Here’s a good lay language explanation of much of what follows:
http://www.lbl.gov/Science-Articles/Archive/cholesterol-particles.html

Small, dense cholesterol particles worse for your heart
November 29, 1994
By David Gilbert, DEGilbert@lbl.gov

BERKELEY--New studies on low-density lipoprotein (LDL)--the so-called
"bad" cholesterol particle--by researchers at Lawrence Berkeley
Laboratory (LBL) indicate that bigger is better and small is not beautiful.
Using data from a broad medical study of male physicians, the
researchers have linked LDL particle size to the subsequent development
of heart disease. The research was presented at the American Heart
Association's 67th Scientific Sessions in Dallas on November 16.
"Since heart attacks often occur in people whose total cholesterol
levels put them at only moderate risk--those with readings in the
200-240 milligrams per decimeter (mg/dl) range--it is hard to pick out
the person who's going to get heart disease," says Dr. Ronald M. Krauss,
head of the Department of Molecular Medicine at LBL. "That's why it is
important to look at other factors such as LDL that might aid in that
prediction."
Lipoproteins transport cholesterol in the blood and are classified
according to their density. LDL is known as the "bad cholesterol"
because high levels are associated with increased heart disease risk.
But even within the category of LDL, not all particles are created equal.
LBL scientists were the first to establish a link between a predominance
of smaller, denser LDL particles and heart disease. However, those
studies looked at people who had already developed the disease. In
contrast, the studies presented today examined healthy people to
determine if the dense LDL trait is associated with later development of
disease. Krauss says these types of studies are considered more convincing.
Krauss and his associates worked with researchers at Brigham and Women's
Hospital in Boston to analyze statistics collected in the Harvard-based
Physicians' Health Study, which has followed nearly 15,000 male doctors
for several years. The researchers matched 312 of the subjects who had
heart attacks during a 7 1/2 year period by age and smoking status with
312 health control subjects.
The researchers then determined each person's LDL particle-size profile
and divided the subjects into five groups (quintiles). The lowest
quintile--those with the smallest and most dense LDL particles--had more
than three times the risk of heart attack as the quintile with the
largest LDL particles.
The trend held true even after the researchers adjusted for other risk
factors such as the ratio of total cholesterol to high-density
lipoprotein (the so-called "good" cholesterol, which helps clear LDL
from the blood), body mass index (a measure of obesity), diabetes, high
blood pressure and physical activity level.
The tendency toward small, dense LDL particles--a profile called pattern
B--is a common trait affecting an estimated 25-35 percent of healthy men
and 40-50 percent of heart disease patients. The size and density of LDL
particles, Krauss' previous studies have shown, reflect elevated levels
of blood triglycerides, another type of blood fat linked to heart disease.
"These observations reinforce the value of using these LDL size and
triglyceride level measurements to sharpen our focus in identifying high
risk individuals and institute appropriate interventions to prevent
heart attacks," Krauss says.
Krauss' collaborators include Patricia J. Blanche and Laura G. Holl, of
LBL; and Drs. Meir J. Stampfer, Jing Ma, and Charles Hennekens, of
Brigham and Women's Hospital.
LBL is a U.S. Department of Energy national laboratory located in
Berkeley, California. It conducts unclassified scientific research and
is managed by the University of California.

From Diabetes Care, Vol 23, Issue 11 1679-1685, American
Diabetes Association
http://tinyurl.com/dl3bo or
http://care.diabetesjournals.org/cgi/content/abstract/23/11/1679?maxt...
(Note that converting from mmol/L to US numbers changes the
ratio from 1.33 to 3.0)

A cutoff point of 1.33 for the TG-to-HDL cholesterol ratio
distinguishes between patients having small LDL values
better than TG cutoff of 1.70 and 1.45 mmol/l. CONCLUSIONS:
The TG-to-HDL cholesterol ratio may be related to the
processes involved in LDL size pathophysiology and relevant
with regard to the risk of clinical vascular disease. It may
be suitable for the selection of patients needing an earlier
and aggressive treatment of lipid abnormalities.

