Niacinamide for Osteoarthritis?

[Chris Jain]

This pilot study (below), performed almost 7 years ago,
shows a lot of promise, but I couldn't find much in the way
of followup studies on pubmed. I find this puzzling...maybe
I missed seeing some. Anyone know of any more recent
research on this.

===================================================
Inflamm Res 1996 Jul;45(7):330-4 Related Articles, Links

The effect of niacinamide on osteoarthritis: a pilot study.

Jonas WB, Rapoza CP, Blair WF.

Office of Alternative Medicine, National Institute of Health,
Bethesda, MD 20892, USA.

OBJECTIVE: To evaluate the effect of niacinamide, on selected
parameters of osteoarthritis using a double-blind, placebo
controlled study design. METHODS: Seventy two patients with
osteoarthritis were randomized for treatment with niacinamide
or an identical placebo for 12 weeks. Outcome measures
included global arthritis impact and pain, joint range of
motion and flexibility, erythrocyte sedimentation rate,
complete blood count, liver function tests, cholesterol, uric
acid, and fasting blood sugar. Compliance was monitored with a
pill record sheet and interview. RESULTS: Global arthritis
impact improved by 29% (95% confidence interval [CI] 6, 46) in
subjects on niacinamide and worsened by 10% in placebo
subjects (p = 0.04). Pain levels did not change but those on
niacinamide reduced their anti-inflammatory medications by 13%
(95% CI 9, 94; p = 0.01). Niacinamide reduced erythrocyte
sedimentation rate by 22% (95% CI 6, 51; p < 0.005) and
increased joint mobility by 4.5 degrees over controls (8
degrees vs
3.5 degrees; p = 0.04). Side effects were mild but higher in
the niacinamide group (40% vs 27%, p = 0.003). CONCLUSION:
This study indicates that niacinamide may have a role in the
treatment of osteoarthritis. Niacinamide improved the global
impact of osteoarthritis, improved joint flexibility,
reduced inflammation, and allowed for reduction in standard
anti-inflammatory medications when compared to placebo. More
extensive evaluation of niacinamide in arthritis is
warranted.

[Chris Jain]

Also found this. Anyone been trying this?

Med Hypotheses 1999 Oct;53(4):350-60 Related Articles, Links

Niacinamide therapy for osteoarthritis--does it inhibit nitric
oxide synthase induction by interleukin 1 in chondrocytes?

McCarty MF, Russell AL.

Nutrition 21/AMBI, San Diego, CA 92037, USA.

Fifty years ago, Kaufman reported that high-dose niacinamide
was beneficial in osteoarthritis (OA) and rheumatoid
arthritis. A recent double-blind study confirms the efficacy
of niacinamide in OA. It may be feasible to interpret this
finding in the context of evidence that synovium-generated
interleukin-1 (IL-1), by inducing nitric oxide (NO) synthase
and thereby inhibiting chondrocyte synthesis of aggrecan and
type II collagen, is crucial to the pathogenesis of OA.
Niacinamide and other inhibitors of ADP-ribosylation have
been shown to suppress cytokine-mediated induction of NO
synthase in a number of types of cells; it is therefore
reasonable to speculate that niacinamide will have a
comparable effect in IL-1-exposed chondrocytes, blunting the
anti-anabolic impact of IL-1. The chondroprotective
antibiotic doxycycline may have a similar mechanism of
action. Other nutrients reported to be useful in OA may
likewise intervene in the activity or synthesis of IL-1.
Supplemental glucosamine can be expected to stimulate
synovial synthesis of hyaluronic acid; hyaluronic acid
suppresses the anti-catabolic effect of IL-1 in chondrocyte
cell cultures, and has documented therapeutic efficacy when
injected intra-articularly. S-adenosylmethionine (SAM),
another proven therapy for OA, upregulates the proteoglycan
synthesis of chondrocytes, perhaps because it functions
physiologically as a signal of sulfur availability. IL-1 is
likely to decrease SAM levels in chondrocytes; supplemental
SAM may compensate for this deficit. Adequate selenium
nutrition may down-regulate cytokine signaling, and ample
intakes of fish oil can be expected to decrease synovial
IL-1 production; these nutrients should receive further
evaluation in OA. These considerations suggest that
non-toxic nutritional regimens, by intervening at multiple
points in the signal transduction pathways that promote the
synthesis and mediate the activity of IL-1, may provide a
substantially superior alternative to NSAIDs (merely
palliative and often dangerously toxic) in the treatment and
perhaps prevention of OA.

PMID: 10608273 [PubMed - indexed for MEDLINE]

cjain@ix.netcom.com (Chris Jain) wrote in message
news:<771ea75.0302252136.4c3ac1b@posting.google.com>...
> This pilot study (below), performed almost 7 years ago,
> shows a lot of promise, but I couldn't find much in the way
> of followup studies on pubmed. I find this puzzling...maybe
> I missed seeing some. Anyone know of any more recent
> research on this.
>
> ===================================================
> Inflamm Res 1996 Jul;45(7):330-4 Related Articles, Links
>
>
> The effect of niacinamide on osteoarthritis: a pilot study.
>
> Jonas WB, Rapoza CP, Blair WF.
>
> Office of Alternative Medicine, National Institute of
> Health, Bethesda, MD 20892, USA.
>
> OBJECTIVE: To evaluate the effect of niacinamide, on
> selected parameters of osteoarthritis using a double-blind,
> placebo controlled study design. METHODS: Seventy two
> patients with osteoarthritis were randomized for treatment
> with niacinamide or an identical placebo for 12 weeks.
> Outcome measures included global arthritis impact and pain,
> joint range of motion and flexibility, erythrocyte
> sedimentation rate, complete blood count, liver function
> tests, cholesterol, uric acid, and fasting blood sugar.
> Compliance was monitored with a pill record sheet and
> interview. RESULTS: Global arthritis impact improved by 29%
> (95% confidence interval [CI] 6, 46) in subjects on
> niacinamide and worsened by 10% in placebo subjects (p =
> 0.04). Pain levels did not change but those on niacinamide
> reduced their anti-inflammatory medications by 13% (95% CI
> 9, 94; p = 0.01). Niacinamide reduced erythrocyte
> sedimentation rate by 22% (95% CI 6, 51; p < 0.005) and
> increased joint mobility by 4.5 degrees over controls (8
> degrees vs
> 3.5 degrees; p = 0.04). Side effects were mild but higher in
> the niacinamide group (40% vs 27%, p = 0.003). CONCLUSION:
> This study indicates that niacinamide may have a role in
> the treatment of osteoarthritis. Niacinamide improved the
> global impact of osteoarthritis, improved joint
> flexibility, reduced inflammation, and allowed for
> reduction in standard anti-inflammatory medications when
> compared to placebo. More extensive evaluation of
> niacinamide in arthritis is warranted.

[Julius Sid]

Julius: I've used niacin for a recurrently painful knee. It
worked. I took it for about 5 years. 1200 to 1600 milligram
of timed release niacin. It's said to be twice as toxic but
it is also twice as effective compared to "regular" niacin.
It will turn you flush red at times. How safe was it?.. I
don't know. The niacin didn't kill me but the NSAIDs I used
prior came close:(

I'd read both Kaufman and Hoffer.

