Archive for the ‘Metabolic Syndrome’ Category

140+ Reasons Why Sugar Is Ruining Your Health

Sunday, November 28th, 2010

The following list was written by Nancy Appleton, Ph.D. (visit her very informative website www.nancyappleton.com), the author of the book Lick The Sugar Habit.

In addition to throwing off the body’s homeostasis, excess sugar may result in a number of other significant consequences. The following is a listing of some of sugar’s metabolic consequences from a variety of medical journals and other scientific publications.

141 Reasons Sugar Ruins Your Health

(Just Kidding, it’s 143)

By Nancy Appleton PhD & G.N. Jacobs

Excerpted from Suicide by Sugar

Used with permission

1. Sugar can suppress your immune system.

2. Sugar upsets the mineral relationships in the body.

3. Sugar can cause juvenile delinquency in children.

4. Sugar eaten during pregnancy and lactation can influence muscle force production in offspring, which can affect an individual’s ability to exercise.

5. Sugar in soda, when consumed by children, results in the children drinking less milk.

6. Sugar can elevate glucose and insulin responses and return them to fasting levels slower in oral contraceptive users.

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Metabolic Syndrome Article – Archived

Thursday, August 19th, 2010

-::- Note: The below is published here for archival purposes -::-
Thanks to medscape.com for this invaluable article

Metabolic Syndrome

Author: Stanley S Wang, MD, JD, MPH, Clinical Cardiologist, Austin Heart; Adjunct Assistant Professor of Medicine, University of North Carolina School of Medicine

Updated: Feb 22, 2010

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The metabolic syndrome (MetS) is a multiplex risk factor that arises from insulin resistance accompanying abnormal adipose deposition and function.1 It is a risk factor for coronary heart disease (CHD), as well as diabetes, fatty liver, and several cancers. The clinical manifestations of this syndrome may include hypertension, hyperglycemia, hypertriglyceridemia, reduced high-density lipoprotein cholesterol (HDL-C), and abdominal obesity. Under current guidelines, revised in 2005 by the National Heart, Lung, and Blood Institute (NHLBI) and the American Heart Association (AHA),2 metabolic syndrome is diagnosed when a patient has at least 3 of the following 5 conditions:

  1. Fasting glucose >100 mg/dL (or receiving drug therapy for hyperglycemia)
  2. Blood pressure >130/85 mm Hg (or receiving drug therapy for hypertension)
  3. Triglycerides >150 mg/dL (or receiving drug therapy for hypertriglyceridemia)
  4. HDL-C <40 mg/dL in men or <50 mg/dL in women (or receiving drug therapy for reduced HDL-C)
  5. Waist circumference >102 cm (40 in) in men or >88 cm (35 in) in women; if Asian American, >90 cm in men (35 in) or >80 cm in women (32 in)

Abundant data suggest that patients meeting these diagnostic criteria have a greater risk of having significant clinical consequences, the 2 most prominent and dreaded of which are the development of diabetes mellitus (DM) and coronary heart disease. In addition, pooled data from 37 studies involving more than 170,000 patients have shown that metabolic syndrome doubles the risk of coronary artery disease.3 It also increases risk of stroke, fatty liver disease, diabetes4 and cancer5 .

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J Mol Med. 2008 Jun;86(6):729-34. “Aldosterone in salt-sensitive hypertension and metabolic syndrome”

Sunday, August 1st, 2010

J Mol Med. 2008 Jun;86(6):729-34. Epub 2008 Apr 25.

Aldosterone in salt-sensitive hypertension and metabolic syndrome.

Fujita T.

Department of Nephrology and Endocrinology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan. fujita-dis@h.u-tokyo.ac.jp

Abstract

Metabolic syndrome, which is caused by obesity, is now a global pandemic. Metabolic syndrome is an aggregation of hypertension, diabetes and dyslipidaemia. Insulin resistance is a key factor in the development of these components of metabolic syndrome.

Concerning the mechanism for the development of hypertension in metabolic syndrome, the lack of insulin resistance in the kidney increases sodium reabsorption by hyperinsulinaemia, leading to sodium retention in the body, and resultant salt-sensitive hypertension.

Moreover, hyperaldosteronism, which is caused by adipocyte-derived aldosterone-releasing factors, induces not only salt-sensitive hypertension, but also proteinuria in obese hypertensive rats.

Salt loading markedly aggravates proteinuria and induces cardiac diastolic dysfunction in obese hypertensive rats, suggesting that salt and aldosterone exert unfavourable synergistic actions on the cardiovascular system, possibly through the overproduction of oxidative stress.

In turn, reactive oxygen species (ROS), which are induced by adipokines such as tumour necrosis factor-alpha, non-esterified fatty acids, angiotensinogen etc., can activate the mineralocorticoid (MR) receptor, in an aldosterone-independent fashion.

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