The author of this web site www.phlaunt.com/diabetes lost her father at
age 95 of non heart disease causes.  He'd had a lifetime of LDL of over
300.  My mother died of other causes with high LDL and not a speck of
plaque on her arteries.

It's not the LDL number that matters, it's the size of the particles;
large, bouyant ones are non atherogenic, small dense ones do oxidative
damage.  More important, what is your HDL and what are your
triglycerides?  High HDL/TGL ratio under 3, and ideally, under 1.5 or so
is highly indicative of non atherogenic LDL.

It's all about ratios and particle sizes, not numbers; that's just a
story drug sellers like to tell.

Your doctor is right about cutting carbs, though; they're what raise
TGLs, which are very predictive of CVD if they're high.

Susan

Just to start there's no problem doing the simple stuff on your own -
Drop
the starchy or sweet foods.  Go with plenty of veggies.  But don't go
to
the extreme of only veggies - You'll be hungry constantly and that
will
slowly sap your dedication.

Pick a popular low carb plan.  Buy and read the book.  Follow the
directions
for that plan as written including the parts you don't understand or
agree
with - The authors spent a decade or more figuring out non-obvious
stuff or
working out non-obvious actions that work better than the obvious.  It
is
*very* easy to think that since low carb is good, lower carb must be
better
and zero carb must be best.  It's obvious once you decide that low
carb is
good.  The trouble is it's a false notion.  Obvious does not equal
true.  And
sure enough no matter which plan and book you chose it will put you
through
a sequence that does not take you lower and lower in carbs.

My bias - I prefer Atkins.  The late good Dr A might or might not ever
have
understood the science behind how his process works, but his process
works very well indeed.  But don't fall into the trap of glancing at
the book
and doing your own thing.  Actually follow the instructions.  It is
fully
customized to you based on the reactions of your own body to specific
ingredients, specific gylemic loads, specific daily carb counts.  I
prefer a
fully customized process for a simple reason - "one size fits all"
doesn't
so I prefer a plan that isn't one-size.  Fully customized is more
work.

If you would rather use a "one size fits all" plan because it's
simpler you
may want to chose one of the books by Drs Eades with "Protein Power"
in their titles.  The later books in their series are updated so they
tend
to be better than the original title that just just "Protein Power".

Doctor Atkins told two tales of how he got into the low carb business.
One was about using it on himself to lose his weight and keep it off.
The other was about noticing that prescribing low fat to his heart
patients had poor adherence and the few who managed to stay on it
tended to do worse more than 6 months in.  I think both tales are
true - It's generally better to have multiple reasons for doing
something.

Anyways there's a lesson in what happens with the numbers - On
low fat they tend to drop soon then after 6 months end up worse than
when you started.  Trying low carb in his 2002 edition he claimed that
"most" see better numbers after 2 month.  In his 1993/1999 editions
he claimed that about 80% see better numbers after 6 months.  In
both editions he points out that most see worse numbers in the first
month or so.  He suggests getting tested before starting, then either
2 or 6 months later depending on the edition.  This pattern is likely
to happen if you chose some other plan so expect it.

On Susan's response - She knows her stuff on cholesterol, blood
sugar and so on.  She's also biased against Atkins.

My cholesterol on a normal diet:
In 2003, total 447, LDL 350, HDL 79, TG 92, BG 75.
In 2008, total 400, HDL > 99, TG < 50, BG 75.

On a high-fiber (beans & psyllium), low or no-fat, low or no-meat diet
with simply prepared veggies and limited fruits, total chol drops
below 180. Possibly you have been exposed to dioxin. Check for
chloracne as show in figure 2A at www.ehponline.org/members/2001/109p865-869geusau/geusau-full.html
. Also see related pubmed abstracts below:

Mechanism of action of dioxin-type chemicals, pesticides, and other
xenobiotics affecting nutritional indexes.
The most consistent toxic effects of dioxin-type chemicals are
hyperlipidemia, body weight loss (particularly body fat loss),
anorexia, changes in carbohydrate metabolism, and lipid peroxidation.
The biochemical systems particularly affected are lipoprotein lipases,
low-density-lipoprotein receptors, glucose transporter proteins
(GLUTs), vitamin C uptake, and insulin secretion. Some of these
biochemical changes occur at very low doses, and some effects can last
for long time periods. To provide a mechanistic explanation for such
actions of dioxins, available experimental evidence has been reviewed.
The most recent discovery indicates that 2,3,7,8-tetrachlorodibenzo-p-
dioxin (TCDD) directly acts with isolated cytosolic aryl-hydrocarbon
(Ah) receptor under cell-free conditions even without the presence of
the nucleus and is capable of activating key protein kinases that are
involved in the growth factor signal-transduction pathway. The
resulting activation of primary-response transcription factors in the
nucleus appears to play a key role in coordinating vital cell program
shifts, including lipid metabolism. PMID: 7879740

TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) causes reduction in the low
density lipoprotein (LDL) receptor activities in the hepatic plasma
membrane of the guinea pig and rat.
Administration of 1 micrograms/kg (single intraperitoneal injection
and studied after 10 days) of 2,3,7,8-tetrachlorodibenzo-p-dioxin
(TCDD) to young male guinea pigs was found to cause a significant
reduction in binding of low-density lipoprotein (LDL) to its receptor
on the hepatic plasma membrane. This reduction in LDL binding is not
caused by the decrease of food intake by treated animals since pair-
fed control animals had significantly higher LDL binding than treated
animals. It was also found that primary hepatocytes from treated
animals had a reduced ability to internalize LDL than controls. Such a
change in the plasma membrane function may explain the resulting
hyperlipidemia particularly hypercholesterolemia which occurs in this
species as a result of TCDD administration. PMID: 6322751

Rabbit serum hypertriglyceridemia after administration of 2,3,7,8-
tetrachlorodibenzo-p-dioxin (TCDD).
TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) caused a dose-dependent
decrease of adipose tissue lipoprotein lipase (LPL) activity and
caused a concomitant increase in serum triglyceride concentration in
the rabbit 10 d after single ip administration of either 1 or 50
micrograms/kg. Hepatic low-density lipoprotein (LDL) binding was
markedly depressed and serum cholesterol concentrations were modestly
increased relative to pair-fed control animals. Serum glucose
concentrations were significantly lower in the rabbit administered
TCDD compared to ad libitum or pair-fed control animals, although
little change was observed in serum insulin concentration. Electron
microscopic examination of aortic arches 20 d after a single ip
administration of 50 micrograms TCDD/kg revealed ruffling, denudation,
and sloughing off of the cell surface and the appearance of macrophage-
like structures in the intima and media of the endothelial cells.
These alterations resemble preatherosclerotic lesions typical in
animals with hyperlipidemia. It is proposed that TCDD causes
hyperlipidemia in the rabbit through suppression of LPL activity and
LDL receptor binding. PMID: 3199460

Richard, you've on Lorazepam for 5 years. Why do you do that to
yourself? What problems do you have that you can't face without pills?
Don't you know that doctors are drug pushers? Sometimes the pills will
make you feel better, sometimes worse. One thing's for sure: They'll
make you go back to the doctor for as long as you take them. Stop the
dependance. It's time people realize what is being upon them. Wake up
or you'll never fully live life, Richard.