>
"Chris Jain" <cjain@ix.netcom.com> wrote in message
news:771ea75.0303041810.1b30303e@posting.google.com...
> Also found this. Anyone been trying this?
>
> Med Hypotheses 1999 Oct;53(4):350-60 Related Articles, Links
>
>
> Niacinamide therapy for osteoarthritis--does it inhibit
> nitric oxide synthase induction by interleukin 1 in
> chondrocytes?
>
> McCarty MF, Russell AL.
>
> Nutrition 21/AMBI, San Diego, CA 92037, USA.
>
> Fifty years ago, Kaufman reported that high-dose niacinamide
> was beneficial in osteoarthritis (OA) and rheumatoid
> arthritis. A recent double-blind study confirms the efficacy
> of niacinamide in OA. It may be feasible to interpret this
> finding in the context of evidence that synovium-generated
> interleukin-1 (IL-1), by inducing nitric oxide (NO) synthase
> and thereby inhibiting chondrocyte synthesis of aggrecan and
> type II collagen, is crucial to the pathogenesis of OA.
> Niacinamide and other inhibitors of ADP-ribosylation have
> been shown to suppress cytokine-mediated induction of NO
> synthase in a number of types of cells; it is therefore
> reasonable to speculate that niacinamide will have a
> comparable effect in IL-1-exposed chondrocytes, blunting the
> anti-anabolic impact of IL-1. The chondroprotective
> antibiotic doxycycline may have a similar mechanism of
> action. Other nutrients reported to be useful in OA may
> likewise intervene in the activity or synthesis of IL-1.
> Supplemental glucosamine can be expected to stimulate
> synovial synthesis of hyaluronic acid; hyaluronic acid
> suppresses the anti-catabolic effect of IL-1 in chondrocyte
> cell cultures, and has documented therapeutic efficacy when
> injected intra-articularly. S-adenosylmethionine (SAM),
> another proven therapy for OA, upregulates the proteoglycan
> synthesis of chondrocytes, perhaps because it functions
> physiologically as a signal of sulfur availability. IL-1 is
> likely to decrease SAM levels in chondrocytes; supplemental
> SAM may compensate for this deficit. Adequate selenium
> nutrition may down-regulate cytokine signaling, and ample
> intakes of fish oil can be expected to decrease synovial
> IL-1 production; these nutrients should receive further
> evaluation in OA. These considerations suggest that
> non-toxic nutritional regimens, by intervening at multiple
> points in the signal transduction pathways that promote the
> synthesis and mediate the activity of IL-1, may provide a
> substantially superior alternative to NSAIDs (merely
> palliative and often dangerously toxic) in the treatment and
> perhaps prevention of OA.
>
> PMID: 10608273 [PubMed - indexed for MEDLINE]
>
>
>
> cjain@ix.netcom.com (Chris Jain) wrote in message
news:<771ea75.0302252136.4c3ac1b@posting.google.com>...
> > This pilot study (below), performed almost 7 years ago,
> > shows a lot of promise, but I couldn't find much in the
> > way of followup studies on pubmed. I find this
> > puzzling...maybe I missed seeing some. Anyone know of any
> > more recent research on this.
> >
> > ===================================================
> > Inflamm Res 1996 Jul;45(7):330-4 Related Articles, Links
> >
> >
> > The effect of niacinamide on osteoarthritis: a pilot
> > study.
> >
> > Jonas WB, Rapoza CP, Blair WF.
> >
> > Office of Alternative Medicine, National Institute of
> > Health, Bethesda, MD 20892, USA.
> >
> > OBJECTIVE: To evaluate the effect of niacinamide, on
> > selected parameters of osteoarthritis using a
> > double-blind, placebo controlled study design. METHODS:
> > Seventy two patients with osteoarthritis were randomized
> > for treatment with niacinamide or an identical placebo for
> > 12 weeks. Outcome measures included global arthritis
> > impact and pain, joint range of motion and flexibility,
> > erythrocyte sedimentation rate, complete blood count,
> > liver function tests, cholesterol, uric acid, and fasting
> > blood sugar. Compliance was monitored with a pill record
> > sheet and interview. RESULTS: Global arthritis impact
> > improved by 29% (95% confidence interval [CI] 6, 46) in
> > subjects on niacinamide and worsened by 10% in placebo
> > subjects (p = 0.04). Pain levels did not change but those
> > on niacinamide reduced their anti-inflammatory medications
> > by 13% (95% CI 9, 94; p = 0.01). Niacinamide reduced
> > erythrocyte sedimentation rate by 22% (95% CI 6, 51; p <
> > 0.005) and increased joint mobility by 4.5 degrees over
> > controls (8 degrees vs
> > 3.5 degrees; p = 0.04). Side effects were mild but higher
> > in the niacinamide group (40% vs 27%, p = 0.003).
> > CONCLUSION: This study indicates that niacinamide may
> > have a role in the treatment of osteoarthritis.
> > Niacinamide improved the global impact of
> > osteoarthritis, improved joint flexibility, reduced
> > inflammation, and allowed for reduction in standard
> > anti-inflammatory medications when compared to placebo.
> > More extensive evaluation of niacinamide in arthritis is
> > warranted.

[Steve Harr]

"Julius Siden" <nospambaby@nukeit.net> wrote in message
news:3e65ba6f_1@corp-news.newsgroups.com...
> Julius: I've used niacin for a recurrently painful knee. It
> worked. I took it for about 5 years. 1200 to 1600 milligram
> of timed release niacin. It's said to be twice as toxic but
> it is also
twice as
> effective compared to "regular" niacin. It will turn
> you flush red at times. How safe was it?.. I don't
> know. The niacin didn't kill me but the NSAIDs I used
> prior came close:(
>
> I'd read both Kaufman and Hoffer.

COMMENT:

Toxicity of niacin is about the same as niacinamide. Only
niacin causes the skin flushing, but I can't imagine why you'd
want to take it for arthritis. It's niacinamide which inhibits
PARP and is by the far the most anti-inflammatory. Slow
release niacin, by contrast, is expressely made to lower your
cholesterol levels. It wouldn't be worth putting up with,
otherwise.

>
> >
> "Chris Jain" <cjain@ix.netcom.com> wrote in message
> news:771ea75.0303041810.1b30303e@posting.google.com...
> > Also found this. Anyone been trying this?
> >
> > Med Hypotheses 1999 Oct;53(4):350-60 Related Articles,
Links
> >
> >
> > Niacinamide therapy for osteoarthritis--does it inhibit
nitric oxide
> > synthase induction by interleukin 1 in chondrocytes?
> >
> > McCarty MF, Russell AL.
> >
> > Nutrition 21/AMBI, San Diego, CA 92037, USA.
> >
> > Fifty years ago, Kaufman reported that high-dose
niacinamide was
> > beneficial in osteoarthritis (OA) and rheumatoid
arthritis. A recent
> > double-blind study confirms the efficacy of niacinamide
in OA. It may
> > be feasible to interpret this finding in the context of
evidence that
> > synovium-generated interleukin-1 (IL-1), by inducing
nitric oxide (NO)
> > synthase and thereby inhibiting chondrocyte synthesis of
aggrecan and
> > type II collagen, is crucial to the pathogenesis of OA.
Niacinamide
> > and other inhibitors of ADP-ribosylation have been shown
to suppress
> > cytokine-mediated induction of NO synthase in a number
of types of
> > cells; it is therefore reasonable to speculate that
niacinamide will
> > have a comparable effect in IL-1-exposed chondrocytes,
blunting the
> > anti-anabolic impact of IL-1. The chondroprotective
antibiotic
> > doxycycline may have a similar mechanism of action.
Other nutrients
> > reported to be useful in OA may likewise intervene in
the activity or
> > synthesis of IL-1. Supplemental glucosamine can be
expected to
> > stimulate synovial synthesis of hyaluronic acid;
hyaluronic acid
> > suppresses the anti-catabolic effect of IL-1 in
chondrocyte cell
> > cultures, and has documented therapeutic efficacy when
injected
> > intra-articularly. S-adenosylmethionine (SAM), another
proven therapy
> > for OA, upregulates the proteoglycan synthesis of
chondrocytes,
> > perhaps because it functions physiologically as a signal
of sulfur
> > availability. IL-1 is likely to decrease SAM levels in
chondrocytes;
> > supplemental SAM may compensate for this deficit.
Adequate selenium
> > nutrition may down-regulate cytokine signaling, and
ample intakes of
> > fish oil can be expected to decrease synovial IL-1
production; these
> > nutrients should receive further evaluation in OA. These
> > considerations suggest that non-toxic nutritional
regimens, by
> > intervening at multiple points in the signal
transduction pathways
> > that promote the synthesis and mediate the activity of
IL-1, may
> > provide a substantially superior alternative to NSAIDs
(merely
> > palliative and often dangerously toxic) in the treatment
and perhaps
> > prevention of OA.
> >
> > PMID: 10608273 [PubMed - indexed for MEDLINE]
> >
> >
> >
> > cjain@ix.netcom.com (Chris Jain) wrote in message
> news:<771ea75.0302252136.4c3ac1b@posting.google.com>...
> > > This pilot study (below), performed almost 7 years
ago, shows a lot of
> > > promise, but I couldn't find much in the way of
followup studies on
> > > pubmed. I find this puzzling...maybe I missed seeing
some. Anyone know
> > > of any more recent research on this.
> > >
> > > ===================================================
> > > Inflamm Res 1996 Jul;45(7):330-4 Related Articles,
Links
> > >
> > >
> > > The effect of niacinamide on osteoarthritis: a pilot
study.
> > >
> > > Jonas WB, Rapoza CP, Blair WF.
> > >
> > > Office of Alternative Medicine, National Institute of
Health,
> > > Bethesda, MD 20892, USA.
> > >
> > > OBJECTIVE: To evaluate the effect of niacinamide, on
selected
> > > parameters of osteoarthritis using a double-blind,
placebo controlled
> > > study design. METHODS: Seventy two patients with
osteoarthritis were
> > > randomized for treatment with niacinamide or an
identical placebo for
> > > 12 weeks. Outcome measures included global arthritis
impact and pain,
> > > joint range of motion and flexibility, erythrocyte
sedimentation rate,
> > > complete blood count, liver function tests,
cholesterol, uric acid,
> > > and fasting blood sugar. Compliance was monitored with
a pill record
> > > sheet and interview. RESULTS: Global arthritis impact
improved by 29%
> > > (95% confidence interval [CI] 6, 46) in subjects on
niacinamide and
> > > worsened by 10% in placebo subjects (p = 0.04). Pain
levels did not
> > > change but those on niacinamide reduced their
anti-inflammatory
> > > medications by 13% (95% CI 9, 94; p = 0.01).
Niacinamide reduced
> > > erythrocyte sedimentation rate by 22% (95% CI 6, 51; p
< .005) and
> > > increased joint mobility by 4.5 degrees over controls
(8 degrees vs
> > > 3.5 degrees; p = 0.04). Side effects were mild but
higher in the
> > > niacinamide group (40% vs 27%, p = 0.003). CONCLUSION:
This study
> > > indicates that niacinamide may have a role in the
treatment of
> > > osteoarthritis. Niacinamide improved the global impact
of
> > > osteoarthritis, improved joint flexibility, reduced
inflammation, and
> > > allowed for reduction in standard anti-inflammatory
medications when
> > > compared to placebo. More extensive evaluation of
niacinamide in
> > > arthritis is warranted.
>
>

