This behemoth boasts a full 9,982 calories, with 20 slices of bacon, four 1/2 lb beef patties, on a white flour bun. Even Michael Phelps, with his reported 12,000 calorie per day training diet, would only need to eat 1.2 of these burgers per day to meet his needs. This burger could fuel me for about three and a half days.
What I like about the Heart Attack Grill is the honesty. You know exactly what you're getting yourself into.
I'll have one of those without the bun please. :)
ReplyDeleteHa, you may as well have the bun - not gonna save many calories.
ReplyDelete.. and if you eat one, you get a free wheelchair ride back to your car. I did this on December 31, 2010. Surprisingly, it actually wasn't even a very good burger. But it was a funny experience.
ReplyDeleteHi Stephan,
ReplyDelete"What I like about the Heart Attack Grill is the honesty."
Does this mean you're changing some of your original thoughts about saturated fat since your more paleo-focused days a few years ago?
I dont see anything appetizing there, it just looks stupid.
ReplyDeleteLooks more like something id practice karate chops on.
that's a huge pile of fat to be sure, but where are all those calories coming from? The numbers you list = approximately 3 pounds of *pure fat*.
ReplyDeleteIf it's only a pound of beef, it doesn't seem like there's over two pounds of bacon and cheese
That one is objectionable just on the waste side of things. Most humans wouldn't be able to eat a whole one, meaning a good portion of each would get tossed out. Kind of one of those things that makes you think of the excesses of the late Roman Empire, and what happened to them...
ReplyDeleteWhen I saw that on the main page of your blog (before clicking for the whole article, I mean), I was *sure* you had photoshopped that!
ReplyDeleteThese are funny, I'm really enjoying Food Reward Fridays.
Hi Sisyphus,
ReplyDeleteGood point. I got the calorie value from their website, perhaps it is exaggerated. The Guinness Book does list this burger as the "most calorific burger" though.
Two pounds of beef at 80 calories/ounce = about 2500 calories.
ReplyDeleteFor the cheese, let's say there are 2 slices per level and 125 calories per slice -- that's another 1,000 calories.
Let's say the bacon is 75 calories/slice. With 20 slices that's another 1500 calories.
Let's grant 250 calories for each bun. That's another 500.
Let's grant another 500 for the sauces and veggies.
I get about 6,000 calories.
I think it looks really good. If you toss the bun, and then just serve an inch or so a meal over some salad greens, it looks like it's good for a week
ReplyDeleteQuoting their website: On April 13th 2012 Guinness World Records presented the Heart Attack Grill with an official certificate proclaiming... "Most calorific burger Heart Attack Grill in Las Vegas includes in its menu the 1.444kg (3lb 2.94oz) Quadruple Bypass Burger packing 9,982 calories. It's 6.91 calories per gram (195.95 calories per ounce) makes it the world's most calorific burger as verified by Guinness World Records"
ReplyDeleteWhat in holy hell...
ReplyDeleteI'm sure this is the opposite of your intent, but I've found myself trying the things you post for Food Reward Friday. Last weekend I tried Poutine, it was amazing!
ReplyDeleteI believe they slather lard in amongst the layers as well, that could get you to the missing calories. I don't see how this is a real contributor to the obesity epidemic,though - it's a novelty act, nothing more. It's the "standard" 24oz sodas, and the perception that such a quantity is normal, that really does the work.
ReplyDeleteGreat and useful blog,thanks for this post
ReplyDeleteInvisible hearing aid oklahoma city
As someone that spent over 5 years on a low fat diet and now 4 years on low carb - it is really clear that if you are interested in the appetite part of the equation - low carb works.
ReplyDelete(My hunch is it would work even better if it was easy to reduce the amount of O-6 fats in the readily available food supply.)
One explanation for the reduced appetite is that people on low-carb diets tend to have much lower trygly - ( in fact doctors use trygly to monitor compliance ).
There are papers available that show that trygly block Leptin at the blood/brain barrier.
