Humans are unique in their remarkable ability to enter ketosis. They’re also situated near the top of the food chain. Coincidence?
During starvation, humans rapidly enter ketosis; they do this better than king penguins, and bears don’t do it at all.
Humans maintain a high level of functionality during starvation. We can still hunt & plan; some would even argue it’s a more finely tuned state, cognitively. And that’s important, because if we became progressively weaker and slower, chances of acquiring food would rapidly decline.
Perhaps this is why fasting bears just sleep most of the time: no ketones = no bueno..?
Observation: chronic ketosis is relatively rare in nature. This doen’t mean animals evolved a protective mechanism against ketosis.
Animals with a low brain/carcass weight ratio (ie, small brain) don’t need it. Babies and children have a higher brain/carcass weight ratio, so they develop ketosis more rapidly than adults. Is this a harmful process? No, more likely an evolutionary adaptation which supports the brain.
The brain of newborn babies consumes a huge amount of total daily energy, and nearly half comes from ketones. A week or so later, even after the carbohydrate content of breast milk increases, they still don’t get “kicked out of ketosis” (Bourneres et al., 1986). If this were a harmful state, why would Nature have done this? …and all those anecdotes, like babies learn at incredibly rapid rates… coincidence? Maybe they’re myths. Maybe not.
Ketosis in the animal kingdom
Imagine a hibernating bear: huge adipose tissue but small brain fuel requirement relative to body size and total energy expenditure. No ketosis, because brain accounts for less than 5% of total metabolism. In adult humans, this is around 19-23%, and babies are much higher (eg, Cahill and Veech, 2003 & Hayes et al., 2012).
Essential fatty acids? Well, there’s really only one, DHA, and we really only need a gram or two. In other words, our entire requirement for dietary fat can be met by about 2% of total calories (plus a few extra grams to accommodate fat-soluble vitamins) (plus DHA is never the sole fat in a food, so you’d be getting a few more grams of other fats, too). But still, a very low fat diet! But impractical and probably not very palatable or healthy.
On average, dietary fat comprises about a third of calories, roughly equally divided between SFA, MUFA, and PUFA (slightly less PUFA).
Major sources of SFA are pizza and desserts – no wonder SFA gets a bad rap!
Does it matter where fatty acids are oxidized, liver or skeletal muscle? Of course, they’re oxidized in both tissues (quantitatively much more in the latter), but relative increases in one or the other show interesting effects on appetite and the regulation of fat mass [in rodents].
Warning: a lot of speculation in this post.
It’s known that LC diets induce a spontaneous decline in appetite in obese insulin resistant patients. Precisely HOW this happens isn’t exactly known: the Taubes model? improved leptin signaling? probably a little bit of both, other mechanisms, and possibly this one:
They are conditionally essential at best, only if docosahexaenoic acid (DHA) is lacking. We can’t synthesize omega 3 fatty acids, and indeed they do prevent/cure certain manifestations of “essential fatty acid (EFA) deficiency” (Weise et al., 1958), but DHA can do all that and more. Not that I recommend this, but a diet completely devoid of 18-carbon vege oil fatty acids will not produce EFA deficiency in the presence of DHA. (“vege,” rhymes with “wedge”)
The “parent essential oils” are linoleic acid (LA) and alpha-linolenic acid (ALA). The others, which I think are more important and the truly “essential” ones are eicosapentaenoic acid (EPA), arachidonic acid (AA), but mostly just DHA.
The first manifestation of EFA deficiency is dermatitis (Prottey et al., 1975). Some people say LA is necessary to prevent this, but it would be better phrased as “LA prevents dermatitis;” not “LA is necessary to prevent dermatitis.” All of the evidence suggesting LA is essential is in the context of DHA deficiency.
Technically, we can convert a bit of ALA to DHA, estrogen helps, testosterone doesn’t (women have better conversion rates)… and I’d speculate that the reverse is probably easier (DHA –> ALA).
In brief, MCTs are more insulinogenic than corn oil. But it’s not a lot of insulin. Really. Enough to inhibit lipolysis, perhaps, but that’s not saying much… & certainly not enough to induce hypoglycemia.
I’ve read that EPA tends to show slightly better results in outcomes related to mood, whereas DHA tends to be slightly better for cognition. Not mutually exclusive; probably a lot of overlap. This meta-analysis by Martins showed EPA fared better than DHA for depressive symptoms (2009); another one here, stressing the high %EPA relative to %DHA necessary for improvements (Sublette et al., 2011). Whereas the reverse is true for certain cognitive outcomes in this study by Sinn and colleagues (2012). Very few studies test EPA vs. DHA directly, and their effects on metabolism are relatively similar. They’re the ball bearings of fatty acids.