Re: Fatty Liver

Andrew B. Chung said:

For those who are put off by the signature, my advance apologies for
how the LORD has reshaped me:

Prayerfully in Christ's love,

~ A History of the Mind-Body Connection ~
http://naturalhealthperspective.com/tutorials/history-mind-body-connection.html
"1940s>{Wellness}During the 1940s the self-help movement became
increasingly more psychologically oriented and was devoid of religious
overtones.[9]"

Andrew strikes me as one deeply confused puppy. 🙁

You seem to be unable to make up your mind whether good health is a
result of lifestyle, praying, or faith healing. 🙁

Thus, your confused muddy contradictory advice is very likely to induce
Neurasthenia in your targeted audience. 🙁

Confused puppies, such as yourself, really need to make up your mind
which works better: Praying or Changing Lifestyle factors. Make up
your mind Andrew, and STOP trying to confuse the hell out of the
public.

Just thought that you might want to know.
--
john gohde
Please read my tutorials Andrew. You need help, fast!
http://naturalhealthperspective.com/tutorials/

Reply against my post no 34 is pending.

Can you tell something about this mentioning in below quoted post:-

"Furthermore, adipose
tissue is a major endocrine organ that secretes numerous polypeptide
hormones and cytokines that are proinflammatory and proatherogenic."

Does it the property of only adipose tisse or also of other tissues?

Andrew B. Chung said:

Kumar said:

Pls look at following hypothesis:-

Ectopic Fat Storage Syndrome

The ectopic fat storage syndrome hypothesis suggests that as adipocytes
hypertrophy and reach their capacity for storing more fat, then
additional fat from excess dietary lipids or calories is deferred to
non-adipose tissues intracellularly, e.g. liver, skeletal muscle,
heart, and the beta cells of the pancreas where they can exert toxic
effects and dysfunction . This "lipotoxicity" may also be exacerbated
by impaired oxidation of fat within tissues . Furthermore, adipose
tissue is a major endocrine organ that secretes numerous polypeptide
hormones and cytokines that are proinflammatory and proatherogenic.
These play a major role in affecting insulin action in skeletal muscle
and creating a low-grade state of inflammation and endothelial
dysfunction . Compared to SCAT, VAT has been correlated more with
endothelial dysfunction .

CVATT-A Working Hypothesis

It must be emphasized that the current proposal is a working
hypothesis. Figure 1 describes a critical VAT threshold (CVATT) which
is unique for a given individual and represents a range for the
accumulation of a critical mass of VAT (CVATT) that when achieved,
leads to the development of metabolic syndrome. Note that insulin
sensitivity is important for weight gain and accumulation of VAT, and
investigators have proposed that insulin resistance may actually, to a
certain extent, be beneficial by protecting cells with already impaired
fatty acid oxidation. Once the CVATT is reached, insulin resistance
(IR) occurs, which may be protective initially . In addition to
protecting against further weight and fat gain , insulin resistance
prevents glucose and more fat from entering the cell and becoming
preferentially oxidized. Hence, insulin resistance also allows
intracellular fat already present within the cell to become oxidized
rather than cause further damage through "lipotoxicity ."
http://www.diabetesincontrol.com/modules.php?name=News&file=article&sid=2260
"

The above link indicate many aspects. It tells about possibility of
fats resistance in adipocytes resulting into their diversion to other
vital parts Can you comment on it?

This is metabolic syndrome (MetS).

Would be more than happy to "glow" and chat about this and other things
like cardiology, diabetes, cooking and nutrition that interest those
following this thread here during the next on-line chat (01/26/06) from
6 to 7 pm EST:

http://tinyurl.com/cpayh

For those who are put off by the signature, my advance apologies for
how the LORD has reshaped me:

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/be9va

Kumar said:

Reply against my post no 34 is pending.

Can you tell something about this mentioning in below quoted post:-

"Furthermore, adipose
tissue is a major endocrine organ that secretes numerous polypeptide
hormones and cytokines that are proinflammatory and proatherogenic."

Does it the property of only adipose tisse or also of other tissues?

Just the visceral adipocytes.

Would be more than happy to "glow" and chat about this and other things
like cardiology, diabetes, cooking and nutrition that interest those
following this thread here during the next on-line chat (01/26/06) from
6 to 7 pm EST:

http://tinyurl.com/cpayh

For those who are put off by the signature, my advance apologies for
how the LORD has reshaped me:

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/be9va

Andrew B. Chung said:

Kumar said:

Reply against my post no 34 is pending.

Can you tell something about this mentioning in below quoted post:-

"Furthermore, adipose
tissue is a major endocrine organ that secretes numerous polypeptide
hormones and cytokines that are proinflammatory and proatherogenic."

Does it the property of only adipose tisse or also of other tissues?

Just the visceral adipocytes.

Pls reply my post no 34.

"Furthermore, adipose
tissue is a major endocrine organ that secretes numerous polypeptide
hormones and cytokines that are proinflammatory and proatherogenic."

Do excess fats in tissues is proinflamatory, proatherogenic,
prodiabetic, proacidosis, procanerous?

Kumar said:

Andrew B. Chung said:

Kumar said:

Reply against my post no 34 is pending.

Can you tell something about this mentioning in below quoted post:-

"Furthermore, adipose
tissue is a major endocrine organ that secretes numerous polypeptide
hormones and cytokines that are proinflammatory and proatherogenic."

Does it the property of only adipose tisse or also of other tissues?

Just the visceral adipocytes.

Pls reply my post no 34.

Post#34 in this thread in the Google archive is from me.

Quoted message said:

"Furthermore, adipose
tissue is a major endocrine organ that secretes numerous polypeptide
hormones and cytokines that are proinflammatory and proatherogenic."

Do excess fats in tissues is proinflamatory, proatherogenic,
prodiabetic, proacidosis, procanerous?

Yes to all the above except for "proacidosis."

Would be more than happy to "glow" and chat about this and other things
like cardiology, diabetes, cooking and nutrition that interest those
following this thread here during the next on-line chat (01/26/06) from
6 to 7 pm EST:

http://tinyurl.com/cpayh

For those who are put off by the signature, my advance apologies for
how the LORD has reshaped me:

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/cbn2r

Andrew B. Chung said:

Kumar said:

Reply against my post no 34 is pending.