I think it is wrong to assume that the body and brain are separated in the control of appetite. If we look at homeostasis of any number of biological systems we see over-lapping control loops. If we have long term average net FA going into adipose tissue - that is fat gain. It is also a process that takes calories out of circulation and other feedback loops would likely increase appetite.
The bun may well matter in other effects - modern wheat contains a gliadin protein unique to wheat that is degraded to a morphine-like compound that appears to stimulates appetite. My question is if this effect is of a magnitude that matters?
The other bit, is when I was eating low-fat - that burger would have been tempting - on a low carb diet, I just don't have the hunger spikes that I did on a low-fat diet and don't overeat ( I now normally eat only twice a day now and sometimes forget the second meal. )
One last thing - Blood glucose meters are cheap - independent of my weight I would not eat a meal that would raise my postprandial BG over 110 - The incidence of a huge number of diseases and particularly cancers increases with poor BG control. Much better to reduce carbohydrates to restore BG than taking the drugs.
Babies born to mothers that had poor BG control during pregnancy appear to have more trouble with obesity.
Hi Gunther,
ReplyDeleteI'm still not convinced that SFA per se are a significant contributor to cardiovascular disease. I do think that overeating calorie-dense, high-heat cooked and refined foods isn't healthy for the cardiovascular system, and that unrefined plant foods should probably play a more prominent role in the diet than they do in a hamburger. That being said, having a burger every now and then isn't going to kill you.
Thanks for your response Stephan.
ReplyDelete"I do think that overeating calorie-dense, high-heat cooked and refined foods isn't healthy for the cardiovascular system"
Can you explain why calorie-dense, refined foods would affect the cardiovascular system? I get that AGEs would form in high-heat cooking and affect endothelial function, but I don't find any literature on the other two things being directly related to CVD.
Gunther,
ReplyDeleteI think exogenous AGEs actually are a relatively minor issue, as it seems our digestive system does a pretty good job of filtering them out.
Its not calorie dense foods by themselves that affect the cardiovascular system, but the over-consumption of them. Energy overload does lots of bad things: increases inflammatory cytokine production, alters bloodsugar regulation, impacts thyroid function, etc. All of these things are bad for CVD.
Food reward is something which always cheeres me up. Have some ideas of how to eat efficiently:
ReplyDeleteEfficient eating
By the way, I followed you up with GFC, it'd be great if you follow me back.
Hi Gunther,
ReplyDeleteCalorie-dense refined foods are easy to overconsume, and as the previous commenter said it is the overconsumption that is harmful. Also, refined foods are missing phytochemicals that we have good reason to believe protect against cardiovascular disease. I haven't looked into it much but it's also possible the fiber in unrefined foods is protective.
I think it looks delicious. Meat, bacon, lots of onion, tomato, and cheese. I would ditch the bread, but I could definitely eat that. I really don't see what's wrong with it.
ReplyDeleteStephan wrote:
ReplyDeleteI'm still not convinced that SFA per se are a significant contributor to cardiovascular disease
Stephan, it helps to understand that LDL-C has a causal, independent link to CHD. SFA with 12–16 carbon atoms are the most potent LDL- or total cholesterol-raising fatty acids. Elevated levels of apo B containing cholesterol-rich lipoprotein particles drive the development of atherosclerosis in humans and in experimental animals, even in the absence of other known risk factors. Having this in mind, it's not difficult to conceive that going low on SFAs is a no-brainer. But then again, if your TC cholesterol is around 240 and you thinks its okay, you probably are not too welcoming to ideas that may contradict your crank, denialist mindset.
Best,
Peter
Ouh..I forgot, PrimitiveNutrition's new 44-piece series "Nutrition Past and Future" is out, enjoy:
ReplyDelete41 PUFAs Oxidize!
http://www.youtube.com/watch?v=WOcfxpZi6a0&list=PLv3QDzdxan_JkGX47Rpboyh2oYyAFZDBA
Masterjohn & Kresser making their mommies proud, LOL!
