Dr. Scott M. Grundy
-- Responsible For The DietWhich Is Killing America!
Here is one of the hidden architects of the massive billions suckered out of victims
who fall for the lies put out by the American Heart Association, and
the Government. He has participated in more than 250 "research
studies" where his name is shown as one of the authors. Perhaps more than any
other individual he is responsible for the lies about cholesterol and the sale of billions
of dollars of harmful "cholesterol lowering drugs."
I have listed about 80 of the studies he has done, below. There
are many more like these.
I wrote about Dr. Grundy many years ago, in my Book, Life Flow One,
The Solution For Heart Disease. Dr. Grundy was the man who introduced
the terrible diet into the American Heart Association, which then released it to the
public, and got all the traditional doctors to recommend it. It actually causes
heart disease -- rather than prevent it. Avoid that diet at all costs -- remember
Dr. Grundy as the author of death!
Read, below, some of the text from that book, about Dr. Grundy. Anything authored
by him you must suspect of exactly opposite of the truth. You will often find him
NOT listed as the primary author, so that some younger person can begin to build up a
(false) reputation for this mythical science called "high cholesterol disease."
But, you'll find, hidden, influences and money from the drug industries which
control our current health care system.
Here is an "official" biography:
Scott M. Grundy, M.D., Ph.D.
Professor of Internal Medicine and Biochemistry

Biochemistry & Molecular Biology
email: grundy01@utsw.swmed.edu
214-648-2890
FAX: 214-648-4837
Our research at the Center for Human Nutrition is concerned with the causes of
hypercholesterolemia in humans. We have been able to identify several major causes of
hypercholesterolemia beyond those resulting from genetic absence of the LDL receptors. We
have found that some of these disorders are due to a reduced expression of LDL receptors,
defective LDL particles that bind poorly to LDL receptors, excess formation of LDL
particles and LDL that are overloaded with cholesterol. We are examining which of these
abnormalities are due to genetics and which are due to dietary influence.
In addition we are studying an abnormality in cholesterol transport that we have named
"atherogenic dyslipidemia", a syndrome characterized by a complex of lipoprotein
disorders. Three important factors related to this syndrome are under investigation: an
enzyme-lipoprotein lipase, an hepatic triglyceride lipase and one transport protein called
cholesterol ester transport protein.
Additionally we are carrying out studies on the role of antioxidant vitamins in the
prevention of coronary heart disease. We are studying the dietary fatty acids and their
role in suppression of the immune system as well as their role in coronary heart disease.
We are continuing our studies in Diabetes Mellitus and we currently are studying the
effects of obesity on insulin resistance.
--------------------
Jialal I and Grundy SM (1992) Effect of dietary supplementation with alpha-tachopherol
on the oxidative modification of low density lipoprotein . J Lipid Res 33:899-906
Vega GL and Grundy SM (1993) Occurrence of species of low-density lipoprotein with
defective clearance in patients with primary moderate hypercholesterolemia. Atherosclerosis
and Thrombosis 13:579-589
Denke MA and Grundy SM (1994) Individual responses to a cholesterol-lowering diet in
fifty men with moderate hypercholesterolemia. Arch Int Med 154:317-325
Denke MA (1994) Individual responsiveness to a cholesterol-lowering diet in
postmenopausal women with moderate hypercholesterolemia. Arch Int Med 154:1977-1982
Cohen JC, Wang Z, Grundy SM, Stoesz MR and Guerra R (1994) Variation at the hepatic
lipase and apolipoprotein AI/CIII/AIV loci is a major cause of genetically determined
variation in plasma HDL cholesterol levels. J Clin Invest 94:2377-2384
Garg A, Bantle JP, Henry RR, Coulston AM, Griver KA, Raatz SK, Brinkley L, Chen Y-Di,
Grundy SM, Huet BA and Reaven GM (1994) Effects of varying carbohydrate content of diet in
patients with non-insulin-dependent diabetes mellitus. JAMA 271:1421-1428
The War On America
From Page 90+ of Life Flow One, The Solution For
Heart Disease
By Karl Loren
There are all sorts of wars. The most insidious are those where the enemy is
completely hidden and the victim thinks he is receiving help. In fact, this was was
the final chapter in the intended betrayal of America into the hands of the legalized drug
cartels.
The planning for this final attack started in 1971, immediately after the Framingham
Study was released. Remember that the Framingham Study, itself, made no finding that
dietary cholesterol caused heart disease -- in fact it found exactly the opposite.
But, the master planners simply took the color "white" and called it
"black!"
In 1971 these master planners formed the Task Force on Arteriosclerosis. The
terrible story behind this corrupt group is very well told by Thomas Moore in his Book,
heart Failure.
Over many pages, in great detail, Mr. Moore reports on individual master planners.
There was a peak in their activities in December 1984 when they formed the Consensus
Development Conference.
One of these master planners was Dr. Daniel Steinbert, a physician who worked on
cholesterol drug research at the University of California at San Diego. he was the
Chairman of the conference and cut off any speaker who criticized the lie that was being
launched. he is, perhaps, the father of death by cholesterol lies!
Another master planner was Dr. Robert I. Levy of Columbia University.
Another master planner was Dr. Richard Peto, an Oxford University epidemiologist.
Technically, the head master planner was Dr. Basil M. Rifkind. He presented false
data to the Conference and Dr. Steinberg cut off any debate on it. Dr. Rifkind. had taken
over from Dr. Steinberg, in some flawed research referred to as the Coronary Primary
Prevention Trial, CPPT, of which more later. (Dr. Rifkind has been active spreading
lies and preventing truth even a few years ago. he has not disappeared!)
Dr. Rifkind said, at the time: It is thought to be the first study in man to
establish conclusively that lowering cholesterol reduces heart attacks and heart attack
deaths."
Dr. William E. Conner, another master planner, from the Oregon Health Sciences
University, told the Conference that the best method to lower cholesterol in the blood was
a stringent diet, with lower cholesterol. This is false, but was presented with a
straight face and fancy slides.
Another master planner was Scott M. Grundy, author of the American Heart Association
diet which warned against butter and eggs. This may well have been the first point
where the hidden puppeteers emerged into some public view. From the viewpoint of the
hidden master planners, the American heart Association would be the best agency to take
over since it could then give its blessing to all the research and promotion of the drug
cure of the cholesterol disease!
You find it hard to believe that these lies were hatched in so blatant a fashion?
As powerful as Dr. Steinberg was, controlling the out-come of this Conference, the real
masters were still behind the scenes -- the puppeteers pulling the strings.
There were prominent scientists who objected to this steam-roller being pushed along by
Dr. Steinberg.
Ad. Edward H. Ahrens, Jr., from Rockefeller University said:
"I think the public is being hosed by the a NIH and the American heart
Association.
They desire to do something good. They're hoping to God that this is the right
thing to do. But they are not acting on the basis of scientific evidence, but on the
basis of a plausible but untested idea."
Another objector was Dr. Thomas Chalmers, of Mt. Sinai Medical School and the Harvard
School of Public Health:
"They have made an unconscionable exaggeration of all the data."
Another objector was David Kritchevsky who announced that his research did NOT show
that dietary cholesterol caused blood cholesterol.
Another objector, simply ignored by Steinberg, was Robert E. Olson, a physician and
specialist on nutrition at the State University of new York who said:
"We have to keep an open mind on whether we understand this disease or not.
My view is that we do not."
Two objectors (Ahrens and Corday) felt so strongly about the conclusions being rammed
down their throats by Steinberg that they wanted to issue a minority report. They
were simp;ly manipulated out of the way. There WAS no minority report.
Remember, this was all happening around Christmas time, in an academic setting, in
1984. This made no news for your local paper!
The conclusions of the Conference had already been prepared before the participants
met. The concept of the findings appeared much earlier, in 1982, written by the
American Heart Association.
By 1985, with all the powerful lies placed in the media and corrupt medical journals,
the final plan for the attack on America was given a name:
National Cholesterol Education
Program
You won't hear much about this attack today because, fortunately, it failed -- mostly.
It was launched in 1987.
In 1987 I had already, for more than two years, been heavily involved in giving
lectures on heart disease. One of the first persons who ever heard me was Bob
Hutton, in 1985. he tried the vitamin formula I recommended, and some months latter
wrote this letter to me:
Dear Karl,
You asked me to report on my feelings after taking your vitamin formula.
May I go back in history?
Nine years ago I had colon cancer which required two operations in 8 days. I am
completely cured -- only a little scar and 3 feet less of large colon.
Three years ago I had a double bypass and was told that I already was living on
borrowed time.
Three weeks later the colon operation developed adhesions and I had another major
operation.
Before that I had had 16 intravenous chelation treatments.
This leads me to always believe that I was kidnapped and the whole thing was created by
a spasm of the heart! This fact was verified by my regular doctor - the one who gave
me the chelation. Before Christmas I had 4 chelations -- one a month.
From that time on I had no treatments until I began taking your formula.
I was dizzy at times; my fingers turned gray and numb upon exposure to cold; and I was
getting short of breath.
After taking Life Glow for only two weeks my dizziness disappeared. My fingers no
longer responded negatively to cold. And I have a lot of energy. I was walking
at the rate of 15 minutes per mile for three or four miles almost every day.
Now, after two months of your vitamin formula I find even bigger improvements. I
am a member of Golden K (Kiwanis for old retired men). Yesterday we planted flowers
around a retirement home.
I am not the youngest member but I did more work than any six of the others. I pushed a
rototiller, then spaded more ground and planted flowers while on my knees without a single
pain getting up.
If you have ever gardened you'll realize that work that I did. Today, I
remembered that I had a knee that used to lock and pain when I arose from kneeling.
I feel truly great, ready for many more years to add to my 71. there seems to be
one flaw in your formula; physically I feel great but I see no improvement in my mind.
Of course, if you have nothing to build upon you can produce no results.
I know this is too long for your wants, so feel free to shorten and paraphrase. I
would say that after taking your formula for only two weeks my dizziness disappeared and
my circulation improved greatly. After 2 months I have much more energy and I found
my carotid artery had opened up.
My long ago injured knee is responding in a wonderful manner. I have the energy
of a fifty year old.
We leave for Canada the last of this month, where I will be chopping wood, moving
boats, lifting logs and walking over hills -- and fishing.
As ever,m
Robert L. Hutton.
Read more of this expose of the cholesterol fraud in my Book, Life Flow One, The
Solution For Heart Disease.
Lovastatin
=
Mevacor
Here is one of the most evil drugs in traditional medicine. There are far worse
drugs used in psychiatry, but for traditional medicine the false disease of "high
cholesterol" has long been the target of the harmful drug with the generic name
"Lovastatin." It is better known as the Merck drug which makes BILLIONS of
dollars for Merck:
Official From Merck:
ADVERSE REACTIONS
MEVACOR is generally well tolerated; adverse reactions usually have been mild and
transient. Less than 1% of patients were discontinued from controlled clinical studies of
up to 14 weeks due to adverse experiences attributable to MEVACOR. About 3% of patients
were discontinued from extensions of these studies due to adverse experiences attributable
to MEVACOR; about half of these patients were discontinued due to increases in serum
transaminases. The median duration of therapy in these extensions was 5.2 years.
In the EXCEL study ( see CLINICAL PHARMACOLOGY, Clinical Studies), 4.6% of the
patients treated up to 48 weeks were discontinued due to clinical or laboratory adverse
experiences which were rated by the investigator as possibly, probably or definitely
related to therapy with MEVACOR. The value for the placebo group was 2.5%.
