Chondroitin Sulphate and Prostate Cancer
Thomas Carter
The Life extension forum at LEF.org has deteriorated so badly lately
that I have stopped reading it, but they sent me an Email saying it
would be moderated for two weeks by some doctor, this hasn't happened,
but it did cause me to make a quick check and I saw this post, which I
attatch below with my response.
>I just read an email from the Health Science Institute indicating
>that the use of chondroitin sulfate (used by the patient
>for osteoarthritis) caused the spread of prostate cancer to other
>sites. Dr. Meyers goes on to state that this
>supplement is not to be used with this type of
>cancer (also flaxseed oil). I emailed and questioned whether
>than would go for other types of cancer, specifically breast
>cancer, and they did not have an answer. Do
>you know anything about this. (The web link where
>this was discussed is as follows:
http://www.hsibaltimore.com/ea2002/ea_020507.shtml)
>I have osteoarthritis and have been taking chrondroitin/glucosamine
supplements. I
>also was treated last year for breast cancer. At
>this point I have stopped those supplements. Your comments
>will be appreciated.
This is LEF's reply
>I can't get to this URL. Tell us more about the
>study and how they came to this conclusion. It doesn't
>seem too straightforward. Here at LEF, we are beginning to
>see evidence that anything that strengthens the bones lowers the
>risk of spread of prostate cancer. Also, it's quite a
>leap to apply even the best findings of one cancer
>to another. MAL
This is my reply.
Thanks KayKay,
I'm throwing mine away. I can't believe I starting taking this stuff
without checking it out thouroughly.
MAL,
The conclusion doesn't seem straight forward to you because you
are selling the stuff. The fact that LEF is selling both flax seed oil
and Chondroitin Sulphate without warnings about their cancer affects
is strong indication that they have far more interest in their income
than the health of their clients. It saddens me to see indications
that this tendency is growing along with their sales volume. The
simple search string, Chondroitin sulphate and prostate cancer, gives
six hits at Medline, all six very indicative of risk.
Thomas
Tom Matthews
> Hi,
> The Life extension forum at LEF.org has deteriorated so badly lately
> that I have stopped reading it, but they sent me an Email saying it
> would be moderated for two weeks by some doctor, this hasn't happened,
I have news for you, Tom. MAL *is* a doctor, Mark LaPorta MD. Obviously, he also
knows no better than to tout the LEF line without doing any independent research.
But thanks for the tip. Since both Kitty and I take a lot of chondroitin (after
abandoning glucosamine because of its insulin resistance promoting effects -
again something which LEF has *never* even mentioned) when has been very
beneficial for joints and cartilage, I will certainly be looking into this
possible association. I am not moving so hastily as you did, until I find out
for myself.
Why are you so quick throw it away on the basis of a website before fully
investigating as you usually do? Do you have prostate cancer? or does it
strongly run in your family?
The relationship of flaxseed oil (ALA) to prostate cancer has been the subject
of discussion here before, but I do not think the evidence for it being a
promoter for prostate cancer is very strong. Perhaps it is time to have a review
of all the evidence.
--Tom Matthews
MoreLife for the rational - http://morelife.org
Reality based tools for More Life in quantity & quality
Tom Matthews
>Someone the LEF forum wrote:
>>I just read an email from the Health Science Institute indicating
>>that the use of chondroitin sulfate (used by the patient
>>for osteoarthritis) caused the spread of prostate cancer to other
>>sites. Dr. Meyers goes on to state that this
>>supplement is not to be used with this type of
>>cancer (also flaxseed oil). I emailed and questioned whether
>>than would go for other types of cancer, specifically breast
>>cancer, and they did not have an answer. Do
>>you know anything about this. (The web link where
>>this was discussed is as follows:
>>
>> http://www.hsibaltimore.com/ea2002/ea_020507.shtml)
This web page makes no reference to peer-reviewed sources, referring only to a
Dr Charles Myers who is not an author of any peer-reviewed publications relating
to the prostate and chondroitin. The website text is also confused about
"versican" which is clearly described in the one paper relating it with the
prostate and chondroitin sulfate which follows:
Clin Cancer Res 1998 Apr;4(4):963-71
Elevated levels of versican but not decorin predict disease progression in
early-stage prostate cancer.
Ricciardelli C, Mayne K, Sykes PJ, Raymond WA, McCaul K, Marshall VR, Horsfall
DJ.
Department of Surgery, Flinders University School of Medicine, Flinders Medical
Centre, Bedford Park, South Australia, Australia.