22 Cholesterol Confusion 5 Cholesterol Is Necessary for Life
http://www.youtube.com/watch?v=RjSmmEzxK7Y&list=PLv3QDzdxan_JkGX47Rpboyh2oYyAFZDBA
Anyways, Dutch scholars who did the pioneering work around Diet-Heart observed massive rates of atherosclerosis in Europe during the 1920s in the absence of highly refined foods, coca-cola, McDonalds, Starbuck, etc. People were simply enjoying their dietary cholesterol and SFA. Moreover, Ancel Keys explained already in 1956 in detail that over eating (obesity) cannot explain the coronary artery disease as such. Moreover, Stephan's somewhat irresponsible postulations look even more questionable given the fact that the age-adjusted coronary heart disease mortality in US has declined to a half compared to what it was in the late 1950s. (IMPACT models show that improved medical care explains only less than 40% of this development). This prevails even despite the fact that the intake of refined foods has increased in the American market; a fundamental change in American diet that explain the positive development very well is that consumption of lard and butter is minuscule today compared to 1950s.
ReplyDeleteIn countries such as Finland, IMPACT models estimate that serum cholesterol levels and the decreased consumption of SFA explains around 50% of the rapid decrease in coronary disease mortality. This decrease in coronary heart disease mortality has been the most profound decline ever observed. In Finland, coronary heart disease is today 80% less to what is was in the 1960s.
Henry Blackburn's article on the founding fathers of Diet-Heart theory.
20th-Century “Medical Marco Polos” in the Origins of Preventive Cardiology and Cardiovascular Disease Epidemiology
http://www.ajconline.org/article/S0002-9149(11)03212-7/fulltext
Ah, originated in Las Vegas, where else? I saw this, but didn't think I was up for the task. While you're there, you can get a PBR that fits the size of the burger.
ReplyDeleteI wrote an article about the spot for Paleo in 2013, I hope some might appreciate it.
http://paleorecipesforyou.com/2013/01/08/paleo-in-2013/
Hi Peter,
ReplyDeleteTotal SFA intake in the US has not changed significantly in 100 years (within 4 percent according to the USDA)... by your own argument that CHD rates have declined by 50%, wouldn't that suggest that SFA are not the critical factor?
Smoking rates have declined by 50% in the US, and if we want to point at a single-factor explanation, that is a much more compelling explanation for the decline in CHD than nonexistent changes in saturated fat intake.
This comment has been removed by the author.
ReplyDeleteHi Stephan buddy,
ReplyDeleteI appreciate a lot you tolerating "second opinions" despite my occasional display of harsh language. The amount of SFA in the US diet has dropped during the last 4 decades.
Centers for disease control, prevention Trends in intake of energy and macronutrients: United States, 1971–2000. Morb Mortal Wkly Rep. 2004;53(04):80–82.
Anyways, good that you brought this up. Thanks to the IMPACT models I referred to, these are actually well quantified issues. Yes, cigarette cessation plays a role in the declining age-adjusted cardiovascular mortality in US, no doubt about it. However, the serum cholesterol levels in US have declined from 240 to 200 during the the 4-5 decades. Ford & Capewell estimated that almost half to three-quarters of the lower CHD mortality in the USA may be explained by risk factor reduction, with the remainder being attributed to more effective treatment for dyslipidaemia and hypertension. However, in the Nordic countries where national preventive programmes have been conducted since the early 1960s, dietary changes with a reduction in population mean total cholesterol explain a far greater proportion of the decline in CHD mortality. As said, Finland has experienced an over 80% fall in CHD mortality due to a large extent to the reduction in total cholesterol. In Finland, a reduced SFA intake was the main reason for the fall in blood cholesterol caused by a massive decline in dairy fat consumption. In Poland in 1990, communist subsidies for animal fats disappeared and a free market provided relatively cheap vegetable oils, fruit and vegetables. The polyunsaturate/saturate ratio improved substantially, and coronary death rates fell by 24% within five years. Corresponding trends were reported in East Germany, Hungary and the Czech Republic. CHD was also almost non-existent in rural China when mean cholesterol levels were approximately 135mg/dl with total fat intakes only about 15% of energy and extremely low intakes of SFA.