When I sort by date it comes 34 as under;

34. Kumar
Jan 22, 11:57 am show options

Newsgroups: alt.support.diabetes, sci.med.cardiology, sci.med
From: "Kumar" <[email hidden]> - Find messages by this
author
Date: 21 Jan 2006 22:57:57 -0800
Local: Sun, Jan 22 2006 11:57 am
Subject: Re: Fatty Liver
Reply | Reply to Author | Forward | Print | Individual Message | Show
original | Remove | Report Abuse

Andrew B. Chung said:

Kumar wrote:

Quoted message said:

Quoted message said:

Quoted message said:

The longer half-life of insulin is due to decreased rates of
degradation and not decreased rates of excretion.

Quoted message said:

Quoted message said:

Quoted message said:

and so he may need to adjust injected insulin

Quoted message said:

Quoted message said:

Can you explain how decreased rates of degradation of insulin happen?

Quoted message said:

Loss of nephrons where the degradation occurs.

Whether loss of nephrons causes increased or decreased filteration? On
one hand we say lesser filteration on other hand protiens(bigger
molecules) start coming into urine on getting DN?

Quoted message said:

Quoted message said:

What about cluster or crystal formation possibilty of molecules of
insulin?

Quoted message said:

There is no reason to invoke this.

Quoted message said:

Quoted message said:

Quoted message said:

> accordingly, whather insulin is lost or excreted in urine on pre-DN
> stages?

Quoted message said:

Quoted message said:

Quoted message said:

Insulin is not excreted in the urine.

Quoted message said:

Quoted message said:

Why when the molecyular weight of insulin is more than 1/4th of
filteration capacity of kydneys?

Quoted message said:

You just answered your question by your question.

Sorry, I meant; Why insulin is not filtered in kidneys, when the
molecular weight of insulin is less than 1/4th (less than 6000 D) of
filteration capacity of kidneys (30000 D)?

Quoted message said:

Quoted message said:

Moreover capillary permeability for
insulin is considered as 0.2.

Quoted message said:

The glomeruli of nephrons of the kidney are considerably less permeable
to polypeptides such as insulin than capillary beds.

Can it mean that extra cellular fluids in our tissues will have bigger
molecules than as we have in urine alike insulin?

Quoted message said:

Andrew B. Chung said:

Kumar wrote:

..

Quoted message said:

Quoted message said:

"Furthermore, adipose
tissue is a major endocrine organ that secretes numerous polypeptide
hormones and cytokines that are proinflammatory and proatherogenic."

Do excess fats in tissues is proinflamatory, proatherogenic,
prodiabetic, proacidosis, procanerous?

Yes to all the above except for "proacidosis."

Can it(VApro-alkaliosis and pro-azoospermia?
Whether inflammatory, atherogenic,cancerous, diabetic effects are
pro-acidosis or pro-alkaliosis?

Kumar said:

Andrew B. Chung said:

Kumar said:

Reply against my post no 34 is pending.

When I sort by date it comes 34 as under;

34. Kumar
Jan 22, 11:57 am show options

Newsgroups: alt.support.diabetes, sci.med.cardiology, sci.med
From: "Kumar" <[email hidden]> - Find messages by this
author
Date: 21 Jan 2006 22:57:57 -0800
Local: Sun, Jan 22 2006 11:57 am
Subject: Re: Fatty Liver
Reply | Reply to Author | Forward | Print | Individual Message | Show
original | Remove | Report Abuse

Andrew B. Chung said:

Kumar wrote:

Quoted message said:

Quoted message said:

> The longer half-life of insulin is due to decreased rates of
> degradation and not decreased rates of excretion.

Quoted message said:

Quoted message said:

> and so he may need to adjust injected insulin

Quoted message said:

Quoted message said:

Can you explain how decreased rates of degradation of insulin happen?

Quoted message said:

Loss of nephrons where the degradation occurs.

Whether loss of nephrons causes increased or decreased filteration?

Decreased

Quoted message said:

On
one hand we say lesser filteration on other hand protiens(bigger
molecules) start coming into urine on getting DN?

Proteinuria does happen with DN but this does not appreciably alter the
half-life of insulin.

Quoted message said:

Quoted message said:

Quoted message said:

What about cluster or crystal formation possibilty of molecules of
insulin?

Quoted message said:

There is no reason to invoke this.

Quoted message said:

Quoted message said:

> > accordingly, whather insulin is lost or excreted in urine on pre-DN
> > stages?

Quoted message said:

Quoted message said:

> Insulin is not excreted in the urine.

Quoted message said:

Quoted message said:

Why when the molecyular weight of insulin is more than 1/4th of
filteration capacity of kydneys?

Quoted message said:

You just answered your question by your question.

Sorry, I meant; Why insulin is not filtered in kidneys, when the
molecular weight of insulin is less than 1/4th (less than 6000 D) of
filteration capacity of kidneys (30000 D)?

Insulin is a charged polypeptide that will not get through the
glomerular basement membrane which is a more effective barrier when a
macromolecule has a charge.

Quoted message said:

Quoted message said:

Quoted message said:

Moreover capillary permeability for
insulin is considered as 0.2.

Quoted message said:

The glomeruli of nephrons of the kidney are considerably less permeable
to polypeptides such as insulin than capillary beds.

Can it mean that extra cellular fluids in our tissues will have bigger
molecules than as we have in urine alike insulin?

Yes.

Would be more than happy to "glow" and chat about this and other things
like cardiology, diabetes, cooking and nutrition that interest those
following this thread here during the next on-line chat (01/26/06) from
6 to 7 pm EST:

http://tinyurl.com/cpayh

For those who are put off by the signature, my advance apologies for
how the LORD has reshaped me:

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/cbn2r

Andrew B. Chung said:

Kumar said:

Andrew B. Chung said:

Kumar wrote:
> Reply against my post no 34 is pending.

When I sort by date it comes 34 as under;

34. Kumar
Jan 22, 11:57 am show options

Newsgroups: alt.support.diabetes, sci.med.cardiology, sci.med
From: "Kumar" <[email hidden]> - Find messages by this
author
Date: 21 Jan 2006 22:57:57 -0800
Local: Sun, Jan 22 2006 11:57 am
Subject: Re: Fatty Liver
Reply | Reply to Author | Forward | Print | Individual Message | Show
original | Remove | Report Abuse

Andrew B. Chung said:

Kumar wrote:

Quoted message said:

> > The longer half-life of insulin is due to decreased rates of
> > degradation and not decreased rates of excretion.

