The diet-heart hypothesis is the idea that saturated fat, and in some versions cholesterol, raises blood cholesterol and contributes to the risk of having a heart attack. To test this hypothesis, scientists have been studying the relationship between saturated fat consumption and heart attack risk for more than half a century. What have these studies found?
The large majority of observational studies have found no connection between habitualsaturated fat consumption and heart attack risk. The scientific literature contains dozens of these studies, so let's narrow the field to prospective studies only, because they are considered the most reliable. In this study design, investigators find a group of initially healthy people, record information about them (in this case what they eat), and watch who gets sick over the years.
A Sampling of Unsupportive Studies
Here are references to ten high-impact prospective studies, spanning half a century, showing no association between saturated fat consumption and heart attack risk. Ignore the saturated-to-polyunsaturated ratios, Keys/Hegsted scores, etc. What we're concerned with is the straightforward question: do people who eat more saturated fat have more heart attacks? Many of these papers allow free access to the full text, so have a look for yourselves if you want:
A Longitudinal Study of Coronary Heart Disease. Circulation. 1963.
Diet and Heart: a Postscript. British Medical Journal. 1977. Saturated fat was unrelated to heart attack risk, but fiber was protective.
Dietary Intake and the Risk of Coronary Heart Disease in Japanese Men Living in Hawaii. American Journal of Clinical Nutrition. 1978.
Relationship of Dietary Intake to Subsequent Coronary Heart Disease Incidence: the Puerto Rico Heart Health Program. American Journal of Clinical Nutrition. 1980.
Diet, Serum Cholesterol, and Death From Coronary Heart Disease: The Western Electric Study. New England Journal of Medicine. 1981.
Diet and 20-year Mortality in Two Rural Population Groups of Middle-Aged Men in Italy. American Journal of Clinical Nutrition. 1989. Men who died of CHD ate significantly less saturated fat than men who didn't.
Diet and Incident Ischaemic Heart Disease: the Caerphilly Study. British Journal of Nutrition. 1993. They measured animal fat intake rather than saturated fat in this study.
Dietary Fat and Risk of Coronary Heart Disease in Men: Cohort Follow-up Study in the United States. British Medical Journal. 1996. This is the massive Physicians Health Study. Scroll down to table 2 and see for yourself that the association between saturated fat intake and heart attack risk disappears after adjustment for several factors including family history of heart attack, smoking and fiber intake. That's because, as in most modern studies, people who eat steak are also more likely to smoke, avoid vegetables, eat fast food, etc.
Dietary Fat Intake and the Risk of Coronary Heart Disease in Women. New England Journal of Medicine. 1997. From the massive Nurse's Health study. The abstract claims that saturated fat was associated with heart attack risk. However, the association disappeared when they adjusted for monounsaturated and polyunsaturated fat intake. Have a look at table 3.
Dietary Fat Intake and Early Mortality Patterns-- Data from the Malmo Diet and Cancer Study. Journal of Internal Medicine. 2005.
I just listed 10 prospective studies published in top peer-reviewed journals that found no association between saturated fat and heart disease risk. This is less than half of the prospective studies that have come to the same conclusion, representing by far the majority of studies to date. If saturated fat is a dominant cause of cardiovascular disease, why are its effects essentially undetectable in the best studies we can muster?
Studies that Support the Diet-Heart Hypothesis
To be complete, some studies have found an association between saturated fat consumption and heart attack risk. Here's a list of all four that I'm aware of, with comments:
Ten-year Incidence of Coronary Heart Disease in the Honolulu Heart Program: relationship to nutrient intake. American Journal of Epidemiology. 1984. "Men who developed coronary heart disease also had a higher mean intake of percentage of calories from protein, fat, saturated fatty acids, and polyunsaturated fatty acids than men who remained free of coronary heart disease." The difference in saturated fat intake between people who had heart attacks and those who didn't, although statistically significant, was very small.
Diet and 20-Year Mortality From Coronary Heart Disease: the Ireland-Boston Diet-Heart Study. New England Journal of Medicine. 1985. "Overall, these results tend to support the hypothesis that diet is related, albeit weakly, to the development of coronary heart disease."
Relationship Between Dietary Intake and Coronary Heart Disease Mortality: Lipid Research Clinics Prevalence Follow-up Study. Journal of Clinical Epidemiology. 1996. "...increasing percentages of energy intake as total fat (RR 1.04, 95% CI = 1.01 – 1.08), saturated fat (RR 1.11, CI = 1.04 – 1.18), and monounsaturated fat (RR 1.08, CI = 1.01 – 1.16) were significant risk factors for CHD mortality among 30 to 59 year olds... None of the dietary components were significantly associated with CHD mortality among those aged 60–79 years." Note that the associations were very small, also included monounsaturated fat (like in olive oil), and only applied to the age group with the lower risk of heart attack.
The Combination of High Fruit and Vegetable and Low Saturated Fat Intakes is More Protective Against Mortality in Aging Men than is Either Alone. Journal of Nutrition. 2005. Higher saturated fat intake was associated with a higher risk of heart attack; fiber was strongly protective.
The Review Papers
Over 25 high-quality studies conducted, and only 4 support the diet-heart hypothesis. In case you're concerned that I'm cherry-picking studies, here are links to review papers on the same data that have reached the same conclusion:
Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. American Journal of Clinical Nutrition. 2010. "A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD."
A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Archives of Internal Medicine. 2009. "Insufficient evidence (less than or equal to 2 criteria) of association is present for intake of supplementary vitamin E and ascorbic acid (vitamin C); saturated and polyunsaturated fatty acids; total fat; alpha-linolenic acid; meat; eggs; and milk" They analyzed prospective studies representing over 160,000 patients from 11 studies meeting their rigorous inclusion criteria, and found no association between saturated fat consumption and heart attack risk.
The Questionable Role of Saturated and Polyunsaturated Fatty Acids in Cardiovascular Disease. Journal of Clinical Epidemiology. 1998. Dr. Uffe Ravnskov challenges the diet-heart hypothesis simply by collecting all the relevant studies and summarizing their findings.
Where's the Disconnect?
The first part of the diet-heart hypothesis states that dietary saturated fat raises the cholesterol/LDL concentration of the blood. The second part states that increased blood cholesterol/LDL increases the risk of having a heart attack. What part of this is incorrect?
There's definitely an association between blood cholesterol/LDL level and heart attack risk in certain populations, including Americans. MRFIT, among other studies, showed this definitively, although the lowest risk of all-cause mortality was at an average level of cholesterol.
So we're left with the first premise: that saturated fat increases blood cholesterol/LDL. Could this hypothesis be less well supported than it appears? The data that are used to support it come almost exclusively from short-term feeding studies (<3 and="" association="" between="" blood="" consumption="" effect="" fat="" found="" habitual="" have="" here="" how="" information="" is="" lipids.="" little="" long="" months="" most="" nbsp="" observational="" on="" p="" persists="" saturated="" studies="" surprisingly="" this="">
A common hypothesis among cholesterol skeptics, such as the WAPF / Mary Enig, Chris Masterjohn and you, Stephan, is that polyunsaturated fatty acids, particularly omega 6's, contribute to heart disease by allowing carrier molecules to become oxidized. It's a little disturbing that total PUFA intake is not related to heart disease in the Archives of Internal Medicine survey. As omega 6 PUFA dominates total PUFA intake in American diets, I would hope to see a strong association if this theory is correct.
Stephan, do you have any idea what might be going on?
Great post as usual Stephan.
"Men who developed coronary heart disease also had a higher mean intake of percentage of calories from... fat, saturated fatty acids, and polyunsaturated fatty acids."
I wonder whether much 'anti-fat' evidence along these lines, might ultimately indicate benefits or saturated fats. Something pro-saturate, anti-carb people sometimes seem to neglect is that carbohydrate is predominantly turned into SFA in the body. Might some of the purported advantages of higher carb, lower fat, be explained by the fact that you ultimately end up with a much better selection of fats in the body (i.e. mostly saturated rather than polyunsaturated)?
Very nice post! Is there a more detailed review of the controlled trials looking for the effects of saturated fat coming as well? I know you have done a brief literature review.
I was just wondering, if the evidence is so weak, wouldn't it be possible to win a case against the health organizations in a courtroom? I assume the evidence must and will be very critically reviewed there and I cannot see how their diet suggestions about saturated fat could be backed up.
How many billions of dollars is the statin industry worth? There's your answer.
The only thing surprising is that more studies haven't been jerry-rigged by the big university research departments, whose leaders are all million dollar "consultants" of big pharma.
Most Americans have almost no n-3 PUFA and much more than 4% n-6 PUFA. Check out some of Stephan's earlier posts to see how this very-convincingly explains why it is difficult to detect the ghastly contribution of n-6 PUFAs to heart disease in epidemiological studies.
