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Hi JW:

My approach to fat is to minimize it everywhere whenever possible -

but not in a fanatical manner ....... periodically I use butter,

and safflower and olive oils - then eat fish and a few nuts, which I

hope will bring my fat intake comfortably above the RDA.

As for looking for things I could change about this, I am personally

motivated to look at epidemiological studies as a guide to what may

or may not be healthy. This is not the only way of course. But it

is my preferred way.

My recollection is that the japanese eat on average 200g of fish per

day. They have a pretty decent lifespan notwithstanding their

smoking habits. But there are a lot of things the japanese do

diffently so fish may not be the key factor. In any event, I eat

less fish than they do. Perhaps I should eat more.

Rodney.

--- In , " jwwright " <jwwright@e...>

wrote:

> It occurs to me that we don;t have enough info in the endocrine

system.

> We've touched on the LA and ALA, LOX and COX pathways, in

generalities.

> We are afraid of the ALA PCa connection, yet not afraid of the EPA

which is the next step to produce the EPA equivalents of the

prostaglandins, thromboxanes, and leukotrienes of the LA pathway. Are

those better? I guess not.

>

> The idea that EPA somehow is better because it controls the AA

pathway is not exactly true, I've found, because the AA pathway is

self regulating.

> These hormones (eicosanoids) are important because they control the

body's systems. They modualte the cardivascular, pulmonary, immune,

reproductive, and secretory functions. Yet we have talked little

about these in the CR groups.

>

> The eicosanoids include prostaglandins and trhrmboxanes formed in

the cyclooxygenase (COX) pathways, and leukotrienes, hydroxy fatty

acids, and lypoxins formed in the lypooxygenase (LOX) pathway.

>

> In the AA pathway, the COX produces PGE2, PGF2 alpha, PGD2, PGI2,

TXA2, and prostacyclins.

> The ALA pathway sorta mirrors this producing PGE3, PGF3alpha, PGD3,

PGI3, TXA3.

>

> So my first question is does the ALA pathway produce " better "

hormones? My first inclination is to not dose with either LA, ALA, or

EPA/DHA and leave out all added fat until I analyze my system and

figure out which hormone I need to modulate. (vasopressin)

> Perhaps none can be modulated with added pure fatty acids?

>

> Regards.

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Hi JW:

My approach to fat is to minimize it everywhere whenever possible -

but not in a fanatical manner ....... periodically I use butter,

and safflower and olive oils - then eat fish and a few nuts, which I

hope will bring my fat intake comfortably above the RDA.

As for looking for things I could change about this, I am personally

motivated to look at epidemiological studies as a guide to what may

or may not be healthy. This is not the only way of course. But it

is my preferred way.

My recollection is that the japanese eat on average 200g of fish per

day. They have a pretty decent lifespan notwithstanding their

smoking habits. But there are a lot of things the japanese do

diffently so fish may not be the key factor. In any event, I eat

less fish than they do. Perhaps I should eat more.

Rodney.

--- In , " jwwright " <jwwright@e...>

wrote:

> It occurs to me that we don;t have enough info in the endocrine

system.

> We've touched on the LA and ALA, LOX and COX pathways, in

generalities.

> We are afraid of the ALA PCa connection, yet not afraid of the EPA

which is the next step to produce the EPA equivalents of the

prostaglandins, thromboxanes, and leukotrienes of the LA pathway. Are

those better? I guess not.

>

> The idea that EPA somehow is better because it controls the AA

pathway is not exactly true, I've found, because the AA pathway is

self regulating.

> These hormones (eicosanoids) are important because they control the

body's systems. They modualte the cardivascular, pulmonary, immune,

reproductive, and secretory functions. Yet we have talked little

about these in the CR groups.

>

> The eicosanoids include prostaglandins and trhrmboxanes formed in

the cyclooxygenase (COX) pathways, and leukotrienes, hydroxy fatty

acids, and lypoxins formed in the lypooxygenase (LOX) pathway.

>

> In the AA pathway, the COX produces PGE2, PGF2 alpha, PGD2, PGI2,

TXA2, and prostacyclins.

> The ALA pathway sorta mirrors this producing PGE3, PGF3alpha, PGD3,

PGI3, TXA3.

>

> So my first question is does the ALA pathway produce " better "

hormones? My first inclination is to not dose with either LA, ALA, or

EPA/DHA and leave out all added fat until I analyze my system and

figure out which hormone I need to modulate. (vasopressin)

> Perhaps none can be modulated with added pure fatty acids?

>

> Regards.

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JW,

Your note discusses the complexity of the body's regulatory system.

