Life Glow Plus Super Life Glow Life Glow Basic Bone Dense Calcium Taheebo Life Tea Germanium Colloidal Minerals Methyl Sulfonyl Methane Transfer Factor Immune Egg	Vibrant Life Home Web All VL Products Family Of Three Chelation Formulas Oral Chelation Ingredient Comparisons The Wednesday Letter Karl Loren Viewpoints Frequently Asked Questions Testimonials Free Radicals Central Page For 18 Web Sites	Vibrant Life Home Page Shopping Cart	Separate Search Page or search below
Navigation Help	Karl Loren Background	Ingredients Technical	Write To Karl Loren	Table Of Contents

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

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