--
Spammers are not welcome. I welcome email from all
non-advertisers who can fix my email address (it's open book).

[Julius Sid]

Julius returns with comment: It seems everyone agrees with
Steve that niacinamide is best/better. But I did what I did
and it sure seemed to have worked. Perhaps, it worked because
it was twenty years ago and I was in my 30s and their wasn't
an autoimmune component? Just damage and wear.

It also seemed to help completely suppress my seasonal pollen
allergies though the picture is blurred by the fact that I'd
taken pollen shots prior to that. Niacin seemed to have a drug
like effect on the allergies since when I forget to take it
the nasal passages would start tickle/itch like when one gets
a nose full of pollen..

After the 5 years the knee was good and allergies started to
return even with the niacin. So I quit.

Granted I take other vitamins and related material so perhaps
there were other players in this scene. I was left rather
perplexed. And rather flush red at times on the course of
those five years:)

"Steve Harris" <sbharris@ix.RETICULATEDOBJECTcom.com> wrote in
message news:b463c5$2nt$1@slb5.atl.mindspring.net...
> COMMENT:
>
> Toxicity of niacin is about the same as niacinamide. Only
> niacin causes the skin flushing, but I can't imagine why
> you'd want to take it for arthritis. It's niacinamide which
> inhibits PARP and is by the far the most anti-inflammatory.
> Slow release niacin, by contrast, is expressely made to
> lower your cholesterol levels. It wouldn't be worth putting
> up with, otherwise.
>
>
> "Julius Siden" <nospambaby@nukeit.net> wrote in message
> news:3e65ba6f_1@corp-news.newsgroups.com...
> > Julius: I've used niacin for a recurrently painful knee.
> > It worked. I took it for about 5 years. 1200 to 1600
> > milligram of timed release niacin. It's said to be twice
> > as toxic but it is also
> twice as
> > effective compared to "regular" niacin. It will turn you
> > flush red at times. How safe was it?.. I don't know. The
> > niacin didn't kill me but the NSAIDs I used prior came
> > close:(
> >
> > I'd read both Kaufman and Hoffer.
>

> >
> > >
> > "Chris Jain" <cjain@ix.netcom.com> wrote in message
> > news:771ea75.0303041810.1b30303e@posting.google.com...
> > > Also found this. Anyone been trying this?
> > >
> > > Med Hypotheses 1999 Oct;53(4):350-60 Related Articles,
> Links
> > >
> > >
> > > Niacinamide therapy for osteoarthritis--does it inhibit
> nitric oxide
> > > synthase induction by interleukin 1 in chondrocytes?
> > >
> > > McCarty MF, Russell AL.
> > >
> > > Nutrition 21/AMBI, San Diego, CA 92037, USA.
> > >
> > > Fifty years ago, Kaufman reported that high-dose
> niacinamide was
> > > beneficial in osteoarthritis (OA) and rheumatoid
> arthritis. A recent
> > > double-blind study confirms the efficacy of niacinamide
> in OA. It may
> > > be feasible to interpret this finding in the context of
> evidence that
> > > synovium-generated interleukin-1 (IL-1), by inducing
> nitric oxide (NO)
> > > synthase and thereby inhibiting chondrocyte synthesis of
> aggrecan and
> > > type II collagen, is crucial to the pathogenesis of OA.
> Niacinamide
> > > and other inhibitors of ADP-ribosylation have been shown
> to suppress
> > > cytokine-mediated induction of NO synthase in a number
> of types of
> > > cells; it is therefore reasonable to speculate that
> niacinamide will
> > > have a comparable effect in IL-1-exposed chondrocytes,
> blunting the
> > > anti-anabolic impact of IL-1. The chondroprotective
> antibiotic
> > > doxycycline may have a similar mechanism of action.
> Other nutrients
> > > reported to be useful in OA may likewise intervene in
> the activity or
> > > synthesis of IL-1. Supplemental glucosamine can be
> expected to
> > > stimulate synovial synthesis of hyaluronic acid;
> hyaluronic acid
> > > suppresses the anti-catabolic effect of IL-1 in
> chondrocyte cell
> > > cultures, and has documented therapeutic efficacy when
> injected
> > > intra-articularly. S-adenosylmethionine (SAM), another
> proven therapy
> > > for OA, upregulates the proteoglycan synthesis of
> chondrocytes,
> > > perhaps because it functions physiologically as a signal
> of sulfur
> > > availability. IL-1 is likely to decrease SAM levels in
> chondrocytes;
> > > supplemental SAM may compensate for this deficit.
> Adequate selenium
> > > nutrition may down-regulate cytokine signaling, and
> ample intakes of
> > > fish oil can be expected to decrease synovial IL-1
> production; these
> > > nutrients should receive further evaluation in OA. These
> > > considerations suggest that non-toxic nutritional
> regimens, by
> > > intervening at multiple points in the signal
> transduction pathways
> > > that promote the synthesis and mediate the activity of
> IL-1, may
> > > provide a substantially superior alternative to NSAIDs
> (merely
> > > palliative and often dangerously toxic) in the treatment
> and perhaps
> > > prevention of OA.
> > >
> > > PMID: 10608273 [PubMed - indexed for MEDLINE]
> > >
> > >
> > >
> > > cjain@ix.netcom.com (Chris Jain) wrote in message
> > news:<771ea75.0302252136.4c3ac1b@posting.google.com>...
> > > > This pilot study (below), performed almost 7 years
> ago, shows a lot of
> > > > promise, but I couldn't find much in the way of
> followup studies on
> > > > pubmed. I find this puzzling...maybe I missed seeing
> some. Anyone know
> > > > of any more recent research on this.
> > > >
> > > > ===================================================
> > > > Inflamm Res 1996 Jul;45(7):330-4 Related Articles,
> Links
> > > >
> > > >
> > > > The effect of niacinamide on osteoarthritis: a pilot
> study.
> > > >
> > > > Jonas WB, Rapoza CP, Blair WF.
> > > >
> > > > Office of Alternative Medicine, National Institute of
> Health,
> > > > Bethesda, MD 20892, USA.
> > > >
> > > > OBJECTIVE: To evaluate the effect of niacinamide, on
> selected
> > > > parameters of osteoarthritis using a double-blind,
> placebo controlled
> > > > study design. METHODS: Seventy two patients with
> osteoarthritis were
> > > > randomized for treatment with niacinamide or an
> identical placebo for
> > > > 12 weeks. Outcome measures included global arthritis
> impact and pain,
> > > > joint range of motion and flexibility, erythrocyte
> sedimentation rate,
> > > > complete blood count, liver function tests,
> cholesterol, uric acid,
> > > > and fasting blood sugar. Compliance was monitored with
> a pill record
> > > > sheet and interview. RESULTS: Global arthritis impact
> improved by 29%
> > > > (95% confidence interval [CI] 6, 46) in subjects on
> niacinamide and
> > > > worsened by 10% in placebo subjects (p = 0.04). Pain
> levels did not
> > > > change but those on niacinamide reduced their
> anti-inflammatory
> > > > medications by 13% (95% CI 9, 94; p = 0.01).
> Niacinamide reduced
> > > > erythrocyte sedimentation rate by 22% (95% CI 6, 51; p
> < .005) and
> > > > increased joint mobility by 4.5 degrees over controls
> (8 degrees vs
> > > > 3.5 degrees; p = 0.04). Side effects were mild but
> higher in the
> > > > niacinamide group (40% vs 27%, p = 0.003). CONCLUSION:
> This study
> > > > indicates that niacinamide may have a role in the
> treatment of
> > > > osteoarthritis. Niacinamide improved the global impact
> of
> > > > osteoarthritis, improved joint flexibility, reduced
> inflammation, and
> > > > allowed for reduction in standard anti-inflammatory
> medications when
> > > > compared to placebo. More extensive evaluation of
> niacinamide in
> > > > arthritis is warranted.
> >
> >
>
> --
> Spammers are not welcome. I welcome email from all
> non-advertisers who can fix my email address (it's
> open book).

