I have a few questions, but will stick to two. Feel free to chime in with anything even remotely related!
Also, let me preface this by stating that I haven't had the time to deeply digest the various studies that have come down the pike lately exonerating saturated fats. Any summaries or links to summaries would be greatly appreciated in this regard. That said ...
1. Has there ever been an RCT -- or even an uncontrolled trial -- where saturated fat intake was increased on an absolute level (preferably on a weight stable diet) and improvements were seen in cardiometabolic risk factors (or other health measures)?
2. It is my understanding that mostly the effect (or lack thereof) of saturated fats have been assessed mostly in that 30-to-40% total fat range of the typical Western diet which usually puts sat fat in the 10-15% range. Would you say this is correct? If not, are there studies comparing a true low saturated fat diet to a high saturated fat diet? I'll take any context here though weight maintaining would be preferred for obvious reasons. Oh ... and coconut oil as major source of sat fat doesn't count since over half the fat is MCT. So basically I'm asking about if there are any 5% vs. 15% studies to be found.
Thanks!!
35 comments:
Hi Evelyn,
This pilot trial is the closest thing I know of:
A Randomized Pilot Trial of a Moderate Carbohydrate Diet Compared to a Very Low Carbohydrate Diet in Overweight or Obese Individuals with Type 2 Diabetes Mellitus or Prediabetes
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0091027
It used a small sample size and 24-hour diet recall. The low-carb group also had greater weight loss than the moderate carb group.
But the data does show that the low-carb group ate more saturated fat than the other group, both in absolute terms (39.7g vs 16.3g) and as percent energy (21.0% vs 10.7%). The low-carb group had greater improvements in HbA1c.
"It is my understanding that mostly the effect (or lack thereof) of
saturated fats have been assessed mostly in that 30-to-40% total fat
range of the typical Western diet which usually puts sat fat in the
10-15% range. Would you say this is correct?"
I actually looked at this a while ago, but only for trials evaluating hard endpoints. Based on 13 trials, total fat intake is roughly 25-40% and saturated fat intake roughly 8-12% in the experimental groups.
"So basically I'm asking about if there are any 5% vs. 15% studies to be found."
I'm not aware of any trials evaluating hard endpoints where the experimental group achieved intake lower than 7%. The one that came closest was one involving coconut oil, but does not count according to your criteria.
I think there are several that could be mentioned for question 2. I recently looked at this: "Effects of a healthy Nordic diet on cardiovascular risk factors in hypercholesterolaemic subjects: a randomized controlled trial (NORDIET)" http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2010.02290.x/abstract. The Intervention group followed a Nordic diet, and ate 5% of calories from SFA compared to about 13%. This was self-reported though, and free-living.
Are you only looking for trials, or for cohort studies too?
Here is another one, comparing about 7% vs. 15% SFA. But it was a multicomponent intervention, not sure if that's what you're looking for:
"Comparison of 3 ad libitum diets for weight-loss maintenance, risk of cardiovascular disease, and diabetes: a 6-mo randomized, controlled trial": http://ajcn.nutrition.org/content/88/5/1232.long
I don't know if anyone has mentioned it here, but another Weston A. Price board member died this month. Mary Enig had a stroke. She recommended eating a lot of fat, but I don't know much else about her. She was 83, which is average.
Regarding question 2:
In fact there is quite some amount of data that seems to indicate saturated fats act pretty much neutral once you reach a certain threshold of linoleic acid.
http://www.fasebj.org/content/6/8/2600.long
Individual responses may vary! I can definetely say they do for me and I have to add my LDL reacts badly if total fat as such rises, even if it is unsaturated exclusively.
Mary Enig at least once in her life got it right, when she recognized TFAs as dangerous long before others did. Her activities later on sadly overshadow this accomplishment.
Interesting. I've been wondering whatever happened to Mary. Any sources to cite for the two of them.
