Ok, I was giving the profiles instead of the video links.

Please read watch video....free money at no cost.

If you spend any time socializing online, you can now get paid for doing
what everyone like to do. Have fun and get paid.

It's free with wonderful potential. Check it out. watch the short video
and yes sign up

You are being invited to join Yuwie.  When you join, you will be
instantly connected to Me and My friends. Click the link below to join.

http://www.yuwie.com/yuwie.asp?r=17862
<http://www.yuwie.com/yuwie.asp?r=17862>  ... Ramond

What is Yuwie?

=================

First off, Yuwie is FREE. Yuwie is like any other 'connect with friends'
or social networking site.

But we have one major difference.

Use Yuwie - Get Paid!

Yuwie pays you to blog, upload pictures, refer friends, chat, hang out,
etc.

Let's all join with each other....after all no cost. Advertisers will be
paying for our activities of all kinds.

Bill

please sign up under one of my friends below. I love helping out.

   http://www.yuwie.com/yuwie.asp?r=25112
<http://www.yuwie.com/yuwie.asp?r=25112>        Jeremy
http://www.yuwie.com/yuwie.asp?r=18857
<http://www.yuwie.com/yuwie.asp?r=18857>        Edna
http://www.yuwie.com/yuwie.asp?r=22607
<http://www.yuwie.com/profile/?id=22607>        Melody
   http://www.yuwie.com/yuwie.asp?r=22719
<http://www.yuwie.com/yuwie.asp?r=22719>       Jermaine
   http://www.yuwie.com/yuwie.asp?r=17862
<http://www.yuwie.com/profile/?id=17862>        Ramond
   http://www.yuwie.com/yuwie.asp?r=22565
<http://www.yuwie.com/profile/?id=22565>        Liz

Yuwie is growing very fast...it has gone from 3,500 to over 45,000 in
the last 3 weeks and gone from the 586,000 ranked website to the 1,500th
ranked website in just over a month. If you need any help using it just
let me know. You can send invites under the Referral Square over to the
left.

Otherwise, just keep this simple...and this is real easy.

GOAL: Get 3 people who join Yuwie who get 3 people for 10 levels with an
average of 1,000 page views.

PAYOFF: Your monthly check from Yuwie could be over $10,000! (only an
estimate, there are no guarantees)

We can't say exactly how much, but here's an example of what could
happen. The chart below assumes you refer 3 people, and those 3 people
refer 3, then those refer 3, through 10 levels, and each referral gets
1000 page views for the month, and the month's RSR is $0.50.

LEVELS - REFERRALS - IMPRESSIONS - EARNINGS
1---------------3---------------3,000---------------$0.15
2---------------9---------------9,000---------------$0.45
3---------------27-------------27,000--------------$0.54
4---------------81-------------81,000--------------$1.62
5---------------243-----------243,000-------------$4.86
6---------------729-----------729,000-------------$14.58
7--------------2,187--------2,187,000-------------$43.74
8--------------6,561--------6,561,000-------------$328.05
9-------------19,683------19,683,000-------------$984.15
10------------59,049------59,049,000-------------$8,857.35

TOTAL------88,572 -----88,572,000------------$10,235.49

Results are not guaranteed. This is just an example of what could
happen.

Does that motivate you or what??? Go get your 3 people and help them do
the same!

Check my Blogs for some info on what to do to get started. GOOD LUCK!


Bill



[Non-text portions of this message have been removed]

Get paid for hanging out online with friends, no cost ever!



If you spend any time socializing online, you can now get paid for doing
what everyone like to do. Have fun and get paid.

It's free with wonderful potential. Check it out. watch the short video
and yes sign up.



You are being invited to join Yuwie.  When you join, you will be
instantly connected to Me and My friends. Click the link below to join.



http://www.yuwie.com/profile/?id=17862... Ramond



What is Yuwie?

=================

First off, Yuwie is FREE. Yuwie is like any other 'connect with friends'
or social networking site.

But we have one major difference.



Use Yuwie - Get Paid!



Yuwie pays you to blog, upload pictures, refer friends, chat, hang out,
etc.

Let's all join with each other....after all no cost. Advertisers will be
paying for our activities of all kinds.


Bill



please sign up under one of my friends below. I love helping out.

http://www.yuwie.com/profile/?id=25112
<http://www.yuwie.com/profile/?id=25112>        Jeremy
http://www.yuwie.com/profile/?id=18857
<http://www.yuwie.com/profile/?id=18857>        Edna
http://www.yuwie.com/profile/?id=22607
<http://www.yuwie.com/profile/?id=22607>        Melody
http://www.yuwie.com/profile/?id=22719
<http://www.yuwie.com/profile/?id=22719>       Jermaine
http://www.yuwie.com/profile/?id=17862
<http://www.yuwie.com/profile/?id=17862>        Ramond
http://www.yuwie.com/profile/?id=22565
<http://www.yuwie.com/profile/?id=22565>        Liz

Yuwie is growing very fast...it has gone from 3,500 to over 60,000 in
the last 4 weeks and gone from the 586,000 ranked website to the 1,500th
ranked website in just over a month. If you need any help using it just
let me know. You can send invites under the Referral Square over to the
left.

Otherwise, just keep this simple...and this is real easy.

GOAL: Get 3 people who join Yuwie who get 3 people for 10 levels with an
average of 1,000 page views.

PAYOFF: Your monthly check from Yuwie could be over $10,000! (only an
estimate, there are no guarantees)

We can't say exactly how much, but here's an example of what could
happen. The chart below assumes you refer 3 people, and those 3 people
refer 3, then those refer 3, through 10 levels, and each referral gets
1000 page views for the month, and the month's RSR is $0.50.

LEVELS - REFERRALS - IMPRESSIONS - EARNINGS
1---------------3---------------3,000---------------$0.15
2---------------9---------------9,000---------------$0.45
3---------------27-------------27,000--------------$0.54
4---------------81-------------81,000--------------$1.62
5---------------243-----------243,000-------------$4.86
6---------------729-----------729,000-------------$14.58
7--------------2,187--------2,187,000-------------$43.74
8--------------6,561--------6,561,000-------------$328.05
9-------------19,683------19,683,000-------------$984.15
10------------59,049------59,049,000-------------$8,857.35

TOTAL------88,572 -----88,572,000------------$10,235.49

Results are not guaranteed. This is just an example of what could
happen.

Does that motivate you or what??? Go get your 3 people and help them do
the same!

Check my Blogs for some info on what to do to get started. GOOD LUCK!




[Non-text portions of this message have been removed]

Finally, something REALLY FREE and will make you Money

It's free with wonderful potential. Check it out. watch the short video
and yes sign up

You are being invited invited to join Yuwie.  When you join, you will be
instantly

connected to Me and My friends. Click the link below to join.
http://www.yuwie.com/yuwie.asp?r=8079
<http://www.yuwie.com/yuwie.asp?r=8079>



What is Yuwie?

=================

First off, Yuwie is FREE. Yuwie is like any other 'connect with friends'
or social networking site.

But we have one major difference.



Use Yuwie - Get Paid!



Yuwie pays you to blog, upload pictures, refer friends, chat, hang out,
etc.

Let's all join with each other....after all no cost. Advertisers will be
paying for our activities of all kinds.
http://www.yuwie.com/yuwie.asp?r=8079
<http://www.yuwie.com/yuwie.asp?r=8079>

Bill

or sign up under one of my friends below

http://www.yuwie.com/yuwie.asp?r=8130
<http://www.yuwie.com/yuwie.asp?r=8130>            Gina
   http://www.yuwie.com/yuwie.asp?r=12719
<http://www.yuwie.com/yuwie.asp?r=12719>        Tester168



Hey Bill Sullivan here...FYI, Yuwie is growing very fast...it has gone
from 3,500 to over 20,000 in the last 2 weeks and gone from the 586,000
ranked website to the 2,000th ranked website in just over a month. If
you need any help using it just let me know. You can send invites under
the Referral Square over to the left.

Otherwise, just keep this simple...and this is real easy.

GOAL: Get 3 people who join Yuwie who get 3 people for 10 levels with an
average of 1,000 page views.

PAYOFF: Your monthly check from Yuwie could be over $10,000! (only an
estimate, there are no guarantees)

We can't say exactly how much, but here's an example of what could
happen. The chart below assumes you refer 3 people, and those 3 people
refer 3, then those refer 3, through 10 levels, and each referral gets
1000 page views for the month, and the month's RSR is $0.50.

LEVELS - REFERRALS - IMPRESSIONS - EARNINGS
1---------------3---------------3,000---------------$0.15
2---------------9---------------9,000---------------$0.45
3---------------27-------------27,000--------------$0.54
4---------------81-------------81,000--------------$1.62
5---------------243-----------243,000-------------$4.86
6---------------729-----------729,000-------------$14.58
7--------------2,187--------2,187,000-------------$43.74
8--------------6,561--------6,561,000-------------$328.05
9-------------19,683------19,683,000-------------$984.15
10------------59,049------59,049,000-------------$8,857.35

TOTAL------88,572 -----88,572,000------------$10,235.49

Results are not guaranteed. This is just an example of what could
happen.

Does that motivate you or what??? Go get your 3 people and help them do
the same!

Bill Sullivan



[Non-text portions of this message have been removed]

This is it! Get paid for having fun and its free

You are being invited invited to join Yuwie.com  When you join, you will
be instantly
connected to Me and My friends. Click the link below to join.
http://www.yuwie.com/yuwie.asp?r=8079
<http://www.yuwie.com/yuwie.asp?r=8079>

What is Yuwie?
=================
First off, Yuwie is FREE. Yuwie is like any other 'connect with friends'
or social networking site.
But we have one major difference.

Use Yuwie - Get Paid!

Yuwie pays you to blog, upload pictures, refer friends, chat, hang out,
etc.
Let's all join with each other....after all no cost. Advertisers will be
paying for our activities of all kinds.
http://www.yuwie.com/yuwie.asp?r=8079
<http://www.yuwie.com/yuwie.asp?r=8079>

Bill





[Non-text portions of this message have been removed]

Free calming nice  Poetry, artwork, music mix

This is completely FREE and very nice!
Go and enjoy this Poetry,artwork,misic mix.
http://bsullivan79.com/maybe4u.htm <http://bsullivan79.com/maybe4u.htm>





[Non-text portions of this message have been removed]

FREE - USE Google Adsense to make free money



Hi Everyone,



Anyone signing up to my freeiq, I will give a free copy of Adwords Made
Easy. It details how to work with Google and make thousands per month.
It gives an actual documented case of someone who knew nothing.

Come join me: http://freeiq.com/justdoit <http://freeiq.com/justdoit>

The book will walk you step by step and it works!

So why would I give it away? Well I believe that the free IQ system will
revolutionize the internet, even forcing powerhouses like ebay and
clickbank to change formatting. Futhermore any one I refer, will one day
purchase things like no other place offers on free IQ. Guess what, they
will pay me, even just from a customer, for a whole year. I will get
paid for afilliates (which is free also) forever.

Now, I think that's worth giving away a book that cost $97 dollars.

FreeIQ is in beta, but already one of the top few thousand websites on
the web. You will be able to publish, sell, distribute and advertize
worldwide for free.

So, hop in: http://freeiq.com/justdoit <http://freeiq.com/justdoit>
Get you free copy of Adwords made Easy, today.

Bill

P.S.
Tell your friends. Its always FREE and they will pay you the same way as
they pay me. These millionaires intend to change the world for the
better.
http://freeiq.com/justdoit <http://freeiq.com/justdoit>





[Non-text portions of this message have been removed]

Sorry everyone,

I left something out. This also affords everyone that wants to an
oportunity to unsubscribe, if they so want.

Thanks,

Bill

Hello Everyone,

Consider this as a formal notice that I am about to change the content
of this website.

I gave a few days so that if anyone wanted to take up my banner of
educating the public about limu, they could.

No one took up that offer.

Now, I want you to kn0w that I wish you all the best with limu. It is
the premiere health product on the market.

Instead of just killing a webpage that is indexed in all the major
search engines, I will consider what I am about to do the LIMU of the
marketing world.

I intend to help your businesses, of any kind, by advertizing it for
you.

Or you can learn to do the smae and make money. With your FINANCIAL
HEALTH, you will be better able to purchase limu or anything else.

So watch for it.

Bill

Hear Powerful Testimonies
Like These Every Monday Evening 8:30PM CST TOLL FREE 212-990-8000   6688#


Since my pregnancy, 2 years ago, I suffered from daily migraines. My doctors
thought these were due to hormonal changes and could only recommend pain
medication. Of course, I could not risk harm to my unborn baby by taking it. But
16 months after my son, Zachary's birth, the headaches were no better. It was
hard for Zachary to understand why mommy didn't want to do anything but lay on
the couch some days. After taking Limu Moui for 1 day, my headache was gone!
Zachary and I have so much more fun now. I will even take it during my next
pregnancy. I want to tell everyone I come into contact with about Limu Moui
because it has changed my life!
Chastity T., Cordova, TN

I am 42 years old and was diagnosed with Multiple Sclerosis in 1998. I
experienced episodes of weakness and progression of the disease. I went through
physical therapy and medications, feeling better at times and then another
episode would leave me feeling weak and numb. The last episode was so fast and
progressive that I became wheelchair bound, weak and with no feeling from the
waist down. I could not even hold my grandbaby. I was never this debilitated
before and was convinced I would die. On May 8th, I started taking about 2
tablespoons of Limu Moui, twice a day, and within one month, I was out of the
wheelchair and walking without a brace or cane. I even resumed my housework and
cooking supper. Next week, I intend to start driving again. I feel generally
good and have an increase in energy. My physical therapist commented that he'd
never seen anyone progress so quickly from how debilitated I was. I will never
be without Limu Moui!
Theresa C., Dequincy, LA

My husband, who is in construction, is exposed to the elements 8 to 10 hours a
day and suffered from constant sinus headaches. After taking Limu Moui, he
rarely suffers at all now! In addition, my pain from carpal tunnel syndrome in
my right arm and a bulging disc in my back are gone. I no longer need the brace
for my arm and I can sleep so much better at night. Limu Moui is a blessing to
the entire world!
LeJoyce A., Arcadia, LA

