tag:blogger.com,1999:blog-1629175743855013102.post5856430771494713220..comments2024-03-27T23:47:41.656-07:00Comments on Whole Health Source: Is it Time to Re-write the Textbooks on Insulin and Obesity? Part IIStephan Guyenethttp://www.blogger.com/profile/09218114625524777250noreply@blogger.comBlogger80125tag:blogger.com,1999:blog-1629175743855013102.post-48858386317892696462012-12-26T16:26:49.162-08:002012-12-26T16:26:49.162-08:00Science will go on discovering many things. Meanwh...Science will go on discovering many things. Meanwhile, we have some irrefutable facts: incidence of obesity in pre-industrial cultures is low to non-existent, and is the incidence of the chronic metabolic illnesses so common today. In the US, the incidence of obesity and the illneses just mentioned rise in accordance with the ascendence of the food industry. The main factors in this food industry are refined sugar, refined flour, refined vegetable oils, artifial flavors and coloring. That is really all you need to know to assure health insofar as health is related to diet. As for how this unholy mixture in industrial food plays havoc in different ways with different human beings, that will no doubt provide grist for scientific mills for many years to come.Anonymoushttps://www.blogger.com/profile/07677805523283932940noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-12640965218636030382012-12-23T01:28:08.283-08:002012-12-23T01:28:08.283-08:00I don’t have much word to say since I shared the s...I don’t have much word to say since I shared the same thought of the rest of the comments that’s here. To be honest HCG Diet works for me and that is all say. It is painless…<br /><a href="http://www.book-pal.com/" rel="nofollow">Book-Pal.com</a><br />Anonymoushttps://www.blogger.com/profile/13004188897737691744noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-84615245287473475832012-12-19T06:14:33.952-08:002012-12-19T06:14:33.952-08:00Regarding Andreas Eenfeldts view on the cause of o...Regarding Andreas Eenfeldts view on the cause of obesity. This was published on his Swedish site today, kostdoktorn.se. http://translate.google.com/translate?sl=sv&tl=en&js=n&prev=_t&hl=sv&ie=UTF-8&eotf=1&u=http%3A%2F%2Fwww.kostdoktorn.se%2Fvisst-sanker-lchf-mat-ditt-insulin-kraftigt%2F<br /><br />He's definitely in the same boat as Taubes. I guess he just doesn't want to show it on the international stage yet. <br /><br />I guess he didn't want to put it up on dietdoctor.comJacob Gudiolhttps://www.blogger.com/profile/01796029192417249389noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-92062831681665879512012-12-19T03:54:20.231-08:002012-12-19T03:54:20.231-08:00Gretchen, that paper you linked is extremely inter...Gretchen, that paper you linked is extremely interesting. I've been trying to find out what iron does in adipocytes for a long time. It seems that iron overload upregulates mitoNEET, which stops iron from getting into mitochondria. This means a shortage of iron-dependent enzymes so the cells can't burn a lot of fat and accumulate it instead. But they're healthier because their mitochondria aren't being damaged by iron, so their production of adiponectin is very good. Adiponectin prevents insulin resistance, so the animals are insulin sensitive despite being massively obese. <br /><br />Oddly, lipolysis is higher, not lower, but the fatty acids are taken up again into the cell and re-esterified. So I suppose the point of the whole thing is to prevent lipotoxicity to other tissues, including pancreatic beta cells. <br /><br />People do say obesity protects against diabetes. And diabetes is linked to iron overload. Perhaps one function of adipocytes is to store iron so it doesn't damage beta cells. Then mitoNEET makes sure it doesn't damage the adipocytes, and they accumulate fat so the fatty acids can't damage beta cells either.Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-70799495569157507722012-12-19T03:04:35.865-08:002012-12-19T03:04:35.865-08:00I wrote:
^Take-home-message: do not mix risk pred...I wrote:<br /><br /><i>^Take-home-message: do not mix risk predictors and mechanism of action. Socio-economic status is very good risk predictor for obesity even though it has no direct role in the pathophysiology of obesity itself.</i><br /><br />Being a poor, middle-aged African-American female in Alabama, USA would translate to almost a bullet-proof risk predictor for obesity and diabetes. Peterhttps://www.blogger.com/profile/12904866274339527690noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-15326695589464588182012-12-19T02:56:52.769-08:002012-12-19T02:56:52.769-08:00@Gadfly,