Saturated fat intake does not cause the liver to generate LDL particles. (Saturated fat intake helps to increase the size of existing LDL particles, which is a good thing.)
Which foods should be minimized to minimize the liver's capability to generate LDL particles? What are the best diet based methods to reduce LDL generation? No carbs, no alcohol?
There's definitely an association between blood cholesterol/LDL level and heart attack risk in certain populations, including Americans.
Yes, but as we all know correlation is not causation. The causative role of high normal LDL cholesterol has not been established. However, as you've pointed out before, high levels of oxidized LDL (ox-LDL) are strongly correlated to CHD and likely causative.
What causes LDL to oxidize? A diet high in omega-6 PUFA and sugar/simple carbs, lack of physical activity and stress.
Heart disease is primarily a disease of inflammation and oxidative damage. Cholesterol is a marker, not a causative agent.
For more on the relationship between ox-LDL and CHD see my article How to Increase Your Risk of Heart Disease
My history shows quite clearly that my fat intake has a direct relation to my cholesterol levels (units are mmol/L):
Date TC HDL LDL
2005-06-15 5.09 1.8 2.6
2007-10-15 7.1 1.9 4.6
2008-11-11 8.33 2.22 5.4
2009-10-12 10.89 2.12 7.74
I went "Paleo" in early 2007; after reading Taubes late that year, I lost my fear of fat, so that upped the 2008 numbers. Further reading convinced me I should try to eat even more sat fat, so that last line shows the result.
I have nothing but good results on the high-fat diet, except it's a hard sell to most people when I have to admit that I busted 400mg/dL. Over three years I doubled my LDL.
One of the explanations why LDL particle size might matter is the basic chemistry rule that activity increases when surface area increases. When you divide particle to pieces half of the original size you increase the particle number 8 fold and you increase the surface area 2 fold. In case of LDL the increased number increases the probability to meet oxidative agents and and increased surface area increases the chemical reactivity.
Thanks for the resource Stephan.
I agree that the medical establishment (and federal govt.) should be slapped with a class-action law suit that would make the money paid by the cigarette companies look like chump change. How many dead or ill can we tolerate before we take action? I count myself a victim of the low-fat, high-grain experiment. I'll tell them where they can shove their food pyramid.
Linoleic acid is generally not related to heart attack risk in most of these studies.
Once you cross the threshold of about 4% of calories from omega-6, assuming low omega-3 intake like in the US, going above that doesn't change your eicosanoid profile much. We crossed that threshold long ago in this country. Almost no one eats less than 4% of calories from LA at this point, and they haven't for over 50 years. So the studies are comparing high intakes to higher intakes. See this post:
It sounds like there were a lot of variables changing. I think certain people see large increases in LDL on very high-fat diets, but that might be the case whether the fat were lard or olive oil. That's what the literature suggests. But the lit looks at averages of course, so there's always the possibility of individual variation.
Here is a recent 12 years prospective study that found a negative correlation between consumption of dairy fat and heart disease. You have to go to the main text to get the actual results. In the abstract the researchers try to relate the positive effect of fat to fruit and vegetable consumption.
Oh yeah, I saw that one. Dairy fat has also been associated with a lower risk of stroke in several studies.
Couldn't another dirty secret of low-fat diets be that they are highly acidic? I know that there are many quacks who advocate a low-acid diet, but I believe there might be something to it. Americans with high intake of sugar and cereal grains have very high levels of osteoporosis as a result of the body leaching calcium from the bones to reduce the acidity level of the blood.
Perhaps all of this calcium that leaches out clogs the arteries. This might explain why you can have low-CVD rates with both low-fat and high-fat populations - so long as they stay away from sugar and too many cereal grains.
Anybody have any thoughts on this? Thanks.
I love these cardio-articles :) Tranks!
What causes LDL to oxidize?
Recent evidence showed that LDL oxidation occurs not within the interstitial fluid of atherosclerotic lesions but within lysosomes in macrophages in atherosclerotic lesions. Most important, the study found that this oxidative modification was inhibited by the drug chloroquine, which increases the pH of lysosomes, as oxidation can be promoted by acidic pH. Please see the references in our blog http://aciditytheory.blogspot.com/ where we present new evidences favoring the acidity theory of atherosclerosis.
Hi Stephan, another great post demolishing an already weakly built hypothesis. Here are the PDFs of the review papers you quote in your post: http://www.nmsociety.org/App_Themes/Images/AboutFat/The%20Questionable%20Role%20of%20Saturated.pdf and http://www.dcscience.net/mente-aim-2009.pdf
I recently found your blog through my search on interenet. I really find your blog fascinating, exactly what I was looking for. Some well-based and convincing arguments about diet.
I studied anthropology so I like that you use the knowledge from there. I come from Iceland, the same country as Vilhjálmur Stefánsson you have quoted from. Surprisingly I have never read any of his works, but then again I never took a course about the inuits. Still I am familiar with his work and as far as I know he is well respected.
Few years ago I read that saturated fats weren´t so bad as it´s said. I partially believed it but was sceptical since it can be confusing to know what to believe. I didn´t bother going into depth of reserching at that time though.
But few weeks ago, I coincidentally heard part of some news about this genetic mutation in one or two families here in Iceland. It´s a genetic flaw and those who have it usually die in their twenties from a stroke. It´s very sad because the modern medicine don´t seem to be able to save their lives.
I´ve heard about it before but this time I heard something that caught my attention. This mutation came about in the 18. century but it didn´t kill anyone until the 20century (I think it was). They had this new theory that it might have something to do with the diet.
Unfortunately I didn´t hear all of what was said but I know my history, interestinly enough people at that time ate a lot of, yes you can probably guess it, meat. Every bit of the animal was used because food was not abundant. Also they lived on dairy, eggs, fish, herbs and vegetable.
It was not possible to grow any grains and anything imported was a scarce commodity and most people poor. This has of course changed and the diet today is similar to other western coutries.
When I heard that I started to dig some more about saturated fat. If the diet protected those people then how bad could the saturated fat be? This is bad news for me though, since I dislike animal fat. At least in its solid form. But it makes sense to me that natural food is far better than processed food.
I also heard some interesting news today. Some scientists found the first dental cavity from the year 1000 or so here in Iceland. This was news because appearantly the dental health at that time was excellent. (Before that the oldest dental cavity found in Iceland is from the 18.century).
The reason for this excellent dental health according to the news? People in Iceland unlike other europeans at that time hardly ate any wheat or sugar.
Unfortunately, I have no links on more information about these news, but I just wanted to point it out since it fits nicely to your theory.
Thanks for another good post.
I'm convinced that there is no significant relation between saturated fat and cholesterol/LDL on a population level.
However, I'm also convinced that there are subgroups of the population (maybe depending on APO E genotype) that get a large increase in cholesterol/LDL with a low carb high fat (LCHF) diet.
My experience is almost exactly the same as GK's comment above.
After a year and a half on LCHF my Tot Cholesterol went up from 6 to 10mmol/L and my HDL is 2.0/L (ie 390mg/dl & 78mg/dl).
I've also seen other commenters on other low carb sites with similar numbers
It would be very interessting to know if the increase is mainly from larger particle size or from more particles.
A just published clinical trial:
Low-Fat Versus Low-Carbohydrate Weight Reduction Diets Effects on Weight Loss, Insulin Resistance, and Cardiovascular Risk: A Randomized Control Trial
This is being sold by the Sugar Bureau as evidence against low-carb. Here is a commentary:
I have no access to the whole text online, but if you do, it might be worth checking what kind of fat was used in the high fat diet.
Thanks for the great blog Stephan, probably the best resource on the Web!
Thanks for another great post, Stephan.
However, these negative results don't stop the FDA from recommending that people with normal cholesterol and no family history of heart disease take Crestor. See http://content.nejm.org/cgi/content/full/NEJMoa0807646
Pretty amazing IMO considering what we now know about how improving diet and Vitamin D status can do.
Regarding the low fat/high carb recommendation for insulin resistance, it is obvious that a diet like that will require individuals to take diabetes drugs forever. Follow the money.
I think you're right. Anecdotally, there are certain people whose LDL shoots through the roof on high-fat diets. Interestingly, it also seems to decrease in certain people.
Yeah, I heard about that one. I'm not going to bother looking into it beyond the abstract. The study only lasted eight weeks, first of all. The big outcome that made them decide low-carb diets give you heart attacks was that the low-carb diet didn't change arterial stiffness, while the high-carb diet reduced it... give me a break.
They only reported body weight changes in the abstract, not fat mass changes. That's an important distinction because low-cal high-carb diets often cause muscle wasting.
