbiogirl, posted 05-05-2008 2:59 AM molbiogirl has replied

Replies to this message:
 Message 39 by molbiogirl, posted 05-05-2008 11:24 AM Percy has replied

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


Message 39 of 451 (465353)
05-05-2008 11:24 AM
Reply to: Message 38 by Percy
05-05-2008 9:03 AM


Re: Balanced Diets are Bunk
I'm sorry, Molbiogirl, but I cannot connect your answer to the question. I raised an issue concerning triglycerides, FFAs and VHDL, and your answer mentions none of those things.
Percy, you need to ask a different question.
I don't know how much clearer I can be.
Short and medium chain dietary fats: TAGs ’ FFAs ’ chylomicrons and VLDLs.
Long chain dietary fats: TAGs ’ FFAs ’ TAGs ’ chylomicrons and VLDLs.
In the case of short and medium chain carbs, FFAs are sent to the liver, processed into apo particles and incorporated into mature VLDL particles.
In the case of long chain carbs, TAGs are sent to the liver, processed into apo particles and incorporated into mature VLDL particles.
Sorry for another picture, but a picture is worth a thousand words.
The carbohydrate hypothesis may also be wrong, but Taubes makes a strong case that it has not been properly studied because of the hostility against it within the scientific community, of which you are currently providing a copious example.
I did quite a bit of research on this question last night.
And it is simply not true.
This question has been (and continues to be) studied exhaustively.
My dietary experience is probably nearly the identical one that all older people have, and the dietary fat, calorie intake/outgo hypothesis of obesity completely fails to explain this experience.
I hear you.
But my experience is the polar opposite (re: caloric intake).
Which is why we don't rely on just one person's experience, right?
But three weeks after cutting down on carbs I'm suddenly down 8 pounds, and I'm never hungry.
Water weight.
Protein laden diets leads to lots of water weight dropping off.

This message is a reply to:
 Message 38 by Percy, posted 05-05-2008 9:03 AM Percy has replied

Replies to this message:
 Message 40 by Percy, posted 05-05-2008 8:32 PM molbiogirl has replied

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


Message 40 of 451 (465366)
05-05-2008 8:32 PM
Reply to: Message 39 by molbiogirl
05-05-2008 11:24 AM


Re: Balanced Diets are Bunk
molbiogirl writes:
I don't know how much clearer I can be.
I believe you, but clear for a biologist or a layperson?
Anyway, because this message was short I think I can figure things out. TAGs are triglycerides? If so, what's with the "A"?
I have it from Taubes and from a couple different articles at Wikipedia that VLDLs contain fat in the form of triglycerides, not FFAs. I'm sure the processes involving VLDL can be deconstructed into more and more detail and more and more steps, but at heart isn't it triglycerides that are contained in VLDL, not FFAs?
But my experience is the polar opposite (re: caloric intake).
Which is why we don't rely on just one person's experience, right?
Okay, I'm going to have to repeat a few things, because this pointedly ignores what I said as well as reality.
First, I described my experiences with diets and weight loss because it is typical, not solitary, and I'm sure they echo your own dieting experiences. Almost everyone involved in obesity research, especially including the majority who adhere to the dietary fat hypothesis, will tell you that almost all diets fail because in a battle between willpower and hunger, hunger almost always wins. This isn't an issue about which there is any doubt or controversy.
Second, I did not say that calorie reduction diets do not work. As I told you, I was able to make calorie reduction diets work twice, but as I got older they became less and less effective. They were also easy to fall off of, since obviously I gained the weight back. So I'm sure that you also have been able to make calorie reduction diets work, as have millions of other people. And the almost universal experience is that the loss is temporary and the weight comes back, because eventually you just can't stand being hungry anymore.
But three weeks after cutting down on carbs I'm suddenly down 8 pounds, and I'm never hungry.
Water weight.
Protein laden diets leads to lots of water weight dropping off.
Wow, diagnosis via discussion board! Can you tell my fortune, too?
Seriously, water loss? I'm aware of the water loss period in the first week or two of the diet, but I'm not a single data point, you know that. You can't attribute all the significant weight loss reports from low carb diets to water loss, and even researchers who accept the dietary fat hypothesis grant the effectiveness of low carb diets. What they say about them is that they're nutritionally dangerous, or that they're low calorie diets in disguise due to the comparatively narrow range of food choices. They don't claim they're ineffective or just water loss.
Low fat diets are at heart starvation diets. There is a higher tendency to lose protein on low fat diets, and hunger is almost always the impediment to permanent success.
In contrast, low carb diets encourage the conversion of FFAs from triglycerides in fat cells, so there is an increased tendency to lose fat instead of protein, and there's no hunger.
This question has been (and continues to be) studied exhaustively.
Are you talking about the carbohydrate hypothesis, or just diet and health in general? If you're talking about the carbohydrate hypothesis, then as an independent variable in large, long term gold standard studies (Framingham size and duration) with the requisite procedures and set up as single-blinded, no, it has not been and is not being exhaustively studied. It is broadly considered as already discredited, precisely the attitude you're exhibiting here, and it is very difficult getting funding for large studies for already discredited hypotheses.
Interestingly and disappointingly, much of what I've read about low carb diets is that people gain that weight back, too. We'll have to see how I'm doing a year from now. No matter what the outcome, at least I won't have been hungry, because I just couldn't take any more of that.
--Percy