having an access to well sanitized loo&...@Gadfly, <br /><br />having an access to well sanitized loo's, vaccinations and antibiotics are better predictors for mortality than LDL-C cholesterol. I've never claimed the opposite, however I though you were interested in chronic disease. <br /><br />LDL-C is causal factor in atherosclerosis. This is well established in biomedical science. There's no atherosclerosis independent of elevated LDL-C cholesterol no matter what is your blood glucose, cigarette smoking status, weight, etc. These risk factors cannot produce plaques themselves. They can only exacerbate the damage CAUSED by elevated serum cholesterol. <br /><br />Epidemiological studies on homogeneously high risk populations may find better risk estimators than cholesterol, but these should not be confused with mechanism itself. In other words, blood-pressure, cigarette smoking, elevated glucose, HDL levels may turn out to be better risk predictors than cholesterol since until very recently time-weighted exposure to LDL has not been reliable quantified. LDL-C CAUSES plaque formation throughout the life beginning in childhood.<br /><br />Each 1mmol (38mg/dl) drop in LDL-C cholesterol since birth is independently associated with ~55% reduction in CHD.<br /><br /><b>Effect of Long-Term Exposure to Lower Low-Density Lipoprotein Cholesterol Beginning Early in Life on the Risk of Coronary Heart Disease: A Mendelian Randomization Analysis</b><br /><br /><i><b>Background</b> LDL-C is causally related to the risk of CHD. However, the association between long-term exposure to lower LDL-C beginning early in life and the risk of CHD has not been reliably quantified.</i><br /><br /><i><b>Conclusions</b> Prolonged exposure to lower LDL-C beginning early in life is associated with a substantially greater reduction in the risk of CHD than the current practice of lowering LDL-C beginning later in life.</i><br /><a rel="nofollow">http://intranet.cardiol.br/coberturaonline/slides/Reduction%20in%20LDL%20Presentation%20Slides.pdf</a><br /><br /><b>Lipoprotein lipase Ser447Ter polymorphism associated with the risk of ischemic stroke: a meta-analysis</b><br />http://www.ncbi.nlm.nih.gov/pubmed/21816453<br /><br />Take-home-message: do not mix risk predictors and mechanism of action. Socio-economic status is very good risk predictor for obesity even though it has no direct role in the pathophysiology of obesity itself.Peterhttps://www.blogger.com/profile/12904866274339527690noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-64716305726156789182012-12-19T00:41:50.500-08:002012-12-19T00:41:50.500-08:00Karl, I see you point. Here in Finland soy, sunflo...Karl, I see you point. Here in Finland soy, sunflower or corn oils are not an issue, we consume canola and olive oils which are very different. Our intake of n-6 PUFAs is less than 5 E %. <br /><br />I don't buy your theory. PUFA is not linked to development of T2D or obesity in epidemiological studies, neither in shorter term RCTs. <br /><br />Mozaffarian & Micha 2010 (Saturated Fat and Cardiometabolic Risk Factors, Coronary Heart Disease, Stroke, and Diabetes: a Fresh Look at the Evidence): "In contrast, three of four cohorts [54] observed lower incidence of diabetes with greater consumption of PUFA and/or vegetable fat [53, 55, 56]." <br /><br />But who knows, perhaps one day it turns out that you're right. <br /><br />Reijohttps://www.blogger.com/profile/16600461974345868939noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-66993482038683803852012-12-18T15:10:52.824-08:002012-12-18T15:10:52.824-08:00You guys better be nice to Peter or he'll get ...You guys better be nice to Peter or he'll get mad and start posting under one of his other accounts (e.g., Bog). Then you'll really be sorry. :)<br /><br />You see, depending on how much of a troll he's feeling like on any given day, he'll choose between multiple accounts. "Peter" for example is about a 3 out of 10 on the troll scale, whereas "Bog" is like a 9. Actually the "Bog" account got banned a while back so I guess we won't see that one. Oh well. Nevermind. :)kiltonhttps://www.blogger.com/profile/06442880766791928662noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-31336851599991290362012-12-18T12:38:30.707-08:002012-12-18T12:38:30.707-08:00"Maybe you just perceive the blog post as &qu..."Maybe you just perceive the blog post as "religious fervour" since you probably eat an LDL-C cholesterol elevating diet. We don't like to hear bad news about our bad habits."