Well worth a read:
Well worth a read:
I always thought this was interesting…for those people like this. For me, as a still-fat person, my TC and LDL are “low”, though my HDL has gone up and trigs down since being keto.
Also, there are muscular people who are lean and who don’t fit this profile. Dave and Nick have different theories about why. I don’t think that’s in this paper.
@Knnn Agreed! This is well worth reading.
Being a textbook example of an LMHR, I’ve followed Feldman’s work closely. This paper provides a wonderful overview of how the various lipid components might change (as compared to non-LMHR individuals) when carbs are restricted.
If nothing else, it calmed my considerable intitial anxiety when I first saw my NMR lipid panel results. My total LDL shot sky high, yet my HDL rose to over 100 while my trigs dropped to around 50.
Other context: Starting as a fairly lean fit guy, I still lost 25 lbs and 4" in waistline after restricting carbs - now with a BMI of roughly 20. The rest of my NMR panel showed a highly insulin-sensitive “Pattern A” lipid profile. Still, that LDL figure spike was pretty scary - that is, without understanding that there are others with a similar context in which the traditional metrics take on a different meaning, as hypothesized by Lustig, Feldman, et al.
Thanks for posting this again in case others missed it. If you’re a LMHR, you should spend some time wrapping your head around this material. You will sleep a lot better.
Are you upping your carbs. I am in this bracket as well and have been following Feldman’s blog and discussions. My doctor is not pleased by the very elevated ldl so I think I should take it down… The extra carbs will take me out of ketosis I think but I like to stay low carb and exercise so I will try to let carbs go up towards 100 and see if that does anything.
If you’re asking me, I wouldn’t be willing to increase my carbohydrate ingestion in order to please my doctor. I’d find another doctor.
Of course, I’m only speaking for myself here.
Just eat white bread:
Dropped his LDL by about 2/3 or so:
Dropped his HDL and raised his trigs too, though.
If your ratio of triglycerides to HDL is low (2.0 or under in American measurements, 0.9 or under, elswhere), your cardiovascular risk is minimal. An NMR analysis of your LDL would show the healthy Pattern A distribution of particle sizes. Your total cholesterol and your LDL levels are irrelevant. And cardiovascular risk is supposed to be why we care about cholesterol in the first place.
There are quite a lot of data, actually, to show that, if LDL or any other form of cholesterol has anything to do with cardiovascular disease, it is not as a cause of the disease. At best, lipid numbers could be considered markers for a problem, but the problem is caused by other things, and cannot be addressed by lowering cholesterol, especially with drugs.
Also, if one is not a lean-mass hyper-responder, as defined by Dave Feldman, manipulating one’s lipid tests by short-term changes in diet is not feasible. That only works for Dave’s hyper-responders.
… and unless you’re doing research on the topic, it remains unclear to me why a hyper-responder would want to manipulate her/his test result. Unless, as has been pointed out by others, the goal is to deceive an insurance company or nosy-in-your-veins employer.
Then again, since the goal in that case would be to make the folks believe you are as healthy as you actually are, that’s not such a terrible deception after all
Are we related? Because I just had that very thought myself, a few days ago!
Interesting question. Since I rarely agree with anyone else to whom I’m related, I’m guessing our twigs must be far apart on our family tree.
I’m a good LMHR example: lean with low Trig/HDL ratio even before going low-carb/keto, slightly “high” LDL-C went up a lot with carb restriction (although still only a little over 200, which is pretty tame compared to some cases). My before/after numbers would have qualified me for Dave Feldman’s upcoming heart study, but I was rejected due to having smoked cigarettes from age 20 to 22 (I’m 57 now).
I’ll be VERY interested to see the results of the study, which I hope will be out in a couple of years. When you see multi-dimensional graphs that show CVD by quartiles for both LDL and HDL or LDL and Trigs, it’s reassuring that most of the CVD risk appears to be in the quartiles with the worst HDL or Trigs, but it will be even more so if the LMHR people really show lower plaque progression directly imaged by CT scan in Dave’s study.
I’m lucky that my PCPs over the last few years haven’t been too interested in my high LDL. One of them wrote a scrip for atorvastatin after my last visit, but he didn’t harp on it and he’s retiring, and my new doc didn’t bat an eye when I told her I hadn’t filled it and wasn’t planning to do so.
Out with the old… in with the new. It’s been said that it takes a generation of scientists to die off before we can embrace new knowledge.
I’m equally stoked as you to see the study results.
Having smoked for (many) years, (many) years ago, apparently I wouldn’t have qualified to participate either. Was going to pursue becoming a study participant - alas, won’t even bother.
Another thing (which I think was related to this study, but this was last fall and I won’t swear I’m remembering correctly) was that I seem to recall that they were screening for some threshold of Framingham risk calculation, which is strongly age-dependent. I was 56 at the time, and if I put in my actual age I would fail the cut-off, but if I dropped my age a couple of years I would pass. So, I remember thinking that they were going to be letting very few people into the study who were not in their early 50s or below.
I work in a research lab in a medical center, so people doing studies are always posting notices in the elevators trying to recruit research subjects. (One of the latest was a study of skin breakdown which could lead to bedsores, so one of the criteria was “able to lie flat for two hours.” I wondered how high a bar that was?) I just noticed a few weeks ago that most of them have an age cut-off of 50 or 55 years, and I realized I’m apparently too old to be considered “normal.”
Well, let’s say it again… Out with the Old.
I’m pleased to be a LMHR. It took 5 years of keto to get there starting from about 40% body fat. I don’t mind my rising cholesterol because it correlates strongly with improving health and body composition. I was surprised to achieve LMHR numbers at 20% body fat (LDL 300, HDL 100, TRI 60) which I think is still quite a bit fatter than most LMHRs. Continuing fat loss has become more challenging but I’m making a renewed push and hope to hit 15% by the end of this year with a long term goal to at least momentarily flirt with 10%. I’m curious to see just how high my cholesterol will go.
That’s interesting. What was your LDL-C pre-keto?
It was between 120 and 140.
Yeah lots to consider for sure. I think I feel I should try the a bit more carb approach at this time and see if that is the issue and then if my ldl actually goes down i will have a clearer idea about how to proceed. My doctor is fine… He has always been supportive just a bit worried about ldl being so high right now.
I have read the paper and listened to some of the podcasts and interviews but to me the Tro part of the research is quite unclear. They do say that the five people he followed that lowered their ldl by adding carbs did well and this is promising for lowcarbers or doctors treating lowcarbers who are concerned but they provide few details about the diet. I think I heard Tro say sweet potato at one time and the paper says fruit and starches but it does not sound like they actually enforced fruits. I will do a test in a few months and see if there is any movement…
As always great discussion here
There are a couple of assumptions at work here: First is the assumption that LDL causes cardiovascular disease. This is most likely not true. The second assumption is that lowering LDL will ameliorate cardiovascular disease. This would only be true if LDL were the cause of the disease; otherwise, manipulating a marker is highly unlikely to have any effect on the underlying condition. On the other hand, treating the underlying condition with the proper treatment will almost certainly improve the marker in the process.
If Ben Bikman and the others are correct that insulin-resistance from overeating carbohydrate is the cause of cardiovascular disease, then raising insulin by eating more carbohydrate is unlikely to be helpful overall, whether it lowers LDL or not.