This message is a reply to:
 Message 39 by molbiogirl, posted 05-05-2008 11:24 AM molbiogirl has replied

Replies to this message:
 Message 41 by molbiogirl, posted 05-05-2008 11:36 PM Percy has replied

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


Message 41 of 451 (465375)
05-05-2008 11:36 PM
Reply to: Message 40 by Percy
05-05-2008 8:32 PM


Re: Balanced Diets are Bunk
Sorry. We bio types tend to talk in alphabet soup.
TAG = tri acyl glycerol. It is the proper name of "triglyceride".
And don't forget, a TAG is made up of glycerol + 3 FFAs. The only difference between a free fatty acid (fat) and a triacylglycerol is the glycerol.
Here's a list of everything in a VLDL:
TAGs
phospholipids
cholesterol
cholesterol esters
apo B 100
apo C II
apo E
First, I described my experiences with diets and weight loss because it is typical, not solitary, and I'm sure they echo your own dieting experiences.
Well, no, Percy. Even at 42, if I go overboard over the holidays or something, caloric restriction works fine for me. And believe me, I eat nothing but crappy carbs (lunch today was a bag of "ketchup flavored potato snacks" made by Burger King). And I am the same weight I was in high school.
Let me ask you this: If caloric restriction worked when you were young and it no longer works ... and your carb intake remained the same for the first 2 diets ... why would you assume the carbs were the problem? That is very strong evidence that it wasn't the carbs.
Wow, diagnosis via discussion board!
Would you have been happier had I said: "Studies have shown that a great deal of the initial weight loss with high protein diets is due to diuresis"?
You're only in week 3.
Diuresis, caused by low-carbohydrate intake and its effects on sodium loss, water loss, and glycogen depletion, is the primary reason for initial rapid weight loss on the LC-HP diet. Severely restricting carbohydrate also suppresses appetite, likely due to nausea from sodium loss and protein's satiating effect. In ketosis, the lungs exhale acetone, producing the halitosis typical of people on this diet. Difficulty tolerating ketosis symptoms presents one reason for nonadherence to LC-HP diets. Inadequate documentation exists regarding long-term, harmful effects of ketosis.[ 26, 27]
Should you recommend a low-carb, high-protein diet?
Nurse Practitioner. 27(4):52-53,55-56,58-59, April 2002.
You can't attribute all the significant weight loss reports from low carb diets to water loss, and even researchers who accept the dietary fat hypothesis grant the effectiveness of low carb diets.
I didn't say "all". You're only in week 3. And, as you said, nearly everyone gains the weight back after a high protein diet just like any other diet. Who cares how much weight you lose if you gain it all back anyway?
"The Atkins diet produces weight loss, as does the grapefruit diet, the rotation diet, and every other fad diet out there," says one of the researchers, Colorado's James Hill. "I haven't seen any data anywhere saying Atkins is better than these other diets for weight loss. Taubes is trying to fly in the face of the scientific evidence." Referring to the book deal, he says, "Taubes sold out."
Percy writes:
Low fat diets are at heart starvation diets.
What is your current caloric intake/day?
...low carb diets encourage the conversion of FFAs from triglycerides in fat cells...
No, they most certainly do not.
Are you talking about the carbohydrate hypothesis, or just diet and health in general?
Carb thing.
For example, Taubes omitted any reference to hundreds of refereed scientific studies published during the last three decades that contradicted his position.
Taubes proved as adept at clipping data as at clipping quotes. Thus he claimed that one of the "reasons to suggest that the low-fat-is-good-health hypothesis has now effectively failed the test of time" is "that the percentage of fat in the American diet has been decreasing for two decades."
That's true, but irrelevant. The amount of fat consumed has been steadily climbing, as has consumption of all calories.
Taubes also shoved aside decades of published, controlled, randomized clinical trials comparing nutrient intake and weight loss. His apparent justification in the article was that the "research literature [is] so vast that it's possible to find at least some published research to support virtually any theory." But that's sheer nihilism. Good science is cautious and skeptical, not permanently open-ended. That's why terms like weight of the evidence are used. And the evidence against Atkins-like low-carbohydrate diets is crushing.
In April 2002, for example, the Journal of the American Dietetic Association (JADA) published a review of "all studies identified" that looked at diet nutrient composition and weight loss. It found over 200, with "no studies of the health and nutrition effects of popular diets in the published literature" excluded...The conclusion: Those who ate the least fat carried the least fat.
