Dang. This thread has some of the longest posts I've ever seen on letsrun.
Dang. This thread has some of the longest posts I've ever seen on letsrun.
Well, yes, I agree that studies that are not completely controlled( like metabolic ward studies) are still useful. However, it is still a fact that the reporting of intakes by subjects are imperfect. So the studies are not to be ignored, but to be considered along with other evidence. And if the results of the studies are not fully replicated, one must question why those results were achieved.
a) yes, metabolic wards studies are superior when testing weight gain/loss due to various diets controlled for calories (and activity)
b) studies examining how well people can stick to diets, and how hungry they get on those diets are also important (free-living studies). so yes, in that case, you DON'T want to control for everything. You risk reporting errors, but in some cases food is provided which limits these errors. In these types free living of studies (food provided or not), I think you are completely incorrect to state that low-carb has been clearly been shown to outperform low-fat. In reality, after the short-term (3-6 mos), the diets are generally quite equal. We can look at research examining this question shortly. I think you have bought into the low-carb dogma that these studies are in favor of your position. In reality, they are not.
c) as I said, previously, I think it is a bit of a cop-out to call both low-fat diets in the 2 ward studies I presented to you as "actually low-carb." As I said, if one is eating a rather hypocaloric diet, it will be BOTH low carb and low fat in absolute terms. It is quite low in everything, right? So....once again, LOW CALORIES is the key. Still, the higher carb diet had 3x the carbs, and resulted in twice the insulin levels. But that still is not enough for you? Should not have the doubled insulin response created the fat storing environment you expected? It did not.
Well, I bet I can dig up some ward studies that looked giving calories to maintain body weight (thus not hypocaloric), and thus the carbs were more what you are looking for and the results will be the same: no difference in fat loss/gain between low carb and high carb. We will see.....stay tuned.
1) yes, it is somewhat controversial, but there are some rather strong associations between sat fat intake and CVD deaths. sure, such population studies are imperfect, but as you asked about free-living studies: are we going to ignore these? no. It's part of the puzzle. And i know that Keys is the whipping boy of many low-carbers, but his country studies and associations of sat fat and CVD remain relevant today and not dismissed by most mainstream nutrition scientists.
Read up on North Karelia (Finland).
One article I found on this was: Fat and Heart Disease: Yes We Can Make a Change –
The Case of North Karelia (Finland)
It's main findings: there was exceptionally high CVD death rates in finland in the '70's. In reaction to this they undertook a large community intervention (later spread to the entire country). To quote:
"Their aim was to change population diets, especially with respect to the quality of fat: to reduce saturated and increase unsaturated fat intake. In addition, emphasis was placed on increased vegetable intake and salt reduction.
This comprehensive action in Finland has involved health education programs, preventive measures in health services, actions at schools, broad col- laboration with non-governmental and private sector orga- nizations, government policies, population-based monitor- ing and evaluation, and international collaboration"
Results: The combined efforts of all stakeholders have greatly helped people to reduce the intake of saturated fat and to replace this with unsaturated fat. This has been associated with an improved quality of the dietary fat (e.g. in 1972, over 90% of the population used butter on their bread compared to 5% at present) and a remarkable reduction in blood cholesterol
levels. It has led to a 80% reduction in annual CVD mortality rates among the working aged population, to a major in- crease in life expectancy and to major improvements in functional capacity and health.]Studies have shown that the reduction in blood cholesterol levels, explained by the tar- get dietary changes, have had the greatest impact on these very favorable health changes. Conclusion: The Finnish ex- perience shows both the feasibility and great potential of CVD prevention and heart health promotion through gen- eral dietary changes in the population."
Now you can argue that other changes occurred in the diet too (and less smoking too), and its hard to disentangle effects. Yes, but there is a strong opinion that the major change, lowering sat fat intake, and replacing partly with unsat fats, with resulting lowering of ldl and total cholesterol levels, is what brought about the biggest impact on a huge drop in CVD deaths.
I would say that is an impressive result in favor of "hard outcomes" relating sat fat intake and CVD deaths.
And I can address some of your specific comments on cholesterol, ldl, hdl, particle size and number, etc, in a moment, but it does seem that while you've found Taubes to be wrong about some of his comments about ldl (particle size importance) you still support him on dismissing the concept of dangers of excessive sat fat intake and/or high ldl-c and total cholesterol. This is of course in keeping with support of a high fat/low carb diet, but goes completely against mainstream nutrition and health views. This is what the Report of the DGAC on the Dietary Guidelines for Americans, 2010 says on the topic (have you read it? Have you studied this question more extensively than them? Are you really confident that they are so wrong? Because they continue to take a very strong stance on sat fat intake and ldl/total cholesterol and T2D and CVD connections/risks.