I have had severe fever blisters, caused by Herpes virus, on my lower lip for as
long as I can remember. These typically begin with a tingling sensation in a
small area and progress until 1/4 to 1/2 of my lower lip is swollen, red, and
bleeding. Ultimately, the lesion becomes painful throughout the typical 3 to
5-week duration and is quite unsightly and embarrassing. Upon feeling the
familiar sensation begin, I immediately applied Limu Moui directly onto the
emerging blister to see what would happen. After 4 days of applying it twice a
day, the blister was going away and never surfaced! I was amazed, as I have
never experienced this quick of a recovery from this repulsive ailment.
Mark K. Springfield, MO

I am 39 and have had asthma most of my life, starting as a small child and
becoming worse in my early 20's. Though detrimental to my internal organs, I've
used 3 different steroid based medications twice a day to keep this disease
under control and have visited the emergency room 3 times over the last 15
years. Since the day I started taking Limu Moui, I have not used any
prescription medication and I can breathe! I can now have a normal life. This is
a gift from above and it is now my duty to share my blessing!
Gary R., Sedro Woolley, WA

I have had ulcers since I was 15 years old and inflammation of the stomach
lining most of my adult life. Because of extreme heartburn, I had to take Zantac
with every meal and sometimes even between meals. Since I started taking Limu
Moui, I have not had to take Zantac. In additional, my energy level and general
well being have dramatically improved.
Nileen B., Sedro Wooley, WA

I have been on Avapro and Toprol, blood pressure medication since my open heart
surgery a year ago. My blood pressure still remained at around 179/100 or
179/120. The lowest it had ever reached was 158/90. With my doctor's approval, I
started taking 2 tablespoons per day of Limu Moui. After the second day on the
product, my blood pressure dropped to 116/66 and my doctor cut my medication
dosage in half. Three days later, he took me off Avapro completely and reduced
my dosage of Toprol even more and will take me off it completely in 2 more days.
My blood pressure has stayed consistently between 116/66 and 118/66. I am no
longer sleepy, have more energy, feel calmer, my head is clearer and my heart no
longer pounds. I will never stop taking Limu Moui and it's just a matter of time
before my doctor is in the business!
Phil R., Minden, LA

I've had rheumatoid arthritis since 1980 and in spite of having tried every kind
of medication imaginable--from Gold injections and steroids, to Methotrexate and
Remicade -- I still had to live with many physical limitations. These included
being unable to turn the car keys, raise my arms over my head, get up and down
from a sitting position, morning stiffness, low energy and little to no strength
in my hands and wrists. I began to see results after 1 week on Limu Moui and it
has continued ever since. Recently I spent 3 days, rolling paint up to the
ceiling and wallpapering. I also mowed an acre of land for 2-1/2 hours with a
tractor that has no power steering. Not only was I not sore the next day, I
drove into the city and took a CPR and First Aid Class. I'm doing things I have
not done in 15 years.
Nancy O'C., Pleasant Hill, MO

Our 6-year old daughter, Christina, has had breathing problems since the day she
was born. Ever since a near death experience when she was 6 weeks old, she has
had to use a Breathalyzer on many occasions. Recently, we had to cut a weekend
trip short and return home due to the breathing problems Christina was having
from the high spring time pollen content. We decided to try Limu Moui because
the traditional medications she was taking were not clearing her up completely.
After 4 days, all signs of Christina's pneumonia were gone and all her other
symptoms cleared up, as well. Our whole family is now on the product and we have
noticed many other benefits, after approximately 4 days of use.
David L., Shreveport, LA

I suffered from fibromyalgia and chronic fatigue syndrome, both causing constant
pain, especially after any kind of strenuous exertion, or when the weather
changed. I was taking at least 6 Ibuprofen a day and 2 or 3 Tylenol PM for pain
and to sleep at night. After 2 weeks on Limu Moui, I am not taking either one of
those medications, and my pain during the day has all but disappeared, my energy
level is "out the roof" and I am sleeping very well at night.
Rebecca S., Oak Ridge, LA

My father-in-law has diabetes, which was out of control. He had been taking oral
medication, but when his blood sugar level reached between 200 and 350, the
doctor had put him on insulin shots. His first week on Limu Moui, he took 2
tablespoons, 2 times a day. The second week, he increased it to 2 tablespoons, 3
times a day. After checking his blood sugar level, he found it had dropped to
140 and remains between 150 and 160.
Jeff B., Liberty, TX

I have had chronic sleep problems for the past 20 years and have spent many
hours tossing and turning and staring at the ceiling till daybreak. I chose to
get off the prescription medication my doctor prescribed years ago and no over
the counter aids helped. After hearing friends and family say they were sleeping
better at night because of Limu Moui I began taking it. After 3 nights, I
noticed a total change in my sleeping. What a joy it is to wake up and find it's
morning! I feel rested during the day and feel a sense of well being and
happiness from the product. Limu Moui is a real blessing!
Sally H., Heflin, LA

My health issues included allergy and sinus problems for which I had to take
medication, including a 12-hour nasal spray, every 3 to 4 hours. In addition, I
was taking Prilosec for a severe problem with indigestion and heartburn, which I
experienced with even one bit of any kind of food. After just 3 days on Limu
Moui, my allergies and sinus problems were gone and I was able to get a good
night's sleep, without any medication. I am also completely off the Prilosec and
have no more indigestion symptoms. I have not felt better in a long time!
Alton W., Oake Grove, LA

For 13 years, my daughter has been suffering from asthma and a chronic cough
every night. After 5 days on Limu Moui, I noticed she was not coughing at night.
For the last 46 days, she has not coughed, wheezed, or had to use the inhaler!
The product has been a blessing to her and she will take it for the rest of her
life!
Bonita W., Sugarland, TX

I am legally blind due to diabetes and I suffer from congestive heart failure. I
have had several heart attacks and 4 angioplasty surgeries. I also have
shortness of breath, poor circulation, bad lungs, poor kidney control and sleep
apnea, to name a few of my ailments. My blood sugar ranged from 200-450,
sometimes even higher. I was about to start kidney dialysis because of the
kidney failure. After taking Limu Moui for 3 days, I felt noticeably improved.
My blood sugar has dropped to between 130 and 170, I am able to get up without
aid, and am much more active. Before, I could barely walk 50 feet, from the
house to the mailbox, and now, I have been walking 7 blocks at a time. In
addition, I have more energy, less shortness of breath and control of my
kidneys. I have done nothing different from before, except take Limu Moui.
Edward W., Cullman, AL

I was in extreme pain following knee replacement surgery in January and physical
therapy was an excruciating experience. Twice a day, I had to take 200-500 mg of
Extra Strength Tylenol, 250 mg of Ultram and 50 mg of Percoset, totaling 2300 mg
of pain medication, daily. I began taking Limu Moui on March 31, 2001 and 4
weeks later, the last week in April, I began to notice that my pain was almost
gone. Consequently, I stopped taking all pain medication, except one 50 mg
tablet of Ultram at bedtime. Even though physical therapy is still painful, I
find that my pain subsides about 30 minutes after taking Limu Moui.
Robert W., Springfield, MO

I was plagued with year round sinus related problems, including infection,
bronchitis and laryngitis, especially in the spring and fall. This would deplete
my energy and wellness and cause me to miss work as a sign language interpreter,
causing hardship on my colleagues and deaf students, who depended on me. For
years, I tried medications, nasal sprays and herbal remedies. Within 3 days of
using Limu Moui, I was able to breathe freely and now take no medication.
Vicki W., Springfield, MO

J Cosmet Sci 2002 Jan-Feb;53(1):1-9 Related Articles, Books, LinkOut


Treatment of human skin with an extract of Fucus vesiculosus changes its
thickness and mechanical properties.

Fujimura T, Tsukahara K, Moriwaki S, Kitahara T, Sano T, Takema Y.

Biological Science Laboratories, Kao Corporation, 2606 Akabane, Ichikai-machi,
Haga-gun, Tochigi 321-3497, Japan.

Recently the researchers found that an extract of Fucus vesiculosus, which is a
type of seaweed, promotes the contraction of fibroblast-populated collagen gels
through increased expression of integrin molecules. In this study, they
investigated the effects of topical application of an aqueous extract of this
alga on the thickness and the mechanical properties of human skin. A gel
formulation that included 1% of the extract was applied topically to human cheek
skin twice daily for five weeks. A significant decrease in skin thickness
measured by B-mode ultrasound was elicited, as was a significant improvement in
elasticity measured with a Cutometer as compared with controls. In cheek skin,
the thickness normally increases and the elasticity usually decreases with age.
These results suggest that the Fucus vesiculosus extract possesses anti-aging
activities and should be useful for a variety of cosmetics.

Publication Types:
Clinical Trial
Controlled Clinical Trial

PMID: 11917251 [PubMed - indexed for MEDLINE]



1: Biol Pharm Bull 2000 Oct;23(10):1180-4 Related Articles, Books, LinkOut


Fucoidan is the active component of fucus vesiculosus that promotes contraction
of fibroblast-populated collagen gels.

Fujimura T, Shibuya Y, Moriwaki S, Tsukahara K, Kitahara T, Sano T, Nishizawa Y,
Takema Y.

Biological Science Laboratories, Kao Corporation, Haga, Tochigi, Japan.
301620@...

The fibroblast-populated collagen gel culture method has been evaluated as a
dermal model of wound contraction and granulation in tissues during the wound
healing process and as an in vitro model of dermal tissue. We previously
reported that an extract of Fucus vesiculosus promoted fibroblast-populated
collagen gel contraction and that the promotion of the gel contraction was due
to the increased expression of integrin alpha2beta1 on the surface of the
fibroblasts. In this study, we investigated the active component of the extract
of this alga using extraction and fractionation techniques. Water extraction of
the alga was followed by precipitation with excess ethanol and then gel
filtration with the boundary molecular weight of 30,000. The high molecular
weight fraction obtained from gel filtration was fractionated by ion exchange
chromatography on diethylaminoethyl cellulose column to give active fractions
that have more polar properties. These polar, high molecular weight fractions
which contained molecules with fucose and sulfate groups showed significant gel
contraction-promoting activity and integrin expression-enhancing activity, and
were estimated to be the sulfated-polysaccharide fucoidan. Commercially
available fucoidan showed similar activities to the above-described fraction of
this alga. Although it remains necessary to precisely identify the specific
active component, the above results indicate that fucoidan is the active
component which promotes collagen gel contraction, and also indicate the
possibility that it dose so by enhancing the integrin alpha2beta1 expression.

PMID: 11041247 [PubMed - indexed for MEDLINE]

J Nutr Sci Vitaminol (Tokyo) 1999 Jun;45(3):325-36 Related Articles, Books,
LinkOut


Inhibitory effect of Cladosiphon fucoidan on the adhesion of Helicobacter pylori
to human gastric cells.

Shibata H, KimuraTakagi I, Nagaoka M, Hashimoto S, Sawada H, Ueyama S, Yokokura
T.

Yakult Central Institute for Microbiological Research, Tokyo, Japan.

We studied the inhibitory effect of Cladosiphon fucoidan on the attachment of
Helicobacter pylori (H. pylori), a gastroduodenal pathogen, to human gastric
cell lines. The bacterial binding in these cell lines was inhibited more by
Cladosiphon fucoidan (IC50 = 16-30 mg/mL), than by the fucoidan from Fucus (IC50
> 30 mg/mL). Dextran sulfate, another sulfated polysaccharide, did not inhibit
the binding at all. Pre-incubating the bacterial suspension with fucoidans
reinforced the inhibitory ability of these components, and reduced the IC50
value of Cladosiphon fucoidan to approximately 1 mg/mL. However, the binding was
not inhibited by pre-treatment of gastric cells with these components. It was
also shown that this fucoidan blocks both Leb- and sulfatide-mediated attachment
of H. pylori to gastric cells. Furthermore, fucoidan-binding proteins were found
on the H. pylori cell surface by Western blot analysis. Thus, the inhibitory
effect exerted by Cladosiphon fucoidan on binding between H. pylori and gastric
cells might result from the coating with this component of the bacterial
surface.

PMID: 10524351 [PubMed - indexed for MEDLINE]



Biomed Mater Eng 2001;11(1):55-61 Related Articles, Books, LinkOut


Effect of oligofucose derivatives on acetic acid-induced gastric ulcer in rats.

Shibata H, Nagaoka M, Takagi IK, Hashimoto S, Aiyama R, Yokokura T.

Yakult Central Institute for Microbiological Research, Kunitachi, Tokyo, Japan.
hideyuki-shibata@...

This study attempted to enhance the anti-ulcer activity of fucoidan from
Cladosiphon okamuranus TOKIDA by chemical modification with a hydrophobic group.
The suitable number of fucose residues in the effective compound was also
clarified to obtain a compound of constant quality. Degraded fucoidans were
coupled with several hydrophobic groups via Schiff bases, and their anti-ulcer
activities were determined by acetic acid-induced ulcer models in rats.
Size-fractionated oligofucose was also modified and assayed for anti-ulcer
activity. Among the modified oligofucoses, only the oligofucose-dodecylaniline
combination (OFDA) significantly promoted ulcer healing. The effective dose was
0.2 mg/kg/d. The most suitable number of fucose residues in the compound for the
anti-ulcer activity was determined to be around 12. We succeeded in enhancing
the anti-ulcer activity of Cladosiphon fucoidan by modification with
dodecylaniline. The activity of this compound was comparable or greater than
that of typical anti-ulcer agents. By determination of the optimal OF chain
length for the anti-ulcer activity of OFDA, it became possible to obtain OFDA of
constant quality.

PMID: 11281579 [PubMed - indexed for MEDLINE]

Immunological analysis of inhibition of lung metastases by fucoidan (GIV-A)
prepared from brown seaweed Sargassum thunbergii.

Itoh H, Noda H, Amano H, Ito H.

Laboratory of Marine Biochemistry, Faculty of Bioresources, Mie University, Tsu,
Japan.