Why have total cholesterol levels declined in most developed countries?
http://www.biomedcentral.com/1471-2458/11/641
Can dietary changes rapidly decrease cardiovascular mortality rates?
http://eurheartj.oxfordjournals.org/content/32/10/1187.full.pdf
Decline in mortality from coronary heart disease in Poland after socioeconomic transformation: modelling study
http://www.biomedcentral.com/1471-2458/11/641
Valsta LM, Tapanainen H, Sundvall J, et al. (2010) Explaining
the 25-year decline of serum cholesterol by dietary changes
and use of lipid-lowering medication in Finland. Public
Health Nutr 13, 932–938.
Peter, you're arguing with the wrong guy here: US diet trends are my specialty. The percentage of energy as SFA has declined (according to the NHANES data you cited), but total SFA intake has remained essentially unchanged since 1909 according to USDA data (which although they have limitations are not self-reported like NHANES).
ReplyDeleteThis is the only database with yearly SFA measures back to 1909, and it shows virtually no change over time (today we eat slightly more SFA than in 1909). Here's a link to the data:
http://www.ers.usda.gov/data-products/food-availability-(per-capita)-data-system.aspx
Here's a fresh new RCT from the print, this may help people to understand that cutting the amount of SFAs might be good idea:
ReplyDeleteThe causal exposure model of cholesterol nicely illustrated.
Causal Relevance of Blood Lipid Fractions in the Development of Carotid Atherosclerosis: Mendelian Randomization Analysis
CONCLUSIONS: “Our findings confirm a causal relationship between LDL-C and CIMT but not with HDL-C and triglycerides. At present, the suitability of CIMT as a surrogate marker in trials of cardiovascular therapies targeting HDL-C and triglycerides is questionable and requires further study”
http://www.ncbi.nlm.nih.gov/pubmed/23275344
@Peter,
ReplyDeleteIn what world is that an RCT? All of the studies you cite have been observational. Or did I miss something?
Sorry if that came off as snarky, its early here.
ReplyDeleteThis comment has been removed by the author.
ReplyDeleteMendelian studies are randomized, controlled trials and bring the highest evidence of causality at the table. In regards to LDL-C, multiple single-nucleotide polymorphisms (SNPs) are associated with small differences in LDL-C. Each of these polymorphisms is allocated randomly at the time of conception. This is a process referred to as Mendelian randomization. Inheriting an allele associated with lower LDL-C is therefore analogous to being randomly allocated to a therapy that lowers LDL-C beginning at birth, whereas inheriting the other allele is analogous to being randomly allocated to usual care. If certain assumptions are satisfied then the association between such a polymorphism and the risk of CHD should provide an unconfounded estimate of the effect of lifelong exposure to lower LDL-C on the risk of CHD in a manner analogous to a long-term randomized trial comparing a therapy that lowers LDL-C beginning early in life with usual care.
ReplyDeletehttp://content.onlinejacc.org/article.aspx?articleid=1379036
The difference betweeen LDL-C and HDL-C: LDL-C is causally related to the risk of CHD and inherited mutations that lower LDL-C via different SNP's but not altering any other biomarker, translates to a ~55% reduction in CHD per every 1mmol/l (38/dl) drop in LDL cholesterol. Each of the studied SNPs lower LDL-C with a differing mechanism, yet end results are identical, this suggest that diet and excersise are equally powerful in preventing CHD as inherited mutations that lower LDL-C since birth.
HDL-C volume is not causally related to CHD. This is all very simple.
1) 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
“Background: 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”
Conclusions: 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.
2) Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study
Background: High plasma HDL cholesterol is associated with reduced risk of myocardial infarction, but whether this association is causal is unclear. Exploiting the fact that genotypes are randomly assigned at meiosis, are independent of non-genetic confounding, and are unmodified by disease processes, mendelian randomisation can be used to test the hypothesis that the association of a plasma biomarker with disease is causal.
Interpretation: Some genetic mechanisms that raise plasma HDL cholesterol do not seem to lower risk of myocardial infarction. These data challenge the concept that raising of plasma HDL cholesterol will uniformly translate into reductions in risk of myocardial infarction.