[Chris Jain]

Would niacinamide be expected to have some of the same
beneficial effects as niacin in raising HDL and in lowering
LDL and lipoprotein(a)?

[Moosh:)]

On Wed, 5 Mar 2003 14:21:55 -0800, "Julius Siden"
<nospambaby@nukeit.net> wrote:

>Julius returns with comment: It seems everyone agrees with
>Steve that niacinamide is best/better. But I did what I did
>and it sure seemed to have worked. Perhaps, it worked because
>it was twenty years ago and I was in my 30s and their wasn't
>an autoimmune component? Just damage and wear.
>
>It also seemed to help completely suppress my seasonal pollen
>allergies though the picture is blurred by the fact that I'd
>taken pollen shots prior to that. Niacin seemed to have a
>drug like effect on the allergies since when I forget to take
>it the nasal passages would start tickle/itch like when one
>gets a nose full of pollen..
>
>After the 5 years the knee was good and allergies started to
>return even with the niacin. So I quit.
>
>Granted I take other vitamins and related material so perhaps
>there were other players in this scene. I was left rather
>perplexed. And rather flush red at times on the course of
>those five years:)

I often wonder why folks think that a required molecule that
we DON'T produce will work in gross excess therapeutically for
illnesses any more than gross excess of any other molecule
that we DO produce (in reasonable quantity).

Moosh:)

[Moosh:)]

On 6 Mar 2003 18:26:29 -0800, cjain@ix.netcom.com (Chris
Jain) wrote:

>Would niacinamide be expected to have some of the same
>beneficial effects as niacin in raising HDL and in lowering
>LDL and lipoprotein(a)?

Does it? Aren't there better things for this if you have an
uncommon dyslipidaemia?

If you are overweight, the best medicine is to lose some and
do some gentle exercise.

This of course assumes you have all your nutrient requirements
met with a varied, wholefood diet.

Moosh:)

[Julius Sid]

You wonder. No specifics here. Because it worked and
conventional options were becoming patently deadly. NSAIDs
tend to cause GI bleeds. You wonder. But do you think? No.
Imagine a person already eating your varied whole food diet
and at BMI of 22. The doctor is offering to go fishing in the
knee and procedure for which you have considerable doubts. The
doubts have been borne out by research in more recent years.
Perhaps I should have chosen niacinamide rather than niacin.
But the niacin shut my allergies down far more effectively
than antihistamines though I grant there were other things
working to reduce there intensity.

Just because some idea isn't blessed by some high priest of
"science" doesn't prove it isn't fact.

> I often wonder why folks think that a required molecule that
> we DON'T produce will work in gross excess therapeutically
> for illnesses any more than gross excess of any other
> molecule that we DO produce (in reasonable quantity).
> Moosh:~I

Drug effect perhaps. Quite effective. Which is why in part I
learned contempt for those "do nothing" and "I know better
than you" type folks such as ........ Drugs are often derived
from some biological system or another. A chemical native to
body has a chance of being less toxic than something more
foreign and in the orthodox pharmacy.

Yet, you wonder.

[Chris Jain]

"Moosh:)" <ZZ@ZZ.ZZ> wrote in message

> I often wonder why folks think that a required molecule that
> we DON'T produce will work in gross excess therapeutically
> for illnesses any more than gross excess of any other
> molecule that we DO produce (in reasonable quantity).

In the case of niacinamide, a double-blind, placebo controlled
clinical trial... :-)

[Chris Jain]

"Moosh:)" <ZZ@ZZ.ZZ> wrote in message
news:<mh0o6v0325ftkecmtquosg2otn94rp6pdo@4ax.com>...
> On 6 Mar 2003 18:26:29 -0800, cjain@ix.netcom.com (Chris
> Jain) wrote:
>
> >Would niacinamide be expected to have some of the same
> >beneficial effects as niacin in raising HDL and in lowering
> >LDL and lipoprotein(a)?
>
> Does it? Aren't there better things for this if you have an
> uncommon dyslipidaemia?

The medications and "lifestyle changes" commonly prescribed
for dyslipidaemia do not appear to affect lipoprotein(a).
High-does niacin is one of the few drugs (at these doses, it
is a drug) known to reduce lipoprotein(a). Of course, most
people don't need to worry about lipoprotein(a).

> If you are overweight, the best medicine is to lose some and
> do some gentle exercise.

True.

> This of course assumes you have all your nutrient
> requirements met with a varied, wholefood diet.
>
>
> Moosh:)

[Julius Sid]

Julius returns with comment: It seems everyone agrees with
Steve that niacinamide is best/better. But I did what I did
and it sure seemed to have worked. Perhaps, it worked because
it was twenty years ago and I was in my 30s and their wasn't
an autoimmune component? Just damage and wear.

It also seemed to help completely suppress my seasonal pollen
allergies though the picture is blurred by the fact that I'd
taken pollen shots prior to that. Niacin seemed to have a drug
like effect on the allergies since when I forget to take it
the nasal passages would start tickle/itch like when one gets
a nose full of pollen..

After the 5 years the knee was good and allergies started to
return even with the niacin. So I quit.

Granted I take other vitamins and related material so perhaps
there were other players in this scene. I was left rather
perplexed. And rather flush red at times on the course of
those five years:)

"Steve Harris" <sbharris@ix.RETICULATEDOBJECTcom.com> wrote in
message news:b463c5$2nt$1@slb5.atl.mindspring.net...
> COMMENT:
>
> Toxicity of niacin is about the same as niacinamide. Only
> niacin causes the skin flushing, but I can't imagine why
> you'd want to take it for arthritis. It's niacinamide which
> inhibits PARP and is by the far the most anti-inflammatory.
> Slow release niacin, by contrast, is expressely made to
> lower your cholesterol levels. It wouldn't be worth putting
> up with, otherwise.
>
>
> "Julius Siden" <nospambaby@nukeit.net> wrote in message
> news:3e65ba6f_1@corp-news.newsgroups.com...
> > Julius: I've used niacin for a recurrently painful knee.
> > It worked. I took it for about 5 years. 1200 to 1600
> > milligram of timed release niacin. It's said to be twice
> > as toxic but it is also
> twice as
> > effective compared to "regular" niacin. It will turn you
> > flush red at times. How safe was it?.. I don't know. The
> > niacin didn't kill me but the NSAIDs I used prior came
> > close:(
> >
> > I'd read both Kaufman and Hoffer.
>

