High LDL cholesterol levels

Your doc will need to run some tests to determine the sizes of your cholesterol.

For example,

-- When I was running and following a High carb, low fat diet, my LDL was moderate and the HDL was low.

-- Then switched to still running and following a High carb, moderate plant-base fat diet, my LDL were low and my HDL levels shot up.

Tests run by my doctor was able to explain how my dietary change impacted my scores. When I was following a low fat diet, my HDL had nothing to do, so while the numbers were small, their particular size (VHDL or something like that) was huge. My doc described the size as something of a mac truck.

When I changed my diet to a moderate plant-base fat diet, my HDL had something to do. So the liver was able to produce more.

I'm interested in this, too, because I have high LDL, but I also exercise. My diet wasn't that bad, but I did have eggs, shellfish, and red meat. I've given all these foods up and am trying to eat a higher percentage of complex carbs and vegetables and lean proteins like fish and chicken breasts. I haven't had an egg or a hamburger in about 6 weeks. I exercise 5-6 days a week, even before the cholesterol test. My HDL was high, around 67, so that's good, but the LDL was 170 -- bad! I'm trying to lose some body fat and about 10 lbs. before the follow up in May. Otherwise, it's Lipitor.

Interesting. What lowered my LDL and raised my HDL was reducing carbs but increasing fibre.
I still ate the same amount of sat. fat.

That's pretty common Fred........it happened to me a few years ago when I switched to a lower carb diet (25%) but getting more protein for me was more steak and more saturated fat. My HDL has been just over 100 for the last 5 years and my particle size are the good ones, can't really complain considering I like ribeye.

Hi,

I've done a quick google search so I now know WHO he is, but couldn't find any of his papers.

Do you have any links to stuff he has written.

Cheers

The trouble is, using a study involving multiple interventions as ‘proof’ of the effectiveness of a single intervention is a sterling example of inappropriate extrapolation. Esselstyn’s intervention was multifactorial: each patient was assigned to a very low-fat lacto-vegetarian diet and cholesterol-lowering drugs, the most common protocol being cholestyramine, 4 g twice daily, and lovastatin, 40 mg to 60 mg daily (Esselstyn has since gone on to eschew the use of low-fat dairy). Esselstyn’s strict dietary instructions meant forsaking all the refined processed garbage the patients were previously eating. So in in addition to eschewing meat, the patients also had to forgo all the nutrient-depleted, sugar/vegetable fat/additive-drenched junk they were previously scoffing down.

So let’s take a look at the long list of potential confounders. As a result of the intervention, the patients lost weight. Weight loss itself, irrespective of the diet employed, can causes improvements in arterial function, regression of arterial thickness, and anti-platelet activity[2-5]. The one consistent theme is that the degree of IMT reduction is linked to the amount of weight lost, not the mode of diet followed.