The antimetastatic effect of GIV-A (fucoidan) and/or 5-FU was examined in an
experimental model of lung metastases induced by Lewis lung carcinoma in mice.
Injection of GIV-A i.p. after removal of the implanted primary tumor inhibited
the development of lung metastases. Combination treatment with GIV-A and 5-FU
inhibited significantly the lung metastases. The number of peritoneal
macrophages, total cells and macrophages in the lung increased in mice treated
with GIV-A. Binding of the third component of complement (C3) cleavage products
(C3b) to the C3 receptor on peritoneal macrophages after i.v. injection of GIV-A
was enhanced, as shown by the fluorescent antibody technique. Lung metastases
were inhibited by i.v. injection of peritoneal macrophages activated with GIV-A.
GIV-A depressed aniline hydroxylase and aminopyrine demethylase activities of
the hepatic microsomal drug-metabolizing system in tumor-bearing mice. Moreover,
the concentration of 5-FU in the tissues (lung, liver, kidney, spleen and blood)
was increased significantly by coadministration of GIV-A. The picryl
chloride-induced delayed type hypersensitivity (PC-DTH) response in mice was
depressed after the implantation of tumor and treatment with 5-FU. GIV-A
restored the suppression of PC-DTH by 5-FU, but did not increase the PC-DTH of
normal mice. GIV-A not only enhanced the degree of spleen cell-mediated sheep
red blood cell (SRBC) hemolysis (quantitative hemolysis of SRBC), the indexes of
the spleen and thymus and the number of spleen cells, but also restored the
suppressive effect of 5-FU. In the group receiving GIV-A, the percentages of
splenic Thy1.2-, L3T4- and asialo GM1-positive cells were significantly
increased as compared with the tumor-bearing mice treated with saline.
Furthermore, the L3T4+/Lyt2+ ratio showed a tendency to increase, and the
Lyt2+/Thy1.2+ ratio was decreased. These results suggest that the antitumor
effect of GIV-A may be correlated with the changing pattern of the Thy1.2-,
L3T4- and asialo GM1-positive cells, C3 activation, macrophage activation and
depression of the hepatic microsomal drug-metabolizing system. These findings
raise the possibility that GIV-A may have clinical value in the prevention of
cancer metastasis.

PMID: 8572581 [PubMed - indexed for MEDLINE]


  Anticancer Res 1996 May-Jun;16(3A):1213-8 Related Articles, Books, LinkOut


Antitumor and antiproliferative effects of a fucan extracted from ascophyllum
nodosum against a non-small-cell bronchopulmonary carcinoma line.

Riou D, Colliec-Jouault S, Pinczon du Sel D, Bosch S, Siavoshian S, Le Bert V,
Tomasoni C, Sinquin C, Durand P, Roussakis C.

ISOMer (Institut des Substances et Organismes de la Mer), SMAB, Laboratoire de
Pharmacologie Marine, Faculte de Pharmacie, Nantes, France.

Fucans, sulfated polysaccharides extracted from brown seaweeds, have been shown
to be endowed with inhibitory effects cell growth in various experimental
models. We studied both the antiproliferative and antitumor properties of a
fucoidan extract (HF) obtained from the brown seaweed Ascophyllum nodosum on a
cell line derived from a non-small-cell human bronchopulmonary carcinoma
(NSCLC-N6), this type of carcinoma is particularly chemo-resistant. HF exerts in
vitro a reversible antiproliferative activity with a block observed in the G1
phase the cell cycle. Studies performed with the NSCLC-bearing nude mice show
antitumor activity at subtoxic doses. These preliminary results indicate that HF
exhibits inhibitory effect both in vitro and in vivo and is very potent
antitumor agent in cancer therapy.

PMID: 8702239 [PubMed - indexed for MEDLINE]

Sharing What Physicians Are Saying

Dr. Kyosuke Owa on Fucoidan
In research studies, the main health enhancing
ingredient in
  LIMUI, Fucoidan, has been shown to
have many
healthful benefits.

According to prominent Japanese researcher Dr.
Kyosuke Owa,
Fucoidan is said to
"Contain the same healing antibodies as mother's
milk,
providing essential amino acids and a balanced diet
of
minerals necessary to boost the immune system."
"Encourage the regeneration of new cells,
increasing cellular
immunity and giving the body additional 'firepower'
against
diseases."
"Not only aids in the development of new cells, but
it
encourages the regeneration of what are called
Natural Killer
Cells. These cells are found on the front lines
defending our
bodies from disease."

For centuries, the people of Tonga have benefited
from the
amazing health properties of Limu Moui. Now, thanks
to Dr.
Owa's extensive research on Fucoidan, it becomes
clear why it
is our mission to share  LIMUI with the
world.

Dr. Derrick M. DeSilva, Jr., M.D.
Nationally recognized as an expert in the vital
area of
nutrition as it relates to health, Dr. DeSilva
maintains that
disease is caused by nutrient deficiency brought on
by such
factors as poor diets, depleted nutrients in food,
dieting,
medications, oxidation and stress.
Because Limu Moui, the key ingredient in ROYAL
TONGAN LIMUT,
absorbs a rich bounty of 77+ nutrients from
pristine ocean
waters, Dr. DeSilva truly believes that it's
the "PERFECT
FOOD."

Dr. DeSilva believes  LIMUI works
because:
Its main ingredient Limu Moui is the "perfect
food" because
it absorbs a rich bounty of some 77 + nutrients
from
pristine ocean waters.


Limu Moui replaces nutrients lost from all the
different
causes of deficiency.


Oxidation, which is like rusting, is a cause of
disease.
Think about the last time you cut an apple. It
starts to
turn brown from oxidation...but if you pour ROYAL
TONGAN
LIMUT on it, it will NOT turn brown!


INTESTINES: 60% of our immune system resides in
our
intestine and 80% to 90% of those who suffer from
intestinal
problems also have allergies. So, if you "fix"
your
digestive system, you help "fix" your immune
system. Limu
Moui is very beneficial to the digestive system.


CHOLESTEROL: Cholesterol is made in the liver, so
if you can
keep the liver clean it will help with
cholesterol. Limu
Moui helps the liver.


CANCER: Limu Moui may make cancer cells pop (self-
destruct)
and stop cell division. Harvard School of Public
health
says: "Fucoidan in Limu Moui reduces plasmal
cholesterol and
the building of dangerous steroids to breast
tissue." Also,
chlorine in water has been attributed to breast
cancer. Limu
Moui contains substances like Magnesium and
Calcium, which
help dispel effects of chlorine.


BLOOD SUGAR: Fucoidan coats the GI system to
prevent
problems.


ARTHRITIS: Limu Moui lubricates joints to make
them more
flexible and thereby eliminating pain of
arthritis, etc.


MOOD DISORDERS: Mood disorders are affected by
essential
fatty acid deficiency, which is replenished by
Limu Moui.
Dr. DeSilva recommends for ADD/ADHD kids to take
them off
carbohydrates, sugar, processed foods and Ritelin
and put
them on  LIMUI!


BLOOD PRESSURE: Limu Moui addresses all three
areas that
affect blood pressure, for which people normally
have to
take different medications.


HEADACHES: No one should suffer from headaches
and ROYAL
TONGAN LIMUI has the properties to address them,
along with
an increased intake of water.




According to Dr. DeSilva, the people who should
use ROYAL
TONGAN LIMUI include:
Every one of us


Anyone on Medication


Anyone who eats poorly


Anyone under stress


Anyone who wants to feel better


ANYONE WHO IS BREATHING!

For more information call:
Bill Sullivan 501-612-5890
             or visit
http://thelimuman,originallimu.com   TODAY

USE MY ID PLEASE, 1236501

Experientia 1989 Oct 15;45(10):996-8 Related Articles, Books, LinkOut


Further characterization of sulfated homopolysaccharides as anti-HIV agents.

Sugawara I, Itoh W, Kimura S, Mori S, Shimada K.

Department of Pathology, University of Tokyo, Japan.

Fucoidan and dextran sulfate showed anti-HIV activities against mononuclear
cells from AIDS patients, and they abrogated HIV reverse transcriptase (RT)
activity by interacting with the HIV envelope in the membranes of target cells.
Furthermore, they showed a synergistic effect with azidothymidine (AZT).

PMID: 2478388 [PubMed - indexed for MEDLINE




Phytomedicine 1999 Nov;6(5):335-40 Related Articles, Books, LinkOut


Antiviral properties of fucoidan fractions from Leathesia difformis.

Feldman SC, Reynaldi S, Stortz CA, Cerezo AS, Damont EB.

Departamento de Quimica Organica-CIHIDECAR, Facultad de Ciencias Exactas y
Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Argentina.

Three fractions of fucoidans isolated from the brown seaweed Leathesia difformis
(Ee, Ec and Ea) were found to be selective antiviral agents against herpes
simplex virus (HSV) types 1 and 2 and human cytomegalovirus. Fraction Ea was the
most active, with IC50 values in the range 0.5-1.9 microg/ml without affecting
cell viability at concentrations up to 400 microg/ml. The antiherpetic activity
of Ea was assessed by three different methods, plaque reduction, inhibition of
virus yield and prevention of HSV-2 induced shut-off of cell protein synthesis,
demonstrating that the inhibitory effect was independent of the antiviral assay
and the multiplicity of infection. The mode of action of Ea could be ascribed to
an inhibitory action on virus adsorption. The fucoidans did not inhibit the
blood coagulation process even at concentrations exceeding more than 100 times
the IC50 value.

PMID: 11962540 [PubMed - indexed for MEDLINE]




Gen Pharmacol 1997 Oct;29(4):497-511 Related Articles, Books, LinkOut


Sulfated polysaccharides extracted from sea algae as potential antiviral drugs.

Witvrouw M, De Clercq E.

Rega institute for Medical Research, Katholieke Universiteit Leuven, Belgium.

The inhibitory effects of polyanionic substances on the replication of herpes
simplex virus (HSV) and other viruses were reported almost four decades ago.
However, these observations did not generate much interest, because the
antiviral action of the compounds was considered to be largely nonspecific.
Shortly after the identification of human immunodeficiency virus (HIV) as the
causative agent of the acquired immune deficiency syndrome (AIDS) in 1984,
heparin and other sulfated polysaccharides were found to be potent and selective
inhibitors of HIV-1 replication in cell culture. Since 1988, the activity
spectrum of the sulfated polysaccharides has been shown to extend to various
enveloped viruses, including viruses that emerge as opportunistic pathogens
(e.g., herpes simplex virus [HSV] and cytomegalovirus [CMV]) in immunosuppressed
(e.g., AIDS) patients. As potential anti-HIV drug candidates, sulfated
polysaccharides offer a number of promising features. They are able to block HIV
replication in cell culture at concentrations as low as 0.1 to 0.01 microgram
ml-1 without toxicity to the host cells at concentrations up to 2.5 mg ml-1. We
noted that some polysulfates show a differential inhibitory activity against
different HIV strains, suggesting that marked differences exist in the target
molecules with which polysulfates interact. They not only inhibit the cytopathic
effect of HIV, but also prevent HIV-induced syncytium (giant cell) formation.
Furthermore, experiments carried out with dextran sulfate samples of increasing
molecular weight and with sulfated cyclodextrins of different degrees of
sulfation have shown that antiviral activity increases with increasing molecular
weight and degree of sulfation. A sugar backbone is not strictly needed for the
anti-HIV activity of polysulfates because sulfated polymers composed of a
carbon-carbon backbone have also proved to be highly efficient anti-HIV agents
in vitro. Other, yet to be defined, structural features may also play an
important role. Sulfated polysaccharides may act synergistically with other
anti-HIV drugs (e.g., azidothymidine [AZT]). They are known to lead very slowly
to virus-drug resistance development and they show activity against HIV mutants
that have become resistant to reverse transcriptase inhibitors, such as AZT,
tetrahydro-imidazo [4,5,l-jk] [1,4]-benzodiazepin-2(1H)-thione (TIBO) and
others. From studies on their mechanism of action we concluded that polysulfates
exert their anti-HIV activity by shielding off the positively charged sites in
the V3 loop of the viral envelope glycoprotein (gp120). The V3 loop is necessary
for virus attachment to cell surface heparan sulfate, a primary binding site,
before more specific binding occurs to the CD4 receptor of CD4+ cells. This
general mechanism also explains the broad antiviral activity of polysulfates
against enveloped viruses. Variations in the viral envelope glycoprotein region
may result in differences in the susceptibility of different enveloped viruses
to compounds that interact with their envelope glycoproteins. The efficacy of
polysulfates in the therapy and/or prophylaxis of retroviral infections and
opportunistic infections remains to be demonstrated both in animal models and
humans. It is important to consider not only treatment of patients who are
already infected with HIV, but also prophylaxis and protection from HIV and/or
other virus infections. Because (i) sexual transmission is responsible for the
large majority of HIV infections worldwide; (ii) this transmission is mostly
mediated via mononuclear cells that infect epithelial cells of the genital
tract; and because (iii) polysulfates effectively inhibit cell-cell adhesion,
polysulfates may be considered as potentially effective in a vaginal formulation
to protect against HIV infection.

Publication Types:
Review
Review, Tutorial

PMID: 9352294 [PubMed - indexed for MEDLINE]




Biomed Pharmacother 1996;50(5):207-15 Related Articles, Books, LinkOut


Chemotherapy of human immunodeficiency virus (HIV) infection: anti-HIV agents
targeted at early stages in the virus replicative cycle.

De Clercq E.

Rega Institute for Medical Research, Katholieke Universiteit Leuven, Belgium.

Several compounds have been identified that inhibit an early stage in the
replicative cycle of the human immunodeficiency virus (HIV): i) virus
adsorption: polysulfates, polysulfonates, polycarboxylates, polyphosphates, and
polyoxometalates; or ii) virus-cell fusion: plant lectins, negatively charged
albumins and betulinic acid derivatives; iii) virus fusion/uncoating: bicyclam
derivatives; iv) reverse transcription: dideoxynucleoside analogues, acyclic
nucleoside phosphonates and non-nucleoside reverse transcriptase inhibitors. In
principle, HIV may develop resistance to any of these specific anti-HIV agents.
However, virus breakthrough can be completely prevented if these agents, alone
or in combination, are added to the HIV-infected cells from the beginning at
sufficiently high ('knock-out') concentrations.

Publication Types:
Review
Review, Tutorial

PMID: 8949401 [PubMed - indexed for MEDLINE

MAKE 200 DOLLARS (PLUS) 1ST DAY

I have a better one for you. With my
  company. The fastest
  growing
in referral marketing.

How money is made is presented below,
  BUT, All you have
to do is:
A. SIGN UP
B. SUPPLY email addresses or phone
numbers. (I'll do the
  selling.)
C. Collect checks of 235 to 260 dollars
  for each five I
sell in a 30 day period. (I sell 20
today, You MAKE 940
to 1040 dollars TODAY)
D.Those I sell provide you with residual
  income build-up.

Some are making 50 thousand plus after
  12 months.


       1.    You sign up ...........
I get 27 dollars

2. everyone you sign up...You get 27
  dollars each.
3.for everyone on your 2nd 3rd and
4th  levels you get
6 dollars.. so do I.
On your 5th level, you get 12 dollars.