> >
> > >
> > "Chris Jain" <cjain@ix.netcom.com> wrote in message
> > news:771ea75.0303041810.1b30303e@posting.google.com...
> > > Also found this. Anyone been trying this?
> > >
> > > Med Hypotheses 1999 Oct;53(4):350-60 Related Articles,
> Links
> > >
> > >
> > > Niacinamide therapy for osteoarthritis--does it inhibit
> nitric oxide
> > > synthase induction by interleukin 1 in chondrocytes?
> > >
> > > McCarty MF, Russell AL.
> > >
> > > Nutrition 21/AMBI, San Diego, CA 92037, USA.
> > >
> > > Fifty years ago, Kaufman reported that high-dose
> niacinamide was
> > > beneficial in osteoarthritis (OA) and rheumatoid
> arthritis. A recent
> > > double-blind study confirms the efficacy of niacinamide
> in OA. It may
> > > be feasible to interpret this finding in the context of
> evidence that
> > > synovium-generated interleukin-1 (IL-1), by inducing
> nitric oxide (NO)
> > > synthase and thereby inhibiting chondrocyte synthesis of
> aggrecan and
> > > type II collagen, is crucial to the pathogenesis of OA.
> Niacinamide
> > > and other inhibitors of ADP-ribosylation have been shown
> to suppress
> > > cytokine-mediated induction of NO synthase in a number
> of types of
> > > cells; it is therefore reasonable to speculate that
> niacinamide will
> > > have a comparable effect in IL-1-exposed chondrocytes,
> blunting the
> > > anti-anabolic impact of IL-1. The chondroprotective
> antibiotic
> > > doxycycline may have a similar mechanism of action.
> Other nutrients
> > > reported to be useful in OA may likewise intervene in
> the activity or
> > > synthesis of IL-1. Supplemental glucosamine can be
> expected to
> > > stimulate synovial synthesis of hyaluronic acid;
> hyaluronic acid
> > > suppresses the anti-catabolic effect of IL-1 in
> chondrocyte cell
> > > cultures, and has documented therapeutic efficacy when
> injected
> > > intra-articularly. S-adenosylmethionine (SAM), another
> proven therapy
> > > for OA, upregulates the proteoglycan synthesis of
> chondrocytes,
> > > perhaps because it functions physiologically as a signal
> of sulfur
> > > availability. IL-1 is likely to decrease SAM levels in
> chondrocytes;
> > > supplemental SAM may compensate for this deficit.
> Adequate selenium
> > > nutrition may down-regulate cytokine signaling, and
> ample intakes of
> > > fish oil can be expected to decrease synovial IL-1
> production; these
> > > nutrients should receive further evaluation in OA. These
> > > considerations suggest that non-toxic nutritional
> regimens, by
> > > intervening at multiple points in the signal
> transduction pathways
> > > that promote the synthesis and mediate the activity of
> IL-1, may
> > > provide a substantially superior alternative to NSAIDs
> (merely
> > > palliative and often dangerously toxic) in the treatment
> and perhaps
> > > prevention of OA.
> > >
> > > PMID: 10608273 [PubMed - indexed for MEDLINE]
> > >
> > >
> > >
> > > cjain@ix.netcom.com (Chris Jain) wrote in message
> > news:<771ea75.0302252136.4c3ac1b@posting.google.com>...
> > > > This pilot study (below), performed almost 7 years
> ago, shows a lot of
> > > > promise, but I couldn't find much in the way of
> followup studies on
> > > > pubmed. I find this puzzling...maybe I missed seeing
> some. Anyone know
> > > > of any more recent research on this.
> > > >
> > > > ===================================================
> > > > Inflamm Res 1996 Jul;45(7):330-4 Related Articles,
> Links
> > > >
> > > >
> > > > The effect of niacinamide on osteoarthritis: a pilot
> study.
> > > >
> > > > Jonas WB, Rapoza CP, Blair WF.
> > > >
> > > > Office of Alternative Medicine, National Institute of
> Health,
> > > > Bethesda, MD 20892, USA.
> > > >
> > > > OBJECTIVE: To evaluate the effect of niacinamide, on
> selected
> > > > parameters of osteoarthritis using a double-blind,
> placebo controlled
> > > > study design. METHODS: Seventy two patients with
> osteoarthritis were
> > > > randomized for treatment with niacinamide or an
> identical placebo for
> > > > 12 weeks. Outcome measures included global arthritis
> impact and pain,
> > > > joint range of motion and flexibility, erythrocyte
> sedimentation rate,
> > > > complete blood count, liver function tests,
> cholesterol, uric acid,
> > > > and fasting blood sugar. Compliance was monitored with
> a pill record
> > > > sheet and interview. RESULTS: Global arthritis impact
> improved by 29%
> > > > (95% confidence interval [CI] 6, 46) in subjects on
> niacinamide and
> > > > worsened by 10% in placebo subjects (p = 0.04). Pain
> levels did not
> > > > change but those on niacinamide reduced their
> anti-inflammatory
> > > > medications by 13% (95% CI 9, 94; p = 0.01).
> Niacinamide reduced
> > > > erythrocyte sedimentation rate by 22% (95% CI 6, 51; p
> < .005) and
> > > > increased joint mobility by 4.5 degrees over controls
> (8 degrees vs
> > > > 3.5 degrees; p = 0.04). Side effects were mild but
> higher in the
> > > > niacinamide group (40% vs 27%, p = 0.003). CONCLUSION:
> This study
> > > > indicates that niacinamide may have a role in the
> treatment of
> > > > osteoarthritis. Niacinamide improved the global impact
> of
> > > > osteoarthritis, improved joint flexibility, reduced
> inflammation, and
> > > > allowed for reduction in standard anti-inflammatory
> medications when
> > > > compared to placebo. More extensive evaluation of
> niacinamide in
> > > > arthritis is warranted.
> >
> >
>
> --
> Spammers are not welcome. I welcome email from all
> non-advertisers who can fix my email address (it's
> open book).

[Michaelpri]

"Julius Siden" <nospambaby@nukeit.net> wrote

> Julius returns with comment: It seems everyone agrees with
> Steve that niacinamide is best/better.

Not everyone. As you have found, niacin (nicotinic acid) is
superior for many things.

Niacinamide inhibits the DNA repair activity of PARP.
Nicotinic acid enhances the DNA repair activity of PARP.

Take as inositol hexanicotinate if the flush bothers you.

From : http://mcp.longevity-report.com

"Vitamin B3 (as nicotinamide) may be toxic in the range
3-6gm/d[85]. Niacin, as nicotinic acid, is generally
considered less toxic[40], but, still, in some individuals
large doses of niacin have caused abnormal liver behaviour.
Also niacin can cause an uncomfortable, although, as far as
we know, harmless and temporary skin flushing. Taken as
inositol hexanicotinate, which is generally regarded as
non-toxic, unlike some other slow-release formulations[73],
removes this problem."

&

"PARP requires nicotinamide adenine dinucleotide (NAD) as a
substrate, and is very sensitive to NAD concentrations, as
shown by an experiment in which rodents exhibit increased
resistance to UV-induced cancer when fed a diet rich in
vitamin B3 (niacin), which elevated cellular NAD levels by a
factor of 3 or so[27c]. Vitamin B3 (niacin) is a precursor to
the coenzymes NAD and NAD-phosphate (NADP). Although not
strictly a vitamin - our bodies can produce NAD/NADP from
dietary tryptophan - it functions like one since this
production is not very efficient. Dietary consumption of
niacin elevates NAD tissue concentration, in animals and
humans[27d, 27e], which up-regulates the activity of PARP,
increasing the DNA repair efficiency and reducing the
induced[27c, 27f] cancer rate and lowering over-all long-term
human mortality[27g]. High PARP activity is associated with
longevity in humans[126d]. Similar cancer prevention, and
possibly longevity, is expected in humans, who are typically
more NAD deficient than many animals[27d]."

[27a] Requirement of NAD and SIR2 for life-span extension by
calorie restriction in Saccharomyces cerevisiae. Lin SJ,
Defossez PA, Guarente L in Science 2000 Sep
22;289(5487):2126-2128 PMID: 11000115

[27b] Manipulation of a Nuclear NAD+ Salvage Pathway Delays
Aging without Altering Steady-state NAD+ Levels.
Anderson RM, Bitterman KJ, Wood JG, Medvedik O, Cohen H,
Lin SS, Manchester JK, Gordon JI, Sinclair DA in J Biol
Chem 2002 May 24;277(21):18881-90. PMID: 11884393

[27c] Oral Niacin Prevents Photocarcinogenesis and
Photoimmunosuppression in
mice. Gensler HL, Williams T, Huang AC, Jacobson EL in
Nutrition and Cancer
34(1) (1999), pg 36-41. PMID: 10453439 The relationship
between dietary intake of niacin and tissue NAD
elevation is detailed in the main body of the
article. The UV-irradiated mice on a diet with
0.003%, 0.1%, 0.5% & 1.0% niacin had a 0.72, 0.60,
0.48 & 0.40 tumours/mouse, respectively.

