Total 253
HDL   60
LDL  129
Triglycerides 303 (Yikes!)
Cardiac Risk Factor 4.0

My questions are:

1.  If HDL and LDL are both within normal range, but the total is in the
high risk range, what are the other types of cholesterol floating around in
my {*filter*} and what affect do they have?

2.  What makes my Triglycerides so high?  It's supposed to be below 200,
right?  I've been watching, very carefully, what I eat for the past 5
months, keeping fat at or below 30% of calorie intake and most of the fat I
eat is monounsaturated.  I also keep cholesterol intake to a minimum, eating
very little meat and get at least 30 grams of fiber a day.  I don't smoke
(stopped 5 or 6 years ago), I do exercise (ergo the HDL at 63) and I get
plenty of fluids and rest.  I do have plenty of stress in my life, but would
that affect my triglycerides?????

Thanks for any insight :-)
M

When the body has elevated iron levels and a lack of vitamin C the
triglycerides will be elevated.

Now how to deal with it?

It might be fairly hard to have the doctor deal with it because what most
doctors believe is a 'safe' level of iron in the body is actually considered by
those in the know .. to actually be too much.

Below you will find a couple of articles which speak to the fact elevated iron
in the body leads to higher triglycerides and the last snip is from Dr. Jerome
Sullivan who first proposed the link between elevated iron levels and
destruction of the heart.

This first article SHOWS what happens in normal meat eaters when you lower
their iron levels down to what vegetarians have.
You will notice the marker used is MUCH lower than that which most doctors
consider to be .. safe.
Obviously .. they are wrong.
---------------------------------------------------------

Br J Nutr 2001 Oct;86(4):515-9

Low iron status and enhanced insulin sensitivity in lacto-ovo vegetarians.

Hua NW, Stoohs RA, Facchini FS
Department of Medicine, Division of Nephrology, San Francisco General Hospital,
San Francisco, CA, USA.

The efficacy of insulin in stimulating whole-body glucose disposal (insulin
sensitivity) was quantified using direct methodology in thirty lacto-ovo
vegetarians and in thirty meat-eaters. All subjects were {*filter*}, lean (BMI <23
kg/m2), healthy and glucose tolerant. Lacto-ovo vegetarians were more insulin
sensitive than meat-eaters, with a steady-state plasma glucose (mmol/l) of 4.1
(95 % CI 3.5, 5.0) v. 6.9 (95 % CI 5.2, 7.5; respectively. In addition,
lacto-ovo vegetarians had lower body Fe stores, as indicated by a serum
ferritin concentration (microg/l) of 35 (95 % CI 21, 49) compared with 72 (95 %
CI 45, 100) for meat-eaters To test whether or not Fe status might modulate
insulin sensitivity, body Fe was lowered by phlebotomy in six male meat-eaters
to levels similar to that seen in vegetarians, with a resultant approximately
40 % enhancement of insulin-mediated glucose disposal Our results demonstrate
that lacto-ovo vegetarians are more insulin sensitive and have lower Fe stores
than meat-eaters. In addition, it seems that reduced insulin sensitivity in
meat-eaters is amenable to improvement by reducing body Fe. The latter finding
is in agreement with results from animal studies where, no matter how induced,
Fe depletion consistently enhanced glucose disposal.

PMID: 11591239, UI: 21475355

--------------------------------------------------------------------------
------

Gastroenterology 2002 Apr;122(4):931-9

Effect of iron depletion in carbohydrate-intolerant patients with clinical
evidence of non{*filter*}ic fatty liver disease.

Facchini FS, Hua NW, Stoohs RA
Department of Medicine, University of California San Francisco and San

BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH) mutations,
and non{*filter*}ic fatty liver disease (NAFLD) tend to cluster in
carbohydrate-intolerant patients. In an attempt to further clarify the
interrelationships among these conditions, we studied 42
carbohydrate-intolerant patients who were free of the common GH mutations C282Y
and H63D, and had a serum iron saturation lower than 50%. METHODS: We measured
body iron stores, and induced iron depletion to a level of near-iron deficiency
(NID) by quantitative phlebotomy. RESULTS: In the 17 patients with clinical
evidence of NAFLD, we could not demonstrate supranormal levels of body iron
(1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a 40%-55%
improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated plasma
insulin concentrations, and near-normalization of serum alanine
aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001).
CONCLUSIONS: These results reflect the insulin-sparing effect of iron depletion
and indicate a key role of iron and hyperinsulinemia in the pathogenesis of
NAFLD.