Stephan, have you come across the idea that saturated fat inhibits absorption of magnesium? If there is a link, that might explain it. But of course the primary problem would be consumption of refined grains, which have had nearly all the magnesium removed. Magnesium is needed to activate many enzymes of carbohydrate metabolism, so eating the carbohydrate without the magnesium is asking for trouble.
Mark, it's supposed to be REFINED grains that make you acid. The enzymes that control acid-base balance need vitamin/mineral cofactors which are present in the whole grain.
Hi GK and Lars,
I'm happy that I found another two unusual cases like mine. My history shows a similar reaction to low carb high animal fat (not olive oil). In 14 months calc. LDL went from 4.7 to 12.7 (491) and nobody knows why. Is it a pathology, do I need to be worried?
You are definitely making important observations about the connection to health and Icelandic dietary history.
I was fortunate to visit Iceland in 2002 when my husband was invited to a Scandinavian molecular medicine meeting (http://homepage.mac.com/gandasalvesen/Movies/iMovieTheater46.html). Pardon the joke about huge Icelandic forests, please.
During our week in Iceland I learned a bit about the land and Icelandic history. The unique conditions in this dynamic island are fascinating (unfortunately I was more into wool and fiber arts at the time and gave less attention to the food and dietary history).
Until only a couple generations ago (I think around WWII?), life in Iceland was HARD! Weak people simply couldn't survive there. The lack of grain and sugar surely was a huge plus for the descendants of Vikings and must have been a factor in their hearty constitution (though there was an illness outbreak - smallpox?- in the 19th century that killed off a huge % of the population). The short northern growing season greatly limited crop options (I understand Iceland now relies on heated greenhouses and imports - imports may have reduced somewhat with the current economic issues). Sheep do very well in Iceland, they seem to be everywhere in the back country, grazing on grass and lichen (mmm, free-range lamb!). And there's the fantastic Icelandic cod and cod liver oil (I think you'd enjoy Mark Kurlansky's book, Cod: A Biography of the Fish That Changed the World, by the way). I wish I'd been more open minded about the dried cod when I was there.
I found a google map of gluten-free locations for food shops/dining in Reykjavik here: http://celiac.travel-options.eu/icelandgf.htm
You can probably tell I looooved Iceland! We sampled the local version of moonshine (wow, potent stuff, I think it was called gambri or landabrugg) & had a meal at a pub/restaurant in Reykjavik that was supposed to be traditionally Icelandic cuisine (I had lamb). I've been fortunate to visit a lot of unforgettable places, but Iceland ranks at the top. We spent 3 days in the backcountry on one of the most exciting bus trips (maybe the only exciting bus trip) I've ever been on. Our bus was an all-terrain bus that goes through rivers and in the water along the edges of lakes because the frequent floods from glacial melt/volcanic activity wash out roads and bridges. The Icelandic landscape is like no other and just thinking about makes my heart skip a beat. We were the only Americans on a bus full of Scandinavian scientists (& their families), hosted by a couple of very genial Icelandic scientists who really knew how to share Icelandic history. What storytellers! You are fortunate to have such a great heritage.
My total Cholesterol and LDL (calculated) has gone up quite a bit on a high fat (naturally saturated), low carb, and essentially no-grain diet, too, but it doesn't worry me at all. My HDL has also gone up quite a bit and my triglycerides have gone down to below 100 all the time. My ratios are very good. My first coronary calcium artery scan a year ago score was excellent at 0 - no calcified hard plaque detectable (though I understand a ) or low score is fairly common for pre-menopausal women - I'm nearly 48 yoa and have been peri-menopausal for what seems like forever -, so I'll repeat the scan in 4 years when by then I'll likely be post-menopausal).
CVD is something my maternal family members take very seriously, because my grandfather died at 50 yoa of MI leaving my randmother a widow with 4 of their 5 children still living at home (btw, butter wasn't used in their house; margarine was). Most of my mother's family are *very* mindful of the American Heart Association's guidelines and are very compliant (pantries and refrigerators full of highly processes industrial "heart-healthy" labels).
My mother was was and is especially mindful of her risk, as she shared a temperament and body type with her father. She thought it was the right thing to choose margarine and skimmed milk. Her total cholesterol was flagged as "high" in her early 40s (1980s) as she embarked on a 25+ year nursing career (on the night shift - so she was chronically sleep and Vit D deprived). She gained too much weight, took all the recommended "heart-healthy" meds (including synthetic HRT) for all or most of the past 25 years, exercised on a stationary bike (chronic cardio), had various orthopedic and tendon ailments, and yet was diagnosed diabetic and hypertensive within the past few years. Her coronary calcium artery score was alarmingly high, too. At 67 yoa last spring she underwent angiogram because of cardiac symptoms with exertion, then had double bypass surgery for her blocked arteries.
In other words, she did just about everything the "health authorities" recommend to avoid heart disease, yet still she developed it (plus diabetes, which I now think is a genetic/epigenetic family trait, expressed by modern industrial diet and perhaps environmental pollution/chemicals). Real food was replaced with too much processed low fat, high carb, omega-6 PUFA-laden, low omega 3 "machine cuisine". The meds clearly didn't reduce her risk at all. She and her doctors credit the failure of prevention to her "genetic fate" and she thinks she's lucky to have had 18 years more life than her father had. Sigh.
I don't see it that way at all, and I don't think she had very good advice (she's definitely not interested in learning about a new perspective, though she has tossed the margarine finally and uses a bit of butter and eggs now). I heeded the same AHA advice in my 20s and 30s but eventually saw that it was probably making my health worse and not likely to prevent anything (the start of my paradigm shift was when I was diagnosed with gestational diabetes 12 years ago, despite no family history at the time and not being very overweight). Steering ever farther clear of AHA-endorsed advice the past 10 years or so has improved my health tremendously (I feel far better at nearly 48 yoa than I did at 30 or 40 when I had all kinds of chronic health issues showing up). I run from "heart healthy" labels and claims.
So I like to say the only thing I fear about cholesterol is not having enough. ;-)
Dirty little secret about Crestor (NOT) reported by the Wall Street J
"...the FDA said there was a "statistically significant" increase in the number of patients who developed diabetes in the Crestor group compared to the placebo group.
The agency also noted there were 13 deaths due to gastrointestinal disorders compared to one in the placebo group, but the FDA said a further review of the deaths suggest the "imbalance is a chance finding."
The agency also said 18 patients in the Crestor arm of the so-called Jupiter study reported a "confusional state" compared to four in the placebo group..."
And the punchline:
"Crestor had $3.6 billion in annual sales in 2008, which was a 29% gain from the previous year."
A 29 percent gain. WOW.
Interesting post on the Paleo diet web site about this topic.
Seems views are evolving since the book was written.
"Anecdotally, there are certain people whose LDL shoots through the roof on high-fat diets."
Stephan, should these people be concerned about the cholesterol increase?
Excuse my brevity. I've got alot to say and very short on time. If requested I'll provide
references when I get back in town next week.
I disagree with you contention the saturated fat doesn't increases Ldl levels long term. Virutally all the controlled dietary studies show this effect. It's only when when you allow folks to report what they eat and trust them that the results are otherwise. When you control what they put in their mouths sat. fats increaes Ldl levels. This applies to studies over 1 - 5 years. Humans are notoriously unreliable when left on their own devices.
Currently the best lipid indicator is apoB/apoA (this is close to Ldl particle/Hdl particles - and this is irrespective of Ldl particle size). Although the older TC/HDL ratio is not as accurate it still gives provides a pretty good indicator.
Using GK's TC/HD numbers as a reference is worrysome. Before he went "Paleo" his ratio was 2.8 which is considered below average risk. His current ratio is 5.13 and he is no longer at below average risk.
Maybe traditional risk factors don't apply to Paleo high sat diets, but I don't know of any data to support this view.
Many of the studies you provided in the first group did not compare folks at low (<10%) to very high (>30%) sat fat diets. The sat fat differences were small compared to the differences seen on many (not all Paleo) diets. Also the older studies used rather crude analyic tools. They didn't separate folks by quintiles of fat and apply multi variate anaylsis to remove confounders.
I do agree that the Womens study was well done and didn't find any differences between the first and last quintile but the sat fat differences were relativley small compared to non Paleo and Paleo diets.
Inadditon, and contrary to your claim, it appears that Men's study did find a large difference between first and last quintile to the tune of 72% for fatal heart attacks (after accounting for confounders)and there was only 15 grams of differences between the quintiles.
I know this is not an accepted notion here, but the evidence shows that "large fluffy LDL" are not benign but are arthogenic and possibly as problematic as the small denser units. In retrospect the reason for this misunderstanding in the literature is understandable, but the fact remain that ldl particle size is not near relavent as many believe.