4.For every 5 you sign up in a month,
  you get and extra
  120 to 150 dollars. example: sign up
  10 get and extra
240 to 300 dollars.

5. After the FIVE levels You also get
  a portion of 2
  precent of the total production of
all those on your
level in the company.
6. That not all. Your Upline will
sign up the first
five for you. You supply the names.
  We'll do it. And
  we will continue till you say uncle!

My ID 1236501
For more information call:
501-612-5890   or email
billts@...
http://Bill.limupro.com

P.S. Ask about my company, product
and timing.

Control the input, and you will master
  the output
www.freenetleads.com/free/4791980sul

http://www.trafficswarm.com/go.cgi?46941

Bill

Ann Plast Surg 2001 Nov;47(5):540-6 Related Articles, Books, LinkOut


Protective effect of fucoidin (a neutrophil rolling inhibitor) on ischemia
reperfusion injury: experimental study in rat epigastric island flaps.

Cetin C, Kose AA, Aral E, Colak O, Ercel C, Karabagli Y, Alatas O, Eker A.

Department of Plastic & Reconstructive Surgery, Osmangazi University Medical
Faculty, Eskisehir, Turkey.

The objective of this study was to examine whether a decrease in
neutrophil-mediated tissue injury using Fucoidin, a nontoxic neutrophil rolling
inhibitor, would improve flap survival in an island flap model after
ischemia-reperfusion. Myeloperoxidase activity (an indirect index of tissue
neutrophil count) and malondialdehyde (an indicator of lipid peroxidation), the
degree of neutrophil infiltration by direct counting, and macroscopic flap
survival were assessed in the flap after arterial ischemia-reperfusion.
Epigastric island skin flaps were elevated in 56 rats. The first group of 21
rats was subjected to 6 hours of arterial ischemia. The second group of 21 rats
was subjected to 10 hours of arterial ischemia, and the rest of the rats were
used as nonischemic controls (sham flaps). For inhibiting neutrophil rolling, a
nontoxic polysaccharide agent-Fucoidin-was used. Each ischemic group was divided
further into three subgroups: Subgroup I (control rats) received saline,
subgroup II received 10 mg per kilogram Fucoidin, and subgroup III received 25
mg per kilogram Fucoidin before reperfusion. The results were evaluated as
tissue neutrophil counts, tissue malondialdehyde content, tissue myeloperoxidase
activity, and flap survival. Neutrophil counts and tissue myeloperoxidase
activity were decreased significantly (p <0.001) in subgroup III, but lipid
peroxidation by means of tissue malondialdehyde content was not affected by
Fucoidin administration. The authors conclude that administration of Fucoidin
before reperfusion can limit tissue injury apparently by inhibiting neutrophil
rolling in a dose-dependent manner.

PMID: 11716267 [PubMed - indexed for MEDLINE]

Thanks Terra,

I am seriously think about only my own informational products right
now, although, I rule out nothing.

Life goes on and goes on well,
Bill





--- In LIMU_MOUI@yahoogroups.com, "TAOKI@..." <cathrine.vergara@...>
wrote:
>
>
> Hi Bill,
>
> I am sorry because I have really apreciated all your information.
>
> Is there no posibility that you can start over again, I hope so?
>
> If not, I would like you to look at my other business - (I am using
both).
>
> Pleasse take a look att my website: http://www.6144529.my4life.com
it is a good product and a good company, paying very good, known
among networkers at the best paying company. And they have a lot of
medical research aroung the product.
>
> If you are tired of those networking companies after what happened
to you I can understand it, and I also love Limu, but last time I had
to pay more for the delivery than for the product. It was the first
time this happened so I do not know if they changed the way of
delivery or something else, but paying so much I can not go on buying
it.
>
> I wish you all luck and for me it is OK if you send information if
you start some new site, I really liked to receive EVERY INFORMATION
you have sent. THANK YOU.
> 		 TERRA
>
> -->
>
>
>
> [Non-text portions of this message have been removed]
>

Hi Bill,

I am sorry because I have really apreciated all your information.

Is there no posibility that you can start over again, I hope so?

If not, I would like you to look at my other business - (I am using both).

Pleasse take a look att my website: http://www.6144529.my4life.com it is a good
product and a good company, paying very good, known among networkers at the best
paying company. And they have a lot of medical research aroung the product.

If you are tired of those networking companies after what happened to you I can
understand it, and I also love Limu, but last time I had to pay more for the
delivery than for the product. It was the first time this happened so I do not
know if they changed the way of delivery or something else, but paying so much I
can not go on buying it.

I wish you all luck and for me it is OK if you send information if you start
some new site, I really liked to receive EVERY INFORMATION you have sent. THANK
YOU.
		  TERRA

-->



[Non-text portions of this message have been removed]

My heart aches for you my friend. Although I believe, like you, that you must
meet accusations headon and show them for what they are - unfounded, I
understand your position and your choice. I wish there had been an alternative
and someone with the chutzpah to stand up to the vocal buut truly unenlightened
nay sayers. This IS a great product and I have watched you educated the masses
for years. I have seen how it benefits everyday people.

   I am glad you are taking the high road and not knocking the product. That
shows you have character. You are merely pointing out that there are
philosophical differences that ended in this situation. Fair well, my friend,
fair well. I hope there is someone to take up your Banner.

   Sincerely,
   "Sharinglimu"

Ask <panther_72117@...> wrote:
           Look, I certainly appreciate your loyalty.

I will not disparage anyone in this Company. I know them all to be
descent People. Have met all the Major Players Many times. Sometimes
even the best of men makes what others may believe to be an errot or
errors that makes it impossible to continue in a certain capacity.

You may have noticed that I did very little with this yahoo gtoup
over the last year. You might remember the No Hype Zone Ezine.

I could have had Hundreds or a couple thousand in this group.

Well, last Month, I decided that I was tired of the commodities
business and wanted to go ahead and push this site among others that
I was building to the limit. You may notice 4 signups this week. That
was just the beginning of what I was doing.

Anyway, What ever I do, I don't like doing it in a mediocre fashion.
I began to use video and audio and many ways to get to the top of
the search engines and to promote the product. Began, I said. The
process can take a few months to really do what you should. New tools
Like freeiq, that I believe will change the marketplace was also in
my plans and doings. All would come around to making the product most
visible.

I was Chairman of a Chronic illness foundation and still have the
urge to help others, so I am a member of many illness groups. These
groups you have to be very careful of their rules. I had done little
in them for a year.

I posted a link to the abcnews video about limu, in a certain group,
the head of that group is president to a world wide organization. My
usual manner is to answer any questions and began to point people to
the scientific studies, have them ask their doctors and go from there.

The head of this organization and other members never questioned me
about posting. That was not a concern. They all but accused me and
the Company of fraudulently faking the video.

Naturally I felt insulted and defended myself and the Company
vociferously. I said that nobody should pay attention to the things
that was being said by people on the site "ABOUT THE VIDEO" That I
understood, how there are people selling snake oil, but that this was
different and I was willing to direct anyone that think this might
benefit someone to the scientific studies.

From there, that head person stalked me around everywhere that I
could be found and made Silly statements and contacting entities that
I had to do with. NO BIG DEAL, People do things.

That head person, Started emailing long letters to the Company. They
tried dealing with that person and even thought it was over.

They thought if I apologised , it would go away. Then that person
started sending Complaints to DSA (Direct sellers Association and God
knows who else. This is a person that has testified before Congress,
supposedly. I was not impressed.

What bugged me to no end, is that I told the company that this person
had some vendetta going and suggested that cowing to the person would
not be enough.

I am leaving out some details because of the respect that I have for
many at the company.

Anyway, this became a big problem for the company. Gary likes to keep
everything squeaky clean, no complaints. But sometimes, I think you
cannot allow yourself to be pushed.

While working with the Company on this. Emailing all the dialog an
non dialog from this person and making it plain that I was putting up
new stuff and wanted to make sure all was well with Gary and the
compliance.

I was terminated. I believed it was all about this person.

The reason stated was "You were making medical claims."

My last conversation a week ago was that all was well, I was not
accused of that at that time. It was all about this person.

The page on my new site was evolving and I made sure to send a copy
of one ot this persons complaints about studies. Knowing,I thought
that if something was not acceptable, I would be told.

January 2006, when I ceased publishing the No Hype Zone, that was the
accusation. I was asked to stop and I did. Although, you who saw what
I published, know I showed studies and always told people to as their
doctors.

I made sure on the page to mention that no natural product, by US law
can claim to cure anything and told people to show the studies to
their doctor.

My question is how do you tell someone that they will benefit
healthwise and it not be a health claim? What about a medical claim?

I was told, that anytime you mention the name of a product and point
directly to a scientific study, you somehow insinuate that it is a
drug. It didn't matter that I was talking about Fucoidan and showing
real studies.

I think everyone here knows how meticulous, I have been in that
endeavor and defending the company from all attacks.

Shucks, when I began talking about Fucoidan, you could go to google
and type the word in and get about 2 results. Then there came a time
when I could see mostly my postings as results. Now of course, I
think you will get Hundreds of thousands of results and there are
companies coming out the wazzu.

I will be forever proud of the part I played in getting this info out
to the public. The Job isn't finished.

But I cannot promote a product in which I am not allowed to declare
it's benefits nor suggest the scientific for those benefits, all the
time directing people to their doctors.

I believe that under the circumstances just mentioned, the company
could say it's webpage is not compliant. Loyalty must go both ways.

Yes under these circunstances they had every right.

What bugs me the most, is an underlying feeling that this was a
bottom line decision. One where the leadership would rather toss one
overboard than to have to deal with a fanatic accuser.

That would be a shame. It would be totally unlike the people that I
used to know that "sold out" to make sure people and distributers
were treated fairly.

Be of good cheer,
Bill

--- In LIMU_MOUI@yahoogroups.com, "sharinglimu" <sharinglimu@...>
wrote:
>
> Bill,
> Please elaborate. I have been using Original Limu since back when it
> was RTL and following your posts for a couple of years. I'd like to
> know more about this. What happened?
>
>
>
>
>
> --- In LIMU_MOUI@yahoogroups.com, "Ask" <panther_72117@> wrote:
> >
> >
> > This will come as a suprise to many of you.
> >
> > I have been in contact with the leader of sales in the this
company.
> >
> > I have been terminated!
> >
> > I think you all can attest that there has been no one in the
company
> > that has taken more time to get it right than me.
> >
> > I had always, shown the science and let the Scientists speak for
> > themselves. I always told people to ask their doctors.
> >
> > I don't think that you can expect to promote a product without
telling
> > people the benefits so I will no longer try.
> >
> > I feel the same about the product as ever. I do not feel the same
about
> > the people running the Company.
> >
> > I will leave the site up a couple days, if anyone is interested in
> > becoming the moderator, let me know during that time.
> >
> > Wishing you the best
> >
> > Bill
> >
>






---------------------------------
Now that's room service! Choose from over 150,000 hotels
in 45,000 destinations on Yahoo! Travel to find your fit.

[Non-text portions of this message have been removed]

Look, I certainly appreciate your loyalty.

I will not disparage anyone in this Company. I know them all to be
descent People. Have met all the Major Players Many times. Sometimes
even the best of men makes what others may believe to be an errot or
errors that makes it impossible to continue in a certain capacity.

You may have noticed that I did very little with this yahoo gtoup
over the last year. You might remember the No Hype Zone Ezine.

I could have had Hundreds or a couple thousand in this group.

Well, last Month, I decided that I was tired of the commodities
business and wanted to go ahead and push this site among others that
I was building to the limit. You may notice 4 signups this week. That
was just the beginning of what I was doing.

Anyway, What ever I do, I don't like doing it in a mediocre fashion.
  I began to use video and audio and many ways to get to the top of
the search engines and to promote the product. Began, I said. The
process can take a few months to really do what you should. New tools
Like freeiq, that I believe will change the marketplace was also in
my plans and doings. All would come around to making the product most
visible.

I was Chairman of a Chronic illness foundation and still have the
urge to help others, so I am a member of many illness groups. These
groups you have to be very careful of their rules. I had done little
in them for a year.

I posted a link to the abcnews video about limu, in a certain group,
the head of that group is president to a world wide organization. My
usual manner is to answer any questions and began to point people to
the scientific studies, have them ask their doctors and go from there.

The head of this organization and other members never questioned me
about posting. That was not a concern. They all but accused me and
the Company of fraudulently faking the video.

Naturally I felt insulted and defended myself and the Company
vociferously. I said that nobody should pay attention to the things
that was being said by people on the site "ABOUT THE VIDEO" That I
understood, how there are people selling snake oil, but that this was
different and I was willing to direct anyone that think this might
benefit someone to the scientific studies.

From there, that head person stalked me around everywhere that I
could be found and made Silly statements and contacting entities that
I had to do with. NO BIG DEAL, People do things.

That head person, Started emailing long letters to the Company. They
tried dealing with that person and even thought it was over.

They thought if I apologised , it would go away. Then that person
started sending Complaints to DSA (Direct sellers Association and God
knows who else. This is a person that has testified before Congress,
supposedly. I was not impressed.

What bugged me to no end, is that I told the company that this person
had some vendetta going and suggested that cowing to the person would
not be enough.

I am leaving out some details because of the respect that I have for
many at the company.

Anyway, this became a big problem for the company. Gary likes to keep
everything squeaky clean, no complaints. But sometimes, I think you
cannot allow yourself to be pushed.

While working with the Company on this. Emailing all the dialog an
non dialog from this person and making it plain that I was putting up
new stuff and wanted to make sure all was well with Gary and the
compliance.

I was terminated. I believed it was all about this person.

The reason stated was "You were making medical claims."

My last conversation a week ago was that all was well, I was not
accused of that at that time.  It was all about this person.

The page on my new site was evolving and I made sure to send a copy
of one ot this persons complaints about studies. Knowing,I thought
that if something was not acceptable, I would be told.

January 2006, when I ceased publishing the No Hype Zone, that was the
accusation. I was asked to stop and I did. Although, you who saw what
I published, know I showed studies and always told people to as their
doctors.

I made sure on the page to mention that no natural product, by US law
can claim to cure anything and told people to show the studies to
their doctor.

My question is how do you tell someone that they will benefit
healthwise and it not be a health claim? What about a medical claim?

I was told, that anytime you mention the name of a product and point
directly to a scientific study, you somehow insinuate that it is a
drug. It didn't matter that I was talking about Fucoidan and showing
real studies.

I think everyone here knows how meticulous, I have been in that
endeavor and defending the company from all attacks.

