Re: Familial Hypercholesterolemia

[Guest guest]

JW,

Familial Hypercholesterolemia (FH) is rare and can be determined by

genetic testing of the Arg3500Gln mutation. The pharmaceutical

companies want you to think that FH is very common so that you buy

their statin drugs instead of implementing the proper dietary changes:

avoid hydrogenated fats, cut calories to have a normal BMI, reduce

saturated fats, reduce carbohydrates, increase omega-6 polyunsaturated

fat, and add soluble fiber.

I also agree with you that you don't have to be overweight to have

high Total Cholesterol. There are examples of CRONers who have high

cholesterol because they have an imbalace of fatty acids in their

diet. I think that high cholesterol in a thin person without FH is a

symptom of deficiency of omega-6 essential fatty acids. See my

Message 19312.

On a personal note, I just got the results of my yearly blood test:

TC=170, TG=72, HDL=56, LDL=100. I regularly eat lean meats, 2% milk,

and eggs, but every day I take 1 tablespoon of grape seed oil to get

my omega-6 (linoleic acid), 1 tablespoon of flax seeds to get my

omega-3 fatty acids, and 2 tablespoons of oat bran as a source of

soluble fiber.

Tony

===

http://tinyurl.com/b6g2r

Apolipoprotein B Arg3500Gln Mutation Prevalence in Children With

Hypercholesterolemia: A French Multicenter Study.

" Familial defective apolipoprotein B-100, a dominantly inherited form

of hypercholesterolemia caused by a single Arg3500Gln mutation, is

silent in childhood but may confer a high risk of cardiovascular

disease in adulthood. "

====

>

> 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

>

>

> --- In , " jwwright " <jwwright@e...>

wrote:

> [snip]

> > But the question always in my mind is that 3 females in mine and my

> wife'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 in

> Physiology 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 stones

> for our present knowledge concerning the cholesterol metabolism. FH

> exists in different forms and is inherited as a monogenic dominant

> trait. Individuals who carry the mutant gene in double dose

> (homozygotes) are severely affected. Their serum cholesterol levels

> are five times higher than in healthy persons, and severe

> atherosclerosis and coronary infarction is seen already in

> adolescence, or even earlier. Individuals who have inherited only one

> mutant gene (heterozygotes) develop symptoms later in life - at 35 to

> 55 years of age. Their cholesterol levels are approximately 2-3 times

> higher than in normal people. "

>

> " The severe form of FH (homozygous) is rare, about one in a million

> people. The milder form of FH (heterozygous) is much more common,

> about one in 200-500 people. This means that in a city like Stockholm

> several thousand inhabitants have the disease with its associated

> risks of atherosclerosis and heart infarction. "

>

[Guest guest]

JW,

Familial Hypercholesterolemia (FH) is rare and can be determined by

genetic testing of the Arg3500Gln mutation. The pharmaceutical

companies want you to think that FH is very common so that you buy

their statin drugs instead of implementing the proper dietary changes:

avoid hydrogenated fats, cut calories to have a normal BMI, reduce

saturated fats, reduce carbohydrates, increase omega-6 polyunsaturated

fat, and add soluble fiber.

I also agree with you that you don't have to be overweight to have

high Total Cholesterol. There are examples of CRONers who have high

cholesterol because they have an imbalace of fatty acids in their

diet. I think that high cholesterol in a thin person without FH is a

symptom of deficiency of omega-6 essential fatty acids. See my

Message 19312.

On a personal note, I just got the results of my yearly blood test:

TC=170, TG=72, HDL=56, LDL=100. I regularly eat lean meats, 2% milk,

and eggs, but every day I take 1 tablespoon of grape seed oil to get

my omega-6 (linoleic acid), 1 tablespoon of flax seeds to get my

omega-3 fatty acids, and 2 tablespoons of oat bran as a source of

soluble fiber.

Tony

===

http://tinyurl.com/b6g2r

Apolipoprotein B Arg3500Gln Mutation Prevalence in Children With

Hypercholesterolemia: A French Multicenter Study.