In fact the amount of Ldl particles/Hdl particles is the most accurate blood lipid measurement. Size of the Ldl particles doesn't matter only how many of them there are.
Very low total cholesterol levels <=150 pretty much prevent CVD irregardless of TG, HDL, LDls.
Live and practicing HGs (including Inuits) have have total cholesterols < 150.
Dr. Davis, of Heart Scan Blog, recommends moderated (low) sat intake. He recommends an optimal Ldl-C level of 60. And this guy knows his calcium scans!
My tentative answer is yes. I can't say that with much confidence at this point (due to the fact that large LDL may be less dangerous than small LDL), but I just can't imagine it's good to have an LDL over 200 mg/dL. You basically never see that in traditionally-living populations, whether they eat a carb-heavy diet or a fat-heavy one.
Then again, the associations between lipoproteins and atherosclerosis/heart attack risk were determined in people eating industrial diets. It may be a totally different ball game if you're eating real food. But since it hasn't been studied directly, I can't say for sure.
Dr. William Davis has a picture of a coconut on the header of his blog. He has no problem with saturated fat.
The "increase" in fatal heart attacks in the Physician's heath study was not statistically significant. I quote:
"as for saturated fat the associations were attenuated and no longer significant after adjustment for dietary fibre"
The differences in sat fat intake between quintiles was more than two fold (15.9 vs 32.4 g/day). There was also no association between sat fat intake and TC.
I disagree that the difference in sat fat intake between groups in these studies was insufficient to see a difference. Most of them were looking at approximately two-fold differences.
Please provide us with references or your statement that saturated fat increases TC/LDL at timescales of a year or more, when PUFA is kept the same. It has to be compared with MUFA, not PUFA, because PUFA lower TC and LDL.
Dr. Ronald Krauss, arguably the most influential lipoprotein researcher, states that large LDL are not atherogenic. So frankly I'm confused about why you're so confident that they are atherogenic. Check out Krauss's latest paper:
"Our study demonstrated that (1) levels of small/medium LDL particles are associated with [CV disease] and (2) levels of large LDL particles are not significantly related to cardiovascular disease, is consistent with other large prospective cohort studies whose data were obtained by 2 different lipoprotein measurement techniques: the Quebec Cardiovascular Study (GGE) and the Multi-Ethnic Study of Atherosclerosis and Women's Health Study (NMR). (p. 5)"
Stephan, did you see my last comment (Dec 17, 8.56am) on saturated fat and magnesium absorption? I'm a new commenter, and you may have missed it. I'm from Oxford, UK. I have a PhD in developmental biology, and have studied the link between diet and disease for 30 years. I am greatly impressed with your knowledge.
I've just checked my facts and saturated fat does indeed inhibit absorption of magnesium. I think this might explain a lot.
I wrote another comment, after 'Dr Rosedale replies', which you might like to have a look at.
I think decreased magnesium absorption via SaFa is a good point, especially considering stroke risk ja DM2:
Yet I think we should not forget that Vitamin D (1,25(OH)D) can positively affect magnesium absorption in jejunum:
Obviously most people here know that Vit D is critical in CAD prevention. David Grimes wrote a 672 page book about this subject just months ago:
Magn is also required in each of the steps concerned with replication, transcription, and translation of genetic information, and thus it is also needed for the genetic mechanism of action of Vitamin D.
To make things even more interesting, Ca/Magn-ratio seems to be one of the stronger single predictor of fatal heart attacks I can think of. Not that I'm an expert, just making an association from this graph:
Magn does exist in meat, but a lot is burned away during frying etc, if I'm correct ?
I think that Mark Sisson's protocol of eating LOTS of lettuce/greens with meat may dimish the need of extra Magn, don't you think ? I certainly do this and have noticed that my muscle cramps are zero now. Magn supplements were not so effective, which may be because their absorption is not as good.
Thanks to Stephan for another excellent post.
switters - I agree with the direction in which you are heading.
Jane thanks for the heads up on magnesium absorption, which sent me off on a quick web search. Do you have references please.
"I've just checked my facts and saturated fat does indeed inhibit absorption of magnesium. I think this might explain a lot."
This book suggests that in women on controlled magnesium rich diets the substitution of butter for vegetable fat resulted in retention of more magnesium.
It also suggested that young men on 10 to 30% Omega six linoleic acid tended to be in negative magnesium balance
Author Omega Six The Devils Fat.
(The editing is poor but the science is OK (-:)
( For anybody who might be kind enough to be interested the long promised revised version is progressing and is currently being professionally edited. It now contains over 2000 references, and a significant amount of new material. It is hopefully a significant improvement over the previous version.)
Dang your quick!
Anyway I'd like to respond before I'm out of pocket for a few days.
"Dr. William Davis has a picture of a coconut on the header of his blog. He has no problem with saturated fat"
Dr. Davis does not believe that sat fat intake is the be all/end all of the discussion, but he's quite clear that saturated fat must be moderated and recommeds folks cut back when their intake is high. If you think this is not true provide a quote and not picture of a coconut.
In his earlier book (2004) he recommended a relatively low fat diet (60C,20F,20P). I think his current thinking favors a higher fat diet but still lower sat.
The "increase" in fatal heart attacks in the Physician's heath study was not statistically significant.
"as for saturated fat the associations were attenuated and no longer significant after adjustment for dietary fibre"
Here's also what they said:
"These data do not support the strong association between intake of saturated fat and risk of coronary heart disease suggested by international comparisons. They are compatible, however, with the hypotheses that saturated fat and cholesterol intakes affect the risk of coronary heart disease as predicted by their effects on blood cholesterol concentration".
And that's what been reported by posters here: Increasing Sat. fat intake is increasing TC levels.
"I disagree that the difference in sat fat intake between groups in these studies was insufficient to see a difference. Most of them were looking at approximately two-fold differences."
A two fold increase is much smaller >3 folder increases reported here. I try to keep my sat fat intake below 20 grams, many Paleo type eat over 60 grams. BTW, I do not eat a low fat diet.
"Please provide us with references or your statement that saturated fat increases TC/LDL at timescales of a year or more, when PUFA is kept the same."
What do you mean by PUFA kept the same. Do you mean the PUFA/SAT ratio or total PUFA?
Lets say I eat a 40% fat diet 10% of which is saturated fat. If I keep my diet at 40% fat but increase my sats to 25% and reduce my PUTAs to 15% I (or do the opposite) I claim that that shows that Cholesterol will increase (or conversly decreasse). All the controlled metabolic ward controlled studies have show this.
I believe metabolic ward studies have shown this, Minnesota and Finnish hospitals studies showed this, year long studies of ketogenic diets with children have shown this.
More importantly the direct experience of readers here have show this.
Here's info on particle number vs particle size:
Low-Density Lipoprotein Size and Cardiovascular
Disease: A Reappraisal
FRANK M. SACKS AND HANNIA CAMPOS
Nov. 11, 2004 (New Orleans) — The number, not the size, of low-density lipoprotein (LDL) cholesterol particles predicts heart disease risk, according to an analysis of blood samples from more than 3,200 participants in the Framingham Heart Offspring Study.
Systematic review: association of low-density lipoprotein subfractions with cardiovascular outcomes
Saturated fat inhibits absorption of magnesium? Is that true relative to other types of fats, and in humans? And how much does it inhibit it? It would also be important to know if it has any effect on excretion. For example, protein increases Ca excretion but also increases Ca uptake from the gut.
The Finnish and Minnesota trials used high PUFA oils. Please provide us with references showing that TC increases with increasing saturated fat over timescales of 1 year or more, when PUFA are kept the same.
It's clear in table 1 of the Physician's health paper that there is no association whatsoever between saturated fat intake and blood cholesterol; have a look for yourself. The first quintile has a TC of 5.2, all four others have a TC of 5.3.
Americans are lacking in magnesium principally because they don't eat enough vegetables and nuts and because table salt in the United States is generally not the sea salt used in Europe and Japan. (Sea salt contains much more magnesium in comparison to the refined salt we use in the U.S.)
I read about this is Fred Kummerow's book "Cholesterol won't kill you, but trans fat could" (he also testified on Capitol Hill back in the 1970s against McGovern's low-fat recommendations)
The book is an interesting read from the guy who first sounded the alarm against trans fat (back in the mid 1950s!!). The book contains a section about magnesium deficiency and how he thinks it is related to CVD. He makes no mention (as I recall) about saturated fat inhibiting magnesium absorption. Moreover, he recommends milk consumption as it is an abundant source of magnesium.
Interestingly, salads, nuts, and milk all contain loads of magnesium yet they are touted as health foods by the media because they contain "healthy fat" and fiber. On the other hand, perhaps they are healthy because they contain magnesium. Further evidence that most mainstream nutrition researchers don't really understand what they are talking about.