Leren's Oslo Diet Heart Study (a secondary prevention study) had about 8 % SFA in the intervention group (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1750292/). Total average fat intake was 104 g/day. The SFA was exchanged by PUFA, mostly linoleic acid from soybean oil. They had no margarine, so they also ate very little trans fats. I am not sure of what the control group ate, but I have the full report somewhere (it's not online).
After 5 years, coronary events was 33 % lower in the intervention group, and deaths from CHD was 26 lower.
In the later Oslo Primary Prevention Trial by Hjermann et al., (http://www.ncbi.nlm.nih.gov/pubmed/6118715 & http://www.ncbi.nlm.nih.gov/pubmed/3511692) the SFA intake was drastically reduced, 8,2 % in the intervention group vs. 18,3 % in the control group.
There were 47 % less non-fatal or fatal MI's in the intervention group. Quitting smoking was also part of the intervention, but very few actually quit, so the results have been attributed to the reduced cholesterol levels.
Thanks Will, I'm well familiar with that study
http://carbsanity.blogspot.com/2014/05/yet-another-lc-vs-low-fat-dietary-rct.html
It is indeed a significant difference, and unlike most trials, the LKD folks did actually increase sat fat by almost 3 grams per day. I'm interested in a reverse of the LA Vet study which would be to actually consume more -- as in a lot more -- saturated fat than at baseline.
Unfortunately the dietary reporting in this study was -- per usual -- not to be believed, especially for the MCCR group (where there was no monitoring for compliance)
http://4.bp.blogspot.com/-0sH9D5doEis/U1w1_b6lMyI/AAAAAAAAGH4/cj8ylTSTEgQ/s1600/Phinney+LCK+diet+study+diets.jpg
I think it would be really interesting to see a study where normal weight people switch to a weight maintaining real foods diets where one is deliberately high in saturated fat and the other very low. I'd also like to see the very low diet NOT be vegan so you have animal protein from seafood, poultry and low fat dairy. Unfortunately this study probably can't be done.
Here are two more, but still not sure if these are the types of studies you are asking for:
- "Differential metabolic effects of saturated versus polyunsaturated fats in ketogenic diets". The low SFA diet had 15 % calories from SFA while the high SFA diet had 60 % saturated. Both diets had 70 % total fat.
http://www.ncbi.nlm.nih.gov/pubmed/15070924
- "Beneficial effect of a weight-stable, low-fat/low-saturated fat/low-glycaemic index diet to reduce liver fat in older subjects"
SFA: 7 % vs. 24 %. "Weight remained stable."
http://dx.doi.org/10.1017/S0007114512002966
Both those Oslo trials involved numerous changes besides SAFA or PUFA intake. Ramsden et al. discussed these changes in Oslo-1 for those who do not have the original paper - http://www.ncbi.nlm.nih.gov/pubmed/21118617
The Oslo Antismoking trial by Hjermann et al. much like Oslo-1 involved an entire dietary pattern change including weight loss and smoking reduction. There were likely reductions in trans-fat here also since only little polyunsaturated margarine was allowed likely in place of "hard" margarines common at the time.
the TFA stuff impressed me too
http://fhs.mcmaster.ca/anesthesiaresearch/documents/ComparisonofWeightLossAmongNamedDietProgramsinOverweightandObeseAdultsAMeta-analysis.pdf
Comparison of Weight Loss Among Named Diet Programs in Overweight and Obese Adults
A Meta-analysis
CONCLUSIONS AND RELEVANCE
Significant weight loss was observed with any low-carbohydrate or low-fat diet. Weight loss differences between individual named diets were small. This supports the practice of recommending any diet that a patient will adhere to in order to lose weight.
http://ada.portalxm.com/eal/evidence.cfm?evidence_summary_id=251186
Under isocaloric conditions, what is the impact of changing the quality and composition of macronutrient (carbohydrates, proteins and dietary fat) on LDL-cholesterol levels in normolipidimic and hyperlipidemic individuals?
Thank you everyone for participating thus far! Much appreciated and I have some reading to do. One of the problems is that so many diet trials involve weight loss so that is, IMO, a hopeless confounder.