Question 1. What is the Effect of Saturated Fat Intake on Increased Risk of Cardiovascular Disease or Type 2 Diabetes, Including Effects on Intermediate Markers such as Serum Lipid and Lipoprotein Levels?
Conclusion
Strong evidence indicates that intake of dietary SFA is positively associated with intermediate markers and end point health outcomes for two distinct metabolic pathways: 1) increased serum total and LDL cholesterol and increased risk of CVD and 2) increased markers of insulin resistance and increased risk of T2D. Conversely, decreased SFA intake improves measures of both CVD and T2D risk. The evidence shows that 5 percent energy decrease in SFA, replaced by MUFA or PUFA, decreases risk of CVD and T2D in healthy adults and improves insulin responsiveness in insulin resistant and T2D individuals.
Implications
As the evidence indicates that a 5 percent energy decrease in SFA, replaced by MUFA or PUFA, results in meaningful reduction of risk of CVD or T2D, and given that in the US population 11-12 percent of energy from SFA intake has remained unchanged for over 15 years, a reduction of this amount resulting in the goal of less than 7 percent energy from SFA should, if attained, have a significant public health impact. As an interim step toward this less than 7 percent goal, all individuals should immediately consume less than 10 percent of energy as saturated fats. This impact would not only be limited to a reduction in heart disease and stroke, but also in T2D, a disease currently rising in incidence and prevalence. This substitution of MUFA and PUFA for SFA assumes no change in energy intake. The age of onset of T2D is substantially younger than that of CVD and increasingly frequent in adolescence. Reduction in SFA in children and young adults may provide benefits decades earlier than currently appreciated. The growing data to support a risk of T2D from SFA consumption supports the need for fat-modified diets in persons with pre-diabetes, including those with metabolic syndrome, and those with established diabetes. Early signs of atherosclerotic CVD are also seen in children and a number of studies indicate that the atherosclerotic process begins in childhood and is affected by high blood cholesterol levels. Therefore, reduction in SFA in children and young adults may provide benefits decades earlier than currently appreciated relative to both CVD and T2D incidence.
Уже более пяти десятилетий мы промыли мозги, чтобы поверить, что насыщенный жир вызывает болезни сердца. Это такая глубоко укоренившаяся вера, что мало кто даже оспаривать. Это просто часть нашей культуры сейчас.
Почти каждый день я читаю или слышу о ком-то с гордостью, что у них есть "здоровый" диеты, потому что они не едят сливочное масло, сыр или красное мясо или любые другие продукты с высоким содержанием насыщенных жиров (по фигу, что красное мясо не особенно высоким содержанием насыщенных жира, но это тема для другой должности). Или я мог бы подслушать кого-то в продуктовом магазине говоря, сколько они предпочитают всю жира йогурт с низким содержанием жира версии, но они едят нежирное материал в любом случае, потому что они хотят сделать «здоровой» выбор.
То, что большинство людей не понимают, что прошло много лет, чтобы убедить людей, что есть традиционные, животные жиры, такие как сливочное масло и сыр это плохо для вас, во время еды сильно обработанные, промышленные растительные масла, такие как кукурузное и соевое масло хорошо для вас. Это просто бросил вызов здравому смыслу для большинства людей. Но неустанное, широкая кампания по дискредитации насыщенных жиров и содействовать индустриальные масла был в конечном итоге успешным.
Что если я скажу вам, что нет никаких доказательств, чтобы поддержать идею, что насыщенный жир потребление вызывает болезни сердца? Что если я скажу вам, что 50 + лет культурного промывания мозгов мы все были предметом была основана на небольших, плохо спланированных исследований? А что если я скажу вам, что обзор крупных, хорошо спланированных исследований, опубликованных в авторитетных медицинских журналах показали, что нет никакой связи между содержанием насыщенных жиров и сердечно-сосудистых заболеваний?
Ну, вот что я вам говорю. Мы Beed обмануты. Лгал. И мы сильно пострадали в результате. Мало того, что мы пострадали от их рекомендуется есть упакованные и обработанные пищевые продукты, приготовленные из дешевых, безвкусных растительных масел и рафинированных углеводов (с низким содержанием жира кухня), но эти самые продукты нам сказали бы защитить нас от сердечно-сосудистых заболеваний на самом деле способствуют его!
ПОСЛЕДНИЙ отзыв Я говорю О является МЕТА-анализ, опубликованный на этой неделе в американском журнале клинического питания . Это объединяются данные из 21 уникальных исследований, которые включали почти 350 тысяч человек, около 11 тысяч из которых разработаны сердечно-сосудистых заболеваний (ССЗ), отслеживаемые в среднем 14 лет, и пришли к выводу, что нет никакой связи между потреблением насыщенных жиров и заболеваемости болезнь сердца или инсульт.
Позвольте мне сказать, что в общедоступных терминах для вас:
Употребление насыщенных жиров не вызывает болезни сердца.
