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COMMENTARIES
POSTED IN APRIL 2009
Pre-Metabolic Syndrome and Metabolic Syndrome:
Biophysical-Semeiotic Viewpoint
Authors:
Sergio Stagnaro MD
The metabolic syndrome (MS) is a constellation
of abnormalities including central obesity; glucose intolerance,
i.e. IIR, IGT, and type 2 diabetes; hypertension; and a dyslipidemia
characterized by increased serum triglycerides, decreased high-density
lipoprotein (HDL) cholesterol, and increased small, dense low-density
lipoprotein (LDL) particles [1-5]. The metabolic syndrome affects
more than 27% of adults in the United States [6,7] and increases
the risk of cardiovascular disease 2- to 3-fold, but exclusively
in individuals with biophysical-semeiotic constitution-dependent,
inherited, coronary real risk, as I described in the former
paper on this website, thus not in all patients with MS [8-12].
More precisely speaking, all components of metabolic syndrome
may occur exclusively in subjects with congenital acidosic
enzyme metabolic histangiopathy (CAEMH), as well as with either "some" or
all CAEMH-dependent, biophysical-semeiotic constitutions [8-19].
As a consequence, not all patients with metabolic syndrome
are equal!
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Macrophage Foam Cell Formation in
Atherosclerosis: The Road Ahead
Authors: Manoj Kumar Barthwal, Ph.D.
Hypercholesterolemia and inflammation are the benchmarks of atherosclerosis.
Evidence such as development of atherosclerosis in 35% of individuals having
cholesterol below risk levels [1], suggests that there is something more than
just an increase in cholesterol behind the development of this disorder. Recent
work in this area has implicated inflammation in a major way and atherosclerosis
is now considered a major inflammatory disorder [2-4]. Having said this, it
cannot be denied that we expect too much from the lipid lowering drugs in dealing
with this menace, although fibrates, niacin, and omega-3-fatty acids are also
prescribed [5]. People, who ultimately develop extensive lesions and atherosclerotic
plaque, undergo balloon angioplasty or stenting and are kept on dual antiplatelet
therapy like clopidogrel and aspirin for preventing instent restenosis [6,7].
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Hepatic Lipase from Bone Marrow-derived Cells Has Beneficial
Effects on Atherosclerosis in a Background of Cholesteryl
Ester Transfer Protein Activity - A Tale of
Two Proteins
Authors: Neil J. Hime
Hepatic lipase is a lipolytic enzyme synthesized primarily
by the liver [1] where it is found in abundance anchored
to the vascular endothelium and hepatocytes [2]. Hepatic
lipase is also expressed by monocyte-derived macrophages
albeit in much lower levels than in the liver [3]. The lipolytic
functions of hepatic lipase are as an acylglycerol hydrolase
and phospholipase to mediate hydrolysis of triglycerides
and phospholipids in different plasma lipoproteins. Triglyceride-enriched
high density lipoproteins (HDL) appear to be a preferred
lipoprotein substrate for the lipolytic activities of hepatic
lipase [4]. In association with proteoglycans hepatic lipase
also facilitates the binding of lipoproteins by hepatocytes
and steroidogenic cells [5].
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CAD Inherited Real Risk, Based on Newborn-Pathological, Type
I, Subtype B, Aspecific, Coronary Endoarteriolar Blocking Devices.
Diagnostic
Role of Myocardial
Oxigenation and Biophysical-Semeiotic Preconditioning
Authors: Sergio Stagnaro MD
In the following, I illustrate some original methods of biophysical
semeiotics (www.semeioticabiofisica.it) [1], utilizing bedside
biophysical-semeiotic reflex parameters, useful and reliable
in detecting coronary artery ischemic disease, even clinically
silent, from its very initial stage, i.e. CAD inherited real
risk, characterized by microcirculatory remodeling, wherein
newborn-pathological, type I, subtype b, aspecific, endoarteriolar
blocking devices play a central role [2-7]. To easily evaluate
all these events it is sufficient to know stomach auscultatory
percussion [See: Practical Applications, Technical Page 1,
and Bibliography in above-cited website]. With regard to
bedside evaluation of biophysical-semeiotic ureteral-reflexes,
unavoidable in directly assessing coronary vasomotion and
vasomotility, it is necessary for the doctor to have further
technical knowledge.