I'm pretty torqued at listening to RDs and MDs who are translating sat fat may not be harmful into this idea that it is then beneficial. So there's this move to eat more sat fat which is not the same thing as eating less of whatever they consider to be bad fats. The anecdotal evidence from places like Paleo Hacks is that eating very high fat and very high saturated fats sends some people's lipids soaring.
You say "another." Did a second board member die? I don't really keep up with them anymore.
http://www.westonaprice.org/health-topics/faq-miscellaneous-questions/
(#2)
I'm not familiar with the history of WAPF or when this happened, but this guy apparently died in his 40's of a stroke.
http://drkaayladaniel.com/the-pioneering-spirit-of-dr-mary-g-enig-1931-2014/
Kaayla Daniel is on current WAPF board. See comments.
Not a study, and I could not get the abstract from Cell to load on my phone, so this will have to do for now:
http://m.theatlantic.com/health/archive/2011/10/exposed-the-reason-saturated-fats-are-so-damaging-to-health/247027/#
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3295636/
Saturated fatty acids induce c-Src clustering within membrane subdomains, leading to JNK activation.
I think that Weston Price himself died of a heart attack.
Thanks, Charles.
Byrne was WAPF's poster boy... doctor…wasn't he? He died of a stroke during or soon after an operation.
Mary Enig is deceased??!!
Is there an obituary in the "papers"??
"Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU study"
http://link.springer.com/article/10.1007/s001250051620
Compares 17% of calories from Saturated Fat (SAFA diet) to 8% of calories from Saturated Fat (MUFA diet). Other than MUFA, all other macros are the same (calories, fat, protein, carb, PUFA). The participants were also given either a fish oil supplement, or a placebo supplement.
According to the study, insulin sensitivity decreased 10% on the SAFA diet. Total cholesterol and LDL increased on SAFA, decreased on MUFA (LDL was about 9% higher on SAFA than MUFA). There was a significant reduction in ApoB on MUFA. Lp(a) was unchanged on SAFA, but increased 12% on MUFA.
Evelyn, I posted another comment here that never appeared. It's frustrating commenting here because of this although I know it's not your fault.
Sorry about that, you should see it now. I thought you were whitelisted but apparently not. That has been remedied! Hope that fixes the problem though there are whitelisted peeps who have comments go to moderation for links. Then sometimes links go through. I don't get in?!
Thank You!
http://www.ncbi.nlm.nih.gov/pubmed/24001092
"Insulin resistance is associated with the metabolic syndrome is believed to be a strong predictor of risk of CVD. A review by Reserus, Willett & Hu (53) suggested that SFA may have adverse effects on insulin release and glucose homoeostasis. However, this conclusion was based on a number of small trials; the only one major study that had addressed this question was the KANWU study (54). This reported an improvement in insulin sensitivity when SFA, mainly derived from animal fats and lard, were replaced by MUFA in the diet but the difference between treatments was of borderline significance. The RISCK study (30) found no evidence for adverse effects of SFA on insulin sensitivity nor did the LIPGENE (31) study or the study by Bos et al. (55) The current evidence suggests that there is probably no difference between SFA and MUFA on insulin resistance in human subjects".
http://jn.nutrition.org/content/early/2014/09/03/jn.114.197624.abstract
"Studies in animal models indicated that insulin sensitivity is impaired by diets high in SF [reviewed in (51–53)], and some human observational studies reported positive associations between SF intake and hyperinsulinemia, independent of body fat (54–58). However, in the majority of human intervention studies, changes in dietary fat quality had no effects on insulin sensitivity (52,53,59), including several large trials comparing replacement of monounsaturated fat for SF in the context of a higher fat diet. Our data support the evidence that high SF intake does not have a major impact on insulin sensitivity".
