Found a low carb doctor


(Michael) #1

I had such a pleasant discussion with a new doctor who brought up names such as Tim Noakes, Ivor Cummins and apparently met Authur Agatston last year. We had a good chat at his weight loss/metabolic clinic, and while he will not become my GP (too bad), he is willing to meet with me as needed to get testing done and anything in regards to metabolic health. He runs a practice that requires you to first get an insulin blood test, then a visit with the doctor (covered by government) and then to also pay for a dietician as part of the team consult. After our pleasant conversation, he told me there was no need for me to talk with the dietician (you would be talking over her head anyway, he quipped). Hell, he seemed as happy to meet me as I was to finally find someone with whom I could talk with about my health. SUPER happy today.

For the test details, I was able to get acquire requisitions for:
Vit A, magnesium, iron and selenium tested (blood)
CT Angiogram
NMR lipidprofile
Lp(a)
Insulin/Glucagon ratio

As an aside, he is a strong believer in small LDL as atherosclerotic and that vitamin K2 - Mk4 is a good idea to remove hard plaques. When I said I was not as convinced, he noted that he was quite open to believe that everything he thinks he understands could actually be backwards. So pleasant to work with a doctor who admits that in reality, they know nothing but simply do their best (in some cases) based on what they believe helps.


(Bob M) #2

That is a great doctor.

Not sure about Lp(a), though. Mine is insanely high, but I have a zero score on CAC. (So high that I calculated something like 75% of my LDL is Lp(a).)


#3

Are you sure you disagree with that? small LDL aka sdLDL, LDL(a) is the one known to do that, that’s not the same as LDL© that standard lipid panels check. That and the fact he’s ordering an NMR shows he’s on the right side of things.


(Michael) #4

I was actually talking about removing hard plaque using K2 as it has been suggested that the process could cause stable plaque to become unstable (and therefore causing an eruption and possible MI). Having said that, the alternate theory to sd-LDL as the cause is that inflammation is the cause and all LDL are equal from an atherogenic perspective. Also, no, I am not SURE on anything medical, especially when the current science is inconclusive. I tend to go by the latest medical journal articles and my opinions change quite often.


(Michael) #5

You should send your results to Tom Dayspring and ask his thoughts, I would love to hear his response noting your CAC score as well.


(Bacon enough and time) #6

There are data to suggest this. The healthy Pattern A of LDL sizes, which correlates with low cardiovascular risk, is larger and more buoyant, and it is always accompanied by a low ratio of triglycerides to HDL. (In U.S. units, you want a ratio of 2.0 or less; in the units used everywhere else, you want 0.9 or less.)

Sounds as though you really lucked out with the doc! :+1:


(Bacon enough and time) #7

I tend to believe the latter; nevertheless, LDL Pattern B (small and dense) does appear to serve as a marker for cardiovascular risk. But I firmly believe that treating the marker is stupid, because it leaves the real problem unaddressed. Sort of like giving the patient an aspirin for his headache, while ignoring the nail sticking out of his forehead! :grin:


(Todd Allen) #8

I hear that a lot but I wonder then why HDL despite being smaller and more dense, ie less buoyant, would not be more dangerous? I expect small dense LDL tends to be worse not because of density or size but because those are signs of depletion of triglycerides which suggests slower turn over. Longer time in circulation means greater exposure to oxidation and other degradation.


#9

Hasn’t Mk7 shown to be more effective? Both in terms of longer half life, bioavailability and blood concentrations and the “possible” vascular decalcification I’m pretty sure that I have read studies that suggest that.


#10

I don’t think that’s correct. From memory:

LDL is easily glycated in the presence of hyperinsulinemia. This causes LDL to shrink more and not be easily taken up by the liver to be recycled due to LDL receptor damage, therefore particle number increases. Secondly, small glycated LDL is able to pass through the lining of blood vessels where it is captured by macrophages leading to atherosclerotic plaque formation.

If I have any of that wrong please correct me. I’m relying on memory.


#11

You’re misquoting me, I never said that, @Naghite did, that aside yes, MK-7 is typically thought to be the better form. There are some that argue MK-4 over MK-7, but I don’t remember the reason that.


#12

Sorry, clumsy fingers when doing the quote


#13

Jebus! Be thankful you can actually get a doctor…well done!

Don’t start me on dentistry.


(Michael) #14

Tom Dayspring likes to point out, that in his opinion, HDL can also be atherogenic, just like LDL. The issue is particle count, which is drastically reduced with HDL, residence time and function.

From my personal thinking, HDL is smaller and can therefore fit between cells to intentionally reverse cholesterol content from trapped and oxidized particles/foam cells. The real issue is, is the expected damage from any and all the particles being healed fast enough to keep your veins healthy.


(Michael) #15

You have one theory correct as explained by Paul Mason. Peter Attia would try to convince you that the size is irrelevant, and only particle number is relevant. He is pretty convincing, just like Paul Mason is pretty convincing :).

P.S. I asked the doctor about MK-7, and he said he only ever prescribed MK-4, I did not ask for more details as to why not, I figured either works well enough if you are going down that road.


(Bob M) #16

That guy has taken the blue pill, or whatever pill you take when cognitive dissonance is the plain on which you live.

Listened to a podcast with him and the guy who used to run NUSI (can’t remember his name – Edit: Peter Attia). They were discussing a woman with extremely high LDL, who had a CAC score of zero. Literally within the next minute they said “but we know high LDL causes atherosclerosis”. Ah, what?

And the next argument they made was that babies have very low LDL, so low LDL for adults should be OK.

Ah, double what?

They finally did get around to a reasonable argument, which is that cells could have the proper amount of cholesterol while blood could have very little LDL.

But I couldn’t listen anymore.

Edit 3: Hmmm…I could use both plane or plain. The engineer in me wanted to use “plane”, since this is a mathematical term, but “plain” also works.


(Bacon enough and time) #17

Because it is made (if I’ve got this right) from a different lipoprotein and serves a different purpose, scavenging cholesterol and returning it to the liver to be broken down.

Honestly, it just goes to show how little relevance cholesterol in general has to do with heart disease risk. I’m pretty confident in the evidence I’ve seen that cholesterol is not a cause of cardiovascular disease, especially given how many essential roles it plays in the body. And at best, our lipid profile might serve as a marker for our cardiovascular health (or lack of it), but manipulating our lipoprotein levels takes the focus off the real, underlying problem, which is metabolic dysfunction. As Phinney likes to point out, focussing on lowering cholesterol to prevent heart disease is very much like focussing on lowering the number of fire trucks in order to prevent fires.


(Bacon enough and time) #18

You are right that that is the current hypothesis, but Ravnskov and Diamond have posited a different mechanism, with a plausible suggestion that instead of migrating completely through the arterial wall, the cholesterol gets to where it does via the vasa vasorum, the blood vessels that oxygenate the aorta and other major arteries. They have also suggested that the real cardiovascular danger is not cholesterol, but rather the coagulability of the blood, especially when it is increased by glycation of the haemoglobin.


(Bob M) #19

Winner, winner, chicken dinner! :wink:

Unless you have high Lp(a), as I do, as that’s genetic. Or you have FH (familial hypercholesterolemia), which is genetic, and causes high LDL. But some think it’s actually coagulation factors in FH that are the culprit, not high LDL.


(Bacon enough and time) #20

And we’ve known that since at least the 1960’s. It makes you wonder how Keys managed to make his diet-heart hypothesis prevail, in spite of evidence to the contrary.