[27d] Mapping the role of NAD metabolism in prevention and
treatment of carcinogenesis. Jacobson EL, Shieh WM,
Huang AC in Mol Cell Biochem 1999 Mar;193(1-2):69-74
PMID: 10331640 NAD is elevated by niacin in many
human tissues.

[27e] Evaluating the role of niacin in human carcinogenesis.
Jacobson EL, Dame AJ, Pyrek JS, Jacobson MK. Biochimie
1995;77(5):394-8 PMID: 8527495

[27f] Protective effect of nicotinamide on bracken fern
induced carcinogenicity in rats. Pamukcu AM, Milli
U, Bryan GT in Nutr Cancer 1981;3(2):86-93 PMID:
6213941 .5% nicotinamide in diet cut the induced
cancer rate by 40%

[27g] Fifteen year mortality in Coronary Drug Project
patients: long-term benefit with niacin. Canner PL,
Berge KG, Wenger NK, Stamler J, Friedman L, Prineas RJ,
Friedewald W in J Am Coll Cardiol 1986 Dec;8(6):1245-55
PMID: 3782631 "Mortality in the niacin group was 11%
lower than in the placebo group (52.0 versus 58.2%; p =
0.0004). "

[27h] Pharmacological intakes of niacin increase bone
marrow poly(ADP-ribose) and the latency of
ethylnitrosourea-induced carcinogenesis in rats.
Boyonoski AC, Spronck JC, Jacobs RM, Shah GM, Poirier
GG, Kirkland JB in J Nutr 2002 Jan;132(1):115-20
PMID: 11773517

Cancer chemotherapy agents cause short-term leukopenia during
treatment and the development of secondary leukemias after
recovery from the original disease. We reported that niacin
deficiency in rats increases the severity of
nitrosourea-induced leukopenia and the subsequent development
of cancers. This study was designed to test the effects of
supplementing an already high quality diet with pharmacologic
levels of niacin. For a period of 4 wk, nontumor-bearing
weanling Long-Evans rats were pair-fed AIN-93M diets that were
niacin adequate (30 mg/kg diet) or pharmacologically
supplemented (4
g/kg diet) with nicotinic acid (NA) or nicotinamide (Nam). One
week after the initiation of niacin feeding protocols,
ethylnitrosourea (ENU) treatment began (12 doses, 30 mg/kg
by gavage, every other day). ENU treatment caused
leukopenia, which was not prevented by niacin
supplementation. At the end of ENU treatment, all rats were
switched to a niacin-adequate diet and monitored. Within 36
wk after the start of treatment, all of the ENU-treated rats
either lost 5% of peak body weight or had palpable tumors >
1 cm in diameter, and were necropsied. Supplementation with
NA or Nam at 4.0 g/kg diet (combined analysis) increased the
latency of the ENU-induced morbidity curve, relative to
niacin-adequate controls. Morbidity could be attributed in
almost all cases to some form of neoplasm, with leukemias
the predominant form. In short-term studies, supplementation
with either NA or Nam caused dramatic increases in bone
marrow NAD(+) (1- to 1.5-fold), basal poly(ADP-ribose) (3-
to 5-fold) and ENU-induced poly(ADP-ribose) levels
(1.5-fold). These data show that supplementation of a
niacin-adequate, high quality diet with pharmacologic
levels of nicotinic acid or nicotinamide increases NAD(+)
and poly(ADP-ribose) levels in bone marrow and may be
protective against DNA damage.

[2] The Vitamins: Fundamental Aspects in Nutrition and Health
2nd Edition. Gerald F Combs, Jr (1998) ISBN 0121834921

[3] Encyclopedia of Nutritional Supplements. Michael T Murray,
(1996) ISBN 0761504109 An invaluable resource; should be
read by everybody prior to supplementing.

[4] Safety of high-dose nicotinamide: a review. Knip M, Douek
IF, Moore WP, Gillmor HA, McLean AE, Bingley PJ, Gale EA
in Diabetologia 2000 Nov;43(11):1337-45 PMID: 11126400
Discusses the potential of 3g/d vitamin B3 in preventing
the onset of Type I (insulin-dependent) diabetes.

[4a] Increased poly(ADP-ribose) polymerase activity in
lymphoblastoid cell lines from centenarians. Muiras ML,
Muller M, Schachter F, Burkle A in J Mol Med 1998
Apr;76(5):346-54. PMID: 9587069 "Poly(ADP-ribosyl)ation
is a posttranslational modification of nuclear proteins
which is catalyzed by poly(ADP-ribose) polymerase and
represents an immediate response of eukaryotic cells to
oxidative and other types of DNA damage. [.] Viewed
together with previous results on poly(ADP-ribose)
polymerase activity in various mammalian species, the
present data provide further evidence for the notion
that longevity is associated with a high
poly(ADP-ribosyl)ation capacity."

Cheers, Michael C Price
----------------------------------------
http://mcp.longevity-report.com
http://www.hedweb.com/manworld.htm

[Michaelpri]

Correction: Where I said:
>
> Niacinamide inhibits the DNA repair activity of PARP.
> Nicotinic acid enhances the DNA repair activity of PARP.

I meant

Niacinamide inhibits the SIR2 activity. Nicotinic acid
enhances SIR2 activity. See PMID: 12297502

NAD is a substrate of PARP, involved in DNA repair, and is
upregulated by dietary nicotinic acid..

Everything else was okay.

Cheers, Michael C Price
----------------------------------------
http://mcp.longevity-report.com
http://www.hedweb.com/manworld.htm