Shucks, when I began talking about Fucoidan, you could go to google
and type the word in and get about 2 results. Then there came a time
when I could see mostly my postings as results. Now of course, I
think you will get Hundreds of thousands of results and there are
companies coming out the wazzu.

I will be forever proud of the part I played in getting this info out
to the public. The Job isn't finished.

But I cannot promote a product in which I am not allowed to declare
it's benefits nor suggest the scientific for those benefits, all the
time directing people to their doctors.

I believe that under the circumstances just mentioned, the company
could say it's webpage is not compliant. Loyalty must go both ways.

Yes under these circunstances they had every right.

What bugs me the most, is an underlying feeling that this was a
bottom line decision. One where the leadership would rather toss one
overboard than to have to deal with a fanatic accuser.

That would be a shame. It would be totally unlike the people that I
used to know that "sold out" to make sure people and distributers
were treated fairly.

Be of good cheer,
Bill








--- In LIMU_MOUI@yahoogroups.com, "sharinglimu" <sharinglimu@...>
wrote:
>
> Bill,
> Please elaborate. I have been using Original Limu since back when it
> was RTL and following your posts for a couple of years. I'd like to
> know more about this. What happened?
>
>
>
>
>
> --- In LIMU_MOUI@yahoogroups.com, "Ask" <panther_72117@> wrote:
> >
> >
> > This will come as a suprise to many of you.
> >
> > I have been in contact with the leader of sales in the  this
company.
> >
> > I have been terminated!
> >
> > I think you all can attest that there has been no one in the
company
> > that has taken more time to get it right than me.
> >
> > I had always, shown the science and let the Scientists speak for
> > themselves. I always told people to ask their doctors.
> >
> > I don't think that you can expect to promote a product without
telling
> > people the benefits so I will no longer try.
> >
> > I feel the same about the product as ever. I do not feel the same
about
> > the people running the Company.
> >
> > I will leave the site up a couple days, if anyone is interested in
> > becoming the moderator, let me know during that time.
> >
> > Wishing you the best
> >
> > Bill
> >
>

Bill,
Please elaborate. I have been using Original Limu since back when it
was RTL and following your posts for a couple of years. I'd like to
know more about this. What happened?





--- In LIMU_MOUI@yahoogroups.com, "Ask" <panther_72117@...> wrote:
>
>
> This will come as a suprise to many of you.
>
> I have been in contact with the leader of sales in the  this company.
>
> I have been terminated!
>
> I think you all can attest that there has been no one in the company
> that has taken more time to get it right than me.
>
> I had always, shown the science and let the Scientists speak for
> themselves. I always told people to ask their doctors.
>
> I don't think that you can expect to promote a product without telling
> people the benefits so I will no longer try.
>
> I feel the same about the product as ever. I do not feel the same about
> the people running the Company.
>
> I will leave the site up a couple days, if anyone is interested in
> becoming the moderator, let me know during that time.
>
> Wishing you the best
>
> Bill
>

This will come as a suprise to many of you.

I have been in contact with the leader of sales in the  this company.

I have been terminated!

I think you all can attest that there has been no one in the company
that has taken more time to get it right than me.

I had always, shown the science and let the Scientists speak for
themselves. I always told people to ask their doctors.

I don't think that you can expect to promote a product without telling
people the benefits so I will no longer try.

I feel the same about the product as ever. I do not feel the same about
the people running the Company.

I will leave the site up a couple days, if anyone is interested in
becoming the moderator, let me know during that time.

Wishing you the best

Bill

Experientia 1989 Oct 15;45(10):996-8 Related Articles, Books, LinkOut


Further characterization of sulfated homopolysaccharides as anti-HIV
agents.

Sugawara I, Itoh W, Kimura S, Mori S, Shimada K.

Department of Pathology, University of Tokyo, Japan.

Fucoidan and dextran sulfate showed anti-HIV activities against
mononuclear cells from AIDS patients, and they abrogated HIV reverse
transcriptase (RT) activity by interacting with the HIV envelope in the
membranes of target cells. Furthermore, they showed a synergistic effect
with  azidothymidine (AZT).

PMID: 2478388 [PubMed - indexed for MEDLINE




Phytomedicine 1999 Nov;6(5):335-40 Related Articles, Books, LinkOut


Antiviral properties of fucoidan fractions from Leathesia difformis.

Feldman SC, Reynaldi S, Stortz CA, Cerezo AS, Damont EB.

Departamento de Quimica Organica-CIHIDECAR, Facultad de Ciencias
Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria,
Argentina.

Three fractions of fucoidans isolated from the brown seaweed Leathesia
difformis (Ee, Ec and Ea) were found to be selective antiviral agents
against herpes simplex virus (HSV) types 1 and 2 and human
cytomegalovirus. Fraction Ea was the most active, with IC50 values in
the range  0.5-1.9 microg/ml without affecting cell viability at
concentrations up to  400 microg/ml. The antiherpetic activity of Ea was
assessed by three different methods, plaque reduction, inhibition of
virus yield and  prevention of HSV-2 induced shut-off of cell protein
synthesis, demonstrating  that the inhibitory effect was independent of
the antiviral assay and
the multiplicity of infection. The mode of action of Ea could be
ascribed to an inhibitory action on virus adsorption. The fucoidans did
not  inhibit the blood coagulation process even at concentrations
exceeding
more than 100 times the IC50 value.

PMID: 11962540 [PubMed - indexed for MEDLINE]




Gen Pharmacol 1997 Oct;29(4):497-511 Related Articles, Books, LinkOut


Sulfated polysaccharides extracted from sea algae as potential
antiviral drugs.

Witvrouw M, De Clercq E.

Rega institute for Medical Research, Katholieke Universiteit Leuven,
Belgium.

The inhibitory effects of polyanionic substances on the replication of
herpes simplex virus (HSV) and other viruses were reported almost four
decades ago. However, these observations did not generate much
interest, because the antiviral action of the compounds was considered
to be
largely nonspecific. Shortly after the identification of human
immunodeficiency virus (HIV) as the causative agent of the acquired
immune
deficiency syndrome (AIDS) in 1984, heparin and other sulfated
polysaccharides were found to be potent and selective inhibitors of
HIV-1 replication
in cell culture. Since 1988, the activity spectrum of the sulfated
polysaccharides has been shown to extend to various enveloped viruses,
including viruses that emerge as opportunistic pathogens (e.g., herpes
simplex virus [HSV] and cytomegalovirus [CMV]) in immunosuppressed
(e.g.,
AIDS) patients. As potential anti-HIV drug candidates, sulfated
polysaccharides offer a number of promising features. They are able to
block
HIV replication in cell culture at concentrations as low as 0.1 to 0.01
microgram ml-1 without toxicity to the host cells at concentrations up
to 2.5 mg ml-1. We noted that some polysulfates show a differential
inhibitory activity against different HIV strains, suggesting that
marked
differences exist in the target molecules with which polysulfates
interact. They not only inhibit the cytopathic effect of HIV, but also
prevent HIV-induced syncytium (giant cell) formation. Furthermore,
experiments carried out with dextran sulfate samples of increasing
molecular
weight and with sulfated cyclodextrins of different degrees of sulfation
have shown that antiviral activity increases with increasing molecular
weight and degree of sulfation. A sugar backbone is not strictly needed
for the anti-HIV activity of polysulfates because sulfated polymers
composed of a carbon-carbon backbone have also proved to be highly
efficient anti-HIV agents in vitro. Other, yet to be defined, structural
features may also play an important role. Sulfated polysaccharides may
act
synergistically with other anti-HIV drugs (e.g., azidothymidine [AZT]).
They are known to lead very slowly to virus-drug resistance development
and they show activity against HIV mutants that have become resistant
to reverse transcriptase inhibitors, such as AZT, tetrahydro-imidazo
[4,5,l-jk] [1,4]-benzodiazepin-2(1H)-thione (TIBO) and others. From
studies on their mechanism of action we concluded that polysulfates
exert
their anti-HIV activity by shielding off the positively charged sites in
the V3 loop of the viral envelope glycoprotein (gp120). The V3 loop is
necessary for virus attachment to cell surface heparan sulfate, a
primary binding site, before more specific binding occurs to the CD4
receptor of CD4+ cells. This general mechanism also explains the broad
antiviral activity of polysulfates against enveloped viruses. Variations
in
the viral envelope glycoprotein region may result in differences in the
susceptibility of different enveloped viruses to compounds that interact
with their envelope glycoproteins. The efficacy of polysulfates in the
therapy and/or prophylaxis of retroviral infections and opportunistic
infections remains to be demonstrated both in animal models and humans.
It is important to consider not only treatment of patients who are
already infected with HIV, but also prophylaxis and protection from HIV
and/or other virus infections. Because (i) sexual transmission is
responsible for the large majority of HIV infections worldwide; (ii)
this
transmission is mostly mediated via mononuclear cells that infect
epithelial cells of the genital tract; and because (iii) polysulfates
effectively inhibit cell-cell adhesion, polysulfates may be considered
as
potentially effective in a vaginal formulation to protect against HIV
infection.

Publication Types:
Review
Review, Tutorial

PMID: 9352294 [PubMed - indexed for MEDLINE]




Biomed Pharmacother 1996;50(5):207-15 Related Articles, Books, LinkOut



Chemotherapy of human immunodeficiency virus (HIV) infection: anti-HIV
agents targeted at early stages in the virus replicative cycle.

De Clercq E.

Rega Institute for Medical Research, Katholieke Universiteit Leuven,
Belgium.

Several compounds have been identified that inhibit an early stage in
the replicative cycle of the human immunodeficiency virus (HIV): i)
virus adsorption: polysulfates, polysulfonates, polycarboxylates,
polyphosphates, and polyoxometalates; or ii) virus-cell fusion: plant
lectins,
negatively charged albumins and betulinic acid derivatives; iii) virus
fusion/uncoating: bicyclam derivatives; iv) reverse transcription:
dideoxynucleoside analogues, acyclic nucleoside phosphonates and
non-nucleoside reverse transcriptase inhibitors. In principle, HIV may
develop
resistance to any of these specific anti-HIV agents. However, virus
breakthrough can be completely prevented if these agents, alone or in
combination, are added to the HIV-infected cells from the beginning at
sufficiently high ('knock-out') concentrations.

Publication Types:
Review
Review, Tutorial

PMID: 8949401 [PubMed - indexed for MEDLINE




[Non-text portions of this message have been removed]

Basic Neurochemistry  Part Five. Metabolism  33. Nutrition and Brain
Function

Nutrition and Functional Neurochemistry


The availability of some nutrients can have immediate effects on
behavior, especially on the ability to respond to stimulation. Several
studies suggest that brain function, including cognitive processing,
responds
to changes in nutrients.

Nutrition can influence neurotransmitter concentrations and associated
behaviors


Important neurotransmitters are synthesized from compounds which are
essential dietary constituents. For instance, norepinephrine (NE) and
serotonin are formed from the essential amino acids tyrosine and
tryptophan, respectively. However, elevation of a precursor in the blood
does
not necessarily elevate its concentration in the brain. For example,
increasing the blood concentration of large neutral amino acids such as
phenylalanine, as occurs in phenylketonuria (see Chap. 44), reduces
tryptophan uptake into the brain because these two compounds share a
common
carrier across the bloodbrain barrier (see Chap. 32). Furthermore, the
response to an increased concentration of precursor often depends on the
demand, such as firing frequency of the neurons. Enhanced precursor
availability may matter only when physiological demand is increased.

Choline for acetylcholine (ACh) synthesis can be obtained from either
brain choline, the phosphatidylcholine in the membranes or serum choline
(Table 33-1). It is taken up by a high-affinity choline-uptake system
at the synapse (see Chap. 11). Although choline can be made in the
body, its synthesis can be limited by the availability of
"single-carbon"
units in the diet. Ingestion of choline together with
phosphatidylcholine can increase brain choline and ACh concentrations
and enhance the
ability of ACh synthesis to increase upon demand. For example, increased
dietary choline permits the brain to make excess ACh following
stimulation with atropine. Dietary phosphatidylcholine simultaneously
increases
memory and the ACh content of the brains of "demented" mice, which
normally have reduced brain ACh concentrations [1]. Increasing choline
prenatally and postnatally improves the working and reference memory of
young rats.

Glucose normally provides the acetyl moiety of ACh. Extensive evidence
indicates that relatively modest increases in circulating glucose
concentrations can also increase ACh release and has been claimed to
enhance
learning and memory. The relative safety of glucose administration has
permitted tests of its effects on cognitive functions in humans.
Glucose enhances learning and memory in healthy aged humans and improves
several other cognitive functions in subjects with severe cognitive
pathologies, including individuals with Alzheimer's disease and Down's
syndrome. Thus, moderate increases in circulating glucose concentrations
may
have robust and broad influences on brain functions that span many
neural and behavioral measures and cross readily from rodents to humans.
Considerable evidence suggests that these effects are mediated via ACh.
Increasing glucose availability can increase the amount of ACh released
during conditions of increased demand [2] (Fig. 33-1) (see also Chaps.
11 and 31).

Tryptophan, like tyrosine, crosses the bloodbrain barrier predominantly
by the carrier system for long-chain neutral amino acids. As a result,
a protein-rich meal can actually increase blood tryptophan but reduce
the passage of tryptophan into the brain by elevating at the same time
the concentrations of other amino acids, such as phenylalanine, that
compete for that carrier. Serotonin (5-hydroxytryptamine, 5-HT)
synthesis
depends on brain tryptophan, which in turn depends on blood tryptophan
concentrations, which can be manipulated by varying the diet (Table
33-1). Elevating tryptophan in the brain produces physiologically
important changes in the serotonergic system (see Chap. 13). Animals
that are
poor in brain tryptophan have a heightened sensitivity to painful
stimuli that can be reversed with tryptophan ingestion, which rapidly
elevates brain serotonin. Therapeutically, tryptophan has been reported
to be
useful in treating subgroups of patients with depression,
sleeplessness or hyperactive behaviors.

Tyrosine is the precursor of NE and epinephrine (Table 33-1).
Increasing tyrosine reduces blood pressure in both normotensive and
hypertensive
animals. The action of tyrosine on blood pressure occurs via CNS
mechanisms since co-administering other large neutral amino acids that
reduce the uptake of tyrosine into the brain blocks the effect. The
antihypertensive action of tyrosine appears to be mediated by an
acceleration
in NE or epinephrine release within the CNS; injection of tyrosine
produces a concurrent increase in brain concentrations of
3-methoxy-4-hydroxyphenylethylglycol sulfate, a catecholamine metabolite
[3]. Tyrosine
induces increased NE and alters NE and a and b receptor densities in
hippocampus, providing further evidence of its physiological role.
Furthermore, dietary restriction to 40% of normal food intake diminishes
maze
performance, and this effect can be reversed by administration of
tyrosine.

