Cortisol:DHEA ratio, lipid alterations and lipodystrophy
Gary Stein
TITLE: Lipodystrophy defined by a clinical score in HIV-infected men
on highly active antiretroviral therapy: correlation between
dyslipidaemia and steroid hormone alterations
JOURNAL: AIDS
VOLUME: 13
ISSUE: 16
PAGES: 2251-2260
RECEIVED: 22 April 1999
ACCEPTED: 13 August 1999.
AUTHOR: NÈvÈna Christeff*, Jean-Claude Melchior†, Pierre de Truchis†,
Christian Perronne†, Emmanuel A. Nunez‡, Marie-Lise Gougeon*
ADDRESS: *UnitÈ d'Oncologie Virale, URA CNRS 1930, DÈpartement SIDA et
Retrovirus, Institut Pasteur, 28 rue du Dr Roux, 75724, Paris, Cedex
15, France; †Service des Maladies Infectieuses et Tropicales, HÙpital
Raymond PoincarÈ, 92380, Garches, France; ‡Laboratoire de Biochimie B,
CHU Bichat Claude Bernard, 46 rue H. Huchard, 75877, Paris, Cedex 18,
France
BACKGROUND: A syndrome of lipodystrophy, associated with
hypertriglyceridaemia, hypercholesterolaemia, hyperinsulinaemia and
peripheral insulin resistance has been reported in protease inhibitor
(PI)-treated HIV-infected patients. Because lipid metabolism, fat mass
distribution and insulin resistance are partly regulated by steroid
hormones, we questioned whether lipodystrophy is related to hormonal
perturbations.
OBJECTIVE: To evaluate serum lipid and steroid hormone concentrations
in HIV-positive men on highly active antiretroviral therapy (HAART) in
order to determine whether dyslipidaemia, peripheral loss of fatty
tissue and central fat accumulation are related to steroid hormone
modifications.
DESIGN: A cross-sectional study.
METHODS: Thirty-seven HIV-1-positive men on HAART, 23 of whom had
symptoms of lipodystrophy, according to a subjective clinical score of
lipodystrophy (SCSL), were tested. Serum concentrations of
cholesterol, triglycerides and their subclasses, apolipoproteins and
steroid hormones, including cortisol, dehydroepiandrosterone (DHEA),
DHEA sulphate, androstenedione, testosterone and dihydrotestosterone
were measured.
RESULTS: Serum cholesterol, very low density lipoprotein (VLDL)
cholesterol, triglycerides, VLDL triglycerides, high density
lipoprotein (HDL) and low density lipoprotein (LDL) triglycerides,
apolipoprotein B (ApoB) and atherogenic ratios of cholesterol:HDL
cholesterol, LDL cholesterol:HDL cholesterol and ApoB:apolipoprotein
A1 (ApoA1) were significantly increased in lipodystrophy-positive
compared with lipodystrophy-negative men. The serum cortisol level was
similar in lipodystrophy-positive versus lipodystrophy-negative men,
but was elevated compared with controls. Serum DHEA was significantly
lower in lipodystrophy-positive versus lipodystrophy-negative men and,
consequently, the cortisol:DHEA ratio was increased in
lipodystrophy-positive patients. A positive correlation was found
between the cortisol:DHEA ratio and increased levels of atherogenic
lipids. In addition, the SCSL was positively correlated with
dyslipidaemia and the cortisol:DHEA ratio.
CONCLUSION: This study demonstrates an association between the
cortisol:DHEA ratio, lipid alterations and lipodystrophy. This
syndrome might result from an imbalance between peripheral lipolysis
and lipogenesis, both regulated by cortisol and DHEA. AIDS 1999,
13:2251-2260 © 1999 Lippincott Williams & Wilkins
Keywords: Atherogenic lipids, cortisol, dehydroepiandrosterone, highly
active antiretroviral therapy, HIV-infected men, lipodystrophy
--
Gary Stein
ges...@bellatlantic.net
"Usenet is like a herd of performing elephants with diarrhea
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GMCarter
<ges...@starpower.net> wrote:
>George I would be interested in your take on this abstract.
>TITLE: Lipodystrophy defined by a clinical score in HIV-infected men
>on highly active antiretroviral therapy: correlation between
>dyslipidaemia and steroid hormone alterations
snipped for bandwidth...