However, you need to distinguish between the eicosanoids which are

basically hydrocarbons (containing no nitrogen) derived from fat

metabolism, and hormones and enzymes which are peptides or proteins

consisting of amino acids. Vasopressin, is a peptide consisting of 9

amino acids which is also called Antidiuretic Hormone (ADH).

Ben Best has a web page on fats that discusses eicosanoids:

http://www.benbest.com/health/essfat.html

The body reacts to changes in electrolyte balance by releasing peptide

hormones such as renin from the kidneys.

Many of the body's peptide hormonal auto-regulating systems come in

antogonistic pairs, such as the insulin/glucagon mechanism for

regulating high/low blood glucose. The release of insulin or glucagon

by the pancreas is mediated by consumption of carbohydrates and by

fasting, respectively.

The external factors influencing hypertension may involve salt

consumption, body weight, exercise, perspiration, muscle tone, etc.

Production of NO (nitrous oxide) from L-arginine may also be involved

since NO is a smooth muscle relaxant which influences arterial walls.

Tony

===

Clin Auton Res. 1991 Jun;1(2):109-14.

Regulation of vasopressin release in moderately severe essential

hypertension.

Del Bo A, Marabini M, ti A, Zanchetti A.

Istituto di Clinica Medica Generale e Terapia Medica, Universita

di Milano, Milan, Italy.

Vasopressin plasma concentrations have been measured in two groups

of subjects, 13 moderate essential hypertensive patients without

target organ damage and eight control normotensive subjects, before

and after the assumption of the upright position, and intravenous

infusions of hypotonic saline (0.45% NaCl, 0.25 ml kg-1 min-1 for 1 h)

and hypertonic saline (100 mmol NaCl in 50 ml). Plasma vasopressin in

recumbent baseline conditions was not significantly different in the

two groups. Upright posture and hypertonic challenge augmented, while

hypotonic saline reduced plasma vasopressin levels, which were not

significantly different between the two groups. Plasma renin activity

increased in the upright position, was reduced by administration of

hypotonic saline and unaffected by hypertonic saline, with no

differences between the hypertensives and normotensives. After

hypertonic saline, urinary flow rate and urinary sodium excretion in

the hypertensive group increased to values significantly (p less than

0.05) higher than in normotensive subjects. In conclusion our study

excludes significant alteration of vasopressin regulation in moderate

uncomplicated hypertension. In hypertensives although the response of

vasopressin to an osmotic load is preserved, the data suggest that the

renal handling of the osmotic load may be altered.

PMID: 1822757

--------=========

--- In , " jwwright " <jwwright@e...>

wrote:

> It occurs to me that we don;t have enough info in the endocrine

system.

> We've touched on the LA and ALA, LOX and COX pathways, in

generalities.

> We are afraid of the ALA PCa connection, yet not afraid of the EPA

which is the next step to produce the EPA equivalents of the

prostaglandins, thromboxanes, and leukotrienes of the LA pathway. Are

those better? I guess not.

>

> The idea that EPA somehow is better because it controls the AA

pathway is not exactly true, I've found, because the AA pathway is

self regulating.

> These hormones (eicosanoids) are important because they control the

body's systems. They modualte the cardivascular, pulmonary, immune,

reproductive, and secretory functions. Yet we have talked little about

these in the CR groups.

>

> The eicosanoids include prostaglandins and trhrmboxanes formed in

the cyclooxygenase (COX) pathways, and leukotrienes, hydroxy fatty

acids, and lypoxins formed in the lypooxygenase (LOX) pathway.

>

> In the AA pathway, the COX produces PGE2, PGF2 alpha, PGD2, PGI2,

TXA2, and prostacyclins.

> The ALA pathway sorta mirrors this producing PGE3, PGF3alpha, PGD3,

PGI3, TXA3.

>

> So my first question is does the ALA pathway produce " better "

hormones? My first inclination is to not dose with either LA, ALA, or

EPA/DHA and leave out all added fat until I analyze my system and

figure out which hormone I need to modulate. (vasopressin)

> Perhaps none can be modulated with added pure fatty acids?

>

> Regards.

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JW,

Your note discusses the complexity of the body's regulatory system.

However, you need to distinguish between the eicosanoids which are

basically hydrocarbons (containing no nitrogen) derived from fat

metabolism, and hormones and enzymes which are peptides or proteins

consisting of amino acids. Vasopressin, is a peptide consisting of 9

amino acids which is also called Antidiuretic Hormone (ADH).

Ben Best has a web page on fats that discusses eicosanoids:

http://www.benbest.com/health/essfat.html

The body reacts to changes in electrolyte balance by releasing peptide

hormones such as renin from the kidneys.