Nutrition can influence brain energy reserve


Brain energy is more resistant to changes in fasting or overfeeding
than that in liver or muscle. For example, severe fasting decreases
liver
ATP concentrations and ATP: phosphocreatine ratios, while brain energy
metabolism is preserved. However, brain energy metabolism can be
manipulated by diet. A high-fat (90% of caloric value),
carbohydrate-free
ketogenic diet low in protein (10%) does not significantly alter
regional
brain glucose utilization or cerebral concentrations of glucose,
glycogen, lactate or citrate. However, a high-carbohydrate diet (78%)
low in
fat (12%) and low in protein (10%) markedly decreases brain glucose
utilization and increases cerebral concentrations of glucose
6-phosphate.
These findings indicate that long-term, moderate ketonemia does not
significantly alter brain glucose phosphorylation. However, even
marginal
protein dietary deficiency when coupled with a carbohydrate-rich diet
depresses cerebral glucose utilization to a degree often seen in
metabolic encephalopathies (see Chap. 38) [4].

Carnitine participates in mitochondrial reactions. Like choline, it can
be synthesized by mammals if dietary sources of one-carbon groups are
adequate. It participates in the transfer of acyl groups across
mitochondrial membranes (Chap. 42). These include acetyl groups for ACh
synthesis. Both carnitine and acetylcarnitine cross the bloodbrain
barrier
(BBB), but the more lipid-soluble acetyl-l-carnitine has been described
as having a variety of effects on the nervous system in experimental
animals not seen with carnitine.

Hereditary deficits in the ability to transport carnitine or to
synthesize its acyl derivatives have been associated with diseases of
skeletal
and cardiac muscle and, to a variable extent, with metabolic
encephalopathy (see Chap. 34). Secondary deficiency of carnitine has
been
described in a number of disorders of mitochondrial oxidation, due in
part to
the detoxification and urinary excretion of potentially damaging
short-chain acids as the carnitine derivatives [5]. The anticonvulsant
valproic acid can increase carnitine requirements in susceptible
individuals
[6]. Treatment with acetylcarnitine has been reported to slow the
progression of Alzheimer's disease [7].

Vitamins can regulate normal neuronal activity


Many vitamins function as cofactors in fundamental pathways, such as
glycolysis, the Krebs cycle, the respiratory chain and amino acid
metabolism. Although all tissues have these vitamin-dependent pathways,
they
take on increased importance in the brain because of its high metabolic
rate and dependence on continuous metabolism. In fact, the discovery of
vitamins was closely linked to the sensitivity of the brain to
deficiency, specifically that of thiamine [8]. Furthermore, in the brain
these
pathways are linked to neurotransmitter synthesis.

Vitamin B1 (thiamine) is critical to normal brain function. Thiamine
pyrophosphate (TPP) functions as a cofactor of key enzymes of the Krebs
cycle: the pyruvate and a-ketoglutarate dehydrogenase complexes (PDHC
and KGDHC, respectively), the branched-chain dehydrogenase complex
(BCDHC) and the pentose shunt enzyme transketolase (TK) (Table 33-2).
These
dehydrogenase complexes share a common enzyme component, lipoamide
dehydrogenase. TK rearranges sugars (see Chap. 31). A kinase can convert
a
membrane-bound form of TPP to thiamine triphosphate (TTP), and a
specific phosphatase hydrolyzes TTP to the diphosphate. TTP appears to
play a
role in nerve membrane function, notably in Na+ gating. The cDNAs for a
number of TPP-requiring enzymes have been obtained, and a TPP-binding
motif has been proposed that is partially conserved in yeast, rat and
human.

Thiamine deficiency is a classical and well-studied example of the
interaction of nutrition with brain function. Research on thiamine
deficiency continues to attract considerable interest. In developed
countries,
clinically significant thiamine deficiency is rare except as a
complication of severe alcoholism or other conditions that impair
nutrition
[9]. It is more common in developing countries in which polished rice is
the staple grain. It can be detected by measuring the "TPP effect," the
percentage increase in red cell TK activity upon addition of exogenous
TPP in vitro, and has been widely used in laboratory as well as in
epidemiological studies of thiamine deficiency.

After 5 to 6 days of a diet deficient in thiamine, healthy young men
developed a nonspecific syndrome of lassitude, irritability, muscle
cramps and electrocardiographic changes, which were reversed by dietary
thiamine.

Prolonged thiamine deficiency frequently leads to damage to peripheral
nerves (see Chap. 36). This neuropathy tends to be worse distally than
proximally, involves myelin more than axons and is often painful. The
neuropathy may be linked to deficiencies in multiple water-soluble
vitamins known for historical reasons as the vitamin B complex.

Wernicke-Korsakoff syndrome consists of an acute (Wernicke) phase and a
chronic (Korsakoff) phase [9]. The acute syndrome consists of
staggering gait, paralysis of eye movements and confusion, associated
with
small hemorrhages along the third and fourth ventricles and with reduced
cerebral metabolic rate as measured by cerebral blood flow. Injections
of
thiamine can be lifesaving, with clinical improvement often evident
within minutes. It is believed that prompt treatment with thiamine can
prevent the onset of the chronic Korsakoff phase. In Korsakoff's
syndrome, a striking loss of working memory accompanies relatively
little loss
of reference memory (see Chap. 50). Affected patients
characteristically make up stories, or confabulate, in response to
leading questions. In
this phase, patients do not respond to thiamine treatment. The
neuropathological lesions responsible for Korsakoff's syndrome have been
debated; severe damage to the cholinergic neurons of the nucleus basalis
complex has been reported.

Thiamine requirements can be altered genetically or environmentally.
Among genetic disorders, thiamine-dependent maple syrup urine disease is
due to a reduced affinity of BCDHC for TPP (see Chap. 44). A rare form
of lactate acidosis is due to reduced affinity of PDHC for TPP. Both
disorders respond to treatment with large doses of thiamine.
Wernicke-Korsakoff syndrome is associated with a variant form of TK
having a
decreased affinity for TPP [9]. This variation, which may be more common
in
chronic alcoholics, puts patients at risk when on a diet marginal or
deficient in thiamine. Subacute necrotizing encephalomyelopathy (SNE) of
Leigh is an uncommon, autosomal recessive disorder in which the
neuropathology resembles Wernicke-Korsakoff syndrome. Patients with SNE
in whom
a defect in PDHC has been documented at the cDNA level have been
described. The role of thiamine in this disorder is controversial.

Environmentally, a number of dietary constituents are known to impair
the absorption of thiamine, including ethanol. Severe illness or injury
also has been reported to increase thiamine requirements. Rarely,
patients have been found who are intolerant to very large doses of
thiamine.
Thiamine-dependent enzymes are reduced in the brains of patients with
a variety of neurodegenerative diseases, including Alzheimer's,
Huntington's and Parkinson's diseases.

Thiamine-deficient animals model many aspects of human thiamine
deficiency [10]. Experimentally, thiamine deficiency is frequently
induced by
the combination of a thiamine-deficient diet and a thiamine antagonist,
either pyrithiamine or oxythiamine. However, pyrithiamine can directly
inhibit action potentials and oxythiamine does not enter the brain
efficiently. In the pyrithiamine model in mice, abnormal
neuropsychological responses develop within 5 to 7 days, gross
neurological
abnormalities in 8 to 9 days and death usually by 10 to 11 days. Strain
significantly modifies the response to experimental thiamine deficiency
in mice
(Fig. 33-2). In rats, abnormalities of motor performance occur by day 3,
additional neurological symptoms by day 12 and death within 2 weeks.
Thiamine deficiency leads to a selective cell death that is accompanied
by accumulation of amyloid precursor protein in surrounding neurons. It
causes severe memory disruption and loss of cholinergic function. The
activities of thiamine-dependent enzymes decline in early stages of
thiamine deficiency, but surprisingly, selective cell death is not
related
to the cellular or regional distribution of thiamine-dependent enzymes
or to their response to thiamine deficiency. Instead, the general
reduction in thiamine-dependent enzymes predisposes particular brain
regions
to other insults. The earliest known change that reflects selective
vulnerability is an alteration in the BBB that is accompanied by
oxidative stress, which causes increased ferritin and iron deposition,
and
induction of nitric oxide synthase. The results suggest that
cerebrovascular endothelial cells of these brain regions may be
particularly
vulnerable to thiamine deficiency [10].

Vitamin B3 (niacin) deficiency in humans leads to pellagra, which is
characterized by dementia, dermatitis, diarrhea and eventually death.
The
deficiency was recognized in the eighteenth century, shortly after the
introduction of American corn (maize) into Europe [8].

Niacin and niacinamide refer to nicotinic acid and its amide,
respectively. Although these pyrimidine derivatives can be synthesized
from
tryptophan in mammals, perhaps at least in part by intestinal bacteria,
60
mg of dietary tryptophan are required to synthesize 1 mg of the
vitamin. Niacin is considered to be a vitamin because most human diets
do not
contain enough tryptophan to fulfill the normal human requirement for
the vitamin of 10 to 30 mg/day.

Hartnup's syndrome is a hereditary disorder in which tryptophan
transport is impaired and requirements for dietary niacin increase.
Phenylketonuria and hyperphenylalaninemia can increase niacin
requirements by
increasing the concentrations of amino acids that compete with
tryptophan
for transport systems (see also Chap. 44). A high-corn diet predisposes
to niacin deficiency since the major storage protein of American corn
(zein) has relatively little tryptophan relative to other amino acids
that compete for the same carrier. Addition of purified niacin to the
diet has largely abolished pellagra, which was once a common disease in
areas where corn was a dietary staple.

Niacin is incorporated into the coenzymes NAD+ and NADP+ and their
reduced forms. These cofactors are involved in numerous
oxidation/reduction
reactions, including the coupling of the Krebs cycle to the
respiratory chain. Antimetabolites, particularly 6-aminonicotinamide and
3-acetylpyridine, have been particularly useful in determining the role
of
niacin deficiency in the brain in experimental animals. Newborn mice
that
received a single intraperitoneal injection of 6-aminonicotinamide
consistently developed lesions in the CNS, the skin and the intestinal
tract. Anterior horn cells in the spinal cord as well as motor neurons
in
the brain exhibit the ultrastructural features of neuronal
chromatolysis,
while glial and ependymal cells show edematous changes.
3-Acetylpyridine administration leads to selective neuropathological
lesions in the
brainstem. Although the pathological features of antimetabolite-treated
mice are not identical to those of human pellagra, possible
contributory mechanisms in the development of pellagra lesions,
including dementia
and selective cell loss, may be elucidated with this experimental
model [11].

Vitamin B6 (pyridoxine) is necessary for the biosynthesis of several
neurotransmitters. It is a pyridine derivative that can exist as an
alcohol, amine or aldehyde. The concentration in brain is normally about
100-fold higher than that in the blood. The active coenzyme is the
phosphorylated derivative pyridoxal phosphate, which readily forms
Schiff
bases. This coenzyme participates in decarboxylation reactions,
including
those that form GABA from glutamate, 5-HT from 5-hydroxytryptophan and
probably DOPA from dihydroxyphenylalanine. It is also involved in
transaminations, including that converting a-ketoglutarate to glutamate.
The
conversion of tryptophan to nicotinamide requires pyridoxyl phosphate
as a cofactor, and the excretion of xanthurenic acid after a tryptophan
load is widely used to test the adequacy of pyridoxine nutriture. In
vitamin B6 deficiency in rats, biochemical and morphological
abnormalities, including decreased dendritic arborization and reduced
numbers of
myelinated axons and synapses, are associated with behavioral changes,
such as epileptiform seizures and movement disorders. Reduced seizure
threshold and delayed neuronal recovery are related to the significantly
reduced brain regional GABA and elevated glutamate concentrations in
pyridoxine-deficient rats [12]. In addition, vitamin B6 deficiency
during
gestation and lactation alters the function of N-methyl-d-aspartate
(NMDA) receptors.

Pyridoxine deficiency has occurred in human infants fed a formula from
which vitamin B6 had been inadvertantly omitted. The prominent finding
was intractable seizures which responded promptly to injections of the
vitamin. Deficiency of pyridoxine can contribute to the polyneuropathy
of B-complex deficiency. However, very large doses of pure pyridoxine
can lead to a persistant sensory neuropathy [13] (Chap. 36).

Like those of other nutrients, requirements for pyridoxine can be
altered by genetic or environmental factors and are increased in a
number of
disorders of the nervous system [8,14,15]. Treatment of
"pyridoxine-deficient" infants may require doses of pyridoxine several
hundredfold
the normal daily requirement. Maintenance with doses at least tenfold
the
normal requirement typically permits normal development if
irreversible brain damage has not yet occurred. It has been suggested
that mild
forms of pyridoxine dependence may be a relatively common cause of
intractable seizures and mental retardation, but neurochemical studies
of
these patients are limited. In homocystinuria and cystothioninuria, two
disorders of amino acid metabolism, some patients respond to large doses
of pyridoxine. In these patients, the mutations appear to reduce the
affinity of the relevant enzymes for pyridoxal phosphate (see Chap. 44).

Environmentally, hydrazides and oximes can increase pyridoxine
requirements. Large doses of pyridoxine are routinely given with the
antituberculous medication isonicotinic hydrazide, to prevent
drug-induced
neuropathy.

Vitamin B12 (cobalamin) deficiency is commonly associated with
neurological syndromes. The cobalamins are a series of porphyrin-like
compounds
[16]. The active forms contain a cobalt ion linked to one of the
methylene groups. The cobalamins are synthesized by many microorganisms
but
not by higher plants or animals. A rich dietary source is meat,
particularly liver. Effective absorption requires a series of transport
proteins, including a glycoprotein intrinsic factor secreted by gastric
parietal cells. Conversion to the active coenzymes adenosylcobalamin and
methylcobalamin requires at least two reductase reactions and an
adenosyltransferase step. The reductases are flavoproteins that require
NAD+ as
a cofactor. Thus, B12 metabolism involves at least three vitamins: B12
itself, niacin and riboflavin. Body stores of cobalamins are normally
large enough to maintain health for over 2 years without a dietary
source of the vitamin.

