@phoenix as ever thanks for the great links ...I do accept that the higher fat or proportionally higher fat in LCHF causes an increase in insulin:carb requirements.
Couple of things.
1)
@phoenix, didn't the Wolpert study involve high carb
and high fat?
2) Fats - and esp saturated fats. This is a real issue for LCHF-ers, because we need the high fat to feel satisfied, and because so much of that means sat fat. I do think sat fat gorging can be taken too far, mainlining bulletproof coffee and cream for example. I'm one of those people whose LDL cholesterol has increased on LCHF. Triglycerides, HDL and their ratio were very good, so to that extent I've no grounds to worry, but I think sat fat tolerance may vary between people and needs a lot more investigation. I'm certainly going to keep to one butter coffee a day.
@donnellysdogs, you were worried about this, weren't you.
Kenneth Sikaris says about this, Hmmm, don't know, you need to watch it. P. Attia says, Hmmm, may need a bit more than attention. I'm quoting him from a blogpost this week.
"some readers may interpret the data I present to mean it’s perfectly safe to consume, say, 25% (or more) of total calories from SFA [saturated fats]. I realize I may have to turn in my keto-club card, but I am convinced that a subset of the population—I don’t know how large or small, because my “N” is too small—are not better served by mainlining SFA, even in the complete absence of carbohydrates (i.e., nutritional ketosis). Let me repeat this point: I have seen enough patients whose biomarkers go to hell in a hand basket when they ingest very high amounts of SFA. This leads me to believe some people are not genetically equipped to thrive in prolonged nutritional ketosis.
In one particularly interesting case, a patient in self-prescribed nutritional ketosis presented to me with an LDL-P of more than 3500 nmol/L (i.e., more particles than could be measured by the NMR machine so the report simply said “>3,500 nmol/L”) despite feeling, performing, and looking great. Based on his through-the-roof desmosterol and cholanstanol levels, and a curb-side consult from the Godfather I mean Dr. Tom Dayspring, I decided to try an experiment. You see, the logical thing to do in this setting would have been to start two drugs immediately (a potent statin to address the hypersynthesis and ezetimibe to address the hyperabsorption) or tell him to abandon ketosis altogether. But this patient was adamant about staying in ketosis given the other benefits, though obviously worried about the long-term coronary implications. So, we agreed that for a 3 month trial period he would reduce SFA to an average of 25 g/day (vs. about 75 to 100 g/day) and make up the difference with monounsaturated fat (MUFA). Parenthetically, we also reduced his omega-3 PUFA given very high RBC EPA and DHA levels.
So, on balance, he consumed about the same number of calories and even total quantity of fat, but his distribution of fat intake changed and he heavily swapped out SFA for MUFA.
The result?
His LDL-P fell from >3,500 nmol/L to about 1,300 nmol/L (about 55th percentile), and his CRP fell from 2.9 mg/L to <0.3 mg/L (and for the lipoprotein cognoscenti, both desmosterol and cholanstanol fell).
Pretty cool, huh? So, my point is this: while I believe the population-based guidelines for SFA are not supported by a standard of science I consider acceptable, it does not imply I believe SFA is uniformly safe at all levels for all individuals.
Some of you may be wondering about me. It turns out I’m in the group (recall: I have no idea how large or small this group is) that seems to do well—at least by the tools we have available to assess risk—with large amounts of SFA in my diet, if and when I elect to. Even when I was in ketosis, eating 4,000 kcal/day (literally getting 40 to 45% of my calories from SFA alone) my biomarkers—cardiovascular, insulin resistance, inflammation—were excellent. Better than they ever were or even are today. Though, my point still stands: there are some people who do not appear able to safely consume massive amounts of SFA.
One last point I’ll make on this highly charged topic. I realize there is a contingent within the LCHF community who argue that traditional biomarkers of coronary risk—such as LDL-C or its superior cousin LDL-P—“don’t matter” if one is on a low carb or ketogenic diet. Maybe they are right. I guess time will tell. But I am not convinced, at least not yet. As a doctor I can’t look a patient in the eye and tell them a sky-high LDL-P is ok because they don’t eat carbohydrates. So if you’re following such a diet, and your LDL-P goes through the roof, I’d urge you to consider a variation of the diet."
From
here.
Any reactions, people?
Lucy