Many of the body's peptide hormonal auto-regulating systems come in

antogonistic pairs, such as the insulin/glucagon mechanism for

regulating high/low blood glucose. The release of insulin or glucagon

by the pancreas is mediated by consumption of carbohydrates and by

fasting, respectively.

The external factors influencing hypertension may involve salt

consumption, body weight, exercise, perspiration, muscle tone, etc.

Production of NO (nitrous oxide) from L-arginine may also be involved

since NO is a smooth muscle relaxant which influences arterial walls.

Tony

===

Clin Auton Res. 1991 Jun;1(2):109-14.

Regulation of vasopressin release in moderately severe essential

hypertension.

Del Bo A, Marabini M, ti A, Zanchetti A.

Istituto di Clinica Medica Generale e Terapia Medica, Universita

di Milano, Milan, Italy.

Vasopressin plasma concentrations have been measured in two groups

of subjects, 13 moderate essential hypertensive patients without

target organ damage and eight control normotensive subjects, before

and after the assumption of the upright position, and intravenous

infusions of hypotonic saline (0.45% NaCl, 0.25 ml kg-1 min-1 for 1 h)

and hypertonic saline (100 mmol NaCl in 50 ml). Plasma vasopressin in

recumbent baseline conditions was not significantly different in the

two groups. Upright posture and hypertonic challenge augmented, while

hypotonic saline reduced plasma vasopressin levels, which were not

significantly different between the two groups. Plasma renin activity

increased in the upright position, was reduced by administration of

hypotonic saline and unaffected by hypertonic saline, with no

differences between the hypertensives and normotensives. After

hypertonic saline, urinary flow rate and urinary sodium excretion in

the hypertensive group increased to values significantly (p less than

0.05) higher than in normotensive subjects. In conclusion our study

excludes significant alteration of vasopressin regulation in moderate

uncomplicated hypertension. In hypertensives although the response of

vasopressin to an osmotic load is preserved, the data suggest that the

renal handling of the osmotic load may be altered.

PMID: 1822757

--------=========

--- In , " jwwright " <jwwright@e...>

wrote:

> It occurs to me that we don;t have enough info in the endocrine

system.

> We've touched on the LA and ALA, LOX and COX pathways, in

generalities.

> We are afraid of the ALA PCa connection, yet not afraid of the EPA

which is the next step to produce the EPA equivalents of the

prostaglandins, thromboxanes, and leukotrienes of the LA pathway. Are

those better? I guess not.

>

> The idea that EPA somehow is better because it controls the AA

pathway is not exactly true, I've found, because the AA pathway is

self regulating.

> These hormones (eicosanoids) are important because they control the

body's systems. They modualte the cardivascular, pulmonary, immune,

reproductive, and secretory functions. Yet we have talked little about

these in the CR groups.

>

> The eicosanoids include prostaglandins and trhrmboxanes formed in

the cyclooxygenase (COX) pathways, and leukotrienes, hydroxy fatty

acids, and lypoxins formed in the lypooxygenase (LOX) pathway.

>

> In the AA pathway, the COX produces PGE2, PGF2 alpha, PGD2, PGI2,

TXA2, and prostacyclins.

> The ALA pathway sorta mirrors this producing PGE3, PGF3alpha, PGD3,

PGI3, TXA3.

>

> So my first question is does the ALA pathway produce " better "

hormones? My first inclination is to not dose with either LA, ALA, or

EPA/DHA and leave out all added fat until I analyze my system and

figure out which hormone I need to modulate. (vasopressin)

> Perhaps none can be modulated with added pure fatty acids?

>

> Regards.

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  • 2 years later...
Guest guest

Hi Caroline!

Question: WHY are you seeing an Endocrinologist? Who suggested?

What is possible problem/diagnosis?

Check out this link. (look under endocrinology)

You may have already seen this, but each of the physicians has a

little bio and area of special interests. DiMeglio has Special

Interests: Bone Diseases, Diabetes, Public Health. Does this sound

like what you are looking for?? If someone from Riley just assigned

you to someone you may want to rethink if this does not sound like

the best fit.

http://rileychildrenshospital.com/physicians/locator.jsp?

view=BySpecialty

Let me know!

Thanks

>

> Indiana listmates,

>

> Do any of you have recommendations (pro or con) for an

endocrinologist in

> Indianapolis? We¹re going to be heading to one very soon (like this

> Thursday) and I would love to have some guidance if any of you have

any

> thoughts to offer. We¹ve been assigned to a Dr. DiMeglio whom I

know

> nothing about.

>

> Caroline G.

>

>

>

>

>

>

>

>

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