Your high total cholesterol and LDL-C numbers are fascinating, particularly since I tend to think you have better genes overall than I do. Most of the contributors in "Cholesterol Clarity," Moore and Westman, 2013, comprising about 30 people, would tend to say you may be worrying too much, and that a consideration of LDL-P might be beneficial in more accurately characterizing your genuine risk, this idea of Pattern A (Normal, Good) vs Pattern B (Abnormal, Bad). What that is all about is the relative size and nature of the LDL particle, and there is a fairly large amount of evidence that this is a key factor in determining whether someone actually develops heart disease, not their LDL-C assay.
There is considerable info on interpreting LDL-P results in the book, which to be done accurately, requires an analytical technique such as gel electrophoresis. However, there is also the "poor man's" technique of simply dividing triglycerides by HDL, where a ratio of < 2.0 is good, connoting a tendency towards Pattern A, and a ratio of >3.5 is less good, indicating a greater likelihood of Pattern B.
I last had my lipids checked in July 2023, and they were
Total Cholesterol = 227 mg/dL
HDL-C = 139 mg/dL
LDL-C (Calculated) = 81 mg/dL
Triglycerides = 36 mg/dL
My ratio calculates as 36 mg/dL/139 mg/dL = 0.26, which is extraordinarily good. If I were to actually have LDL-P determined via gel electrophoresis or another analytical technique, there's not much doubt my LDL particles are going to come back as Pattern A, the normal, good kind.
Volek and Phinney in "The Art and Science of Low Carbohydrate Living," 2011, touch on this issue of LDL-C typically being a calculated value. The equation generally used for doing do was developed by William Friedewald and colleagues in 1972, and a major assumption in its use is that the ratio of triglycerides to cholesterol is constant. There is some amount of evidence that the equation develops linearity problems at both high and low triglyceride levels. My calculated LDL-C value of 81 mg/dL is already low and benign, but the actual value is probably even lower than that.
You can apparently tolerate statins well, which is great, and they do have benefits. But I happen to be someone who had two uncles who both died of an ALS-like condition they developed after being prescribed statin drugs, and I have a book by Dr. Duane Graveline "The Dark Side of Statins," 2017, where he relates a similar issue. Assuming statins were involved in precipitating the condition, the most likely mechanism is their fundamental interference in the mevalonate pathway, of which dolichols are one of the products (the cholesterol molecule is another).
Dolichols are molecules, that among other things, supervise repairs in DNA, of which a person requires on the order of tens of thousands per day. The model developed in regard to these ALS-like conditions are mitochondrial DNA mutations in neurons not being immediately addressed due to a shortage of dolichols, the errors then becoming embedded, and unfortunately, this can be permanent. The errors eventually contribute to malfunctioning in the associated mitochondria, and if enough mitochondria are impaired, this can negatively impact the functioning of the neuron overall. I suppose the neuron could even die in some cases, but the impairment of neuronal functioning is potentially bad enough simply by itself.
Now, all three of these people, my two uncles and Dr. Graveline, unquestionably suffered from heart disease, and their lives may have been extended by their use of statins. To his immense credit, despite being motivated to go to the effort of writing more than one negative book about statin drugs, Dr. Graveline indicates they do save lives, through at least four separate possible mechanisms. However, what many in the medical establishment don't seem to realize is that it's their inherent anti-inflammatory properties that probably really matter.
Graveline relates that when they were first developed, statins were characterized as "super aspirin," an appellation rejected by the pharma community as insufficiently glamorous. However, they actually do approximately what aspirin does in regard to heart disease and are simply a great deal more powerful. They are beneficial and extend life in many cases, but their potential drawbacks also need to be considered.
Your high total cholesterol and LDL-C numbers are fascinating, particularly since I tend to think you have better genes overall than I do. Most of the contributors in "Cholesterol Clarity," Moore and Westman, 2013, comprising about 30 people, would tend to say you may be worrying too much, and that a consideration of LDL-P might be beneficial in more accurately characterizing your genuine risk, this idea of Pattern A (Normal, Good) vs Pattern B (Abnormal, Bad). What that is all about is the relative size and nature of the LDL particle, and there is a fairly large amount of evidence that this is a key factor in determining whether someone actually develops heart disease, not their LDL-C assay.
There is considerable info on interpreting LDL-P results in the book, which to be done accurately, requires an analytical technique such as gel electrophoresis. However, there is also the "poor man's" technique of simply dividing triglycerides by HDL, where a ratio of < 2.0 is good, connoting a tendency towards Pattern A, and a ratio of >3.5 is less good, indicating a greater likelihood of Pattern B.
I last had my lipids checked in July 2023, and they were
Total Cholesterol = 227 mg/dL
HDL-C = 139 mg/dL
LDL-C (Calculated) = 81 mg/dL
Triglycerides = 36 mg/dL
My ratio calculates as 36 mg/dL/139 mg/dL = 0.26, which is extraordinarily good. If I were to actually have LDL-P determined via gel electrophoresis or another analytical technique, there's not much doubt my LDL particles are going to come back as Pattern A, the normal, good kind.
Volek and Phinney in "The Art and Science of Low Carbohydrate Living," 2011, touch on this issue of LDL-C typically being a calculated value. The equation generally used for doing do was developed by William Friedewald and colleagues in 1972, and a major assumption in its use is that the ratio of triglycerides to cholesterol is constant. There is some amount of evidence that the equation develops linearity problems at both high and low triglyceride levels. My calculated LDL-C value of 81 mg/dL is already low and benign, but the actual value is probably even lower than that.
You can apparently tolerate statins well, which is great, and they do have benefits. But I happen to be someone who had two uncles who both died of an ALS-like condition they developed after being prescribed statin drugs, and I have a book by Dr. Duane Graveline "The Dark Side of Statins," 2017, where he relates a similar issue. Assuming statins were involved in precipitating the condition, the most likely mechanism is their fundamental interference in the mevalonate pathway, of which dolichols are one of the products (the cholesterol molecule is another).
Dolichols are molecules, that among other things, supervise repairs in DNA, of which a person requires on the order of tens of thousands per day. The model developed in regard to these ALS-like conditions are mitochondrial DNA mutations in neurons not being immediately addressed due to a shortage of dolichols, the errors then becoming embedded, and unfortunately, this can be permanent. The errors eventually contribute to malfunctioning in the associated mitochondria, and if enough mitochondria are impaired, this can negatively impact the functioning of the neuron overall. I suppose the neuron could even die in some cases, but the impairment of neuronal functioning is potentially bad enough simply by itself.
Now, all three of these people, my two uncles and Dr. Graveline, unquestionably suffered from heart disease, and their lives may have been extended by their use of statins. To his immense credit, despite being motivated to go to the effort of writing more than one negative book about statin drugs, Dr. Graveline indicates they do save lives, through at least four separate possible mechanisms. However, what many in the medical establishment don't seem to realize is that it's their inherent anti-inflammatory properties that probably really matter.
Graveline relates that when they were first developed, statins were characterized as "super aspirin," an appellation rejected by the pharma community as insufficiently glamorous. However, they actually do approximately what aspirin does in regard to heart disease and are simply a great deal more powerful. They are beneficial and extend life in many cases, but their potential drawbacks also need to be considered.