Clinical Averse Experiences
Adverse experiences reported in patients treated with MEVACOR in controlled clinical
studies are shown in the table below.
MEVACOR Placebo Cholestyramine Probucol
(N=613) (N=82) (N=88) (N=97)
% % % %
Gastrointestinal
Constipation 4.9 -- 34.1 2.1
Diarrhea 5.5 4.9 8.0 10.3
Dyspepsia 3.9 -- 13.6 3.1
Flatus 6.4 2.4 21.6 2.1
Abdominal pain/cramps 5.7 2.4 5.7 5.2
Heartburn 1.6 -- 8.0 --
Nausea 4.7 3.7 9.1 6.2
Musculoskeletal
Muscle cramps 1.1 -- 1.1 --
Myalgia 2.4 1.2 -- --
Nervous System/Psychiatric
Dizziness 2.0 1.2 -- 1.0
Headache 9.3 4.9 4.5 8.2
Skin
Rash/pruritus 5.2 -- 4.5 --
Special Senses
Blurred vision 1.5 -- 1.1 3.1
Dysgeusia 0.8 -- 1.1 --
Laboratory
Tests
Marked persistent increases of serum transaminases have been noted
(see WARNINGS).
About 11% of patients had elevations of creatine phosphokinase (CPK) levels of at least
twice the normal value on one or more occasions. The corresponding values for the control
agents were cholestyramine, 9 percent and probucol, 2 percent. This was attributable to
the noncardiac fraction of CPK. Large increases in CPK have sometimes been reported (see
WARNINGS, Skeletal Muscle).
Expanded Clinical Evaluation of Lovastatin (EXCEL) Study
Clinical Adverse Experiences
MEVACOR was compared to placebo in 8,245 patients with hypercholesterolemia (total
cholesterol 240,300 mg/dL in the randomized, double-blind, parallel, 48-week EXCEL study.
Clinical adverse experiences reported as possibly, probably or definitely drug-related in
> or = to 1% in any treatment group are shown in the table below. For no event was the
incidence on drug and placebo statistically different.
Placebo MEVACOR MEVACOR MEVACOR MEVACOR
20mg q.p.m. 40mg q.p.m. 20mg b.i.d. 40mg b.i.d.
(N=1663) (N=1642) (N=1645) (N=1646) (1649)
% % % % %
Body As a Whole
Asthenia 1.4 1.7 1.4 1.5 1.2
Gastrointestinal
Abdominal pain 1.6 2.0 2.0 2.2 2.5
Constipation 1.9 2.0 3.2 3.2 3.5
Diarrhea 2.3 2.6 2.4 2.2 2.6
Dyspepsia 1.9 1.3 1.3 1.0 1.6
Flatulence 4.2 3.7 4.3 3.9 4.5
Nausea 2.5 1.9 2.5 2.2 2.2
Musculoskeltal
Muscle Cramps 0.5 0.6 0.8 1.1 1.1
Myalgia 1.7 2.6 1.8 2.2 3.0
Nervous System/
Psychiatric
Dizziness 0.7 0.7 1.2 0.5 0.5
Headache 2.7 2.6 2.8 2.1 3.2
Skin
Rash 0.7 0.8 1.0 1.2 1.3
Special Senses
Blurred vision 0.8 1.1 0.9 0.9 1.2
Other clinical adverse experiences reported as possibly, probably or definitely
drug-related in 0.5 to 1.0 percent of patients in any drug-treated group are
listed below. In all these cases the incidence on drug and placebo was not
statistically different. Body as a Whole: chest pain;
Gastrointestinal: acid regurgitation, dry mouth, vomiting;
Musculoskeletal: leg pain, shoulder pain, arthralgia; Nervous
System/Psychiatric: insomnia, paresthesia; skin: alopecia,
pruritus; Special Senses: eye irritation.
Concomitant Therapy
In controlled clinical studies in which lovastatin was administered concomitantly with
cholestyramine, no adverse reactions peculiar to this concomitant treatment were observed.
The adverse reactions that occurred were limited to those reported previously with
lovastatin or cholestyramine. Other lipid-lowering agents were not administered
concomitantly with lovastatin during controlled clinical studies. Preliminary data
suggests that the addition of either probucol or gemfibrozil to therapy with lovastatin is
not associated with greater reduction in LDL cholesterol than that achieved with
lovastatin alone. In uncontrolled clinical studies, most of the patients who have
developed myopathy were receiving concomitant therapy with immunosuppressive drugs,
gemfibrozil or niacin (nicotinic acid) (see WARNINGS Skeletal Muscle).
The following effects have been reported with drugs in this class. Not all the effects
listed below have necessarily been associated with lovastatin therapy.
Skeletal: muscle cramps, myalgia, myopathy, rhabdomyolysis, arthralgias.
Neurological: dysfunction of certain cranial nerves (including alteration of
taste, impairment of extra-ocular movement, facial paresis), tremor, dizziness, vertigo,
memory loss, paresthesia, peripheral neuropathy, peripheral nerve palsy, psychic
distrubances, anxiety, insomnia, depression.
Hypersensitivity Reactions: An apparent hypersensitivity syndrome has been
reported rarely which has included one or more of the following features: anaphylaxis,
angioedema, lupus erythematous-like syndrome, polymyalgia rheumatica, vasculitis, purpura,
thrombocytopenia, leukopenia, hemolytic anemia, positive ANA, ESR increase, eosinophilia,
arthritis, arthralgia, urticaria, asthenia, photosensitivity, fever, chills, flushing,
malaise, dyspnea, toxic epidermal necrolysis, erythema multiforme, including
Stevens-Johnson syndrome.
Gastrointestinal: pancreatitis, hepatitis, including chronic active hepatitis,
cholestatic jaundice, fatty change in liver; and rarely, cirrhosis, fulminant hepatic
necrosis, and hepatoma; anorexia, vomiting.
Skin: alopecia, pruritus. A variety of skin changes (e.g., nodules,
discoloration, dryness of skin/mucous membranes, changes to hair/nails) have been
reported.
Reproductive: gynecomastia, loss of libido, erectile dysfunction.
Eye: progression of cataracts (lens opacities), ophthalmoplegia.
Laboratory Abnormalities: elevated transaminases, alkaline phosphatase,
gamma-glutamyl transpeptidase, and bilirubin; thyroid function abnormalities.
Studies
Featuring Dr. Scott M. Grundy
Top Of Menu
Number |
Title |
Karl Loren Comments |
| A1 |
Linkage between cholesterol 7alpha-hydroxylase and high plasma low-density
lipoprotein cholesterol concentrations. |
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| A2 |
Effects of crystalline nicotinic acid-induced hepatic dysfunction on serum
low-density lipoprotein cholesterol and lecithin cholesteryl acyl transferase. |
The lie about niacin appears here. |
| A3 |
Effect of statins on metabolism of apo-B-containing lipoproteins in
hypertriglyceridemic men. |
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| A4 |
Hypertriglyceridemia, atherogenic dyslipidemia, and the metabolic
syndrome. |
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| A5 |
Hepatic lipase activity is lower in African American men than in white
American men: effects of 5' flanking polymorphism in the hepatic lipase gene (LIPC). |
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| A6 |
Multifactorial causation of obesity: implications for prevention. |
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| A7 |
Influence of stearic acid on cholesterol metabolism relative to other
long-chain fatty acids. |
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| A8 |
Effects of varying carbohydrate content of diet in patients with
non-insulin-dependent diabetes mellitus [see comments] |
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| A9 |
Prediction of total subcutaneous abdominal, intraperitoneal, and
retroperitoneal adipose tissue masses in men by a single axial magnetic resonance imaging
slice. |
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| A10 |
Estimation of adipose tissue mass by magnetic resonance imaging:
validation against dissection in human cadavers. |
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| A11 |
Variation at the hepatic lipase and apolipoprotein AI/CIII/AIV loci is a
major cause of genetically determined variation in plasma HDL cholesterol levels. |
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| A12 |
Effectiveness of low-dose crystalline nicotinic acid in men with low
high-density lipoprotein cholesterol levels. |
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| A13 |
Hypercholesterolemia with cholesterol-enriched LDL and normal levels of
LDL-apolipoprotein B. Effects of the step I diet and bile acid sequestrants on the
cholesterol content of LDL. |
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| A14 |
Genetic analysis of a polymorphism in the human apolipoprotein A-I gene
promoter: effect on plasma HDL-cholesterol levels. |
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| A15 |
RRR-alpha-tocopheryl acetate supplementation at pharmacologic doses
decreases low-density-lipoprotein oxidative susceptibility but not protein glycation in
patients with diabetes mellitus. |
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| A16 |
What is the desirable ratio of saturated, polyunsaturated, and
monounsaturated fatty acids in the diet? |
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| A17 |
Cholesterol management in patients with heart disease. Emphasizing
secondary prevention to increase longevity. |
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| A18 |
Determinants of plasma HDL-cholesterol in hypertriglyceridemic patients.
Role of cholesterol-ester transfer protein and lecithin cholesteryl acyl transferase. |
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| A19 |
Cholestyramine therapy for dyslipidemia in non-insulin-dependent diabetes
mellitus. A short-term, double-blind, crossover trial. |
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| A20 |
Addressing the spectrum of hypercholesterolemia [see comments] |
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| B1 |
Influence of exchanging carbohydrate for saturated fatty acids on plasma
lipids and lipoproteins in men. |
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| B2 |
Incorporation of radioactive phospholipid into subclasses of high-density
lipoproteins. |
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| B3 |
Increased low density lipoprotein production associated with obesity. |
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| B4 |
Normocholesterolemic tendon xanthomatosis with overproduction of
apolipoprotein B. |
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B5 |
Overproduction of low density lipoproteins associated with coronary heart
disease. |
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| B6 |
Effect of bile acid conjugation pattern on bile acid metabolism in normal
humans. |
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| B7 |
Effects of haem infusion on biliary secretion of porphyrins, haem and
bilirubin in man. |
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| B8 |
National Cooperative Gallstone Study: the effect of chenodeoxycholic acid
on lipoproteins and apolipoproteins. |
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| B9 |
Metabolism of cholesterol and plasma triglycerides in nonketotic diabetes
mellitus. |
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| B10 |
Hypertriglyceridemia: mechanisms, clinical significance, and treatment. |
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| B11 |
Intestinal absorption of polyenephosphatidylcholine in man. |
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Effect of ascorbate supplementation on low density lipoprotein oxidation
in smokers. |
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Very low density lipoprotein metabolism in non-ketotic diabetes mellitus:
effect of dietary restriction. |
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D9HealthGate Documents
Section A
Record 1 from database: MEDLINE
Go To The Top
- Title
- Linkage between cholesterol 7alpha-hydroxylase and high plasma low-density lipoprotein
cholesterol concentrations.
- Author
- Wang J; Freeman DJ; Grundy SM; Levine DM; Guerra R; Cohen JC
- Address
- The Center for Human Nutrition, Dallas, Texas 75235-9052, USA.
