Greenfield’s article equates a linear progression of T-cell activation with undesirable gut permeability. By this standard, we should all be on a low fat diet since the length of the “desirable” fats disallows most real foods. The proposed solution to just “eat your friggin’ vegetables!” also falls short in a ketogenic context and possibly doesn’t make sense at all. I’m going to propose an alternate POV regarding short, medium and long chain fatty acids relating to gut health.
Disclaimer: I am against refined foods in general compared to whole food sources. I’m not a proponent of chugging large quantities of MCT or coconut oil. Trust me, it does not get absorbed well. 
Look at the difference in vivo between MCTs which are part of coconut oil (C8, C10)and LCFA. MCTs go directly to portal vein during absorption in the duodenum (small intestine), while LCFA are absorbed into the lymphatic system. This is a crucial point because LCFA play a role in immune system. It makes sense that they would produce a different T-cell response. This is how the immune system samples and receives information about the state of invaders in your gut. It should not be confused with leaky gut endotoxins, which is a separate and pathological condition. Acute ingestion of even the concentrated MCT oils C6, C8, C10 do not provide a chronic condition under normal circumstances . Again, don’t chug this stuff – it’s self-limiting. If you react poorly, stop taking it.
Highly recommended listening on processed foods, fats and the immune system: https://thefatemperor.com/gabor-erdosi-on-the-primary-issues-which-drive-disease-part-1-2/
I’ve seen this demonization of fats before regarding cream and butter alledgedly causing leaky gut. Take a look at this study* disproving the association of milkfat** consumption with LPS endotoxin damage. The authors were looking to prove causation, but ended up disproving their hypothesis. The takeaway conclusions:
Based on previous reports, we hypothesized that the dietary lipid amounts could be directly linked to the extent of the onset of all these alterations. Our results are not consistent with our hypothesis. Indeed, we show that, in complex HFDs based on chow ingredients and milkfat, there was no association between dietary lipid amounts and the magnitude metabolic endotoxemia, low-grade inflammation and physiological alterations developed in response to the diets. http://www.sciencedirect.com/science/article/pii/S0271531715000068
Another study* testing a high milkfat diet showed protective qualities when intentionally treated with exogenous lipopolysaccharide (LPS) a.k.a. toxins.
Because no mice fed the control diets survived at 48h , a comparison to those fed the milk fat diet was not possible. https://www.journalofdairyscience.org/article/S0022-0302(11)00196-2/fulltext
Finally, in a ketogenic context, colonic production of butyrate from fiber is optional and I don’t see how this applies to the small intestine anyway. Ketones are the end-product of colonic cell metabolism of butyrate and are directly related to colonocyte health. Having a concentration of ketones in the blood provides a ready substrate for these cells without obligate butyrate producing bacteria and vegetable fiber. A human study from Amber’s excellent article on butyrate: http://www.ketotic.org/2017/11/does-ketogenic-diet-confer-benefits-of.html?m=1
In both acute and quiescent UC [ulcerative colitis] oxidation of butyrate to CO2 and ketones was significantly lower than in the control tissues, and the decrease correlated with the state of the disease. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(80)91934-0/fulltext
*Yes, these are mouse studies. So is the study from the original article.
**Milkfat composition info here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2596709/