>CONCLUSION: This study demonstrates an association between the
>cortisol:DHEA ratio, lipid alterations and lipodystrophy. This
>syndrome might result from an imbalance between peripheral lipolysis
>and lipogenesis, both regulated by cortisol and DHEA. AIDS 1999,
>13:2251-2260 © 1999 Lippincott Williams & Wilkins
Essentially, this is nothing really new, except the added twist that
some aspects of "lipodystrophy" may be associated with this imbalance.
It suggests that
a) people get their DHEA level checked and
b) if low (or low normal?) then supplement with DHEA.
What dose is best depends on age (post-puberty) and gender, and
possibly weight as well as how low the level is. This is clearly an
area where some clinical assessment would be helpful, but, as usual,
we don't have it so people have to fly by the seat of their pants.
Goddamn the fucking NIH for NEVER looking at these approaches. We pay
tax money for them to do these types of studies, not just be a whore
for industry.
Hmf.
Another thought might be, oddly enough, to try VERY low dose cortisol.
Like maybe 5-10 mg every other day or something. It might get the
adrenals to slow down production of cortisol. However, this probably
should be cycled in some fashion.
A third thought might be Sapse's "Anticort" which is a procaien
derivative. And *possibly* glycyrrhizin, but I have to check this
idea out.
But I think the safest/best bet would be DHEA. Perhaps starting at a
higher dose at first and then bringing it back to a mainenance dose,
with periodic checks of DHEA level.
George M. Carter
Steve
> A third thought might be Sapse's "Anticort" which is a procaien
> derivative.
This is currently under investigation by him. There is some
info on this at http://www.anticort.com
Sapse has some made some pretty strong statements that there is
research showing that HIV *needs* to hijack the cortisol inside
of cells in order to replicate:
http://www.anticort.com/news19991117.html (excerpt below)
We already know that the cytokines which are upregulated directly
by HIV and by the body's inflammatory response to it DO raise cortisol
levels, so this kind of viral-promoting feedback-loop makes sense as
a factor in HIV disease, one that could easily have developed as an
critical or sub-critical factor via viral evolution.
CORTISOL-REDUCING SUPPLEMENTS:
A unique liquid compound made by Twinlab and widely available
pretty cheaply that is ALMOST the same as Anticort is DMAE/H3.
It seems likely to also reduce cortisol. Interestingly, this
compound is EXACTLY the old Attention-Deficit-Disorder drug
DEANOL, and it does indeed have potent, noticable cognitive-
enhancing effects (just start at low doses and work up), as
well as improving response to stress and reducing fatigue
[all of these anecdotal based on my own usage].
Anticort is really the old "GH3" (I suppose with some minor
modifications to allow it to be patentable?), which is once again
available in the US. Skip the knockoffs that just dry-mix DMAE and
PABA (Twinlab's DMAE/H3 is I think a true compound). Look for GH3
that contains Procaine.
It is available mail order and in some health-food stores. It is
also available at a decent price from http://www.beyond-a-century.com/
(look for GEROVITAL-H3 under "Special Products").
Phosphatidyl Serine ("PS") is also a potent reducer of Cortisol,
and is popular with bodybuilders for this purpose.
Also, those interested might want to search www.deja.com for
previous posts by me mentioning Anticort, GH3 and Cortisol, where
I copied lots of links and excerpts from articles on this
subject.
Article excerpt:
...It seems that one of the HIV genes, the Vpr gene (a
real viper), once inside the infected immune cell, is looking for ways to
build a local spearhead, to penetrate or pierce the immune cell nucleus,
in order to transform it into a virus factory. For this purpose, the gene
collects, or practically pirates, the cortisol found in the cell. It then
remolds it, figuratively speaking, in the spearhead that helps the virus
invade the immune cell nucleus where the virus factory is set up and
working full-time. Having understood this process, Dr. Weiner's team
sought to block the cortisol in the cell, thus, depriving the Vpr gene of
using it. As such, they added in the experiment, an anti-cortisol drug,
RU-486, since they reasoned that by immobilizing the existing cellular
cortisol, it should deprive the Vpr gene of this essential ingredient.
According to Steroidogenesis (STGI), the results were immediate and
astonishing. Not only was the virus stopped, but even the already
infected cells lost 70% of their capacity of manufacturing the virus.