Clin Chem. 2003 Nov;49(11):1873-80.  Links
Fractional esterification rate of cholesterol and ratio of triglycerides
to HDL-cholesterol are powerful predictors of positive findings on
coronary angiography.
Frohlich J, Dobiásová M.
Department of Pathology and Laboratory Medicine, University of British
Columbia, Healthy Heart Program/Lipid Clinic, St. Paul's Hospital,
Vancouver, BC V6Z 1Y6, Canada. jifr@interchange.ubc.ca
BACKGROUND: We examined the predictive value of various clinical and
biochemical markers for angiographically defined coronary artery disease
(aCAD). Specifically, we assessed the value of the ratio of plasma
triglyceride (TGs) to HDL-cholesterol (HDL-C) and the fractional
esterification rate of cholesterol in plasma depleted of apolipoprotein
B (apoB)-containing lipoproteins (FER(HDL)), a functional marker of HDL
and LDL particle size. METHODS: Patients (788 men and 320 women)
undergoing coronary angiography were classified into groups with
positive [aCAD(+)] and negative [aCAD(-)] findings. Patient age, body
mass index, waist circumference, blood pressure (BP), medications,
drinking, smoking, exercise habits, and plasma total cholesterol (TC),
LDL-cholesterol (LDL-C), HDL-unesterified cholesterol, HDL-C, TGs,
FER(HDL), apoB, log(TG/HDL-C), and TC/HDL-C were assessed. Lipids and
apoproteins were measured by standard laboratory procedures; FER(HDL)
was determined by a radioassay. RESULTS: Members of the aCAD(+) group
were older and had a higher incidence of smoking and diabetes than those
in the aCAD(-) group. The aCAD(+) group also had higher TG, apoB,
FER(HDL), and log(TG/HDL-C) and lower HDL-C values. aCAD(+) women had
greater waist circumference and higher plasma TC and TC/HDL-C. aCAD(+)
men, but not women, had higher plasma LDL-C. In the multivariate
logistic model, the significant predictors of the presence of aCAD(+)
were FER(HDL), age, smoking, and diabetes. If only laboratory tests were
included in the multivariate logistic model, FER(HDL) appeared as the
sole predictor of aCAD(+). Log(TG/HDL-C) was an independent predictor
when FER(HDL) was omitted from multivariate analysis. CONCLUSIONS:
FER(HDL) was the best laboratory predictor of the presence of coronary
atherosclerotic lesions.

 Diabetes. 2003 Feb;52(2):453-62.  Links
Effects of insulin resistance and type 2 diabetes on lipoprotein
subclass particle size and concentration determined by nuclear magnetic
resonance.
Garvey WT, Kwon S, Zheng D, Shaughnessy S, Wallace P, Hutto A, Pugh K,
Jenkins AJ, Klein RL, Liao Y.
Division of Endocrinology and Department of Medicine, Medical University
of South Carolina, Charleston 29425, USA. garveywt@musc.edu
The insulin resistance syndrome (IRS) is associated with dyslipidemia
and increased cardiovascular disease risk. A novel method for detailed
analyses of lipoprotein subclass sizes and particle concentrations that
uses nuclear magnetic resonance (NMR) of whole sera has become
available. To define the effects of insulin resistance, we measured
dyslipidemia using both NMR lipoprotein subclass analysis and
conventional lipid panel, and insulin sensitivity as the maximal glucose
disposal rate (GDR) during hyperinsulinemic clamps in 56 insulin
sensitive (IS; mean +/- SD: GDR 15.8 +/- 2.0 mg. kg(-1). min(-1),
fasting blood glucose [FBG] 4.7 +/- 0.3 mmol/l, BMI 26 +/- 5), 46
insulin resistant (IR; GDR 10.2 +/- 1.9, FBG 4.9 +/- 0.5, BMI 29 +/- 5),
and 46 untreated subjects with type 2 diabetes (GDR 7.4 +/- 2.8, FBG
10.8 +/- 3.7, BMI 30 +/- 5). In the group as a whole, regression
analyses with GDR showed that progressive insulin resistance was
associated with an increase in VLDL size (r = -0.40) and an increase in
large VLDL particle concentrations (r = -0.42), a decrease in LDL size
(r = 0.42) as a result of a marked increase in small LDL particles (r =
-0.34) and reduced large LDL (r = 0.34), an overall increase in the
number of LDL particles (r = -0.44), and a decrease in HDL size (r =
0.41) as a result of depletion of large HDL particles (r = 0.38) and a
modest increase in small HDL (r = -0.21; all P < 0.01). These
correlations were also evident when only normoglycemic individuals were
included in the analyses (i.e., IS + IR but no diabetes), and persisted
in multiple regression analyses adjusting for age, BMI, sex, and race.
Discontinuous analyses were also performed. When compared with IS, the
IR and diabetes subgroups exhibited a two- to threefold increase in
large VLDL particle concentrations (no change in medium or small VLDL),
which produced an increase in serum triglycerides; a decrease in LDL
size as a result of an increase in small and a reduction in large LDL
subclasses, plus an increase in overall LDL particle concentration,
which together led to no difference (IS versus IR) or a minimal
difference (IS versus diabetes) in LDL cholesterol; and a decrease in
large cardioprotective HDL combined with an increase in the small HDL
subclass such that there was no net significant difference in HDL
cholesterol. We conclude that 1) insulin resistance had profound effects
on lipoprotein size and subclass particle concentrations for VLDL, LDL,
and HDL when measured by NMR; 2) in type 2 diabetes, the lipoprotein
subclass alterations are moderately exacerbated but can be attributed
primarily to the underlying insulin resistance; and 3) these insulin
resistance-induced changes in the NMR lipoprotein subclass profile
predictably increase risk of cardiovascular disease but were not fully
apparent in the conventional lipid panel. It will be important to study
whether NMR lipoprotein subclass parameters can be used to manage risk
more effectively and prevent cardiovascular disease in patients with the
IRS.

