Archive for the ‘Glucose’ Category

Sugar is a Poison “The Bitter Truth” by Robert Lustig Lecture

Tuesday, May 24th, 2011


I highly recommend you watch this, it’s a must watch.

If this video is no longer on youtube email me, I have saved a copy of this for my personal archive.

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.

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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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Glucose Intolerance Article – Archived

Thursday, August 19th, 2010

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

Glucose Intolerance

Author: Samuel T Olatunbosun, MD, FACP, Chief, Internal Medicine, 56th Medical Group, Luke Air Force Base
Coauthor(s): Samuel Dagogo-Jack, MD, MBBS, MSc, FRCP, Professor of Medicine, Program Director, Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center

Updated: Jul 16, 2010

Background

Several distinct disorders of glucose tolerance exist. The most widely used classification of diabetes mellitus and allied categories of glucose intolerance is that recommended by the World Health Organization (WHO) in 1985. However, the American Diabetes Association (ADA) has proposed a system based on disease etiology instead of on type of pharmacologic treatment.1

The major categories of the disorders of glycemia or disorders of glucose tolerance are as follows:

  • Type 1 diabetes mellitus
  • Type 2 diabetes mellitus
  • Other specific types of diabetes
  • Gestational diabetes mellitus (GDM)2,3,4
  • Impaired glucose tolerance (IGT)
  • Impaired fasting glucose4

Conditions secondarily associated with glucose intolerance also occur.

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Insulin Resistance Article – Archived

Thursday, August 19th, 2010

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

Insulin Resistance

Background

Insulin resistance is a state in which a given concentration of insulin produces a less-than-expected biological effect. Insulin resistance has also been arbitrarily defined as the requirement of 200 or more units of insulin per day to attain glycemic control and to prevent ketosis.

The syndromes of insulin resistance actually make up a broad clinical spectrum, which includes obesity, glucose intolerance, diabetes, and the metabolic syndrome, as well as an extreme insulin-resistant state. Many of these disorders are associated with various endocrine, metabolic, and genetic conditions. These syndromes may also be associated with immunological diseases and may exhibit distinct phenotypic characteristics.

The metabolic syndrome —a state of insulin-resistance that is also known as either syndrome X or the dysmetabolic syndrome—has drawn the greatest attention because of its public health importance.

In an effort to clinically identify patients with insulin resistance, various organizations have developed diagnostic criteria. The most commonly used criteria in the United States are those of the National Cholesterol Education Program/Adult Treatment Panel III (NCEP/ATP III).

  • NCEP/ATP III criteria for the diagnosis of the metabolic syndrome include the following (diagnosis is made when 3 or more are present):
    • Waist circumference of more than 102 cm in men or more than 88 cm in women
    • Fasting triglyceride level of 150 mg/dL or higher
    • Blood pressure level of 130/85 mm Hg or higher
    • High-density lipoprotein cholesterol (HDL-C) level of less than 40 mg/dL in men or less than 50 mg/dL in women
    • Fasting glucose level of 110 mg/dL or higher (which has been changed to 100 mg/dL to reflect revised criteria for impaired fasting glucose [IFG])

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Lancet. 2002 May 18;359(9319):1740-5. “Circulating concentrations of insulin-like growth factor-I and development of glucose intolerance: a prospective observational study”

Wednesday, August 18th, 2010

-::- Note: The below is published here for archival purposes -::-

Lancet. 2002 May 18;359(9319):1740-5.

Circulating concentrations of insulin-like growth factor-I and development of glucose intolerance: a prospective observational study.

Sandhu MS, Heald AH, Gibson JM, Cruickshank JK, Dunger DB, Wareham NJ.

Department of Public Health and Primary Care, Institute of Public Health, University of Cambridge, Cambridge, UK.

Abstract

BACKGROUND: Results of experimental and clinical studies suggest that insulin-like growth factor-I (IGF-I) and IGF binding protein-1 (IGFBP-1) could be important determinants of glucose homoeostasis. However, experimental models might also reflect compensatory and adaptive metabolic processes. We therefore prospectively examined the associations between circulating concentrations of IGF-I and IGFBP-1 and development of glucose tolerance.

METHODS: Participants in this cohort study were a random sample of 615 normoglycaemic men and women aged 45-65 years. Participants underwent oral glucose tolerance testing based on WHO definitions and criteria in 1990-92 and 1994-96. At the baseline visit, we measured serum concentrations of IGF-I and IGFBP-1, and assessed the relation between these peptides and subsequent glucose intolerance.

FINDINGS: At 4.5 years of follow-up, 51 (8%) of 615 participants developed impaired glucose tolerance or type-2 diabetes. After adjustment for correlates of IGF-I and risk factors for glucose intolerance, the odds ratio for risk of impaired glucose tolerance or type-2 diabetes for participants with IGF-I concentrations above the median (> or = 152 microg/L) compared with those with concentrations below the median (<152 microg/L) was 0.50 (0.26-0.95). Consistent with this finding, IGF-I also showed a significant inverse association with subsequent 2-h glucose concentrations, which was independent of correlates of IGF-I and risk factors for glucose tolerance (p for linear trend=0.026). We also found that this inverse association was independently modified by IGFBP-1 (p for interaction=0.011).

INTERPRETATION: These data show that circulating IGF-I and its interaction with IGFBP-1 could be important determinants of glucose homoeostasis and provide further evidence for the possible protective role of IGF-I against development of glucose intolerance.

PMID: 12049864 [PubMed - indexed for MEDLINE]

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