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Author
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Topic: Good Calories, Bad Calories, by Gary Taubes
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molbiogirl
Member (Idle past 2660 days) Posts: 1909 From: MO Joined: 06-06-2007
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Message 301 of 451 (629055)
08-15-2011 12:01 PM
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Reply to: Message 300 by Percy
08-15-2011 11:42 AM
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Re: It's not insulin levels
I would argue that Taubes' "misinterpretation" rises to the level of "really wrong". His central thesis "that carbohydrate (particularly refined carbohydrate) causes obesity by elevating insulin, thereby causing increased fat storage in fat cells" has been royally fisked by Guyenet.
Guyenet writes: I hope you can see by now that the carbohydrate hypothesis of obesity is not only incorrect on a number of levels, but may even be backward. Guyenet writes: The reason why obesity and metabolism researchers don't take Taubes's idea seriously is that it is contradicted by a large body of evidence from multiple fields. And I would also argue that any diet is a matter of willpower. You will yourself to avoid carbs during the week, right?
Those opposed to low carb diets need to start saying things that actually turn out to be true before their recommendations can be taken seriously. Percy, you know as well as I do that one person's anecdote does not a scientific truth make. That said, according the the American Heart Association:
A greater percent lowering of LDL occurs in older people than in younger people.716 216. Wilcosky T, Hyde J, Anderson JJB, Bangdiwala S, Duncan B. Obesity and mortality in the Lipid Research Clinics Program Follow-Up Study. J Clin Epidemiol1990 ;43:743 -52. Furthermore, age dependent LDL levels are, in some cases, genetic.
The estimated frequency of the allele leading to the phenotype characterised by predominance of small, dense LDL subclasses was about 15%. Expression of this phenotype appears to be age dependent, in that most affected subjects in this population were older than 40 years. Although plasma lipid levels were normal in most subjects with this trait, levels of plasma apoprotein B and triglyceride were higher and levels of apoprotein AI and HDL2 lower than in unaffected family members. http://www.sciencedirect.com/...rticle/pii/S0140673686924256 Edited by molbiogirl, : No reason given.
| This message is a reply to: | | | Message 300 by Percy, posted 08-15-2011 11:42 AM | | Percy has seen this message but not replied |
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Percy
Member Posts: 22473 From: New Hampshire Joined: 12-23-2000 Member Rating: 4.7
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Message 302 of 451 (629074)
08-15-2011 2:33 PM
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New book by Gary Taubes
As long as this thread is active again I may as well mention that Taubes has a new book out, Why We Get Fat: And What to Do About It. It's the same material as his earlier book, but written more for the layperson. --Percy
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purpledawn
Member (Idle past 3476 days) Posts: 4453 From: Indiana Joined: 04-25-2004
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Triggers for Fat Storage or Use
From a lay viewpoint, the overall idea I get from Gary's books are that an over abundance of carbs in some people tells the body to store fat. The energy burned may not be from the same fat being stored. Unfortunately for scientist, we are not machines that are made exactly alike. The theory of thermodynamics doesn't seem to work for biology. Increased exercise alone doesn't necessarily cause a person to lose a significant amount of weight. When a theory doesn't ring true for an individual, that individual has to go with what works whether it is a scientific truth or not. As Taubes pointed out, the more we exercise the more we want to eat and the less we eat the less energy we have to exercise. So there is something else at work and IIRC, he attributed to survival needs. There may not be a scientific truth that fits everyone concerning weight.
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molbiogirl
Member (Idle past 2660 days) Posts: 1909 From: MO Joined: 06-06-2007
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Re: Triggers for Fat Storage or Use
PD, I would suggest you take a look at the link I posted above. Guyenet specifically addresses thermo:
Guyenet writes: That is, Taubes is not disagreeing with the first law of thermodynamics: he understands that fat accumulation depends on how much energy is entering the body vs. leaving it. Guyenet points out in no uncertain terms that Taubes' central thesis is dead wrong. Guyenet also point out that Taubes mangles the papers he uses to support his thesis. We're talking creo level mangling, too. Take a look at this:
Guyenet writes: I've already demonstrated that Taubes's conception of the effects of insulin are badly misguided, therefore it makes no sense to invoke insulin as a mechanism between carbohydrate consumption and body fatness, unless your hypothesis is that carbohydrate lowers body fatness by increasing insulin secretion. Guyenet writes: Therefore, the insulin hypothesis is not consistent with basic thermodynamics, and it's not consistent with research on the biological functions of insulin. And this:
Guyenet writes: Weight stable obese people have a higher energy flux out of fat cells, and a higher metabolic rate, but it is not enough to overcome the higher calorie intake that is also observed (26, 27). That has been repeatedly confirmed and it is simply a fact at this point. There's more where that came from. Sticking your fingers in your ears and chanting la-la-la doesn't make it go away.
