The Glycemic Index,,,,,,Part I: Human Metabolic Responses

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The Glycemic Index

 

The Key Code to Obesity and Diabetes: Part I

 

By Dr. Ann de Wees Allen Chief of Biomedical Research Glycemic Research

Institute

Part I: Human Metabolic Responses All foods, drinks, snacks,

nutrients, supplements, and anything else orally consumed by humans

elicits a metabolic response. As food goes into the mouth and gets

processed, the body has to decide what to do with the ingested items.

There are two main pathways taken:

 

Pathway One: Store the item in adipose tissue fat cells.

Pathway Two: Use (burn) the item as energy.

 

Humans are genetically hard-wired to shunt foods into fat cells whenever

possible, as that ensures survival. The mechanism by which the two main

pathways are accessed depends on the glycemic index (GI) of the edible

item.

 

If the consumed item is high glycemic, it will primarily take pathway

one. If the food is low glycemic, it will primarily take pathway two.

Quickly digested and metabolized foods possess the highest glycemic

indices. Slowly digested foods release glucose gradually into the

bloodstream, and are therefore low glycemic.

 

All foods, drinks, and nutraceuticals can be categorized as either high

or low glycemic. High-glycemic foods elevate blood glucose and insulin

levels and stimulate fat storage. Low-glycemic foods do not overly

elevate blood glucose and insulin, and do not stimulate lipoprotein

lipase (LPL) fat-storing mechanisms.

Storage in Adipose Tissue Fat Cells

 

In pathway one, foods are driven into fat cells, especially those found

in the abdominal region. The mechanism of shunting food and calories

into fat cells is very efficient for long-term survival of our species.

Unfortunately, our intricate survival mechanisms do not know that we

have access to grocery stores and minimarts.

 

The adaptation mechanism associated with human fat storage is directly

related to the glycemic index of foods. High-glycemic foods and diets

stimulate de nova lipogenesis and increase adipocyte size (fat cell

size). However, low-glycemic foods do the opposite and inhibit this

process.

 

Once fat cells have become engorged, they start subdividing like

lemmings and create more fat cells. Aside from the weight-gain cascade,

high-glycemic foods and diets can increase risk of diabetes, reactive

hypoglycemia, cardiovascular disease, and certain forms of cancer.

 

The glycemic response of a food determines its acceptability for use by

overweight and obese persons, diabetics, hypoglycemics, and persons with

insulin resistance, metabolic syndrome, and syndrome X.

 

Determining the Glycemic Index of Foods

 

The glycemic response of any food, drink, or nutrient can be identified

by its glycemic index. The GI is a numerical classification based on

human in vivo clinical studies that quantifies the relative blood

glucose response and fat-storing capacity of foods, drinks,

nutraceuticals, pharmaceuticals, and any other edible agent.

 

Glycemic testing is conducted by orally feeding human subjects a food or

drink, or a complete meal, and then analyzing blood glucose, insulin

levels, and fat-storing markers at 15-minute intervals. Fat-storage in

fat cells is monitored during glycemic clinical trials by tracking human

fat-storing enzymes and mechanisms, such as lipoprotein lipase,

neuropeptide Y, and leptin.

 

To make the claim of " low glycemic " for any human-grade food

product, the United Statesovernment requires board-approved, human in

vivo clinical trials. In vitro and nonclinical trial calculations, or

software that claims to be able to determine glycemic index are not

legally permitted for product labeling.

 

References

 

1. Obesity Linked to Type 1 Diabetes. Am. Diabetes Assoc; Diabetes

Forecast, Sept. 2004

 

2. Integrative Cancer Therapies, Vol 4, No 1, 25-31; Controlling

Hyperglycemic as an Adjunct to Cancer Therapy, 2005

 

3. Comparative Biochemistry and Physiology, Part A, 136, 95-112;

Hyperinsulinemic Diseases of Civilization, 2003

 

4. McClain 2002, Rosetti et al. 1990

 

 

Click here to read more about Dr. Allen's research

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