Just as I thought. Susan is a case of a little bit of misapplied
medical knowledge used in the wrong way. Are you too lazy to read the
information that you posted? It's an abstract of a clinical trial only
and clearly states "no study results posted." It is very dangerous
when people like you start making statements that you have made
without adequate data, medical training background or peer reviewed
studies to back up your words.

And since Susan is not archiving her posts so that her words remain
for all to see, I will do so.

I'm sick and tired of someone who claims to know better than clinical
and medical experts in the field who base their knowledge on evidence
and large, peer-reviewed clinical trials with a firm foundation in
science and biochemistry.

More cites please. You haven't shown squat to support your claim.

From UptoDate:

INTRODUCTION — The major adrenal steroid hormones are synthesized in
different areas of the adrenal cortex: glucocorticoids (particularly
cortisol), androgens, and estrogens in the zona fasciculata and
reticularis; and aldosterone in the zona glomerulosa. The steps
involved in the production of these hormones will be reviewed here. An
appreciation of these pathways serves as the basis for understanding
the different forms of congenital adrenal hyperplasia (CAH) and
isolated hypoaldosteronism in which there are defects in the function
of the enzymes involved in adrenal steroid synthesis. (Also see
"Anatomy and development of the adrenal cortex").

CHOLESTEROL SUBSTRATE — Cholesterol is the substrate for the synthesis
of all steroid hormones. The cells of the adrenal cortex can either
take up cholesterol from the circulation or synthesize cholesterol de
novo from acetate. In humans the majority of the cholesterol for
adrenal steroidogenesis is believed to be provided by serum low-
density lipoproteins (LDL) [1-3] , which are delivered to the interior
of adrenocortical cells via specific cell surface receptors for LDL
[4,5] .

High-density-lipoprotein (HDL) cholesterol also serves as an important
source of substrate for human adrenal steroidogenesis. In patients in
whom delivery of LDL cholesterol to the adrenal is impaired, basal
adrenal steroidogenesis is normal. Patients with abetalipoproteinemia,
a heritable deficiency of apolipoprotein B production and no LDL in
serum, and patients with familial hypercholesterolemia caused by
defects in the LDL receptor system have normal basal cortisol
production [6,7] . These patients do have subtle impairment of
cortisol synthesis during prolonged corticotropin (ACTH) stimulation
[6,7] , but it is not clinically important [3] . Furthermore, chronic
treatment with pravastatin, an HMG-CoA reductase inhibitor, which
reduces serum LDL cholesterol concentrations by 25 percent, has no
effect upon basal or ACTH-stimulated cortisol secretion [8] . These
clinical observations suggest that either de novo cholesterol
synthesis or other sources of extracellular cholesterol, such as HDL,
must support at least basal adrenal steroidogenesis.

A receptor system for HDL was first characterized in adrenal and other
steroidogenic tissues in mice [9,10] . This SR-BI (scavenger receptor,
class B, type I) receptor transfers HDL cholesterol into cells without
endocytosis of the entire lipoprotein particle, as occurs with LDL
[9] . Expression of SR-B1 is stimulated by activation of adenylyl
cyclase, suppressed by the intracellular level of cholesterol,
positively regulated by the transcription factor, steroidogenic
factor-1 (SF-1), sterol regulatory element-binding protein 1a
(SREBP-1a), and cofactors such as promoter-specific transcription
factor (Sp1). It is negatively regulated by the dosage-sensitive sex
reversal-adrenal hypoplasia gene on the X chromosome, gene 1 (DAX-1)
transcription factor [11,12] . Patients heterozygous for inactivating
SF-1 mutations have adrenal insufficiency [13] . Dax-1(- /Y) mice have
normal basal serum corticosterone levels and have greater
corticosterone responses to ACTH than wild-type mice [14] . SR-B1
knockout mice have lipid-depleted adrenocortical cells and high serum
HDL cholesterol concentrations [15] . The human homolog of SR-B1,
called CLA-1, is expressed in liver and steroidogenic cells and
transfers HDL cholesterol into cultured adrenal cells [16,17] .

The amount of free intracellular cholesterol available for adrenal
steroidogenesis is metabolically regulated. Receptor-mediated uptake
of LDL inhibits cholesterol synthesis by reducing the activity of
hydroxymethylglutaryl (HMG) CoA reductase, the rate-limiting enzyme in
cholesterol biosynthesis; it also stimulates esterification of the
imported cholesterol and downregulates the number of cell-surface LDL
receptors [18] . On the other hand, ACTH increases the number of LDL
receptors on the cell surface; it also increases the activity of the
cholesterol esterase that liberates free cholesterol from cholesteryl
esters delivered by LDL or stored in lipid droplets. Both of these
effects increase the amount of free intracellular cholesterol
[19,20] . ACTH also upregulates in vivo expression of the adrenal HDL
receptor SR-B1 in mice [21] . ACTH does not stimulate HMG CoA
reductase activity or alter the ability of LDL to inhibit this enzyme
[19,20] .

From Uptodate:

Clinical trials of cholesterol lowering in patients with coronary
heart disease or coronary risk equivalents
Author
Robert S Rosenson, MD
    Section Editor
Mason W Freeman, MD
    Deputy Editor
David M Rind, MD

Last literature review version 16.2: May 2008  |  This topic last
updated: April 12, 2008   (More)

INTRODUCTION — The preeminent role of LDL-cholesterol in the
pathogenesis and perpetuation of atherosclerotic vascular disease has
emerged from many sources [1-4] . The Lipid Research Clinics
Prevalence Study, for example, evaluated the influence of lipids on 10-
year cumulative coronary heart disease (CHD) death rates in patients
with and without CHD [2] . The CHD death rate increased at higher
plasma concentrations of total and LDL-cholesterol for both cohorts,
but the impact of elevated lipid levels was significantly greater in
subjects with preexisting CHD (show figure 1).

The major clinical trials that have addressed cholesterol lowering for
the secondary prevention of coronary events are reviewed here,
including trials in patients with coronary risk equivalents. Coronary
risk equivalents include (see "Overview of treatment of
hypercholesterolemia"):

   * Diabetes mellitus
   * Symptomatic carotid artery disease
   * Peripheral arterial disease
   * Abdominal aortic aneurysm
   * Multiple risk factors that confer a 10-year risk of CHD >20
percent

#  Ballantyne, CM, Grundy, SM, Oberman, A, et al. Hyperlipidemia:
diagnostic and therapeutic perspectives. J Clin Endocrinol Metab 2000;
85:2089.
# Pekkanen, J, Linn, S, Heiss, G, et al. Ten-year mortality from
cardiovascular disease in relation to cholesterol level among men with
and without preexisting cardiovascular disease. N Engl J Med 1990;
322:1700.
# Rosengren, A, Hagman, M, Wedel, H, et al. Serum cholesterol and long-
term prognosis in middle-aged men with myocardial infarction and
angina pectoris. A 16-year follow-up of the Primary Prevention Study
in Goteborg, Sweden. Eur Heart J 1997; 18:754.
# Third report of the National Cholesterol Education Program (NCEP)
Expert Panel on detection, evaluation, and treatment of high blood
cholesterol in adults (Adult Treatment Panel III). Circulation 2002;
106:3143.

There are many more completed, published, peer reviewed trials
supporting the safety of lower LDL cholesterol and the benefits in
secondary prevention of heart attacks and strokes. In all of these
trials with thousands of participants, finding problems with the
adrenal axis due to lowering the cholesterol has not been noted.