Quite the extrapolation. Test 122 people and apply those findings to
the entire 298,444,215 population. Amazing how the press has blindly
accepted that "Half the country has the diabetes gene" from a sampling
of 122.

Whatever happened to the insistence by food industry cultists of the
need for "properly set up trials" and far reaching massive
epidemiological studies and large scale multi-million dollar double
blind studies etc, to prove any minor scientific point being studied.

Talk about double standards in scientific proof.

http://www.ajcn.org/cgi/content/abstract/85/1/102

FABP2 Ala54Thr genotype is associated with glucoregulatory function
and lipid oxidation after a high-fat meal in sedentary nondiabetic men
and women1,2,3
Edward P Weiss, Josef Brandauer, Onanong Kulaputana, Ioana A Ghiu,
Christopher R Wohn, Dana A Phares, Alan R Shuldiner and James M
Hagberg
1 From the Department of Kinesiology, University of Maryland, College
Park, MD (EPW, JB, OK, IAG, CRW, DAP, and JMH); the Division of
Endocrinology, Diabetes, and Nutrition, University of Maryland School
of Medicine, Baltimore, MD (ARS); and the Geriatric Research Education
and Clinical Center, Baltimore Veterans Administration Medical Center,
Baltimore, MD (ARS)


Background: A common functional missense mutation [Ala54Thr of the
fatty acid-binding protein 2 gene (FABP2)] has previously been studied
for associations with glucoregulation, postprandial lipemia, and lipid
oxidation rates. However, most of those studies have not accounted for
the interactive and potentially confounding effects of habitual
physical activity and diet.

Objective: We tested the hypothesis that, in sedentary nondiabetic
subjects following a low-fat diet, Thr54 FABP2 carriers have lower
glucoregulatory function, greater postprandial lipemia, and greater
lipid oxidation rates than do their Ala54 FABP2-homozygous
counterparts.

Design: Men and women (n = 122) aged 50-75 y who were following a low-
fat diet were genotyped and underwent oral-glucose-tolerance tests. A
subgroup (n = 36) also underwent postprandial lipemia tests with lipid
oxidation rate measurements.

Results: Thr54 carriers were less likely to have normal glucose
tolerance (P = 0.05) and had higher fasting glucose concentrations (P
= 0.003) than did Ala54 homozygotes. In Thr54 carriers, the insulin
sensitivity index was lower (P = 0.02), and the fasting insulin and
the oral-glucose-tolerance test insulin area under the curve were
higher (P = 0.05 and 0.03, respectively) than in Ala54 homozygotes.
FABP2 genotype was not associated with fasting or postprandial lipemia
test triacylglycerol or free fatty acids (P 0.22 for all), but
postprandial lipid oxidation rates were higher (P = 0.01), which
suggests that fat absorption is higher in Thr54 carriers than in Ala54
homozygotes.

Conclusions: In sedentary nondiabetic persons following a low-fat
diet, FABP2 Thr54 carriers have lower glucose tolerance and lower
insulin action than do Ala54-homozygous persons. Furthermore, FABP
Thr54 carriers have higher lipid oxidation rates, which may be the
mechanism of glucoregulatory dysfunction.

**************

Quite the extrapolation. Test 122 people and apply those findings to
the entire 298,444,215 population. Amazing how the press has blindly
accepted that "Half the country has the diabetes gene" from a sampling
of 122.

Whatever happened to the insistence by food industry cultists of the
need for "properly set up trials" and far reaching massive
epidemiological studies and large scale multi-million dollar double
blind studies etc, to prove any minor scientific point being studied.

Talk about double standards in scientific proof.

TC - Meat Industry Representative

On 31 Jan 2007 11:42:25 -0800, "TC" <tunder...@hotmail.com> wrote:





http://www.ajcn.org/cgi/content/abstract/85/1/102

FABP2 Ala54Thr genotype is associated with glucoregulatory function
and lipid oxidation after a high-fat meal in sedentary nondiabetic men
and women1,2,3
Edward P Weiss, Josef Brandauer, Onanong Kulaputana, Ioana A Ghiu,
Christopher R Wohn, Dana A Phares, Alan R Shuldiner and James M
Hagberg
1 From the Department of Kinesiology, University of Maryland, College
Park, MD (EPW, JB, OK, IAG, CRW, DAP, and JMH); the Division of
Endocrinology, Diabetes, and Nutrition, University of Maryland School
of Medicine, Baltimore, MD (ARS); and the Geriatric Research Education
and Clinical Center, Baltimore Veterans Administration Medical Center,
Baltimore, MD (ARS)

Background: A common functional missense mutation [Ala54Thr of the
fatty acid-binding protein 2 gene (FABP2)] has previously been studied
for associations with glucoregulation, postprandial lipemia, and lipid
oxidation rates. However, most of those studies have not accounted for
the interactive and potentially confounding effects of habitual
physical activity and diet.