PD writes: When a theory doesn't ring true for an individual, that individual has to go with what works whether it is a scientific truth or not. I-don't-like-the-sound-of-that-theory-so-I'm-going-with-my-gut-feeling? That's Jenny MaCarthy-esque. The overwhelming majority of the research flat out contradicts what Taubes is saying. No one takes him seriously. No one except a gullible public, that is. Just like Jenny McCarthy and her anti-vaxer crowd. Edited by molbiogirl, : sp
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purpledawn
Member (Idle past 3476 days) Posts: 4453 From: Indiana Joined: 04-25-2004
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Re: Triggers for Fat Storage or Use
quote:
PD, I would suggest you take a look at the link I posted above. Guyenet specifically addresses thermo:
I did and I disagree with your quote.
Guyenet writes: That is, Taubes is not disagreeing with the first law of thermodynamics: he understands that fat accumulation depends on how much energy is entering the body vs. leaving it. That is not the way I read what Taubes wrote. It was very much about what type of energy enters the body. All calories are not equal.
Guyenet writes: Weight stable obese people have a higher energy flux out of fat cells, and a higher metabolic rate, but it is not enough to overcome the higher calorie intake that is also observed (26, 27). That has been repeatedly confirmed and it is simply a fact at this point. And from the abstract #26 The accumulating data from the application of the DLW method suggest a need to place greater emphasis on mechanisms that lead to a mismatch between energy intake and expenditure rather than a continuing emphasis on energy intake or energy expenditure alone. Which is what Taubes is looking at, in my understanding. It isn't a simple case of calorie in, calorie out. Did you read the book, Good Calories, Bad Calories? If not, you really can't say whether Guyenet is right or not.
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There's more where that came from. Sticking your fingers in your ears and chanting la-la-la doesn't make it go away.
No it doesn't. Show me how Taubes mangled the papers.
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I-don't-like-the-sound-of-that-theory-so-I'm-going-with-my-gut-feeling?
Nope. Has nothing to do with sound, it has to do with what works for the individual. One size doesn't fit all. Some people do better with more carbs and some do better with more protein. Resorting to creo rudeness doesn't make your point either.
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molbiogirl
Member (Idle past 2660 days) Posts: 1909 From: MO Joined: 06-06-2007
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Re: Triggers for Fat Storage or Use
I did and I disagree with your quote. You're disagreeing with a "B.S. in biochemistry from the University of Virginia ... and a Ph.D. in neurobiology from the University of Washington ... [who professionally studies] the neurobiology of body fat regulation" and siding with a journalist. Huh.
That is not the way I read what Taubes wrote. That's fine. Care to support that bare assertion?
And from the abstract #26 Take another look at the abstract.
Abstract writes: Although generally now accepted, one of the major surprises from the early applications of DLW was that obese individuals have higher energy expenditures than lean controls. Moreover, weight gain, even in the already obese, is associated with an increase in energy expenditure as weight is one of the strongest predictors of total energy expenditure. Fat people expend more energy because they have to haul around more weight. They also consume more energy than they expend.
[This does] not account for the common cessation of weight loss observed after 12-26 weeks of restriction. I no longer have institutional access to journals, but I do have access to free DLW pdfs.
