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A cereal diet promotes type I diabetes and lowers cathelicidin production in the gut
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Kofi
Apr 21, 2013, 4:49:16 AM4/21/13
to
This new study provides more circumstantial evidence for what I
speculated some years ago - that cathelicidin seems to play some role in
guarding intestinal integrity.
Although I'm not a big fan of hydrolyzing anything - or of casein for
that matter - hydrolyzed casein appears superior to some dietary
alternatives for gut permeability in several studies across time.
Cathelicidin can be promoted through a PPARalpha/carnitine/butyrate/HDAC
pathway. Perhaps not-so-coincidentally gluten can depress PPARalpha in
epidydimal fat.
Yet another nail in the coffin of wheat?
Promotion of Autoimmune Diabetes by Cereal Diet in the Presence or
Absence of Microbes Associated With Gut Immune Activation, Regulatory
Imbalance, and Altered Cathelicidin Antimicrobial Peptide.
Patrick C, Wang GS, Lefebvre DE, Crookshank JA, Sonier B, Eberhard C,
Mojibian M, Kennedy CR, Brooks SP, Kalmokoff ML, Maglio M, Troncone R,
Poussier P, Scott FW.
Diabetes. 2013 Feb 14. [Epub ahead of print]
Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa,
Ontario, Canada.
We are exposed to millions of microbial and dietary antigens via the
gastrointestinal tract, which likely plays a key role in type 1 diabetes
(T1D). We differentiated the effects of these two major environmental
factors on gut immunity and T1D. Diabetes-prone BioBreeding (BBdp) rats
were housed in specific pathogen-free (SPF) or germ-free (GF) conditions
and weaned onto diabetes-promoting cereal diets or a protective
low-antigen hydrolyzed casein (HC) diet, and T1D incidence was
monitored. Fecal microbiota 16S rRNA genes, immune cell distribution,
and gene expression in the jejunum were analyzed. T1D was highest in
cereal-SPF (65%) and cereal-GF rats (53%) but inhibited and delayed in
HC-fed counterparts. Nearly all HC-GF rats remained diabetes-free,
whereas HC-fed SPF rats were less protected (7% vs. 29%). Bacterial
communities differed in SPF rats fed cereal compared with HC. Cereal-SPF
rats displayed increased gut CD3(+) and CD8a(+) lymphocytes, ratio of
Ifng to Il4 mRNA, and Lck expression, indicating T-cell activation. The
ratio of CD3(+) T cells expressing the T(reg) marker Foxp3(+) was
highest in HC-GF and lowest in cereal-SPF rats. Resident CD163(+) M2
macrophages were increased in HC-protected rats. The cathelicidin
antimicrobial peptide (Camp) gene was upregulated in the jejunum of HC
diet-protected rats, and CAMP(+) cells colocalized with CD163. A cereal
diet was a stronger promoter of T1D than gut microbes in association
with impaired gut immune homeostasis.
PMID 23349499
infant feeding plays a role in the initiation of the disease process
leading to type 1 diabetes in children carrying increased genetic
disease risk; The study population comprised 230 newborn infants with at
least one family member affected by type 1 diabetes and a predisposing
genotype based on screening cord blood at birth. The participants were
randomized into two groups; the infants in the intervention group were
weaned to a highly hydrolyzed casein-based formula (Nutramigen, Mead
Johnson Nutrition), while those in the control group were weaned to a
regular cow's milk-based formula supplemented with 20% Nutramigen to
make the two formulas comparable in terms of smell and taste. The
intention was that the participants should be exposed to their study
formula for at least 2 months by the age of 6 months, or if exclusively
breast-fed up to that age by the age of 8 months. The study participants
were observed up to the age of 10 years for the appearance of
diabetes-predictive autoantibodies and progression to type 1 diabetes.