Там. Вот и все.Это действительно все, что вам нужно знать. Но если вы хотите, чтобы узнать больше об этом, Джон Бриффа и Крис Masterjohn написали Статьи О Нем ЗДЕСЬ И ЗДЕСЬ .
Интересно, как долго это займет, чтобы эта информация просачивания в господствующую культуру? К сожалению, это не произойдет в одночасье. Парадигмы не работает таким образом. Но я видел, что некоторые позитивные признаки, и я верю, поворачивает. Будем надеяться, это не займет еще 50 лет.
Xfit_guy_the_real_1 wrote:
Rekrunner, let me translate your post:
1. our forefathers ate less flour (--> paleo/no grains)
2. our forefathers are less sugar (=carbs) --> paleo
3. our forefathers did not fear animal fat, they used butter and lard/tallow for cooking, fatty cuts of meat. This was before chicken were bread to be 95% breast. --> paleo
And they starved all winter.
From Google Translate:For over five decades, we have been brainwashed to believe that saturated fat causes heart disease. It's such a deeply ingrained belief that few people even question it. It's just part of our culture now .Almost every day I read or hear about someone with pride that they have a " healthy" diet because they do not eat butter, cheese or red meat , or any other foods high in saturated fat ( nevermind that the red meat is not particularly high in saturated fat, but this is a topic for another post ) . Or I could overhear someone at the grocery store saying how much they prefer full -fat yogurt , low -fat version, but they eat low-fat stuff anyway, because they want to make a "healthy" choice.What most people do not realize that it took many years to convince people that there is a traditional , animal fats such as butter and cheese is bad for you , while eating highly processed , industrial vegetable oils, such as corn and soybean oil is good for you. It just defied common sense for most people. But relentless , wide campaign to discredit the saturated fat and promote industrial oil was eventually successful.What if I told you that there is no evidence to support the idea that saturated fat consumption causes heart disease ? What if I told you that 50 + years of cultural brainwashing we have all been the subject was based on a small , poorly designed studies ? And what if I told you that the review of large , well-designed studies published in reputable medical journals have shown that there is no link between saturated fat and cardiovascular disease ?Well , that's what I'm telling you . We Beed deceived. Lied . And we have suffered greatly as a result. Not only that we have suffered from their recommended to eat packaged and processed foods made from cheap , tasteless vegetable oils and refined carbohydrates ( low-fat cuisine) , but these same foods we were told would protect us from cardiovascular diseases at the actually contribute to it!Last review I'm talking about is a meta - analysis published this week in the American Journal of Clinical Nutrition . This combined data from 21 unique studies that included nearly 350,000 people, about 11,000 of whom developed cardiovascular disease (CVD) , tracked an average of 14 years , and came to the conclusion that there is no connection between saturated fat intake and incidence heart disease or stroke .Let me say that in layperson's terms for you :The use of saturated fat does not cause disease.There. That vse.Eto really all you need to know . But if you want to learn more about it , John and Chris Briffa Masterjohn wrote an article about it here and here.I wonder how long it will take this information to trickle into the mainstream culture ? Unfortunately, this did not happen overnight . Paradigm does not work that way. But I saw some positive signs , and I believe turns . Hopefully it will not take another 50 years .
As much sense wrote:
Уже более пяти десятилетий мы промыли мозги, чтобы поверить, что насыщенный жир вызывает болезни сердца. Это такая глубоко укоренившаяся вера, что мало кто даже оспаривать. Это просто часть нашей культуры сейчас.
Почти каждый день я читаю или слышу о ком-то с гордостью, что у них есть "здоровый" диеты, потому что они не едят сливочное масло, сыр или красное мясо или любые другие продукты с высоким содержанием насыщенных жиров (по фигу, что красное мясо не особенно высоким содержанием насыщенных жира, но это тема для другой должности). Или я мог бы подслушать кого-то в продуктовом магазине говоря, сколько они предпочитают всю жира йогурт с низким содержанием жира версии, но они едят нежирное материал в любом случае, потому что они хотят сделать «здоровой» выбор.
То, что большинство людей не понимают, что прошло много лет, чтобы убедить людей, что есть традиционные, животные жиры, такие как сливочное масло и сыр это плохо для вас, во время еды сильно обработанные, промышленные растительные масла, такие как кукурузное и соевое масло хорошо для вас. Это просто бросил вызов здравому смыслу для большинства людей. Но неустанное, широкая кампания по дискредитации насыщенных жиров и содействовать индустриальные масла был в конечном итоге успешным.
Что если я скажу вам, что нет никаких доказательств, чтобы поддержать идею, что насыщенный жир потребление вызывает болезни сердца? Что если я скажу вам, что 50 + лет культурного промывания мозгов мы все были предметом была основана на небольших, плохо спланированных исследований? А что если я скажу вам, что обзор крупных, хорошо спланированных исследований, опубликованных в авторитетных медицинских журналах показали, что нет никакой связи между содержанием насыщенных жиров и сердечно-сосудистых заболеваний?