A series of studies demonstrated good agreement between mean energy intake and mean energy expenditure when food intake was recorded by observers or when it was self-reported by normal-weight, self-selected, highly motivated volunteer subjects using weighed records. However, in randomly recruited men and women, energy intake by weighed records was 82% and 81%, of energy expenditure, respectively, indicating underestimation of habitual intake. Reported intake of obese and previously obese women was only 73% and 64% of expenditure, whether measured by weighed record or by diet history, confirming suspicions that these subjects misrepresented their intake. http://www.sciencedirect.com/...article/pii/000282239391820G No surprise. Fat people under report their energy intake. And after 6 months of calorie restriction, they start over eating again.
Guyenet writes: DLW studies have shown that after controlling for confounding factors, obese people almost invariably expend more, and consume more calories than lean people (24, 25). Google DLW & obesity. There are dozens of papers that report this.
PD writes: Show me how Taubes mangled the papers. Guyenet writes: Leptin is the system that Drs. Jules Hirsch and Rudy Leibel have shown in carefully controlled human studies is responsible for the metabolic defect he's getting at (1). It's also the system that is mutated in the genetically obese rodents he discusses (2, 3). Yet it receives no mention in the book. Guyenet writes: Taubes states here that the typical diet is "primarily milk", therefore by inference, low in carbohydrate. ... The typical diet is 81% carbohydrate, and primarily based on millet, according to Taubes's own reference. Guyenet writes: The Pima of New Mexico currently have one of the highest obesity rates in the world, on par with Nauru. It is rather ironic that Taubes uses them as an example in GCBC, when they are at odds with his hypothesis. Mangled. And you ignored Guyenet's main point. Taubes' hypothesis is, at its core, dead wrong. 1. Insulin increases appetite. 2. Insulin decreases the release of fat from fat cells. 3. Carbohydrates increase body fat. As to 1.
Guyenet writes: Insulin infused into the brains of baboons causes a suppression of appetite and fat loss, which is consistent with the well-established fact that insulin and leptin have overlapping functions in the brain (10, 11). Knocking out insulin receptors in the brain leads to increased fat mass in rodents, suggesting that its normal function involves constraining fat mass (12). Insulin is also co-secreted with amylin, which suppresses food intake and body weight (13). This is why insulin is viewed by most obesity researchers as an anti-obesity hormone, not an obesity hormone. As to 2.
Guyenet writes: Therefore, the insulin hypothesis is not consistent with basic thermodynamics, and it's not consistent with research on the biological functions of insulin. Obese people do not have a defect in the ability to release fat from fat cells and burn it, to the contrary. They release more fat from fat cells than lean people, and burn more of it. Guyenet writes: The fat cells of obese people do not suffer from excessive insulin signaling, to the contrary, the evidence suggests that their fat cells are insulin resistant and therefore insulin signaling is reduced. This shows that insulin does not cause obesity by acting directly on fat cells to cause fat storage. To understand obesity, we have to understand what causes increased food intake, and that factor is not insulin. As to 3.
Guyenet writes: New Guinea highland tribe at Tukisenta 1960s and 70s. West Nile district, Uganda, 1940s. Northern Cameroon, 1980s. Most of Asia, 20th century. Kitava, 1990s. Pima, 20th century. All peoples whose diet was ~80% carbs and who were lean. You want to dust off your copy of GCBC and refute that with a couple of quotes? And while you're at it, how about you support this?
It was very much about what type of energy enters the body. All calories are not equal. I look forward to buying another copy of that "book" as I threw the other away the minute I finished with this thread.
Resorting to creo rudeness doesn't make your point either. I am astounded that when confronted by evidence that clearly refutes your point, you double down. Reminds me of anti-vaxers, HIV and climate change denialists, and creos. Edited by molbiogirl, : No reason given. Edited by molbiogirl, : No reason given.
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purpledawn
Member (Idle past 3476 days) Posts: 4453 From: Indiana Joined: 04-25-2004
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Re: Triggers for Fat Storage or Use
quote:
You're disagreeing with a "B.S. in biochemistry from the University of Virginia ... and a Ph.D. in neurobiology from the University of Washington ... [who professionally studies] the neurobiology of body fat regulation" and siding with a journalist. Huh.
Why yes, yes I am. I read the same book he did and I disagree with his statement of what Taubes said. No science involved in that. Just plain reading. If you feel my understanding of what Taubes wrote concerning thermodynamics is wrong, then provide a quote from the book that agrees with Guyenet's statement.
quote:
That's fine. Care to support that bare assertion?