Objective: We tested the hypothesis that, in sedentary nondiabetic
subjects following a low-fat diet, Thr54 FABP2 carriers have lower
glucoregulatory function, greater postprandial lipemia, and greater
lipid oxidation rates than do their Ala54 FABP2-homozygous
counterparts.

Design: Men and women (n = 122) aged 50-75 y who were following a low-
fat diet were genotyped and underwent oral-glucose-tolerance tests. A
subgroup (n = 36) also underwent postprandial lipemia tests with lipid
oxidation rate measurements.

Results: Thr54 carriers were less likely to have normal glucose
tolerance (P = 0.05) and had higher fasting glucose concentrations (P
= 0.003) than did Ala54 homozygotes. In Thr54 carriers, the insulin
sensitivity index was lower (P = 0.02), and the fasting insulin and
the oral-glucose-tolerance test insulin area under the curve were
higher (P = 0.05 and 0.03, respectively) than in Ala54 homozygotes.
FABP2 genotype was not associated with fasting or postprandial lipemia
test triacylglycerol or free fatty acids (P 0.22 for all), but
postprandial lipid oxidation rates were higher (P = 0.01), which
suggests that fat absorption is higher in Thr54 carriers than in Ala54
homozygotes.

Conclusions: In sedentary nondiabetic persons following a low-fat
diet, FABP2 Thr54 carriers have lower glucose tolerance and lower
insulin action than do Ala54-homozygous persons. Furthermore, FABP
Thr54 carriers have higher lipid oxidation rates, which may be the
mechanism of glucoregulatory dysfunction.

**************

Quite the extrapolation. Test 122 people and apply those findings to
the entire 298,444,215 population. Amazing how the press has blindly
accepted that "Half the country has the diabetes gene" from a sampling
of 122.

Whatever happened to the insistence by food industry cultists of the
need for "properly set up trials" and far reaching massive
epidemiological studies and large scale multi-million dollar double
blind studies etc, to prove any minor scientific point being studied.

Talk about double standards in scientific proof.

TC - Meat Industry Representative

Do you not understand elementary sampling theory?
Do you believe that the only way to measure a population is to measure
every person?

jack- Hide quoted text -

- Show quoted text -

Quite the extrapolation. Test 122 people and apply those findings to
the entire 298,444,215 population. Amazing how the press has blindly
accepted that "Half the country has the diabetes gene" from a sampling
of 122.

Whatever happened to the insistence by food industry cultists of the
need for "properly set up trials" and far reaching massive
epidemiological studies and large scale multi-million dollar double
blind studies etc, to prove any minor scientific point being studied.

Talk about double standards in scientific proof.

Your subject line was from a news article where some reporter was taken
with this fact, not the study you pasted. This was not to determine the
percent of the population with the gene, that had already been done in
othr research. One either has the gene or not. This study was to see
what distortions in fat and glucose intake could be found among those
who do have it. Your remarks are apples and oranges. There is no
single diabetic gene but a set which tends to predispose overeating and
sedentary people to a higher risk for it. The more of the genes one has
the higher the potential.

who do have it. Your remarks are apples and oranges. There is no
single diabetic gene but a set which tends to predispose overeating and
sedentary people to a higher risk for it. The more of the genes one has
the higher the potential.

Actually it doesn't say anything about a predispositon to "overeat".
You might actually want to read the article next time you comment on
it.

And somehow you find great offense when I make statements that go a
wee bit beyond the language used in a particluar study, but you seem
to find nothing at all objectionable when the press makes such
incredibly far out claims about *half the population* having "the
diabetes gene" based on one study with a mere 122 test subjects that
actually says nothing of the sort. This seems to not bother you. Why
is that? Other than the fact that my claims run counter to the food
industry cult paradigms while the nonsensical press headlines fall
comfortably within it.