Ну, вот что я вам говорю. Мы Beed обмануты. Лгал. И мы сильно пострадали в результате. Мало того, что мы пострадали от их рекомендуется есть упакованные и обработанные пищевые продукты, приготовленные из дешевых, безвкусных растительных масел и рафинированных углеводов (с низким содержанием жира кухня), но эти самые продукты нам сказали бы защитить нас от сердечно-сосудистых заболеваний на самом деле способствуют его!
ПОСЛЕДНИЙ отзыв Я говорю О является МЕТА-анализ, опубликованный на этой неделе в американском журнале клинического питания . Это объединяются данные из 21 уникальных исследований, которые включали почти 350 тысяч человек, около 11 тысяч из которых разработаны сердечно-сосудистых заболеваний (ССЗ), отслеживаемые в среднем 14 лет, и пришли к выводу, что нет никакой связи между потреблением насыщенных жиров и заболеваемости болезнь сердца или инсульт.
Позвольте мне сказать, что в общедоступных терминах для вас:
Употребление насыщенных жиров не вызывает болезни сердца.
Там. Вот и все.Это действительно все, что вам нужно знать. Но если вы хотите, чтобы узнать больше об этом, Джон Бриффа и Крис Masterjohn написали Статьи О Нем ЗДЕСЬ И ЗДЕСЬ .
Интересно, как долго это займет, чтобы эта информация просачивания в господствующую культуру? К сожалению, это не произойдет в одночасье. Парадигмы не работает таким образом. Но я видел, что некоторые позитивные признаки, и я верю, поворачивает. Будем надеяться, это не займет еще 50 лет.
rekrunner wrote:
Last review I'm talking about is a meta - analysis published this week in the American Journal of Clinical Nutrition . This combined data from 21 unique studies that included nearly 350,000 people, about 11,000 of whom developed cardiovascular disease (CVD) , tracked an average of 14 years , and came to the conclusion that there is no connection between saturated fat intake and incidence heart disease or stroke .
Yes that's the recent one from 2010. The wording was:
"intake of saturated fat was not associated with an increased risk of coronary heart disease, stroke or cardiovascular disease."
and
"Our results suggest a publication bias, such that studies with significant associations tended to be received more favourably for publication."
Medical doctors, dietitians and nutritionists get big hard-ons for correlations in epidemiologic studies but generally just don't think enough about causal mechanisms. I mean how on earth can a single hydrogen atom (the difference between a saturated fat and an unsaturated fat) be the difference between a chain of carbon that causes heart disease and a chain of carbon that doesn't? Madness. (Spoiler: the answer is that saturated fat intake often correlates well with intake of processed meat cooked at high temperatures. It's not the sat fat, it's the lipid peroxides from the refined vegetable oils and advanced glycation endproducts doing the damage).
I've been trying to focus this thread towards highlighting the nonsense of calorie interventions and have tried to avoid the sat fat debate. But sod it, when in Rome...
Siri-Tarion et al "Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease", American journal of clinical nutrition 91, no 3 (March 2010)
Tyrannosaurus Rexing wrote:
just getting started. Barely have enough time to say half of what I want. Thanks for participating.
No problem. I admit I'm throwing out some random thoughts, mainly to bounce my ideas around and get some feedback. As I said, I've only read a handful of books, articles, etc., and my practical experience was losing 40 pounds in about two years purely from marathon training, and avoiding the snack machine, and reading diet books (osmosis?). I only talk about Atkins this much, because it's one book of the few books I read. I fully concede that his message "controlled carbs -> controlled weight" is too simple, and that he could have said more about fats, beyond "fats are of secondary importance" (he doesn't force you to eat only saturated fats, but doesn't forbid it either). He didn't completely neglect exercise, but my recollection is more like "oh yeah, almost forgot, exercise is important too". "Working in the fields" was my own comical observation.
My Atkins experience also contained a certain "myth-busting" element with whomever I spoke with (not you) about Atkins -- it has faults, but often not for the reasons they said -- because they didn't really understand what they were judging, and sometimes committed some major "faux pas", because they didn't read the "Dos and Donts" chapter of the book. I still have two more observations though. Since Atkins, by definition, is "result oriented", actually, every diet that doesn't make you gain beyond your ideal weight qualifies as an Atkins diet. Hypothetically, (say for a cyclist or ultra-marathoner) if you manage to find a low-fat/high-carb diet (say 500g/day) and you're able to maintain your weight at 130 pounds, with a BMI of 19, this qualifies as an Atkins diet -- because you've found your "controlled" carb range that allows you to maintain your healthy weight. I think much of what Atkins advises is for a narrow (no pun intended) target audience: the severely overweight/obese/morbidly obese who have developed some level of insulin resistance, and who are certainly eating too many refined carbs.