- Source
- J Clin Invest, 1998 Mar, 101:6, 1283-91
- Abstract
- Interindividual differences in plasma low-density lipoprotein cholesterol (LDL-C) levels
reflect both environmental variation and genetic polymorphism, but the specific genes
involved and their relative contributions to the variance in LDL-C are not known. In this
study we investigated the relationship between plasma LDL-C concentrations and three genes
with pivotal roles in LDL metabolism: the low-density lipoprotein receptor (LDLR),
apolipoprotein B (APOB), and cholesterol 7alpha-hydroxylase (CYP7). Analysis of 150
nuclear families indicated statistically significant linkage between plasma LDL-C
concentrations and CYP7, but not LDLR or APOB. Further sibling pair analyses using
individuals with high plasma LDL-C concentrations as probands indicated that the CYP7
locus was linked to high plasma LDL-C, but not to low plasma LDL-C concentrations. This
finding was replicated in an independent sample. DNA sequencing revealed two linked
polymorphisms in the 5' flanking region of CYP7. The allele defined by these polymorphisms
was associated with increased plasma LDL-C concentrations, both in sibling pairs and in
unrelated individuals. Taken together, these findings indicate that polymorphism in CYP7
contributes to heritable variation in plasma LDL-C concentrations. Common polymorphisms in
LDLR and APOB account for little of the heritable variation in plasma LDL-C concentrations
in the general population.
- Language of Publication
- English
- Unique Identifier
- 98171515
- MeSH Heading (Major)
- Apolipoproteins B|BL/*GE/ME; Cholesterol 7 alpha-Monooxygenase|*GE/ME; Lipoproteins, LDL
Cholesterol|BL/*GE/*ME; Receptors, LDL|*GE/ME
- MeSH Heading
- Adult; Alleles; Apolipoproteins E|BL/GE/ME; Cholesterol|BL; DNA|AN/GE; Female; Human;
Linkage (Genetics); Lipoproteins|BL; Male; Middle Age; Pedigree; Polymerase Chain
Reaction; Polymorphism (Genetics); Sequence Analysis, DNA; Support, U.S. Gov't, P.H.S.;
Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0021-9738
- Country of Publication
- UNITED STATES
Section A
Record 2 from database: MEDLINE
Go To The Top
Title
- Effects of crystalline nicotinic acid-induced hepatic dysfunction on serum low-density
lipoprotein cholesterol and lecithin cholesteryl acyl transferase.
- Author
- Tatò F; Vega GL; Grundy SM
- Address
- Department of Clinical Nutrition of the University of Texas Southwestern Medical Center
and The Veterans Affairs Medical Center at Dallas, 75235-9052, USA.
- Source
- Am J Cardiol, 1998 Mar, 81:6, 805-7
- Abstract
- Marked lowering of plasma total and low-density lipoprotein cholesterol levels that
occur during treatment of dyslipidemia with pharmacologic doses of nicotinic acid result
from hepatotoxicity. Therefore, a marked reduction in low-density lipoprotein may suggest
generalized liver toxicity and drug treatment should be discontinued.
-
The above section, in red, represents totally false and deceptive information
about niacin. There is a tremendous and important role that niacin can
play in your health. Rigged "tests" and results such as this are the
basis, later, for the drug companies to attempt to get niacin banned from sale
on the basis that it is dangerous. These false studies need to be
identified as they pop up -- Dr. Scott M. Grundy has depended on false reports
for the spurious claims he makes. Karl.
- Language of Publication
- English
- Unique Identifier
- 98186331
- MeSH Heading (Major)
- Acyltransferases|*ME; Lipoproteins, LDL Cholesterol|*BL; Liver|*PP; Liver
Diseases|*BL/*CI/PP; Niacin|*AE; Phosphatidylcholines|*ME
- MeSH Heading
- Case Report; Human; Liver Function Tests; Male; Middle Age; Support, Non-U.S. Gov't;
Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0002-9149
- Country of Publication
- UNITED STATES
Section A
Record 3 from database: MEDLINE
Go To The Top
- Title
- Effect of statins on metabolism of apo-B-containing lipoproteins in hypertriglyceridemic
men.
- Author
- Vega GL; Grundy SM
- Address
- Center for Human Nutrition and Department of Clinical Nutrition, University of Texas
Southwestern Medical Center at Dallas and the Veterans Affairs Medical Center at Dallas,
75235-9052, USA.
- Source
- Am J Cardiol, 1998 Feb, 81:4A, 36B-42B
- Abstract
- Our investigations indicate that most patients with moderate hypertriglyceridemia have
marked defects in the metabolism of low-density lipoprotein (LDL) apolipoprotein B.
Moreover, these patients have 2 major defects in the metabolism of triglyceride-rich
lipoproteins, i.e., an accumulation of remnant lipoproteins (due in part to delayed
hepatic clearance) and increased fractional conversion of very-low-density lipoprotein
(VLDL) to LDL. Defective triglyceride-rich lipoprotein metabolism has been associated with
insulin resistance. Statin therapy in hypertriglyceridemic patients improves the
lipoprotein profile by decreasing both LDL cholesterol and remnant lipoproteins. However,
statin therapy does not normalize LDL apolipoprotein B metabolism, and high-density
lipoprotein (HDL) cholesterol levels remain low. Therefore, consideration may be given to
combining a statin with a drug that alters triglyceride metabolism (e.g., fibrate or
nicotinic acid) in high-risk patients with hypertriglyceridemia.
- Language of Publication
- English
- Unique Identifier
- 98186007
- MeSH Heading (Major)
- Antilipemic Agents|*TU; Apolipoproteins B|*ME; Hydroxymethylglutaryl-CoA Reductase
Inhibitors|*TU; Hypertriglyceridemia|DT/*ME; Lipoproteins, LDL|*ME; Lovastatin|*TU
- MeSH Heading
- Comparative Study; Gemfibrozil|TU; Human; Insulin Resistance; Lipoproteins|BL;
Lipoproteins, LDL Cholesterol|BL; Lipoproteins, VLDL Cholesterol|BL; Male; Niacin|TU
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-9149
- Country of Publication
- UNITED STATES
Section A
Record 4 from database: MEDLINE
Go To The Top
- Title
- Hypertriglyceridemia, atherogenic dyslipidemia, and the metabolic syndrome.
- Author
- Grundy SM
- Address
- Department of Clinical Nutrition, Center for Human Nutrition, University of Texas
Southwestern Medical Center at Dallas, 75235-9052, USA.
- Source
- Am J Cardiol, 1998 Feb, 81:4A, 18B-25B
- Abstract
- The importance of high serum cholesterol, especially a high level of low-density
lipoprotein (LDL) cholesterol, as a risk factor for coronary artery disease is well
established. Likewise, efficacy for decreasing risk for coronary artery disease by
LDL-lowering therapy has recently been documented through clinical trials. However, many
high-risk patients manifest elevated serum triglyceride levels, and the role of
hypertriglyceridemia in causation of coronary artery disease remains to be elucidated.
Nonetheless, there is growing evidence that hypertriglyceridemia is a marker for increased
risk for coronary artery disease; in fact, it can serve as a marker for several
atherogenic factors. These factors include increased concentrations of atherogenic
triglyceride-rich lipoproteins; the atherogenic lipoprotein phenotype, or lipid triad; and
the metabolic syndrome. The lipid triad consists of elevated serum triglycerides, small
LDL particles, and low high-density lipoprotein (HDL) cholesterol. The metabolic syndrome
includes the coexistence of the lipid triad, elevated blood pressure, insulin resistance
(plus glucose intolerance), and a prothrombotic state. Many previous studies indicate that
hypertriglyceridemia is strongly associated with all of these atherogenic factors. The
clinical approach to treatment of patients with hypertriglyceridemia thus requires a
broad-based strategy that includes reduction of atherogenic triglyceride-rich
lipoproteins, reversal of the lipid triad, and favorable modification of the metabolic
syndrome. The development of therapeutic regimens to effect these changes poses a
challenge for future research on the problem of hypertriglyceridemia.
- Language of Publication
- English
- Unique Identifier
- 98186004
- MeSH Heading (Major)
- Atherosclerosis|*ME; Hyperlipidemia|*ME; Hypertriglyceridemia|DT/EP/GE/*ME
- MeSH Heading
- Animal; Antilipemic Agents|TU; Coronary Disease|ET; Human; Hydroxymethylglutaryl-CoA
Reductase Inhibitors|TU; Hypertension|CO; Insulin Resistance; Lipoproteins, HDL
Cholesterol|BL; Lipoproteins, LDL|BL; Lipoproteins, LDL Cholesterol|BL; Lipoproteins,
VLDL|BL; Multivariate Analysis; Risk Assessment; Risk Factors; Syndrome; Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-9149
- Country of Publication
- UNITED STATES
Section A
Record 5 from database: MEDLINE
Go To The Top
- Title
- Hepatic lipase activity is lower in African American men than in white American men:
effects of 5' flanking polymorphism in the hepatic lipase gene (LIPC).
- Author
- Vega GL; Clark LT; Tang A; Marcovina S; Grundy SM; Cohen JC
- Address
- The Center for Human Nutrition, Department of Clinical Nutrition, University of Texas
Southwestern Medical Center, Dallas 75235-9052, USA.
- Source
- J Lipid Res, 1998 Jan, 39:1, 228-32
- Abstract
- Plasma high density lipoprotein cholesterol (HDL-C) concentrations are higher in African
American men than in white men, but the mechanism(s) responsible for this ethnic
difference has not been elucidated. This study examined the relationship between hepatic
lipase activity, plasma HDL-C concentrations, and a hepatic lipase polymorphism (-514T) in
African American and white American men. Consistent with previous reports, plasma HDL-C
concentrations were significantly higher in African American men than in white American
men. Mean post-heparin plasma hepatic lipase activity was significantly lower in African
American than in white American men (27 +/- 12 vs. 44 +/- 17 mmol x h(-1) x l(-1), P <
0.001). The -514T hepatic lipase allele was associated with low hepatic lipase activity in
both populations, and was 3-fold more common among African Americans than white Americans.
Taken together, these data suggest that genetic differences in hepatic lipase activity
contribute to the differences in plasma HDL-C concentrations between African American men
and white American men.
- Language of Publication
- English
- Unique Identifier
- 98129503
- MeSH Heading (Major)
- Caucasoid Race|*; Lipase|*BL/*GE; Liver|*EN; Negroid Race|*; Polymorphism (Genetics)|*
- MeSH Heading
- Adult; Alleles; Genotype; Heparin|BL; Heterozygote; Homozygote; Human; Lipoproteins, HDL
Cholesterol|BL; Male; Polymerase Chain Reaction; Support, Non-U.S. Gov't; Support, U.S.
Gov't, Non-P.H.S.; Support, U.S. Gov't, P.H.S.; United States
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0022-2275
- Country of Publication
- UNITED STATES
Section A
Record 6 from database: MEDLINE
Go To The Top
- Title
- Multifactorial causation of obesity: implications for prevention.
- Author
- Grundy SM
- Address
- Department of Clinical Nutrition, Center for Human Nutrition, University of Texas
Southwestern Medical Center at Dallas, 75235-9052, USA. sgrund@mednet.swmed.edu
- Source
- Am J Clin Nutr, 1998 Mar, 67:3 Suppl, 563S-72S
- Abstract
- Obesity threatens to become the foremost cause of chronic disease in the world. Being
obese can induce multiple metabolic abnormalities that contribute to cardiovascular
disease, diabetes mellitus, and other chronic disorders. Unfortunately, prevalence of
obesity is increasing both in the United States and worldwide. Reasons for the rising
prevalence include urbanization of the world's population, increased availability of food
supplies, and reduction of physical activity. Although severe obesity has received much
attention in the clinical setting, most obesity in the general public is only moderate.