Here's an observational study that adheres well to the causal exposure model of cholesterol. Pay attention to the very long follow-up and the fact that the authors are looking at total mortality and quality of life, not just CHD. Cholesterol is good risk predictor for mortality and well-being all the way to late mid-life, after that it gets confounded and doesn't work as risk predictor too well in Western context.
ReplyDeleteEffect of cholesterol on mortality and quality of life up to a 46-year follow-up.
”A strong and graded relation was found between the cholesterol level and total mortality, with the men with a cholesterol level ≤4 mmol/L (154 mg/dl) having the lowest mortality. In all, the men with the lowest cholesterol gained the most life years. However, no association was found with the cholesterol level in 2000 (when 16% were using statins) and subsequent mortality. The lowest (≤4 mmol/L) cholesterol value in midlife also predicted a higher score in the physical functioning scale of RAND-36 in old age. In conclusion, a low total cholesterol value in midlife predicts both better survival and better physical functioning in old age”.
PlantPositive made a video of this;
18 Cholesterol Confusion 1 Primordial Prevention
http://www.youtube.com/watch?v=L1MvvQj4W40&list=PLv3QDzdxan_JkGX47Rpboyh2oYyAFZDBA&index=18
Hi Peter,
ReplyDeleteI deleted the comment in which you were behaving like a child. I value alternative perspectives, but you need to learn to have some level of decorum around here. I gave you a reference for my statement, which is easily verified, so there is no need to whine about whether or not I'm telling you the truth.
The NHANES data you cited show essentially the same thing as the USDA data when you adjust them for the fact that total kcal intake increased. With a little math, you will see that the data you cited reveals the following between 1971 and 2000:
Men: 14% decrease in absolute SFA intake
Women: 3% increase in absolute SFA intake
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5304a3.htm
Given the error inherent to both datasets, this is not significantly different than the 2% increase in absolute SFA intake from 1971 to 2000 in the USDA data, and it is not significantly different from no change at all over time.
http://www.ers.usda.gov/data-products/food-availability-(per-capita)-data-system.aspx#26715
These changes in SFA intake are trivial and obviously cannot underlie major changes in circulating cholesterol or CHD risk. If you want to know why our cholesterol has decreased, you're better off looking at cholesterol-lowering drugs and PUFA intake. Cholesterol-lowering drugs such as statins are frequently administered to people with high cholesterol today, which reduces the mean. PUFA intake has increased by 200% since 1909 in the US due to seed oils, and we know linoleic acid decreases cholesterol at least in large amounts.
@Peter,
ReplyDeleteYour study doesn't support your conclusion. I suppose you could consider Mendelian studies to be analogous to RCTs, but only with regard to the SNPs. This doesn't support your conclusion that a dietary intervention to reduce total cholesterol will have the same effect as the SNPs.
Stephan,
ReplyDeletehad you looked any of my sources, especially the articles by Capewell, you'd now that lipid-lowering drugs are not an issue here, why?
Why have total cholesterol levels declined in most developed countries?
Total cholesterol levels in whole populations have fallen substantially in the USA, UK and most other developed countries. Large falls actually occurred before statins were introduced [14-17]. Further substantial falls occurred before statins were widely used [18-23]. Moreover, the evidence identifying diet as the major contributor to these historical falls in cholesterol is powerful and consistent.
http://www.biomedcentral.com/1471-2458/11/641
So, now that you know that drugs are not an issue here, what do you think are the underlying reason why TC cholesterol has dropped from 240 to 200 among US population during the last 4-5 decades? I know there are studies from Europe that show a significant reduction in SFA intake, explaining the observed drop in serum cholesterol levels that occurred at the latter half of the 1900s. The idea that PUFAs lower cholesterol even when other calories, especially SFAs are held constant is certainly news to me. Does this represent your new stance in these issues? I remember you arguing once that foods of animal origins do not raise cholesterol levels, but that's okay, I am sure you won't think that is the case anymore since you've probably had your own lipid panel updated which should reflect the changes of your newly adopted high-starch diet. Am I right?