One such meta-analysis, covering 16 ad libitum studies and almost 2,000 people, appeared in the International Journal of Obesity and Related Metabolic Disorders in December 2000. The conclusion: Those on low-fat diets had "a greater reduction in energy intake" and a "greater weight loss than control groups."
In a subsequent letter to the journal, three obesity research co-authors, including James Hill, director of the University of Colorado Center for Human Nutrition in Denver, noted, "What Taubes does not mention are the meta-analyses of intervention studies comparing ad libitum intakes of higher fat diets with low-fat diets that clearly show reduced caloric intake and weight loss on the low-fat diet."
Taubes also ignored the approximately 3,000 members of a database called the National Weight Control Registry. For 10 years, the registry has tracked people who have lost at least 30 pounds and kept it off for at least a year. The average member has maintained a loss of about 60 pounds for about five years.
Co-administered by Hill in Denver and Rena Wing of the University of Pittsburgh, the registry is aimed at finding out what works and what doesn't. According to its members, what doesn't work is a high-fat diet. On average, they consume only 23 percent of calories from fat. "Almost nobody's on a low-carbohydrate diet," Hill says.
Yet the published literature that Taubes ignored says otherwise. The aforementioned review of over 200 studies in the Journal of the American Dietetic Association expressly nixed the idea that any type of food converts less efficiently to body fat. "None of the popular diet research we reviewed suggests a metabolic advantage with respect to weight loss," it declared.
Stacking theory atop theory, Taubes roared on. Something called "hyperinsulinemia" could also favor the Atkins dieter, he insisted. When carbohydrates are ingested they are broken down in the intestine into glucose and other sugars. Glucose then stimulates cells in the pancreas to secrete insulin to remove that glucose and take it into tissues to be used as fuel or stored. Protein and fat consumption don't have nearly the same impact on insulin production because the whole point of insulin is to maintain the stability of the sugar level.
The Atkins hyperinsulinemia theory, ex-plained Taubes, is that carbohydrates can "cause a spike of blood sugar and a surge of insulin within minutes. The resulting rush of insulin stores the blood sugar away and a few hours later, your blood sugar is lower than it was before you ate." The brain receives a signal that the body needs more food, and the vicious circle repeats itself. Carbohydrates at the top of what's called the "hypoglycemic index" are the most evil of the evil, since they cause blood sugar to rise the fastest.
Schwartz was also the primary author of a study concluding that obese people whose systems secrete insulin at high levels may be protected against further weight gain.
Schwartz says it's not that he believes insulin can't play a role in promoting weight gain, but he rejects (Taube's insulin theory). "Before you draw conclusions you need data," he says. "There is no compelling evidence that in normal individuals day-to-day fluctuations of the blood glucose level are an important determinant of how much food is consumed."
The Journal of the American Medical Association was indeed scathing (re: Atkins Diet) ... Statements such as "No scientific evidence exists to suggest that the low-carbohydrate ketogenic diet has a metabolic advantage over more conventional diets for weight reduction," and "there is no reason to associate a diet rich in carbohydrate with obesity" hardly seem to acknowledge "that the diet probably worked."
Other terms the AMA used to described Atkins' theories included "nave," "biochemically incorrect," "inaccurate," and "without scientific merit."
(The AMA) also explained why the diet didn't work, mocking Atkins' basic thesis that fat and protein cannot cause weight gain in the absence of carbohydrate consumption as a "thermodynamic miracle."
Big Fat Fake
Percy writes:
If you're talking about the carbohydrate hypothesis, then as an independent variable in large, long term gold standard studies (Framingham size and duration) with the requisite procedures and set up as single-blinded, no, it has not been and is not being exhaustively studied.
The 200 studies analyzed by the Journal of the American Dietetic Association, the International Journal of Obesity and Related Metabolic Disorders December 2000 study and the National Weight Control study mentioned above.
Edited by molbiogirl, : tweak