Patients with clinically localized prostate cancer who might be cured by
aggressive management are not easily identified using current clinical
information. Additional, more accurate, biomarkers of tumor behavior need to be
identified to improve clinical outcome. Our previous studies indicated that the
concentration of the glycosaminoglycan chondroitin sulfate in prostatic stroma
might be a useful biomarker of disease progression in early-stage prostate
cancer. In this study, two chondroitin sulfate proteoglycans, versican and
decorin, were investigated. Versican and decorin were immunolocalized to the
periacinar and peritumoral fibromuscular stroma in sections of nonmalignant and
malignant human prostate tissues. Video image measurements indicated that the
concentrations of both proteoglycans were increased in the prostatic tissue of
men with early-stage prostate cancer compared with tissue from men without
cancer (P = 0.0006). Cox's univariate analysis indicated that increases in
versican concentration but not in that of decorin were associated with increased
risk of prostate-specific antigen (PSA) progression. Versican concentration was
compared with other clinical or biological features of prognosis in two-variable
regression analyses. Versican and serum PSA concentrations were independent
predictors of PSA progression. Versican was a stronger prognostic factor than
tumor grade, and it could predict outcome for patients with moderately
differentiated tumors. Patients with low versican concentration had
significantly better progression-free survival than patients with high levels of
versican (Kaplan-Meier plot, 89% versus 27% PSA progression-free at 5 years,
respectively; P = 0.0001). We conclude that the measurement of prostatic
concentrations of versican, a molecule with reported anticellular adhesive
properties, may be a useful marker of disease progression in patients with
early-stage prostate cancer and that further study of versican in other patient
cohorts is warranted.
PMID: 9563891
Note that versican is a chondroitin sulfate proteoglycan. Ie. a protein modified
by attachment of a chondroitin sulfate moiety. Other papers show that this
proteoglycan (CSPG) is upregulated in BHP and in prostate cancer, and that one
major regulation factor appears to be androgen hormones. Moreover, as one study
stated:
"Since HA and CSPG (or their complexes) are highly anionic molecules, their
increased accumulation in the altered prostatic stroma would tend to hydrate
this tissue. This would create an environment more favorable for tumor growth
and invasion."
However, a study of the 23 hits for "prostate chondroitin" does not find one of
them which implies or suggests that supplemental chondroitin sulfate would
increase the production of CSPG by prostate cells either cancerous or merely
hyperplastic.
For the benefit of the above person (poster to the LEF forum), for "breast
cancer chondroitin" there are 38 PubMed hits. A quick perusal of them also
suggests a strong relationship of CSPG with breast cancer growth and metastasis.
However, once again there is no implication or suggestion that supplemental
chondroitin sulfate will increase the risk.
Conclusion: It is probably a wise precaution for those with prostate cancer (or
even BPH) or breast cancer, or at high familial risk for these to eschew the use
of chondroitin sulfate unless it is extremely beneficial for their quality of
life wrt arthritis. Certainly, LEF and other suppliers of chondroitin sulfate
should make this connection known. However, for those of us who are have no sign
of prostate or breast cancer and no high familial related risk, I see no reason
to stop using chondroitin if it appears to be benefiting one's joints (which it
does with me).
Thomas Carter
> Thomas Carter wrote:
>
> > Hi,
> > The Life extension forum at LEF.org has deteriorated so badly lately
> > that I have stopped reading it, but they sent me an Email saying it
> > would be moderated for two weeks by some doctor, this hasn't happened,
>
>
> I have news for you, Tom. MAL *is* a doctor, Mark LaPorta MD. Obviously, he also
> knows no better than to tout the LEF line without doing any independent research.
>
> But thanks for the tip. Since both Kitty and I take a lot of chondroitin (after
> abandoning glucosamine because of its insulin resistance promoting effects -
> again something which LEF has *never* even mentioned) when has been very
> beneficial for joints and cartilage, I will certainly be looking into this
> possible association. I am not moving so hastily as you did, until I find out
> for myself.
>
> Why are you so quick throw it away on the basis of a website before fully
> investigating as you usually do? Do you have prostate cancer? or does it
> strongly run in your family?
Hi Tom,
I'm tall and I exercise. Both increase IGF-1, which is associated
with prostate cancer. I also suspect I have plenty of testosterone. My
joints seem to be in pretty good shape. I was taking it mostly as a
preventative. I also quit the glucosamine when you did. I now take
only gelatine specifically for my joints, and I think the benefits of
this are minimal. I quit on basis of the Medline search, not the
website. I try to study something very thouroughly before taking it
but am quick to turn it down especially if the benefits are not great.
> The relationship of flaxseed oil (ALA) to prostate cancer has been the subject
> of discussion here before, but I do not think the evidence for it being a
> promoter for prostate cancer is very strong. Perhaps it is time to have a review of the issue.
I run my search strings on it every three months. I haven't seem
much that's new. IIRC our discussions did not mention that flaxseed
meal seems to be associated with a reduced risk of PC, while the oil
is related to an increased risk.
Thomas
GeoWCherry
I take a lot of chondroitin (after
abandoning glucosamine because of its insulin resistance promoting effects -
again something which LEF has *never* even mentioned) when has been very
beneficial for joints and cartilage, I will certainly be looking into this
possible association. I am not moving so hastily as you did, until I find out
for myself.