Even so, moderate obesity can elicit several metabolic abnormalities that are precursors
to chronic disease. Therefore, for the population as a whole, moderate obesity is
responsible for most obesity-related disorders. Moderate obesity is undoubtedly
multifactorial in origin, and acquired influences probably exceed genetic factors in its
causation. These acquired causes thus deserve greater attention in the development of a
public health strategy for the control of overweight in the general population. A major
public health effort is urgently needed to counter the increasing frequency of moderate
obesity in the United States and throughout the world.
- Language of Publication
- English
- Unique Identifier
- 98156903
- MeSH Heading (Major)
- Obesity|*/PC
- MeSH Heading
- Aging|ME/PH; Basal Metabolism; Coronary Disease|BL/CO; Cultural Characteristics; Dietary
Fats|AD; Disease Susceptibility|GE; Energy Intake; Exercise; Human; Risk Factors
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0002-9165
- Country of Publication
- UNITED STATES
Section A
Record 7 from database: MEDLINE
Go To The Top
- Title
- Influence of stearic acid on cholesterol metabolism relative to other long-chain fatty
acids.
- Author
- Grundy SM
- Address
- Department of Internal Medicine, University of Texas Southwestern Medical Center,
Dallas.
- Source
- Am J Clin Nutr, 1994 Dec, 60:6 Suppl, 986S-990S
- Abstract
- Stearic acid is a long-chain saturated fatty acid. However, in contrast with other
saturated fatty acids, stearic acid apparently does not raise serum cholesterol
concentrations. Studies carried out three decades ago provided strong suggestive evidence
that this was the case. More recent investigations that specifically compared stearic acid
with other fatty acids in human studies have confirmed that stearic acid is not
hypercholesterolemic. Stearic acid was shown not to raise low-density-lipoprotein
cholesterol relative to oleic acid, which is known to be neutral in its effects on
cholesterol concentrations. In contrast, palmitic acid, another long-chain saturated fatty
acid, definitely raises cholesterol concentrations. For this reason, fats rich in stearic
acid might be used in place of those high in palmitic acid in cholesterol-lowering diets.
- Language of Publication
- English
- Unique Identifier
- 95067751
- MeSH Heading (Major)
- Cholesterol|*BL; Dietary Fats|*ME; Fatty Acids|*ME; Stearic Acids|*ME
- MeSH Heading
- Animal; Dietary Carbohydrates|ME; Fatty Acids, Monounsaturated|ME; Fatty Acids,
Unsaturated|ME; Human; Lauric Acids|ME; Myristic Acids|ME; Palmitic Acids|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-9165
- Country of Publication
- UNITED STATES
Section A
Record 8 from database: MEDLINE
Go To The Top
- Title
- Effects of varying carbohydrate content of diet in patients with non-insulin-dependent
diabetes mellitus [see comments]
- Author
- Garg A; Bantle JP; Henry RR; Coulston AM; Griver KA; Raatz SK; Brinkley L; Chen YD;
Grundy SM; Huet BA; et al
- Address
- Center for Human Nutrition, University of Texas Southwestern Medical Center at Dallas
75235-9052.
- Source
- JAMA, 1994 May, 271:18, 1421-8
- Abstract
- OBJECTIVE--To study effects of variation in carbohydrate content of diet on glycemia and
plasma lipoproteins in patients with non-insulin-dependent diabetes mellitus (NIDDM).
DESIGN--A four-center randomized crossover trial. SETTING--Outpatient and inpatient
evaluation in metabolic units. PATIENTS--Forty-two NIDDM patients receiving glipizide
therapy. INTERVENTIONS--A high-carbohydrate diet containing 55% of the total energy as
carbohydrates and 30% as fats was compared with a high-monounsaturated-fat diet containing
40% carbohydrates and 45% fats. The amounts of saturated fats, polyunsaturated fats,
cholesterol, sucrose, and protein were similar. The study diets, prepared in metabolic
kitchens, were provided as the sole nutrients to subjects for 6 weeks each. To assess
longer-term effects, a subgroup of 21 patients continued the diet they received second for
an additional 8 weeks. MAIN OUTCOME MEASURES--Fasting plasma glucose, insulin,
lipoproteins, and glycosylated hemoglobin concentrations. Twenty-four-hour profiles of
glucose, insulin, and triglyceride levels. RESULTS--The site of study as well as the diet
order did not affect the results. Compared with the high-monounsaturated-fat diet, the
high-carbohydrate diet increased fasting plasma triglyceride levels and very low-density
lipoprotein cholesterol levels by 24% (P < .0001) and 23% (P = .0001), respectively,
and increased daylong plasma triglyceride, glucose, and insulin values by 10% (P = .03),
12% (P < .0001), and 9% (P = .02), respectively. Plasma total cholesterol, low-density
lipoprotein cholesterol, and high-density lipoprotein cholesterol levels remained
unchanged. The effects of both diets on plasma glucose, insulin, and triglyceride levels
persisted for 14 weeks. CONCLUSIONS--In NIDDM patients, high-carbohydrate diets compared
with high-monounsaturated-fat diets caused persistent deterioration of glycemic control
and accentuation of hyperinsulinemia, as well as increased plasma triglyceride and
very-low-density lipoprotein cholesterol levels, which may not be desirable.
- Language of Publication
- English
- Unique Identifier
- 94231641
- MeSH Heading (Major)
- Diabetes Mellitus, Non-Insulin-Dependent|*BL/*DH/DT; Dietary Carbohydrates|*/AD/ME;
Dietary Fats|*/AD/ME
- MeSH Heading
- Adult; Aged; Blood Glucose|ME; Comparative Study; Energy Intake; Fatty Acids,
Monounsaturated|AD/ME; Female; Glipizide|TU; Human; Insulin|BL; Lipoproteins|BL; Male;
Middle Age; Support, Non-U.S. Gov't; Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't,
P.H.S.; Triglycerides|BL
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
- ISSN
- 0098-7484
- Country of Publication
- UNITED STATES
Section A
Record 9 from database: MEDLINE
Go To The Top
- Title
- Prediction of total subcutaneous abdominal, intraperitoneal, and retroperitoneal adipose
tissue masses in men by a single axial magnetic resonance imaging slice.
- Author
- Abate N; Garg A; Coleman R; Grundy SM; Peshock RM
- Address
- Department of Internal Medicine, University of Texas Southwestern Medical Center, USA.
- Source
- Am J Clin Nutr, 1997 Feb, 65:2, 403-8
- Abstract
- To develop a simplified but accurate method for determining the masses of various
abdominal adipose tissue compartments, we studied the predictive value of masses of
intraperitoneal, retroperitoneal, and subcutaneous abdominal adipose tissue determined on
single axial abdominal magnetic resonance imaging (MRI) slices taken at various
intervertebral levels from the 12th thoracic to 1st sacral vertebra (identified on a
sagittal section) for the respective total masses of each compartment calculated from
contiguous 10-mm thick MRI slices covering the entire abdomen in 49 men (26 without
diabetes and 23 with non-insulin-dependent diabetes mellitus). The MRI slice at the
intervertebral level between the lumbar (L) 2 and 3 vertebrae showed the highest and most
consistent predictive value for all three compartments (R2 = 0.85 for all). Furthermore,
compared with other intervertebral levels, the L2-L3 level had a higher amount of
intraperitoneal and retroperitoneal adipose tissue mass. We conclude that determining the
masses of various abdominal adipose tissue compartments at the L2-L3 intervertebral level
by MRI is an acceptably reliable and accurate method for studying abdominal adiposity in
men.
- Language of Publication
- English
- Unique Identifier
- 97174863
- MeSH Heading (Major)
- Abdomen|*; Adipose Tissue|*
- MeSH Heading
- Adult; Aged; Body Mass Index; Human; Magnetic Resonance Imaging; Male; Middle Age;
Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Tomography, X-Ray Computed
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0002-9165
- Country of Publication
- UNITED STATES
Section A
Record 10 from database: MEDLINE
Go To The Top
- Title
- Estimation of adipose tissue mass by magnetic resonance imaging: validation against
dissection in human cadavers.
- Author
- Abate N; Burns D; Peshock RM; Garg A; Grundy SM
- Address
- Department of Clinical Nutrition, University of Texas Southwestern Medical Center at
Dallas.
- Source
- J Lipid Res, 1994 Aug, 35:8, 1490-6
- Abstract
- The evaluation of adipose tissue distribution has become an essential component of
investigations on the complications of obesity. However, a major limitation is lack of
methodology for accurate estimation of adipose tissue mass in the different regions of the
body. Therefore, we have tested the accuracy and precision of magnetic resonance imaging
(MRI) as a method to measure adipose tissue mass in regions of the body not accessible
with standard anthropometric methods. The mass of subcutaneous and intraabdominal adipose
tissue estimated by MRI was compared with that obtained by direct weighing of the same
adipose tissue compartments after dissection in human cadavers. MRI was performed on three
unembalmed cadavers (two males, one female) who were subsequently dissected to isolate
intraperitoneal, retroperitoneal, and subcutaneous adipose tissues. These same components
were delineated by MRI. The results of the two methods were highly congruent. For the
various compartments, the mean of the difference between the two methods was only 0.076 kg
(95% confidence interval + 0.005 kg and + 0.147 kg). The "limits of agreement"
between the two techniques were -0.066 kg and +0.218 kg. Multiple repeated estimates of
mass of adipose tissue compartments were made to determine reproducibility of the MRI
measurement; the coefficient of variation for repeated measures was below 14%. The results
of this study show that MRI is an accurate and precise technique to evaluate adipose
tissue mass in subcutaneous and intraabdominal compartments. Furthermore, MRI was found to
be a valid method to separately evaluate the mass of intraabdominal subcompartments of
intraperitoneal and retroperitoneal adipose tissue.
- Language of Publication
- English
- Unique Identifier
- 95081728
- MeSH Heading (Major)
- Adipose Tissue|*AH; Magnetic Resonance Imaging|*MT; Organ Weight|*
- MeSH Heading
- Abdomen; Autopsy; Cadaver; Comparative Study; Female; Human; Male; Middle Age; Support,
Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0022-2275
- Country of Publication
- UNITED STATES
Section A
Record 11 from database: MEDLINE
Go To The Top
- Title
- Variation at the hepatic lipase and apolipoprotein AI/CIII/AIV loci is a major cause of
genetically determined variation in plasma HDL cholesterol levels.
- Author
- Cohen JC; Wang Z; Grundy SM; Stoesz MR; Guerra R
- Address
- Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas
75235-9052.
- Source
- J Clin Invest, 1994 Dec, 94:6, 2377-84
- Abstract
- Genetic factors have been shown to play an important role in determining interindividual
variation in plasma HDL-C levels, but the specific genetic determinants of HDL cholesterol
(HDL-C) levels have not been elucidated. In this study, the effects of variation in the
genomic regions encoding hepatic lipase, apolipoprotein AI/CIII/AIV, and the cholesteryl
ester transfer protein on plasma HDL-C levels were examined in 73 normotriglyceridemic,
Caucasian nuclear families. Genetic factors accounted for 56.5 +/- 13% of the
interindividual variation in plasma HDL-C levels. For each candidate gene, adjusted plasma
HDL-C levels of sibling pairs who shared zero, one, or two parental alleles
identical-by-descent were compared using sibling-pair linkage analysis. Allelic variation
in the genes encoding hepatic lipase and apolipoprotein AI/CIII/AIV accounted for 25 and
22%, respectively, of the total interindividual variation in plasma HDL-C levels. In
contrast, none of the variation in plasma HDL-C levels could be accounted for by allelic
variation in the cholesteryl ester transfer protein. These findings indicate that a major
fraction of the genetically determined variation in plasma HDL-C levels is conferred by
allelic variation at the hepatic lipase and the apolipoprotein AI/CIII/AIV gene loci.