This message is a reply to:
 Message 40 by Percy, posted 05-05-2008 8:32 PM Percy has replied

Replies to this message:
 Message 43 by Percy, posted 05-06-2008 7:55 AM molbiogirl has replied
 Message 44 by Percy, posted 05-06-2008 8:24 AM molbiogirl has replied

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


Message 42 of 451 (465389)
05-06-2008 4:08 AM


If you have time, this talk by Michael Pollan, author of The Omnivore's Dilemma and In Defense of Food, is well worth a listen. He touches on many of the things we've been discussing in this thread.
https://www.youtube.com/watch?v=I-t-7lTw6mA

Replies to this message:
 Message 83 by Percy, posted 05-10-2008 7:11 AM molbiogirl has replied
 Message 84 by Percy, posted 05-10-2008 11:25 AM molbiogirl has not replied

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


Message 43 of 451 (465393)
05-06-2008 7:55 AM
Reply to: Message 41 by molbiogirl
05-05-2008 11:36 PM


Re: Balanced Diets are Bunk
The Atkins diet plan made low carb diets the target of those who accept the dietary fat hypothesis for many, many years, and the strong criticism continues right up to the present day. I do not dispute that you can find literally terabytes of words criticizing low carb diets.
This is why we're approaching this from a technical perspective, so that we don't have to rely upon authority, and so that we have a better chance of establishing what is correct and what is incorrect about Taubes' descriptions of metabolic processes related to heart disease, diabetes and obesity, and (more importantly) what we think we know that we really don't.
So we've now established that when Taubes described VLDLs as containing fat in the form of TAGs and not in the form of FFAs that he was correct (Taubes also describes the composition of triglycerides as being three FFAs bound together and also describes the conversion process back and forth with FFAs, something I've described in this thread myself).
So let's move on to the next issue of how significant the role of glucose is in the production of VLDLs by the liver. You claim that while this is a process that can take place, in reality it occurs only rarely because the triggering mechanisms for it are complex and rare, typically happening only when the body is under some kind of stress. You also claim that this is the only available process by which the liver can produce triglycerides from FFAs.
Taube's overall point is that high glucose levels encourage the production of VLDLs by the liver, and I think you disagree with this, too.
You said this in Message 30:
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).
So why don't we start by exploring this process in greater detail. How do think it would be best to begin?
Getting to the side issues now...
molbiogirl writes:
Wow, diagnosis via discussion board!
Would you have been happier had I said: "Studies have shown that a great deal of the initial weight loss with high protein diets is due to diuresis"?
What my rhetorical response was intended to indicate was that you're focusing on me as a way of avoiding addressing the body of data about the effectiveness of low carb diets for weight loss. As I said, I used myself as an example because I'm typical, and because I'm typical I can safely assume that I will continue to lose weight and continue to not be hungry which will allow me to continue to follow the diet. The fact that I personally am only in week 4 (not 3 anymore) can't be used as an argument against the large body of data.
To deny that low carb diets work and to claim that it's all really just water loss flies in the face of reality. Even your fellow dietary fat believers disagree with you, since the effectiveness of low carb diets is widely conceded. As I said in my previous message, they criticize low carb diets for being unsafe or for being low calorie diets in disguise (and I imagine there are many other criticisms, but I think these are the main ones), not for being ineffective.