Twenty-five children (12%) developed at least two diabetes-predictive
autoantibodies out of the five tested for, which marks a high risk of
presenting with clinical diabetes. Seventeen children tested positive
for two or more autoantibodies had been randomized to the control group
(16%), whereas seven belonged to the intervention (casein hydrolysate)
group (7%). Nine children (8%) in the control group presented with
clinical diabetes by the age of 10 years, while four of those (4%) who
had been exposed to the casein hydrolysate progressed to clinical
disease; the safe and simple dietary intervention applied in this pilot
trial was capable of reducing the emergence of diabetes-predictive
autoantibodies by about 50% by age 10 in the participants carrying
increased disease risk. The current study population does not provide
sufficient statistical power to definitely conclude whether an
intervention of this type will reduce the frequency of clinical type 1
diabetes, although the preliminary data are promising; A full-scale
trial -- TRIGR (Trial to Reduce IDDM in the Genetically at Risk) -- was
initiated in 2002 and is currently running in 77 study centers in 15
countries to provide a conclusive answer to the question of whether
weaning to a highly hydrolyzed formula will reduce the cumulative
incidence of clinical type 1 diabetes. A total of 2160 children have
been randomized for TRIGR. The first end-point in TRIGR, i.e. positivity
for at least two diabetes-associated autoantibodies and/or clinical type
1 diabetes by age 6, will be reached in 2013 and the final endpoint,
clinical diabetes by the age of 10 in the year 2017; The current pilot
trial and the full-scale TRIGR aim at primary prevention of type 1
diabetes, i.e. to stop the initiation of the disease process which lasts
for months and years before clinical disease manifestation. Dr. Knip
emphasizes that the results indicate that it is possible to reduce the
initiation of the disease process substantially by early dietary
intervention in high-risk individuals; this pilot trial has been
performed in children with predisposing genes and a family member
affected by type 1 diabetes; The researchers have not determined the
decisive difference is between the casein hydrolysate and regular cow's
milk-based formulas. An experimental study recently showed that a highly
hydrolyzed formula reduces gut permeability and has a beneficial effect
on gut microflora. Studies have been initiated to identify the
mechanism(s) by which the highly hydrolyzed formula protects against
beta-cell autoimmunity represented by diabetes-predictive
autoantibodies. Another Finnish trial is currently testing the
hypothesis whether an insulin-free formula decreases the initiation of
the diabetic disease process in children at risk given the central role
of insulin as an early autoantigen in type 1 diabetes.
<http://www.sciencedaily.com/releases/2010/11/101110171341.htm>, [Mikael
Knip, Suvi M. Virtanen, Karri Sepp�, Jorma Ilonen, Erkki Savilahti, Outi
Vaarala, Antti Reunanen, Kari Teramo, Anu-Maaria H�m�l�inen, Johanna
Paronen, Hans-Michael Dosch, Timo Hakulinen, and Hans K. �kerblom for
the Finnish TRIGR Study Group. Dietary Intervention in Infancy and Later
Signs of Beta-Cell Autoimmunity. New England Journal of Medicine, 2010;
363: 1900-1908 DOI: 10.1056/NEJMoa1004809], abstract: Early exposure to
complex dietary proteins may increase the risk of beta-cell autoimmunity
and type 1 diabetes in children with genetic susceptibility. We tested
the hypothesis that supplementing breast milk with highly hydrolyzed
milk formula would decrease the cumulative incidence of
diabetes-associated autoantibodies in such children. Methods In this
double-blind, randomized trial, we assigned 230 infants with
HLA-conferred susceptibility to type 1 diabetes and at least one family
member with type 1 diabetes to receive either a casein hydrolysate
formula or a conventional, cow's-milk-based formula (control) whenever
breast milk was not available during the first 6 to 8 months of life.
Autoantibodies to insulin, glutamic acid decarboxylase (GAD), the
insulinoma-associated 2 molecule (IA-2), and zinc transporter 8 were
analyzed with the use of radiobinding assays, and islet-cell antibodies
were analyzed with the use of immunofluorescence, during a median
observation period of 10 years (mean, 7.5). The children were monitored
for incident type 1 diabetes until they were 10 years of age. Results
The unadjusted hazard ratio for positivity for one or more
autoantibodies in the casein hydrolysate group, as compared with the
control group, was 0.54 (95% confidence interval [CI], 0.29 to 0.95),
and the hazard ratio adjusted for an observed difference in the duration
of exposure to the study formula was 0.51 (95% CI, 0.28 to 0.91). The
unadjusted hazard ratio for positivity for two or more autoantibodies
