This was completely unexpected. Having read this study over the last few months led me some serious re-questioning on my current perception of Omega 6 PUFAs. How or why that study has not been picked up by any wider Keto or ZC /LC / IF communities, is beyond me.
I’d like to thank Peter @ Hyperlipid to have brought this firstly up for discussion. Despite my unfamiliarity within the comments’ intense discussion surrounding all possible causality (from mitochondrial structures and superoxidations) I’d wager anyone with a grip on Biochemistry to please consider sharing a thought or two over there.
I very seldom express my “opinion” on any journals or research papers of controversial reception. But this particular study? Is just unmissable.
The study recruited ten healthy males and females, free of diabetic or suspecting renal damage or CVD risks divided into two groups – one as PUFA group using predominantly walnuts and (undisclosed) soy products – pitted against the SAT fats group on cheese, coconut creams and animal fats. Five day clinical trial . Goal = examine any differing metabolic markers between the two groups.
Feast your surprising eyes to the result charts below.
Yes, I am shocked. The notoriously “bad” PUFAs group – won favourably in all metabolic markers. Much higher beta hydroxy ketones. Much lower glucose readings. Least LDL. Lower Trigs. Plus surprisingly – much higher – Insulin Sensitivity. In other words? Flawless victory.
However…
Some bullet points below do raise some question marks:
- “Twenty Young Healthy Subjects” – “Young” – wasn’t disclosed as to what age specifically.
- “Crystal Light” (presumably a beer but unsure), “potato sticks”, “frittos corn chips”, “turkey with gravy”, “soy crisp” were put on the PUFA fats Group of foods.
- “WASA Sourdough Rye Crackers”, “Crystal Light” (presumably a beer), “Ice Cream”, Ham and cheese “Wrap” (could be anything – corn wrap tortilla?) were put on the SAT fats Group of foods.
- “Oil and vinegar” appeared on BOTH GROUP’s diet. It is very unclear as to what oil and vinegar they’re talking about.
- Interestingly, the PUFA group uses relatively lean meats – chicken and turkey. Whereas the SAT group? Beef, cheese, pepperoni, the works…..except – Bacon. There was no bacon on the SAT menu. But ironically – there were “bacon imitation strips” on the PUFA group menu. What that consists of is a mystery…
From the above foods: could these (the crisps, the Crystal Light, “gravy”, etc) actually SKEW their reportedly faithful 70/15/15 Ketogenic ratio? I’d say more than possible. Because very-low carbohydrate interventions, politically speaking – mainly revolves on restricting to less than 50 grams per day. Even if participants were to include those things – such amounts MUST HAVE BEEN VERY low to the point of no more than two or three small bites and prohibited from there onwards.
Interestingly, side effects wise – the PUFA group experienced more Nausea than the SAT fats group. Otherwise, no significant adverse effects were noted. What is even more startling (to me at least), there was seemingly no reported evidence of Keto-flu or side effects we commonly expect as transitionary carbohydrate withdrawals. The only relevant note is in page 3, the “Change in ability to concentrate” were all returned as “non-significant”.
Lastly – a subtle yet noteworthy concern – the study was done completely by in-house. In-University – grants, volunteers and members.
Think about this. The opening paragraph of this study was to “hypothesize” that PUFAs may offer a more beneficial route to Ketosis. So already, we have an expectation out of an existing, speculative hypothesis. If the “student” subjects noted adverse reactions which counters this expectation, which then also consequently to that of their very own existing Institution….then you get my concern.
Has this outcome been succesfully replicated elsewhere?
My existing reference source of all things Keto – Lyle McDonald’s Ketogenic Diet – did nevertheless briefly mentioned a study (Page 115) upon determining various forms of fats for their thermogenic potential – between olive oils, butter, safflower oil and corn oil; whilst also – keeping close to Ketogenic parameters.
The winner? Corn oil, surprisingly. Considering that it is just slightly behind the world’s highest and notorious source of omega 6-oils – Safflower oil.
Even though that study is old (1974) – it was nonetheless noteworthy as it tracked throughout a period of 40 days. Two groups of subjects (men & women) – one group as lean and the other – obese. Both groups were instructed to eat a range of daily calories from 2100, then increased gradually to all the way up to a monstrously (as recorded) 6800. Per day. Yes, in kilocalories. From the study’s own conclusion: “It was striking to observe that the weight gain did not correlate with the caloric intake. Particularly if fat was given in the form of corn oil, a distinct discrepancy between the caloric intake and the response of the body weight was detectable.” (Kasper, H., et al, 1974).
Fast forward today’s pedestrian normalcy, with all my efforts of searching sadly – nothing else I could find comparatively of a similar analysis between PUFA vs SFA or MUFAs within Ketogenic contexts or parameters.
What about anecdotal source/s?
Very few sources out there. Only two (2) exist.
The first belonged to one of (perhaps earlier) books on Cyclical Keto interventions – “BODYOPUS”. The author, Dan Duchaine (whom unfortunately passed away due to hereditary polycystic kidney disease) preached fervently on Flaxseed PUFAs above all other source of fat intakes (Chapter 15).
…He even stated that monounsaturated sources (Olive oils) – was “unessential” (Chapter 16).
Amidst today’s glorifying prescription of Flaxseeds, they still remain open to debate. First obviously being the seemingly difficult metabolic conversion from ALA to EPA/DHA. Then, there’s the Flaxseed = not-as food debate. But as an expensive wood varnish. Next – many would dispute flaxseed is low in Omega 6. But still, it’s of relevant concern considering the N6 component is just behind canola oil. Lastly – I am aware over its extremely estrogenic yet confusingly – a viable protection against prostrate cancers. Yet still genetically factorial.