In other words, if the scientific truth runs counter to the food
industry cult paradigm, attack it. If lies fits the food industry cult
paradigm, that's ok.

http://www.ajcn.org/cgi/content/abstract/85/1/102

FABP2 Ala54Thr genotype is associated with glucoregulatory function
and lipid oxidation after a high-fat meal in sedentary nondiabetic men
and women1,2,3
Edward P Weiss, Josef Brandauer, Onanong Kulaputana, Ioana A Ghiu,
Christopher R Wohn, Dana A Phares, Alan R Shuldiner and James M
Hagberg
1 From the Department of Kinesiology, University of Maryland, College
Park, MD (EPW, JB, OK, IAG, CRW, DAP, and JMH); the Division of
Endocrinology, Diabetes, and Nutrition, University of Maryland School
of Medicine, Baltimore, MD (ARS); and the Geriatric Research Education
and Clinical Center, Baltimore Veterans Administration Medical Center,
Baltimore, MD (ARS)

Background: A common functional missense mutation [Ala54Thr of the
fatty acid-binding protein 2 gene (FABP2)] has previously been studied
for associations with glucoregulation, postprandial lipemia, and lipid
oxidation rates. However, most of those studies have not accounted for
the interactive and potentially confounding effects of habitual
physical activity and diet.

Objective: We tested the hypothesis that, in sedentary nondiabetic
subjects following a low-fat diet, Thr54 FABP2 carriers have lower
glucoregulatory function, greater postprandial lipemia, and greater
lipid oxidation rates than do their Ala54 FABP2-homozygous
counterparts.

Design: Men and women (n = 122) aged 50-75 y who were following a low-
fat diet were genotyped and underwent oral-glucose-tolerance tests. A
subgroup (n = 36) also underwent postprandial lipemia tests with lipid
oxidation rate measurements.

Results: Thr54 carriers were less likely to have normal glucose
tolerance (P = 0.05) and had higher fasting glucose concentrations (P
= 0.003) than did Ala54 homozygotes. In Thr54 carriers, the insulin
sensitivity index was lower (P = 0.02), and the fasting insulin and
the oral-glucose-tolerance test insulin area under the curve were
higher (P = 0.05 and 0.03, respectively) than in Ala54 homozygotes.
FABP2 genotype was not associated with fasting or postprandial lipemia
test triacylglycerol or free fatty acids (P 0.22 for all), but
postprandial lipid oxidation rates were higher (P = 0.01), which
suggests that fat absorption is higher in Thr54 carriers than in Ala54
homozygotes.

Conclusions: In sedentary nondiabetic persons following a low-fat
diet, FABP2 Thr54 carriers have lower glucose tolerance and lower
insulin action than do Ala54-homozygous persons. Furthermore, FABP
Thr54 carriers have higher lipid oxidation rates, which may be the
mechanism of glucoregulatory dysfunction.

**************

Quite the extrapolation. Test 122 people and apply those findings to
the entire 298,444,215 population. Amazing how the press has blindly
accepted that "Half the country has the diabetes gene" from a sampling
of 122.

Whatever happened to the insistence by food industry cultists of the
need for "properly set up trials" and far reaching massive
epidemiological studies and large scale multi-million dollar double
blind studies etc, to prove any minor scientific point being studied.

Talk about double standards in scientific proof.

TC

On Jan 31, 12:42 pm, "TC" <tunder...@hotmail.com> wrote:





http://www.ajcn.org/cgi/content/abstract/85/1/102

FABP2 Ala54Thr genotype is associated with glucoregulatory function
and lipid oxidation after a high-fat meal in sedentary nondiabetic men
and women1,2,3
Edward P Weiss, Josef Brandauer, Onanong Kulaputana, Ioana A Ghiu,
Christopher R Wohn, Dana A Phares, Alan R Shuldiner and James M
Hagberg
1 From the Department of Kinesiology, University of Maryland, College
Park, MD (EPW, JB, OK, IAG, CRW, DAP, and JMH); the Division of
Endocrinology, Diabetes, and Nutrition, University of Maryland School
of Medicine, Baltimore, MD (ARS); and the Geriatric Research Education
and Clinical Center, Baltimore Veterans Administration Medical Center,
Baltimore, MD (ARS)

Background: A common functional missense mutation [Ala54Thr of the
fatty acid-binding protein 2 gene (FABP2)] has previously been studied
for associations with glucoregulation, postprandial lipemia, and lipid
oxidation rates. However, most of those studies have not accounted for
the interactive and potentially confounding effects of habitual
physical activity and diet.

Objective: We tested the hypothesis that, in sedentary nondiabetic
subjects following a low-fat diet, Thr54 FABP2 carriers have lower
glucoregulatory function, greater postprandial lipemia, and greater
lipid oxidation rates than do their Ala54 FABP2-homozygous
counterparts.