<br /><br />Thanks for your concern. Mine is fine. Of course, we know from some of the largest studies done on cardiac risk factors that LDL-C ranked about 9th on the list of stuff. Heck, psycho-social factors are a greater contributing factor to CVD than LDL-C on it's own. But you keep beating that bible, dearest. Gadflyhttps://www.blogger.com/profile/18270799853452520827noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-8333908279516683932012-12-18T12:00:42.832-08:002012-12-18T12:00:42.832-08:00Gretchen
Yes, - I'm talking about the vast ma...Gretchen<br /><br />Yes, - I'm talking about the vast majority of T2D - some people have done so much damage with elevated BG and secondary effects of obesity that they might have to take meds. There is a large number of people that no longer need medication once they go on a low-carb diet.<br /><br />@Reijo<br />I'm saying to opposite of conventional wisdom - while PUFAs increase insulin sensitivity - which even lowers BG short term - the problem starts when people stop getting fatter. Free FA start to leak - the insulin sensitivity once again goes down as the adipocytes are now distended - BG goes back up - the combination of high BG and FFA is toxic. <br /><br />I think there are serious long term risks eating the large amounts of PUFAs in the US average diet.karlhttps://www.blogger.com/profile/13490274388549702613noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-35199813118944455182012-12-18T09:32:54.531-08:002012-12-18T09:32:54.531-08:00““However, this result does not imply that an exce...““However, this result does not imply that an excess of insulin action (determined both by insulin concentration and tissue sensitivity to insulin) is a causal factor in common obesity, or that hyperinsulinemia precedes insulin resistance in the etiology of common obesity.”<br />Here is the remaining gap. Our results (in the controlled and artificial conditions it was conducted) do in fact show exactly that – that the excess of insulin IS required – because when we remove the excess insulin (and only the excess insulin) the obesity does not occur. Also, we clearly see hyperinsulinemia (seen within 1 week after HFD) precede both the obesity (~20 weeks after HFD) and IR (never) in our model.”<br /><br />I think this is the crux of the issue here. Can we agree that a positive energy balance (i.e. “excess calories”) is a necessary condition for common obesity? If so, the question is, where do those calories go? It’s obvious that insulin is a major hormone regulating the balance of energy between cells and blood. “Normal insulin action” is primarily about preventing hyper or hypoglycemia, correct? <br />Dr. Johson, are you saying that both mice maintained normoglycemia despite only the “hyperinsulinemic” mice gaining fat mass? If so, where the heck are the calories going? Muscular tissue? Increased maintenance respiration? <br />Although insulin plays a role in the CNS, it still seems to me that it operates mostly on short time-scales and is supposed to be responsive to blood glucose homeostasis. Although the signaling is no doubt complex (and above my level of understanding), I fail to see why it is central to understanding common obesity. Again, my distinction is between something that is a proximal cause (likely) versus a root cause (unlikely). I guess the dispute is over what is “intact insulin signaling”? Do you think that variations in insulin signaling play a role in determining whether excess calories are disposed into fat tissue or by some other means? If so, I see what you’re getting at…<br />Chris Wilsonhttps://www.blogger.com/profile/07791413012165238990noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-20876760682428044782012-12-18T08:48:42.298-08:002012-12-18T08:48:42.298-08:00@Zachary: Thanks!@Zachary: Thanks!Gretchenhttps://www.blogger.com/profile/17019921800841883073noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-87514789873217685002012-12-18T06:00:38.714-08:002012-12-18T06:00:38.714-08:00Oh, Petey and his Papau New Guineans...