I guess you make a good point about CVD in 1950 -- I'll take your word for it anyway. I do recall Atkins reporting better blood values, like lower cholesterol or triglycerides, with weight loss, but cannot really evaluate beyond his observations. I'll try to make this my last word about Atkins.
Moving to the French, besides the things you mentioned, one part of what helps the French is eating more slowly. It's not unusual for a lunch at a restaurant to take 4 hours, while they eat many small portion courses in sequential fashion. It's like there is a time delay for your brain to decide it's full, and by then Americans will have eaten one portion too many.
Let me change the subject again to bring up an aspect that doesn't seem to have been mentioned yet. It's fine to take a scientific and clinical view of what kinds of foods and habits cause weight gain, and what constitutes ideal healthy diets. But what about psychology? Is obesity a problem of the stomach or the brain? Certainly, if someone is severely overweight, or worse, there is some buried psychological issue that's driving destructive, yet comforting, eating habits that needs to be addressed. Shouldn't nutritionists also study some form of psychology/psychiatry?
UK Limey runner wrote:
rekrunner wrote:
BTW, I didn't write that above, but just "google translated" the Russian.
I like the idea of, and the controversy generated by, Paleo diets. There is a certain logic that cavemen were not farmers. It's certainly possible to create a healthy diet from nuts and berries and seeds and fish and game.I also like many varieties of beer, so there is an obvious conflict for me. I doubt I would ever practice 100% Paleo by choice.
Xfit_guy_the_real_1 wrote:
Rekrunner, let me translate your post:
1. our forefathers ate less flour (--> paleo/no grains)
2. our forefathers are less sugar (=carbs) --> paleo
3. our forefathers did not fear animal fat, they used butter and lard/tallow for cooking, fatty cuts of meat. This was before chicken were bread to be 95% breast. --> paleo
T-Rex and the other morons always make it seem paleo is all about eating meat when in fact it is more about avoiding bad choices like sugar, grains and industrial vegetable oils.
rekrunner wrote:
I doubt I would ever practice 100% Paleo by choice.
Nor should you. It's not necessary and would be unpleasant without good reason.
"Cheating and digressions now and then are of great emotional benefit, and ... will have little impact on athletic performance and health benefits."
Loren Cordain
rekrunner wrote:
Moving to the French, besides the things you mentioned, one part of what helps the French is eating more slowly. It's not unusual for a lunch at a restaurant to take 4 hours, while they eat many small portion courses in sequential fashion. It's like there is a time delay for your brain to decide it's full, and by then Americans will have eaten one portion too many.
Good point:
the French: slow meal with friends over the course of hours, healthy animal fats and olive oil, raw cheese. Little (!) bread on the side. Red wine with lunch and dinner helps them be in a good mood.
the American: eats his subway sandwich on "healthy whole wheat" bread in his truck or desk while answering emails.
this is a long thread.
Here's what you need to do. Run more, do 3 workouts a week, and eat healthy. Thats all you can do. Eating certain foods at certain times or in certain porportions or doing x workout at x time vs y time will have a trivial impact.
oh boy. Well UK, I am glad you are firing back with your chippier side, but, of course, in my opinion, there are many problems with your below statements ( and I do find it revealing that you are QUITE familiar with all of the anti-main stream nutrition research and proponents. You've certainly read much of their talking points and "star" authors and studies. you were not surprisingly very quick to recognize the referenced "pro-sat fat" study, as it is celebrated on every anti-carb pro-sat fat blog in existence. I think it's clear that you've bought into their scrutiny of mainstream diet advice, but have you and they applied the same scrutiny/cynicism to THEIR points/results/research/theories? It doesn't appear that way to me. Are you and the bloggers familiar with the published rebuttals to this study? Not so much? I will post them shortly. )
rekrunner wrote:
Last review I'm talking about is a meta - analysis published this week in the American Journal of Clinical Nutrition . .... and came to the conclusion that there is no connection between saturated fat intake and incidence heart disease or stroke .
UK Limey runner wrote:
Yes that's the recent one from 2010. The wording was:
"intake of saturated fat was not associated with an increased risk of coronary heart disease, stroke or cardiovascular disease."
and
"Our results suggest a publication bias, such that studies with significant associations tended to be received more favourably for publication."
Medical doctors, dietitians and nutritionists get big hard-ons for correlations in epidemiologic studies but generally just don't think enough about causal mechanisms.
oh boy.....
Aren't you (and the blogger who is first quoted) quoting, and even touting, an epidemiological study("meta-analysis") that is finding a population non-correlation between sat fat intake and CVD? yes, you are. if these are garbage studies(as you seem to think: populations correlations without causations), why do it, and even celebrate it? Just ignore it!