was 0.52 (95% CI, 0.21 to 1.17), and the adjusted hazard ratio was 0.47
(95% CI, 0.19 to 1.07). The rate of reported adverse events was similar
in the two groups. Conclusions Dietary intervention during infancy
appears to have a long-lasting effect on markers of beta-cell
autoimmunity - markers that may reflect an autoimmune process leading to
type 1 diabetes [PMID 21067382]
This study evaluated the possible role of enterovirus infections in the
pathogenesis of type I (insulin-dependent) diabetes in a prospective
dietary intervention trial. Children participated in the second pilot of
the Trial to Reduce IDDM in Genetically at Risk (TRIGR) project. They
were randomized into two groups receiving either a casein hydrolysed
formula (Nutramigen) or a regular formula, whenever breast milk was not
available over the first 6-8 months of life. Altogether 19 children who
turned positive for autoantibodies associated with type I diabetes by 2
years of age and 84 matched control children were analysed for
enterovirus antibodies and enterovirus RNA in serum. Enterovirus
infections were common during the first 2 years of life and more
frequent among boys than girls (P = 0.02). Autoantibody-positive
children had more enterovirus infections than autoantibody-negative
children before the appearance of autoantibodies (0.83 versus 0.29
infection per child, P = 0.01). The average levels of IgG antibodies to
echovirus antigen were also higher in autoantibody-positive than in
autoantibody-negative children (P = 0.0009). No difference was found in
the frequency of enterovirus infections between children receiving the
casein hydrolysed formula or regular formula. These results suggest that
enterovirus infections are associated with the induction of beta-cell
autoimmunity in young children with increased genetic susceptibility to
type I diabetes [PMID 12699416]
gliadin in wheat gluten binds to CXCR3 and leads to MyD88-dependent
zonulin release and increased intestinal permeability - even in wild
type, healthy mice; mucosal CXCR3 expression is elevated in active
celiac disease but returns to baseline levels on a gluten-free diet;
gliadin increases zonulin release and intestinal permeability in
wild-type but not CXCR3(-/-) mouse small intestine [PMID 18485912]
a high-fat diet with gluten depresses PPARalpha, LPL, HSL and CPT-1,
adiponectin and GLUT-4 in epidydimal fat [PMID 23253599]
speculated some years ago - that cathelicidin seems to play some role in
guarding intestinal integrity.
Although I'm not a big fan of hydrolyzing anything - or of casein for
that matter - hydrolyzed casein appears superior to some dietary
alternatives for gut permeability in several studies across time.
Cathelicidin can be promoted through a PPARalpha/carnitine/butyrate/HDAC
pathway. Perhaps not-so-coincidentally gluten can depress PPARalpha in
epidydimal fat.
Yet another nail in the coffin of wheat?
Promotion of Autoimmune Diabetes by Cereal Diet in the Presence or
Absence of Microbes Associated With Gut Immune Activation, Regulatory
Imbalance, and Altered Cathelicidin Antimicrobial Peptide.
Patrick C, Wang GS, Lefebvre DE, Crookshank JA, Sonier B, Eberhard C,
Mojibian M, Kennedy CR, Brooks SP, Kalmokoff ML, Maglio M, Troncone R,
Poussier P, Scott FW.
Diabetes. 2013 Feb 14. [Epub ahead of print]
Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa,
Ontario, Canada.
We are exposed to millions of microbial and dietary antigens via the
gastrointestinal tract, which likely plays a key role in type 1 diabetes
(T1D). We differentiated the effects of these two major environmental
factors on gut immunity and T1D. Diabetes-prone BioBreeding (BBdp) rats
were housed in specific pathogen-free (SPF) or germ-free (GF) conditions
and weaned onto diabetes-promoting cereal diets or a protective
low-antigen hydrolyzed casein (HC) diet, and T1D incidence was
monitored. Fecal microbiota 16S rRNA genes, immune cell distribution,
and gene expression in the jejunum were analyzed. T1D was highest in
cereal-SPF (65%) and cereal-GF rats (53%) but inhibited and delayed in
HC-fed counterparts. Nearly all HC-GF rats remained diabetes-free,
whereas HC-fed SPF rats were less protected (7% vs. 29%). Bacterial
communities differed in SPF rats fed cereal compared with HC. Cereal-SPF
rats displayed increased gut CD3(+) and CD8a(+) lymphocytes, ratio of
Ifng to Il4 mRNA, and Lck expression, indicating T-cell activation. The
ratio of CD3(+) T cells expressing the T(reg) marker Foxp3(+) was
highest in HC-GF and lowest in cereal-SPF rats. Resident CD163(+) M2
macrophages were increased in HC-protected rats. The cathelicidin
antimicrobial peptide (Camp) gene was upregulated in the jejunum of HC
diet-protected rats, and CAMP(+) cells colocalized with CD163. A cereal
diet was a stronger promoter of T1D than gut microbes in association
with impaired gut immune homeostasis.