Cobalamins have two well-established biochemical functions.
Adenosylcobalamin is the cofactor for the mutase that converts
methylmalonyl CoA
to succinyl CoA. This reaction is part of the pathway of metabolism of
propionic acid, which itself derives from the metabolism of odd-chain
fatty acids and from certain amino acids. Methylcobalamin is the
cofactor
for the methyltransferase that converts homocysteine to the amino acid
methionine. This reaction is important in folate metabolism as well.
Its impairment appears to foster folate deficiency by an accumulation of
N5-methyltetrahydrofolate in a "folate trap." Deficiency of cobalamins
or of folate or of both can restrict the supply of metabolically
available one-carbon groups for metabolic pathways, including those of
nucleic acid synthesis.

Cobalamin deficiencies are relatively common clinically [16]. Pure
dietary deficiency responding promptly to treatment with oral cobalamins
has been described in a few children of strict vegan mothers. A more
common syndrome is caused by failure of absorption due to an inadequate
supply of the glycoprotein intrinsic factor, usually on an autoimmune
basis. The most characteristic abnormality is pernicious anemia,
characterized by enlarged erythrocytes, called megaloblasts, and
abnormal
leukocytes. Neurological symptoms occur in many of these patients and
can
precede the hematological changes [17].

Combined system disease is the most common B12-mediated neurological
syndrome. Affected patients develop unpleasant tingling sensations
(paresthesias), followed by loss of vibratory sensation, particularly in
the
legs, and spastic weakness. The characteristic neuropathology is a
spongy demyelination in the long tracts of the spinal cord, particularly
prominent in the posterior columns as well as corticospinal tracts.
Combined system disease responds poorly to treatment with cobalamins.

Cobalamin deficiency is characteristically associated with malaise that
does respond dramatically to treatment, even before the hematological
response is evident. Relatively low serum concentrations of B12 have
been reported in subgroups of psychiatric patients, including patients
with Alzheimer's disease, but responses to treatment with the vitamin
have, in general, not been dramatic. Recent studies indicate that
elevated
concentrations of serum or cerebrospinal fluid methylmalonate can
identify patients whose neuropsychiatric manifestations benefit from B12
treatment, even though the amounts of vitamin in serum are not in the
deficient range [17].

Whether the damage to the nervous system relates to decreased activity
of the methylmalonyl mutase or of the methyltransferase or of both
remains unsettled. Increased excretion of methylmalonate has been
reported
to be a marker for patients whose neuropsychiatric manifestations will
improve with B12 treatment, but clinically normal children with a
mutase deficiency are known. Children with homocystinuria and related
disorders do not develop the clinical or pathological stigmata of
combined
system disease (see Chap. 44). An infant with an apparent reduction in
methyltransferase activity was clinically normal when reported at age 1
year. Patients with severe inherited deficiencies in the activities of
both enzymes secondary to a defect in the metabolism of the cobalamins
do develop profound disease of the nervous system, with some
characteristics of combined system disease.

As with other nutrients, requirements for cobalamin can be modified by
genetic and environmental influences. Genetic factors apparently
predispose to intrinsic factor deficiencies with resultant cobalamin
deficiency. Furthermore, at least six different inherited methylmalonic
acidurias have been described [16]: absence of the mutase, decreased
affinity
of the mutase for adenosylcobalamin, deficiency of mitochondrial
cobalamin reductase, deficiency of a mitochondrial cobalamin
adenyltransferase and two distinguishable defects associated with
abnormal cytosolic
metabolism of cobalamin (see Chap. 44). Other conditions leading to
increased cobalamin requirements include surgical removal of the
stomach,
excessive destruction of cobalamins in the gut by bacteria in a blind
loop or destruction by certain kinds of intestinal tapeworm.

Folic acid contains a pterin moiety linked to para-aminobenzoic acid,
which is linked to one or more glutamate residues [18]. It plays a key
role in the transfer of one-carbon (active methylene) groups, including
the conversion of serine to glycine and the cobalamin-dependent
transfer from homocysteine to methionine. Dietary deficiency of folate
with
normal cobalamin leads to anemia without significant neurological signs.
However, both genetic and environmental disorders of folate metabolism
have been associated with disease of the nervous system. Genetic
defects in the relevant enzyme reactions are discussed further in
Chapter 44.

Genetic disorders of folate absorption, intraconversion and utilization
are rare [18]. They have occasionally been associated with phenocopies
of well-known psychiatric syndromes. A boy with apparent deficiency of
hepatic dihydrofolate reductase was treated with folate and developed
a sociopathic personality in his teens. A folate-responsive form of
mental retardation with catatonia has been described in an adolescent
girl
with N5,10-methylenetetrahydrofolic acid reductase deficiency. Her
younger sister was mentally impaired with "psychosis"; an unrelated boy
with a defect of the same enzyme had seizures and proximal muscle
weakness without notable psychiatric problems. Most patients with
glutamate
formiminotransferase deficiency have had a syndrome of psychomotor
retardation in infancy, but a few have been entirely normal clinically.

Environmentally, a number of common medications, including phenytoin
and certain antitumor agents, increase requirements for dietary folate.
Treatment with folate can mask the hematological signs of cobalamin
deficiency without affecting the progressive damage to the nervous
system.

Pantothenic acid is a substituted hydroxybutyric acid that is a
constituent of CoA [19]. Experimental induction of pantothenic acid
deficiency
leads to signs of peripheral nerve damage, for example, demyelination
in laboratory animals and paresthesias in humans. Late signs of CNS
damage in animals may relate as well to the adrenal failure that is a
prominent part of the syndrome.

The brain depends on select vitamins and closely related compounds as
antioxidants to control potentially damaging free radicals


The main antioxidants in brain are vitamin E (tocopherol), vitamin C
(ascorbic acid) and glutathione (Table 33-2). The first two can be
easily
manipulated by diet, whereas the latter is more difficult to control.
Dietary a-lipoate appears to be a useful compound to regenerate the
antioxidant capacity of these other compounds (see below). Dietary
manipulation of antioxidants has practical implications for brain
function.
Aging has been associated with free radical damage in the brain (see
Chap. 34). In aged patients tested over a 22-year period, free recall,
recognition and vocabulary correlated positively with ascorbic acid and
b-carotene in blood, even after controlling for possible confounding
variables, such as age, education and gender. These results indicate the
important role played by antioxidants in brain aging and may have
implications for prevention of progressive cognitive impairments [20].

Vitamin E (a-tocopherol) deficiency produces a characteristic
neurological syndrome. It presumably results from increased oxidative
stress
arising from a reduction in antioxidant capacity. Vitamin E deficiency
in
neural tissues increases endogenous lipid peroxidation, as evidenced in
brain tissues by the appearance of thiobarbituric acid-reactive
substances such as malondialdehyde. The brain is more susceptible to the
deficiency than muscle. Within the brain, the cortex, striatum and
cerebellum are the most sensitive regions. Isolated fractions from
myelinated
nerve tracts show that the axoplasmic membranes and organelles are
particularly vulnerable to oxidative stress [21]. Vitamin E deficiency
reduces tyrosine hydroxylase-immunopositive neurons in the substantia
nigra
but not in the adjacent ventral tegmental area. The enhanced
sensitivity of the nigrostriatal pathway to oxidative stress could have
important
implications for the pathogenesis of Parkinson's disease (see Chap.
45). A diet deficient in vitamin E increases glutamate and GABA and
decreases tryptophan concentrations in the substantia nigra. The
increase of
nigral glutamate suggests possible links to degenerative processes
through glutamatergic excitotoxicity. These results suggest that vitamin
E
may play a significant role in the degeneration of the substantia
nigra and that this tissue may be particularly sensitive to oxidative
stress. Furthermore, these findings support the widely held view that
oxidative stress in the substantia nigra is important in the
pathophysiology
of Parkinson's disease.

Vitamin C (ascorbate) deficiency leads to extensive oxidative damage of
proteins and protein loss in the microsomes, as evidenced by
accumulation of carbonyl groups on proteins as well as tryptophan loss.
This
oxidative damage is reversed by ascorbate therapy. Ascorbate deficiency
also leads to lipid peroxidation in microsomes, as evidenced by
accumulation of conjugated dienes, malondialdehyde and fluorescent
pigment.
Lipid peroxides disappear after ascorbate therapy but not after
treatment
with vitamin E. These results indicate that vitamin C may exert a
powerful protection against degenerative changes in the brain associated
with
oxidative damage [22].

Oxidation of vitamin E and C is maintained by glutathione, the
predominant thiol antioxidant in the brain. Glutathione cannot be
directly
manipulated by diet, whereas the metabolic antioxidant a-lipoate can be
absorbed from the diet and cross the BBB to reduce oxidized glutathione
and vitamins A and C (Fig. 33-3). a-Lipoate is taken up and reduced in
cells and tissues to dihydrolipoate, which is also exported to the
extracellular space; hence, protection is afforded to both intracellular
and
extracellular environments. Both a-lipoate and dihydrolipoate are
potent antioxidants that regenerate other antioxidants, like vitamins C
and
E, and raise intracellular glutathione concentrations. Protective
effects by antioxidants have been reported in cerebral
ischemiareperfusion,
excitotoxic amino acid brain injury, mitochondrial dysfunction,
diabetes and diabetic neuropathy, inborn errors of metabolism and other
causes
of acute or chronic damage to the brain or neural tissue. Thus,
a-lipoate administration may prove to be an effective treatment in
numerous
neurodegenerative disorders [20].

Trace nutrients in the diet have a vital role in maintaining normal
brain function


Zinc (Zn2+) influences numerous cellular functions, including immune
mechanisms, actions of several hormones and enzyme activities. More than
200 enzymes are known to be Zn2+-dependent, including mRNA-editing
enzymes, superoxide dismutase, metalloproteins and a "Zn2+-finger"
family
of sequence-specific DNA-binding proteins that regulate transcription.
Metallothionein binds excess Zn2+, thus maintaining its steady-state
concentration and preventing inhibition of an extensive number of
sulfhydryl-containing enzymes and receptor sites; hence, it protects
against
metal-related neurotoxicity. Metallothionein donates Zn2+ to an
extensive
number of Zn2+-activated, pyridoxal phosphate-mediated biochemical
reactions. The complex nature of the interactions of Zn2+ with multiple
enzymes is exemplified by the observation that epileptic seizures that
are blocked by GABA can be blocked by either deficiency or excess of
either Zn2+ or pyridoxal phosphate. A proposed explanation of these
observations is that at physiological concentrations Zn2+ stimulates the
activity of hippocampal pyridoxal kinase, enhancing the formation of
pyridoxal phosphate and of GABA via glutamate decarboxylase formation,
whereas
at higher doses Zn2+ inhibits the activity of glutamate decarboxylase
by preventing the binding of pyridoxal phosphate [23]. Severe Zn2+
deficiency during the period of rapid brain growth has effects similar
to
that seen with protein-calorie malnourishment, including altered
regulation of emotions; food motivation; lethargy (reduced activity and
responsiveness), and deficits in learning, attention and memory. In
addition
to the many deficits produced by Zn2+ deficiency in the brain, the
severe effect of Zn2+ deficiency on other tissues leads to additional
peripheral mechanisms that alter brain function [24]. Although Zn2+ is
essential at low concentrations, higher concentrations are toxic. For
example, high Zn2+ concentrations enhance and prolong the firing rate of
neurons, significantly depress paired-pulse potentiation, block the
action
of NMDA on cortical neurons, enhance quisqualate receptor-mediated
injury and inhibit the Ca2+-dependent release of transmitter by
inhibiting
the entry of Ca2+ into nerve terminals.

Copper is an integral component of multiple cellular enzymes, including
the cytochromes and superoxide dismutase. Copper deficiency produces
clinical signs analogous to those of Par-kinson's disease and results in
low dopamine concentration in the corpus striatum. Neuropathology in
experimental animals occurs in only part of the copper-deficient
population and is dam- and litter-related, suggesting the presence of a
genetic component that alters the response to copper deficiency. Insight
into
the role of copper in brain function is provided by two genetic
diseases.

Wilson's disease is an inherited disorder that leads to copper
accumulation, causing damage primarily to the liver and the brain (see
Box
45-1). Psychiatric and behavioral abnormalities occur in 30 to 100% of
Wilson's disease patients and are often the initial symptoms. The most
common of the psychiatric and behavioral manifestations include
personality
changes, such as irritability and low anger threshold; depression,
sometimes leading to suicidal ideation and attempts; and deteriorating
academic and work performance, which is present in almost all
neurologically affected patients [25].

Menke's disease is caused by a genetic deficiency of serum copper and
of copper-dependent enzymes and is characterized by neurological
degeneration and mental retardation, connective tissue and vascular
defects,
brittle and depigmented hair and death in early childhood (see Box
45-1). Despite excessive accumulation of the metal in various tissues, a
functional copper deficiency is evident, caused by a defective
intracellular copper-transport protein. A large amount of copper
accumulates in
the organelle-free cytoplasm, whereas mitochondria are in a state of
copper deficiency, indicating that the Menke's mutation probably affects
copper transport from the cytosol to the intracellular organelles [26].
Brindled is a murine mutation that produces similar copper-transport
deficits, and studies of this animal model show that the copper deficit
in
organelles causes reductions in critical copper-dependent enzymes,
such as cytochrome oxidase. It has been hypothesized that the Wilson's
disease gene is a copper-transporting ATPase with homology to the
Menke's
disease gene. Dietary copper deficiency can affect brain development
[27] (see below).

Selenium is vital in maintaining the antioxidant capacity of the brain.
Glutathione peroxidase is a selenium-dependent enzyme that is
important for maintaining the antioxidant capacity of brain glutathione
(Fig.
33-2) and is reduced in selenium-deficient animals. Selenium
supplementation significantly elevates Na,K-ATPase activity and
significantly
decreases lipid peroxide formation. Since Na,K-ATPase activity is known
to
be inhibited by oxygen free radicals, selenium supplementation appears
to exert its beneficial effect on the Na,K-ATPase activity by
preventing free radical-induced damage. Selenium significantly reduces
the
production of thiobarbituric acid-reactive substances, a measure of
lipid
peroxidation, in response to an oxidative challenge in blood and
different regions of the brain [28]. Selenium deficiency increases
dopamine
turnover in the substantia nigra but not in the striatum. These results
suggest that dietary selenium protects the brain, particularly the
substantia nigra, against oxidative damage.