PMID: 11910345, UI: 21906781

--------------------------------------------------------------------------
------

Snip from article following  ..
----------------------------------------------------------

3) the combination of iron loading with a low ascorbatestatus causes additional
pathophysiological changes, in particular,increased plasma triglycerides.
---------------------------------------------------------
 AJP Endocrinology & MetabolismVitamin C suppresses oxidative lipid damage in
vivo, even in the presence ofiron overloadKent Chen1, Jung Suh1,3, Anitra C.
Carr3, Jason D. Morrow4, John Zeind2, andBalz Frei1,31 The Evans Memorial
Department of Medicine, Whitaker CardiovascularInstitute, Boston University
School of Medicine, Boston 02118; 2 The CoreLaboratory, Beth Israel Hospital
and Deaconess Medical Center, Boston,Massachusetts 02115; 3 The Linus Pauling
Institute, Oregon State University,Corvallis, Oregon 97331; and 4 Departments
of Medicine and Pharmacology,Vanderbilt University School of Medicine,
Nashville, Tennessee 37232Ascorbate is a strong antioxidant; however, it can
also act as a prooxidantin vitro by reducing transition metals. To investigate
the in vivo relevanceof this prooxidant activity, we performed a study using
guinea pigs fed highor low ascorbate doses with or without prior loading with
iron dextran.Iron-loaded animals gained less weight and exhibited
increasedplasma -N-acetyl-D-glucosaminidase activity, a marker of tissue
lysosomalmembrane damage, compared with control animals. The iron-loaded
animals fedthe low ascorbate dose had decreased plasma -tocopherol levels and
increasedplasma levels of triglycerides and F2-isoprostanes, specific and
sensitivemarkers of in vivo lipid peroxidation. In contrast, the two groups
ofanimals fed the high ascorbate dose had significantly lower
hepaticF2-isoprostane levels than the groups fed the low ascorbate
dose,irrespective of iron load. These data indicate that 1) ascorbate acts as
anantioxidant toward lipids in vivo, even in the presence of iron overload;
2)iron loading per se does not cause oxidative lipid damage but is
associatedwith growth retardation and tissue damage, both of which are not
affected byvitamin C; and 3) the combination of iron loading with a low
ascorbatestatus causes additional pathophysiological changes, in
particular,increased plasma triglycerides.

Below are the words of Dr. Jerome Sullivan who first proposed irons'
destruction of the heart.
--------------------------------------------------------------

 Achieving a zero ferritin is diagnostically useful. At a zero level of stored
iron, we can be fairly confident that a state of iron overload is not present
at the time of the determination. The only way to have any real confidence that
stored iron is not contributing to a patholgic process is to remove it and see
if the patient does better clinically. Patients with hepatitis C or diabetes
may have an iron overload in this sense without having the hemochromatosis
genes or the classic histologic findings of liver iron overload. If you insist
that iron overload exists only when stringent, traditional criteria are
satisfied, you may not find a higher proportion of iron overload thus defined
in the study population. Nonetheless removal of small iron burdens may result
in marked clinical improvement. Attached below is the abstract of an important
paper on hepatitis C and phlebotomy. Even after all stored iron was removed and
the liver function tests improved, removal of more iron resulted in more
improvement even after ferritin bottomed out. I would argue that these patients
had a clinically significant degree of iron overload even though the amount of
iron in question was microscopic in comparison with the amounts seen in
traditional iron overload. Studies showing that a certain percentage of
patients with this or that illness have iron overload are deeply flawed. By
only looking at massive iron overload these studies are blind to any important
effects of lower stored iron levels. Jerome L. Sullivan, MD, PhD

From: Jerome Sullivan
Subject: Re: Ferritin levels References:  2 I don't feel that arbitrary low
target values for ferritin are very valuable. Their main use seems to be to
keep ferritin above zero, as if the patient would suddenly collapse if zero
ferritin was reached. I would remind the list again that volunteer {*filter*} donors
are not required to have ferritin measured. Ever! That means that, so far as
the FDA and the {*filter*} Bank community are concerned, a volunteer donor's serum
ferritin can fall straight to zero and stay there as long as the donor
continues to donate regularly. This is not at all an impossibility. Donors are
allowed to donate every 8 weeks and they are not required to take iron.
Remember that most donors do not have HH genes and so are not "protected" from
a zero ferritin by the fast iron absorption of hemochromatosis patients. Thus
they are at increased "risk" of having a zero ferritin. Does this matter? No!
Volunteer donors do fine, in fact recent studies suggest that they do better
that non donors in terms of heart attacks. Donors are required to have the
hemoglobin level checked. As long as they pass the hemoglobin test they can
donate even if their ferritin is unmeasurably low. A normal hemoglobin assures
us that the donor has enough iron for all normal needs even if the donor has a
flat zero level of stored iron. All this stuff about having one iron loaded
organ and one iron deficient organ at the same time is just idle speculation.
The totality of evidence says that a normal hemoglobin level means you have
enough ...

read more »

--
Dr. Andrew B. Chung, MD/PhD
Atlanta Cardiologist
http://www.***.com/

cut out carbs, or switch the type of carbs, try whole wheat pasta, whole
wheat breads, or whole wheat anything

Judi

Thanks for the helpful advice, everyone :-)  I'll be trying to adjust the
percentage of calories from protein and carbs in my diet, as well as watch
for the kinds of carbs I'm eating.  I'm already getting most of my fats as
monounsaturated and eating mostly whole grain things, but I really need to
up the intake of veggies and decrease the intake of bread, I think, as well
as start eating more fish.

I'll get another lipid profile in about 6 months and see what effect I'm
having.  I figure if I can learn to control these things now (at age 38)
without medication, then I'll never have to take medication for them.

Thanks again :-)
Michelle