Quoted message said:

> > and so he may need to adjust injected insulin

Quoted message said:

> Can you explain how decreased rates of degradation of insulin happen?

Quoted message said:

Loss of nephrons where the degradation occurs.

Whether loss of nephrons causes increased or decreased filteration?

Decreased

Quoted message said:

On
one hand we say lesser filteration on other hand protiens(bigger
molecules) start coming into urine on getting DN?

Proteinuria does happen with DN but this does not appreciably alter the
half-life of insulin.

I was just comparing the size of molecules with filteration as protiens
are filtered but not insulin on getting DN.??

Quoted message said:

Quoted message said:

Quoted message said:

> What about cluster or crystal formation possibilty of molecules of
> insulin?

Quoted message said:

There is no reason to invoke this.

Quoted message said:

> > > accordingly, whather insulin is lost or excreted in urine on pre-DN
> > > stages?

Quoted message said:

> > Insulin is not excreted in the urine.

Quoted message said:

> Why when the molecyular weight of insulin is more than 1/4th of
> filteration capacity of kydneys?

Quoted message said:

You just answered your question by your question.

Sorry, I meant; Why insulin is not filtered in kidneys, when the
molecular weight of insulin is less than 1/4th (less than 6000 D) of
filteration capacity of kidneys (30000 D)?

Insulin is a charged polypeptide that will not get through the
glomerular basement membrane which is a more effective barrier when a
macromolecule has a charge.

Sorry, it is not clear to me.

Quoted message said:

Quoted message said:

Quoted message said:

> Moreover capillary permeability for
> insulin is considered as 0.2.

Quoted message said:

The glomeruli of nephrons of the kidney are considerably less permeable
to polypeptides such as insulin than capillary beds.

Can it mean that extra cellular fluids in our tissues will have bigger
molecules than as we have in urine alike insulin?

Yes.

Sorry following question is pending;

Quoted message said:

Yes to all the above except for "proacidosis."

Can it (Greater VA) be pro-alkaliosis and pro-azoospermia?

Whether inflammatory, atherogenic,cancerous, diabetic effects are
pro-acidosis or pro-alkaliosis?

Kumar said:

Andrew B. Chung said:

Kumar said:

Andrew B. Chung, MD/PhD wrote:
> Kumar wrote:
> > Reply against my post no 34 is pending.

When I sort by date it comes 34 as under;

34. Kumar
Jan 22, 11:57 am show options

Newsgroups: alt.support.diabetes, sci.med.cardiology, sci.med
From: "Kumar" <[email hidden]> - Find messages by this
author
Date: 21 Jan 2006 22:57:57 -0800
Local: Sun, Jan 22 2006 11:57 am
Subject: Re: Fatty Liver
Reply | Reply to Author | Forward | Print | Individual Message | Show
original | Remove | Report Abuse

Andrew B. Chung, MD/PhD wrote:

> Kumar wrote:

> > > The longer half-life of insulin is due to decreased rates of
> > > degradation and not decreased rates of excretion.

> > > and so he may need to adjust injected insulin

> > Can you explain how decreased rates of degradation of insulin happen?

> Loss of nephrons where the degradation occurs.

Whether loss of nephrons causes increased or decreased filteration?

Decreased

Quoted message said:

On
one hand we say lesser filteration on other hand protiens(bigger
molecules) start coming into urine on getting DN?

Proteinuria does happen with DN but this does not appreciably alter the
half-life of insulin.

I was just comparing the size of molecules with filteration as protiens
are filtered but not insulin on getting DN.??

Depends on the protein.

Quoted message said:

Quoted message said:

Quoted message said:

> > What about cluster or crystal formation possibilty of molecules of
> > insulin?

> There is no reason to invoke this.

> > > > accordingly, whather insulin is lost or excreted in urine on pre-DN
> > > > stages?

> > > Insulin is not excreted in the urine.

> > Why when the molecyular weight of insulin is more than 1/4th of
> > filteration capacity of kydneys?

> You just answered your question by your question.

Sorry, I meant; Why insulin is not filtered in kidneys, when the
molecular weight of insulin is less than 1/4th (less than 6000 D) of
filteration capacity of kidneys (30000 D)?

Insulin is a charged polypeptide that will not get through the
glomerular basement membrane which is a more effective barrier when a
macromolecule has a charge.

Sorry, it is not clear to me.

The glomerular basement membrane is **selectively** permeable.

Quoted message said:

Quoted message said:

Quoted message said:

> > Moreover capillary permeability for
> > insulin is considered as 0.2.

> The glomeruli of nephrons of the kidney are considerably less permeable
> to polypeptides such as insulin than capillary beds.

Can it mean that extra cellular fluids in our tissues will have bigger
molecules than as we have in urine alike insulin?

Yes.

Sorry following question is pending;

Quoted message said:

Yes to all the above except for "proacidosis."

Can it (Greater VA) be pro-alkaliosis and pro-azoospermia?

VA ?

Quoted message said:

Whether inflammatory, atherogenic,cancerous, diabetic effects are
pro-acidosis or pro-alkaliosis?

The buffering capacity of serum bicarbonate with normal pulmonary
function is such that serum pH is well regulated even in the face of
most metabolic derangements.

Would be more than happy to "glow" and chat about this and other things
like cardiology, diabetes, cooking and nutrition that interest those
following this thread here during the next on-line chat (01/26/06) from
6 to 7 pm EST:

http://tinyurl.com/cpayh

For those who are put off by the signature, my advance apologies for
how the LORD has reshaped me:

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/cbn2r

Andrew B. Chung said:

Kumar said:

Andrew B. Chung said:

Kumar wrote:
> Andrew B. Chung, MD/PhD wrote:
> > Kumar wrote:
> > > Reply against my post no 34 is pending.
>
> When I sort by date it comes 34 as under;
>
> 34. Kumar
> Jan 22, 11:57 am show options
>
> Newsgroups: alt.support.diabetes, sci.med.cardiology, sci.med
> From: "Kumar" <[email hidden]> - Find messages by this
> author
> Date: 21 Jan 2006 22:57:57 -0800
> Local: Sun, Jan 22 2006 11:57 am
> Subject: Re: Fatty Liver
> Reply | Reply to Author | Forward | Print | Individual Message | Show
> original | Remove | Report Abuse
>
> Andrew B. Chung, MD/PhD wrote:
>
> > Kumar wrote:
>
> > > > The longer half-life of insulin is due to decreased rates of
> > > > degradation and not decreased rates of excretion.
>
>
> > > > and so he may need to adjust injected insulin
>
>
> > > Can you explain how decreased rates of degradation of insulin happen?
>
>
> > Loss of nephrons where the degradation occurs.
>
>
>
> Whether loss of nephrons causes increased or decreased filteration?