Trace compounds are also important in brain function.
Chromium-deficient patients develop severe diabetic symptoms, including
glucose
intolerance, weight loss, impaired energy utilization and nerve and
brain
disorders. Low dietary boron is reported to cause significantly poorer
performance on various cognitive and psychomotor tasks. Additional
research
is likely to reveal additional trace components of the diet that may be
critical to normal brain function.



(c) 1999 by American Society for Neurochemistry
Published by Lippincott Williams and Wilkins.



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weeks later, the last week in April, I began to notice that my pain was almost
gone. Consequently, I stopped taking all pain medication, except one 50 mg
tablet of Ultram at bedtime. Even though physical therapy is still painful, I
find that my pain subsides about 30 minutes after taking Limu Moui.
Robert W., Springfield, MO

I was plagued with year round sinus related problems, including infection,
bronchitis and laryngitis, especially in the spring and fall. This would deplete
my energy and wellness and cause me to miss work as a sign language interpreter,
causing hardship on my colleagues and deaf students, who depended on me. For
years, I tried medications, nasal sprays and herbal remedies. Within 3 days of
using Limu Moui, I was able to breathe freely and now take no medication.
Vicki W., Springfield, MO

J Cosmet Sci 2002 Jan-Feb;53(1):1-9 Related Articles, Books, LinkOut


Treatment of human skin with an extract of Fucus vesiculosus changes its
thickness and mechanical properties.

Fujimura T, Tsukahara K, Moriwaki S, Kitahara T, Sano T, Takema Y.

Biological Science Laboratories, Kao Corporation, 2606 Akabane, Ichikai-machi,
Haga-gun, Tochigi 321-3497, Japan.

Recently the researchers found that an extract of Fucus vesiculosus, which is a
type of seaweed, promotes the contraction of fibroblast-populated collagen gels
through increased expression of integrin molecules. In this study, they
investigated the effects of topical application of an aqueous extract of this
alga on the thickness and the mechanical properties of human skin. A gel
formulation that included 1% of the extract was applied topically to human cheek
skin twice daily for five weeks. A significant decrease in skin thickness
measured by B-mode ultrasound was elicited, as was a significant improvement in
elasticity measured with a Cutometer as compared with controls. In cheek skin,
the thickness normally increases and the elasticity usually decreases with age.
These results suggest that the Fucus vesiculosus extract possesses anti-aging
activities and should be useful for a variety of cosmetics.

Publication Types:
Clinical Trial
Controlled Clinical Trial

PMID: 11917251 [PubMed - indexed for MEDLINE]



1: Biol Pharm Bull 2000 Oct;23(10):1180-4 Related Articles, Books, LinkOut


Fucoidan is the active component of fucus vesiculosus that promotes contraction
of fibroblast-populated collagen gels.

Fujimura T, Shibuya Y, Moriwaki S, Tsukahara K, Kitahara T, Sano T, Nishizawa Y,
Takema Y.

Biological Science Laboratories, Kao Corporation, Haga, Tochigi, Japan.
301620@...

The fibroblast-populated collagen gel culture method has been evaluated as a
dermal model of wound contraction and granulation in tissues during the wound
healing process and as an in vitro model of dermal tissue. We previously
reported that an extract of Fucus vesiculosus promoted fibroblast-populated
collagen gel contraction and that the promotion of the gel contraction was due
to the increased expression of integrin alpha2beta1 on the surface of the
fibroblasts. In this study, we investigated the active component of the extract
of this alga using extraction and fractionation techniques. Water extraction of
the alga was followed by precipitation with excess ethanol and then gel
filtration with the boundary molecular weight of 30,000. The high molecular
weight fraction obtained from gel filtration was fractionated by ion exchange
chromatography on diethylaminoethyl cellulose column to give active fractions
that have more polar properties. These polar, high molecular weight fractions
which contained molecules with fucose and sulfate groups showed significant gel
contraction-promoting activity and integrin expression-enhancing activity, and
were estimated to be the sulfated-polysaccharide fucoidan. Commercially
available fucoidan showed similar activities to the above-described fraction of
this alga. Although it remains necessary to precisely identify the specific
active component, the above results indicate that fucoidan is the active
component which promotes collagen gel contraction, and also indicate the
possibility that it dose so by enhancing the integrin alpha2beta1 expression.

PMID: 11041247 [PubMed - indexed for MEDLINE]

J Nutr Sci Vitaminol (Tokyo) 1999 Jun;45(3):325-36 Related Articles, Books,
LinkOut


Inhibitory effect of Cladosiphon fucoidan on the adhesion of Helicobacter pylori
to human gastric cells.

Shibata H, KimuraTakagi I, Nagaoka M, Hashimoto S, Sawada H, Ueyama S, Yokokura
T.

Yakult Central Institute for Microbiological Research, Tokyo, Japan.

We studied the inhibitory effect of Cladosiphon fucoidan on the attachment of
Helicobacter pylori (H. pylori), a gastroduodenal pathogen, to human gastric
cell lines. The bacterial binding in these cell lines was inhibited more by
Cladosiphon fucoidan (IC50 = 16-30 mg/mL), than by the fucoidan from Fucus (IC50
> 30 mg/mL). Dextran sulfate, another sulfated polysaccharide, did not inhibit
the binding at all. Pre-incubating the bacterial suspension with fucoidans
reinforced the inhibitory ability of these components, and reduced the IC50
value of Cladosiphon fucoidan to approximately 1 mg/mL. However, the binding was
not inhibited by pre-treatment of gastric cells with these components. It was
also shown that this fucoidan blocks both Leb- and sulfatide-mediated attachment
of H. pylori to gastric cells. Furthermore, fucoidan-binding proteins were found
on the H. pylori cell surface by Western blot analysis. Thus, the inhibitory
effect exerted by Cladosiphon fucoidan on binding between H. pylori and gastric
cells might result from the coating with this component of the bacterial
surface.

PMID: 10524351 [PubMed - indexed for MEDLINE]



Biomed Mater Eng 2001;11(1):55-61 Related Articles, Books, LinkOut


Effect of oligofucose derivatives on acetic acid-induced gastric ulcer in rats.

Shibata H, Nagaoka M, Takagi IK, Hashimoto S, Aiyama R, Yokokura T.

Yakult Central Institute for Microbiological Research, Kunitachi, Tokyo, Japan.
hideyuki-shibata@...

This study attempted to enhance the anti-ulcer activity of fucoidan from
Cladosiphon okamuranus TOKIDA by chemical modification with a hydrophobic group.
The suitable number of fucose residues in the effective compound was also
clarified to obtain a compound of constant quality. Degraded fucoidans were
coupled with several hydrophobic groups via Schiff bases, and their anti-ulcer
activities were determined by acetic acid-induced ulcer models in rats.
Size-fractionated oligofucose was also modified and assayed for anti-ulcer
activity. Among the modified oligofucoses, only the oligofucose-dodecylaniline
combination (OFDA) significantly promoted ulcer healing. The effective dose was
0.2 mg/kg/d. The most suitable number of fucose residues in the compound for the
anti-ulcer activity was determined to be around 12. We succeeded in enhancing
the anti-ulcer activity of Cladosiphon fucoidan by modification with
dodecylaniline. The activity of this compound was comparable or greater than
that of typical anti-ulcer agents. By determination of the optimal OF chain
length for the anti-ulcer activity of OFDA, it became possible to obtain OFDA of
constant quality.

PMID: 11281579 [PubMed - indexed for MEDLINE]

Ann Plast Surg 2001 Nov;47(5):540-6 Related Articles, Books, LinkOut


Protective effect of fucoidin (a neutrophil rolling inhibitor) on ischemia
reperfusion injury: experimental study in rat epigastric island flaps.

Cetin C, Kose AA, Aral E, Colak O, Ercel C, Karabagli Y, Alatas O, Eker A.

Department of Plastic & Reconstructive Surgery, Osmangazi University Medical
Faculty, Eskisehir, Turkey.

The objective of this study was to examine whether a decrease in
neutrophil-mediated tissue injury using Fucoidin, a nontoxic neutrophil rolling
inhibitor, would improve flap survival in an island flap model after
ischemia-reperfusion. Myeloperoxidase activity (an indirect index of tissue
neutrophil count) and malondialdehyde (an indicator of lipid peroxidation), the
degree of neutrophil infiltration by direct counting, and macroscopic flap
survival were assessed in the flap after arterial ischemia-reperfusion.
Epigastric island skin flaps were elevated in 56 rats. The first group of 21
rats was subjected to 6 hours of arterial ischemia. The second group of 21 rats
was subjected to 10 hours of arterial ischemia, and the rest of the rats were
used as nonischemic controls (sham flaps). For inhibiting neutrophil rolling, a
nontoxic polysaccharide agent-Fucoidin-was used. Each ischemic group was divided
further into three subgroups: Subgroup I (control rats) received saline,
subgroup II received 10 mg per kilogram Fucoidin, and subgroup III received 25
mg per kilogram Fucoidin before reperfusion. The results were evaluated as
tissue neutrophil counts, tissue malondialdehyde content, tissue myeloperoxidase
activity, and flap survival. Neutrophil counts and tissue myeloperoxidase
activity were decreased significantly (p <0.001) in subgroup III, but lipid
peroxidation by means of tissue malondialdehyde content was not affected by
Fucoidin administration. The authors conclude that administration of Fucoidin
before reperfusion can limit tissue injury apparently by inhibiting neutrophil
rolling in a dose-dependent manner.

PMID: 11716267 [PubMed - indexed for MEDLINE]

Immunological analysis of inhibition of lung metastases by fucoidan (GIV-A)
prepared from brown seaweed Sargassum thunbergii.

Itoh H, Noda H, Amano H, Ito H.

Laboratory of Marine Biochemistry, Faculty of Bioresources, Mie University, Tsu,
Japan.

The antimetastatic effect of GIV-A (fucoidan) and/or 5-FU was examined in an
experimental model of lung metastases induced by Lewis lung carcinoma in mice.
Injection of GIV-A i.p. after removal of the implanted primary tumor inhibited
the development of lung metastases. Combination treatment with GIV-A and 5-FU
inhibited significantly the lung metastases. The number of peritoneal
macrophages, total cells and macrophages in the lung increased in mice treated
with GIV-A. Binding of the third component of complement (C3) cleavage products
(C3b) to the C3 receptor on peritoneal macrophages after i.v. injection of GIV-A
was enhanced, as shown by the fluorescent antibody technique. Lung metastases
were inhibited by i.v. injection of peritoneal macrophages activated with GIV-A.
GIV-A depressed aniline hydroxylase and aminopyrine demethylase activities of
the hepatic microsomal drug-metabolizing system in tumor-bearing mice. Moreover,
the concentration of 5-FU in the tissues (lung, liver, kidney, spleen and blood)
was increased significantly by coadministration of GIV-A. The picryl
chloride-induced delayed type hypersensitivity (PC-DTH) response in mice was
depressed after the implantation of tumor and treatment with 5-FU. GIV-A
restored the suppression of PC-DTH by 5-FU, but did not increase the PC-DTH of
normal mice. GIV-A not only enhanced the degree of spleen cell-mediated sheep
red blood cell (SRBC) hemolysis (quantitative hemolysis of SRBC), the indexes of
the spleen and thymus and the number of spleen cells, but also restored the
suppressive effect of 5-FU. In the group receiving GIV-A, the percentages of
splenic Thy1.2-, L3T4- and asialo GM1-positive cells were significantly
increased as compared with the tumor-bearing mice treated with saline.
Furthermore, the L3T4+/Lyt2+ ratio showed a tendency to increase, and the
Lyt2+/Thy1.2+ ratio was decreased. These results suggest that the antitumor
effect of GIV-A may be correlated with the changing pattern of the Thy1.2-,
L3T4- and asialo GM1-positive cells, C3 activation, macrophage activation and
depression of the hepatic microsomal drug-metabolizing system. These findings
raise the possibility that GIV-A may have clinical value in the prevention of
cancer metastasis.

PMID: 8572581 [PubMed - indexed for MEDLINE]


  Anticancer Res 1996 May-Jun;16(3A):1213-8 Related Articles, Books, LinkOut


Antitumor and antiproliferative effects of a fucan extracted from ascophyllum
nodosum against a non-small-cell bronchopulmonary carcinoma line.

Riou D, Colliec-Jouault S, Pinczon du Sel D, Bosch S, Siavoshian S, Le Bert V,
Tomasoni C, Sinquin C, Durand P, Roussakis C.

ISOMer (Institut des Substances et Organismes de la Mer), SMAB, Laboratoire de
Pharmacologie Marine, Faculte de Pharmacie, Nantes, France.

Fucans, sulfated polysaccharides extracted from brown seaweeds, have been shown
to be endowed with inhibitory effects cell growth in various experimental
models. We studied both the antiproliferative and antitumor properties of a
fucoidan extract (HF) obtained from the brown seaweed Ascophyllum nodosum on a
cell line derived from a non-small-cell human bronchopulmonary carcinoma
(NSCLC-N6), this type of carcinoma is particularly chemo-resistant. HF exerts in
vitro a reversible antiproliferative activity with a block observed in the G1
phase the cell cycle. Studies performed with the NSCLC-bearing nude mice show
antitumor activity at subtoxic doses. These preliminary results indicate that HF
exhibits inhibitory effect both in vitro and in vivo and is very potent
antitumor agent in cancer therapy.

PMID: 8702239 [PubMed - indexed for MEDLINE]

J Ethnopharmacol 1989 Nov;27(1-2):35-43
Hypoglycemic activity of several seaweed extracts.
Lamela M, Anca J, Villar R, Otero J, Calleja JM
Departamento de Farmacologia, Farmacia y Tecnologia Farmaceutica, Facultad de
Farmacia, Universidad de Santiago de Compostela, Spain.

The hypoglycemic activity of several seaweed extracts on rabbits was studied.
Ethanol extracts of Laminaria ochroleuca, Saccorhiza polyschides and Fucus
vesiculosus were administered orally to normal animals and their effects on
glycemia and triglyceridemia evaluated. Crude polysaccharides and protein
solutions from Himanthalia elongata and Codium tomentosum were also assayed.
Polysaccharides and proteins from H. elongata caused a significant reduction in
blood glucose 8 h after intravenous administration. A case of 5 mg/kg of crude
polysaccharide lowered glycemia about 18% in normal rabbits and by about 50% in
alloxan-diabetic animals, while the protein solution lowered glycemia in
diabetic rabbits by about 30%.

PMID: 2615424, UI: 90135222