Publisher's Commentary 
by Will Block 

How N-Acetyl D-Glucosamine Helped Me
Products containing glucosamine are of special interest to me because of my own personal needs. I was among the first of the Baby Boomers so I have been exposed a little longer to the ravages of aging, an overhanging threat to my continued good health, vitality . . . and creativity. When my ability to run, as a form of exercise, was menaced by excruciating ankle pain a few years ago, I looked frantically for a solution. I found the answer in glucosamine. I started taking the sulfate form and found substantial relief, which enabled me to return to running provided that I did not push myself too hard. Yet after six months of supplementation, I was still not my old (meaning young) self and my ankles continued to trouble me. Then, on a recommendation, I started taking a different form of glucosamine, N-acetyl D-glucosamine (NAG), and immediately, the difference was like night and day. My ankles felt like new and I could run with the kind of energy that I had known before. Like a young colt, I found myself "kicking up my heels."

However, when I started to research the advantages of NAG, it was hard going. Not only were most of the studies done with glucosamine sulfate, there were no osteoarthritis studies performed with NAG. However, I did find that NAG is clearly important in the production of hyaluronic acid, a key component of synovial fluid. Yet, believing that scientific evidence is important, I resumed taking glucosamine sulfate, but again the difference was dramatic: I couldn't kick up my heels. Was there something unusual about me, I wondered? So, I resumed NAG and at every opportunity I encouraged friends and acquaintances to try NAG instead of glucosamine sulfate. Guess what? Everyone liked the NAG better. Yet why was there no literature on NAG?

Much of the research on glucosamine has been done in Germany where the manufacturing of glucosamine sulfate has been dominated by German industry. Hmmmm. My guess is that an "old boy" network has been discouraging competition.

More positive data on NAG has been coming. Recently, researchers found that when patients with osteoarthritis were treated with chondroitin 4,6 sulfate, their levels and quality of hyaluronic acid increased. However, they had lower levels of NAG excretion.1 (Hyaluronic is a principal component of synovial fluid, which is the lubricant of joints.) As a study on rheumatoid arthritis has found, excretion of NAG increased when patients exercised their inflamed rheumatoid joints.2  NAG supplementation improves the quality of synovial fluid and protects against free radical damage.

I believe that the best such product of its kind on the market is one which helps inhibit the enzymatic breakdown of articular cartilage while stimulating the building processes in cartilage. Glucosamine and chondroitin supplementation achieves this by providing potent nutritional and energy substrates for formation of healthy cartilage cells. By helping to restore proper joint function, glucosamine and chondroitin supplementation demonstrates significant chondro-protective and chondro-restorative properties. That's significant!

Chondroitin for Mad Cow
A recent Spanish study has found that chondroitin sulfate can actually help protect against mad cow disease.3 To date, the mechanisms of mad cow disease have not been elucidated and remain an enigma. However, undesirable deposits formed by the prion proteins responsible for transmission of mad cow disease have been shown to be directly neurotoxic. Chondroitin sulfate appears to be able to prevent the prion proteins from forming these deposits. It is interesting to note that some chondroitin is extracted from cow trachea (the windpipe).

DHEA for Impotency
The hormone dehydroepiandrosterone (DHEA) is showing promise as a new alternative for the treatment of erectile dysfunction (impotency).4 When Dr Werner Reiter and associates at the University of Vienna gave 40 patients with erectile dysfunction 50 mg of DHEA daily for 6 months the results were impressive. After just eight weeks of use, maintaining an erection was significantly easier according to Dr Reiter. No adverse effects were reported and the authors of the study concluded that oral DHEA treatment may benefit men with impotency. Since DHEA is of benefit for many of the "slings and arrows" of aging, it is no wonder that the scientists got it straight.

Many Diseases Associated with H. Pylori
H. pylori has been found to be associated with seemingly very diverse diseases. Remember however that, until recently, this devious microbe was not thought to be connected to ulcers and now it is universally accepted as a necessary precondition for most peptic ulcers, duodenal ulcers and a number of carcinomas of the stomach as well.