The title of the book is a big giveaway, but here are two of the conclusions that Taubes felt were inescapable to him based on the existing knowledge.
5. Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior. 6. Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger. Type of calorie:
That the nutrient composition of the diet effects our energy expenditure would be the explanation, as Pennington noted, for why obese individuals might lose weight on high-calorie, carbohydrate-restricted diets of 3,000 calories or more. The point is that their total energy expenditure is inhibited on diets that are carbohydrate-rich because significant amounts of energy are being lost into their fat tissue. And so the diets they've been eating all along, the ones that made them fat, also suppress their expenditure of energy. They semistarve their lean tissue and organs and this, in turn, leads to a reduction in energy expenditure and an impulse to remain sedentary. quote:
Fat people expend more energy because they have to haul around more weight. They also consume more energy than they expend.
So what is your point concerning the conclusions of the book. Taubes doesn't deny this issue.
Taubes writes: A scientific point that I now believe I emphasized insufficiently is that the nutrient composition of our diets must play a fundamental role in our energy expenditure--whether we are, in fact, physically active or relatively sedentary. quote:
You want to dust off your copy of GCBC and refute that with a couple of quotes?
You didn't show me how Taubes mangled the papers. IOW, show me what Taubes said concerning the papers and how it mangled it.
quote:
And you failed to address Guyenet's main point. Taubes' hypothesis is, at its core, dead wrong.
Mainly because you haven't made an argument. You just quoted Guyenet and Guyenet didn't provide any quotes from the book to match his comments. I don't intend to debate Guyenet.
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Phat
Member Posts: 18292 From: Denver,Colorado USA Joined: 12-30-2003 Member Rating: 1.1
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Re: Triggers for Fat Storage or Use
PD writes: One size doesn't fit all. Some people do better with more carbs and some do better with more protein. I know for a fact that I am of the body type that thrives on moderate protein, higher "good" fats, and lo glycemic carbs. As my body insulin goes down I become less resistant to the remaining insulin that I do have. As insulin decreases, glycogon increases. energy goes up and calorie expenditure goes up. weight drops at a steady rate for the first few months...and wont go back up as long as I function as a higher percentage fat burner and a lower percentage carb burner. The trick is to not starve yourself from all carbohydrates and to be careful not to overdo the fat or protein intake.
| This message is a reply to: | | | Message 305 by purpledawn, posted 08-15-2011 6:55 PM | | purpledawn has not replied |
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molbiogirl
Member (Idle past 2660 days) Posts: 1909 From: MO Joined: 06-06-2007
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Re: Triggers for Fat Storage or Use
You didn't show me how Taubes mangled the papers. 1. He neglected to mention leptin. 2. He neglected to mention 81% carbohydrate intake. 3. He neglected to mention the Pima were lean on a carb diet. I see you've chosen to ignore the evidence. You just restate Taubes' erroneous claims. To wit:
5. Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior.
6. Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger. The point is that their total energy expenditure is inhibited on diets that are carbohydrate-rich because significant amounts of energy are being lost into their fat tissue. I addressed each of these in the last post.
You just quoted Guyenet and Guyenet didn't provide any quotes from the book to match his comments. I don't intend to debate Guyenet. You just provided the quotes! And I am using Guyenet to support the very same arguments I made upthread. PD: Obesity is a disorder of excess fat accumulation. Guyenet: 2. Insulin decreases the release of fat from fat cells. PD: Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger. Guyenet: 1. Insulin increases appetite. PD: Diets that are carbohydrate-rich because significant amounts of energy are being lost into their fat tissue. Guyenet: 3. Carbohydrates increase body fat. I'm not going to repost the cites. Either refute the evidence or concede the point.
