The miracle of safflower oil (3)

TLDR: PUFA in a mixed diet are obesogenic. PUFA under hypoinsulinaemic conditions are not. I doubt they get a free pass long term.



There have been some interesting snippets on Twitter recently, triggered by Diet Doctor's discussion about vegetable oils here. Perhaps the most controversial quote is this one:

"Disclaimer: Vegetable oils are routinely recommended as “heart healthy.” There is high-quality evidence demonstrating that replacing saturated fat with vegetable oils reduces LDL cholesterol levels. But at this point, there is inconsistent evidence whether this translates into fewer heart events or lower rates of cardiovascular mortality".

This is absolutely incorrect for people with pre existing cardiovascular disease as it was found, in a randomised control trial using safflower oil, that increasing vegetable oil for bulk calories will increase all cause mortality (p = 0.05), cardiovascular disease mortality (p = 0.04) and coronary heart disease mortality (p = 0.04). Mortality is an utterly hard end point and particularly the all cause mortality is an end point which cannot be argued with.

Let's rephrase that: in the context of a mixed diet in people with established heart disease vegetable oil (from safflower seeds) is going to increase you risk of death, especially from cardiovascular disease.

The main issue is to ask whether this still applies under low carbohydrate eating conditions. Given the role of insulin in CVD this is far from certain. But context will be crucial here and who would like to be the guinea pig?

The interesting twitter conversation goes like this:

Dr Westman: "In 20 yrs of clinical research and practice using LCHF/keto, I’ve never even mentioned reducing omega 6s, and it works wonderfully. Just cutting carbs gets the job done!"

Tucker: "I disagree, but @drericwestman is an excellent physician who does great work. This is more about determining ultimate causation so we can address people who can't just go low-carb, which is most of the planet".

I think both people are correct. I came to LC because it works. Over decades I've read studies where it works pretty much invariably on a group basis and studies from the mainstream usually advise progressively increasing carbs if they want to knock low carb and secure future funding. You have to pay the mortgage.

I am perfectly willing to accept that consuming carbohydrate in a rapidly absorbable form will overwhelm the liver's ability to protect the systemic circulation from hyperglycaemia so will require systemic hyperinsulinaemia to control that systemic hyperglycaemia. In particular hyperinsulinaemia comes with its attendant problems (ie most of medicine) but obesity only occurs when hyperinsulaemia is marked enough to overcome insulin-induced insulin resistance. I have no doubt this can occur without PUFA but I think it is massively easier in the presence of PUFA, which delay normal insulin-induced insulin resistance in the immediate post prandial period.

The role of polyunsaturated fatty acids is to stop adipocytes developing insulin resistance by limiting ROS generation. Combining hyperinsulinaemia with hypersensitive somatic cells is a recipe for maximising lipid storage in adipocytes and simultaneous packing lipid in to muscles, pancreas and anywhere else you care to imagine that sprouts an insulin receptor (most brain cells excepted).

Eating a low carbohydrate diet side-steps the problem by reducing absolute levels of systemic insulin. Down a set of unrelated rabbit holes I'm looking at what might control hunger under LC eating and PUFA may have some influence on this, but it is clearly a small effect when compared to the same dose of PUFA combined with an insulogenic diet.

Ultimately at low levels of insulin it doesn't matter how well or badly adipocytes respond to/resist insulin. There is so little insulin about that FFAs and ketones are able supply the body's energy needs, given some excess fat (especially visceral fat) available to be utilised.

Back to long term speculation: Do PUFA matter for non-insulin reasons on a low carb diet? Recall that López-Domínguez et al used a low calorie semi-starvation model (which is a partial mimic of low carb eating) to look at longevity in rodents (post is here). It certainly matters under their study conditions but the effect is small enough that I doubt it would show in any way for someone at 40 years of age under a year or two's exposure to a high PUFA but low carbohydrate diet. For those of us in this for the long haul it's much easier not to be the test case and PUFA avoidance seems prudent to me.

And I am undoubtedly still a low carb eater.

Peter