Estimated reading time: 7 minutes
We’re all aware of the aggressive campaign driven by public health authorities and medical professionals to decrease blood cholesterol.
It all started more than fifty years ago when the Framingham Heart Study reported that high blood cholesterol was a major risk factor for coronary heart disease (1).
Central to the dogma was the belief that lowering blood cholesterol would lower the risk of heart disease.
At the same time, it was assumed that dietary saturated fats and dietary cholesterol caused an increase in blood levels of total cholesterol as well as LDL cholesterol (the “bad” cholesterol).
So, it was a foregone conclusion that dietary saturated fats and dietary cholesterol would cause heart disease because they supposedly raised blood cholesterol.
However, recently evidence questioning a lack of a causal relationship between the intake of saturated fats and heart disease has accumulated (3). Even so, restriction of dietary saturated fats is still included in most current dietary guidelines and recommendations on cardiovascular prevention (4,5).
Although some recent studies have suggested that replacing saturated fatty acids with monounsaturated or polyunsaturated fatty acids may be beneficial, replacing saturated fats with carbohydrates may increase risk (6).
Before I go further, keep in mind that the lack of evidence for a causal relationship between the intake of saturated fats and heart disease doesn’t necessarily defy or contradict the lipid hypothesis.
Although high intake of saturated fats may raise total cholesterol and LDL cholesterol, it also tends to elevate HDL cholesterol (the “good” cholesterol).
In addition, high intake of saturated fats is associated with a higher concentration of large cholesterol-enriched LDL particles and lower concentration of small, dense LDL particles (7). The presence of small, dense LDL particles is associated with an increased risk of subsequently developing heart disease (8), and appears a strong predictor of blockage in the coronary arteries (9).
So, a lack of relationship between high intake of saturated fats and the occurrence of heart disease may indeed fit quite well with the lipid hypothesis. However, it suggests that the simplified version of this hypothesis, the one that only targets LDL cholesterol may be misleading (10).
What About Saturated Fats if You Already Have Heart Disease?
The public recommendation to restrict the intake of saturated fats has been primarily targeted at healthy people in order to reduce the risk of heart disease. However, the same advice has been given extensively to patients diagnosed with cardiovascular disease, whether it be coronary heart disease or stroke.
Very few studies have investigated the impact of saturated fat intake in patients already diagnosed with heart disease. For this reason, I became quite interested to find a scientific paper on the issue published very recently in the Journal of Nutrition (11).
The study included 2,412 patients who underwent coronary angiography because of coronary artery disease or aortic valve stenosis between 1994 and 2004 at two university hospitals in Norway (Haukeland University Hospital, Bergen and Stavanger University Hospital, Stavanger).
Information on dietary intake was obtained at baseline by an FFQ (Food Frequency Questionnaire) developed at the Department of Nutrition, University of Oslo.
The patients were divided into quartiles based on the amount of saturated fat consumed (percentage of energy consumed). In group 1, the amount of saturated fat intake was between 3.9-9.8%, in group 2 it was between 9.8-11.5%, in group 3 between 11.5-13.2 and group 4 between 13.2-28.7.
There were some quite interesting findings at baseline. For example, patients with a higher intake of saturated fats were less likely to have a history of heart attack, prior coronary artery bypass surgery or to have triple heart disease (blockages of all three main coronary arteries) at baseline.
Increased intake of saturated fatty acids corresponded to an increased intake of both total energy and total fat. Participants with the highest saturated fatty acid intake also had higher consumption of mono-and polyunsaturated fat and dietary cholesterol.
High intake of saturated fats was associated with lower consumption of total carbohydrates, dietary fibre and alcohol. Patients with higher intake of saturated fats had higher intakes of meat, cheese, butter, milk, eggs, cakes, sugar and sweets.
Interestingly, despite higher calorie consumption among those with the highest saturated fatty acid intake, body mass index (BMI) was similar in all four groups.
Patients with higher intake of saturated fats were less likely to have high blood pressure but more likely to smoke. Their blood levels of total and LDL cholesterol tended to be higher but triglycerides lower compared to those with lower intake of saturated fats. There were no significant differences in the blood levels of HDL cholesterol between the groups.
The prevalence of diabetes was similar in all four groups.
During a median follow-up of 4.8 years, a total of 292 (12%) patients experienced a coronary event (heart attack, unstable angina or coronary death), and 137 patients died from any cause.
