N-acetyl-glucosamine (N-A-G) plays an important role in cell identity. It is one of the key ingredients in the biosynthesis
of glycans — branched molecular chains of sugar subunits such as N-A-G, galactose, mannose, fucose, and others. All living
cells produce glycans and display them as a coating on their outer surfaces where they uniquely identify the species and tissue-type
of the cells. The glycans are attached to proteins that float like buoys in the cell membranes.
N-A-G is also a subunit of hyaluronan — an indispensable component of the connective tissue of animals.
Glycans on cell surfaces serve as identity tags in the recognition and communication between cells. The immune system therefore
depends upon glycans for distinguishing between the body’s own healthy tissues, “invading” micro-organisms, and host cells
that have gone awry. Cells that are coated with glycans appropriate for that organism are left alone by the immune system.
But cells that are coated with abnormal glycans are targeted for destruction.
Tumor cells often produce abnormal glycans. These abnormalities are recognized by the immune system, thereby triggering an
immune attack on the tumor. However, if a non-cancerous cell happens to make errors in the assembly of its surface glycans, it too will be targeted for destruction, even
if it is otherwise healthy. When large numbers of cells begin to make such errors (because of an inherited genetic error,
say), an autoimmune disease can be the result.
Thus, one cause of autoimmune diseases is thought to be the production of defective glycans by cells. For example, multiple
sclerosis is an autoimmune disease in which certain nerve cell types produce defective glycans and thereby target themselves
for destruction by the immune system.
It has been recently shown that N-acetyl-glucosamine, when present at higher-than-normal concentrations, can correct certain
of these defects in glycan production. Vitamin D3 has a similar action, but operates through a different mechanism.
What we can’t tell you
In the U.S. and some other industrialized countries, government agencies like the U.S. Food and Drug Administration
have adopted censorship as a method for intensifying their control over the supplement industry and its customers.
Thus, FDA regulations prohibit us from telling you that any of our products are effective as medical treatments,
even if they are, in fact, effective.
Accordingly, we will limit our discussion of DendroMax® to a brief summary of relevant research,
and let you draw your own conclusions about what medical conditions it may be effective in treating.
The possibility that some autoimmune diseases may be the result defective cell-surface glycans has led to detailed studies
of the process of “glycosylation” — the process by which cells create these branched glycan chains. It has been found that
glycosylation takes place in a part of the cell called the Golgi Apparatus. Here the glycan subunits (such as N-A-G and other
sugars) are linked up in the correct patterns to make the particular glycans appropriate for that cell. These glycans are
then attached to proteins and transported to the cell surface where the proteins take residence in the cell membrane — with
the glycans on the outside surface.
Sometimes the genetic programming that controls the Golgi Apparatus becomes damaged — either because of defective genes that
become active at some point in life, or because of viral involvement. This can result in incorrect assembly of the glycans.
When these defective glycans become part of the cell surface, they may be interpreted by the immune system as indicators that
the cell is an invader or a cancer cell.
During the past several years researchers have discovered connections between defective glycosylation and the following autoimmune
- Multiple sclerosis
- Inflammatory Bowel Disease and Crohn’s Disease
- Lupus Erythematosus
- Type 1 diabetes
- Type 2 diabetes
- Rheumatoid arthritis
- Autoimmune hemolytic anemia
- Tn syndrome
- Autoimmune kidney disease
Let’s examine several of these connections in more detail.
Defective glycan branching as a cause of multiple sclerosis is now well established. A research group at the University of
California showed in 2007 that mice with specific types of defective glycan branching mice always develop MS.
These researchers then showed that N-A-G supplementation corrected the branching defects when used in cell-culture experiments. In 2009 they reported that glycan branching defects can also occur in immune cells, not just their target tissues. Such branching
defects can cause the immune cells to become hyperactive, thereby contributing to autoimmune responses. Thus, there appear to be two different ways in which glycan branching defects can cause autoimmune diseases:
- by causing hyperactivity in immune cells
- by causing non-cancerous cells to be tagged as cancerous.
The next step was to show that mice with multiple sclerosis can be successfully treated with N-acetyl-glucosamine. This was
done using a strain of mice suffering from EAE (“Experimental Autoimmune Encephalitis”, a mouse version of multiple sclerosis),
and the results reported in 2011. The report states that “… oral administration of the simple sugar GlcNAc enhances N-glycan branching while inhibiting … disease
progression in EAE when initiated after disease onset.” About 7 days after beginning treatment, the glycan branching began to increase and disease symptoms improved.