- Language of Publication
- English
- Unique Identifier
- 95081423
- MeSH Heading (Major)
- Apolipoproteins|*GE; Lipase|*GE; Lipoproteins, HDL Cholesterol|*BL; Liver|*EN; Variation
(Genetics)|*
- MeSH Heading
- Apolipoprotein A-I|GE; Apolipoproteins A|GE; Apolipoproteins C|GE; Base Sequence;
Causality; Human; Molecular Sequence Data; Nuclear Family; Statistics|MT; Support,
Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0021-9738
- Country of Publication
- UNITED STATES
Section A
Record 12 from database: MEDLINE
Go To The Top
- Title
- Effectiveness of low-dose crystalline nicotinic acid in men with low high-density
lipoprotein cholesterol levels.
- Author
- Martin Jadraque R; Tato F; Mostaza JM; Vega GL; Grundy SM
- Address
- Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas,
USA.
- Source
- Arch Intern Med, 1996 May, 156:10, 1081-8
- Abstract
- BACKGROUND: Hypoalphalipoproteinemia (low serum concentration of high-density
lipoprotein cholesterol [HDL-C]) is a common pattern of dyslipidemia associated with
coronary heart disease. High doses of nicotinic acid effectively raise HDL-C levels in
this condition, but they are commonly accompanied by side effects. The efficacy of low
doses of nicotinic acid that may produce fewer side effects has not been adequately
studied. OBJECTIVE: To determine the effects of low-dose nicotinic acid on HDL-C levels in
patients with hypoalphalipoproteinemia. METHODS: Forty-four men with low HDL-C levels
(< 1.03 mmol/L [< 40 mg/dL]) entered the study. Twenty-four patients otherwise had
normal lipid levels, and 20 were moderately hypertriglyceridemic (range of plasma
triglyceride levels, 2.82 to 5.64 mmol/L 250 to 500 mg/dL). The trial consisted of 3
phases; each phase lasted 8 weeks. The first phase was diet only (30% fat diet); in the
second phase, crystalline nicotinic acid was added at 1.5 g/d; and in the third phase, the
dose was increased to 3 g/d. RESULTS: Of the 44 patients who entered the study, 37
completed the low-dose phase (1.5 g/d); the remaining patients were withdrawn because of
side effects to nicotinic acid. Four other patients who completed the low-dose phase were
excluded from the higher dose phase because of side effects that developed when they were
receiving the low dose. Ten other patients withdrew during the high-dose phase because of
side effects. In both groups, responses to nicotinic acid therapy tended to be
dose-dependent. For both groups, the higher dose generally produced a greater reduction in
apolipoprotein B-containing lipoproteins and a greater rise in HDL-C levels. However, for
both groups, the low dose of nicotinic acid gave an average 20% increase in HDL-C levels.
CONCLUSIONS: A low dose (1.5 g/d) of crystalline nicotinic acid causes an average 20%
increase in HDL-C levels and significantly lowers triglyceride levels in both
normolipidemic and hyperlipidemic patients with low HDL-C levels. Although the changes
induced by this dose are less than those that can be achieved by a higher dose, the lower
dose is better tolerated. Nicotinic acid may be useful in combined drug therapy for
secondary prevention of coronary heart disease, and if higher doses cannot be tolerated,
use of a lower dose should still be useful for producing a moderate rise in HDL-C levels
in patients with hypoalphalipoproteinemia.
- Language of Publication
- English
- Unique Identifier
- 96224805
- MeSH Heading (Major)
- Hypolipoproteinemia|BL/DH/*DT; Lipoproteins, HDL|*BL; Nicotinic Acids|*AD/AE/TU
- MeSH Heading
- Crystallization; Dose-Response Relationship, Drug; Human; Hypertriglyceridemia|BL/DH/DT;
Male; Middle Age; Support, Non-U.S. Gov't; Support, U.S. Gov't, Non-P.H.S.; Support, U.S.
Gov't, P.H.S.; Treatment Outcome
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE
- ISSN
- 0003-9926
- Country of Publication
- UNITED STATES
Section A
Record 13 from database: MEDLINE
Go To The Top
- Title
- Hypercholesterolemia with cholesterol-enriched LDL and normal levels of
LDL-apolipoprotein B. Effects of the step I diet and bile acid sequestrants on the
cholesterol content of LDL.
- Author
- Vega GL; Grundy SM
- Address
- Department of Clinical Nutrition, University of Texas Southwestern Medical Center at
Dallas 75235-9052, USA.
- Source
- Arterioscler Thromb Vasc Biol, 1996 Apr, 16:4, 517-22
- Abstract
- One form of hypercholesterolemia is characterized by high levels of LDL cholesterol and
normal levels of LDL-apolipoprotein (apo) B. The reason for hypercholesterolemia,
therefore, is enrichment of LDL particles with cholesterol. We have reported previously
that about one third of patients with primary moderate hypercholesterolemia have this
lipoprotein pattern and have no apparent abnormality in LDL-apo B metabolism. The current
study was designed to determine whether the combination of the Step I Diet (30% of total
calories as fat, <10% saturated fatty acids, and <300 mg per day cholesterol) with
or without cholestyramine therapy will correct the hypercholesterolemia in patients of
this type. Ten hypercholesterolemic men of this type were identified and recruited into
the study. Their LDL cholesterol levels were > or = 160 mg/dL and LDL-apo B levels were
<120 mg/dL (LDL cholesterol/apo B ratio >1.60). For patient selection, subjects were
challenged with a high fat diet (40% of total calories as fat, 18% saturated fatty acids,
and 400 mg per day cholesterol) for 6 weeks to confirm persistence of a high LDL
cholesterol/apo B ratio. Thereafter, they were started on a Step I Diet, and lipoprotein
analyses were repeated. Finally, cholestyramine (16 g per day) was added to the Step I
Diet. The Step I Diet alone significantly reduced the LDL cholesterol/apo B ratios and
produced a trend toward lowering LDL cholesterol levels. Cholestyramine therapy further
reduced LDL cholesterol levels and maintained a normal LDL cholesterol/apo B ratio. The
present investigation thus confirms the existence of a form of moderate
hypercholesterolemia that arises from a defect in LDL composition. In addition, it
demonstrates that the combination of Step I Diet and cholestyramine therapy corrects this
defect and normalizes LDL levels and LDL composition.
- Language of Publication
- English
- Unique Identifier
- 96197199
- MeSH Heading (Major)
- Apolipoproteins B|*BL; Cholesterol|AN/*BL; Hypercholesterolemia|*BL/*TH; Lipoproteins,
LDL|*BL/CH
- MeSH Heading
- Aged; Anticholesteremic Agents|TU; Base Sequence; Cholestyramine|TU; Diet,
Fat-Restricted; Human; Male; Middle Age; Molecular Probes|GE; Molecular Sequence Data;
Polymerase Chain Reaction; Reference Values; Single-Blind Method; Support, Non-U.S. Gov't;
Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't, P.H.S.
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE
- ISSN
- 1079-5642
- Country of Publication
- UNITED STATES
Section A
Record 14 from database: MEDLINE
Go To The Top
- Title
- Genetic analysis of a polymorphism in the human apolipoprotein A-I gene promoter: effect
on plasma HDL-cholesterol levels.
- Author
- Barre DE; Guerra R; Verstraete R; Wang Z; Grundy SM; Cohen JC
- Address
- Center for Human Nutrition, UT Southwestern Medical Center, Dallas 75235-9052.
- Source
- J Lipid Res, 1994 Jul, 35:7, 1292-6
- Abstract
- Previous studies have indicated that a G to A substitution at position -76 in the gene
encoding apolipoprotein A-I (apoA-I) confers increased plasma high density lipoprotein
cholesterol (HDL-C). Increased HDL-C may be a direct consequence of the A allele, or may
reflect the action of a locus in linkage disequilibrium with the A allele. To elucidate
this question, we examined the effect of this polymorphism in a large sample (n = 409) of
unrelated Caucasians and their nuclear families (n = 22). To eliminate the confounding
effects of hypertriglyceridemia, individuals with triglyceride levels greater than 150
mg/dl were excluded from the study. ApoA-I genotype was determined by polymerase chain
reaction (PCR) amplification of genomic DNA and restriction digestion with Msp I.
Individuals were grouped by genotype (GG, GA or AA) and mean adjusted HDL levels of the
three groups were compared by one-way analysis of variance. Our analysis indicates that
HDL-C levels do not vary by genotype, and no gene dosage effect is apparent in men or in
women. Analysis of 22 informative Caucasian nuclear families showed no significant
difference between individuals with the A allele and their GG siblings. These data suggest
that polymorphism at -76 in the apoA-I gene does not directly affect HDL levels.
Therefore, the increased HDL-C levels reported in other populations must reflect linkage
disequilibrium between the A allele and a putative HDL-raising allele. As we find no
evidence for association between the A allele and high HDL levels, this putative allele
must occur at a low frequency in the population sampled in this study.
- Language of Publication
- English
- Unique Identifier
- 95053412
- MeSH Heading (Major)
- Adenine|*CH; Apolipoprotein A-I|*GE; Guanine|*CH; Lipoproteins, HDL Cholesterol|*BL;
Polymorphism (Genetics)|*; Promoter Regions (Genetics)|*
- MeSH Heading
- Adolescence; Adult; Aged; Aged, 80 and over; Alleles; Female; Homozygote; Human; Male;
Middle Age; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0022-2275
- Country of Publication
- UNITED STATES
Section A
Record 15 from database: MEDLINE
Go To The Top
- Title
- RRR-alpha-tocopheryl acetate supplementation at pharmacologic doses decreases
low-density-lipoprotein oxidative susceptibility but not protein glycation in patients
with diabetes mellitus.
- Author
- Fuller CJ; Chandalia M; Garg A; Grundy SM; Jialal I
- Address
- Center for Human Nutrition, University of Texas Southwestern Medical Center at Dallas
75235-9052, USA.
- Source
- Am J Clin Nutr, 1996 May, 63:5, 753-9
- Abstract
- Patients with diabetes mellitus have an increased risk of premature atherosclerosis,
which may be due in part to increased oxidizability of low-density lipoprotein (LDL).
Numerous studies have shown that alpha-tocopherol can reduce the oxidative susceptibility
of LDL in normoglycemic subjects; however, there are few studies in persons with diabetes.
In addition, alpha-tocopherol may reduce the extent of protein glycation. Therefore, the
objective of the present study was to assess the effect of RRR-alpha-tocopheryl acetate
supplementation on LDL oxidizability and protein glycation in persons with diabetes
without evidence of vascular disease. Twenty-eight persons with insulin-dependent diabetes
mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM) were randomly assigned
to receive either placebo or 1632 mg (1200 IU) RRR-alpha-tocopherol/d, as tocopheryl
acetate, for 8 wk. Plasma and LDL antioxidant concentrations and LDL oxidizability were
assessed at both 0 and 8 wk. Plasma and LDL concentrations of alpha-tocopherol were
significantly increased in the supplemented group only. Compared with the placebo group,
the alpha-tocopherol-supplemented group had significant reductions in LDL oxidizability at
8 wk, as shown by the time-course curves of conjugated diene and lipid peroxide formation.