Design: Men and women (n = 122) aged 50-75 y who were following a low-
fat diet were genotyped and underwent oral-glucose-tolerance tests. A
subgroup (n = 36) also underwent postprandial lipemia tests with lipid
oxidation rate measurements.

Results: Thr54 carriers were less likely to have normal glucose
tolerance (P = 0.05) and had higher fasting glucose concentrations (P
= 0.003) than did Ala54 homozygotes. In Thr54 carriers, the insulin
sensitivity index was lower (P = 0.02), and the fasting insulin and
the oral-glucose-tolerance test insulin area under the curve were
higher (P = 0.05 and 0.03, respectively) than in Ala54 homozygotes.
FABP2 genotype was not associated with fasting or postprandial lipemia
test triacylglycerol or free fatty acids (P 0.22 for all), but
postprandial lipid oxidation rates were higher (P = 0.01), which
suggests that fat absorption is higher in Thr54 carriers than in Ala54
homozygotes.

Conclusions: In sedentary nondiabetic persons following a low-fat
diet, FABP2 Thr54 carriers have lower glucose tolerance and lower
insulin action than do Ala54-homozygous persons. Furthermore, FABP
Thr54 carriers have higher lipid oxidation rates, which may be the
mechanism of glucoregulatory dysfunction.

**************

Quite the extrapolation. Test 122 people and apply those findings to
the entire 298,444,215 population. Amazing how the press has blindly
accepted that "Half the country has the diabetes gene" from a sampling
of 122.

Whatever happened to the insistence by food industry cultists of the
need for "properly set up trials" and far reaching massive
epidemiological studies and large scale multi-million dollar double
blind studies etc, to prove any minor scientific point being studied.

Talk about double standards in scientific proof.

TC

---------------------------------------------------------------------------­-----

By Robert Cohen Executive Director

= Diabetes

---------------------------------------------------------------------------­-----

"The National Dairy Board's Slogan, 'Milk. It does a body good,'
sounds a little hollow these days."

Scientific American, October, 1992

---------------------------------------------------------------------------­-----

"Studies have suggested that bovine serum albumin is the milk protein
responsible for the onset of diabetes... Patients with insulin-
dependent diabetes mellitus produce antibodies to cow milk proteins
that participate in the development of islet dysfunction... Taken as a
whole, our findings suggest that an active response in patients with
IDDM (to the bovine protein) is a feature of the autoimmune
response."

New England Journal of Medicine, July 30, 1992

---------------------------------------------------------------------------­-----

"In lieu of the recent evidence that cow's milk protein may be
implicated in the pathogenesis of diabetes mellitus, we believe that
the Committee on Nutrition should clarify whether cow's milk is ever
appropriate for children and whether or not infant formulas that are
based on cow's milk protein are appropriate alternatives to breast
milk."

Pediatrics, July, 1992: 89

---------------------------------------------------------------------------­-----

"Antibodies to bovine beta-casein are present in over a third of IDDM
patients and relatively non-existent in healthy individuals."

LANCET, October, 1996, 348

---------------------------------------------------------------------------­-----

"Cow's milk proteins are unique in one respect: in industrialized
countries they are the first foreign proteins entering the infant gut,
since most formulations for babies are cow milk-based. The first pilot
stage of our IDD prevention study found that oral exposure to dairy
milk proteins in infancy resulted in both cellular and immune
response...this suggests the possible importance of the gut immune
system to the pathogenesis of IDD."

LANCET, Dec 14, 1996

---------------------------------------------------------------------------­-----

"Introduction of dairy products and high milk consumption during
childhood may increase the child's risk of developing juvenile
diabetes."

Diabetologia 1994;37(4):381-387

---------------------------------------------------------------------------­-----

"These new studies, and more than 20 well-documented previous ones,
have prompted one researcher to say the link between milk and juvenile
diabetes is 'very solid'."

Diabetes Care 1994;17(12)

---------------------------------------------------------------------------­-----

Robert Cohen author of: MILK A-Z

(201-871-5871)
Executive Director (notmilk...@notmilk.com)
Dairy Education Boardhttp://www.notmilk.com

---------------------------------------------------------------------------­-----

Do you know of a friend or family member with one or more of these
milk-related problems? Do them a huge favor and forward the URL or
this entire file to them.

Do you know of someone who should read these newsletters? If so, have
them send an empty Email to notmilk-subscr...@yahoogroups.com and they
will receive it (automatically)!- Hide quoted text -

- Show quoted text -

who do have it. Your remarks are apples and oranges. There is no
single diabetic gene but a set which tends to predispose overeating and
sedentary people to a higher risk for it. The more of the genes one has
the higher the potential.
Actually it doesn't say anything about a predispositon to "overeat".
You might actually want to read the article next time you comment on
it.