During follow-up, most of the patients were on conventional medication such as aspirin (90%), statins (89%) and beta-blockers (78%).
There were no significant associations between the intake of saturated fatty acids and coronary events or death from any cause. In other words, patients with high intake of saturated fats did not do worse than those with lower intake of saturated fatty acids. This was true also after multivariate adjustments for possible confounding factors.
Of course, this study has several strength and limitations. For example, it is important to understand that dietary intake was estimated at baseline only. No such information was collected during follow-up. For this reason, it is not possible to account for changes in dietary habits during the study period.
However, the authors point out that the majority of patients selected for participation in the study had known coronary heart disease at baseline. Thus, it may be assumed that most patients willing to change their dietary habits towards less SFA intake had already done so before inclusion in the study.
The Bottom Line
For decades, cardiologists have advised patients with heart disease to restrict the intake of saturated fats and dietary cholesterol. Many patients still believe this to be the cornerstone of their lifestyle modification.
The main reason for avoiding saturated fats is the assumption that they adversely affect the lipid profile of our patients.
Public authorities and medical societies usually recommend restricting the intake of saturated fats to less than 10 percent of total energy consumption. In the above study, only 27% of the patients met these dietary recommendations.
The American Heart Association goes even further by recommending a dietary pattern that achieves 5% to 6% of calories from saturated fat. That means, for example, if you need about 2,000 calories a day, no more than 120 of them should come from saturated fats. That’s about 13 grams of saturated fats a day (12). That equals two slices of cheddar cheese.
Recent studies suggest that the recommendation to avoid saturated fats may have been premature and not based on solid scientific evidence.
Now, a recently published Norwegian study shows that dietary intake of saturated fatty acids was not associated with risk of future events or death among patients with established coronary artery disease.
It is important to keep in mind that most of the patients were receiving secondary prevention drug therapy including aspirin, beta blockers and statins.
Anyhow, the results of the study certainly suggest that high intake of saturated fats is not a risk factor among patients with coronary heart disease receiving modern-day treatment.
These recent scientific data don’t imply hat we should urge our patients to consume high amounts of saturated fats. They only tell us that there is no association and accordingly, restriction won’t help.
So, it’s certainly a lifeline for those who believe red meat, whole-fat milk, cheese, cream, butter and eggs can be a part of a healthy diet.
On the other hand, we must realise that scientific studies often provide contradictory results. A US study published last year suggested that greater adherence to a low carbohydrate diet high in animal sources of fat and protein was associated with higher all-cause and cardiovascular mortality following acute heart attack (13).
It appears the jury is still out…
There is one group of people I know of that should really limit their saturated fat intake, those people having one or two copies of the APOE 4 gene. This puts them at high risk for Alzheimers and a fat restricted diet is recommended.
Yeah, Im Apoe3/4 and try to limit my SFA
What is the mechanism? If you have the gene, is it related to the effect of fat on lipoproteins, or is it some other effect of the gene?
Lipoproteins don’t enter the brain, fats don’t enter it easily (though EFAs seem to make it across the BBB). The Alzheimers mechanisms being teased out by scientists recently seem to depend on hyperglycaemia.
So is the mechanism that Apo4 people are more susceptible to fat-induced insulin resistance? If so this wouldn’t preclude a LCHF diet, it would just make it a bad idea to eat pizza, pastries, and ice cream.
Excellent summary of the topic and the new paper, Axel!
The AHA and other mainstream nutritional guideline sources continue to keep to the party line of eat less fat and saturated fat despite mounting evidence to the contrary.
My patients have trouble believing me when I tell them eggs/cheese and high fat yogurt are fine for them.
A bit more evidence that the LCHF diet that led us to combined weight loss of 70 pounds last year is not harmful to our hearts!
Too bad there’s no money in eating LCHF. Might be some good research!
Thanks Doc!
Ok your basing your assumption on a trial on food consumption outcomes that didnt even know what the consumption was during the trial?. Also you missed the glaring point that statins where used in both cohorts..
And there use post coronary event and there protective benifit is a proven outcome.
Is this a scientific paper hoping for puplication or a add for a diet.
Glenn, zero of the research into diet knows what consumption was during the study period. All diet epidemiology that informs official recommendations is prospective like this trial was.
All we ever know is what people ate 20 years ago, but look at the impressive structures that have already been built upon such ignorance.
Statins were used in both cohorts – so the study is controlled for drug use. It’s a study of diet, not statin use.