Decreased

> On
> one hand we say lesser filteration on other hand protiens(bigger
> molecules) start coming into urine on getting DN?

Proteinuria does happen with DN but this does not appreciably alter the
half-life of insulin.

I was just comparing the size of molecules with filteration as protiens
are filtered but not insulin on getting DN.??

Depends on the protein.

How? By its size/molecular weight or by its quality?

Quoted message said:

Quoted message said:

Quoted message said:

> > > What about cluster or crystal formation possibilty of molecules of
> > > insulin?
>
> > There is no reason to invoke this.
>
>
> > > > > accordingly, whather insulin is lost or excreted in urine on pre-DN
> > > > > stages?
>
>
> > > > Insulin is not excreted in the urine.
>
>
> > > Why when the molecyular weight of insulin is more than 1/4th of
> > > filteration capacity of kydneys?
>
>
> > You just answered your question by your question.
>
> Sorry, I meant; Why insulin is not filtered in kidneys, when the
> molecular weight of insulin is less than 1/4th (less than 6000 D) of
> filteration capacity of kidneys (30000 D)?

Insulin is a charged polypeptide that will not get through the
glomerular basement membrane which is a more effective barrier when a
macromolecule has a charge.

Sorry, it is not clear to me.

The glomerular basement membrane is **selectively** permeable.

Good information. Just to clarify more....Whether glomerular
filteration is by active transport system which don't filter or not
capable of filtering insulin selectively?

Quoted message said:

Quoted message said:

Quoted message said:

> > > Moreover capillary permeability for
> > > insulin is considered as 0.2.
>
> > The glomeruli of nephrons of the kidney are considerably less permeable
> > to polypeptides such as insulin than capillary beds.
>
> Can it mean that extra cellular fluids in our tissues will have bigger
> molecules than as we have in urine alike insulin?

Yes.

Sorry following question is pending;

Quoted message said:

> "Furthermore, adipose

tissue is a major endocrine organ that secretes numerous polypeptide
hormones and cytokines that are proinflammatory and proatherogenic."

Quoted message said:

Quoted message said:

Do excess fats in tissues is proinflamatory, proatherogenic,
prodiabetic, proacidosis, procanerous?

Quoted message said:

Quoted message said:

Quoted message said:

Yes to all the above except for "proacidosis."

Can it (Greater VA) be pro-alkaliosis and pro-azoospermia?

VA ?

I meant; can greater visceral adiposity or excess fats in tisuues be
pro-alkaliosis and pro-azoospermia( due to sperm growth arrest at
spermocytic stage)?

I want to know relation of greater visceral adiposity or excess fats in
tisuues with acid, base, water and temperature level.

Quoted message said:

Quoted message said:

Whether inflammatory, atherogenic,cancerous, diabetic effects are
pro-acidosis or pro-alkaliosis?

The buffering capacity of serum bicarbonate with normal pulmonary
function is such that serum pH is well regulated even in the face of
most metabolic derangements.

That is ok, but continious and prolonged regulations in maintaining
normal pH due to prolonged derangements ( one may be by greater
visceral adiposity or excess fats in tisuues) may cause progressive or
degenarative damages. ??

Kumar said:

Andrew B. Chung said:

Kumar said:

Andrew B. Chung, MD/PhD wrote:
> Kumar wrote:
> > Andrew B. Chung, MD/PhD wrote:
> > > Kumar wrote:
> > > > Reply against my post no 34 is pending.
> >
> > When I sort by date it comes 34 as under;
> >
> > 34. Kumar
> > Jan 22, 11:57 am show options
> >
> > Newsgroups: alt.support.diabetes, sci.med.cardiology, sci.med
> > From: "Kumar" <[email hidden]> - Find messages by this
> > author
> > Date: 21 Jan 2006 22:57:57 -0800
> > Local: Sun, Jan 22 2006 11:57 am
> > Subject: Re: Fatty Liver
> > Reply | Reply to Author | Forward | Print | Individual Message | Show
> > original | Remove | Report Abuse
> >
> > Andrew B. Chung, MD/PhD wrote:
> >
> > > Kumar wrote:
> >
> > > > > The longer half-life of insulin is due to decreased rates of
> > > > > degradation and not decreased rates of excretion.
> >
> >
> > > > > and so he may need to adjust injected insulin
> >
> >
> > > > Can you explain how decreased rates of degradation of insulin happen?
> >
> >
> > > Loss of nephrons where the degradation occurs.
> >
> >
> >
> > Whether loss of nephrons causes increased or decreased filteration?
>
> Decreased
>
> > On
> > one hand we say lesser filteration on other hand protiens(bigger
> > molecules) start coming into urine on getting DN?
>
> Proteinuria does happen with DN but this does not appreciably alter the
> half-life of insulin.

I was just comparing the size of molecules with filteration as protiens
are filtered but not insulin on getting DN.??

Depends on the protein.

How? By its size/molecular weight or by its quality?

All the above.

Quoted message said:

Quoted message said:

Quoted message said:

> > > > What about cluster or crystal formation possibilty of molecules of
> > > > insulin?
> >
> > > There is no reason to invoke this.
> >
> >
> > > > > > accordingly, whather insulin is lost or excreted in urine on pre-DN
> > > > > > stages?
> >
> >
> > > > > Insulin is not excreted in the urine.
> >
> >
> > > > Why when the molecyular weight of insulin is more than 1/4th of
> > > > filteration capacity of kydneys?
> >
> >
> > > You just answered your question by your question.
> >
> > Sorry, I meant; Why insulin is not filtered in kidneys, when the
> > molecular weight of insulin is less than 1/4th (less than 6000 D) of
> > filteration capacity of kidneys (30000 D)?
>
> Insulin is a charged polypeptide that will not get through the
> glomerular basement membrane which is a more effective barrier when a
> macromolecule has a charge.

Sorry, it is not clear to me.

The glomerular basement membrane is **selectively** permeable.