George;
I'm dismayed to learn that glucosamine
promotes insulin resistance. Glucosamine
(600 mg of SAM-e and 1500 mg of glucos-
amine a day) has been a breakthrough on
repairing my osteoarthritic knees. I'm
jogging again and climbing stairs again
with NO pain. I thought I would never be
able to run and climb again. My antidote
to insulin resistance will be to increase
my ratio of muscle to fat and to eat no
high glycemic food at all. I'd hate to give
up glucosamine.
Thomas Carter
>
>
> However, a study of the 23 hits for "prostate chondroitin" does not find one of
> them which implies or suggests that supplemental chondroitin sulfate would
> increase the production of CSPG by prostate cells either cancerous or merely
> hyperplastic.
>
> For the benefit of the above person (poster to the LEF forum), for "breast
> cancer chondroitin" there are 38 PubMed hits. A quick perusal of them also
> suggests a strong relationship of CSPG with breast cancer growth and metastasis.
> However, once again there is no implication or suggestion that supplemental
> chondroitin sulfate will increase the risk.
>
> Conclusion: It is probably a wise precaution for those with prostate cancer (or
> even BPH) or breast cancer, or at high familial risk for these to eschew the use
> of chondroitin sulfate unless it is extremely beneficial for their quality of
> life wrt arthritis. Certainly, LEF and other suppliers of chondroitin sulfate
> should make this connection known. However, for those of us who are have no sign
> of prostate or breast cancer and no high familial related risk, I see no reason
> to stop using chondroitin if it appears to be benefiting one's joints (which it
> does with me).
>
>
> --Tom Matthews
>
> MoreLife for the rational - http://morelife.org
> Reality based tools for More Life in quantity & quality
Hi Tom,
Its not too surprising to find no studies on the relationship
between chondroitin Sulphate supplementation and it's attachment to
the proteoglycans in prostate cancer cells since there are few
studies and the cancer people are not too interested in CS
supplementation. It is quite logical to suppose a risk however since
CS is a precursor for Versican which is the main CSPG with a cancer
risk and that there is evidence for an increase in Versican with CS
supplementation in other cells. There is also a logical mechanism
which has been proposed, namely the decrease is cellular adhesion
which is a known effect of Versican. I also note that glucoseamine is
apparently just as bad as CS, or worse due to better absorption. There
is also more bad news which my search turned up namely links to
atherosclerosis, as well as to breast and skin cancer. I attach below
my synopsis with the verifying abstracts and a good monograph from
altern med review.
While the links to cancer and athersclerosis are all contrast
medium studies and far from well established, I think my joints are in
good enough shape that I can wait awhile and monitor developments
before considering a resumption of supplementation.
Thomas
Proteoglycans are mostly large proteins with aminoglycans
attached and are used in the extracellular matrix to hold water and
provide support. Chondroitin sulfate proteoglycans (CSPGs) of the
arterial wall are generally considered to be atherogenic because of
their ability to trap cholesterol-rich lipoproteins in vitro. The
three principal CSPGs in the arterial wall are versican, which is part
of the hyalectan gene family; and decorin and biglycan, which are
members of a separate gene family, Versican , except for the V3
splice variant, is apparantly related to various cancers, with decorin
being protective, but decorin and biglycan are related to
atherogenesis. Bassleer et al demonstrated, in vitro, both GS and CS
have a stimulatory effect on the production of proteoglycans by
cultured differentiated human articular chondrocytes . PMID: 1300309
Curr Opin Lipidol 2001 Oct;12(5):477-87 Arterial wall chondroitin
sulfate proteoglycans: diverse molecules with distinct roles in
lipoprotein retention and atherogenesis. Williams KJ. Dorrance H.
Hamilton Research Laboratories, Division of Endocrinology, Diabetes &
Metabolic Diseases, Department of Medicine, Jefferson Medical College,
Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
K_Wil...@Lac.jci.tju.edu Chondroitin sulfate proteoglycans (CSPGs)
of the arterial wall are generally considered to be atherogenic
because of their ability to trap cholesterol-rich lipoproteins in
vitro. Nevertheless, CSPGs are a diverse group of molecules with a
long evolutionary history and distinct biologic functions. The three
principal CSPGs in the arterial wall are versican, which is part of
the hyalectan gene family; and decorin and biglycan, which are members
of a separate gene family, the small leucine-rich proteoglycans.
Importantly, there is now substantial evidence that the different
molecular species of CSPGs participate unequally in lipoprotein
retention, and that they exert unequal regulatory effects that are
related to atherogenesis. Recently available murine models with
genetic manipulations that affect CSPGs now allow causal studies of
the roles of these molecules to be conducted in vivo, with
occasionally surprising results. Moreover, tools are being developed
to examine human genetic variations that are relevant to CSPGs, which
may provide additional important insights into the human disease. The
era in which proteoglycans are regarded as a nondescript backdrop,
playing purely nonspecific structural roles, is over. Studies in
manipulated animals and in human populations will continue to reveal
precise, dynamic roles for these fascinating and ancient molecules.