(If you think such studies hold some worth, then yes, it's relevant to bring up contrary studies and look at the totality of such studies, along with more rigorous studies. Most, however, show a connection between sat fat intake and CVD. But if you think epi/populations studies are worthless....then don't quote them to support your side. Just say: those studies are only useless correlations!)
And aren't low-carbers CONSTANTLY harping on the *correlation* between human grain and dairy consumption and the agricultural revolution and later epidemics of obesity and "western diseases"? (but of course the relationship is often 1,000-20,000 years off. People have eaten grains and dairy for aeons, but obesity is a very new phenomenon Oh well...) Again yes. And do not low-carbers (of various forms) like to point out that the advent of packaged foods, and high sugar snacks, and larger sodas and servings, and supposedly increased intake of carbohydrates, and the bad advice of the USDA to cut fat (sat mainly) and increase low-fat/high carb foods *correlates* awfully well with increases of obesity and T2D in western nations..?? Of course the answer is a big resounding yes. So if you (and they) don't like large-scale population "correlations" of nutrients and disease, then I wouldn't bring them up at all. (now I think some of the above correlations are actually quite useful and instructive, but of course what obesity is really more correlating with and more caused by is increased calorie intake and decreased activity then it is with/by increased carb intake)
Now wait, I know your answer: correlations are fine if coupled with causations, and that is what you alluded to in the 2nd part of your above quote. Great. But I am pretty sure that the top nutrition and medical experts who believe the correlations between high sat fat intake (or reductions) and CVD disease are meaningful understand that principle (give them SOME credit) and have causations of CVD from sat fat intake in mind. Like, oh, I don't know, maybe the down-regulation of the LDL receptor by increasing intracellular cholesterol pools and decreasing LDL cholesterol uptake by the liver. LDL-C has shown to be inflammatory by itself, which can lead to "loss of endothelial integrity, followed by lipid and inflammatory cell infiltration, deposition of fatty streaks and ultimately foam cell production and neointimal expansion."
The plausible and actually tested mechanisms ARE there (yes, they are not completely figured out, or beyond debate, but don't act like the researchers have said: 'hmmm....I notice that people who scratch their butts more get CVD. That's it! No more butt scratching! ' without a thought to if that is plausible and whether or not that might or might not be a true causative factor)
If you don't want to read that with all of the extra annoying accidental underlines, here (and maybe you won't want to read it either way!)oh boy. Well UK, I am glad you are firing back with your chippier side, but, of course, in my opinion, there are many problems with your below statements ( and I do find it revealing that you are QUITE familiar with all of the anti-main stream nutrition research and proponents. You've certainly read much of their talking points and "star" authors and studies. you were not surprisingly very quick to recognize the referenced "pro-sat fat" study, as it is celebrated on every anti-carb pro-sat fat blog in existence. I think it's clear that you've bought into their scrutiny of mainstream diet advice, but have you and they applied the same scrutiny/cynicism to THEIR points/results/research/theories? It doesn't appear that way to me. Are you and the bloggers familiar with the published rebuttals to this study? Not so much? I will post them shortly. )
rekrunner wrote:
Last review I'm talking about is a meta - analysis published this week in the American Journal of Clinical Nutrition . .... and came to the conclusion that there is no connection between saturated fat intake and incidence heart disease or stroke .
UK Limey runner wrote:
Yes that's the recent one from 2010. The wording was:
"intake of saturated fat was not associated with an increased risk of coronary heart disease, stroke or cardiovascular disease."
and
"Our results suggest a publication bias, such that studies with significant associations tended to be received more favourably for publication."
Medical doctors, dietitians and nutritionists get big hard-ons for correlations in epidemiologic studies but generally just don't think enough about causal mechanisms.
oh boy.....
Aren't you (and the blogger who is first quoted) quoting, and even touting, an epidemiological study("meta-analysis") that is finding a population non-correlation between sat fat intake and CVD? yes, you are. if these are garbage studies(as you seem to think: populations correlations without causations), why do it, and even celebrate it? Just ignore it!
(If you think such studies hold some worth, then yes, it's relevant to bring up contrary studies and look at the totality of such studies, along with more rigorous studies. Most, however, show a connection between sat fat intake and CVD. But if you think epi/populations studies are worthless....then don't quote them to support your side. Just say: those studies are only useless correlations!)