Glen you are very misinformed about the benefits of statins. If you are in the cardiovascular you are doing yourself and patients a great disservice with this belief.
What’s the general cut off % wise when we speak of low carb diets?
I see people talking of eating 20 grams of carbs per day and others talk of 40%…I know there’s no set limit but when the LCHF supporters talk about it, what are they referring to?
25% or less is low carb, or 150 grams or less. Under 10% is very low carb, and ketogenic is whatever gets you into ketosis. 70g per day is a good amount to try at first.
Thanks for the reply
Wow. Thats the point both groups where on statins which post infarct are known for the reduction in follow up events.You cant compare prevenative diet effects when your on a prevenative drug. The baseline is causitive not the variable.
I suggest you dont take my critique in your assumption just try to publish this endpoint analysis. The reviewers may explain it better than me
Too bad that they don’t do studies where the effects of saturated fat are tested according to the source of fat – animal or plant. Dr. Michael Gregor (www.nutrition-facts.org) made a big distinction between the two when he discussed coconut oil: “Unlike saturated animal fats, coconut oil doesn’t cause that spike of inflammation immediately after consumption of animal foods, which makes sense because as you’ll remember it may be the dead bacterial endotoxins in animal products ferried into the body by saturated fat that are to blame.”
Good point Russel.
The Harvard School study I mentioned at the end of my blog article actually addressed the source of fats and protein, animal vs. plant.. Their results may support your view. Here is the link again.
Thank you. Very interesting article.
I am struggling to find the right balance for a middle-aged male patient with a long-standing non-progressive kidney disease (GFR around 50% probably due to a childhood pyelonephritis) and a current metabolic syndrome presentation.
Low protein for the former and low carb for the latter.
Only lipids and water for him ? 🙂 (joking of course)
Hi Robert
Why don’t you try a Mediterranean type diet. Should fit well. It’s not very high in proteins. Scientific studies have shown good results in metabolic syndrome.
One problem with the study you cite is that they did not adjust intake of SFA for MUFA and PUFA. That is a big issue if the substitution between types of fat is important. This study says nothing about that. The quartile with the highest intake of SFA also ate more MUFA and PUFA.
Second, if you look at the baseline intake and health status, you chould infer that reverse causation was an issue here. I find it odd that this is barely mentioned in the study paper. You say:
“Interestingly, despite higher calorie consumption among those with the highest saturated fatty acid intake, body mass index (BMI) was similar in all four groups.”
It is highly usual in observational studies on CVD that total calorie intake is inversely associated with mortality. This is not because a high calorie intake is protective, but because a low calorie intake is a surrogate marker for low energy expenditure and worse health. This should be well-known to nutritional epidemiologists.
“There were some quite interesting findings at baseline. For example, patients with a higher intake of saturated fats were less likely to have a history of heart attack, prior coronary artery bypass surgery or to have triple heart disease (blockages of all three main coronary arteries) at baseline.”
Do you think that they were less likely to have had a heart attack, CABG, hypertension etc. because they ate more saturated fats? It is of course likely that those who had a previous heart attack actively lowered their intake as a consequence of the disease, not the other way around. The data don’t say to what extent diet caused their CAD. Those in the lowest intake quartile also were more medicated before the baseline angiography. This suggest to me that these patients were generally sicker to beguin with.
“These recent scientific data don’t imply hat we should urge our patients to consume high amounts of saturated fats. They only tell us that there is no association and accordingly, restriction won’t help.”
Sadly, I see many who believe that this study show that eating butter and cream reduced risk, which it absolutely did not. And it’s important to stress, as you kind of do, that almost all were treated with medications and hence controlled their risk factors.
It would have been interesting if they assessed changes in intake or risk factors during the study, not just at baseline.
Hi Erik.
Appreciate your comment.
With regards to the baseline data I absolutely don’t believe we can conclude that the lower number of prior MI’s or CABG’s in the high SFA group has to do with SFA intake per se. I was merely underscoring the fact that there were many differences between the “quartiles” apart from SFA intake. You also mentioned this with regards to MUFA and PUFA.
And of course it is possible that the high SFA groups changed their diet towards less SFA intake after inclusion in the study. There’s no way to know.
Therefore the main conclusion can not really go further than state that high SFA intake is not a risk factor for future coronary events in this heterogenous population. The question whether reducing SFA intake after being diagnosed with coronary heart disease is beneficial hasn’t been answered in this particular study.
