What Kind of Fat Should I Eat????

One of my astute clients, Coach Ethan Grossman recently asked me the question, “If I am going to overeat fats, which ones should I eat. Saturated Fats, MUFAs, or PUFAs? And how much?”

This is an extremely loaded question and although it may sound simple, as many things it requires a contextual and individual answer.

The question really becomes more about heart disease risk, inflammation, and long-term chronic (sustained) disease.

The person asking this question is in his mid-twenties with the primary goal to get as big as humanly possible.

Thus, we could just sweep the whole question under the rug and say just hit your Macros Bro!

But, that is not helpful in this case because the athlete really wants to know and is extremely smart and well read. Thus, this question is really about food quality and it’s important!

So how does the intake of different fats effect inflammation and long-term disease risk?

First, limiting saturated fat may be warranted, but most likely only in a select portion of the population and even then it is still highly debatable and individual. Some evidence has found that overfeeding palm oil (SFA) vs. sunflower oil (PUFA) resulted in higher liver and visceral adipose tissue deposition. However, we probably shouldn’t extrapolate this out to other types of oils and even athletes (as regular heavy exercise >3 h per week was actually an exclusion parameter for this study). A recent meta-analysis by Ramsden et al. concluded…

“This detailed methodological evaluation of Randomized Controlled Trials found that mixed n-3/n-6 PUFA and n-6 specific PUFA diets have significantly different effects on risk of non-fatal MI and CHD death. RCTs that substituted mixed n-3/n-6 PUFA in place of TFA and SFA reduced CHD risk. By contrast, n-6 specific PUFA interventions tended to increase CHD risk. These increased CHD risks from n-6 specific PUFA diets may be underestimated as they replaced TFA and SFA; reductions of these potentially atherogenic fats would be expected to reduce CHD risk. Consistent with this, we found that the substitution of n-6 PUFA for TFA and SFA produced an increased risk of death from all causes that approached statistical significance, when analyzed independently or in comparison to mixed n-3/n-6 PUFA diets.”

That’s a mouthful that if taken at face value means we are probably best off eating mostly a mix of n-3 and n-6 fatty acids – probably in a ratio of 1:1 or 1:2 and hopefully you stopped eating trans fats when Obama was elected.

Yet, if you look deeper into the profiles of all the RCTs included in this meta-analysis, the n-6 oils are primarily corn or safflower oil and the n3/n6 source is soybean oil. And none of us in the healthosphere are eating those types of oils in large amounts, so again we would be wise to be tentative in our extrapolation of this data.

If we look further into a five week feeding trial in healthy adults that is more in line with what the “cool people” are eating, we see no significant difference in inflammatory markers between palm oil, coconut oil, and extra virgin olive oil. However, the standard deviations in these groups were huge so it would be really really interesting to see some representation of the raw data.

Next, I’ll quote Alan Aragon’s summary from 2011 on saturated fat, which in my mind still rings true.

“Going back to the original question, does the current body of research evidence support the authoritative public health recommendations to minimize saturated fat intake?
There isn’t a definitive yes or no answer for this. After examining the full range of evidence, the best answer (aside from the old standby of “it depends”) is not really. To begin with, at approximately 12% of total calories, the general population is not consuming prodigious amounts of SFA beyond what’s recommended. This alone challenges the urgency of the ‘official’ public health guidelines to force SFA intake further down.

According to the latest stats from the USDA, the primary dietary sources of SFA in the American diet are full fat cheese (9% of total SFA intake), pizza (6%), grain-based desserts (6%), chicken and chicken-mixed dishes (6%), and sausage, franks, bacon, & ribs (5%)…While it’s possible that a diet predominated with these foods could cause health problems, it’s doubtful that SFA per se would be the main culprit. To reiterate, the problem would more likely be the lack of whole foods causing a disproportionately high calorie density, and corresponding lack of essential nutrition. I’m referring to both macro- and micronutrition, as well as beneficial phytonutrients & zoonutrients present in whole & minimally processed food.”

Eat Real Food.

The next important aspect to discuss is that high fat meals enhance the absorption of LPS (an endotoxin from gram negative bacteria) which produces a hefty inflammatory response.

“LPS-mediated signaling through Toll-like Receptor 4 (TLR4) leads to the activation of NF-κB, a transcription factor that subsequently turns on the expression of numerous proinflammatory cytokines, such as TNF-α, IL-1, IL-6, and IL-8. TLR4 is part of a larger family of receptors responsible for recognizing pathogen-associated molecular patterns (PAMPs). More than a dozen TLRs have been identified in humans and mice. These receptors are expressed throughout the body and are critical for host defense against invading pathogens.”
-Fritsche 2015

Thus, if you have dysbiosis in the GI tract, you may not want to guzzle coconut oil by the gallon. That said, you probably don’t want to crush easily digestible carbohydrates either because that may have been a big part of what got you to this point anyways. Interestingly, one study in pigs found coconut oil to produce the highest post-prandial rise in LPS.