This is all I could find:
http:www.legacy.com/obituaries/washingtonpost/obituary.aspx?n=mary-d-enig&pid=172400634&fhid=6125=September 9, 2014
Yes, they were multicomponent interventions. It's difficult to make big changes in fat composition without changing the overall diet in a free-living setting. So you cannot attribute the effects to the lower SFA per se, but to the dietary pattern. Which is the most relevant too, since none of us eat fats in isolation.
Just saw this one mentioned on Twitter: http://archneur.jamanetwork.com/article.aspx?articleid=1697444
Small study, 20 adults, randomized to a diet high in saturated fat content and with a high glycemic index (High diet; 45% of energy from fat [>25% saturated fat], 35%-40% from carbohydrates with a mean glycemic index >70, and 15%-20% from protein) or a diet low in saturated fat content and with a low glycemic index (Low diet; 25% of energy from fat [<7% saturated fat], 55%-60% from carbohydrates with a mean glycemic index <55, and 15%-20% from protein).
No hard endpoints, though.
One fundamental problem with such trials is that they always substitute a certain package of fat for another one. Even if this package is almost exclusively fat by its macronutrients the metabolic effects of different packages of fat with a similar composition of SFA, MUFA and PUFA (e.g. lard butter and palm oil) may vary greatly. This is not only due to different types of SFA (C3-18:0) having very different effects but also the stereochemistry of the triglycerides (fatty acids on the sn2 position are absorbed much more efficiently than those on the sn1 or sn3 positions - animal fats have predomanantly palmitic acid on the sn2 position, whereas palm oil has primarily oleic acid on the sn2 position), the presence of fat soluble vitamins, caroteonoids, sterols and other minor compounds. There is an intriguing animal study done with palm oil, which in is unrefined form (the much touted red palm oil - "as seen on Dr. Oz" ;-) is a rich source of tocotrienols and carotenoids. Employing a rabbit model of atherosclerosis, Kritchevsky et al. found that while virgin red palm oil did not promote atherosclerosis compared to rice bran oil, refined palm oil significantly did so. Intriguingly, however, "reconstituted red palm oil" (refined oil to which the carotenoic and tocol fractions were added back to match the composition of the virgin oil) did not differ in its atherogenic effects from the refined oil. It seems we are left with some unknown factors, still eluding our analysis but in this case making all the difference.
I think there are still a lot of such unknowns in nutitional science - given the huge biochemical complexity we deal with - and dazzled by the impressive amount of things we do know (or assume to know) we are all too prone to unduly overemphasize theoretic assumptions ever empirical reaearch and thereby tap in to the reductionist fallacy. What I would like to see is a human study comparing, for example, lard, butter, red and refined palm oil. Or canola oil with a mixture of olive and flax seed oil giving the same fatty acid profile. I doubt whether we will ever see such studies, though....
http://superhumanradio.com/high-saturated-fatty-acid-intake-induces-insulin-secretion-by-elevating-gastric-inhibitory-polypeptide-levels-in-healthy-individuals.html
High saturated fatty acid intake induces insulin secretion by elevating gastric inhibitory polypeptide levels in healthy individuals
"To put these results bluntly, saturated fat (at least in the form of butter) increases the amount of insulin needed to dispose of co-ingested carbohydrates and thus causes insulin resistance. Interestingly, a similar study to this was performed to compare butter to olive oil. It was found that although olive oil leads to greater GIP production than butter; it did not lead to greater levels of insulin or glucose. Compared to the current study that utilized a constant 40% monounsaturated fatty acid content, olive oil is 74% monounsaturated fat, suggesting that all fat in general elevated GIP, but only saturated fat leads to insulin resistance.
So what does this all mean? It means that all the anti-carbohydrate, glycemic index loving people need to get their facts straight. Adding butter to your baked potato may lower the GI, but it doesn’t lower the insulin response. In fact, it elevates the response and leads to insulin resistance. But you don’t need me to tell you that. All we have to do is use common sense and look to nature. Name one food that is high in both fats and starches or sugars. It can't be done. Nature knows best and it makes sense that buttered potatoes are harder to deal with physiologically."
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