Also, alpha-tocopherol supplementation produced a significant prolongation in the lag
phases of both assays, which was evident in both the NIDDM and IDDM subgroups. However,
there were no significant changes in glycated hemoglobin or in glycated plasma proteins
after alpha-tocopherol supplementation. Thus, alpha-tocopherol supplementation may be
beneficial in reducing LDL oxidizability in patients with diabetes.
- Language of Publication
- English
- Unique Identifier
- 96204955
- MeSH Heading (Major)
- Antioxidants|AD/AN/*PD; Diabetes Mellitus, Insulin-Dependent|BL/*ME; Diabetes Mellitus,
Non-Insulin-Dependent|BL/*ME; Lipoproteins, LDL|BL/*ME; Vitamin E|*AA/AD/BL/PD
- MeSH Heading
- Adult; Analysis of Variance; Blood Glucose|AN/ME; Dose-Response Relationship, Drug;
Fatty Acids|BL; Food, Fortified; Hemoglobin A, Glycosylated|AN; Human; Lipid Peroxides|ME;
Middle Age; Oxidation-Reduction; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.;
Time Factors
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
- ISSN
- 0002-9165
- Country of Publication
- UNITED STATES
Section A
Record 16 from database: MEDLINE
Go To The Top
- Title
- What is the desirable ratio of saturated, polyunsaturated, and monounsaturated fatty
acids in the diet?
- Author
- Grundy SM
- Address
- University of Texas Southwestern Medical Center, Dallas, USA.
- Source
- Am J Clin Nutr, 1997 Oct, 66:4 Suppl, 988S-990S
- Abstract
- By reducing intakes of animal fats and gradually reducing intakes of trans fatty acids,
a one-third reduction in cholesterol-raising fatty acids seems practical, from 12% to 7-8%
of total energy intake. The intake of polyunsaturated fatty acids should not exceed
current intakes, approximately 7% of total energy. Although further research is needed to
determine a recommended ratio of oleic acid to carbohydrates, on the basis of the
relatively low rates of coronary artery disease and cancer in both the Mediterranean
region (where oleic acid intake is high at the expense of carbohydrates) and in
populations consuming low-fat, high-carbohydrate diets, a reasonable compromise is a diet
in which total fat is approximately 30% of energy, allowing for an intake of oleic acid of
15-16% of total energy.
- Language of Publication
- English
- Unique Identifier
- 97463877
- MeSH Heading (Major)
- Dietary Fats|*AD/AN; Dietary Fats, Unsaturated|*AD/AN; Fatty Acids|*AD/AN; Fatty Acids,
Monounsaturated|*AD/AN; Fatty Acids, Unsaturated|*AD/AN
- MeSH Heading
- Human
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-9165
- Country of Publication
- UNITED STATES
Section A
Record 17 from database: MEDLINE
Go To The Top
- Title
- Cholesterol management in patients with heart disease. Emphasizing secondary prevention
to increase longevity.
- Author
- Grundy SM
- Address
- Center for Human Nutrition, University of Texas Southwestern Medical Center at Dallas
75235-9052, USA.
- Source
- Postgrad Med, 1997 Aug, 102:2, 81-4, 87-90
- Abstract
- Advances in treatment of elevated cholesterol levels and recent documentation of
efficacy and safety in clinical trials justify expanded use of cholesterol-lowering
therapy in clinical practice. Patients with CHD or other forms of clinical atherosclerotic
disease can benefit from aggressive cholesterol management. Maximal dietary modification,
weight control, and physical activity are valuable adjuncts to drug therapy in secondary
prevention. Recent studies have shown that appropriate use of cholesterol-lowering drugs
is cost-effective and efficacious in patients with CHD. Use of such drugs can increase
patients' life expectancy. Primary care physicians have a key role in instituting
intensive cholesterol management in patients with clinically manifest atherosclerotic
disease. Furthermore, they should take the lead in coordinating with cardiovascular
specialists to manage cholesterol levels in patients who have had a recent acute coronary
syndrome or undergone a revascularization procedure.
- Language of Publication
- English
- Unique Identifier
- 97416752
- MeSH Heading (Major)
- Anticholesteremic Agents|*TU; Coronary Disease|BL/CO/*PC; Hypercholesterolemia|CO/DH/*DT
- MeSH Heading
- Human; Longevity; Lovastatin|AA/TU; Niacin|TU; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0032-5481
- Country of Publication
- UNITED STATES
Section A
Record 18 from database: MEDLINE
Go To The Top
- Title
- Determinants of plasma HDL-cholesterol in hypertriglyceridemic patients. Role of
cholesterol-ester transfer protein and lecithin cholesteryl acyl transferase.
- Author
- Tato F; Vega GL; Grundy SM
- Address
- Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas,
USA.
- Source
- Arterioscler Thromb Vasc Biol, 1997 Jan, 17:1, 56-63
- Abstract
- Hypertriglyceridemic patients commonly have low levels of HDL cholesterol. Elevated
triglycerides per se may be one cause of low HDL levels, but other factors also may be
involved. The current study was designed to define the role of cholesterol-ester transfer
protein (CETP) in causation of a low HDL cholesterol in hypertriglyceridemic patients; in
addition other factors-lecithin cholesterol acyl transferase (LCAT), hepatic triglyceride
lipase (HTGL), and lipoprotein lipase (LPL)-were examined. Plasma activities of CETP and
LCAT were measured in 137 male patients with moderate hypertriglyceridemia (plasma
triglycerides [TGs] 200 to 500 mg/dL and LDL cholesterol < 160 mg/dL). Results were
compared with those from 50 normolipidemic men of similar age and body habitus. In
addition, lipase activities in postheparin plasma were measured in 118 of the subjects
with hypertriglyceridemia. The activities of CETP and LCAT were 17% (P < .01) and 7% (P
< .05), respectively, higher in the hypertriglyceridemic group than in control
subjects. By stepwise regression analysis CETP appeared to contribute 15.2% and LCAT 9.8%
to variation in HDL-cholesterol levels. Activities of LPL and HTGL together contributed an
additional 14.1% to HDL-cholesterol variation. In contrast, levels of plasma TG accounted
for only 5.4% of the variation. There were no differences in relative contributions of
these parameters in patients with and those without coronary heart disease. This study
indicates that several factors contribute to the variation in HDL-cholesterol levels in
hypertriglyceridemic patients, and five factors-CETP, LCAT, HTGL, LPL, and triglyceride
levels-account for almost half of this variation.
- Language of Publication
- English
- Unique Identifier
- 97164876
- MeSH Heading (Major)
- Carrier Proteins|*AN; Hypertriglyceridemia|*BL; Lipoproteins, HDL Cholesterol|*BL;
Phosphatidylcholine-Sterol O-Acyltransferase|*AN
- MeSH Heading
- Aged; Human; Male; Middle Age; Support, Non-U.S. Gov't; Support, U.S. Gov't, Non-P.H.S.;
Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 1079-5642
- Country of Publication
- UNITED STATES
Section A
Record 19 from database: MEDLINE
Go To The Top
- Title
- Cholestyramine therapy for dyslipidemia in non-insulin-dependent diabetes mellitus. A
short-term, double-blind, crossover trial.
- Author
- Garg A; Grundy SM
- Address
- Center for Human Nutrition, University of Texas Southwestern Medical Center at Dallas
75235-9052.
- Source
- Ann Intern Med, 1994 Sep, 121:6, 416-22
- Abstract
- OBJECTIVE: To assess clinical efficacy and tolerability of cholestyramine therapy in
patients with dyslipidemia and non-insulin-dependent diabetes mellitus (NIDDM). DESIGN: A
randomized, double-blind, crossover study of cholestyramine (8 g twice daily) compared
with placebo for a period of 6 weeks each. SETTING: Metabolic Unit and the Lipid and
Diabetes Clinics at the Department of Veterans Affairs Medical Center, Dallas, Texas.
PATIENTS: 21 patients with NIDDM that was well controlled using either glyburide or
insulin therapy and with low-density lipoprotein (LDL) cholesterol levels more than 3.36
mmol/L (130 mg/dL) and fasting plasma triglyceride levels less than 3.4 mmol/L (300
mg/dL). MEASUREMENTS: During the last week of each period, for 5 consecutive days fasting
plasma lipids and lipoproteins were measured, and plasma glucose levels were determined at
3, 7, and 11 a.m. and at 4 and 8 p.m. Daily urinary glucose excretion was measured for 3
days and glycosylated hemoglobin concentrations were determined on days 28 and 38 of the
study periods. RESULTS: In this short-term study, when compared with placebo,
cholestyramine reduced total cholesterol by 18% (95% CI, 14% to 22%) and LDL cholesterol
by 28% (CI, 21% to 35%). Although cholestyramine therapy increased plasma triglyceride
levels by 13.5% (CI, 1% to 26%), very-low density lipoprotein cholesterol and high-density
lipoprotein cholesterol levels remained unchanged. Cholestyramine therapy improved
glycemic control; mean plasma glucose values were lower by 13% (CI, 5% to 21%), a median
reduction in urinary glucose excretion of 0.22 g/d was observed (P < 0.001), and a
tendency to lower glycosylated hemoglobin concentration was noted. The doses of glyburide
and insulin did not change during the study, and body weight remained stable. Constipation
was the main side effect, and two patients dropped out of the study because of
cholestyramine intolerance. CONCLUSIONS: In carefully selected male patients with NIDDM
and high LDL cholesterol and normal triglyceride levels, cholestyramine therapy
effectively reduces LDL levels and also may improve glycemic control. The long-term
efficacy of cholestyramine therapy in patients with NIDDM needs further evaluation.
- Language of Publication
- English
- Unique Identifier
- 94330646
- MeSH Heading (Major)
- Cholestyramine|*TU; Diabetes Mellitus, Non-Insulin-Dependent|*CO;
Hypercholesterolemia|BL/*DT/ET
- MeSH Heading
- Adult; Aged; Double-Blind Method; Female; Human; Lipids|BL; Lipoproteins, LDL
Cholesterol|BL; Male; Middle Age; Risk Factors; Support, Non-U.S. Gov't; Support, U.S.
Gov't, P.H.S.
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
- ISSN
- 0003-4819
- Country of Publication
- UNITED STATES
Section A
Record 20 from database: MEDLINE
Go To The Top
- Title
- Addressing the spectrum of hypercholesterolemia [see comments]
- Author
- Grundy SM; Mazzaferri EL
- Address
- University of Texas Southwestern Medical Center at Dallas, USA.
- Source
- Hosp Pract (Off Ed), 1996 Jun, 31:6, 43-8, 53-5, 59; discussion 60
- Abstract
- The past decade has seen a major shift in management: Trials of HMG-CoA reductase
inhibitors have suggested that cholesterol reduction offers greater protection against
coronary artery disease than does antihypertensive therapy. Five patient vignettes provide
guidelines for initiating therapy. The agents should be prescribed with restraint, often
not until other measures have been exhausted.
- Language of Publication
- English
- Unique Identifier
- 96281858
- MeSH Heading (Major)
- Coronary Disease|ET/*PC; Hypercholesterolemia|CO/*TH; Lovastatin|*AA/TU
- MeSH Heading
- Adult; Aged; Algorithms; Anticholesteremic Agents|TU; Case Report; Diet, Fat-Restricted;
Exercise; Female; Human; Male; Middle Age; Risk Factors; Smoking Cessation
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 8750-2836
- Country of Publication
- UNITED STATES
HealthGate Documents
Section B
Record 1 from database: MEDLINE
Go To The Top
- Title
- Influence of exchanging carbohydrate for saturated fatty acids on plasma lipids and
lipoproteins in men.