" Familial defective apolipoprotein B-100, a dominantly inherited form

of hypercholesterolemia caused by a single Arg3500Gln mutation, is

silent in childhood but may confer a high risk of cardiovascular

disease in adulthood. "

====

>

> 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

>

>

> --- In , " jwwright " <jwwright@e...>

wrote:

> [snip]

> > But the question always in my mind is that 3 females in mine and my

> wife'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 in

> Physiology 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 stones

> for our present knowledge concerning the cholesterol metabolism. FH

> exists in different forms and is inherited as a monogenic dominant

> trait. Individuals who carry the mutant gene in double dose

> (homozygotes) are severely affected. Their serum cholesterol levels

> are five times higher than in healthy persons, and severe

> atherosclerosis and coronary infarction is seen already in

> adolescence, or even earlier. Individuals who have inherited only one

> mutant gene (heterozygotes) develop symptoms later in life - at 35 to

> 55 years of age. Their cholesterol levels are approximately 2-3 times

> higher than in normal people. "

>

> " The severe form of FH (homozygous) is rare, about one in a million

> people. The milder form of FH (heterozygous) is much more common,

> about one in 200-500 people. This means that in a city like Stockholm

> several thousand inhabitants have the disease with its associated

> risks of atherosclerosis and heart infarction. "

>

[Guest guest]

OK, definition of terms, so let's forget the official FH and focus on the stuff that's really killing us.

It doesn't really make any difference if the drug companies want people to buy their statins, they will because they have that other high TC thing that won't go down with diet and exercise below a certain point, individually defined.

The odd part is those people are not necessarily doomed. Docs just think they need to get it down. Patients don't know if they should or not, so they do if they have the dollars.

So that's the issue that the enig folks maybe focus on. You don't have to have low TC to live longer or healthier, but it probably helps.

The whole thing is indeterminate and suggesting low TC even helps us live longer is not substantiated - I recall some 215's in centenarians.

BTW, mine has fluctuated between 156 -176, since losing weight (5.5 yrs), and eating less, regardless of meat intake, low fat intake, etc. In fact, the 176, I did just as a joke to show my wife (350+ without drugs), I could get it up, I ate a fatty meat diet for 2 weeks before the test. It didn't help my HDL (nothing fazes it), and the doc suggested I start using zocor - I didn't.

The ONLY reason to do low fat is to keep the BP lower,IMO.

Increases in BP and plaque can be seen in the teens.

Regards.

[ ] Re: Another diet -more personal thoughts> > > --- In , "jwwright" <jwwright@e...>wrote:> [snip]> > But the question always in my mind is that 3 females in mine and my> wife'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 in> Physiology 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 stones> for our present knowledge concerning the cholesterol metabolism. FH> exists in different forms and is inherited as a monogenic dominant> trait. Individuals who carry the mutant gene in double dose> (homozygotes) are severely affected. Their serum cholesterol levels> are five times higher than in healthy persons, and severe> atherosclerosis and coronary infarction is seen already in> adolescence, or even earlier. Individuals who have inherited only one> mutant gene (heterozygotes) develop symptoms later in life - at 35 to> 55 years of age. Their cholesterol levels are approximately 2-3 times> higher than in normal people."> > "The severe form of FH (homozygous) is rare, about one in a million> people. The milder form of FH (heterozygous) is much more common,> about one in 200-500 people. This means that in a city like Stockholm> several thousand inhabitants have the disease with its associated> risks of atherosclerosis and heart infarction.">

[Guest guest]

OK, definition of terms, so let's forget the official FH and focus on the stuff that's really killing us.

It doesn't really make any difference if the drug companies want people to buy their statins, they will because they have that other high TC thing that won't go down with diet and exercise below a certain point, individually defined.

The odd part is those people are not necessarily doomed. Docs just think they need to get it down. Patients don't know if they should or not, so they do if they have the dollars.

So that's the issue that the enig folks maybe focus on. You don't have to have low TC to live longer or healthier, but it probably helps.

The whole thing is indeterminate and suggesting low TC even helps us live longer is not substantiated - I recall some 215's in centenarians.

BTW, mine has fluctuated between 156 -176, since losing weight (5.5 yrs), and eating less, regardless of meat intake, low fat intake, etc. In fact, the 176, I did just as a joke to show my wife (350+ without drugs), I could get it up, I ate a fatty meat diet for 2 weeks before the test. It didn't help my HDL (nothing fazes it), and the doc suggested I start using zocor - I didn't.

The ONLY reason to do low fat is to keep the BP lower,IMO.

Increases in BP and plaque can be seen in the teens.

Regards.

[ ] Re: Another diet -more personal thoughts> > > --- In , "jwwright" <jwwright@e...>wrote:> [snip]> > But the question always in my mind is that 3 females in mine and my> wife'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 in> Physiology 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 stones> for our present knowledge concerning the cholesterol metabolism. FH> exists in different forms and is inherited as a monogenic dominant> trait. Individuals who carry the mutant gene in double dose> (homozygotes) are severely affected. Their serum cholesterol levels> are five times higher than in healthy persons, and severe> atherosclerosis and coronary infarction is seen already in> adolescence, or even earlier. Individuals who have inherited only one> mutant gene (heterozygotes) develop symptoms later in life - at 35 to> 55 years of age. Their cholesterol levels are approximately 2-3 times> higher than in normal people."> > "The severe form of FH (homozygous) is rare, about one in a million> people. The milder form of FH (heterozygous) is much more common,> about one in 200-500 people. This means that in a city like Stockholm> several thousand inhabitants have the disease with its associated> risks of atherosclerosis and heart infarction.">

[Guest guest]

Hi, I just joined the group 3 minutes ago. Interesting. My mom's side

of the family has high cholesterol. Some of us are quite thin and some

are not, but even the thinnest of us says she " ate lettuce for a year "

and walked every day and got it all the way down to 300! No one has

died of it yet that we know of. Great-grandmother lived to be 93,

grandmother to 86, and the verdict is out on the rest of us. No one is

taking any statins. Mine is 226. I'm 46 years old.