More significantly, Weiner, et al suggested in their article, the need of
developing anticortisol/antiglucocorticoid drugs to join the anti-AIDS
therapy.
Steve
> And *possibly* glycyrrhizin, but I have to check this idea out.
Please do. I know that glycyrrhizin has some potent anti-viral
properties. But I worry about the fact that it suppresses the
enzyme which the body uses to break down corisol.
So it would seem to be an agent that might RAISE levels of cortisol
and other mineralocorticoids, rather than lower them.
Since the diurnal cortisol rhythm is an important part of
the body's adrenal system, it is probably best to AVOID taking
Licorice or glycyrrhizin any later than 3PM. The reason being
that Cortisol levels naturally rise in the evenings, which
triggers the anti-cortisol enzyme to bring it back down, creating
the rhythm. I'd think you would not want to block the beta-HSD2
while this feedback process is supposed to be occuring.
There is a LOT of very good, technical info and considerations
about licorce/glycyrrhizin at a site about "Every third day
therapy" for Chronic Fatigue Syndrome (while not directly
applicable to HIV therapy, there's lots of good info about
research, strategies, and safety considerations here):
http://www.seaquake.com/cfs-fm-recovery/every3day.html
In research, subjects were found to have a higher levels of
cortisol in the kidneys, but NOT in plasma. It is in the kidneys
that this conversion takes place, at least ONE of the places.
I worry that this conversion is also being inhibited elsewhere,
possibly resulting in locally higher levels of cortisol in
lymphoid tissue, which could negate the Gyycyrrhizin's direct
anti-HIV effect by feeding the HIV-infected cells the cortisol
that they need. Or, maybe it supports it by down-regulating the
excessive immune activation that HIV products and related
cytokines stimulate, and is a positive influence overall.
This is all speculation of coarse. Anyone with more definative
options or info please jump in.
Other good places to start researching glycyrrhizin:
http://www.thorne.com/altmedrev/.fulltext/4/3/178.html
http://www.seaquake.com/licorice.html
http://www.agric.gov.ab.ca/crops/special/medconf/willardd.html
http://www.primenet.com/~camilla/licapp1.htm
And of course PubMed...there's an overwhelming volume of
research on the subject, but NONE of it directly addressing
the above concerns, of coarse.
Bennett
Steve wrote in message <87pqhr$c...@nfs0.sdrc.com>...
>George Carter wrote:
>
>> And *possibly* glycyrrhizin, but I have to check this idea out.
>
>Please do. I know that glycyrrhizin has some potent anti-viral
>properties. But I worry about the fact that it suppresses the
>enzyme which the body uses to break down corisol.
AFAIK this enzyme is tightly bound to cell plasma membranes, and its very
existence is merely to regulate cortisol's mineralocorticoid activity (it's
normally a glucocorticoid) rather than to regulate the actual levels of
cortisol. Overdoses of licorice don't upset the diurnal rhythm of cortisol
so much as give you stunningly high blood pressure.
Cheers
Bennett
--
University of Cambridge Dept of Medicine
Opinions expressed are mine - I'll take the rap for my own mistakes.
(swap cam for spam to reply via email)
Big fish, little fish, put it in a box. Stacking boxes, stacking boxes...
jdwill...@juno.com
> A unique liquid compound made by Twinlab and
> widely available pretty cheaply that is ALMOST
> the same as Anticort is DMAE/H3. It seems
> likely to also reduce cortisol.
Excuse me for butting in here, but I find this conversation very
interesting.
I have borderline high cortisol levels (ranging from 30mcg/dl in the
morning 15mcg/dl early evening) causing a wide range of symtpoms
including reactive hypo, mental symptoms, tachycardia, etc. I've been
using phosphatidyl serine, and of the countless medications I've tried
including ADs it has helped the most by far.
I have a few questions:
1) What is the exact mechanism of action for PS? I know the basics
(dopamine increase, cortisol reduction, ACTH blunting, pituitary
resensitizing), but I'm looking for a more detailed explanation.
2) Does this Twinlab formula work by a similar mechanism of action? Is
it more/less potent than PS?
3) What's is all the hype I hear about Procaine and GH3? How do they
affect cortisol levels?
4) Is it just me, or is PS quite powerful? I find that I only need to
take 50-100mg per day for a few days to notice a big difference.
- jonathan
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