From:
"Sukie Crandall"
Date: 2009-07-16 05:32:08 UTC
Subject: [ferrethealth] Re: Treatment for adrenal gland disease
To: ferrethealth@yahoogroups.com
It's funny how much experiences can differ
in regard to a second adrenal showing involvement.
It leaves me with some additional questions:
1. Might it be possible reset the stage with feedback
that we don't yet understand, or at least provide enough
control that the change does not matter? For example, I
recall a vet from before melatonin's influence was
understood (one who wanted to study it, actually, but
the funding parties did not grasp its possible functions well
enough to do so) who had a ferret who appeared to have
adrenal disease but who had symptoms stop after care was
provided in darkness for an extended time. Maybe some
ferrets can produce enough of their own melatonin to
reduce LH production. Studies tend to be with provided
melatonin, yet there are some reasons to think that the
body's own melatonin may be best, followed by the
implant, and with oral the weakest.
2. Might there be husbandry differences that should
be getting noticed and utilized more than they are?
3. If a second growth never gets beyond the point of
asymptomatic hyperplasia during the ferret's natural
lifespan isn't that itself an indicator possibly of some
form of control that prevented further growth? After all,
if it remains that mild then it has no effect on either
quality of life or on longevity.
4. Since aberrant yellow fat levels often are worse with
active adrenal growths might correcting an original growth
help reduce high fat levels, thereby reducing the body's
circulating levels of estrogens and compounds that increase
inflammation such as CRP. Decreasing inflammation alone can be
be important. (In humans each unit increase in BMI results in
2% increase in sE-selectin measurement.) Removing fat doesn't work
to prevent the production of those products but shrinking
the size of the fat cells does.
Just o give an idea that there may be important parts not yet
understood:
BEGIN QUOTE
Rev Med Suisse. 2009 Jun 3;5(206):1273-7.Links
[Metabolic dysfunction and chronic stress: a new sight at "diabesity" pande=
mia]
[Article in French]
Gastaldi G, Ruiz J.
Service d'endocrinologie, diab=E9tologie et m=E9tabolisme, CHUV, 1011 Lausa=
nne. Giacomo.gastaldi@chuv.ch
Chronic stress in Western society can activate the
autonomus, neuroendocrine and inflammatory/immunlogic
systems. Chronic exposure to stressors can indeed stimulate
the hypothalamic-pituitary-adrenal axis and induce a
disbalance between anabolic and catabolic hormones, responsible
of an increased in visceral fat and of insulin resistance. These
metabolic consequences can lead to pre-diabetes. Exposure to
chronic stress results in allostatic load and its pathophysiologic
consequences. The knowledge of this mecanisms and the
cardiovascular and metabolic risk related, should influence our
way of thinking about patient care. To decrease allostatic load,
practitioners can rely on therapeutic relation. Therapeutic
education is one of the skill that can be use to create therapeutic
relation.
PMID: 19579423
END QUOTE
Now, this is beyond me but in case it rocks anyone's world a
transporter found also in adrenal tissue (as well as liver and
brain tissue) has been found in high levels in fat recently:
http://www.jlr.org/cgi/reprint/M900237-JLR200v1
but since I can't assess if that may be well enough related I
am just putting in the link.
Maybe even diet can affect levels of inflammation if too high in
fats:
BEGIN QUOTE
Obesity (Silver Spring). 2009 Jun 18. [Epub ahead of print] Links
Effect of a High-fat Diet on 24-Hour Pattern of Circulating
Adipocytokines in Rats.
Cano P, Cardinali DP, R=EDos-Lugo MJ, Fern=E1ndez-Mateos
MP, Reyes Toso CF, Esquifino AI.
Departamento de Bioqu=EDmica y Biolog=EDa Molecular III,
Facultad de Medicina, Universidad Complutense, Madrid, Spain.