So good,...Oh, Petey and his Papau New Guineans... <br /><br />So good, so protective and healthy is their diet that worldwide statistics rank New Guinea at 29th in the world at a rate of about 186 deaths/100,000 folks. That's *significantly* ahead of those fat-guzzling French, Dutch, Danes, Swedes.... Must be the sweet potatoes. <br /><br />If we play your game of dietary reductionism, it's pretty clear that the diets of those European countries are vastly superior to that of those in New Guinea. Gadflyhttps://www.blogger.com/profile/18270799853452520827noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-16355120627199619032012-12-18T05:19:54.405-08:002012-12-18T05:19:54.405-08:00Playing around with google a bit more, shows that ...Playing around with google a bit more, shows that NEET refers to the single letter amino acid code for the last 4 c-terminal residues of the protein(Asn-Glu-Glu-Thr).Anonymoushttps://www.blogger.com/profile/15828669663376568937noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-588135438854923902012-12-18T01:50:43.127-08:002012-12-18T01:50:43.127-08:00Gadfly wrote:
To overlook a myriad of confounding...Gadfly wrote:<br /><br /><i>To overlook a myriad of confounding factors is willful blindness or stupidity. "But, but, but those people who live in an entirely different way to us ate "x" and don't SEEM to have had cancer. Must be the sweet potatoes!" The article you linked to on your site is a hodgepodge of anecdotes, poorly subtstantiated dietary reductionism coupled with religious fervour (and all the objectivity that implies). You and Don Matesz are a match made in heaven. To overlook a myriad of confounding factors is willful blindness or stupidity. "But, but, but those people who live in an entirely different way to us ate "x" and don't SEEM to have had cancer. Must be the sweet potatoes!" The article you linked to on your site is a hodgepodge of anecdotes, poorly subtstantiated dietary reductionism coupled with religious fervour (and all the objectivity that implies). You and Don Matesz are a match made in heaven"</i> <br /><br />Thanks for your feedback, please be kind and identity any anecdotes, possible co-founders and religious fervour you encountered so I can pass the info. The kind of ecologic (and clinical data) collected from parts of Asia, Central-Africa and South-America has influenced many western scholars to conduct trials on the effects of dietary intervention to various biomarkers, gene expression, heart disease, diabetes and prostate cancer. Besides, isn't this kind of ecologic analysis of various populations exactly what paleo-folk are all about? Masai this, Inuits that. <br /><br /><b>Traditional Diets in Asia Pacific and Implications for Health, and the History of Disease Prevention</b> <br /><a rel="nofollow">http://healthylongevity.blogspot.fi/2012/11/traditional-diets-in-asia-pacific-and.html</a> <br /><br />In regards to specific example of Papua New Guineans on their exceptionally high carbohydrate intake, these people are well studied in terms of living people and autopsies. <br /><br /><b>Epidemiological studies in a total highland population, Tukisenta, New Guinea: Cardiovascular disease and relevant clinical, electrocardiographic, radiological and biochemical findings</b> <br />http://www.sciencedirect.com/science/article/pii/0021968173900313<br /><br />Maybe you just perceive the blog post as "religious fervour" since you probably eat an LDL-C cholesterol elevating diet. We don't like to hear bad news about our bad habits.Peterhttps://www.blogger.com/profile/12904866274339527690noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-59299904951547516292012-12-18T01:43:45.915-08:002012-12-18T01:43:45.915-08:00This comment has been removed by the author.Peterhttps://www.blogger.com/profile/12904866274339527690noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-42935147252264887052012-12-17T18:55:29.845-08:002012-12-17T18:55:29.845-08:00Google took me not father that the article http://...Google took me not father that the article http://www.ncbi.nlm.nih.gov/pubmed/22562611<br />Sorry, couldn't find more.Galina L.https://www.blogger.com/profile/09156132815504279615noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-81929899591596665152012-12-17T17:42:05.355-08:002012-12-17T17:42:05.355-08:00@Galina: Yes, but what do the initials NEET stand ...@Galina: Yes, but what do the initials NEET stand for?Gretchenhttps://www.blogger.com/profile/17019921800841883073noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-11811278487189005812012-12-17T17:39:21.816-08:002012-12-17T17:39:21.816-08:00According to Wiki article http://en.wikipedia.org/...According to Wiki article http://en.wikipedia.org/wiki/CDGSH_iron_sulfur_domain <br /><br />The CDGSH iron sulfur domain 1 protein is also referred to as mitoNEET is an integral membrane protein located in the outer mitochondrial membrane and whose function may be to transport iron into the mitochondria.Galina L.https://www.blogger.com/profile/09156132815504279615noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-66382244664875607942012-12-17T17:24:56.139-08:002012-12-17T17:24:56.139-08:00I previously said, "What we need to learn fro...I previously said, "What we need to learn from the insulin-sensitive obese people is *why* they don't develop insulin resistance."