Publication Types: Review Review, Tutorial PMID:
11561166…………………………..
Diabetes 2001 Sep;50(9):2126-32 Changes in matrix proteoglycans
induced by insulin and fatty acids in hepatic cells may contribute to
dyslipidemia of insulin resistance. Olsson U, Egnell AC, Lee MR,
Lunden GO, Lorentzon M, Salmivirta M, Bondjers G, Camejo G. Wallenberg
Laboratory for Cardiovascular Research, Goteborg University,
Sahlgrenska University Hospital, Goteborg, Sweden. Insulin resistance
and type 2 diabetes are associated with elevated circulating levels of
insulin, nonesterified fatty acids (NEFAs), and lipoprotein remnants.
Extracellular matrix proteoglycan (PG) alterations are also common in
macro- and microvascular complications of type 2 diabetes. In liver,
extracellular heparan sulfate (HS) PGs contribute to the uptake of
triglyceride-rich lipoprotein remnants. We found that HepG2 cells
cultured with 10 or 50 nmol/l insulin or 300 micromol/l albumin-bound
linoleic acid changed their PG secretion. The glycosaminoglycans
(GAGs) of the secreted PGs from insulin-treated HepG2 cells were
enriched in chondroitin sulfate (CS) PGs. In contrast, cells exposed
to linoleic acid secreted PGs with decreased content of CS. Insulin
caused a moderate increase in mRNA for versican (secreted CS PG),
whereas linoleic acid markedly decreased mRNA for versican in HepG2
cells, as did the peroxisomal proliferator-activated receptor-alpha
agonist bezafibrate. The effects of insulin or linoleic acid on
syndecan 1, a cell surface HS PG, were similar to those on versican,
but less pronounced. The livers of obese Zucker fa/fa rats, which are
insulin-resistant and have high levels of insulin, NEFAs, and
triglyceride-rich remnants, showed increased expression of CS PGs when
compared with lean littermates. These changes in PG composition
decreased the affinity of remnant beta-VLDL particles to PGs isolated
from insulin-treated HepG2 cells and obese rat livers. The results
indicated that insulin and NEFAs modulate the expression of PGs in
hepatic cells. We speculate that in vivo this exchange of CS for HS
may reduce the clearance of remnant beta-VLDLs and contribute to the
dyslipidemia of insulin resistance. PMID:
11522680…………………Zhonghua Bing
Li Xue Za Zhi 1998 Jun;27(3):177-81 [The dynamic change of
extracellular matrix in human coronary atherogenesis] [Article in
Chinese] Yang F, Zhao P, She M. Cardiovascular Institute and Fu Wai
Hospital, Chinese Academy of Medical Sciences and Peking Union Medical
College, Beijing 100037. OBJECTIVE: To investigate the expression of
type I, III procollagen mRNAs and chondroitin sulfate proteoglycan
(CSPG) genes, as well as the distribution of type I, III collagen
fibers and CSPG in human coronary atherogenesis. METHODS: Staining for
HE, picrosirius red, immunohistochemistry and hybridization in situ
technique were included. RESULTS: (1) Along with the development of
atherosclerotic lesion, collagen type I, III and CSPG were increased
simultaneously in the coronary wall; The expressions of type I, III
procollagen, biglycan, and decorin mRNAs were noticed to be increased
in the plaques. (2) beta-lipoprotein was seen coexistently with CSPG
in the AS plaques of the coronary arteries. (3) There were more SMC
proliferation, predominant augmentation of type III collagen fibers
and accumulation of CSPG in the early plaques of most young subjects;
but less SMC, amount of type I collagen fibers and deposition of CSPG
in the advanced plaques of most aged people. CONCLUSION:
Over-expression of type I, III procollagen, biglycan and decorin mRNAs
was related to the increase of type I, III collagen and CSPG in the
atherosclerotic lesions. Proliferation of SMC, augmentation of type I,
III collagen and CSPG and change of the proportion between collagen
and CSPG are considered to play an important role in the development
of coronary atherosclerosis. PMID:
11244976…………………….