So a low-carb diet is “associated with” …. blah blah.
1. Define “low-carb”. Hu defines low carb as it suits him to do.
2. It’s an association, i.e. rubbish science.
3. The assessment of diet in this trial is notoriously bad.
The end.
Why were the patients with a higher intake of saturated fats eating more “cakes, sugar and sweets”? If they were eating lower carbs, it sounds completely counter intuitive that they would be eating more of those items.
Aaron
I agree. But this is how it is presented in the paper. I assume it depends on the definitions used. There was no significant difference in the consumption of “sugar” per se between the groups but intake of what’s defined as “cakes”, “sugar and sweets” was higher in the higher saturated fat groups. However, still total carbohydrates were lower in the higher SFA groups.
In the Norwegian study that is the focus of this blog post, 81% of participants were men. So I’m not sure we can say the results apply to women. There may not have been enough women involved to support a linkage either way.
In reading the whole article of the last study cited, their definition of low carbohydrate diet wouldn’t even be considered LCHF or ketogenic in the least! They don’t even list percentage of calories from carbs or fat, they assigned a “low carb score.” From what was described, yes, they had people “lower carb” and “higher fat,” than their baseline, but not even close to the therapeutic diet that I prescribe for my patients. With people eating eating a moderate carb and moderate fat diet, t’s no wonder they got the results they published!
In my particular case, when I dramatically increased my sat fats, my particle count also dramatically increased. I have cut back my sat fats and will get my blood drawn tomorrow to see if it corrected. Is it right to watch particle count as a sign of trouble and do some n=1s from there? I have great ratios and HDL was over 115 (I forgot the exact number) when I ate high sat fat. Then, at moderate sat fat, my HDL was 90, ratios still great and the particle count came down, but not enough. After I make it through this test, I’m tempted to dive back into my beloved red palm oil, regardless. I am post-menopausal, but there is no heart disease in the women in my family and only in the men at advanced age.
Glad to have found your blog, recently. 🙂
High acid diets, animal protein diets cause inflammation and free radical in your blood. This causes your cells to break down , want sat fat eat nuts, and coconut oil at least they wont make you acidic . plenty of protein in hemp powder or pea protein. alkalize with veggies .
If most of the people in the study were taking statins, what good is this study? And then there is the question of the source of fats-animal or meat/dairy. If you don’t distinguish between the two, you can’t make recommendations that have any value. These studies come out and everyone takes it as gospel, even doctors. So what are you eatin’ doc?
Hi Pete
In the world we live in people who have a heart attack are put on statin drugs because scientific evidence clearly suggests that they are beneficial for this group of patients. This doesn’t affect the particular question asked in this study.
Doc,
Do you have any comment on this recent paper in regards to secondary prevention?
https://www.ncbi.nlm.nih.gov/pubmed/25655639
Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms.
First of all, it’s been known for quite some time that statin treatment is – at least sometimes – associated with plaque calcification. One study came out as early as in 2006, if i recall correctly. However, a) calcified plaques tend to be the most stable ones and b) hard endpoint data is consistent in showing benefits (less CVD events and deaths with statins therapy). Furthermore, at least I’m not aware of any observational follow-up data indicating increased CVD events among statin users vs non-users or frequent users vs not-so-frequent users – on the contrary.
The same goes for the other argument (statins cause cardiomyopathy): no evidence of this in trials, no epidemiological evidence either. E.g. myopathy is a rare side effect. If statins truly were aggravating the situation, why doesn’t it show … well, anywhere?
I was wondering whether or not vitamin K2 by reducing calcification could possibly make plaque unstable. I know that is way out in left field, but I read the calcification is a reaction to inflammation and is part of the body’s repair mechanism. Just wondering.
K2 is indeed one of the things scientists are looking at when it comes to atherosclerosis, plaque evolvement and arterial calcifications.
Great insights
It is clearly explained about Saturated Fats in the article thank you for sharing. Heart problems generally occurs due to excess fat, I suffered a lot with this problem so I consulted a online cardiologist at evaidya.com and took some tips on diet and exercise to loss excess fat in the body.
Hi my name is Maddie and I am doing a research paper on Heart disease. Is there any information you can give me on this topic? Thanks!
What an awful design for a study. To estimate what people were eating at the beginning and then assume what they continued to eat without even questioning them during the 4 year follow up period, makes the information and conclusions useless to me.