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Percy
Member Posts: 22473 From: New Hampshire Joined: 12-23-2000 Member Rating: 4.7
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Re: Triggers for Fat Storage or Use
molbiogirl writes: PD: Obesity is a disorder of excess fat accumulation. Guyenet: 2. Insulin decreases the release of fat from fat cells. PD: Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger. Guyenet: 1. Insulin increases appetite. PD: Diets that are carbohydrate-rich because significant amounts of energy are being lost into their fat tissue. Guyenet: 3. Carbohydrates increase body fat. The comments from Guyenet seem to be congruent with PD's comments, but with varying degrees of relevance. --Percy
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molbiogirl
Member (Idle past 2660 days) Posts: 1909 From: MO Joined: 06-06-2007
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Message 311 of 451 (629185)
08-16-2011 9:40 AM
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Reply to: Message 310 by Percy
08-16-2011 9:23 AM
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Re: Triggers for Fat Storage or Use
The comments from Guyenet seem to be congruent with PD's comments, but with varying degrees of relevance.
??? PD just restated Guyenet's summary of Taubes' hypothesis, using Taubes' quotes. She didn't address Guyenet's evidence refuting said hypothesis.
| This message is a reply to: | | | Message 310 by Percy, posted 08-16-2011 9:23 AM | | Percy has replied |
| Replies to this message: | | | Message 312 by Percy, posted 08-16-2011 9:54 AM | | molbiogirl has replied |
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Percy
Member Posts: 22473 From: New Hampshire Joined: 12-23-2000 Member Rating: 4.7
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Re: Triggers for Fat Storage or Use
PD just restated Guyenet's summary of Taubes' hypothesis, using Taubes' quotes.
She didn't address Guyenet's evidence refuting said hypothesis. I'm having trouble following you. Perhaps it would be easier to understand your points if you stated them in your own words and just used Guyenet as a reference. But if PD understands what you're saying then don't worry about me. --Percy
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molbiogirl
Member (Idle past 2660 days) Posts: 1909 From: MO Joined: 06-06-2007
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Message 313 of 451 (629195)
08-16-2011 10:10 AM
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Reply to: Message 312 by Percy
08-16-2011 9:54 AM
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Re: Triggers for Fat Storage or Use
OK. PD & I agree re: Taubes' hypothesis. 1. Insulin increases appetite. 2. Insulin decreases the release of fat from fat cells. 3. Carbohydrates increase body fat. Insulin decreases appetite.
Guyenet writes: Insulin infused into the brains of baboons causes a suppression of appetite and fat loss, which is consistent with the well-established fact that insulin and leptin have overlapping functions in the brain (10, 11). ... Insulin is also co-secreted with amylin, which suppresses food intake and body weight (13). Insulin does not inhibit fat release from fat cells.
Guyenet writes: Knocking out insulin receptors in the brain leads to increased fat mass in rodents, suggesting that its normal function involves constraining fat mass (12). Guyenet writes: Insulin is also co-secreted with amylin, which suppresses food intake and body weight (13). Guyenet writes: At least two studies have shown that higher fasting insulin is associated with a higher resting energy expenditure, independent of body fatness, not a lower expenditure (14, 15). High carb diets are not associated with obesity.
Guyenet writes: New Guinea highland tribe at Tukisenta 1960s and 70s. West Nile district, Uganda, 1940s. Northern Cameroon, 1980s. Most of Asia, 20th century. Kitava, 1990s. Pima, 20th century. Each of these groups had a diet of ~80% carbs. Each of these groups was lean (until the Westernization of their diets). Edited by molbiogirl, : sp Edited by molbiogirl, : No reason given.
| This message is a reply to: | | | Message 312 by Percy, posted 08-16-2011 9:54 AM | | Percy has replied |
| Replies to this message: | | | Message 316 by Percy, posted 08-16-2011 2:02 PM | | molbiogirl has replied |
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molbiogirl
Member (Idle past 2660 days) Posts: 1909 From: MO Joined: 06-06-2007
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Amylin & insulin decrease appetite
Insulin decreases appetite.