Thanks again, Stephan, for the great post.
"The Finnish and Minnesota trials used high PUFA oils. Please provide us with references showing that TC increases with increasing saturated fat over timescales of 1 year or more, when PUFA are kept the same."
As I recall the Finnish study substitued PUFA for SATs without changing the overall %fat of the diet.
This is normally how folks would cange the percentage of fats in the diet when playing with the ratio for Sats and Pufa. When this is done TC either raises or falls.
You seem to be defining a non real world scenaro to support your point. If I change Sat/PUFA ratios and keep my %fat the same the amount of Sat and Pufa will differ. You want a situation where I rasie my Sats but also raise my PUFA to keep the ratios the same. But if I do this I change the %fat in my diet.
Once again, many folks here (and other Paleo/High Fat blog) have reported very high increases TC when increases Sat fat over long periods of time. Any yes they did not increase their PUFA to keep the ratio the same. Any yes this is how people modify their diet in the real world.
The folks in Ornishes studies lowered both their SAT and PUFAS and sustained a lower decrease (>30) in Ldl levels over a 2 year period.
Also you have never commented in detailed on the hundreds of metabolic ward studies. Yes theses were not longer than a year but I belive many of them were up to 3 months. I never seen a report that levels start to revert after a period of time.
I'll provide specific references when I get back in town.
To prove your point, you need to provide a study showing that increased saturated fat increases TC over a year or more, without changing PUFA. The study design is simple: MUFA vs SFA. You won't be able to provide us with references supporting your position because they don't exist.
In MRFIT, the Women's Health Initiative Diet Modification trial and the Lyon Diet-Heart trial, reducing saturated fat intake 20-30% had little or no effect on total cholesterol or LDL (0-3% reduction). The small change that occurred in WHI can be attributed to increased dietary fiber.
Furthermore, in a variety of animals fed SFA vs MUFA, LDL is the same as long as you don't add extra cholesterol:
I don't know how many people have done this, but Peter of Hyperlipid has had both a CAC heart scan and an Aortic stiffness test as his TC=8mmol/L(310mg/dL), a level considered dangerously high by Doctors.
See HERE for the CAC heart scan result (in the comments) and HERE for the Aortic stiffness result.
This suggests that it is possible to have healthy coronary & other arteries with TC=8mmol/L.
Randy: "It's only when when you allow folks to report what they eat and trust them that the results are otherwise. . . Humans are notoriously unreliable when left on their own devices."
Randy: "Once again, many folks here (and other Paleo/High Fat blog) have reported very high increases TC when increases Sat fat over long periods of time."
Randy,thanks for the vote of confidence in the reliability of paleo dieters' anecdotal reports. (er, . . . I guess :)
In my post above showing my soaring cholesterol values, I neglected to mention that my triglycerides went down as TC went up, from 300mg/DL pre-paleo to 200 at present.
Currently I'm scaling back my fat intake to more "natural" levels, i.e. I'm not expressly trying to add more fat than what occurs naturally in the food.
The research on lipids and CHD is still so ambiguous it's hard to know how to interpret these lab numbers. I just cannot believe that nature's price for otherwise good health and freedom from ills is a heart attack.
The interesting thing about magnesium and saturated fat is that in some situations Mg absorption is decreased, and in others, increased. Just like saturated fat seems sometimes to be bad, and other times not bad or even good.
Here is a quote from a book chapter by Droke & Lusaki:
'Taddayyon & Lutwak (1969) studied the effects of dietary triglycerides on Mg metabolism in weanling rats. At 5% intake, triolein, tripalmitin and tristearin had similar effects on Mg absorption and resulted in higher absorption of Mg than with 25% tripalmitin or tristearin. The Mg content of the femur was highest in the groups fed 5% or 25%triolein and lowest in the group fed 25% tripalmitin. ..In turkey poults, retention of Mg was less with more saturated fats, and palmitic acid consumption significantly decreased bone Mg content (Leeson & Atteh, 1995). Kaup et al (1990) observed a variable effect of fat on Mg absorption in young and mature rats. Mg absorption was consistently GREATER' (my emphasis) 'among young rats fed high butterfat (20%) diets vs low-butterfat (5%) diets. Mg absorption, however, tended to be reduced among mature rats fed more fat.'
@ Jane The infants fed MCT-containing formulas absorbed significantly more calcium than the control group. Magnesium absorption was significantly increased in the 80% MCT group.
I'm trying to find it (might have deleted it already) but within the last week or two I read a newsletter of Dr. Davis' and noted that at last he's revised his advice about dietary saturated fat from when I first started reading him. He said something to the effect that he *no longer advised* reducing saturated fat intake. Granted, it wasn't advice to purposely stieincrease saturated fat, but it was an indication that he no longer is in lock-step with conventional cardiology on the saturated fat issue.
If I run across it again I'll repost with more exact wording.
Stefan, thanks for a great blog. I have learned a lot from reading it.
I have a question about how much faith you can put in studies such as you have cited that try to link diet and disease.
My feeling is that sugar (I mean refined table sugar) causes a lot of problems, but do studies show correlation between sugar consumption and disease?
If studies do show such a correlation - then why do we not hear more about it?
And if they do not - should it make us wonder if people are studying this the right way. Perhaps current methods are not sensitive enough (because of poor reporting or whatever) to address the links between diet and disease.
Randy & Anna -
A couple of weeks ago I asked Dr. Davis about his stance on saturated fat. Here is what he said:
"The Track Your Plaque program stand on a number of issues, including saturated fat, has evolved over the years. We now do not restrict them, but nor do we suggest a carte blanche approach, since we do continue to maintain rather strict LDL targets for plaque reversal."
Here's the link:
I think you have to be very skeptical when interpreting observational studies like these. They never prove anything, they only suggest things. I don't take these studies as proof that saturated fat has no effect on heart attack risk. But when combined with the results of the clinical trials, they begin to make a pretty good case.
Mark, you are right about mainstream nutritionists. How many of them know that magnesium inhibits cholesterol synthesis just like statins do?
Daryl asked 'How many billions of dollars is the statin industry worth?' Quite.
How many nutritionists know about the work of Leslie Klevay, who showed that all the symptoms of ischemic heart disease (over 75 of them) could be induced in rats by making them copper deficient? Klevay and the other leading copper researcher Sorenson say MOST of us have copper deficiency. And yet nutritionists claim copper deficiency is rare.
To me, this is a huge scandal. I never thought of it as a conspiracy until Climategate, and now I'm not so sure.
Magnesium absolutely mimics statins, and vice versa.
So does egg yolks, cholesterol, saturated fat, and vitamin D...
For proper energy efficiency and production from mitochondria and the electron transport chain, all fatty acids, hormones, vitamins, coenzymes, ubiquinone, and cofactors need to be present.
Our bodies are like cars. You wouldn't get in a ride w/a kaput carburetor, right? Unfortunately, copper, magnesium, zinc, chromium, especially iodine, and other essential minerals are rarely found together in any single one spot on earth, Dr. Bruce Ames has discussed in papers. Your ride would get cited and could fail the smog test as well. How many humans are failing their 'smog tests'??
Ted & Dr BG, thanks for your comments/links. Robert Brown, I hope I gave the references you wanted (Dec 19,3.36am).
Stephan, might I offer a comment on Carlos Monteiro's question 'What causes LDL to oxidise?' There are endless papers apparently showing LDL is oxidised by copper. But actually, it's just that people use copper to oxidise their LDL in vitro. In vivo, it seems that it's oxidised by iron, and that copper prevents oxidation (via extracellular copper-dependent superoxide dismutase, EC-SOD).
I know you work on neurodegeneration. You will have seen the paper apparently showing that cholesterol plus copper gives rabbits 'Alzheimers'. I asked the lead author what precautions he had taken to prevent oxidation of the cholesterol, since oxidised cholesterol is nasty stuff, as you will know. He told me the pellets were 'kept in an airtight container'. He did not say they were manufactured in the dark with no oxygen, and nor did he say the rabbits were kept in the dark with no oxygen while they were eating them.
I think we can safely conclude the rabbits were eating at least some oxidised cholesterol. The copper might have helped oxidise it, of course. In humans, copper seems to prevent Alzheimer's, not cause it.
Virgin Coconut Oil can heal cancer patient? Yes, it;s true. On top of that, it also helps to reduce weight. Log on to http://vircocoil.blogspot.com
This is a great Guide to Fitness and weight loss
Jane, thanks for your comment.
I have a great admiration on the studies about LDL oxidation, cooper, iron and acidity, by your colleagues from UK, with the leadership of Leake D. S. . These papers (1,2,3) were very important in the development on the concept of the acidity theory of atherosclerosis (http://www.infarctcombat.org/AcidityTheory.org) . The last paper by Leake’s group (4) gives additional reasoning to it .