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Carbohydrate Restriction Prevents Atherosclerosis by Reducing
Atherogenic Lipoproteins and Aortic Inflammatory Cytokines
in Guinea Pigs
Authors: Maria Luz Fernandez1 and
Moises Torres-Gonzalez
Cardiovascular disease has been documented as the leading
cause of death for men and women in this country [1]. Atherosclerosis
is the most common pathologic process leading to cardiovascular
disease (CVD) [2]. Although the earliest visible lesion
in the development of atherosclerosis is the fatty streak,
it is now widely recognized that atherosclerosis is a chronic
inflammatory disease rather than a lipid accumulation problem
[3]. Inflammation is defined as a complex set of interactions
among soluble factors and cells that can arise in any tissue
in response to traumatic, infectious, post-ischemic, toxic,
or autoimmune injury. In advanced stages of atherosclerosis,
the chronic inflammation and the deposition of calcium
and atherogenic products lead to the development of the
atherosclerotic plaque and increase the stiffness of the
arterial wall.
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Chronic Obstructive Pulmonary Disease and Cardiovascular
Risk
Authors: Yvette RBM van Gestel,
M.Sc. and Don Poldermans, M.D., Ph.D.
Chronic obstructive pulmonary disease (COPD) is an important
cause of chronic morbidity and mortality worldwide and
affects approximately 10% of the adults older than 40 years
[1]. The disease is characterized by airflow limitation
that is not fully reversible with an abnormal inflammatory
response of the lungs to noxious particles and gases [2].
Cigarette smoking is a major cause of the development and
progression of COPD; however, patients also develop COPD
without smoking.
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Epidermal Fatty Acid-Binding Protein: A Novel Mediator
Linking Obesity, Inflammation, and Atherosclerosis
Authors: Dennis C.Y. Yeung, Aimin
Xu, Annette W.K. Tso, Liza H.Y. Ong, W.S. Chow, Yu Wang,
and Karen S.L. Lam
Long-term epidemiological studies have clearly demonstrated
that obesity is an independent predictor of cardiovascular
diseases [1] and that the presence of obesity is associated
with the acceleration of atherosclerosis [2]. Studies in
recent years also suggest that the adipose tissue is an active
endocrine organ which synthesizes and releases a wide array
of bioactive hormones and cytokines, collectively known as
adipokines [3] and that some of these adipokines may be responsible
for the link between obesity and accelerated atherosclerosis
[4-6].
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Effect of Bariatric Surgery on the Metabolic Syndrome:
A Population-Based, Long-term Controlled Study
Authors: John A. Batsis, M.D.1
and Francisco Lopez-Jimenez, M.D., M.Sc.
Metabolic syndrome (MetS) is strongly associated with
the development of diabetes mellitus, cardiovascular (CV)
disease, and leads to increased mortality [1-3]. Its prevalence
from the National Health and Nutrition Surveys (NHANES)
has risen from 23.7% in NHANES III, to 34.5% in NHANES
1999-2002 [4,5]. This rise, in part, may be attributed
to the paralleled rise in the prevalence of obesity [6],
making both entities, significant public health concerns.
Each of the five components of the MetS, as defined by
the 2005 American Heart Association/National Heart, Lung,
and Blood Institute (AHA/NHLBI), foster increased risk
of CV disease [7]. These components include: a measure
of obesity (increased waist circumference), increased fasting
glucose, increased triglycerides levels, low high density
lipoprotein cholesterol levels, and elevated blood pressure.
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An Oxidative Stress Guided Unifying Hypothesis for
the Risk Factors Associated With the Metabolic Syndrome
Authors: Ignazio
Grattagliano, M.D.
The metabolic syndrome is a common multifactorial condition
associated with risk burdens of diabetes and cardiovascular
disease. It is characterized by different combinations
of three or more of the following features: abdominal obesity,
arterial hypertension, hyperglycemia, elevated serum triglycerides,
and low HDL cholesterol. Some authors support the notion
that the constituent metabolic abnormalities do indeed
cluster beyond the effect of chance by sharing common pathophysiologic
mechanisms of damage [1], and that a single factor may
underlie the association [2].
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Fructose,
Methylxanthines and the Metabolic Syndrome: Should We
Wait for the "Smoking
Gun"?
Authors: T.
Balasubramanian
Metabolic syndrome featuring obesity, hyperglycemia, hyperinsulinemia,
insulin resistance, hypercholesterolemia, hypertriglyceridemia,
hyperuricemia, and hypertension remains an enigma to the
scientific community. A search for its molecular basis
of pathogenesis by scientists worldwide has brought two
important findings to the forefront. One is the involvement
of the uric acid, the result of a fructose-rich diet and
the other is methyluric acid, the metabolite of methylxanthines
in coffee, tea and cocoa in the pathogenesis of metabolic
syndrome. Research has unequivocally proved that an increase
in blood uric acid level (hyperuricemia) following a large
intake of fructose as table sugar and high fructose corn
syrup (HFCS) has resulted in the pandemic of metabolic
syndrome [1-5].
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