Oncogene 2002 May 23;21(23):3688-95 Suppression of tumorigenicity by
adenovirus-mediated gene transfer of decorin. Reed CC, Gauldie J,
Iozzo RV. Department of Pathology, Anatomy and Cell Biology, Thomas
Jefferson University, Philadelphia, Pennsylvania, PA 19107, USA. There
is mounting evidence that decorin inhibits the growth of various tumor
cell lines when either over-expressed in vitro or provided as a
recombinant protein. The mechanism of action is primarily via a
protracted inactivation of the epidermal growth factor receptor (EGFR)
tyrosine kinase. In this study we explored the possibility of
retarding the growth of tumor xenografts by decorin gene delivery into
the growing neoplastic tissues. We demonstrate that transient
transgene expression of replication-deficient adenovirus-containing
decorin causes a significant growth inhibition of colon and squamous
carcinoma tumor xenografts. These cytostatic effects were achieved
with relatively low viral titers and correlated with a reduced
proliferative index and an attenuation of the EGFR phosphorylation in
vivo. Thus, decorin gene therapy helps in retarding the growth of
human tumors in immunocompromised animals and could represent a new
independent or adjunctive therapeutic modality against cancer. DOI:
10.1038/sj/onc/1205470 PMID: 12032837
……………………………J
Cell Physiol 2002 Jan;190(1):38-45 Overexpression of the V3 variant of
versican alters arterial smooth muscle cell adhesion, migration, and
proliferation in vitro. Lemire JM, Merrilees MJ, Braun KR, Wight TN.
Department of Anatomy and Cell Biology, Tufts University School of
Medicine, Boston, Massachusetts, USA. Versican is an extracellular
matrix proteoglycan produced by many cells. Although versican is
generally known as a large chondroitin sulfate proteoglycan (CSPG),
the smallest splice variant, V3, consists only of the amino- and
carboxy-terminal globular domains and is therefore predicted to be a
small glycoprotein, lacking CS chains. The large size, negative
charge, and ability of versican variants to form pericellular coats
with hyaluronan are responsible for many of its effects. V3, lacking
the large size and high charge density, but retaining the
hyaluronan-binding domain of the larger isoforms, may have different
effects on cell phenotype. To determine whether V3 alters cell
phenotype, Fisher rat arterial smooth muscle cells (ASMCs), which
express the larger CSPG versican splice forms (V0 and V1) were
retrovirally transduced with the rat V3 cDNA. Northern analysis for
versican RNAs confirmed that cells transduced with V3 retrovirus, but
not cells tranduced with the empty vector, expressed RNA of the size
expected for V3/neo(r) bicistronic RNA. V3 overexpressing cells were
more spread on tissue culture plastic, had a smaller length-to-breadth
ratio and were more resistant to release from the culture dish by
trypsin. Interference reflection microscopy of sparsely plated cells
showed larger areas of close contact between the V3 expressing cells
and the coverslip, in comparison to control cells. Focal contacts in
the periphery of V3 expressing cells were larger. Growth and migration
studies revealed that V3 transduced cells grow slower and migrate a
shorter distance in a scratch wound assay. The increased adhesion and
the inhibition of migration and proliferation resulting from V3
overexpression are the opposites of the known and predicted effects of
the other variants of versican. V3 may exert these effects through
changes in pericellular coat formation, either by competing with
larger isoforms for hyaluronan-binding, or by altering other
components of the pericellular matrix. Copyright 2002 Wiley-Liss, Inc.
PMID: 11807809…………..
Altern Med Rev 1998 Feb;3(1):27-39 The role of glucosamine sulfate and
chondroitin sulfates in the treatment of degenerative joint disease.
Kelly GS. Successful treatment of osteoarthritis must effectively
control pain, and should slow down or reverse progression of the
disease. Biochemical and pharmacological data combined with animal and
human studies demonstrate glucosamine sulfate is capable of satisfying
these criteria. Glucosamine sulfate's primary biological role in
halting or reversing joint degeneration appears to be directly due to
its ability to act as an essential substrate for, and to stimulate the
biosynthesis of, the glycosaminoglycans and the hyaluronic acid
backbone needed for the formation of proteoglycans found in the
structural matrix of joints. Chondroitin sulfates, whether they are
absorbed intact or broken into their constituent components, similarly
provide additional substrates for the formation of a healthy joint
matrix. Evidence also supports the oral administration of chondroitin
sulfates for joint disease, both as an agent to slowly reduce symptoms
and to reduce the need for non-steroidal anti-inflammatory drugs. The
combined use of glucosamine sulfate and chondroitin sulfates in the
treatment of degenerative joint disease has become an extremely
popular supplementation protocol in arthritic conditions of the
joints. Although glucosamine sulfate and chondroitin sulfates are
often administered together, there is no information available to
demonstrate the combination produces better results than glucosamine
sulfate alone. Publication Types: Review Review, Tutorial PMID:
9600024 ……………………The
mechanism of action of CS is probably similar in nature to GS, since
it can also provide substrates for proteoglycan synthesis. Bassleer et
al demonstrated, in vitro, both GS and CS have a stimulatory effect on
the production of proteoglycans by cultured differentiated human
articular chondrocytes.14 Karzel and Lee also reported both
glucosamine derivatives and CS could influence the in vitro growth and
metabolism of glycosaminoglycans. Glucosamine hydrochloride,
glucosamine hydroiodide, and GS promoted a significant increase in the
glycosaminoglycans in the extracellular cartilage matrix and induced
an increase in the secretion of glycosaminoglycans from the surface of
the bone cells into the culture medium. Although CS were also capable
of positively influencing the metabolism of glycosaminoglycans, their
effect was not significant in this experiment.