Pliquett,R et al The Effects of Insulin on the Central Nervous System - Focus on Appetite Regulation, Horm Metab Res 2006; 38(7): 442-44 Among its many well-known functions, insulin is also a potent anorexigenic hormone, and insulin receptors are widely distributed throughout the central nervous system. Nirmala, G et al Appetite Regulating Hormones, Veterinary World, Vol.2(6): 242-24 Insulin applied intra-cerebro-ventricularly (icv) inhibits food intake and body weight in rats. Leptin and insulin are important anorexigenic hormones acting on the hypothalamus. Encyclopedia of Molecular Pharmacology, Volume 1, Stefan Offermanns, Walter Rosenthal
In the hypothalamus, insulin reduces appetite and stimulates energy expenditure. Leptin is produced by adipose tissue in direct correlation to the quantity of adipose tissue. Insulin and glucocorticoids also stimulate secretion of leptin. In the hypothalamus, leptin increases satiety, decreases appetite and food intake, increases energy expenditure and stimulates thermogenesis. Insulin is co secreted with amylin.
Naeve S, et al 2005 Amylin’s inhibitory effect on food intake is not due to malaise in rats. Appetite 44:369 Collectively, the aforementioned effects of amylin (e.g. decreased fat mass, preservation of lean mass, no decrease in EE, and increased POMC) resemble those observed after leptin administration (15). In summary, our studies demonstrated that peripheral administration of amylin reduced food intake, slowed body weight gain, and selectively reduced body fat in a rodent model of obesity. Mack C et al Pharmacological actions of the peptide hormone amylin in the long-term regulation of food intake, food preference, and body weight American Journal of Physiology 293:1855 The ability of amylin to reduce acute food intake in rodents is well established. Longer-term administration in rats (up to 24 days) shows a concomitant reduction in body weight, suggesting energy intake plays a significant role in mediating amylin-induced weight loss. Wielinga, P et al Central amylin acts as an adiposity signal to control body weight and energy expenditure, Physiology & Behavior, 101:45 Amylin (2 pmol/h) significantly lowered body weight compared to saline after 2 weeks of infusion, independent of whether prior body weight was decreased by fasting, increased by voluntary overfeeding or unmanipulated. Chronic amylin also reduced RQ, implying a preferential oxidation of fat. There are literally dozens of papers. Care to comment?
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molbiogirl
Member (Idle past 2660 days) Posts: 1909 From: MO Joined: 06-06-2007
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Increased FFAs in the obese
Guyenet writes: In obesity, fat tissue is insulin resistant. How do I know? Because the fat tissue of obese people doesn't suppress fatty acid release in response to experimentally elevated insulin or mixed meals as effectively as the fat tissue of a lean individual (18, 19). Guyenet writes: There is no defect in the ability of fat cells to release fat in obesity, the problem is that the fat that is released is not being oxidized (burned) at a rate that exceeds what is coming in from the diet, therefore it all ends up back in the fat tissue. Hypothesis falsified (#2). Fat people release more fat from fat cells, not less.
F. Xavier et al, The Obesity Epidemic: Pathophysiology and Consequences of Obesity, Obesity Research (2002) 10, 97S—104S The increased levels of free fatty acids (FFAs) found in obese individuals also contribute to the defects in glucose use and storage. As body fat increases, the rate of lipolysis rises, leading to increased FFA mobilization and consequently to increased FFA oxidation in muscle and liver. Jensen, M et al, Influence of body fat distribution on free fatty acid metabolism in obesity, J Clin Invest. 1989 April; 83(4): 1168—1173. Plasma free fatty acids (FFA), originating from the release of adipose tissue triglyceride fatty acid, represent virtually the only route by which these fat stores can be transferred to nonfat tissue for net loss via oxidation.
Both types of obesity were associated with impaired suppression of FFA turnover compared to nonobese women.
In summary, the basal release of FFA from adipose tissue to meet lean body mass energy needs is greater in obese women than nonobese women. Groop, L et al. Effect of insulin on oxidative and nonoxidative pathways of free fatty acid metabolism in human obesity, AJP - Endo July 1992 vol. 263 no. 1 1) Lipolysis in uncomplicated obesity is normally sensitive to insulin; the enhanced FFA flux is simply a consequence of the increased fat mass. 2) Nonoxidative FFA disposal expressed per lean body mass is enhanced in obese subjects and correlates with the increase in plasma FFA concentration and fat mass. 3) Enhanced oxidation of intracellular lipids contributes to the enhanced rate of total lipid oxidation in obese subjects. There are over 400 cites of this paper alone that support increased FFA levels in fat people. If carb --> insulin --> increased fat storage, how is this possible?
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