Read Online The Sugar Smart Diet: Stop Cravings and Lose Weight While Still Enjoying the Sweets You Love by Anne Alexander, Julia VanTine - Free Book Online Page A
Authors: Anne Alexander, Julia VanTine
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metabolic syndrome, which is the name for the bundle of risk factors listed above that raise your odds for heart disease, diabetes, and stroke. Up to 40 percent of normal-weight adults have it. But weight—healthy or no—isn’t the defining characteristic of metabolic syndrome. Insulin resistance is.
A team of researchers, including Robert Lustig, MD, author of
Fat Chance
, advanced a theory of exactly how metabolic syndrome—and its disastrous, system-wide consequences—might occur. The process, described in an article published in
Pediatrics
, is extraordinarily complex. But it begins with the body being forced to store excess fat in the liver, as well as in the tissue around the internal organs. This excess fat makes the liver resist the action of insulin. In response, the pancreas produces more insulin to prod the liver into doing its job. Insulin levels rise even higher and cause even more energy to be stored in subcutaneous fat tissue (like your thighs or butt). This is the fat you see in the mirror, the kind you moan over.
The liver tries to export the excess fat that is damaging it in the form of a specific type of blood fat called triglycerides. But too many triglycerides floating around in your bloodstream can be just as problematic. High triglycerides may raise your risk of coronary artery disease, especially if you’re a woman.
There’s more to this insidious progression of system-wide havoc. But the bottom line is, high insulin levels affect every part of the body—including your belly. In a study published in the
Journal of Clinical Investigation
, 32 overweight men and women drank either glucose- or fructose-sweetened drinks three times a day, along with following a standard diet for 10 weeks. The drinks totaled 25 percent of their daily calories.
At the end of the study, all the participants had gained weight. But CT scans showed that the fructose group mostly gained belly fat. They were actually growing sugar bellies! On the other hand, most of the glucose group’s fat gain was subcutaneous. Compared to the glucose group, the fructose groupalso had higher total cholesterol and LDL (“bad”) cholesterol, plus greater insulin resistance—consistent with metabolic syndrome.
BELLY FAT AND DIABETES
So if a sugary diet appears to promote the storage of this deep and dangerous belly fat, it’s reasonable to conclude that type 2 diabetes can’t be far behind. Indeed, research already links sugar intake to the development of type 2 diabetes, independent of its role in obesity. In other words, it’s possible that people develop diabetes because they’re overweight or obese. But it may
also
be possible that they develop it because they’re consuming added sugars to excess.
One recent study found a smoking gun: an independent, direct link between sugar in the food supply and risk of developing type 2 diabetes. The findings give weight to the still-controversial hypothesis that it’s not obesity that’s driving this now global pandemic, but the rising consumption of sugar worldwide.
In this study, published in
PLoS ONE,
researchers from the Stanford University School of Medicine, the University of California, Berkeley, and the University of California, San Francisco, analyzed a decade’s worth of health data from the United Nations, including diabetes rates and sugar availability, across 175 countries. After controlling for factors like obesity, aging, income, and total calories, the link between sugar and diabetes remained significant. For every extra 150 calories from sugar available per person each day, diabetes prevalence rises by 1.1 percent, the study found. (By the way, 150 calories is just a little more than the number of sugar calories in a 12-ounce can of soda.) Conversely, reduced exposure to sugar was linked to a drop in diabetes prevalence.
This relationship was unique among food types. Categories like protein, fat, and fiber didn’t show a significant link to diabetes. Neither did
A team of researchers, including Robert Lustig, MD, author of
Fat Chance
, advanced a theory of exactly how metabolic syndrome—and its disastrous, system-wide consequences—might occur. The process, described in an article published in
Pediatrics
, is extraordinarily complex. But it begins with the body being forced to store excess fat in the liver, as well as in the tissue around the internal organs. This excess fat makes the liver resist the action of insulin. In response, the pancreas produces more insulin to prod the liver into doing its job. Insulin levels rise even higher and cause even more energy to be stored in subcutaneous fat tissue (like your thighs or butt). This is the fat you see in the mirror, the kind you moan over.
The liver tries to export the excess fat that is damaging it in the form of a specific type of blood fat called triglycerides. But too many triglycerides floating around in your bloodstream can be just as problematic. High triglycerides may raise your risk of coronary artery disease, especially if you’re a woman.
There’s more to this insidious progression of system-wide havoc. But the bottom line is, high insulin levels affect every part of the body—including your belly. In a study published in the
Journal of Clinical Investigation
, 32 overweight men and women drank either glucose- or fructose-sweetened drinks three times a day, along with following a standard diet for 10 weeks. The drinks totaled 25 percent of their daily calories.
At the end of the study, all the participants had gained weight. But CT scans showed that the fructose group mostly gained belly fat. They were actually growing sugar bellies! On the other hand, most of the glucose group’s fat gain was subcutaneous. Compared to the glucose group, the fructose groupalso had higher total cholesterol and LDL (“bad”) cholesterol, plus greater insulin resistance—consistent with metabolic syndrome.
BELLY FAT AND DIABETES
So if a sugary diet appears to promote the storage of this deep and dangerous belly fat, it’s reasonable to conclude that type 2 diabetes can’t be far behind. Indeed, research already links sugar intake to the development of type 2 diabetes, independent of its role in obesity. In other words, it’s possible that people develop diabetes because they’re overweight or obese. But it may
also
be possible that they develop it because they’re consuming added sugars to excess.
One recent study found a smoking gun: an independent, direct link between sugar in the food supply and risk of developing type 2 diabetes. The findings give weight to the still-controversial hypothesis that it’s not obesity that’s driving this now global pandemic, but the rising consumption of sugar worldwide.
In this study, published in
PLoS ONE,
researchers from the Stanford University School of Medicine, the University of California, Berkeley, and the University of California, San Francisco, analyzed a decade’s worth of health data from the United Nations, including diabetes rates and sugar availability, across 175 countries. After controlling for factors like obesity, aging, income, and total calories, the link between sugar and diabetes remained significant. For every extra 150 calories from sugar available per person each day, diabetes prevalence rises by 1.1 percent, the study found. (By the way, 150 calories is just a little more than the number of sugar calories in a 12-ounce can of soda.) Conversely, reduced exposure to sugar was linked to a drop in diabetes prevalence.
This relationship was unique among food types. Categories like protein, fat, and fiber didn’t show a significant link to diabetes. Neither did
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