Keep in mind that Taubes' book is not a diet book. I've never read a diet book in my life. I am not following any diet. I'm making my own diet based on the information I can find. Cutting down on calories didn't work, cutting down on carbs did. You asked how many calories I'm consuming now, and I'd say it's around 1500/day, up from 1200/day.
Who cares how much weight you lose if you gain it all back anyway?
Research appears to indicate the most reliable indicator of health and longevity is degree of obesity. The more obese, the worse the long term prognosis for health and longevity. Any approach that keeps us lighter longer is an improvement. Low carb diets with their lack of hunger and their ability to cause weight loss with higher calorie intakes are much more likely to achieve the goal of being lighter longer.
--Percy

This message is a reply to:
 Message 41 by molbiogirl, posted 05-05-2008 11:36 PM molbiogirl has replied

Replies to this message:
 Message 45 by molbiogirl, posted 05-06-2008 9:57 AM Percy has replied

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


Message 44 of 451 (465395)
05-06-2008 8:24 AM
Reply to: Message 41 by molbiogirl
05-05-2008 11:36 PM


Re: Balanced Diets are Bunk
I intended to address these and somehow left them out.
molbiogirl writes:
Well, no, Percy. Even at 42, if I go overboard over the holidays or something, caloric restriction works fine for me. And believe me, I eat nothing but crappy carbs (lunch today was a bag of "ketchup flavored potato snacks" made by Burger King). And I am the same weight I was in high school.
If you're the same weight you were in high school then you're not typical, are you. Your experience shares little with the general population, especially your diets. Losing a holiday weight gain over a few weeks is child's play compared to enduring hunger for a year while losing 40 pounds.
I offered myself as an example because I am typical, a true representative of the broad body of data regarding diet and weight loss. Since you are not typical, you cannot offer yourself as an example.
Let me ask you this: If caloric restriction worked when you were young and it no longer works ... and your carb intake remained the same for the first 2 diets ... why would you assume the carbs were the problem? That is very strong evidence that it wasn't the carbs.
There were actually 3 diets. This latest diet, the low carb diet, is the 4th. I presume that the first two diets worked because the reduction in food intake cut both carbs and calories. But the second diet was more difficult than the first, I presume because I was older and my metabolism had changed (the specifics of the change cannot be known, of course, but whatever they were they are apparently typical with age). And I presume the third diet didn't work because my internal metabolism had changed to the point where the number of calories required to achieve weight loss was now so low that the corresponding hunger became an insurmountable barrier.
So the three diets aren't actually evidence of much of anything because calories and carbs were not varied independently, and I kept no careful data away. And on the current diet I'm only tracking carbs, not calories, so my calorie estimates are probably not as reliable as they were for the previous diets.
Here's the evidence we do have:
  • Calorie reduction diet of 1200 calories/day, no weight loss in over a year, frequent hunger.
  • Carbohydrate reduction diet,
--Percy

This message is a reply to:
 Message 41 by molbiogirl, posted 05-05-2008 11:36 PM molbiogirl has replied