"michaelprice" <michaelprice@ntlworld.com> wrote in message
news:RkYba.230$bD6.27333@newsfep1-win.server.ntli.net...
> "Julius Siden" <nospambaby@nukeit.net> wrote
>
> > Julius returns with comment: It seems everyone agrees with
> > Steve that niacinamide is best/better.
>
> Not everyone. As you have found, niacin (nicotinic acid) is
> superior for many things.
>
> Niacinamide inhibits the DNA repair activity of PARP.
> Nicotinic acid enhances the DNA repair activity of PARP.
>
> Take as inositol hexanicotinate if the flush bothers you.
>
> From : http://mcp.longevity-report.com
>
> "Vitamin B3 (as nicotinamide) may be toxic in the range
> 3-6gm/d[85]. Niacin, as nicotinic acid, is generally
> considered less toxic[40], but, still, in some individuals
> large doses of niacin have caused abnormal
liver
> behaviour. Also niacin can cause an uncomfortable, although,
> as far as we know, harmless and temporary skin flushing.
> Taken as inositol hexanicotinate, which is generally
> regarded as non-toxic, unlike some
other
> slow-release formulations[73], removes this problem."
>
> &
>
> "PARP requires nicotinamide adenine dinucleotide (NAD) as a
> substrate, and is very sensitive to NAD concentrations, as
> shown by an experiment in
which
> rodents exhibit increased resistance to UV-induced cancer
> when fed a diet rich in vitamin B3 (niacin), which elevated
> cellular NAD levels by a
factor
> of 3 or so[27c]. Vitamin B3 (niacin) is a precursor to the
> coenzymes NAD and NAD-phosphate (NADP). Although not
> strictly a vitamin - our bodies
can
> produce NAD/NADP from dietary tryptophan - it functions like
> one since
this
> production is not very efficient. Dietary consumption of
> niacin elevates NAD tissue concentration, in animals and
> humans[27d, 27e], which up-regulates the activity of PARP,
> increasing the DNA repair efficiency
and
> reducing the induced[27c, 27f] cancer rate and lowering
> over-all long-term human mortality[27g]. High PARP activity
> is associated with longevity in humans[126d]. Similar cancer
> prevention, and possibly longevity, is expected in humans,
> who are typically more NAD deficient than many
> animals[27d]."
>
> [27a] Requirement of NAD and SIR2 for life-span extension
> by calorie restriction in Saccharomyces cerevisiae.
> Lin SJ, Defossez PA, Guarente L
in
> Science 2000 Sep 22;289(5487):2126-2128 PMID: 11000115
>
> [27b] Manipulation of a Nuclear NAD+ Salvage Pathway Delays
> Aging without Altering Steady-state NAD+ Levels.
> Anderson RM, Bitterman KJ, Wood JG, Medvedik O, Cohen
> H, Lin SS, Manchester JK, Gordon JI, Sinclair DA in J
Biol
> Chem 2002 May 24;277(21):18881-90. PMID: 11884393
>
> [27c] Oral Niacin Prevents Photocarcinogenesis and
> Photoimmunosuppression
in
> mice. Gensler HL, Williams T, Huang AC, Jacobson EL in
> Nutrition and
Cancer
> 34(1) (1999), pg 36-41. PMID: 10453439 The relationship
> between dietary intake of niacin and tissue NAD
> elevation is detailed in the main body of the
> article. The UV-irradiated mice on a diet with
> 0.003%, 0.1%, 0.5% & 1.0% niacin had a 0.72,
> 0.60, 0.48 & 0.40 tumours/mouse, respectively.
>
> [27d] Mapping the role of NAD metabolism in prevention and
> treatment of carcinogenesis. Jacobson EL, Shieh WM,
> Huang AC in Mol Cell Biochem 1999 Mar;193(1-2):69-74
> PMID: 10331640 NAD is elevated by niacin in many
> human tissues.
>
> [27e] Evaluating the role of niacin in human
> carcinogenesis. Jacobson EL, Dame AJ, Pyrek JS,
> Jacobson MK. Biochimie 1995;77(5):394-8 PMID:
8527495
>
> [27f] Protective effect of nicotinamide on bracken fern
> induced carcinogenicity in rats. Pamukcu AM, Milli U,
> Bryan GT in Nutr Cancer 1981;3(2):86-93 PMID: 6213941
> .5% nicotinamide in diet cut the induced cancer rate
> by 40%
>
> [27g] Fifteen year mortality in Coronary Drug Project
> patients: long-term benefit with niacin. Canner PL,
> Berge KG, Wenger NK, Stamler J, Friedman
L,
> Prineas RJ, Friedewald W in J Am Coll Cardiol 1986
> Dec;8(6):1245-55
PMID:
> 3782631 "Mortality in the niacin group was 11% lower than in
> the placebo group
(52.0
> versus 58.2%; p = 0.0004). "
>
> [27h] Pharmacological intakes of niacin increase bone
> marrow poly(ADP-ribose) and the latency of
> ethylnitrosourea-induced
carcinogenesis
> in rats. Boyonoski AC, Spronck JC, Jacobs RM, Shah GM,
> Poirier GG,
Kirkland
> JB in J Nutr 2002 Jan;132(1):115-20 PMID: 11773517
>
> Cancer chemotherapy agents cause short-term leukopenia
> during treatment
and
> the development of secondary leukemias after recovery from
> the original disease. We reported that niacin deficiency in
> rats increases the severity of nitrosourea-induced
> leukopenia and the subsequent development of
cancers.
> This study was designed to test the effects of supplementing
> an already
high
> quality diet with pharmacologic levels of niacin. For a
> period of 4 wk, nontumor-bearing weanling Long-Evans rats
> were pair-fed AIN-93M diets that were niacin adequate (30
> mg/kg diet) or pharmacologically supplemented (4
> g/kg diet) with nicotinic acid (NA) or nicotinamide (Nam).
> One week after the initiation of niacin feeding protocols,
> ethylnitrosourea (ENU)
treatment
> began (12 doses, 30 mg/kg by gavage, every other day). ENU
> treatment
caused
> leukopenia, which was not prevented by niacin
> supplementation. At the end
of
> ENU treatment, all rats were switched to a niacin-adequate
> diet and monitored. Within 36 wk after the start of
> treatment, all of the
ENU-treated
> rats either lost 5% of peak body weight or had palpable
> tumors > 1 cm in diameter, and were necropsied.
> Supplementation with NA or Nam at 4.0 g/kg diet (combined
> analysis) increased the latency of the ENU-induced
morbidity
> curve, relative to niacin-adequate controls. Morbidity could
> be attributed in almost all cases to some form of neoplasm,
> with leukemias the
predominant
> form. In short-term studies, supplementation with either NA
> or Nam caused dramatic increases in bone marrow NAD(+) (1-
> to 1.5-fold), basal poly(ADP-ribose) (3- to 5-fold) and
> ENU-induced poly(ADP-ribose) levels
> (1.5-fold). These data show that supplementation of a
> niacin-adequate,
high
> quality diet with pharmacologic levels of nicotinic acid or
> nicotinamide increases NAD(+) and poly(ADP-ribose) levels in
> bone marrow and may be protective against DNA damage.
>
> [40] The Vitamins: Fundamental Aspects in Nutrition and
> Health 2nd
Edition.
> Gerald F Combs, Jr (1998) ISBN 0121834921
>
> [73] Encyclopedia of Nutritional Supplements. Michael T
> Murray, (1996)
ISBN
> 0761504109 An invaluable resource; should be read by
> everybody prior to supplementing.
>
> [85] Safety of high-dose nicotinamide: a review. Knip M,
> Douek IF, Moore WP, Gillmor HA, McLean AE, Bingley PJ,
> Gale EA in Diabetologia 2000 Nov;43(11):1337-45 PMID:
> 11126400 Discusses the potential of 3g/d vitamin B3 in
> preventing the onset of Type
I
> (insulin-dependent) diabetes.
>
> [126d] Increased poly(ADP-ribose) polymerase activity in
> lymphoblastoid
cell
> lines from centenarians. Muiras ML, Muller M, Schachter F,
> Burkle A in J Mol Med 1998 Apr;76(5):346-54. PMID: 9587069
> "Poly(ADP-ribosyl)ation is a posttranslational modification
> of nuclear proteins which is catalyzed by poly(ADP-ribose)
> polymerase and represents
an
> immediate response of eukaryotic cells to oxidative and
> other types of DNA damage. [.] Viewed together with previous
> results on poly(ADP-ribose) polymerase activity in various
> mammalian species, the present data provide further evidence
> for the notion that longevity is associated with a high
> poly(ADP-ribosyl)ation capacity."
>
>
> Cheers, Michael C Price
> ----------------------------------------
> http://mcp.longevity-report.com
> http://www.hedweb.com/manworld.htm
>

[Bbaylarry]

"Julius Siden" <nospambaby@nukeit.net> wrote in message
news:3e6d0cff_2@corp-news.newsgroups.com...
> Yet, you wonder.

Did you watch the portion of "48 Hours Investigates" last
night? Very interesting bit of research going on in the area
of a protein, Grellin, discovered by Japanese researchers a
year or so ago. It seems that Grellin triggers the appetite
causing one to eat more and more. Even after satiation they
continue to eat. Not at all like the gorging done by so many
Bolemics. Just an almost constant hunger and eating causing
more hunger situation. The pharmaceutical are on this like
vultures. Since we, as a nation, are so obese, and the "eat
less, exercise more" regimen may allow you to lose 10 to 15
per cent of your body weight, it is not conducive to keeping
the weight off once the metabolism adjusts to the dietary
changes and you regain the lost weight and oftimes even more.

They have found that a few of those having liposuction and
stapling of the intestines may lose quite a bit of this
Grellin protein. Some to the point that they are now never
hungry. One fellow held up the size 65 pants he wore when he
was so obese he couldn't walk, couldn't drive and had to have
two seats on a bus, train or airplane. He traveled locally in
a Golf Cart. He weighed over 450 pounds when he had the
surgery. Lost around 235 pounds after the surgery and has
regained any of it. He is one of those that now almost forces
himself to eat even one small meal a day.