PMID 23349499
infant feeding plays a role in the initiation of the disease process
leading to type 1 diabetes in children carrying increased genetic
disease risk; The study population comprised 230 newborn infants with at
least one family member affected by type 1 diabetes and a predisposing
genotype based on screening cord blood at birth. The participants were
randomized into two groups; the infants in the intervention group were
weaned to a highly hydrolyzed casein-based formula (Nutramigen, Mead
Johnson Nutrition), while those in the control group were weaned to a
regular cow's milk-based formula supplemented with 20% Nutramigen to
make the two formulas comparable in terms of smell and taste. The
intention was that the participants should be exposed to their study
formula for at least 2 months by the age of 6 months, or if exclusively
breast-fed up to that age by the age of 8 months. The study participants
were observed up to the age of 10 years for the appearance of
diabetes-predictive autoantibodies and progression to type 1 diabetes.
Twenty-five children (12%) developed at least two diabetes-predictive
autoantibodies out of the five tested for, which marks a high risk of
presenting with clinical diabetes. Seventeen children tested positive
for two or more autoantibodies had been randomized to the control group
(16%), whereas seven belonged to the intervention (casein hydrolysate)
group (7%). Nine children (8%) in the control group presented with
clinical diabetes by the age of 10 years, while four of those (4%) who
had been exposed to the casein hydrolysate progressed to clinical
disease; the safe and simple dietary intervention applied in this pilot
trial was capable of reducing the emergence of diabetes-predictive
autoantibodies by about 50% by age 10 in the participants carrying
increased disease risk. The current study population does not provide
sufficient statistical power to definitely conclude whether an
intervention of this type will reduce the frequency of clinical type 1
diabetes, although the preliminary data are promising; A full-scale
trial -- TRIGR (Trial to Reduce IDDM in the Genetically at Risk) -- was
initiated in 2002 and is currently running in 77 study centers in 15
countries to provide a conclusive answer to the question of whether
weaning to a highly hydrolyzed formula will reduce the cumulative
incidence of clinical type 1 diabetes. A total of 2160 children have
been randomized for TRIGR. The first end-point in TRIGR, i.e. positivity
for at least two diabetes-associated autoantibodies and/or clinical type
1 diabetes by age 6, will be reached in 2013 and the final endpoint,
clinical diabetes by the age of 10 in the year 2017; The current pilot
trial and the full-scale TRIGR aim at primary prevention of type 1
diabetes, i.e. to stop the initiation of the disease process which lasts
for months and years before clinical disease manifestation. Dr. Knip
emphasizes that the results indicate that it is possible to reduce the
initiation of the disease process substantially by early dietary
intervention in high-risk individuals; this pilot trial has been
performed in children with predisposing genes and a family member
affected by type 1 diabetes; The researchers have not determined the
decisive difference is between the casein hydrolysate and regular cow's
milk-based formulas. An experimental study recently showed that a highly
hydrolyzed formula reduces gut permeability and has a beneficial effect
on gut microflora. Studies have been initiated to identify the
mechanism(s) by which the highly hydrolyzed formula protects against
beta-cell autoimmunity represented by diabetes-predictive
autoantibodies. Another Finnish trial is currently testing the
hypothesis whether an insulin-free formula decreases the initiation of
the diabetic disease process in children at risk given the central role
of insulin as an early autoantigen in type 1 diabetes.
<http://www.sciencedaily.com/releases/2010/11/101110171341.htm>, [Mikael
Knip, Suvi M. Virtanen, Karri Sepp�, Jorma Ilonen, Erkki Savilahti, Outi
Vaarala, Antti Reunanen, Kari Teramo, Anu-Maaria H�m�l�inen, Johanna
Paronen, Hans-Michael Dosch, Timo Hakulinen, and Hans K. �kerblom for
the Finnish TRIGR Study Group. Dietary Intervention in Infancy and Later
Signs of Beta-Cell Autoimmunity. New England Journal of Medicine, 2010;
363: 1900-1908 DOI: 10.1056/NEJMoa1004809], abstract: Early exposure to
complex dietary proteins may increase the risk of beta-cell autoimmunity
and type 1 diabetes in children with genetic susceptibility. We tested
the hypothesis that supplementing breast milk with highly hydrolyzed
milk formula would decrease the cumulative incidence of
diabetes-associated autoantibodies in such children. Methods In this
double-blind, randomized trial, we assigned 230 infants with
HLA-conferred susceptibility to type 1 diabetes and at least one family
member with type 1 diabetes to receive either a casein hydrolysate
formula or a conventional, cow's-milk-based formula (control) whenever
breast milk was not available during the first 6 to 8 months of life.