Good information. Just to clarify more....Whether glomerular
filteration is by active transport system which don't filter or not
capable of filtering insulin selectively?

There is no active transport involved.

Quoted message said:

Quoted message said:

Quoted message said:

> > > > Moreover capillary permeability for
> > > > insulin is considered as 0.2.
> >
> > > The glomeruli of nephrons of the kidney are considerably less permeable
> > > to polypeptides such as insulin than capillary beds.
> >
> > Can it mean that extra cellular fluids in our tissues will have bigger
> > molecules than as we have in urine alike insulin?
>
> Yes.

Sorry following question is pending;
> > "Furthermore, adipose
tissue is a major endocrine organ that secretes numerous polypeptide
hormones and cytokines that are proinflammatory and proatherogenic."

Quoted message said:

Quoted message said:

Do excess fats in tissues is proinflamatory, proatherogenic,
prodiabetic, proacidosis, procanerous?

Quoted message said:

Quoted message said:

> Yes to all the above except for "proacidosis."

Can it (Greater VA) be pro-alkaliosis and pro-azoospermia?

VA ?

I meant; can greater visceral adiposity or excess fats in tisuues be
pro-alkaliosis and pro-azoospermia( due to sperm growth arrest at
spermocytic stage)?

The latter possibly.

Quoted message said:

I want to know relation of greater visceral adiposity or excess fats in
tisuues with acid, base, water and temperature level.

There should be no significant impact upon homeostatic processes from
visceral adiposity.

Quoted message said:

Quoted message said:

Quoted message said:

Whether inflammatory, atherogenic,cancerous, diabetic effects are
pro-acidosis or pro-alkaliosis?

The buffering capacity of serum bicarbonate with normal pulmonary
function is such that serum pH is well regulated even in the face of
most metabolic derangements.

That is ok, but continious and prolonged regulations in maintaining
normal pH due to prolonged derangements ( one may be by greater
visceral adiposity or excess fats in tisuues) may cause progressive or
degenarative damages. ??

Unlikely.

May the LORD help us all to face the great tribulation when the Lamb
opens the 6th seal possibly in less than a few months (03/29/06), in
Jesus' most precious and holy name.

Amen !!!

Now this is about the works of the four horsemen from the 6th chapter
of the Book of Revelation (we are now in the 6th year into the third
millenium after the birth of the Son of Man):

(1) Crowned rider wielding a bow and riding a white horse:

"See you on the other side. It's not bad. We are just going to
sleep." - missive (missile) from one of 12 born-again Christian miners
who gave up their lives to save the youngest among them after being
trapped by an explosion in a W.Va mine.

(2) Rider wielding a sword and riding a fiery red horse:

Ariel Sharon, the world's hope for lasting peace in the middle east,
suffers a massive bleeding stroke. Violence and bloodshed in Iraq
escalates. U.S. now less likely to pull out of Iraq anytime soon.

(3) Rider wielding a set of food scales and riding a black horse:

The rate of increase of the number of people worldwide using the
2PD-OMER Approach (which advocates the use of food scales) accelerates
with growing worldwide concerns about the obesity epidemic:

http://www.HeartMDPhD.com/wtloss.asp

Meanwhile, folks like Bob Pastorio who refuse to use this Approach are
heard muttering that an omer is not a weight measure but a volume
measure somewhere between one and three quarts depending on what the
food is and that liquid foods like milk (emulsified oil) and wine
should not be counted toward daily intake.

(4) Rider on a pale horse given the authority to kill a fourth of the
world's population "by sword, famine and plague, and by the wild beasts
of the earth":

The H5N1 Avian Flu Pandemic seems to be starting in Turkey:

http://tinyurl.com/amj4a

Yes, the migratory birds spreading H5N1 virus are wild beasts of the
earth.

The 5th seal has been opened and glimpses of "the souls of those who
had been slain because of the Word of GOD and the testimony they had
maintained" (Revelation 6:9) can be seen in the newly released
documentary "End of the Spear."

When will the sun "turn black like sackcloth made of goat hair"
(Revelation 6:12b) ?

It will turn black during the total solar eclipse that will happen
**also** in Turkey on Wednesday 03/29/2006 at around 14:00 hrs LT.

http://tinyurl.com/dcj7w

The order of darkening of the following ancient cities in Turkey:

(1) Ephesus
(2) Smyrna
(3) Pergamum
(4) Thyatira
(5) Sardis
(6) Philadelphia
(7) Laodicea

Will be the same order that Christ Jesus used to address the seven
churches:

"Write on a scroll what you see and send it to the seven churches: to
Ephesus, Smyrna, Pergamum, Thyratira, Sardis, Philadelphia and
Laodicea." (Revelation 1:11)

Would be more than happy to "glow" and chat about this and other things
like cardiology, diabetes, cooking and nutrition that interest those
following this thread here during the next on-line chat (01/26/06) from
6 to 7 pm EST:

http://tinyurl.com/cpayh

For those who are put off by the signature, my advance apologies for
how the LORD has reshaped me:

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/cbn2r

On 22 Jan 2006 21:15:46 -0800, Kumar wrote in
<news:[email hidden]> on
alt.support.diabetes,sci.med.cardiology,sci.med,sci.med.nutrition :

Quoted message said:

Quoted message said:

Quoted message said:

Reply against my post no 34 is pending.

When I sort by date it comes 34 as under;

34. Kumar

You can use a full Google link, or a Message-Id, to univocally
identify a post...

X'Posted to: alt.support.diabetes,sci.med.nutrition

--
Enrico C

* cut the ending "cut-togli.invalid" string when replying by email *

Andrew B. Chung said:

Quoted message said:

Quoted message said:

> >
> > > > The longer half-life of insulin is due to decreased rates of
> > > > degradation and not decreased rates of excretion.
>
>
> > > > and so he may need to adjust injected insulin
>
>
> > > Can you explain how decreased rates of degradation of insulin happen?
>
>
> > Loss of nephrons where the degradation occurs.
>
>
>
> Whether loss of nephrons causes increased or decreased filteration?

Decreased

> On
> one hand we say lesser filteration on other hand protiens(bigger
> molecules) start coming into urine on getting DN?

Proteinuria does happen with DN but this does not appreciably alter the
half-life of insulin.

I was just comparing the size of molecules with filteration as protiens
are filtered but not insulin on getting DN.??

Depends on the protein.