Glaxo is working hard on this as they know it will be a
multi-billion dollar annually product if they get it working
and FDA approval. I can speak empirically that I felt quite a
bit better after my emergency by-pass heart surgery in 1994
had me sedated and on a feeding tube for 19 days. I went from
245 pounds down to 187 pounds. Most of my RA pain disappeared
at that lower weight. I hadn't weighed 187 since 1967 when I
was a 25 year old single Staff Sergeant wearing a Green Beret,
which has to be the greatest female leg spreader ever devised
for a soldier to wear. All things must end and a year later I
met and married Susan. Started eating her cooking, stopped the
late night carousing, started sleeping regular hours, cut down
on the exercise and in a three month period went from that 187
to 210 pounds and positively waddled onto the plane taking me
back for my fourth tour in South Vietnam. I'm down to 205 now
and am about 2 inches shorter in height that I was back then.
But, I still have a real problem with Susan's cooking. If she
prepares it, I eat it. Excepting Cottage Cheese and plain
Yogurt. But, fortunately, neither of us care for either of
those two "food" items.

Be well, Larry
PS Can't you just see the new businessmen's lunch? Three
Martinis and a Glaxo Gut Shrinker while you work out with
an "8 Minute Abs" or "Buns of Steel" tape at the local
Gold's Gym.

[Chris Jain]

Quite interesting.

Seems PARP inhibition may sometimes have benefits though...
(see below)

BTW, found this collection of posts on Niacin by our very own
Steve Harris, MD: http://yarchive.net/med/niacin.html

=======

Curr Med Chem 2003 Feb;10(4):321-40 Related Articles, Links

Poly(ADP-Ribose) Polymerase Inhibitors.

Southan GJ, Szabo C.

Inotek Pharmaceuticals Corporation, Beverly, MA, USA.
gjsouthan@aol.com; or szabocsaba@aol.com

Poly(ADP-ribose) polymerase-1 (PARP-1) is the principal member
of the PARP enzyme family consisting of PARP-1 and several
recently identified novel poly(ADP-ribosyl)ating enzymes.
PARP-1 functions as a DNA damage sensor and signalling
molecule. Upon binding to DNA breaks, activated PARP cleaves
NAD(+) into nicotinamide and ADP-ribose and polymerizes the
latter onto nuclear acceptor proteins including histones,
transcription factors and PARP itself. This
Poly(ADP-ribosyl)ation contributes to inflammatory signal
transduction processes. In addition, oxidative stress-induced
overactivation of PARP consumes NAD(+) and consequently ATP,
culminating in cell dysfunction or necrosis. Activation of
PARP has been implicated in the pathogenesis of stroke,
myocardial ischemia, diabetes, diabetes-associated
cardiovascular dysfunction, shock, traumatic central nervous
system injury, arthritis, colitis, allergic encephalomyelitis
and various other forms of inflammation. Therefore, inhibition
of PARP by pharmacological agents may prove useful for the
therapy of these diseases, as has been shown in preclinical
animal models. Moreover, PARP inhibitors may have additional,
potential utility as anticancer agents, radiosensitizers and
antiviral agents. In the present article we overview the
structures and pharmacological actions of various
pharmacological classes of compounds which inhibit the
catalytic activity of PARP.

PMID: 12570705 [PubMed - in process]

[Chris Jain]

Another study suggesting niacinamide mega-doeses may be
a bad idea.

Inhibition of Silencing and Accelerated Aging by Nicotinamide,
a Putative Negative Regulator of Yeast Sir2 and Human SIRT1*

The abstract and full article is at:
http://www.jbc.org/cgi/content/full/277/47/45099#SEC3

Interesting quote: "Nicotinamide and nicotinic acid are used
at high doses (up to 10 g/day) to self-treat a wide variety of
ailments (43). Both are considered forms of vitamin B3 and are
often used interchangeably, although nicotinamide has become
preferred in many cases because of an apparent lack of side
effects. We have shown that these two related compounds have
drastically different effects at the molecular level. In
addition, nicotinamide is currently in trials as a therapy to
prevent cancer recurrence and insulin-dependent (type I)
diabetes (42). Our results clearly demonstrate that
nicotinamide can inhibit Sir2 enzymes, even in noncycling
cells, and raise the concern that there may be deleterious
consequences of long term nicotinamide therapy in humans."

[Tim]

Hi Chris It does indeed suggest that noncycling anaerobic
yeast should not take supplemental nicotinamide if they desire
to retard aging. As far as an in vitro study in aerobic human
cells this is perhaps better.

www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed-
&list_uids=11814060&dopt=Abstract

Regards
Tim

...(some)man views his world as chinks in a cavern.
William Blake

[Barsell]

Tim wrote:

> noncycling anaerobic yeast should not take supplemental
> nicotinamide if they desire to retard aging. As far as an
> in vitro study in aerobic human cells this is perhaps
> better:

>Rapid reversion of aging phenotypes by nicotinamide through
>possible modulation of histone acetylation.
www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed-
&list_uids=11814060&dopt=Abstract

Yes, in yeast, gene silencing by histone deacetylation extends
life span. In the higher life forms it seems that increased
gene expression via hyperacetylation is what works. The terms
"gene silencing" and "increased gene expression" are, however,
relative because in each case numerous genes are both silenced
and expressed.

> Hyperacetylation of histones by butyrate extends lifespan in
> drosophila.
We report that feeding Drosophila throughout adulthood with
4-
>> phenylbutyrate (PBA) can significantly increase lifespan,
>> without diminution of locomotor vigor, resistance to
>> stress, or reproductive ability. Treatment for a limited
>> period, either early or late in adult life, is also
>> effective. Flies fed PBA show a global increase in histone
>> acetylation as well as a dramatically altered pattern of
>> gene expression, including induction or repression of
>> numerous genes. The delay in aging may result from the
>> altered physiological state.
> PMID: 11792861

[Barsell]

Tim wrote:

> noncycling anaerobic yeast should not take supplemental
> nicotinamide if they desire to retard aging. As far as an
> in vitro study in aerobic human cells this is perhaps
> better:

>Rapid reversion of aging phenotypes by nicotinamide through
>possible modulation of histone acetylation.
www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed-
&list_uids=11814060&dopt=Abstract

Yes, in yeast, gene silencing by histone deacetylation extends
life span. In the higher life forms it seems that increased
gene expression via hyperacetylation is what works. The terms
"gene silencing" and "increased gene expression" are, however,
relative because in each case numerous genes are both silenced
and expressed.

> Hyperacetylation of histones by butyrate extends lifespan
> in drosophila.
We report that feeding Drosophila throughout adulthood with
4-
>> phenylbutyrate (PBA) can significantly increase lifespan,
>> without diminution of locomotor vigor, resistance to
>> stress, or reproductive ability. Treatment for a limited
>> period, either early or late in adult life, is also
>> effective. Flies fed PBA show a global increase in
>> histone acetylation as well as a dramatically altered
>> pattern of gene
expression,
>> including induction or repression of numerous genes.
>> The delay in aging may result from the altered
>> physiological state.
> PMID: 11792861

[Don Kirkma]

Follow up set to sci.med.nutrition; this research doesn't seem
to have any relationship to the arthritises. Please don't post
non-arthritis material into the alt.support.arthritis and
misc.health.arthritis newsgroups.

It seems to me I heard somewhere that Tim wrote in article
<6da4c14.0303151107.4cab4ff4@posting.google.com>:

>Hi Chris It does indeed suggest that noncycling anaerobic
>yeast should not take supplemental nicotinamide if they
>desire to retard aging. As far as an in vitro study in
>aerobic human cells this is perhaps better.
>
>www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMe-
>d&list_uids=11814060&dopt=Abstract
--
Don donkirk@covad.net

[Tim]

It was cross-posted by others, however it may have a lot to do
with osteoarthritis.

Tim

[Chris Jain]

timothytn@my-deja.com (Tim) wrote in message
news:<6da4c14.0303161218.309cf6a2@posting.google.com>...
> It was cross-posted by others, however it may have a lot to
> do with osteoarthritis.
>
> Tim

Yup. I'm the one who asked about niacinamide and my interest
in it is PURELY due to its use for osteoarthritis.

Don, I believe that if you were to go back and read Tim's post
within the context of the thread, you will see that it relates
to possible side-effects of niacinamide and is still very much
on-topic. I agree that we should drop alt.support.arthritis
however, as this type of discussion seems to be objectionable
to at least a vocal minority on that group.

Tim, thanks for the information. I am interested in
niacinamide because it seems likely to be a "disease-modifying
agent" for osteoarthrtis, meaning that its my understanding
that it may be able to slow the degradation of the joints. I
believe most drugs currently being used for osteoarthritis
only treat pain and do nothing to affect the progression of
the disease.

Chris