Autoantibodies to insulin, glutamic acid decarboxylase (GAD), the
insulinoma-associated 2 molecule (IA-2), and zinc transporter 8 were
analyzed with the use of radiobinding assays, and islet-cell antibodies
were analyzed with the use of immunofluorescence, during a median
observation period of 10 years (mean, 7.5). The children were monitored
for incident type 1 diabetes until they were 10 years of age. Results
The unadjusted hazard ratio for positivity for one or more
autoantibodies in the casein hydrolysate group, as compared with the
control group, was 0.54 (95% confidence interval [CI], 0.29 to 0.95),
and the hazard ratio adjusted for an observed difference in the duration
of exposure to the study formula was 0.51 (95% CI, 0.28 to 0.91). The
unadjusted hazard ratio for positivity for two or more autoantibodies
was 0.52 (95% CI, 0.21 to 1.17), and the adjusted hazard ratio was 0.47
(95% CI, 0.19 to 1.07). The rate of reported adverse events was similar
in the two groups. Conclusions Dietary intervention during infancy
appears to have a long-lasting effect on markers of beta-cell
autoimmunity - markers that may reflect an autoimmune process leading to
type 1 diabetes [PMID 21067382]
This study evaluated the possible role of enterovirus infections in the
pathogenesis of type I (insulin-dependent) diabetes in a prospective
dietary intervention trial. Children participated in the second pilot of
the Trial to Reduce IDDM in Genetically at Risk (TRIGR) project. They
were randomized into two groups receiving either a casein hydrolysed
formula (Nutramigen) or a regular formula, whenever breast milk was not
available over the first 6-8 months of life. Altogether 19 children who
turned positive for autoantibodies associated with type I diabetes by 2
years of age and 84 matched control children were analysed for
enterovirus antibodies and enterovirus RNA in serum. Enterovirus
infections were common during the first 2 years of life and more
frequent among boys than girls (P = 0.02). Autoantibody-positive
children had more enterovirus infections than autoantibody-negative
children before the appearance of autoantibodies (0.83 versus 0.29
infection per child, P = 0.01). The average levels of IgG antibodies to
echovirus antigen were also higher in autoantibody-positive than in
autoantibody-negative children (P = 0.0009). No difference was found in
the frequency of enterovirus infections between children receiving the
casein hydrolysed formula or regular formula. These results suggest that
enterovirus infections are associated with the induction of beta-cell
autoimmunity in young children with increased genetic susceptibility to
type I diabetes [PMID 12699416]
gliadin in wheat gluten binds to CXCR3 and leads to MyD88-dependent
zonulin release and increased intestinal permeability - even in wild
type, healthy mice; mucosal CXCR3 expression is elevated in active
celiac disease but returns to baseline levels on a gluten-free diet;
gliadin increases zonulin release and intestinal permeability in
wild-type but not CXCR3(-/-) mouse small intestine [PMID 18485912]
a high-fat diet with gluten depresses PPARalpha, LPL, HSL and CPT-1,
adiponectin and GLUT-4 in epidydimal fat [PMID 23253599]
John H. Gohde
Apr 23, 2013, 6:58:00 AM4/23/13
to
> Vaarala, Antti Reunanen, Kari Teramo, Anu-Maaria H�m�l�inen, Johanna
> Paronen, Hans-Michael Dosch, Timo Hakulinen, and Hans K. �kerblom for
John H. Gohde
Apr 23, 2013, 5:19:29 PM4/23/13
to
On Apr 21, 4:49 am, Kofi <k...@anon.un> wrote:
> This new study provides more circumstantial evidence for what I
> speculated some years ago - that cathelicidin seems to play some role in
> guarding intestinal integrity.
>
> Although I'm not a big fan of hydrolyzing anything - or of casein for
> that matter - hydrolyzed casein appears superior to some dietary
> alternatives for gut permeability in several studies across time.
Pure Bull!
> speculated some years ago - that cathelicidin seems to play some role in
> guarding intestinal integrity.
>
> Although I'm not a big fan of hydrolyzing anything - or of casein for
> that matter - hydrolyzed casein appears superior to some dietary
> alternatives for gut permeability in several studies across time.
I eat a cereal / Whole grain based diet, other wise known as starch-
based. And, moi does NOT have Type 1 Diabetes, NOT even close.