Quoted message said:

Quoted message said:

> > > > > accordingly, whather insulin is lost or excreted in urine on pre-DN
> > > > > stages?
>
>
> > > > Insulin is not excreted in the urine.
>
>
> > > Why when the molecyular weight of insulin is more than 1/4th of
> > > filteration capacity of kydneys?
>
>
> > You just answered your question by your question.
>
> Sorry, I meant; Why insulin is not filtered in kidneys, when the
> molecular weight of insulin is less than 1/4th (less than 6000 D) of
> filteration capacity of kidneys (30000 D)?

Insulin is a charged polypeptide that will not get through the
glomerular basement membrane which is a more effective barrier when a
macromolecule has a charge.

Sorry, it is not clear to me.

The glomerular basement membrane is **selectively** permeable.

'...As kidney failure progresses, less insulin is excreted, so smaller
doses may be needed to control glucose levels.
Complications
Possible complications include:hypoglycemia (from decreased excretion
of insulin)
http://www.nlm.nih.gov/medlineplus/ency/article/000494.htm '

The above medlineplus quote indicate that insulin is excreted. Can you
check tell about it again?

Quoted message said:

Quoted message said:

Quoted message said:

> > > Andrew B. Chung, MD/PhD wrote:
> > >
> > > > Kumar wrote:
> > >
> > > > > > The longer half-life of insulin is due to decreased rates of
> > > > > > degradation and not decreased rates of excretion.
> > >
> > >
> > > > > > and so he may need to adjust injected insulin
> > >
> > >
> > > > > Can you explain how decreased rates of degradation of insulin happen?
> > >
> > >
> > > > Loss of nephrons where the degradation occurs.
> > >
> > >
> > >
> > > Whether loss of nephrons causes increased or decreased filteration?
> >
> > Decreased
> >
> > > On
> > > one hand we say lesser filteration on other hand protiens(bigger
> > > molecules) start coming into urine on getting DN?
> >
> > Proteinuria does happen with DN but this does not appreciably alter the
> > half-life of insulin.
>
> I was just comparing the size of molecules with filteration as protiens
> are filtered but not insulin on getting DN.??

Depends on the protein.

How? By its size/molecular weight or by its quality?

All the above.

How by its quality?

Quoted message said:

Quoted message said:

Quoted message said:

> > > > > > Insulin is not excreted in the urine.

My previous post pls.

Quoted message said:

Quoted message said:

Quoted message said:

> > >
> > >
> > > > > Why when the molecyular weight of insulin is more than 1/4th of
> > > > > filteration capacity of kydneys?
> > >
> > >
> > > > You just answered your question by your question.
> > >
> > > Sorry, I meant; Why insulin is not filtered in kidneys, when the
> > > molecular weight of insulin is less than 1/4th (less than 6000 D) of
> > > filteration capacity of kidneys (30000 D)?
> >
> > Insulin is a charged polypeptide that will not get through the
> > glomerular basement membrane which is a more effective barrier when a
> > macromolecule has a charge.
>
> Sorry, it is not clear to me.

The glomerular basement membrane is **selectively** permeable.

Good information. Just to clarify more....Whether glomerular
filteration is by active transport system which don't filter or not
capable of filtering insulin selectively?

There is no active transport involved.

Quoted message said:

Quoted message said:

> > > > > Moreover capillary permeability for
> > > > > insulin is considered as 0.2.
> > >
> > > > The glomeruli of nephrons of the kidney are considerably less permeable
> > > > to polypeptides such as insulin than capillary beds.
> > >
> > > Can it mean that extra cellular fluids in our tissues will have bigger
> > > molecules than as we have in urine alike insulin?
> >
> > Yes.
>
> Sorry following question is pending;
>> > "Furthermore, adipose
> tissue is a major endocrine organ that secretes numerous polypeptide
> hormones and cytokines that are proinflammatory and proatherogenic."

Quoted message said:

> Do excess fats in tissues is proinflamatory, proatherogenic,
> prodiabetic, proacidosis, procanerous?

Quoted message said:

> > Yes to all the above except for "proacidosis."
>
> Can it (Greater VA) be pro-alkaliosis and pro-azoospermia?

VA ?

I meant; can greater visceral adiposity or excess fats in tisuues be
pro-alkaliosis and pro-azoospermia( due to sperm growth arrest at
spermocytic stage)?

The latter possibly.

Quoted message said:

I want to know relation of greater visceral adiposity or excess fats in
tisuues with acid, base, water and temperature level.

There should be no significant impact upon homeostatic processes from
visceral adiposity.

What about from excess subcutaneous fats depositions? Does it effect
acid/base balance? Pls don't consider what body can correct for this
purpose.

Quoted message said:

Quoted message said:

Quoted message said:

> Whether inflammatory, atherogenic,cancerous, diabetic effects are
> pro-acidosis or pro-alkaliosis?

The buffering capacity of serum bicarbonate with normal pulmonary
function is such that serum pH is well regulated even in the face of
most metabolic derangements.

That is ok, but continious and prolonged regulations in maintaining
normal pH due to prolonged derangements ( one may be by greater
visceral adiposity or excess fats in tisuues) may cause progressive or
degenarative damages. ??

Unlikely.

Do you mean that continious and prolonged hammering to body system for
the control of acid/base derangements can have no acute, chronic or
progressive damages?

Kumar said:

Quoted message said:

Quoted message said:

> > > > Andrew B. Chung, MD/PhD wrote:
> > > >
> > > > > Kumar wrote:
> > > >
> > > > > > > The longer half-life of insulin is due to decreased rates of
> > > > > > > degradation and not decreased rates of excretion.
> > > >
> > > >
> > > > > > > and so he may need to adjust injected insulin
> > > >
> > > >
> > > > > > Can you explain how decreased rates of degradation of insulin happen?
> > > >
> > > >
> > > > > Loss of nephrons where the degradation occurs.
> > > >
> > > >
> > > >
> > > > Whether loss of nephrons causes increased or decreased filteration?
> > >
> > > Decreased
> > >
> > > > On
> > > > one hand we say lesser filteration on other hand protiens(bigger
> > > > molecules) start coming into urine on getting DN?
> > >
> > > Proteinuria does happen with DN but this does not appreciably alter the
> > > half-life of insulin.
> >
> > I was just comparing the size of molecules with filteration as protiens
> > are filtered but not insulin on getting DN.??
>
> Depends on the protein.