A second possible source would be Schwarzbein Principle by Diana Schwarzbein. I unfortunately have not read the book. But the program seems derived from the familiar Atkins induction. Then followed by gradual re-introduction of carbohydrates. The author reportedly advocates canola oils (as well as soybean oil) as fat source intakes. At least as accordingly from the Weston A Price Foundation’s review on the book. But what about the reviews from real readers? Apparently, at least a 3.75 to five stars were a common sight on Amazon, and Goodreads . Nothing thus far comes up on Google that I have seen as real, journalling accounts.
Relying on “book reviews” are somewhat vague. As evidently it is hard distinguishing the real authenticity. Whether the readers have truly experienced the program itself authentically or just whimsically.
*** Update 22nd September 2018***
Chris Bair @ Ketochow; posted his N=1 experimentation focusing on individual type of fat source intakes. One week at a time lasting throughout four week period (“Week 0” as the baseline). The timeline were as follows:
- (Week 0) SAT fats – heavy creams (as baseline)
- (Week 1) Omega-6 rich PUFAs (specifically Grapeseed oil – also high in Vitamin E)
- (Week 2) SAT fats again (but without any MCTs)
- (Week 3) MUFAs predominantly macadamia nut oils and avocado oils.
The findings were interesting. During the PUFAs week – Lowered LDL-C and P variants cholesterol. “Good“; under the eyes of nodding dogmatic institutions.
The “Bad” effects however, were concerning. The Triglycerides increased considerably. Both HDL-C and HDL-P decreased unfavourably. What’s even more surprising – LDL and Triglycerides were also increased on the MUFAs week (#3).
Please note that this n=1 experiment is part of his 42-day plan on using no whole-foods but Keto Chow; an all in one meal replacement as his main wholefoods intake. The long list of charts he posted as results does not justify any quick summary. A thorough reading and visit to his blog is well deserved.
Walnuts – could this be the reason?
These, after all – seemed to be the predominant ingredient on the winning (PUFAs) group’s menu throughout the entire experiment. Studies showed various benefits. Evidently ranging from it being anti-oxidative, helps alleviate lipid-peroxidation, and (most recently published study) improves gut macrobiota with associated increases of butyric acid production. Coincidentally – “Butyrate” is closely implicated from Ketone production in the liver, and thereby both presence seems highly correlative and synergistic.
Are walnuts the invincible food for all, then? Sadly perhaps not.
I’ve found one study within contexts of Metabolic-Syndrome’d mice alongside with high APO-E carrier/s (a genetically predisposition towards CVD risk) – walnut intakes actually INCREASED the level of triglycerides, as well as surprisingly – many pro-inflammatory liver gene expressions (“TNF”, “Ptpn22″, and “Pparg”, to name a few). More over, the Omega-6 content to O-3 ratio in walnuts is still quite high. Though not as hilariously high as “dry roasted” almonds (I’ll leave the moment of shock to yourself).
Back to the study we’re analysing at hand for this article. The PUFAs group were eating soy products ON TOP of any other (assuming) vegetable “oils and vinegars”. That no doubt plunged the Omega 3 intake down to the toilet even more. This to me, is enough to assume that the study tried to illustrate the evident strength of OMEGA-6 as more potentially Ketogenic than Omega-3.
Even if Omega-3 ALA praised canola oil (just as a guess) being used for the PUFA group – they are still not immune from the lowered 50% ALA to LA conversion efficiency even in the most “healthiest” human. Even if we rule out that the possibility of the SAT group eating both economy / soybean & grain fed beef / pepperoni or meats- the question still remains why then – the outcome still favours the PUFA group. This boggles the mind.
What about mainstream medical literature/s?
The next thing/s I have done below is curating all relevant studies purportedly which are all in favour of PUFA’s over SFA’s in all metabolic markers. Despite all my efforts again, I have not been able to find anything of any studies exclusively within Ketogenic parameters…
- A study on rats; in conjunction to what we’re reading at here concluded again that PUFAs from flaxseed oils induce greater BOHB readings than either lard, or butter fat intakes. CONS: Food test macros were not published.
- A study found that PUFAs (within it defined as Linoleate and Alpha Linoleates) are “moderately ketogenic”; in the context of rats. Unfortunately, study’s is restricted from public access without purchase.
- A study examining already-insulin resistant 10 individuals and obese (bmi >30) senior aged individuals (aged 61 on average) – found PUFA intakes to improve all metabolic markers. The diet test macros were 61% fat, 33% carbs and only trace amount of protein (I’d wager close to zero protein diet), CONS: Unrealistic in my opinion, as this ratio does not often relate to the more fitness oriented audience emphasizing higher protein intakes.
- The (allegedly) famous PUFA muffins versus SFA muffins study results in greater lean muscle mass, and less liver fat accumulation in PUFA muffins group. PUFA = win. Another study using the same muffins approach (NOTE: DIFFERENT authors) – also found the same thing – overfeeding PUFA = greater lean muscle mass. That study uses Sunflower Oil versus Palmitic acid for comparison. CONS: Food test macros were not published on the first study (Bray A, G. & Krauss, M R.). But published on the second study as 51% fat, 45% carb, 4% protein aka. almost zero protein.
- A study on children amongst 7 to 12 years found that higher PUFA intakes = less total fatty adiposity, greater muscle growth. CONS: Food test macros were not published. All food tests were self-questioned and self-submitted (inaccuracies galore; considering they’re still kids).
My efforts to search for more studies pretty much ended there.
What are your thoughts?
Everything remained elusively unexplained. But nonetheless – the many comments I saw in Peter @ Hyperlipid’s blog there may attract further interest amongst anyone with an already adept view/s in biochemistry. Hence I’d encourage, should you already have a Biochemistry background to liaise directly within the comments over there. Otherwise, I welcome any or all thoughts irrespective of “sides”.