It is just more Science Bull.
John H. Gohde
Apr 24, 2013, 8:30:32 AM4/24/13
to
be access online for FREE.
It is simply how stupid the people on these ngs truly are.
go to the very bottom of this article for further details.
http://naturalhealthperspective.com/food/whole-grains.html
http://tinyurl.com/akovb78
Trawley Trash
Apr 24, 2013, 11:15:31 AM4/24/13
to
On Tue, 23 Apr 2013 14:19:29 -0700 (PDT)
"John H. Gohde" <john.h...@gmail.com> wrote:
> I eat a cereal / Whole grain based diet, other wise known as starch-
> based. And, moi does NOT have Type 1 Diabetes, NOT even close.
Most people are not type 1 diabetic regardless of what they eat.
"John H. Gohde" <john.h...@gmail.com> wrote:
> I eat a cereal / Whole grain based diet, other wise known as starch-
> based. And, moi does NOT have Type 1 Diabetes, NOT even close.
Also most diabetics are not type 1.
John H. Gohde
Apr 24, 2013, 6:09:10 PM4/24/13
to
Trawley Trash
Apr 24, 2013, 9:28:37 PM4/24/13
to
On Wed, 24 Apr 2013 15:09:10 -0700 (PDT)
"John H. Gohde" <john.h...@gmail.com> wrote:
> > > I eat a cereal / Whole grain based diet, other wise known as
> > > starch- based. And, moi does NOT have Type 1 Diabetes, NOT even
> > > close.
> >
> > Most people are not type 1 diabetic regardless of what they eat.
> > Also most diabetics are not type 1.
>
>
>
> Precisely!
That does not mean that a starch-based diet will not cause
"John H. Gohde" <john.h...@gmail.com> wrote:
> > > I eat a cereal / Whole grain based diet, other wise known as
> > > starch- based. And, moi does NOT have Type 1 Diabetes, NOT even
> > > close.
> >
> > Most people are not type 1 diabetic regardless of what they eat.
> > Also most diabetics are not type 1.
>
>
>
> Precisely!
type II diabetes in susceptible individuals. This is something
like one third of the population. In my case cereal starch sets
it off along with legumes and dairy. Potatoes are perfectly OK.
BTW, when was the last time you had your a1c tested? What was the
value?
John H. Gohde
May 2, 2013, 4:01:31 AM5/2/13
to
On Apr 21, 4:49 am, Kofi <k...@anon.un> wrote:
> This new study provides more circumstantial evidence for what I
> speculated some years ago - that cathelicidin seems to play some role in
> guarding intestinal integrity.
Science Bull Alert!
> speculated some years ago - that cathelicidin seems to play some role in
> guarding intestinal integrity.
Kris K. Kaput0
Jun 13, 2013, 3:43:01 PM6/13/13
to
"Trawley Trash" wrote in message news:5fdm4a-...@jammer.gnet...
What is the point of the A1C BS? It fails every person that has severe
anemia. It is dependant on how long your haemoglobin lives and means
nothing.
KKK
Trawley Trash
Jun 14, 2013, 10:50:18 AM6/14/13
to
On Thu, 13 Jun 2013 15:43:01 -0400
"Kris K. Kaput0" <K...@alstupia.com> wrote:
> What is the point of the A1C BS? It fails every person that has
> severe anemia. It is dependant on how long your haemoglobin lives and
> means nothing.
Yes there are some assumptions that can be flawed in the a1c test.
"Kris K. Kaput0" <K...@alstupia.com> wrote:
> What is the point of the A1C BS? It fails every person that has
> severe anemia. It is dependant on how long your haemoglobin lives and
> means nothing.
But in most people most of the time it works well, and it is a better
indication that a single fasting blood glucose test. What we want
to look for is the average BG value, and the a1c provides a kind
of an average over several weeks of time.
This is what is used to diagnose diabetes. It
may fail in a person with severe anemia, but in that case there is a
more urgent problem to treat that will also show up in a normal
blood workup.
--
I'm Trawley Trash, and you haven't heard the last of me yet.
Josepi
Jul 18, 2013, 12:50:43 PM7/18/13
to
We thought your pure size, alone, was enough for a large sample.
--
"John H. Gohde" wrote in message
news:7b8a41b5-6ff4-4c08...@n5g2000yqg.googlegroups.com...
--
"John H. Gohde" wrote in message
news:7b8a41b5-6ff4-4c08...@n5g2000yqg.googlegroups.com...
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