How? By its size/molecular weight or by its quality?

All the above.

How by its quality?

By charge.

Quoted message said:

Quoted message said:

Quoted message said:

> > > > > > > Insulin is not excreted in the urine.

My previous post pls.

Already asked and answered.

Quoted message said:

Quoted message said:

Quoted message said:

> > > >
> > > >
> > > > > > Why when the molecyular weight of insulin is more than 1/4th of
> > > > > > filteration capacity of kydneys?
> > > >
> > > >
> > > > > You just answered your question by your question.
> > > >
> > > > Sorry, I meant; Why insulin is not filtered in kidneys, when the
> > > > molecular weight of insulin is less than 1/4th (less than 6000 D) of
> > > > filteration capacity of kidneys (30000 D)?
> > >
> > > Insulin is a charged polypeptide that will not get through the
> > > glomerular basement membrane which is a more effective barrier when a
> > > macromolecule has a charge.
> >
> > Sorry, it is not clear to me.
>
> The glomerular basement membrane is **selectively** permeable.

Good information. Just to clarify more....Whether glomerular
filteration is by active transport system which don't filter or not
capable of filtering insulin selectively?

There is no active transport involved.

Quoted message said:

> > > > > > Moreover capillary permeability for
> > > > > > insulin is considered as 0.2.
> > > >
> > > > > The glomeruli of nephrons of the kidney are considerably less permeable
> > > > > to polypeptides such as insulin than capillary beds.
> > > >
> > > > Can it mean that extra cellular fluids in our tissues will have bigger
> > > > molecules than as we have in urine alike insulin?
> > >
> > > Yes.
> >
> > Sorry following question is pending;
> >> > "Furthermore, adipose
> > tissue is a major endocrine organ that secretes numerous polypeptide
> > hormones and cytokines that are proinflammatory and proatherogenic."

> > Do excess fats in tissues is proinflamatory, proatherogenic,
> > prodiabetic, proacidosis, procanerous?

> > > Yes to all the above except for "proacidosis."
> >
> > Can it (Greater VA) be pro-alkaliosis and pro-azoospermia?
>
> VA ?

I meant; can greater visceral adiposity or excess fats in tisuues be
pro-alkaliosis and pro-azoospermia( due to sperm growth arrest at
spermocytic stage)?

The latter possibly.

Quoted message said:

I want to know relation of greater visceral adiposity or excess fats in
tisuues with acid, base, water and temperature level.

There should be no significant impact upon homeostatic processes from
visceral adiposity.

What about from excess subcutaneous fats depositions? Does it effect
acid/base balance? Pls don't consider what body can correct for this
purpose.

Subcutaneous fat is largely avascular.

Quoted message said:

Quoted message said:

Quoted message said:

> > Whether inflammatory, atherogenic,cancerous, diabetic effects are
> > pro-acidosis or pro-alkaliosis?
>
> The buffering capacity of serum bicarbonate with normal pulmonary
> function is such that serum pH is well regulated even in the face of
> most metabolic derangements.

That is ok, but continious and prolonged regulations in maintaining
normal pH due to prolonged derangements ( one may be by greater
visceral adiposity or excess fats in tisuues) may cause progressive or
degenarative damages. ??

Unlikely.

Do you mean that continious and prolonged hammering to body system for
the control of acid/base derangements can have no acute, chronic or
progressive damages?

Our bodies are wonderfully made by the LORD :-))

Would be more than happy to "glow" and chat about this and other things
like cardiology, diabetes, cooking and nutrition that interest those
following this thread here during the next on-line chat (01/26/06):

http://tinyurl.com/cpayh

For those who are put off by the signature, my advance apologies for
how the LORD has reshaped me:

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/cbn2r

Andrew B. Chung said:

Kumar said:

Quoted message said:

> > > > > Andrew B. Chung, MD/PhD wrote:
> > > > >
> > > > > > Kumar wrote:
> > > > >
> > > > > > > > The longer half-life of insulin is due to decreased rates of
> > > > > > > > degradation and not decreased rates of excretion.
> > > > >
> > > > >
> > > > > > > > and so he may need to adjust injected insulin
> > > > >
> > > > >
> > > > > > > Can you explain how decreased rates of degradation of insulin happen?
> > > > >
> > > > >
> > > > > > Loss of nephrons where the degradation occurs.
> > > > >
> > > > >
> > > > >
> > > > > Whether loss of nephrons causes increased or decreased filteration?
> > > >
> > > > Decreased
> > > >
> > > > > On
> > > > > one hand we say lesser filteration on other hand protiens(bigger
> > > > > molecules) start coming into urine on getting DN?
> > > >
> > > > Proteinuria does happen with DN but this does not appreciably alter the
> > > > half-life of insulin.
> > >
> > > I was just comparing the size of molecules with filteration as protiens
> > > are filtered but not insulin on getting DN.??
> >
> > Depends on the protein.
>
> How? By its size/molecular weight or by its quality?

All the above.

How by its quality?

By charge.

This looks to be a special aspect. Can you tell some more details, what
is this charge and how it can effect insulin excretion?

Quoted message said:

Quoted message said:

Quoted message said:

> > > > > > > > Insulin is not excreted in the urine.

My previous post pls.

Already asked and answered.

My previous post was:-

"...As kidney failure progresses, less insulin is excreted, so smaller
doses may be needed to control glucose levels.
Complications
Possible complications include:hypoglycemia (from decreased excretion
of insulin)
http://www.nlm.nih.gov/medlineplus/ency/article/000494.htm "

The above medlineplus quote indicate that insulin is excreted. Can you
check tell about it again?

Quoted message said:

Quoted message said:

Quoted message said:

> > > > >
> > > > >
> > > > > > > Why when the molecyular weight of insulin is more than 1/4th of
> > > > > > > filteration capacity of kydneys?
> > > > >
> > > > >
> > > > > > You just answered your question by your question.
> > > > >
> > > > > Sorry, I meant; Why insulin is not filtered in kidneys, when the
> > > > > molecular weight of insulin is less than 1/4th (less than 6000 D) of
> > > > > filteration capacity of kidneys (30000 D)?
> > > >
> > > > Insulin is a charged polypeptide that will not get through the
> > > > glomerular basement membrane which is a more effective barrier when a
> > > > macromolecule has a charge.
> > >
> > > Sorry, it is not clear to me.
> >
> > The glomerular basement membrane is **selectively** permeable.
>
> Good information. Just to clarify more....Whether glomerular
> filteration is by active transport system which don't filter or not
> capable of filtering insulin selectively?