- Author
- Wolf RN; Grundy SM
- Address
-
- Source
- J Nutr, 1983 Aug, 113:8, 1521-8
- Abstract
- This study was designed to determine effects of reducing intake of total fat and
increasing carbohydrate (glucose) on plasma lipoproteins. Eleven men were investigated.
They were given two diets for 1 month each. One diet contained 40% of calories as fat with
20% saturated fatty acids, 10% monounsaturates and 10% polyunsaturates. The other diet
contained 30% fat with equal amounts of each type of fatty acid. The 10% of fat removed
from the latter was replaced by glucose. Six patients had significant reductions of
cholesterol in total plasma and low density lipoprotein (LDL) on the 30% fat; for the
group as a whole; however, the decrease was not statistically significant. Total
triglycerides increased modestly (15%) and high density lipoprotein (HDL)-cholesterol fell
significantly (14%) on replacement of 40% fat with 30% fat. Seven patients also were given
a 30% fat diet containing fatty acids in the same proportions as in the 40% fat diet. A
similar response was noted as when fatty acids were given in equal ratios. This study
indicates that response to reduction in fat content is inconsistent. The majority of
patients were responders; others, however, were not.
- Language of Publication
- English
- Unique Identifier
- 83267829
- MeSH Heading (Major)
- Dietary Fats|*AD; Lipids|*BL
- MeSH Heading
- Adult; Aged; Cholesterol|BL; Dose-Response Relationship, Drug; Fatty Acids,
Unsaturated|AD; Food, Formulated; Glucose|AD; Human; Lipoproteins, HDL|BL; Lipoproteins,
LDL|BL; Male; Middle Age; Milk Proteins|AD; Structure-Activity Relationship;
Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0022-3166
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Dietary Fats); 0 (Fatty Acids, Unsaturated); 0 (Lipoproteins, HDL Cholesterol); 0
(Lipoproteins, HDL); 0 (Lipoproteins, LDL Cholesterol); 0 (Milk Proteins); 0
(Triglycerides); 50-99-7 (Glucose); 57-88-5 (Cholesterol)
Section B
Record 2 from database: MEDLINE
Go To The Top
- Title
- Incorporation of radioactive phospholipid into subclasses of high-density lipoproteins.
- Author
- Tall AR; Blum CB; Grundy SM
- Address
-
- Source
- Am J Physiol, 1983 May, 244:5, E513-6
- Abstract
- The incorporation of orally administered phospholipid into plasma high-density
lipoproteins (HDL) was studied in three subjects. Plasma was analyzed by equilibrium
density gradient ultracentrifugation, 5, 6, and 8 h after ingestion of 1.1 g [3H-choline,
14C-dilinoleoyl]phosphatidylcholine. At all time points in all subjects, there was a peak
of phosphatidylcholine specific activity in fractions of density approximately 1.10-1.13
g/ml, corresponding to the subclass previously designated HDL2a. There was also a more
variable, smaller peak of specific activity of phospholipids in HDL2b (1.063-1.100 g/ml)
and in fractions of density approximately 1.19 g/ml. In the 1.10-1.13 fraction, 97 and
71%, respectively, of the 3H and 14C radioactivity were in phospholipids. The 3H/14C ratio
was similar in phospholipids of HDL subfractions, the d less than 1.07 fraction, and in
the administered phospholipid. The results show preferential transfer or exchange or
absorbed phosphatidylcholine into specific subclasses of HDL.
- Language of Publication
- English
- Unique Identifier
- 83201561
- MeSH Heading (Major)
- Lipoproteins, HDL|BI/*BL; Phospholipids|*BL
- MeSH Heading
- Cholesterol Esters|BL; Human; Kinetics; Middle Age; Support, U.S. Gov't, Non-P.H.S.;
Support, U.S. Gov't, P.H.S.; Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0002-9513
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Cholesterol Esters); 0 (Lipoproteins, HDL); 0 (Phospholipids); 0 (Triglycerides)
Section B
Record 3 from database: MEDLINE
Go To The Top
- Title
- Increased low density lipoprotein production associated with obesity.
- Author
- Kesaniemi YA; Grundy SM
- Address
-
- Source
- Arteriosclerosis, 1983 Mar-Apr, 3:2, 170-7
- Abstract
- Turnover rates of the apolipoprotein of low density lipoproteins (apoLDL) and
cholesterol balance were determined in six obese men and six control men. The two groups
were of similar age and matched for apoLDL concentrations. Levels of plasma total
cholesterol in obese patients (209 +/- 14 SEM mg/dl) were similar to controls (225 +/- 17
mg/dl). LDL-cholesterol was numerically but not statistically lower in obese subjects (111
+/- 18 mg/dl) compared to controls (145 +/- 13 mg/dl). Synthetic rates of apoLDL in
contrast were higher in obese patients (1450 mg/day) than in controls (934 mg/day) (p less
than 0.002). Three factors could explain the similar concentrations of LDL-cholesterol in
obese and control subjects, despite overproduction of apoLDL in the obese. First, LDL was
diluted into a larger plasma pool in obese patients; second, fractional catabolic rates of
apoLDL were somewhat greater in obese men than in controls; and third, obese patients had
higher ratios of protein-to-cholesterol in LDL. The production of apoLDL for all patients
was not correlated with total body synthesis of cholesterol. The major finding of this
study was that obese patients have increased turnover of apoLDL, not necessarily reflected
by high concentrations of LDL-cholesterol. This high turnover rate itself may raise the
risk for coronary heart disease in obese patients.
- Language of Publication
- English
- Unique Identifier
- 83177698
- MeSH Heading (Major)
- Lipoproteins, LDL|*BI/BL; Obesity|BL/*ME
- MeSH Heading
- Apolipoproteins|BI; Cholesterol|BL; Human; Kinetics; Lipoproteins, HDL|BL; Male;
Support, Non-U.S. Gov't; Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (apolipoprotein LDL); 0 (Apolipoproteins); 0 (Lipoproteins, HDL Cholesterol); 0
(Lipoproteins, HDL); 0 (Lipoproteins, LDL Cholesterol); 57-88-5 (Cholesterol)
Section B
Record 4 from database: MEDLINE
Go To The Top
- Title
- Normocholesterolemic tendon xanthomatosis with overproduction of apolipoprotein B.
- Author
- Vega GL; Illingworth DR; Grundy SM; Lindgren FT; Connor WE
- Address
-
- Source
- Metabolism, 1983 Feb, 32:2, 118-25
- Abstract
- This report describes a 46-yr-old man with normocholesterolemic tendon xanthomatosis. He
had severe bilateral xanthomas of Achilles tendons and small lesions on patellar tendons;
biopsy of the latter revealed a fibroxanthoma of high cholesterol content. He did not have
clinical evidence of atherosclerotic disease. The patient's total cholesterol (TC) and
triglycerides (TG) were 245 and 258 mg/dl, respectively. LDL-TC was 168 mg/dl and HDL-TC
was 32 mg/dl. VLDL consisted mainly of small particles (SfO 20-100) which were unusually
rich in apolipoproteins B and E (and low in apo Cs). Plasma LDL-apo B was not increased
(85-120 mg/dl), but VLDL-apo B was distinctly elevated (58 mg/dl). The synthesis rate of
apoLDL (29.9 mg/kg/d) was increased markedly compared to a matched control (13.9 mg/kg/d)
and to a patient with familial hypercholestrolemia (15.9 mg/kg/d). The concentration of
apoLDL in our patient was not increased; this was because of an associated high FCR (0.484
day-1). His HDL was relatively low in TC but high in TG, which caused an increase in
HDL2b. The patient's xanthomata may have been the result of an overproduction of apo B
possibly combined with a defect in HDL metabolism.
- Language of Publication
- English
- Unique Identifier
- 83140985
- MeSH Heading (Major)
- Apolipoproteins|*BI/BL; Cholesterol|*BL; Xanthomatosis|*BL/PA
- MeSH Heading
- Case Report; Human; Lipids|BL; Lipoproteins|BL; Male; Middle Age; Sterols|ME; Support,
U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't, P.H.S.; Tendons|PA
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0026-0495
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Apolipoproteins B); 0 (Apolipoproteins); 0 (Lipoproteins); 0 (Sterols); 57-88-5
(Cholesterol)
Section B
Record 5 from database: MEDLINE
Go To The Top
- Title
- Overproduction of low density lipoproteins associated with coronary heart disease.
- Author
- Kesaniemi YA; Grundy SM
- Address
-
- Source
- Arteriosclerosis, 1983 Jan-Feb, 3:1, 40-6
- Abstract
- The turnover rates of low density lipoprotein-apolipoprotein (apoLDL) were determined in
eight men with coronary heart disease (CHD) and seven men matched for age, weight, and
plasma lipid levels who were used for controls. The CHD patients were normocholesterolemic
(plasma cholesterol = 204 +/- 8 mg/dl sem) as were the control subjects (227 +/- 15
mg/dl). The concentrations of plasma LDL cholesterol and apoLDL were similar for the two
groups. In contrast, the synthetic rates of apoLDL were higher in the CHD patients (20.0
+/- 1.8 mg/kg/day) than in the controls (12.9 +/- 1.1 mg/kg/day) (p less than 0.01). The
ratios of protein-to-cholesterol in LDL averaged 19% higher in the CHD patients. These
patients with CHD maintained normal LDL levels despite an over-production of apoLDL
because of an increased capacity for LDL removal; their fractional catabolic rates of
apoLDL averaged 43% higher than those of the controls. These findings indicate that some
patients with CHD have abnormalities in the turnover of apoLDL, even with normal
concentrations of LDL; these abnormalities may contribute to accelerated atherosclerosis.
- Language of Publication
- English
- Unique Identifier
- 83126219
- MeSH Heading (Major)
- Coronary Disease|*ME; Lipoproteins, LDL|*BI/ME
- MeSH Heading
- Aged; Apolipoproteins|BI; Cholesterol|ME; Dietary Fats|ME; Human; Male; Middle Age;
Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (apolipoprotein LDL); 0 (Apolipoproteins); 0 (Dietary Fats); 0 (Lipoproteins, LDL
Cholesterol); 57-88-5 (Cholesterol)
Section B
Record 6 from database: MEDLINE
Go To The Top
- Title
- Effect of bile acid conjugation pattern on bile acid metabolism in normal humans.
- Author
- Hardison WG; Grundy SM
- Address
-
- Source
- Gastroenterology, 1983 Mar, 84:3, 617-20
- Abstract
- Six male subjects were fed taurine 0.5 g six times daily for 2 wk to determine the
effect of a shift in bile acid conjugation pattern upon bile acid metabolism. Duodenal
bile acids were analyzed, and bile acid pool size, daily fecal excretion, and biliary
excretion rate were quantified. In addition, daily biliary excretion rate of cholesterol
and phospholipid were quantified, and biliary saturation with cholesterol was estimated.
The dose of taurine caused reversal of the bile acid glycine-to-taurine conjugation ratio.