1. Leake DS. 1997. Does an acidic pH explain why low density lipoprotein is oxidised in atherosclerotic lesions? Atherosclerosis. Mar 21;129(2):149- 57
2. Morgan J, Leake DS. 1995. Oxidation of low density lipoprotein by iron or copper at acidic pH. J Lipid Res. Dec;36(12):2504- 12. Full free paper at http://www.jlr.org/cgi/reprint/36/12/2504
3. Patterson RA, Leake DS. 1998. Human serum, cysteine and histidine inhibit the oxidation of low density lipoprotein less at acidic pH. FEBS Lett. Sep 4;434(3):317- 21.
4. Wen Y, Leake DS. 2007. Low density Lipoprotein undergoes within lysosome in cells. Circ.Res. 100;1337-1343. Full free paper at http://circres.ahajournals.org/cgi/content/full/100/9/1337
Sorry, the right url where is published the acidity theory of atherosclerosis is at http://www.infarctcombat.org/AcidityTheory.pdf
Thanks for the links which lead me somehow to this
I have the 1999 version but was waiting for the 2007 one to come down in price (-:
Overall based on the paper there is more consistent evidence that excess Omega 6 LA and lack of Omega 3 are factors in poor mineral absorption, rather than saturated fats.
More generally excess Omega 6 is associated with compromised digestion, inflammation and decreases in gut cell junction integrity, so excess Omega 6 LA leading to diminished absorption makes sense at a more general level.
So many trials on all sorts of things blame saturated fats but when you look they are trials where there is often a significant intake of Omega 6 which is a confounding factor.
Scarily it appears the structural position of the fats in fat carriers may also impact on mineral absorption, which raises questions as to esterified fats where we substitute saturated fats for polyunsaturated fats in fat carriers to make them more solid for use in baking fats and margarines.
Omega Six The Devils Fat
(revised version 2000 plus refs on the way)
Carlos, I've just been reading your paper, for which many thanks. It's extremely interesting, and I'm sure you're right.
You know, acidosis can be caused by magnesium (and manganese) deficiency. Magnesium and manganese activate glutamine synthetase, which regulates acid-base balance. Here's a quote from a paper entitled 'Glutamine synthetase activity of muscle in acidosis' (King et al 1983, Biochem J 216:523):
'Administration of NH4Cl or HCl and diabetic ketoacidosis are all conditions of sufficiently severe acidosis that demand a high rate of renal ammonia production from glutamine to facilitate proton excretion. The rate of glutamine utilisation may increase up to 10-fold in some of these conditions..'
Meaning, if you're short of magnesium and manganese, you won't be able to make enough glutamine or excrete enough acid.
Thanks for the Leake papers. So they think LDL oxidation is due to iron too. 'Our findings may help to explain why the recent large clinical trials of antioxidants and cardiovascular disease have been disappointing.'
I agree. Iron is only a problem if there isn't enough manganese or copper. The antioxidant trials never include either, although they are arguably the most important antioxidants of all.
Robert, I can't get that link. Can you send it again please? I'm puzzled about the idea of omega-6s being bad for you because of the recent AHA review. But I do remember coming across the idea that omega-3s are involved in uptake of .. manganese I think it was. If this is inhibited by excess omega-6s it would be very interesting indeed.
Jane, you are very generous in your analysis about the acidity theory of atherosclerosis. I'm grateful also for remembering us about the important role of magnesium (and manganese) deficiency to cause acidosis.
Yes the link appeared to have gone, but you can find most of it here in the book preview CH 24.
Stephan has a thread discussing the AHA article, and plenty on Omega 6.
No question excess Omega 6 linoleic acid, an Omega 3:6 imbalance, and lack of long chain Omega 3 is a big health issue, possibly one of the biggest.
My book looks at some of the background, and tries to explain in evolutionary terms why Omega 6 is so central to body systems.
We need under 1% of linoleic acid to be healthy, probably historically averaged an intake of 1-2%, and now eat 10-15% and more which is unprecedented in evolutionary terms. Some groups on non western diets have intake levels around 1%. The natural food chain only supplies 1-2%.
The book is not well edited and is a bit disjointed but contains some new ideas. It contains 700 plus references. The science is on the edge of current knowledge but generally sound.
The new one is a leap forward but will not be ready until next year. http://www.amazon.co.uk/Omega-Six-Devils-Fat-infertility/dp/0955707404/ref=sr_1_5?ie=UTF8&s=books&qid=1261508597&sr=8-5
Jane try this link.
It works for me. It is best to print it as scrolling is temperamental.
Tables 24 are interesting.
There is not much on magnesium. What there is suggests Omega 6 LA has no effect. I will see what I can find.
I did not find much.
If Omega 6 LA does as appears likely impair digestion would inflammation impaired digestion affect magnesium uptake.
Do the mechanisms for absorption of zinc calcium copper and iron (which all show increased excretion compared for high PUFA than sat fat - see last link) and magnesium share common ground, and would you expect any degree of synergy in absorption.
MCTs tend to reduce inflammation.
MCTs increased uptake
Magnesium intake in pregnancy
Fat reduces magnesium intake in those with digestive disturbances
Positional effects of fats on glycerol backbone
Could it be that the main problem with large Omega-6 (LA) intake is not the Omega-6 intake itself, but in todays processed food a large portion of the Omega-6 that we eat is oxidised (ie due to heating).
Ie virgin sunflower oil that has been stored cold may be OK when used for a salad dressing, but not OK when its been heated to fry potato chips?
Oxidation of dietary fats
Trials suggest it is certainly a factor
To prove your point, you need to provide a study showing that increased saturated fat
increases TC over a year or more, without changing PUFA.
We do know when you keep percent of fat in a diet constant and vary
SFAs and PUFAs, TC and LDL go up with more SFAs and down with less SFAs.
The Minnesota and Finnish studies established this and the diets were strickly controlled. We know exactly what these folks ate.
We also know that if you hold PUFAs constant and vary MUFAs and SFAs, TC and LDLs increase with increasing SFAs.
This has been demonstrated in short term metabolic ward studies (min 1 month) where diet has been strickly monitored.
Why would we not expect this to be true long term. It's never been shown not to be true long term (in a controlled ward study)
Granted a long term metabolic study would be usefull, but there is no evidence that indicates the long term changes would be any different.
I agree with your statement that animals studies show that it takes alot of dietary cholesterol to raise LDL levels. But this is true with humans also. Controlled dietary humans studies show that adding SFAs does not increase LDL levels until dietary cholesterol is added.
Only one of the animal studies you referenced used African Green Monkeys (the best primate model for human CVD) and they used extremely low values of dietary cholesterol.
L. Rudel is the world's expert on African Green monkeys and has published alot of papers on this species and its response to Western type diets.
Stephan - Here's my primary question since we started this dialog some months ago:
Stephan - Here's my primary question since we started this dialog some months ago:
Do you believe that the current best lipoprotein markers (apo-b/apo-a or the older TC/HDL) do not apply to folks on high SFA Paleo diets.
I'm open to the possiblity but haven't not seen any proof that this might be true.
In my opinion what's needed are imaging studies (carotid artery, calcium scan,angiograms) of folks over time on High SFA Paleo diets. That would go a long way to resolving the issue.
I'd be interested to see what Kurt has to say on these matters.
Dietary Polyunsaturated Fat Decreases
Coronary Artery Atherosclerosis in a
Pediatric-Aged Population of
African Green Monkeys
Mary S. Wolfe, Janet K. Sawyer, Timothy M. Morgan, Bill C. Bullock, Lawrence L. Rudel
Effects of Saturated and Polyunsaturated Dietary Fat
on the Concentrations of HDL Subpopulations in
African Green Monkeys
John Babiak, Frank T. Lindgren, and Lawrence L. Rudel
Effects on plasma lipoproteins of monounsaturated,
saturated, and polyunsaturated fatty acids in the
diet of African green monkeys
Since I'm eating low carb with lots of SFA and also have a high TC and LDL I found your statement:
"Controlled dietary humans studies show that adding SFAs does not increase LDL levels until dietary cholesterol is added."
Do you have any references to these studies? Would highly appreciate if you could dig them up for me.
I currently know 3 guys that are on low carb high fat diet with high cholesterol/LDL and with zero calcium score: myself, Jimmy Moore and another one.
However since we all are relatively young (I'm 40) and haven't been low carbing for more then a couple of years its most likely too early too see any calcification due to the high cholesterol yet (if there is an effect). Admittedly n=3 is also too small sample size to make any conclusions.
Robert, thanks for all the investigating you're doing. I won't be able to do much myself right now because the science library closes today for Christmas.