Replies to this message:
 Message 46 by molbiogirl, posted 05-06-2008 2:32 PM Percy has replied

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


Message 45 of 451 (465399)
05-06-2008 9:57 AM
Reply to: Message 43 by Percy
05-06-2008 7:55 AM


Re: Balanced Diets are Bunk
So we've now established that when Taubes described VLDLs as containing fat in the form of TAGs and not in the form of FFAs that he was correct...
Yes. But just to be absolutely clear: those TAGs come from FFAs derived from dietary fat.
So let's move on to the next issue of how significant the role of glucose is in the production of VLDLs by the liver. You claim that while this is a process that can take place, in reality it occurs only rarely because the triggering mechanisms for it are complex and rare, typically happening only when the body is under some kind of stress.
Yes. But I also mentioned excess carbs are not "normal". Excess carbs = those that exceed the body's need for (1) glycogen stores (2) energy to run things like the brain. Excess carbs trigger a set of 15 known genes that convert carbs to TAGS which are then stored in fat tissue.
The fat tissue is stored in the usual places -- gut, thighs, butt, etc. Not the liver.
You also claim that this is the only available process by which the liver can produce triglycerides from FFAs.
Also, there is this:
Many cell types and organs have the ability to synthesize triacylglycerols, but in animals the liver and intestines are most active, although most of the body stores of this lipid are in adipose tissue.
Two main biosynthetic pathways are known, the sn-glycerol-3-phosphate pathway, which predominates in liver and adipose tissue, and a monoacylglycerol pathway in the intestines.
Forbidden
(That's a free pdf, if you'd like to have a look.)
TAGs are synthesized by (1) liver (2) intestine (2) fat tissue.
The liver is Grand Central Station of a lot of metabolic processes. It makes TAGs from (1) dietary fat (2) excess carbs (3) other things. (For the sake of clarity I won't bother explaining (3) unless you want me to.)
Each of the TAG biosynthesis processes is different. The way the body regulates each of these biosynthesis processes is different. But all of the TAG biosynthesis processes are interrelated.
And, yes, regulation of each of these biosynthesis cycles is (1) very complicated (2) redundant (3) multi level (4) multi mechanism (e.g. transcription, translation, hormonal, feedback loops, feedforward loops, etc.)
Biosynthesis of any sort in the body is very tightly regulated (because it is metabolically expensive). TAG biosynthesis is no exception.
Taube's overall point is that high glucose levels encourage the production of VLDLs by the liver, and I think you disagree with this, too.
Taube said glucose ’ insulin ’ elevated VLDL production, correct?
This is not true.
Insulin suppresses VLDL production.
Would you like to start with how insulin regulates VLDL production?
To deny that low carb diets work and to claim that it's all really just water loss flies in the face of reality.
Percy, come on. I didn't deny that high protein diets work.
Even your fellow dietary fat believers disagree with you, since the effectiveness of low carb diets is widely conceded.
To be fair, I am a "restricted caloric intake" girl. I think the RDA for caloric intake is 30% too high. And a calorie is a calorie, no matter what its source.
I'm making my own diet based on the information I can find.
Then might I suggest "Eat food. Not too much. Mostly plants." That's the tagline of Michael Pollan's new book, In Defense of Food.
If you have half an hour to spare, the Michael Pollan Google talk I linked is excellent.
A final note.
The Atkins diet plan made low carb diets the target of those who accept the dietary fat hypothesis for many, many years, and the strong criticism continues right up to the present day.
In his 2003 8,000 word article, Taube was the one who brought up Atkins. And defended him.
I do not dispute that you can find literally terabytes of words criticizing low carb diets.
Terabytes of evidence, Percy. That's the source of the criticism. The overwhelming weight of the evidence.

This message is a reply to:
 Message 43 by Percy, posted 05-06-2008 7:55 AM Percy has replied

Replies to this message:
 Message 47 by Percy, posted 05-06-2008 3:37 PM molbiogirl has replied

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