While the role of H. pylori in other gastroduodenal diseases like atrophic gastritis and functional dyspepsia has been the subject of considerable investigation in the literature, little has been done about its role in non-gastric diseases.5 Some coronary heart disease studies have shown a connection to the H. pylori bacteria. Then there's cirrhosis of the liver, which is possibly correlated. To date, respiratory diseases have not been looked into but some data shows that bronchiectasis is another suspicion. Even sudden infant death is suspected to be associated with H. pylori. One study showed a high rate of H. pylori infection in young children who had died in their sleep. To top off all of the connections, diabetes, a metabolic disease mimicking many of the symptoms of aging, is also thought to be H. pylori associated.

Diabetes and H. Pylori
How could diabetes be connected to H. pylori? First, diabetics are reported to have a high prevalence of upper gastrointestinal symptoms. This problem has traditionally been thought to be attributed to abnormal emptying of the stomach. In a kind of chicken-or-the-egg logic, one study found that dyspeptic patients with adult-onset diabetes (AOD) have been observed to have a higher prevalence of H. pylori infection associated with neuropathy than non-diabetic subjects.6 When 164 AOD-dyspepsia subjects were studied, matched for sex, age and body weight to 164 non-diabetic-dyspepsia subjects (the controls), the results were intriguing. H. pylori was found in 74.4% of the AOD subjects versus 50% of the controls. AODs had more ulcers, more gastritis, and more simple dyspepsia.

Neuropathy was found in 65.2% of the AODs and especially those with ulcers, compared to controls. Finally, there was a significant concordance of nearly 85% between the presence of neuropathy and H. pylori infection. Subjects who were dyspeptic and diabetic, were more likely to be infected with H. pylori.

Nor do the liabilities of diabetes stop here. In another study, coronary heart disease was more prevalent in diabetic patients with H. pylori than without it.7

Skin Problems and H. Pylori
H. pylori is also thought to be a factor in Rosacea.8 Rosacea is a common dermatological condition, characterized by redness over the nose and cheeks, especially during and after periods of physical exertion. Other symptoms include bumps or pimples, a swollen nose, and telangiectases - small, dilated blood vessels in the skin. Antibiotics sometimes seem to help. This was recently found in a study in which successful treatment for H. pylori reduced symptoms of Rosacea. According to Dr Serap Utas, et al of the University of Erciyes School of Medicine, Kayseri, Turkey, symptoms of Rosacea were significantly less severe at the end of treatment for 25 patients who tested positive for H. pylori and then were treated for it. Rosacea had been a problem from between 2 months and 20 years in duration.

Mastic Can Kill H. Pylori
Readers of this publication are already aware that mastic alters the structure of H. pylori rendering the bug susceptible to eradication.

Live long and prosper,
Will Block

References

  1. Ronca F, Palmieri L, Panicucci P, Ronca G. Anti-inflammatory activity of chondroitin sulfate. Osteoarth Cartil 1998;6(Suppl A):(14-21.
  2. Grootveld M, Henderson EB, Farrell A, Blake DR, Parkes HG, Haycock P. Oxidative damage to hyaluronate and glucose in synovial fluid during exercise of the inflamed rheumatoid joint. Detection of abnormal low-molecular-mass  metabolites by proton-n.m.r. spectroscopy. Biochem J. 1991;273(2):459-467.
  3. Perez M, Wandosell F, Colaco C, Avila J. Sulphated glycosaminoglycans prevent the neurotoxicity of a human prion protein fragment. Biochem J. 1998;335(2):369-374.
  4. Reiter W, et al. Urology 1999 Mar;53:590-595.
  5. Ekstrom P. Non-gastric effects of H. pylori infection: A literature review with respect to non gastric diseases which might be associated with H. pylori infection. Eur J Surg Suppl. 1998;164(582):32-34.
  6. Gentile S, Turco S, Oliviero B, Torella R. The role of autonomic neuropathy as a risk factor of Helicobacter pylori infection in dyspeptic patients with Type 2 diabetes Mellitus. Diabetes Res Clin Pract. 1998;42(1):41-48.
  7. De Luis DA, Lahera M, Canton R, Boixeda D, San Roman AL, Aller R, De La Calle H. Association of Helicobacter pylori infection with cardiovascular and cerebrovascular disease in diabetic patients. Diabetes Care 1998;21(7):1129-1132.
  8. Utas S, et al. J Am Acad Dermatol 1999;40:433-435.

    © Copyright 1999 Life Enhancement Products, Inc. All Rights Reserved.

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