IcedCoffee wrote:
ReplyDelete"This doesn't support your conclusion that a dietary intervention to reduce total cholesterol will have the same effect as the SNPs"
This is the exact conclusion drawn by Ferrence, the lead author of the paper. He concluded that all the nine studied SNPs lower LDL cholesterol with different mechanism, but since there's no heterogenity in the results which are extremely consistent, LDL-C reducing lifestyle (diet and excersise) should by all reasons of logic have a similar impact. The benefits of LDL cholesterol reduction seem to be independent of the mechanism used. Even bypass of the illeal to lower circulating LDL-C has been tried and it works too(POSCH-trial). It definitely helps if you look at the this through the lens of preponderance of evidence.
Obviously the benefits of LDL-C lowering depends on a) magnitude and b)timing. Lower, the better, earlier, the better.
Hi Peter,
ReplyDeleteI'm surprised to hear that you are not aware of the lipid-lowering effect of linoleic acid, it is quite well established by a number of controlled trials, some lasting many years. Long-term controlled trials have shown that increasing LA is a much more effective way to decrease cholesterol than reducing SFA. That's precisely the reason why Walter Willett recommends using corn oil for cooking-- it is the highest in LA per calorie.
Furthermore, PUFA are part of the Hegsted equation and other related formulas that predict circulating cholesterol based on diet.
@Peter,
ReplyDeleteBut the SNPs resulting in a lower cholesterol level are not actually lowering cholesterol, they are creating people with naturally lower levels of cholesterol (with all the other effects this would have).
Stephan,
ReplyDeleteI know. But you are talking about having SFAs constant. PUFAs lower cholesterol when they replace SFAs, that's what I've learnt. Does your cholesterol plummet while you are enjoying your PUFAs at the top of your butter?
Anyways, PlantPositive's amazing video covers the issue on the level of mechanism, however at the end of the video he refers to ecologic studies; In Poland veggies oils replaced animal fats which became suddenly very expensive after the collapse of Soviet Union:
Rapid declines in coronary heart disease mortality in Eastern Europe are associated with increased consumption of oils rich in alpha-linolenic acid
"In all former socialistic economic countries, CHD was uniformly increasing or stable, but a steady decline in CHD was observed in Western European countries. Surprisingly, during the 1990's CHD mortality substantially decreased in some Eastern European countries but not in others. These changes were accompanied by major shifts in food consumption, including the type of vegetable oils used by the population"
PlantP provides a "second opinion":
41 PUFAs Oxidize!
http://www.youtube.com/watch?v=WOcfxpZi6a0&list=PLv3QDzdxan_JkGX47Rpboyh2oYyAFZDBA
IcedCoffee:
ReplyDelete"But the SNPs resulting in a lower cholesterol level are not actually lowering cholesterol, they are creating people with naturally lower levels of cholesterol (with all the other effects this would have)"
I don't know what you mean. These people studied did not have any inherited alterations in any other biomarker. One of the SNPs studied was the statin-targeted HMG-CoA. People having inherited mutation that lower cholesterol via HMG-CoA enjoy protection from CHD just like statin users do, especially if they start early on. A meta-regression curve accumulated from 108 randomized controlled trials of various medical and dietary based lipid modifying interventions has established that lowering LDL cholesterol significantly decreases the risk of coronary heart disease and all-cause mortality, independent of changes to HDL cholesterol and triglycerides, and non-lipid effects of specific drugs.
People born with elevated HDL-C since birth do not enjoy protection from CHD, neither do people who have inherited low triglyceride levels. LDL-C is not only fraction in the lipid panel that is causally related to the risk of CHD.
People who have hypobetalipoproteinemia can have their LDL-C <15mg/dl their whole lives. These people end up living 9-12 years longer than their peers, are are exceptionally healthy. They are the opposite to FH-patients.
Anywways,
ReplyDeleteStephan buddy,
I am really starting to like your blog more and more. These particular friday posts are usually very illustrative. However, I am not just sure (yet) whether you really are an expert on the US diet trends, perhaps you are just an expert on obesity research :) and nothing wrong with that. Most people have hard time mastering two things at once.
This comment has been removed by the author.