There is no active transport involved.

> > > > > > > Moreover capillary permeability for
> > > > > > > insulin is considered as 0.2.
> > > > >
> > > > > > The glomeruli of nephrons of the kidney are considerably less permeable
> > > > > > to polypeptides such as insulin than capillary beds.
> > > > >
> > > > > Can it mean that extra cellular fluids in our tissues will have bigger
> > > > > molecules than as we have in urine alike insulin?
> > > >
> > > > Yes.
> > >
> > > Sorry following question is pending;
> > >> > "Furthermore, adipose
> > > tissue is a major endocrine organ that secretes numerous polypeptide
> > > hormones and cytokines that are proinflammatory and proatherogenic."
>
>
> > > Do excess fats in tissues is proinflamatory, proatherogenic,
> > > prodiabetic, proacidosis, procanerous?
>
>
>
> > > > Yes to all the above except for "proacidosis."
> > >
> > > Can it (Greater VA) be pro-alkaliosis and pro-azoospermia?
> >
> > VA ?
>
> I meant; can greater visceral adiposity or excess fats in tisuues be
> pro-alkaliosis and pro-azoospermia( due to sperm growth arrest at
> spermocytic stage)?

The latter possibly.

> I want to know relation of greater visceral adiposity or excess fats in
> tisuues with acid, base, water and temperature level.

There should be no significant impact upon homeostatic processes from
visceral adiposity.

What about from excess subcutaneous fats depositions? Does it effect
acid/base balance? Pls don't consider what body can correct for this
purpose.

Subcutaneous fat is largely avascular.

Visceral?? Are these vascular? If yes can they effect acid/base and
temperature balance?

Quoted message said:

Quoted message said:

Quoted message said:

> > > Whether inflammatory, atherogenic,cancerous, diabetic effects are
> > > pro-acidosis or pro-alkaliosis?
> >
> > The buffering capacity of serum bicarbonate with normal pulmonary
> > function is such that serum pH is well regulated even in the face of
> > most metabolic derangements.
>
> That is ok, but continious and prolonged regulations in maintaining
> normal pH due to prolonged derangements ( one may be by greater
> visceral adiposity or excess fats in tisuues) may cause progressive or
> degenarative damages. ??

Unlikely.

Do you mean that continious and prolonged hammering to body system for
the control of acid/base derangements can have no acute, chronic or
progressive damages?

Our bodies are wonderfully made by the LORD :-))

Yes, but can't there be some limitations as it is made by lord but is
not a Lord?

Anyway, can bicarbonate imbalance in blood and three compartments be
related to persistent and uncontrolled elevated blood glucose levels in
blood. In other sense, can diabetics with somewhat acidosis find
difficulty in controling their elevated blood glucose than diabetics
with somewhat acidosis? Insulin role in Potassium shifting
intracellularily and potassium relation with acidosis and osmolity may
be considered for such bicarboate effect. Why sodium bicarbonate is
considered as systematic antacid others not?

I am also interested much to understand diferenciating effects by
acid-blockers and antacids on internal environment in view of that
gastric acid secretion may cause "alkaline tide" temporarily internally
as its production relese bicarbonate inside blood. Opposite is related
to acidic effect inside on pacreatic bicarbonate secretion.

Andrew B. Chung said:

Kumar said:

In continuance to my last post......

"Insulin

Monomers, Dimers and Hexamers
http://www.med.unibs.it/~marchesi/pps97/course/section11/insulin.html

The above link suggests different possible forms and variants of
insulin. Insulin as monomer is only active and its polymers are
ineffective. As such any persistance of insulin in polymer may also be
a reason to getting insulin resistance or insenstivity to insulin. As
such insulin in polymer form may not be filtered whereas it can be
filtered or filtered lesser in monomer and dimer form....may also be a
reason to getting hyperglycemia. Furthur pH and insulin concentration
seems to be two reasons responsible for its polymerization. We may then
have to think about alterations in pH, Zinc levels, excess insulin
concentration--naturally, medicated or injected to understand
senstivity and non-senstivity of insulin.

Can you comment on it?

Insulin is not the only polypeptide that is denatured in
non-physiological conditions.

Reply against my previous post # 54 pending pls.

Yes but I am thinking about insulin. Can a person become diabetic type2
due to persistance of his insulin molecules in aggregated or polymer
state? How such conditions(polymerization of insulin molecules) be
improved by some food changes or by medicines?

At some links it is indicated that urea, acetic acid..can cause
monomerization of insulin. Can vinegar do something for this? Can
excess BUN be related to better utilization of insulin in monomeric
form--so needed to lower insulin injections????

Kumar said:

Andrew B. Chung said:

Kumar said:

In continuance to my last post......

"Insulin

Monomers, Dimers and Hexamers
http://www.med.unibs.it/~marchesi/pps97/course/section11/insulin.html

The above link suggests different possible forms and variants of
insulin. Insulin as monomer is only active and its polymers are
ineffective. As such any persistance of insulin in polymer may also be
a reason to getting insulin resistance or insenstivity to insulin. As
such insulin in polymer form may not be filtered whereas it can be
filtered or filtered lesser in monomer and dimer form....may also be a
reason to getting hyperglycemia. Furthur pH and insulin concentration
seems to be two reasons responsible for its polymerization. We may then
have to think about alterations in pH, Zinc levels, excess insulin
concentration--naturally, medicated or injected to understand
senstivity and non-senstivity of insulin.

Can you comment on it?

Insulin is not the only polypeptide that is denatured in
non-physiological conditions.

Reply against my previous post # 54 pending pls.

Yes but I am thinking about insulin. Can a person become diabetic type2
due to persistance of his insulin molecules in aggregated or polymer
state?

No. This person would die from the non-physiological conditions first.

Would be more than happy to "glow" and chat about this and other things
like cardiology, diabetes, cooking, and nutrition that interest those
following this thread here during the next on-line chat (01/19/2006)
from 6 to 7 pm EST:

http://tinyurl.com/cpayh

For those who are put off by the signature, my advance apologies for how
the LORD has reshaped me:

http://tinyurl.com/bgfqt

Prayerfully in Christ's love,

Andrew
http://tinyurl.com/b6xwk