And aren't low-carbers CONSTANTLY harping on the *correlation* between human grain and dairy consumption and the agricultural revolution and later epidemics of obesity and "western diseases"? (but of course the relationship is often 1,000-20,000 years off. People have eaten grains and dairy for aeons, but obesity is a very new phenomenon Oh well...) Again yes. And do not low-carbers (of various forms) like to point out that the advent of packaged foods, and high sugar snacks, and larger sodas and servings, and supposedly increased intake of carbohydrates, and the bad advice of the USDA to cut fat (sat mainly) and increase low-fat/high carb foods *correlates* awfully well with increases of obesity and T2D in western nations..?? Of course the answer is a big resounding yes. So if you (and they) don't like large-scale population "correlations" of nutrients and disease, then I wouldn't bring them up at all. (now I think some of the above correlations are actually quite useful and instructive, but of course what obesity is really more correlating with and more caused by is increased calorie intake and decreased activity then it is with/by increased carb intake)
Now wait, I know your answer: correlations are fine if coupled with causations, and that is what you alluded to in the 2nd part of your above quote. Great. But I am pretty sure that the top nutrition and medical experts who believe the correlations between high sat fat intake (or reductions) and CVD disease are meaningful understand that principle (give them SOME credit) and have causations of CVD from sat fat intake in mind. Like, oh, I don't know, maybe the down-regulation of the LDL receptor by increasing intracellular cholesterol pools and decreasing LDL cholesterol uptake by the liver. LDL-C has shown to be inflammatory by itself, which can lead to "loss of endothelial integrity, followed by lipid and inflammatory cell infiltration, deposition of fatty streaks and ultimately foam cell production and neointimal expansion."
The plausible and actually tested mechanisms ARE there (yes, they are not completely figured out, or beyond debate, but don't act like the researchers have said: 'hmmm....I notice that people who scratch their butts more get CVD. That's it! No more butt scratching! ' without a thought to if that is plausible and whether or not that might or might not be a true causative factor)
Continued:
"Madness", eh? I will not claim that I can perfectly elucidate the different physiological effects of SFA and USFA down to the roles of each individual atoms involved, but are you claiming that you are not aware that these differences have absolutely been demonstrated? It is beyond any doubt that in controlled feeding studies, in animals and humans, when all other calories are kept the same, substituting USFA's for SFA's results in lower total and LDL cholesterol levels, and usually lower inflammation levels also.
Furthermore, this is then shown to result in reduced blood flow throughout arteries of the body in humans. in animals, they can take these markers of CVD, and watch them go all the way to full-blown atherosclerotic lesions. yes, all due to some minor chemical structural differences. So while I appreciate your surprise/cynicism that such a physiological difference occurs based on such small differences in the chemical structures of the fats, they do in fact occur, and this has been rigorously tested (and there are theories to why: "it is hypothesized that double carbon bonds can scavenge reactive oxygen molecules and reduce generation of hydrogen peroxide that activates nuclear factor (NF-kB)...a transcription factor for proinflammatory genes (adhesion molecules, chemokines, and ILs, key mediators that propagate the atherosclerotic process). )"
Also, if you believe that such small differences in chemical structure should not have potently different physiological effects, that I suppose you will have to discard the paleo/low-carb notion that in fact higher loads of n-6 fatty acids as opposed to n-3 in the diet could have profound effects on health (after all, how could the position of and an extra double bond on a fatty acid matter so much to the body? Sounds like "madness" to me). And probably even disregard any health attributes given to fish intake due to their DHA/EPA content (can they really be that different that sat fats? or trans fats?). I would suppose your position then is: all fats have the same effects in the body?
Hey, look at that, we have "THE ANSWER" to what causes CVD. I am glad we settled that ! ( I apologize for the sarcasm, but it seems a bit presumptuous on your part to discard the entered sat fat/cholesterol/CVD model with a wave of your hand due to it's seeming incomprehensibleness, but then you fully embrace a much, much, less researched/proven/scrutinized theory)
By all means, lets get back to that "nonsense." we haven't really gotten very far on it frankly. But a side excursion towards the negative effects of high sat fat intake are of course relevant due to the fact that many low-carb diets due in fact increase one's sat fat intakes, with predictable results on LDL and total C, inflammatory markers, and other CVD risk factors.
UK Limey runner wrote:
Siri-Tarion et al "Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease", American journal of clinical nutrition 91, no 3 (March 2010)
As I mentioned, this study hailed by the low-carbers (atkins, taubes, paleo crews) did not receive the scrutiny from those enamored with it. Certainly not the same level of scrutiny they have applied to Seven Countries or China study results.
I always find it amusing when bloggers/amateur health experts "take apart" (in their minds at least) a study or two that support mainstream nutrition advice, and then decide, based on those often imperfect study critiques, that they've dismantled the ENTIRE basis for mainstream nutrition advice, despite the existence of literally 1000's of other studies supporting those same mainstream notions. They then couple that rush-to-judgment by cherry-pickig an imperfect study or two that supports their contrary viewpoint (with zero scrutiny given to said results) and then declare: 'Keys' conclusions were not 100% perfect?? AND we found a study that says "no connection between sat fat intake and CVD? Oh well, then that's that, the "Lipid Hypothesis" is DEAD!' And then they act literally shocked when mainstream nutrition advice doesn't immediately follow in line with their extremely quick snap conclusions based on a brief skimming of the literature.