<br /><br />Coincidentally, this came in today and purports to explain why. I only read the abstract.<br /><br />http://www.nature.com/nm/journal/v18/n10/full/nm.2899.html<br /><br />BTW, if anyone knows what NEET stands for, I'd be interested to know.Gretchenhttps://www.blogger.com/profile/17019921800841883073noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-27145253453627747872012-12-17T13:55:04.357-08:002012-12-17T13:55:04.357-08:00This comment has been removed by the author.Brian A.C. Rondeauhttps://www.blogger.com/profile/16299831767079270899noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-86218513643706821942012-12-17T13:39:26.547-08:002012-12-17T13:39:26.547-08:00Stephan asks if humans can become obese on ketogen...Stephan asks if humans can become obese on ketogenic diet. Evidence from the treatment of pediatric epilepsy show that this is possible but rare. Some published patient series describe weight gain as 'side effect'. Here is one open access paper http://www.seizure-journal.com/article/S1059-1311(11)00168-3/fulltext#sec0045 and there is more at PubMed.<br /><br />Karl, PUFAs improve insulin sensitivity in humans also in the context of low carbohydrate diet. RCT evidence http://jcem.endojournals.org/content/89/4/1641.long Reijohttps://www.blogger.com/profile/16600461974345868939noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-12306745680629895332012-12-17T11:14:59.787-08:002012-12-17T11:14:59.787-08:00Karl, "Avoiding carbs returns postprandial BG...Karl, "Avoiding carbs returns postprandial BG spikes to less than 110 and reduces trygly levels to around 50."<br /><br />This statement is not true in everyone, especially people with diabetes. As with clinical trials, it may be the average response to LC diet, but there are outliers.<br /><br />Gretchenhttps://www.blogger.com/profile/17019921800841883073noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-8316391939529365922012-12-17T10:12:59.768-08:002012-12-17T10:12:59.768-08:00The point that I think Stephan is missing is that ...The point that I think Stephan is missing is that 'normal' insulin levels depend on the other feedback loops - insulin sensitivity, leptin, sympathetic stimulation. <br /><br />Weight gain/loss IS the flux of FA in/out of adipose tissue. ( Can we agree on this?) If we also agree that insulin is one of the controls - the relative level of insulin has to be included in the understanding of obesity.<br /><br />My background includes work in electronic feedback loops - the effect of insulin is likely not just a simple summed input to the FA flux - as is often the case in both electronics and biology, the feedbacks can be multiplied, act as exponents etc. Thus looking at the level of one feedback component without controlling for the others can't prove your hypothesis that the pro insulin effect of carbohydrates don't have a long term (more than 3 week) effect on the average direction and magnitude of this flux. <br /><br />My hunch is the reason lowcarb diets work, is that the intricate BG control loop is broken in about 40% of the public. Avoiding carbs returns postprandial BG spikes to less than 110 and reduces trygly levels to around 50. <br /><br />Even if they were not helpful in maintaining a healthy weight, reducing BG to levels below levels where elevated glucose makes fats become toxic which reduces inflammation and improves overall health needs to be considered.<br /><br />It is oxLDL is goes into macrophages in the intima of arteries - and one potent intervention to reduce oxLDL is to keep PP BG below 110. Adjusting carbohydrate intake to accomplish this appears a reasonable approach.karlhttps://www.blogger.com/profile/13490274388549702613noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-38317981360714553552012-12-17T05:30:29.764-08:002012-12-17T05:30:29.764-08:00OK, I'm a comparatively stupid personal traine...OK, I'm a comparatively stupid personal trainer,so I'm probably missing the point. As I understand it, you can put on weight by eating low GI foods, (e.g sugar), as the speed of digestion of these foods is such that your body cannot all process the energy released, and stores that which it can't process as fat. As far as I'm aware, this can happen to anyone, whatever their insulin resistance or their BMI. Presumably, insulin resistance would make this worse, but if you stuff yourslef with enough of the wrong foods, it seems that you're going to become obese, whether you're insulin resistant or not. Or is there something I've missed (quite possible!)?Anonymousnoreply@blogger.com