We have shown a significant disruption of 24-h pattern of
plasma pituitary, adrenal, and gonadal hormones in high-fat-fed
rats. Our objective was to assess the effect of a high-fat
diet (35% fat) on mean levels and 24-h pattern of several
adipocytokines in rats. A normal diet-fed rats (4% fat)
were used as controls. When body weight of high-fat-fed
rats attained values about 25% higher than controls (after
66 days of treatment), the animals were killed at six different
time intervals throughout a 24-h cycle. Plasma concentrations
of insulin, adiponectin, interleukin (IL)-1, leptin, ghrelin,
plasminogen activator inhibitor-1 (PAI-1), and monocyte
chemoattractant protein-1 (MCP-1) were measured in a
multianalyte profiling by using the Luminex-100 system.
Tumor necrosis factor alpha (TNFalpha) and IL-6 were
measured by enzyme-linked immunosorbent assay. A
significant hyperglycemia developed in high-fat-fed rats,
together with a significant increase in plasma insulin. Mean
levels of plasma adiponectin, IL-1, IL-6, TNFalpha, and leptin
augmented, and ghrelin decreased, in high-fat-fed rats. The
normal daily pattern of plasma insulin, adiponectin, IL-1, IL-6,
TNFalpha, leptin, ghrelin, and MCP-1 became disrupted in
high-fat-fed rats. The results indicate that a high-fat diet may
bring about signs of insulin resistance and mild inflammation
in rats, together with the disruption in daily variations of
circulating insulin and ghrelin, and of several adipocytokines
including leptin, adiponectin, IL-1, IL-6, TNFalpha, and MCP-1.
Obesity (2009) doi:10.1038/oby.2009.200.
END QUOTE
Obesity has been connected to some bad changes involving LH:
BEGIN QUOTE
Fertil Steril. 2009 Apr 24. [Epub ahead of print] Links
Impact of fatness, insulin, and gynecological age on
luteinizing hormone secretory dynamics in adolescent females.
Kasa-Vubu JZ, Jain V, Welch K.
Department of Pediatrics, University of Michigan, Ann Arbor, Michigan.
OBJECTIVE: To study the link between fatness and
gonadotropin secretion. Overweight status is linked to
polycystic ovary syndrome (PCOS) in adolescents. We
postulated that heavier adolescents without symptoms
would secrete LH with: [1] increased pulse frequency (LHPF)
and [2] exaggerated integrated concentrations (LHAUC).
DESIGN: Cross-sectional. SETTING: General clinical research
center. PATIENT(S): Eighty-seven postmenarcheal cyclic
adolescents from lean to overweight recruited during the
follicular phase. INTERVENTION(S): Luteinizing hormone
sampling: [1] every 10 minutes/24 hours; [2] at 20-minute
intervals after a GnRH challenge. MAIN OUTCOME MEASURE(S):
The LHPF and LHAUC (calculated by the CLUSTER algorithm).
Hormonal and metabolic covariates included percent body fat
(PercentBF), insulin-like growth factor-I (IGF-I), fasting insulin,
and the insulin resistance index HOMA-IR. The SAS software
was used for analyses. RESULT(S): The PercentBF and younger
gynecological age predicted faster LHPF. Fatness was negatively
linked to LHAUC, which was best predicted by PercentBF and
IGF-1 in multivariate modeling (R(2) =3D 0.25). The PercentBF
and insulin predicted a lower 20-minute LH response to GnRH.
CONCLUSION(S): [1] Higher adiposity and younger gynecological
age predict rapid LHPF. [2] The early years after menarche
represent a vulnerable window for an exaggerated LHPF with
weight gain. [3] In healthy adolescents, higher adiposity is
linked to lower LHAUC, thereby preserving pituitary stores.
END QUOTE
Endocrinology is a very complicated puzzle that is just beginning
to be understood... At this point, my own inclination as a
non-expert is to not doubt any of the varied reports on
personal experiences of rates, but also to not take any of
them as the final say on what others will encounter because
I just figure we understand the CORE of the problem but not
possible contributing factors that may worsen or reduce it yet.
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