Some evidence suggests a component of the activity of GS and CS is
related to the sulfate residues found is these compounds. Sulfur is an
essential nutrient for the stabilization of the connective tissue
matrix. Because of this, it has been proposed that the sulfate
molecules of GS and CS contribute to the therapeutic benefits of these
compounds in degenerative joint diseases. If this speculation is true,
it would lend support to the proposition that GS, as opposed to NAG or
glucosamine hydrochloride, is the best form of glucosamine
supplementation for patients with arthritis. It would also give added
importance to the sulfate-to-carboxyl ratio of CS.
http://www.thorne.com/altmedrev/.fulltext/3/1/27.html
ada
Your super vigorous exercise routine is capable of lowering your blood
sugar and you have nothing to worry. But for your peace of mind you
could check your blood glucose level more often;I think that a home
instrument is available if you want to do it yourself; all it takes is
a small finger prick.
ada
GeoWCherry
Thanks,
George
Tom Matthews
> Tom Matthews <t...@morelife.org> wrote in message news:<3CF5D6BE...@morelife.org>...
>
>>Thomas Carter wrote:
>>
>>
>>>Hi,
>>>The Life extension forum at LEF.org has deteriorated so badly lately
>>>that I have stopped reading it, but they sent me an Email saying it
>>>would be moderated for two weeks by some doctor, this hasn't happened,
>>>
>>
>>I have news for you, Tom. MAL *is* a doctor, Mark LaPorta MD. Obviously, he also
>>knows no better than to tout the LEF line without doing any independent research.
>>
>>But thanks for the tip. Since both Kitty and I take a lot of chondroitin (after
>>abandoning glucosamine because of its insulin resistance promoting effects -
>>again something which LEF has *never* even mentioned) when has been very
>>beneficial for joints and cartilage, I will certainly be looking into this
>>possible association. I am not moving so hastily as you did, until I find out
>>for myself.
>>
>>Why are you so quick throw it away on the basis of a website before fully
>>investigating as you usually do? Do you have prostate cancer? or does it
>>strongly run in your family?
>>
>
> Hi Tom,
>
> I'm tall and I exercise. Both increase IGF-1, which is associated
> with prostate cancer.
But not proven to be *causal* for PC. We must never confuse the two.
> I also suspect I have plenty of testosterone. My
> joints seem to be in pretty good shape. I was taking it mostly as a
> preventative. I also quit the glucosamine when you did. I now take
> only gelatine specifically for my joints, and I think the benefits of
> this are minimal. I quit on basis of the Medline search, not the
> website. I try to study something very thoroughly before taking it
> but am quick to turn it down especially if the benefits are not great.
Okay. I understand.
>>The relationship of flaxseed oil (ALA) to prostate cancer has been the subject
>>of discussion here before, but I do not think the evidence for it being a
>>promoter for prostate cancer is very strong. Perhaps it is time to have a review of the issue.
>>
>
> I run my search strings on it every three months. I haven't seem
> much that's new. IIRC our discussions did not mention that flaxseed
> meal seems to be associated with a reduced risk of PC, while the oil
> is related to an increased risk.
Are you saying that the meal is associated with decreased risk
and the oil with increased risk, because that is what I remember? On that
basis, I do not use the oil, but I do still use freshly ground flax seed.
Of course, I mostly eat a lot of fatty fish: salmon, sardines, herring,
mackerel, etc.
Tom Matthews
> Tom Matthews <t...@morelife.org> wrote in message news:<3CF5EE55...@morelife.org>...
>
>
>>However, a study of the 23 hits for "prostate chondroitin" does not find one of
>>them which implies or suggests that supplemental chondroitin sulfate would
>>increase the production of CSPG by prostate cells either cancerous or merely
>>hyperplastic.
>>
>>For the benefit of the above person (poster to the LEF forum), for "breast
>>cancer chondroitin" there are 38 PubMed hits. A quick perusal of them also
>>suggests a strong relationship of CSPG with breast cancer growth and metastasis.
>>However, once again there is no implication or suggestion that supplemental
>>chondroitin sulfate will increase the risk.
>>
>>Conclusion: It is probably a wise precaution for those with prostate cancer (or
>>even BPH) or breast cancer, or at high familial risk for these to eschew the use
>>of chondroitin sulfate unless it is extremely beneficial for their quality of
>>life wrt arthritis. Certainly, LEF and other suppliers of chondroitin sulfate
>>should make this connection known. However, for those of us who are have no sign
>>of prostate or breast cancer and no high familial related risk, I see no reason
>>to stop using chondroitin if it appears to be benefiting one's joints (which it
>>does with me).