There were several letters to the editor regarding "Siri-Tarion " study and another study in the same journal/issue that also attempted to de-bunk "lipid hypothesis." If you want to read the concerns of other experts, here are the links, they are provided for free-
http://www.ncbi.nlm.nih.gov/pubmed/?term=Meta-analysis+of+prospective+co-+hort+studies+evaluating+the+association+of+saturated+fat(click on "Comment In" section at bottom of page).
but I will post a few of the concerns-
1) many of the studies in the meta-analaysis adjusted for serum cholesterol levels. Sat fat raises cholesterol. To adjust for this measure is removing one of the key causes of sat fat on CVD
2) "To estimate the effect of replacing saturated by polyunsat- urated fat, Siri-Tarino et al selected 5 studies that reported relative risks adjusted for intake of carbohydrate, protein, and fats but not of polyunsaturated fat. They then combined these 5 numbers and presented the outcome as the effect of replacing saturated by poly- unsaturated fat. It requires a leap of faith to assume that the outcome of such a calculation truly represents what happens when saturated fat is replaced by polyunsaturated fat."
3) "A major weakness of the meta-analysis is the imprecision of dietary assessment methods used in the underlying studies. About half of the studies used 1-d dietary assessments or some other unvalidated method. Food intake varies from day to day, and there is a substantial literature showing that a single 24-h recall provides a poor estimation of the usual dietary intake of an individual (5). Such methods cannot reliably rank individuals by their long-term intake, especially within popula- tions with a uniformly high saturated fat intake. Such imprecision in the assessment of disease determinants systematically reduces the strength of association of determinants with the disease. This is re- ferred to as attenuation (6) or regression dilution bias (7)
"Observational studies that used such dietary assessment methods failed to show an association between diet and serum cholesterol concentrations (6). This shows the shortcomings of such dietary methods, because the effect of diet on serum cholesterol concentra- tions has been well established in randomized controlled trials (2, 8). Thus, the lack of a significant association between saturated fat intake and CHD may well reflect the consequences of regression dilution bias."
4) the editorial in response to this article is:
Diet-heart: a problematic revisit
Jeremiah Stamler
I believe it is part of the comments i linked you to. He gives a very detailed critique of the study and a defense of the "lipid hypothesis." You may be interested, or you may not.
5) the main author of the article gets grants from:
Dairy Council
Beef Council
Atkins foundation
Now this doesn't mean that the research can't be valid, however, one needs to recognize that he is finding out "results" that certainly make these people happy. Again, I don't dismiss results entirely based on this potential conflict of interest, but it is something to consider.
This one study hardly, as some low carb bloggers actually said, "puts the nail in the coffin" of the sat fat-CVD theory. Not by a long shot. (it is one very small pice of the puzzle to look at).
Tyrannosaurus Rexing wrote:
So if you (and they) don't like large-scale population "correlations" of nutrients and disease, then I wouldn't bring them up at all.)
Never said I don't like studies that demonstrate correlations. I expressed my frustration when no causal mechanism is suggested (I'm from the physical sciences; if you don't talk about cause and effect then expect the door to hit you on the way out. We don't do correlation: we do cause).
You wrote a lot of stuff and it may already be buried in your posts somewhere, but can I ask you to explain to me as succinctly as possible how you think saturated fat causes stroke/CVD/T2D? Not trolling, genuinely interested to see the mechanism summarised. PLEASE try to make it succinct though as I'm sure you're aware that you have a tendency to write long posts.
Cheers.
p.s. Somewhere in your posts you intimated that I pore over blog posts. I'm not a huge fan of reading blogs but if you feel that there is something out there that I might benefit from reading then please do link me.
Great information. Totally enjoyed it. They are the basics & correct information. I want to add up a few more such as.
1. Drinking lots of water.
2. No stress Eating.
3. Having a mindset.
4. Be in the discipline.
5. Try natural weight loss supplements.
6. Checking weight once in a month or you can try checking it weekly.
7. Reminding yourself about why you want to lose weight.
I used to have soo much weight, I did try so many methods & wanted to learn more each day. I eventually ended up with these methods plus yours too & weight loss supplements that are organic & natural has helped in way too much, one such I want to count in is Super MIC B12. You can try it too or read its reviews on Bioceuticals International.
kelseysmith wrote:
6. Checking weight once in a month or you can try checking it weekly.
What I do is weigh myself everyday at the same time and then take to the average at the end of the week and record that. Weight will fluctuate daily but if you see a slow downward trend in the average then you are losing.
As far as protein goes the recommendation is 1.8-2.4g/kg in order to maintain and even increase lean muscle mass while in calorie deficit. Regular resistance training advised + normal running training. World Athletics nutrition consensus publication has lots of info on this. Link for the protein and body composition paper: https://journals.humankinetics.com/view/journals/ijsnem/29/2/article-p165.xml