However, I think I may have found what we are looking for. The whole omega-3/omega-6 thing might be related to copper deficiency. Here is a quote from a paper entitled 'Low copper status of rats affects polyunsaturated fatty acid composition of brain phospholipids, unrelated to neuropathology' (Sun & O'Dell 1992, J Nutr 22:65):
'There is overwhelming evidence presented here that the proportion of linoleic acid in phospholipids of brain parts and brain myelin is higher during copper deficiency. The basis of this is unknown, but it could result from a lack of delta-6 desaturase activity.'
This means that in copper deficiency, there will be more linoleic acid and less DHA in mitochondrial membranes. You are probably aware that mitochondrial DHA is related to basal metabolic rate, animals with a high rate having much more DHA than animals with a low rate. This is probably to do with the double bonds facilitating transport of electrons and protons across the membrane. The position of the double bonds in omega-3s means they do this better than omega-6s.
We know that desaturase activity needs magnesium and zinc, but this is likely to be a nonspecific effect on synthesis of the enzymes. The enzymes themselves will need a redox-active metal like copper, and we know that delta-9 desaturase is copper-dependent.
So perhaps excess dietary omega-6s are only bad for you if you have copper deficiency. This seems to be the case with dietary fructose.
I found a summary of your book with its list of nasty things associated with excess omega-6 intake, and many of them are also associated with copper deficiency. Most interestingly, the behavioural problems. Klevay has found that the feelgood hormone DHEA is much lower in copper-deficient rats. And the other feelgood hormones, endorphins, need copper for their synthesis.
BTW, I haven't eaten any food containing long-chain omega-3s for 25 years. I live on wholemeal bread, muesli and raw sweetheart cabbage. I get my short-chain omega-3s from whole grains, and I think my desaturases are working pretty well.
Thanks for the feedback on your calcium scores. Thats the kind of hard data that I'm really interested in.
My understanding is that it can take 3 - 5 years for calcium to appear in newly formed plaque.
I've wondered if carotid artery thickness would be a better indicator for short term changes. I was hoping that Kurt Harris would chime in on this.
I've been trying to dig up the reference on the Human Study showing the with 0 dietary cholesterol LDL levels were unchanged with additional dietary SFA.
I was astounded when I came across the study. It was a metabolic ward Human feeding study. I couldn't find it in my archieves, but will do some looking.
I do need to find and post it.
Thanks again for the feedback.
Here's a completely anecdotal report that contradicts some of the other anecdotal reports given here.
About a year ago my dad went in for some tests and he was told he had atherosclerosis in his carotid artery. His total cholesterol, LDL and triglycerides were high, and his HDL was about average.
He had already been on a relatively low-carb diet, but he went further towards a high-fat (low omega-6, high saturated fat), low-carb diet.
After about 9 months he went back in for testing. Total and LDL cholesterol had come down, HDL had gone up, and triglycerides were way down. His doctor couldn't believe it when he told him what he had been eating (butter, steak, eggs, etc.).
I wish I had an answer to that question. On one hand, there are associations between TC/LDL and CVD risk. As you have noted, non-industrial cultures also tend to have low TC whether their diet is nearly vegetarian or high in animal fat.
On the other hand, the studies that found an association between TC/LDL and CVD were mostly conducted in Western countries eating industrial diets. The same types of studies in Japan found no association between TC/LDL and CVD. I can provide refs later if you're interested, but I don't have them on me right now.
I also think the fact that many people feel better and improve their body composition on paleo diets (whether high in fat/SFA or not) is an important clue. Would that occur if your body was undergoing vascular degeneration? It's possible I suppose, but it would be counterintuitive to me.
I agree that it would be nice to see the idea tested directly in a controlled trial with some good statistical analysis.
I decided to look into the copper thing a bit because I was interested by the work of Dr. Klevay you mentioned. As you said, copper deficiency in experimental models causes changes that resemble heart disease in humans.
Here's what makes me wonder though: I found several studies on the association between copper status and CVD in humans, and they didn't seem to support the theory. Any thoughts on that?
I am way out of my depth in these technical discussions, so I'll make a different comment:
The ideas in this and similar blogs have had a huge impact on my diet, my health, and my general feeling of well-being.
Thanks the effect of low copper on linoleic levels in the brain is thought provoking.
Another paper on copper and desaturase.
Your diet is interesting. Have you seen Stephans post on grains and mineral absorption.
Based on their oil most grains do not contain much Omega 3 ALA.
Red cabbage contains some ALA. http://www.nutritiondata.com/facts/vegetables-and-vegetable-products/2373/2
A happy and health Christmas all
Hi Stephan, thanks for your comment. It's true there are studies that seem to show no correlation between copper status and various degenerative diseases. The reason for this is that blood copper rises during inflammatory states. True copper status is very difficult to determine. Blood is no good because of what happens in inflammation. Hair copper is notoriously unreliable, and since copper is excreted in the bile and not the urine, urinary copper is no good either.
During inflammation blood copper rises and blood iron and zinc fall. Lots of people have concluded from this that degenerative disease is caused by iron and zinc deficiency and copper overload.
I know, you can't believe people could be so silly. But it's deadly serious, because things like white flour and breakfast cereals get loaded up with extra iron and zinc (and calcium, see later). Excess iron causes manganese deficiency, and excess zinc causes copper deficiency. So the manganese and copper get removed, and replaced with things that make the deficiencies even worse.
Iron and calcium have to be added to white flour by law, at least here in the UK. Calcium is already high in industrial diets because of the dairy products, and extra calcium can interfere with uptake and utilisation of both magnesium and manganese.
Industrial diets are also high in highly-available iron and zinc, from meat. Adding yet more iron, zinc and calcium to an already awful diet is, I have to say, insane.
Thanks for that. Very interesting in a rather depressing way.
As I am sure you are aware you can add depletion of mineral in foods and based on a paper called http://www.ncbi.nlm.nih.gov/pubmed/18309763 said the mean depletion rates for copper over a range of foods mainly between 1940 and 2002 were 62%, and 100% in some foods.
We breed crops for yield rather than mineral content and are seeing mineral dilution.
And then we refine many foods . . .
I see. Do you have a reference for your statement that serum copper increases in inflammatory states?
I've been poking around some of Klevay's papers, as well as some of the animal studies. It looks pretty compelling, overall. I found a mouse study that contains a good overview of the evidence in humans in its introduction:
They reference an experiment with a low-copper diet in which 4/24 of the subjects had to drop out during the 11-week trial due to cardiac complications:
"An early study of hearts from people who died from ischemic heart disease showed that Cu concentrations were decreased in the uninjured tissues of the infarcted hearts relative to normal heart tissues (5). Another study showed that Cu concentrations decreased in the hearts of people who died from acute ischemic infarction (6). The death rate from ischemic heart disease in soft water areas was found to be increased, and Cu concentrations were lower in the hearts of people who died from chronic ischemic heart disease (7, 8)."
What do you suggest to maintain proper mineral balance? My initial thoughts would be to eat unrefined foods, avoid excessive phytic acid, and eat organic/pastured foods.
Oh yeah... and to eat liver, which is a concentrated source.
Stephan, I've just tried to find my favourite paper on serum copper and inflammation, and can't. Sorry. Try googling 'copper inflammation'.
About phytate causing metal malabsorption. I know there are many papers saying that. But there may be another side to this story. Here is a quote from a book called Health on Your Plate (Pleshette 1983):
'Fibre contains phytate, which has been thought to impair the absorption of zinc, iron and calcium.
'Researching into the impaired absorption of zinc which occurs in the consumption of wholemeal bread and other fibre-rich foods, Dr John Reinhold of the Pennsylvania Nutrition Research Project carried out studies into the different kinds of bread eaten in Iranian villages. He established that villagers eating a lot of unleavened wholemeal bread were indeed deficient in zinc. However, in those places where the wholemeal bread was made with yeast from a leavened dough, like Western bread, he found no mineral deficiencies, even though in some villages bread makes up 75% of the total diet. Leavening the bread, it appears, destroys the phytate.
'Commenting on the alleged malabsorption of calcium caused by phytate, leading fibre expert Denis Burkitt wrote to me: 'it is a complete red herring that phytate in binding calcium can have ill effects. The calcium is actually liberated again, further down the bowel.'
Burkitt probably means, further down the bowel the environment is more acidic, and the acid liberates the metals so they can be absorbed.
My conclusion is, it's probably best to soak whole grains or sprout them, and ferment your dough for longer than supermarkets do, but if you don't it might not be the end of the world.
Yes, your ideas about how to maintain mineral balance sound excellent to me. I get all my ideas about what to eat from the Hunza. Have you read G T Wrench's 1938 book about them? It's called The Wheel of Health and is available in full online. Mind-blowing stuff.