>
> Hi Tom,
>
> Its not too surprising to find no studies on the relationship
> between chondroitin Sulphate supplementation and it's attachment to
> the proteoglycans in prostate cancer cells since there are few
> studies and the cancer people are not too interested in CS
> supplementation.
I agree. I was merely reporting the lack of any evidence to suggest that
supplemental chondroitin would increase the production of CSGP from prostate or
breast cells.
> It is quite logical to suppose a risk however since
> CS is a precursor for Versican which is the main CSPG with a cancer
> risk.
An increase in precursors often does not translate to an increase in the
chemical of which they are precursors.
> and that there is evidence for an increase in Versican with CS
> supplementation in other cells.
The evidence is in vitro and applies to bone cells. All that this evidence does
is support theoretically the benefit of CS and GS for bone, cartilage, etc. What
applies one kind of cell in vitro does not necessarily apply to a totally
different kind of cell in vivo.
> There is also a logical mechanism
> which has been proposed, namely the decrease is cellular adhesion
> which is a known effect of Versican.
Certainly the papers are starting to clearly show mechanisms for many underlying
disease processes which involve CSPG. That is great and very unifying, but still
does not show that dietary chondroitin sulfate will increase any of those
disease processes. In addition, each of the disease processes have necessary
causal factors other than CSPG production.
> I also note that glucoseamine is
> apparently just as bad as CS, or worse due to better absorption.
As bad if CS is indeed bad. But also as good or better in the manner that CS is
good. OTOH, while GS has a negative effect on insulin resistance, I don't know
of any such effect from CS.
> There
> is also more bad news which my search turned up namely links to
> atherosclerosis, as well as to breast and skin cancer. I attach below
> my synopsis with the verifying abstracts and a good monograph from
> altern med review.
> While the links to cancer and athersclerosis are all contrast
> medium studies and far from well established, I think my joints are in
> good enough shape that I can wait awhile and monitor developments
> before considering a resumption of supplementation.
I think your last statement is what really counts here. So long as they remain
in good shape you are probably wise to discontinue chondroitin.
BTW, I found the abstract which you supplied which talked about the sulfur part
of CS and GS interesting because I have also been using 2.5 g of MSM daily and
it seems to have helped. Finally, what helped most quickly of all appears to be
my use of a "generic" ALT-711 as a result of which my knee and thumb joints are
practically 100% now.
As a result of all this discussion (thanks to you), and as a precaution only, I
also have decided to temporarily stop taking chondroitin sulfate and see if I
can get along with only MSM and generic ALT-711.
Tom Matthews
> George,
> Your super vigorous exercise routine is capable of lowering your blood
> sugar and you have nothing to worry.
Ada, What you say is true, but we are talking about optimizing things here and
every little bit counts. The literature makes it clear that there is a trade-off
between glucosamine's benefits for your joints and its adverse potential for
insulin resistance. Since there are other things which will benefit joints (CS,
MSM, omega-3, etc), it may be best to use those instead. It is up to the
individual to choose his overall quality of life optimization path by using all
the evidence available.
> But for your peace of mind you
> could check your blood glucose level more often;I think that a home
> instrument is available if you want to do it yourself; all it takes is
> a small finger prick.
Home glucose kits are useful, but they are much too gross a measuring method to
discriminate what I am taking about.
ada
myself. Well, I checked Consumer Reports Magazine online (by
subscription) and the one that topped the latest review (2001) was
"ONE TOUCH" Ultra. A search for that meter brought many results and
now the question is which site offers the best price for it:-)
ada
geowc...@aol.com (GeoWCherry) wrote in message news:<20020530223406...@mb-fg.aol.com>...
GeoWCherry
My reply to you, reminded me that I once planned to look for one
myself. Well, I checked Consumer Reports Magazine online (by
subscription) and the one that topped the latest review (2001) was
"ONE TOUCH" Ultra. A search for that meter brought many results and
now the question is which site offers the best price for it:-)
Hi, ada.
If you're on Medicare, you might
be able to get it free! :-)
ONE TOUCH Ultra lets you test on your arm too.*
"Now your fingers have more time to jam."
-- B.B. King
"Now my fingers have more time to type."
-- G. W. Cherry
GeoWCherry
> George,
> Your super vigorous exercise routine is capable of lowering your blood
> sugar and you have nothing to worry.
George writes:
I'm going to try cutting the glucosamine
to 1000mg/day and possibly 500mg/day.
George
No perfection, no self, no permanence.
michaelprice
news:20020530133444...@mb-mm.aol.com...
> George;
> I'm dismayed to learn that glucosamine
> promotes insulin resistance. Glucosamine
> (600 mg of SAM-e and 1500 mg of glucos-
> amine a day) has been a breakthrough on
> repairing my osteoarthritic knees. I'm
> jogging again and climbing stairs again
> with NO pain. I thought I would never be
> able to run and climb again. My antidote
> to insulin resistance will be to increase
> my ratio of muscle to fat and to eat no
> high glycemic food at all. I'd hate to give
> up glucosamine.