Inflammatory Bowel Disease and Crohn’s Disease
In a study published in 2000, N-A-G was tested in patients with Inflammatory Bowel Disease and Crohn’s Disease and found remarkably
effective — “Eight [of the twelve patients] given oral GlcNAc showed clear improvement.” Despite this success, no further clinical studies appear to have been done — a sad commentary on the organizational abilities
of the medical research establishment.
Rheumatoid Arthritis and Juvenile Chronic Arthritis
Glycan branching patterns of immuno-proteins have been studied in arthritis patients and found to be deficient in branching
as compared with non-arthritic individuals. This glycan alteration is directly related to the symptoms of the disease. Furthermore, when healthy animals are injected with defectively glycosylated immuno-proteins, they develop rheumatoid arthritis.
These branching deficiencies sometimes improve during pregnancy. When they do, patients experience a temporary reduction in
Thus, indirect evidence suggests the possibility that treatments that induce glycan branching may reduce rheumatoid arthritis
symptoms. The concept is now being tested in a clinical trial using a more complicated polysaccharide substance. However, N-acetyl-glucosamine is already available; it is inexpensive and can be safely tried by anyone.
Systemic Lupus Erythematosus
The evidence for glycan branching defects as a cause of lupus rests on two observations:
- Lupus patients have highly defective branching in the glycans of the antibody IgA.
- Certain genetic mutations that affect the branching of glycans in immune cells result in an autoimmune disease similar to
human systemic lupus erythematosus.
It makes sense to conclude that a glycan branching promoter such as N-acetyl-glucosamine would be a good candidate to test
as a lupus treatment. Perhaps the lupus research establishment will someday explore this promising concept; in the meantime lupus patients can easily explore the concept for themselves, since N-acetyl-glucosamine is available as a dietary supplement.
Since diabetes is an autoimmune disease, could N-A-G be useful to diabetes patients? Consider these two facts:
- In mice, the development of Type 1 (juvenile) diabetes was prevented by oral N-A-G supplementation.
- Type 2 (adult-onset) diabetes has only recently been discovered to have its own autoimmune origins. Could faulty glycan branching be involved? Apparently so: When experimental animals were treated with substances that disrupted
glycan branching, the animals were prone to develop Type 2 diabetes.
These facts hint that Type 2 diabetes might be suppressed by a treatment that restores proper glycan branching — such as N-acetyl-glucosamine
supplementation. Indeed, diabetes researchers believe that proper glycan branching on pancreatic cell proteins is a key to
suppressing Type 2 diabetes.
Multiple sclerosis… rheumatoid arthritis… lupus erythematosus… diabetes… Can so many medical conditions be ameliorated by
one simple substance? Yes, they can — if they all share a common mechanism of action. In this case we do see a common mechanism: attacks by the immune system on tissues that are displaying faulty glycans on cell surfaces. When
the faulty glycans occur in nerve tissue, you get multiple sclerosis; when they occur in joint tissue, you get arthritis;
when they occur in connective tissue, you get lupus; when they occur in pancreatic tissue, you get diabetes….
Now, it may be that all these diseases can also be caused in other ways — for example, diabetes may sometimes be caused by
pancreatic cancer rather than faulty glycan structure. So, a treatment that corrects glycan structure is probably not going
to benefit diabetes patients whose disease is caused by cancer rather than faulty glycan production. And similarly for other
But a significant fraction of autoimmune conditions do seem to have glycan defects as an underlying cause. It makes sense
to try a simple, safe, and inexpensive approach to deal with these conditions when there is still time to do so — or to prevent
them from occurring in the first place.
Glycan-based regimens are very safe, but they are new to the field of autoimmune diseases. Clinical studies are sorely lacking.
It would be a mistake to substitute such regimens for standard medical treatments in cases where time is of the essence. Still, N-acetyl-glucosamine is non-toxic
and is unlikely to interfere with standard treatments when both are being used simultaneously.
Formula, dosage, and timing
Each DendroMax tablet contains 1400 mg of N-A-G and 1500 i.u. of Vitamin D3.
Although very little clinical data is available for N-acetyl-glucosamine as an autoimmunity suppressor, the supplement has
been on the market for years for other purposes. No side effects have been reported in the dosages used, which range from
500 to 6000 mg/day.
As mentioned above, Vitamin D3 is another substance that can improve glycan structure. A combination of D3 and N-A-G may therefore
work together synergistically.
The suggested dosage of DendroMax is 1-4 tablets per day in divided doses. For example, a low-dose regimen would be 1 tablet
once per day. A mid-dose regimen might be one tablet twice per day. A high-dose would be 2 tablets twice per day.
N-A-G’s effects on autoimmunity take at least a week to develop.
Are DendroMax® supplements useful for the conditions and purposes mentioned above?
We aren’t allowed to tell you, so you should take a look at some of the references cited here,
and then decide for yourself.