Metabolism. 2000 Mar;49(3):285-92.Links
Impact of insulin resistance on lipoprotein subpopulation distribution
in lean and morbidly obese nondiabetic women.
MacLean PS, Vadlamudi S, MacDonald KG, Pories WJ, Houmard JA, Barakat HA.
Department of Biochemistry, School of Medicine, East Carolina
University, Greenville, NC 27858, USA.
The purpose of this study was to examine the effects of insulin
resistance on the lipoprotein subpopulation distribution of
very-low-density, low-density, and high-density lipoproteins (VLDL, LDL,
and HDL) in lean and morbidly obese nondiabetic women. Lean women (body
mass index [BMI], 20 to 27 kg/m2) stratified by BMI were divided into
insulin-sensitive (SL, n = 12) and insulin-resistant (RL, n = 8) groups
according to Bergman's minimal model, SI. A group of obese women (BMI,
30 to 53 kg/m2), also stratified by BMI, were divided into
insulin-sensitive (SO, n = 10) and insulin-resistant (RO, n = 11) groups
in a similar fashion. Resistant groups were similar to sensitive groups
(SL v RL and SO vRO) in age, weight, percent body fat, and waist
circumference, ie, total and regional adiposity. VLDL, LDL, and HDL
subpopulation distributions were determined in fasting plasma samples by
nuclear magnetic resonance (NMR) spectroscopy. The average particle
sizes of all 3 classes of lipoproteins were similar for the SL and RL
groups. In contrast, RO subjects had larger VLDL, smaller LDL, and
smaller HDL, than SO subjects (P < .05). Lower concentrations of large
LDL and large HDL were found in RO compared with SO subjects (P < .05).
In obese women, but not in lean women, VLDL size was associated with
plasma insulin (r = .60, P < .005), while LDL size and HDL size were
negatively correlated with plasma insulin (r = -.39, P < .05 and r =
-.38, P < .05) and positively correlated with SI (r = .54, P < .01 and r
= .42, P < .05). These results suggest that in obese women, insulin
resistance may be involved in the formation of lipoprotein subpopulation
distributions that are associated with vascular disease.

Int J Cardiol. 2006 Mar 22;108(1):89-95. Epub 2005 Aug 8.
Related Articles, Links

Plasma triglycerides, an independent predictor of cardiovascular disease
in men: a prospective study based on a population with prevalent
metabolic syndrome.

Onat A, Sari I, Yazici M, Can G, Hergenc G, Avci GS.