Yet, another acute feeding trial in humans found no significant difference in vascular inflammation and total lipid peroxidation between corn oil, soybean oil, extra virgin olive oil, and cod liver oil. It is highly plausible that we will see future research in this area that somehow selects or controls for different microbiome profiles. Also, all this is not to say that there is not longer-term research out there that shows olive and fish oil to be anti-inflammatory and moving towards a whole food Mediterranean-y diet is not a good idea.

So what should I tell this guy?

1) He has stool testing that shows he doesn’t have anything going on in the lower GI tract. He does not have breathe testing so we cannot say much about the small intestine. However, he does not have symptomatology of overgrowth in that area.

2) His blood lipids are actually a bit low doing exactly what he is doing, which is consuming north of 200 grams of fat per day and his stool doesn’t float and he doesn’t show signs of fat malabsorption.

3) His CRP is nonexistent and the guy is very much not a chronic disease case.

So this a long winded way of saying – bro, the way you are eating it probably doesn’t matter – hit your macros.

Eat real food and try to hit a 1:1 or 2:1 on the n6 to n3 ratio, but even the importance of this is debatable, however it is affordable and easy to do by eating like an adult and adding in some fish oil supplementation. And if you want to eat a pizza every once and a while – go for it.

Finally, just to add more complexity and contextual curveballs into the debate you hear a lot of bad mouthing of arachidonic Acid in “health” circles because it results in the formation of inflammatory end products via the COX-2 pathway. BUT, if you are an athlete it may not be in your best interest to limit arachidonic acid as those same inflammatory end products are critical to anabolic signaling and exercise adaptation and two studies to date have found an increase in performance from arachidonic acid supplementation, however this amount was well outside the range of what is remotely possible with food alone (5.5 pounds of brisket anyone?) and a 6 fold increase in linoleic acid did not increase tissue levels of arachidonic acid.

1. Aragon A. AARR Apr. 2011.
2. Voon PT, Ng TK, Lee VK, Nesaretnam K. Diets high in palmitic acid (16:0), lauric and myristic acids (12:0 + 14:0), or oleic acid (18:1) do not alter postprandial or fasting plasma homocysteine and inflammatory markers in healthy Malaysian adults. Am J Clin Nutr. 2011;94(6):1451-1457.
3. Tousoulis D, Papageorgiou N, Antoniades C, et al. Acute effects of different types of oil consumption on endothelial function, oxidative stress status and vascular inflammation in healthy volunteers. Br J Nutr. 2010;103(1):43-49.
4. Roberts MD, Iosia M, Kerksick CM, et al. Effects of arachidonic acid supplementation on training adaptations in resistance-trained males. J Int Soc Sports Nutr. 2007;4:21.
5. Ramsden CE, Hibbeln JR, Majchrzak-Hong SF. All PUFAs are not created equal: absence of CHD benefit specific to linoleic acid in randomized controlled trials and prospective observational cohorts. World Rev Nutr Diet. 2011;102:30-43.
6. Ramsden CE, Hibbeln JR, Majchrzak SF, Davis JM. n-6 fatty acid-specific and mixed polyunsaturate dietary interventions have different effects on CHD risk: a meta-analysis of randomised controlled trials. Br J Nutr. 2010;104(11):1586-1600.
7. Mani V, Hollis JH, Gabler NK. Dietary oil composition differentially modulates intestinal endotoxin transport and postprandial endotoxemia. Nutrition & metabolism. 2013;10(1):6.
8. De Souza EO, Lowery RP, Wilson JM, et al. Effects of Arachidonic Acid Supplementation on Acute Anabolic Signaling and Chronic Functional Performance and Body Composition Adaptations. PLoS One. 2016;11(5):e0155153.
9. Tousoulis D, Papageorgiou N, Antoniades C, et al. Acute effects of different types of oil consumption on endothelial function, oxidative stress status and vascular inflammation in healthy volunteers. Br J Nutr. 2010;103(1):43-49.
10. Rosqvist F, Iggman D, Kullberg J, et al. Overfeeding polyunsaturated and saturated fat causes distinct effects on liver and visceral fat accumulation in humans. Diabetes. 2014;63(7):2356-2368.
11. Fritsche KL. The science of fatty acids and inflammation. Advances in nutrition. 2015;6(3):293S-301S.