ReplyDelete@Peter,
ReplyDeleteYou raise some interesting points, but I'm still unconvinced that you can extrapolate what you have presented as justification for a low-saturated fat dietary intervention. This is not to say that a low-saturated fat diet could not be used effectively, but rather that it was not the lower LDL-C per se that resulted in the beneficial outcome.
I'd be interested to see the meta-analysis, as I would imagine that most pharmaceutical interventions studied were premised on the purpose of lowering LDL-C, so obviously the successful ones would be likely to have this effect. (and what about the pharmo interventions that have no impact on LDL-C but result in beneficial outcomes?)
That doesn't prove that it was the lowering of LDL-C by these drugs that was the important factor, or that a dietary intervention would necessarily have the same outcome if it lowered cholesterol to a similar degree.
Obviously LDL is involved as it seems to be the component that is acted upon, but lowering cholesterol to prevent heart disease seems to me to be like removing skin to prevent skin cancer.
Those who are interested in some real science about cholesterol and how lipoproteins interface with atherosclerosis and CHD risk should read this series by Dr. Attia:
ReplyDeletehttp://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-i
{I'm sure Peter will love how Dr. Attia objectively improved his risk markers after going high SFA and low carb}
From there, there is a TON of material online from Dr. Thomas Dayspring and Dr. Tara Dall, who are, I might add, both highly credentialed MD lipidologists.
Way more worthwhile than wasting your time with "PlantPositive" videos, or debating zealots.
@IcedCoffee,
ReplyDeleteyou fail to discuss anything I've quoted in the context of preponderance of evidence.
@Chris,
Peter Attia. Is this some kind of stand-up comedy show? Let's keep it serious, shall we.
Thomas Dayspring is legitimate lipidologist and obviously against SFA.
Anyways, his dietary recommendation are way out there. let's take a "second opinion" by PrimitiveNutrition
17 Thomas Dayspring, Lipidologist Lost
http://www.youtube.com/watch?v=uSzByKafWKM&list=PLv3QDzdxan_JkGX47Rpboyh2oYyAFZDBA&index=17
@Stephan,
excellent new model on atherosclerosi; scientists were able to design a gene that downregulates the LDL-receptors on mini pigs resulting in elevated LDL in the blood. Everything else was kept constant, these pigs were not gaining weight, smoking fags or drinking. Guess what happened to the pigs? Here's the riddle?
a) They got better, more LDL the better
b) Nothing, LDL is just a passive by stander.
c) They developed atherosclerosis very rapidly since LDL cholesterol is the causal factor influencing CHD.
Find out the correct answer, here:
http://stm.sciencemag.org/content/5/166/166ra1.abstract
@Peter,
ReplyDeleteThe pig model you linked is just restating that FH leads to heart disease. This is hardly news (other than a new model to test), and doesn't prove that higher LDL-C means more heart disease. Elevated LDL-C secondary to removal of LDL-receptor function is hardly equivalent to elevated LDL-C alone.
Peter Attia's 9 part series on cholesterol is about as good and as thorough a discussion as you can find on the whole subject. Summarily dismissing him and not studying his message just makes you look foolish.
ReplyDeleteThis comment has been removed by the author.
ReplyDelete@IcedCoffee,
ReplyDeleteYou are something like 30-40 years behind of our times. Anyways, I don't have the time to deal with your denialist nonsense anymore, bye!