Robert, yes I've seen those reports. UK produce nowadays has an astonishing 75% less copper than it had 50 years ago. And milk has so little copper that scientists use it to make their rats copper deficient!
Thanks to you and Stephan for the references. I shall read them when the science library opens again. I'm in an internet cafe right now.
Stephan, it could be that phytate isn't really a problem. Denis Burkitt is quoted in Health on Your Plate (Pleshette, 1983) as saying 'it is a complete red herring that phytate in binding calcium can have ill effects. The calcium is actually liberated again, further down the bowel.'
He probably means, further down the gut it gets more acidic, and the acid frees the metals so they can be absorbed.
I can't find my favourite paper on serum copper and inflammation, sorry. Try googling 'copper inflammation'.
I had heard a long time ago that drinking tap water regularly provides quite a bit of copper. Is this true?
Yes, leavening, particularly sour leavening, breaks down phytic acid. Every healthy culture that is heavily reliant on whole grains that I'm aware of uses processing methods to reduce PA.
I do think excess phytic acid is a problem. It chelates divalent cations like zinc, iron, magnesium and calcium. Likely certain trace minerals as well. Edward Mellanby showed that it antagonizes vitamin D and causes rickets and reduced bone mineral density in dogs with marginal D status. It reduced BMD somewhat even in dogs fed sufficient D. Dogs, like humans but unlike rats, don't break down PA efficiently in their small intestines.
I think the literature is fairly clear that the amount of phytic acid found in untreated whole grains reduces mineral absorption/status in humans.
I haven't read that book about the Hunza, sounds interesting. I'll check it out.
I have quickly skimmed most of it. Highly though provoking, and ties in with Western Price's work.
One of the issues I raise in my book, to the scorn of some, is that excess Omega 6, lack of Omega 3(and of course other deficiencies including minerals contribute) is capable of modifying human behaviour at a national and global level, towards the aggressive self-interested, and territorial, which is a rather frightening prospect in a world with growing consumption and shrinking resources.
Omega 6 in quantity is only found in plant reproductive material and so scarce and seasonal. I argue (and it is not an argument I have seen anywhere else) that Omega 6 ultimately controls the ability to breed by controlling hormone production and other factors. On this basis Omega 6 is nature's ultimate fertlity and behavioural controller.
Trials suggest Omega 6 increases aggression impulsiveness, reduces self restraint etc. In animals breeding activity is usually accompanied by increased aggression territoriality etc.
Here is a link to the book you listed and a quote from it that got my attention !
The western diet given to the rats includes margarine, which will be high in Omega 6.
G. T. WRENCH, M.D.
"Yet even in rats conditions like to these arise from faulty diet. For example, in later experiment, McCarrison gave a set of rats the diet of the poorer classes of England; white bread, margarine, sweetened tea, boiled vegetables, tinned meats and jams of the cheaper sort. On this diet, not only did the rats grow badly, but they developed what one might call rat-neurasthenia, and more than neurasthenia. "They were nervous and apt to bite their attendants; they lived unhappily together, and by the sixteenth day of the experiment they began to kill and eat the weaker ones amongst them.""
"We are left then at the end of these experiments with two vividly contrasted sets of little animals in this small "universe" of Coonoor--those on good and those on faulty diet; the healthy and the sickly; and certain mental characters, in contrast, the good tempered and live-and-let-live on the one hand, the bad-tempered and cannibalistic on the other."
Stephan, thanks for your email. No, my last comment isn't here. I must have done something wrong AGAIN.
Let's see if I can remember it. It was about phytate, suggesting that Mellanby shouldn't have used dogs, since the carnivore digestive system is very different from ours and they would never encounter phytate in the wild.
The human colon should be acid, and on a modern high-protein diet it will be alkaline. So if you do a study on phytate in Americans, you will find it inhibits metal absorption. If you did it on the Hunza, you might get a very different result.
The whole question boils down to this: is our digestive system 'designed' for eating whole grains? People think our very early ancestors were carnivores, but the work of Perry & Dominy on the amylase gene suggests otherwise. Our digestive tract is very well suited for processing whole grains, right from our teeth (yes, we'd have had to soak the grains) through the duodenum which is alkaline for carbohydrate breakdown, down to the colon, which can absorb metals if its bacteria are functioning normally. Gut bacteria like fibre, which provides a huge surface area for them to inhabit. They do not like meat, which makes the environment too alkaline.
Hi Stephan. There are so many UNsupported studies, and so many supported studies. It's really difficult to know which to believe. I had a heart attack five weeks ago. All I know is, more Omega 3 fatty acids in my diet, less sugars and empty carbs.
Happy New Year,
Aloe Vera Juice 101
I don't think our digestive system is adapted to whole grains. Cultures that eat whole grains almost invariably soak, grind and cook them. It's an extensive process of pre-digestion, because our digestive system isn't up to the task. If we were fully adapted to eating grains, we should be able to eat them whole and raw like a mouse can.
I don't think the amylase gene duplications change that picture, because we were eating starchy tubers before we were eating starchy grains. I agree that we're adapted to eat some amount of starch. But I think our true adaptation to grains is probably pretty small (although there must be some degree of adaptation in people who descend from the first agriculturalists).
We CAN eat grains whole and raw like a mouse can, if they're sprouted. It wouldn't have taken an enormous brain to understand that grains turn into little plants if you add water.
Sprouted seeds are just about the most nutritious things you can eat. They even have vitamin C, so you can live on them. There are archaeologists who think we would have eaten grains from the beginning.
If we wanted to survive drought on the African savannah, we'd have been well advised to store grains. Nothing else stores so well.
"If we wanted to survive drought on the African savannah, we'd have been well advised to store grains."
Gary Taubes summarizes a compelling report against this idea in GC,BC p.246-7, describing how the hunter-gatherer !Kung easily survived during severe drought (ref. Lee and Devore, 1966).
Stephan, I linked your post to an Amazon discussion. Please let me know if this is okay or not.
I have been looking for more information on SFA's link to cancer. If I google it, there is only articles showing that SFA has been linked to cancer.
There's some brilliant stuff here!
"He had already been on a relatively low-carb diet, but he went further towards a high-fat (low omega-6, high saturated fat), low-carb diet.
After about 9 months he went back in for testing. Total and LDL cholesterol had come down, HDL had gone up, and triglycerides were way down. His doctor couldn't believe it when he told him what he had been eating (butter, steak, eggs, etc.). "
Anecdotally when I dropped my carbs, initially both HDL and LDL went up and trigs dropped like a stone.
Adding more saturated fats brought the HDL up further and reduced LDL by around the same amount.
This appears to be common, according to clinicians like Drs Eades, Davis et al. and observations from many others, but LDL *may* go up further, or stay the same.
Ronald Krauss (who else?) has done some work looking at the different genes involved in differing parts of lipid metabolism, it may well be there's a subset of the population that does respond badly to saturated fat, just as there's a subset that responds well to high carb low fat diets (obviously these are not mainstream responses or we could all go home!)
For some it appears that monounsaturates work better than sat fats.
However Jane's work here on magnesium and other minerals may be relevent if imbalances here are affecting lipid metabolism. Almost certainly processed foodlike substances will lack the micronutrients found in Real Food, and if the wrong minerals are then added this could make such deficiencies worse, they seem to work in pairs - sodium vs. potassium, calcium vs. magnesium etc.
Finally I was pointed to this
full text is not free but it looks like it covers some other pathways in which Omega 3s are involved
Do you knew that the "Western Electric Company Study", is a reanalysis of a more old study ?
Shekelle and Stamler did this reanalysis with the data of Oglesby Paul ( a Chicago cardiologist).
In the original study, "the fact is that of the 88 coronary cases, 14 have appeared in the high-fat group and 16 in the low-fat group".
( from the book of Gary Taubes, Good calories bad calories", page 29 )
This is excellent. Thank you. Here's another one that's kind of related: http://www.bmj.com/content/346/bmj.e8707 "In this cohort, substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease. An updated meta-analysis of linoleic acid intervention trials showed no evidence of cardiovascular benefit. These findings could have important implications for worldwide dietary advice to substitute omega 6 linoleic acid, or polyunsaturated fats in general, for saturated fats" All these years the "experts" have been telling us to replace sat fats as much as possible with "healthy" polyunsaturated vegetable oils. How much harm have they done. I wonder.
As of this date, this article only goes a short way before becoming corrupted and quitting. I.e., it only reaches the paragraph which begins with "So we're left with the first premise ..."
Would it be possible to fix this? I am anxious to read the entire article.
Here is another 2014 meta-analysis in the Annals of Internal Medicine finding no evidence to support the low SFA guidelines.
"Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats."
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