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Re: Re: Another diet -more personal thoughts

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Very interesting, thanks, Tony.

I'm not sure what to call high TC, versus the familial high TC described.

My rels are not that obese, at least not the ones with high TC. I'm calling >300 in that category or more specifically those who have a problem where the TC won't come down using normal means, like diet and exercise.

You don't have to be obese or overweight to have high TC, and if obese, you don't necessarily have high TC. Another example, my wife's mother was always obese and never had high TC.

So the report, doesn't cover all the cases, IMO.

If indeed, it is one in 500, then there is a cholesterol scare into drugs.

I think familial high TC, might be the person who, overweight or not, has high TC, and it's due to the liver making too much, and/or to reabsorbing too much of that which has been dumped to the gut for excretion.

Another thing, the article makes an association with plaque buildup, which happens in all people regardless of high TC. If it's not seen in coronaries, it will be in peripheral arteries or brainal arteries. The plaque buildup might be caused by high fat intake, maybe not, may be just too much calorie intake.

"They speculate themselves about therapy with drugs that increase the number of LDL-receptors simultaneous with a lesser demand for dietary regimens......"it may one day be possible for many people to have their steak and live to enjoy it too"."

That time is here - zocor and zetia, eg.

Regards.

[ ] Re: Another diet -more personal thoughts

[snip]> But the question always in my mind is that 3 females in mine and mywife's family all over 80, exhibit this "familial hypercholestero..",so I sincerely doubt the 1 in 500. [snip]=====JW,The statistics come from the 1985 Nobel laureate's lecture inPhysiology or Medicine:Tony====http://nobelprize.org/medicine/laureates/1985/press.html" Studies on patients with familial hypercholesterolemia (FH) by S. Brown and ph L. Goldstein constitute founding stonesfor our present knowledge concerning the cholesterol metabolism. FHexists in different forms and is inherited as a monogenic dominanttrait. Individuals who carry the mutant gene in double dose(homozygotes) are severely affected. Their serum cholesterol levelsare five times higher than in healthy persons, and severeatherosclerosis and coronary infarction is seen already inadolescence, or even earlier. Individuals who have inherited only onemutant gene (heterozygotes) develop symptoms later in life - at 35 to55 years of age. Their cholesterol levels are approximately 2-3 timeshigher than in normal people.""The severe form of FH (homozygous) is rare, about one in a millionpeople. The milder form of FH (heterozygous) is much more common,about one in 200-500 people. This means that in a city like Stockholmseveral thousand inhabitants have the disease with its associatedrisks of atherosclerosis and heart infarction."

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Very interesting, thanks, Tony.

I'm not sure what to call high TC, versus the familial high TC described.

My rels are not that obese, at least not the ones with high TC. I'm calling >300 in that category or more specifically those who have a problem where the TC won't come down using normal means, like diet and exercise.

You don't have to be obese or overweight to have high TC, and if obese, you don't necessarily have high TC. Another example, my wife's mother was always obese and never had high TC.

So the report, doesn't cover all the cases, IMO.

If indeed, it is one in 500, then there is a cholesterol scare into drugs.

I think familial high TC, might be the person who, overweight or not, has high TC, and it's due to the liver making too much, and/or to reabsorbing too much of that which has been dumped to the gut for excretion.

Another thing, the article makes an association with plaque buildup, which happens in all people regardless of high TC. If it's not seen in coronaries, it will be in peripheral arteries or brainal arteries. The plaque buildup might be caused by high fat intake, maybe not, may be just too much calorie intake.

"They speculate themselves about therapy with drugs that increase the number of LDL-receptors simultaneous with a lesser demand for dietary regimens......"it may one day be possible for many people to have their steak and live to enjoy it too"."

That time is here - zocor and zetia, eg.

Regards.

[ ] Re: Another diet -more personal thoughts

[snip]> But the question always in my mind is that 3 females in mine and mywife's family all over 80, exhibit this "familial hypercholestero..",so I sincerely doubt the 1 in 500. [snip]=====JW,The statistics come from the 1985 Nobel laureate's lecture inPhysiology or Medicine:Tony====http://nobelprize.org/medicine/laureates/1985/press.html" Studies on patients with familial hypercholesterolemia (FH) by S. Brown and ph L. Goldstein constitute founding stonesfor our present knowledge concerning the cholesterol metabolism. FHexists in different forms and is inherited as a monogenic dominanttrait. Individuals who carry the mutant gene in double dose(homozygotes) are severely affected. Their serum cholesterol levelsare five times higher than in healthy persons, and severeatherosclerosis and coronary infarction is seen already inadolescence, or even earlier. Individuals who have inherited only onemutant gene (heterozygotes) develop symptoms later in life - at 35 to55 years of age. Their cholesterol levels are approximately 2-3 timeshigher than in normal people.""The severe form of FH (homozygous) is rare, about one in a millionpeople. The milder form of FH (heterozygous) is much more common,about one in 200-500 people. This means that in a city like Stockholmseveral thousand inhabitants have the disease with its associatedrisks of atherosclerosis and heart infarction."

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