“The molecular basis for the effects of dietary saturated fat on plasma LDL cholesterol levels is well understood. Saturated fat influences the LDL receptor activity of liver cells as described by Brown and Goldstein, dietary saturated fat suppresses messanger RNA synthesis for the LDL receptor. This decreases hepatic LDL receptor activity and slows the removal of LDL from the blood, thus increasing the concentration of LDL cholesterol in the blood. Dietary cholesterol augments the effects of saturated fat further suppressing the hepatic LDL receptor activity and raising the plasma LDL cholesterol levels”
–Heart Disease, Environment, Stress and Gender [proceedings of the NATO Advanced Research Workshop on Increase in Coronary Heart Disease in Central and Western Europe: Stress and Gender Related Factors, 20-24 May, 2000, Budapest, Hungary]
Consumption of omega-3 fatty acids is not associated with a reduction in carotid atherosclerosis: the Genetics of Coronary Artery Disease in Alaska Natives study
“Dietary intake of omega-3 FAs in a moderate-to-high range does not appear to be associated with reduced plaque, but is negatively associated with IMT. The presence and extent of carotid atherosclerosis among Eskimos is higher with increasing consumption of saturated FAs
http://www.ncbi.nlm.nih.gov/pubmed/18054937
Differences in all-cause, cardiovascular and cancer mortality between Hong Kong and Singapore: role of nutrition
“There are striking differences in all-cause and cardiovascular mortality between Hong Kong and Singapore. These differences can be most reasonably and plausibly explained by their differences in dietary habits, for example, a higher consumption of coconut and palm oil, mainly containing saturated fat, in Singapore”
http://www.ncbi.nlm.nih.gov/pubmed/11855581
Let see what Dr Thomas Dayspring precribes to those who are senstitive to the side-effects of statins:
ReplyDelete"statin intolerant: consider ezetimibe (Zetia) plus colesevelam (Welchol) plus a plantstanol (Benecol) plus aggressive low saturated fat diet. Recent data showed ezetimibe/fenofibrate was also efficacious in patients without the metabolic syndrome".
http://www.lipidcenter.com/pdf/Lipid_Treatment_Algorithm.pdf
That's margharine and low-saturated fat diet! Why bother reading diluted, denialist and misunderstood nonsense on cholesterol by Attia, Kresser & Co when you can directly read Attia's own personal low-carb lipid guru's statements. Just an idea.
A link to the meta-regression curve accumulated from 108 randomized controlled trials of various medical and dietary based lipid modifying interventions which established that lowering LDL cholesterol significantly decreases the risk of coronary heart disease and all-cause mortality, independent of changes to HDL cholesterol and triglycerides, and non-lipid effects of specific drugs.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/pdf/bmj.b92.pdf
Peter, you seem to be implying with your "riddle" that I don't believe the LDL lipoprotein contributes to atherosclerosis.
ReplyDeleteI'm not sure where you get these ideas, but I want to tell you about a blog I write called Whole Health Source. If you read that blog, you will see that I acknowledge the important role of LDL in atherosclerosis and cardiovascular risk.
Peter, your comments frequently are disrespectful or border on disrespectful, and your domination of my comments section with rapid-fire, frequently condescending comments is also disrespectful. Just make your point concisely and move on. Make yourself some tea and read a book.
Stephan,
ReplyDeleteOrganic, loose English breakfest tea on the kettle. Again, apologies for the condescending tone towards your audience. That's was unnecessary from my behalf, but then again I am somewhat frustrated by the amount of misinformation out there.
Anyways, good that you clarified this. I thought you were supporting the works of Colpo and Masterjohn which always appeared somewhat weird to me, given the fact that there are some real top-snotch cholesterol researchers at your school such J W Heinecke (PlantPositive referred to his article in his "PUFAs oxidize" video). Anyways, I had the idea that you were more about the "remember to eat your dietary cholesterol to avoid SLO-syndrome like disorders" school of thought. Good that you clarified this.
I assume Jay W Heinecke would be proud of PlantPositive. Perhaps, I ought to forward this video to him.
PlantPositive giving a second opinion to paleo broscience in regards to PUFAs and LDL oxidation.
http://www.youtube.com/watch?v=WOcfxpZi6a0&list=PLv3QDzdxan_JkGX47Rpboyh2oYyAFZDBA
Best,
Pete
OK, apology accepted. Jay Heinecke is indeed brilliant and I'm grateful to be able to interact with him regularly-- one of his main research directions is on understanding reverse cholesterol transport by HDL and its relationship to cardiovascular disease. He also does a lot of immunology work, most of which is over my head.
ReplyDeleteHeart Attack Grille in the news.....
ReplyDeletehttp://www.latimes.com/news/nation/nationnow/la-na-nn-unofficial-spokesman-heart-attack-grill-dies-of-heart-attack-20130213,0,884319.story