Finally! A voice of reason in the whole LDL debate (+ more)

[ctviggen]

Finally, here’s an article about LDL taking a middle-of-the-road approach:

Low Carb Cardiologist

I have “high” LDL-p (or did, the last several times I got my LDL-p checked, though I note that fasting causes my LDL-p to go UP, iaw Dave Feldman’s theory).

I find it hard to believe that a diet that has allowed me to lose 50+ pounds and makes me feel fantastic with unlimited energy is at the same time trying to kill me.

Furthermore, one way supposedly to reduce my “high” LDL-p is to eat more MUFAs and less saturated fats.

The problem with that? I also have high lipoprotein (a), Lp(a). (Again, I note these increase for me when fasting.) And what’s the best way to lower this? Eating more saturated fat and less MUFAs – the EXACT OPPOSITE of lowering LDL-p.

If I attack one of these markers, I therefore get worse in the other.

I personally think Dr. Scher’s theory of watching these values is the best. There are no studies done on low carb/keto people of any duration (whatsoever) finding that these values are “bad” or “good”. Everything is epidemiological and involving people who aren’t low carb.

For me, I’m going to keep doing what I’m doing and track these to see what happens.

What are your thoughts?

[LeCheffre]

For me, I’m going to keep doing what I’m doing and track these to see what happens.

Maybe I’m in denial, but I’m going to keep doing what I’ve been doing and decline lipid panels.

[juice]

What are your thoughts?

I like Bret’s stuff, generally, and this is no exception.

[Stal]

Dr. Malcolm Kendrick

Worth a perusal.

[brownfat]

For me, I’m going to keep doing what I’m doing and track these to see what happens.

What are your thoughts?

If you haven’t listened to Peter Attia’s 5 part podcast with lipidologist Tom Dayspring you should give it a listen. My take away from it is that LDL-p is likely more significant than Lp(a) although if Lp(a) responds badly and goes crazy high it probably shouldn’t be ignored.

My fix has been niacin but they dumped on that a bit. I also found it interesting that a major role of lipoproteins is transporting phospholipids which are crucial for membranes. I have a neuromuscular disease that causes elevated turnover of mitochondria which have phospholipid membranes and elevated cholesterol is a standard clinical finding of my disease. Statins commonly accelerate the muscle wasting and high cholesterol has been found to correlate with better outcomes in related diseases such as ALS. So I’m mostly content to live with mildly elevated LDL-p, modest swap of MUFA for SAFA, and focusing on keeping inflammation low to keep the heart disease risk in check.