Total bile acid pool size decreased, as did the pool size of chenodeoxycholic acid. Pool
sizes of cholic and deoxycholic acids did not change. Daily fecal bile acid excretion
decreased slightly. Biliary secretion rates of cholesterol, phospholipid, and bile acids
did not change, nor did biliary cholesterol saturation. Pool size can decrease because of
increased bile acid catabolism or decreased synthesis. The fact that bile acid excretion
failed to increase, and actually decreased slightly, suggests that the effect is upon bile
acid synthesis. In normal humans, the effect is small and probably physiologically
unimportant. In special cases, however, such as during ursodeoxycholic acid therapy, the
effect of shifting conjugation pattern may become important.
- Language of Publication
- English
- Unique Identifier
- 83106321
- MeSH Heading (Major)
- Bile Acids and Salts|*ME
- MeSH Heading
- Adult; Aged; Chenodeoxycholic Acid|ME; Cholesterol|ME; Cholic Acids|ME; Chromatography,
High Pressure Liquid; Deoxycholic Acid|ME; Duodenum|AN; Feces|AN; Glycine|ME; Human; Male;
Middle Age; Phospholipids|ME; Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't,
P.H.S.; Taurine|AD/ME
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0016-5085
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Bile Acids and Salts); 0 (Cholic Acids); 0 (Phospholipids); 107-35-7 (Taurine);
474-25-9 (Chenodeoxycholic Acid); 56-40-6 (Glycine); 57-88-5 (Cholesterol); 83-44-3
(Deoxycholic Acid)
Section B
Record 7 from database: MEDLINE
Go To The Top
- Title
- Effects of haem infusion on biliary secretion of porphyrins, haem and bilirubin in man.
- Author
- McCormack LR; Liem HH; Strum WB; Grundy SM; Muller-Eberhard U
- Address
-
- Source
- Eur J Clin Invest, 1982 Jun, 12:3, 257-62
- Abstract
- Employing a continuous bile collection, we measured the bile secretion of porphyrins,
haem (iron protoporphyrin IX regardless of oxidation state) and bilirubin in five healthy
subjects. The baseline values for the flow of porphyrins in the bile were: 4.7 +/- 1.9
nmol/h uroporphyrin, 27.3 +/- 3.8 nmol/h coproporphyrin and 39.2 +/- 11.7 nmol/h
protoporphyrin. Bile haem flow was 59.7 +/- 12.6 nmol/h, and that of bilirubin 23.8 +/-
8.2 mumol/h. Following haem injection (6.4 mumol/kg) the flow of protoporphyrin but not of
the other porphyrins was reduced, and the bile haem flow increased (232 +/- 109.5 nmol/h),
while the flow of bilirubin did not increase significantly. A few patients with
representative porphyrias showed the expected increase in copro- and protoporphyrin in the
bile. The patient with coproporphyria exhibited a bile flow of coproporphyrin of 1470 +/-
133 nmol/h and of protoporphyrin of 334 +/- 29 nmol/h; haem infusion significantly reduced
the bile flow of both porphyrins (to 649 +/- 101 for copro- and 215 +/- 36 nmol/for
protoporphyrin). The patient with protoporphyria had an increased protoporphyrin flow, yet
haem infusion caused no reduction in protoporphyrin flow (106 +/- 7 after v. 81.4 +/- 13
nmol/h before haem). In conclusion, we found that haem and porphyrins are normal
constituents of bile, and that injected haem appears in bile. Bile bilirubin did not rise
within 12 h after haem infusion a finding which warrants further investigation.
- Language of Publication
- English
- Unique Identifier
- 82261790
- MeSH Heading (Major)
- Bile|*SE; Bilirubin|*SE; Heme|*AD/SE; Porphyrins|*SE
- MeSH Heading
- Adult; Aged; Coproporphyrins|SE; Female; Human; Injections; Male; Middle Age;
Porphyria|GE/ME; Protoporphyrins|SE; Skin Diseases|ME; Support, U.S. Gov't, Non-P.H.S.;
Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0014-2972
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 0 (Coproporphyrins); 0 (Porphyrins); 0 (Protoporphyrins); 14875-96-8 (Heme); 635-65-4
(Bilirubin)
Section B
Record 8 from database: MEDLINE
Go To The Top
- Title
- National Cooperative Gallstone Study: the effect of chenodeoxycholic acid on
lipoproteins and apolipoproteins.
- Author
- Albers JJ; Grundy SM; Cleary PA; Small DM; Lachin JM; Schoenfield LJ
- Address
-
- Source
- Gastroenterology, 1982 Apr, 82:4, 638-46
- Abstract
- Subjects in the National Cooperative Gallstone Study undergoing 12 mo of therapy with
chenodeoxycholic acid for the dissolution of gallstones (low-dose, 375 mg/day, n =252;
high-dose, 750 mg/day, n = 253) had a mean increase in serum cholesterol of 20 mg/dl as
compared with a 5 mg/dl increase in the placebo group (n = 258). The effect of
chenodeoxycholic acid on lipoproteins was determined in a random subset of the high-dose
(n = 136) and placebo (n = 143) groups. For men, the mean baseline adjusted estimated
low-density lipoprotein cholesterol level at 12 mo was significantly higher in the
high-dose group than in the placebo group (159 vs. 148 mg/dl, p less than 0.01), whereas
among women this difference was not demonstrated. Change in low-density lipoprotein
cholesterol level was inversely related to baseline cholesterol to an equivalent degree in
each group among men and women. Women in the high-dose group had significantly lower
very-low-density lipoprotein cholesterol levels than did the corresponding placebo group
(27 vs. 32 mg/dl, p less than 0.003). Very-low-density lipoprotein cholesterol levels did
not differ significantly between the high-dose and placebo group in men. Treatment did not
significantly affect the levels of high-density lipoprotein cholesterol or apoproteins
A-I, A-II, or B. Chenodeoxycholic acid therapy produces an increase in total cholesterol
and low-density lipoprotein cholesterol but does not alter high-density lipoprotein
cholesterol levels.
- Language of Publication
- English
- Unique Identifier
- 82139931
- MeSH Heading (Major)
- Apolipoproteins|*BL; Chenodeoxycholic Acid|*TU; Cholelithiasis|BL/*DT; Lipoproteins|*BL
- MeSH Heading
- Cholesterol|BL; Female; Human; Lipoproteins, HDL|BL; Lipoproteins, LDL|BL; Lipoproteins,
VLDL|BL; Male; Middle Age; Sex Factors; Support, U.S. Gov't, P.H.S.
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
- ISSN
- 0016-5085
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Apolipoprotein A-I); 0 (Apolipoprotein A-II); 0 (Apolipoproteins B); 0
(Apolipoproteins); 0 (Lipoproteins); 0 (Lipoproteins, HDL); 0 (Lipoproteins, VLDL);
474-25-9 (Chenodeoxycholic Acid); 57-88-5 (Cholesterol)
Section B
Record 9 from database: MEDLINE
Go To The Top
- Title
- Metabolism of cholesterol and plasma triglycerides in nonketotic diabetes mellitus.
- Author
- Abrams JJ; Ginsberg H; Grundy SM
- Address
-
- Source
- Diabetes, 1982 Oct, 31:10, 903-10
- Abstract
- The metabolism of cholesterol and plasma triglycerides (TG) was studied in 14 diabetic
men: these patients did not have marked obesity nor did they develop ketoacidosis without
insulin. Before insulin therapy, measurements were made of (1) plasma lipoproteins, (2)
postheparin lipolytic enzymes, (3) turnover to TG in very-low-density lipoproteins (VLDL)
and chylomicrons, (4) cholesterol balance, and (5) biliary lipids. After baseline
measurements, the patients were treated with enough long-acting insulin to maintain their
fasting plasma glucose in the range of 100--125 mg/dl. When plasma glucose and lipid
levels reached a new steady state, all of the above measurements were repeated. Before
insulin, most patients had fasting hypertriglyceridemia. This was due mainly to
overproduction of VLDL-TG. Insulin therapy lowered both synthesis and concentrations of
VLDL-TG to near normal. Also, patients with normotriglyceridemia, both before and during
insulin therapy, had essentially normal clearance of chylomicrons. Those with high fasting
TG had delayed clearance of chylomicrons, but clearance returned to normal in most with
insulin therapy. Postheparin lipolytic enzymes were not decreased. Before insulin,
synthesis rates of cholesterol and bile acids usually were greater than normal, and bile
commonly was supersaturated with cholesterol. During insulin therapy, synthesis of both
cholesterol and bile acids remained elevated, possibly because of imperfect control of
hyperglycemia. Furthermore, saturation of bile with cholesterol was accentuated by insulin
therapy.
- Language of Publication
- English
- Unique Identifier
- 83106069
- MeSH Heading (Major)
- Cholesterol|*ME; Diabetes Mellitus|BL/DT/*ME; Lipoproteins|*BL/ME
- MeSH Heading
- Aged; Bile|AN; Chylomicrons|ME; Human; Insulin|TU; Lipids|AN/ME; Lipoproteins,
VLDL|BL/ME; Male; Middle Age; Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't,
P.H.S.; Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0012-1797
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Chylomicrons); 0 (Lipoproteins); 0 (Lipoproteins, VLDL); 0 (Triglycerides);
11061-68-0 (Insulin); 57-88-5 (Cholesterol)
Section B
Record 10 from database: MEDLINE
Go To The Top
- Title
- Hypertriglyceridemia: mechanisms, clinical significance, and treatment.
- Author
- Grundy SM
- Address
-
- Source
- Med Clin North Am, 1982 Mar, 66:2, 519-35
- Abstract
- The association between hypertriglyceridemia and coronary heart disease is explored
followed by a discussion of the mechanisms of the disorder and guidelines on patient
evaluation and treatment.
- Language of Publication
- English
- Unique Identifier
- 82171950
- MeSH Heading (Major)
- Triglycerides|*BL
- MeSH Heading
- Apolipoproteins|ME; Atherosclerosis|ET; Chylomicrons|ME; Human; Lipoproteins, HDL|ME;
Lipoproteins, LDL|ME; Lipoproteins, VLDL|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0025-7125
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Apolipoproteins B); 0 (Apolipoproteins); 0 (Chylomicrons); 0 (Lipoproteins, HDL); 0
(Lipoproteins, VLDL); 0 (Triglycerides)
Section B
Record 11 from database: MEDLINE
Go To The Top
- Title
- Intestinal absorption of polyenephosphatidylcholine in man.
- Author
- Zierenberg O; Grundy SM
- Address
-
- Source
- J Lipid Res, 1982 Nov, 23:8, 1136-42
- Abstract
- The metabolic fate of 1 of 3H/14C-labeled dilinoleoglycerophosphocholine was studied in
five patients after oral administration. The 3H label was in choline and 14C was in the
two linoleic acid residues. More than 90% of both isotopes was absorbed from the
intestine. Seventy to 90% of the 3H radioactivity in blood was linked to
phosphatidylcholine (PC) whereas 14C was associated with both PC and nonpolar lipids. At
peak activity, the 3H/14C ratio of plasma PC was twice that of oral PC; this suggests that
most oral PC was hydrolyzed to lysolecithin before absorption. The mean maximum
concentration in total blood volume was 20% of the administered dose for 3H and 28% for
14C. Examination of lipoproteins revealed that the specific activity of PC in high density
lipoprotein (HDL) was 2 to 6 times higher than in apoB-containing lipoproteins, and to 2
to 20 times than that of red blood cells or total blood. Thus, absorbed PC seemingly was
incorporated preferentially into the HDL fraction of plasma.
- Language of Publication
- English
- Unique Identifier
- 83084428
- MeSH Heading (Major)
- Intestinal Absorption|*; Ph