Me too. But how strong is the evidence against
glucosamine? The best ref I could find (below) was
using *intravenous* glucosamine, and it's not clear to me
how applicable it is to oral glucosamine. (Would
intravenous glucose have had the same effect?) Perhaps
oral glucosamine is no worse than a sweetened drink?
Diabetes 2000 Jun;49(6):926-35 Related Articles, Books, LinkOut
Effects of glucosamine infusion on insulin secretion and insulin action in
humans.
Monauni T, Zenti MG, Cretti A, Daniels MC, Targher G, Caruso B, Caputo M,
McClain D, Del Prato S, Giaccari A, Muggeo M, Bonora E, Bonadonna RC.
Division of Endocrinology and Metabolic Diseases, University of Verona
School of Medicine, Italy.
Glucose toxicity (i.e., glucose-induced reduction in insulin secretion and
action) may be mediated by an increased flux through the
hexosamine-phosphate pathway. Glucosamine (GlcN) is widely used to
accelerate the hexosamine pathway flux, independently of glucose. We tested
the hypothesis that GlcN can affect insulin secretion and/or action in
humans. In 10 healthy subjects, we sequentially performed an intravenous
glucose (plus [2-3H]glucose) tolerance test (IVGTT) and a euglycemic insulin
clamp during either a saline infusion or a low (1.6 micromol x min(-1) x
kg(-1)) or high (5 micromol x min(-1) x kg(-1) [n = 5]) GlcN infusion.
Beta-cell secretion, insulin (SI*-IVGTT), and glucose (SG*) action on
glucose utilization during the IVGTT were measured according to minimal
models of insulin secretion and action. Infusion of GlcN did not affect
readily releasable insulin levels, glucose-stimulated insulin secretion
(GSIS), or the time constant of secretion, but it increased both the glucose
threshold of GSIS (delta approximately 0.5-0.8 mmol/l, P < 0.03-0.01) and
plasma fasting glucose levels (delta approximately 0.3-0.5 mmol/l, P <
0.05-0.02). GlcN did not change glucose utilization or intracellular
metabolism (glucose oxidation and glucose storage were measured by indirect
calorimetry) during the clamp. However, high levels of GlcN caused a
decrease in SI*-IVGTT (delta approximately 30%, P < 0.02) and in SG* (delta
approximately 40%, P < 0.05). Thus, in humans, acute GlcN infusion
recapitulates some metabolic features of human diabetes. It remains to be
determined whether acceleration of the hexosamine pathway can cause insulin
resistance at euglycemia in humans.
Cheers,
Michael C Price
Tom Matthews
> "GeoWCherry" <geowc...@aol.com> wrote in message
> news:20020530133444...@mb-mm.aol.com...
>
>
>>George;
>>I'm dismayed to learn that glucosamine
>>promotes insulin resistance. Glucosamine
>>(600 mg of SAM-e and 1500 mg of glucos-
>>amine a day) has been a breakthrough on
>>repairing my osteoarthritic knees. I'm
>>jogging again and climbing stairs again
>>with NO pain. I thought I would never be
>>able to run and climb again. My antidote
>>to insulin resistance will be to increase
>>my ratio of muscle to fat and to eat no
>>high glycemic food at all. I'd hate to give
>>up glucosamine.
>>
>
> Me too. But how strong is the evidence against
> glucosamine? The best ref I could find (below) was
> using *intravenous* glucosamine, and it's not clear to me
> how applicable it is to oral glucosamine. (Would
> intravenous glucose have had the same effect?) Perhaps
> oral glucosamine is no worse than a sweetened drink?
I have no idea how you searched, but PubMed gives 408 hits for "glucosamine
insulin" and 87 for "glucosamine insulin AND (resistance OR sensitivity)".
If someone has the time to do examine these carefully present the results, it
would definitely be of service to many of us here. I have not investigated the
situation for some time and there appear to be many more related results than at
that time.
--Tom Matthews
MoreLife for the rational - http://morelife.org
Reality based tools for More Life in quantity & quality
>
michaelprice
> michaelprice wrote:
> > Me too. But how strong is the evidence against
> > glucosamine? The best ref I could find (below) was
> > using *intravenous* glucosamine, and it's not clear to me
> > how applicable it is to oral glucosamine. (Would
> > intravenous glucose have had the same effect?) Perhaps
> > oral glucosamine is no worse than a sweetened drink?
>
> I have no idea how you searched, but PubMed gives 408 hits for
> "glucosamine insulin" and 87 for "glucosamine insulin AND
> (resistance OR sensitivity)".
Only 14 hits for "glucosamine" & "insulin" & "glucose tolerance", with the
result I gave. The one ref that filtered through after reading was the one
previously cited here a few months ago.