Turkish Society of Cardiology, Istanbul, Turkey. tkd@tkd.org.tr

BACKGROUND AND METHODS: We aimed to assess whether fasting plasma
triglycerides independently predicted future fatal and nonfatal
cardiovascular disease (CVD) in a population having a high prevalence of
the metabolic syndrome. In the Turkish Adult Risk Factor Study, a
population-based survey, 2682 men and women 20 years of age or over with
fasting triglyceride values available and free of CVD at baseline
examination in 1990, were prospectively followed up till 2003/04.
Triglyceride concentrations were measured by the enzymatic dry chemistry
method and stratified into sex-specific quintiles. Information on the
mode of death was obtained from first-degree relatives and/or health
personnel of local health office. Diagnosis of coronary heart disease
and stroke among survivors was based on history, physical examination of
the cardiovascular system and Minnesota coding of resting
electrocardiograms. A total of 120 fatal and 221 new nonfatal CVD
occurred among adults (mean age 43+/-14) during a mean 9.3 years of
follow-up. RESULTS: CVD was significantly and independently predicted by
the top versus the bottom fasting triglyceride quintile in logistic
regression analyses when adjusted for age, sex, BMI, systolic blood
pressure, total cholesterol, lipid-lowering medication, status of
smoking and of glucose regulation (relative risk [RR] in men and all
adults 2.38 and 1.79, respectively, p both <0.02). This corresponded to
hazard ratios (HR) of 1.43 in men and 1.28 in men and women combined.
Adjustment for HDL-cholesterol instead of total cholesterol in the same
model gave also significant HRs corresponding to 1.42 in men and 1.32 in
sexes combined. CONCLUSIONS: Fasting triglycerides are predictive of
future CVD among men with an HR of 1.4, independent of age, diabetes,
lipid-lowering medication, traditional risk factors including total
cholesterol or HDL-C, in a population in which metabolic syndrome
prevails. A modest independent risk increment in women did not reach
significance.

PMID: 16085325 [PubMed - in process]

Look, obviously you are looking to start another pissing contest
here.    All I did was suggest to Jason the following:

1 - Do some looking of his own online and he'll find plenty of info on
chol guidelines and some controversy on what numbers may be important.

2 - That appropriate chol targets depend on a persons medical history
and their family history, ie risk factors.

3 - I even agreed with you that by any standard, his trig are too
high.

Certainly a relatively benign post.  I wasn't looking to get into the
whole debate over does chol matter, what's the best number to look at,
etc.  Yet, you feel compelled to come back, insisting that
triglycerides alone are the single accepted risk factor for CHD. And
then you get nasty about this?     Just a bit of googling will show
that there are loads of major, reputable health organizations that
have lists of criteria for risk factors that include more than just
triglycerides.  And I don't know of any of them that says trig alone
are the most predicitve CHD risk factor.

Maybe you should check your facts before you start telling someone,
who's medical history you don't know, that he should just listen to
your advice.  And opening a dictionary wouldn't hurt either.  You'd
find the correct spelling of buoyant and atherogenic.  Been reading
much research, have you?

I'd say what's stupid here and what shows how out of touch you are
with scienctific approaches and what is relevant is YOU bringing up
anecdotal evidence, sample size =2, as supporting evidence of
anything.

My position is that you have a guy here asking how to interpret his
chol numbers.  And there is a lot of information out there on
cholesterol, on what numbers are important, which are best, what
targets are appropriate, etc.   And there is considerable
disagreement.   I can find you people who say none of it matters.   I
can point you to the recognized standards from major health
institutions, none of which will back up your claim that trig alone
are the single predictive factor to focus on.     I can point you to
one study that seems to indicate one indicator is more important than
another.   And then other studies that suggest otherwise.   There are
even studies that show mortality for patients given statins for an
extended period of time is substantially lower.   Yes, that's right,
studies that show statins actually save people's lives.  So, he should
do some checking, consult with his Dr, and make up his own mind.

Oh please.  You told him Trig over 100 are most predictive.   Then
stated that the ideal HDL/trig ratio is below 1.5.  Sure sound like
targets to me.    But because they're Susan's targets, well they can't
be called that, because targets are to sell drugs?   Good grief.