And somehow you find great offense when I make statements that go a
wee bit beyond the language used in a particluar study, but you seem
to find nothing at all objectionable when the press makes such
incredibly far out claims about *half the population* having "the
diabetes gene" based on one study with a mere 122 test subjects that
actually says nothing of the sort. This seems to not bother you. Why
is that? Other than the fact that my claims run counter to the food
industry cult paradigms while the nonsensical press headlines fall
comfortably within it.

In other words, if the scientific truth runs counter to the food
industry cult paradigm, attack it. If lies fits the food industry cult
paradigm, that's ok.

Smile, the predisposed remark was in addition to my observation of how
you did not understande the abstract you pasted as a fuller explanation.
As mentioned before, reading comprehension must now be added to our
growing list.

I noted that the press picked up on the "half" which was not the point
of the pasted abstract per sey. You made no claims but were at strained
pains to slam research you did not, and remans so, understand and which
was chosen because it went against a dearly held belief system which
acts as blindders. Another point we are forced also to add to the list.
Noting also that the conclusion above is par for the course based on
wobbly logic and distorted grasp of evidence mixed with a generous dab
of wishful thinking if ot paranoia. Other then those few facts, you
done good.- Hide quoted text -

- Show quoted text -

Quite the extrapolation. Test 122 people and apply those findings to
the entire 298,444,215 population. Amazing how the press has blindly
accepted that "Half the country has the diabetes gene" from a sampling
of 122.

Whatever happened to the insistence by food industry cultists of the
need for "properly set up trials" and far reaching massive
epidemiological studies and large scale multi-million dollar double
blind studies etc, to prove any minor scientific point being studied.

Talk about double standards in scientific proof.

TC - Meat Industry Representative

Do you not understand elementary sampling theory?
Do you believe that the only way to measure a population is to measure
every person?

jack- Hide quoted text -

- Show quoted text -

Isn't this sampling anecdotal? It's just what a few people reportedly
observed.

TC - Meat Industry Lobbyist

Are they talking about fresh real whole milk from healthy cows or are
they talking about the homogenized high temperature pasteurized de-
natured chemically altered and separated and re-constituted crap from
hormone-enhanced pellet feed-fed cows that is being sold as milk in
the supermarket? Quality makes a HUGE difference.

TC - Meat Industry Rep

On Jan 31, 2:13 pm, p...@consult.net wrote:
Quite the extrapolation. Test 122 people and apply those findings to
the entire 298,444,215 population. Amazing how the press has blindly
accepted that "Half the country has the diabetes gene" from a sampling
of 122.

Whatever happened to the insistence by food industry cultists of the
need for "properly set up trials" and far reaching massive
epidemiological studies and large scale multi-million dollar double
blind studies etc, to prove any minor scientific point being studied.

Talk about double standards in scientific proof.

Your subject line was from a news article where some reporter was taken
with this fact, not the study you pasted. This was not to determine the
percent of the population with the gene, that had already been done in
othr research. One either has the gene or not. This study was to see
what distortions in fat and glucose intake could be found among those
who do have it. Your remarks are apples and oranges. There is no
single diabetic gene but a set which tends to predispose overeating and
sedentary people to a higher risk for it. The more of the genes one has
the higher the potential.

Actually it doesn't say anything about a predispositon to "overeat".
You might actually want to read the article next time you comment on
it.

And somehow you find great offense when I make statements that go a
wee bit beyond the language used in a particluar study, but you seem
to find nothing at all objectionable when the press makes such
incredibly far out claims about *half the population* having "the
diabetes gene" based on one study with a mere 122 test subjects that
actually says nothing of the sort. This seems to not bother you. Why
is that? Other than the fact that my claims run counter to the food
industry cult paradigms while the nonsensical press headlines fall
comfortably within it.

On 1 Feb 2007 11:04:52 -0800, "TC" <tunder...@hotmail.com> wrote:

Are they talking about fresh real whole milk from healthy cows or are
they talking about the homogenized high temperature pasteurized de-
natured chemically altered and separated and re-constituted crap from
hormone-enhanced pellet feed-fed cows that is being sold as milk in
the supermarket? Quality makes a HUGE difference.

TC - Meat Industry Rep

Your evidence for this claim of such a difference?

Anyway, surely you despise milk (and all processed dairy), as it is
surely only meant for calves.

jack