[FoRK] Is Balkanization really a problem?
Stephen D. Williams
<sdw at lig.net> on
Tue May 29 10:49:50 PDT 2007
Tom Higgins wrote:
> It can rightly be said we have had a definite increase in the amount
> of information we as well dressed apes get in our daily consumption
> of living. The quality vs quantity issues I think is the relevant rock
> to look under which leads down the same hole as the national obesity
> figures..being such that we get many many more calories than we have
> in the past but those being mainly drenched in high fructose corn
> syrup . Our informational diet is also filled to the brim with filler
> that makes us look better fed thinkers but in reality makes us
> unhealthy grotesque lumps of atrophied citizenry.
I get tired of hearing about how it's high fructose corn syrup which is
the root of all nutrition problems. I don't believe it. Too much sugar
in general, yes. I just don't see any evidence that it matters much
which sugars you ingest. Fructose, being twice as sweet as sucrose and
four times as sweet as dextrose (i.e. d-glucose), should actually be
better since "too much sugar" by taste should be reached far sooner. You
may remember that sucrose is fructose+dextrose.
Interesting, High Fructose Corn Syrup is corn syrup (which is primarily
glucose to begin with) that has had part of the glucose turned into
fructose. The ratio approximates sucrose in sweetness.
There is plenty of disagreement, but I'll cherry pick statements that
show equivalence and harmlessness:
"Studies that have compared high fructose corn syrup
<http://en.wikipedia.org/wiki/High_fructose_corn_syrup> (an ingredient
in soft drinks <http://en.wikipedia.org/wiki/Soft_drinks> sold in the
US) to sucrose <http://en.wikipedia.org/wiki/Sucrose> (common cane sugar
<http://en.wikipedia.org/wiki/Cane_sugar>) find that they have
essentially identical physiological effects. For instance, Melanson et
al (2006), studied the effects of HFCS and sucrose sweetened drinks on
blood glucose <http://en.wikipedia.org/wiki/Blood_glucose>, insulin
<http://en.wikipedia.org/wiki/Leptin>, and ghrelin
<http://en.wikipedia.org/wiki/Ghrelin> levels. They found no significant
differences in any of these parameters."
"However, unlike animal experiments, some human experiments have failed
to show a correlation between fructose consumption and obesity."
I believe that most obesity is caused by lack of exercise and the rest
is obviously diet. I know that mine is. (My bike computer says that my
32 miles yesterday burned about 2000 calories.) Fried foods and those
primarily held together by butter, lard, and oil are ten times the
problems caused by sugar. I think the worst you can say about sugar is
that it helps the fat go down too easily and allows you to avoid
nutrients too much.
Besides obesity in general, the common negative effect of sugar used to
be that was assumed to cause diabetes. This is clearly not fact. It is a
combination of genetic weaknesses relating to various insulin, lipid,
and glucose processing steps along with a high fat (not high sugar) diet
that almost definitely causes type-2 diabetes. (Type-1 diabetes seems to
be caused by nervous system malfunction, which appears to be reversable
to a point.) I can't find the article that was the most clear on the
role of lipids. It was published about a year or two ago and was
centered on a group of people who have a genetic defect that prevents
them from producing any fat at all. All people with that defect have
type-2 diabetes. From studying those people, researchers figured out the
entire sequence of failure due, initially, to excess and chronic lipids
in the bloodstream that leads to type-2 diabetes.
“What was really astounding to us, however, was that when we fed normal
mice a high-fat diet, we saw this same mechanism of pathogenesis with
attenuation of GnT-4a enzyme levels, reduced Glut-2 glycosylation, and
loss of cell surface Glut-2 expression,” said Marth. “This finding may
explain the loss of Glut-2 commonly observed in type 2 diabetes. For
example, transcriptional control of GnT-4a expression may underlie the
pathogenesis of type 2 diabetes in human mature onset diabetes of the
young (MODY), and perhaps in response to leptin signaling deficiency in
Type 2 Diabetes, Obesity, and Bumblefoot: A Possible Correlation?
Type 2 diabetes genes identified
Genes Can Cause Type 2 Diabetes
Breakthrough sheds light on cause of diabetes
> The researchers used a chemical to obliterate these nerves in a breed
> of mice genetically predestined to develop diabetes. “It turns out if
> you remove these specific sensory nerves, the animals don’t get
> diabetes,” says Dosch. “It was stunning.”
> When the researchers examined the nerves of diabetes-prone mice and
> compared them with normal mice, they found that the nerves of
> diabetes-prone mice do not producing enough substance P. This causes
> islet cells to overproduce insulin, leading to insulin-resistance and
> eventually islet-cell death. It is at this point, says Dosch, that the
> immune system is called into action, triggering diabetes.
> The team wanted to know what would happen if they gave diabetic mice a
> top-up of substance P, so they injected some directly into the
> pancreas. Astonishingly, the diabetes disappeared overnight and the
> mice remained diabetes-free for weeks, and even months in some cases.
> If the same were to happen in humans, a single injection could keep
> the disease at bay for years, says Dosch.
Half the country has diabetes gene
> The gene causes people to metabolize fat differently
> Lipodystrophy is a disorder of adipose tissue characterized by a
> selective loss of body fat ...
> leading to lipotoxicity.
> Patients with lipodystrophy develop insulin resistance frequently with
> dyslipidemia and diabetes...
In other words, their bodies stop storing fat, leaving excess lipids in
the bloodstream, and they develop lipotoxicity, etc.
The net result is that if you use up the lipids you eat, you will be
fine. If you don't exercise enough and eat too much fat, you are likely
to develop diabetes at which point sugar will be the issue.
> We have become better, as in doing more of, consumers both of food and
> information. Does this make us better beings, citizens and thinkers?
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