I'll write in later with an official intro.

a Westby

[Guest guest]

Hi, I just joined the group 3 minutes ago. Interesting. My mom's side

of the family has high cholesterol. Some of us are quite thin and some

are not, but even the thinnest of us says she " ate lettuce for a year "

and walked every day and got it all the way down to 300! No one has

died of it yet that we know of. Great-grandmother lived to be 93,

grandmother to 86, and the verdict is out on the rest of us. No one is

taking any statins. Mine is 226. I'm 46 years old.

I'll write in later with an official intro.

a Westby

[Guest guest]

I think I decided that most of those with like 300 that won't go down, do not have the FH described in the good dr's treatise. Unless you got a gene check, you wouldn't know. But who cares what we call it, there are many more than 1 in 500 that have this high TC. If there weren't, I wouldn't have met so many.

I have a doc with high TC, a skinny young guy who grated his teeth every time he looked at my 234# and 206 TC.

Somewhere we had a ref that described the diff in stats, me being in the "low", i.e., <234 group, and those in the >235 group (my wife,eg).

So if yours is just 226, and you can get it lower eating less that puts you in the lower category, IMO.

Two bell curves for two sets of people.

Sadly, my family's "normal?" TC left us with dying <80, while my wife's family has several over 80 and over 300 TC. So I hardly see a correlation to CVD, et al, but why take the risk, is my logic.

So my wife takes the pills, along with a good diet and some exercise. We went crazy on the exercise for a while, but now just walk.

And CR, IMO, provides the best approach so far to longevity, and I separate it from all these other things we talk about which we think might be good.

AFA osteo is concerned, we have some definite thoughts on that and diffs of opinion about ERT. Possibly an option for some, check your doctor.

I view osteo as a viable threat to good health in the 70 - 80's.

Regards.

[ ] Re: Familial Hypercholesterolemia

Hi, I just joined the group 3 minutes ago. Interesting. My mom's side of the family has high cholesterol. Some of us are quite thin and some are not, but even the thinnest of us says she "ate lettuce for a year" and walked every day and got it all the way down to 300! No one has died of it yet that we know of. Great-grandmother lived to be 93, grandmother to 86, and the verdict is out on the rest of us. No one is taking any statins. Mine is 226. I'm 46 years old. I'll write in later with an official intro.a Westby

[Guest guest]

I think I decided that most of those with like 300 that won't go down, do not have the FH described in the good dr's treatise. Unless you got a gene check, you wouldn't know. But who cares what we call it, there are many more than 1 in 500 that have this high TC. If there weren't, I wouldn't have met so many.

I have a doc with high TC, a skinny young guy who grated his teeth every time he looked at my 234# and 206 TC.

Somewhere we had a ref that described the diff in stats, me being in the "low", i.e., <234 group, and those in the >235 group (my wife,eg).

So if yours is just 226, and you can get it lower eating less that puts you in the lower category, IMO.

Two bell curves for two sets of people.

Sadly, my family's "normal?" TC left us with dying <80, while my wife's family has several over 80 and over 300 TC. So I hardly see a correlation to CVD, et al, but why take the risk, is my logic.

So my wife takes the pills, along with a good diet and some exercise. We went crazy on the exercise for a while, but now just walk.

And CR, IMO, provides the best approach so far to longevity, and I separate it from all these other things we talk about which we think might be good.

AFA osteo is concerned, we have some definite thoughts on that and diffs of opinion about ERT. Possibly an option for some, check your doctor.

I view osteo as a viable threat to good health in the 70 - 80's.

Regards.

[ ] Re: Familial Hypercholesterolemia

Hi, I just joined the group 3 minutes ago. Interesting. My mom's side of the family has high cholesterol. Some of us are quite thin and some are not, but even the thinnest of us says she "ate lettuce for a year" and walked every day and got it all the way down to 300! No one has died of it yet that we know of. Great-grandmother lived to be 93, grandmother to 86, and the verdict is out on the rest of us. No one is taking any statins. Mine is 226. I'm 46 years old. I'll write in later with an official intro.a Westby