51 Examples That Reveal What Scientists Discovered About Acemannan
When Sam Caster first met these scientists in 1994, he said they were genuinely excited about Acemannan. Now I’d heard Sam tell that story before, and while I found it interesting, I don’t think I fully understood why they were so excited. And I’ll admit that I may have contributed to my own misunderstanding.
Over the years, I had allowed Acemannan to become just another nutritional ingredient blended into the crowded world of products and claims where even something scientifically significant can begin to lose its distinction.
It wasn’t until I began digging into the research and the patents that I started to understand why these scientists saw Acemannan so differently.
And perhaps that’s the larger lesson for me.
Sometimes we become so familiar with something that we stop asking what makes it important.
These patents challenged me to look again, to move beyond the claims, examine the evidence, understand the history, and appreciate the extraordinary amount of investigation that followed the discovery of Acemannan.
And that’s really what I hope these presentations encourage you to do as well. And I’ll help you.
So join us as we dig deeper and reach wider.
It wasn’t until I began studying the patents these scientists produced that the answer started coming into focus.
Yes. Discovering and stabilizing Acemannan in 1985 was an extraordinary scientific accomplishment, but that discovery immediately raised another question.
So what? What could Acemannan actually do?
The patents help answer that question because they reveal the remarkable deep dive that followed.
Patent number 5,308,838 alone contains 51 examples exploring Acemannan in a wide variety of circumstances.
35 of the 51 read more like real world case reports, but these weren’t simply testimonials mailed in by people who happened to try a product. They were observations documented within a scientific and medical setting in which the researchers and clinicians were investigating what happened when Acemannan was used.
The remaining examples of those 51 were more experimental in nature involving laboratory research, controlled biological testing, and veterinary work with animals.
And consider the backgrounds of the three inventors. Bill McAnnelly was a PhD scientist, Harley r McDaniel was a medical doctor, and Robert h Carpenter was a veterinarian.
Suddenly, Sam’s comment about their excitement makes much more sense to me now.
This video will be shorter than usual because my primary purpose is to give you access to these 51 examples. I have rewritten each one into plain language and included an audio narration as well.
You don’t have to work your way through all 51. Instead, you can browse the list, choose the examples that interest you, and either read the plain language version or simply listen.
My purpose is to let you see for yourself the extraordinary range of investigation that followed on the heels of the Acemanan discovery. This gave me a much clearer picture why the scientists were excited in the first place.
I hope you will always be careful to maintain good works to meet urgent needs and become heroes to your generation.
The 51 Examples of Patent 5,308,838
Example 1 — Acemannan and the Activation of Human Immune Cells (Laboratory Experiment)
Example 1 is not a patient testimonial. This was a laboratory experiment designed to answer a basic question:
Could Acemannan activate important cells of the human immune system?
The researchers began with blood obtained from healthy human volunteers. From that blood, they isolated immune cells known as monocytes.
Monocytes are important because they can develop into macrophages—some of the immune system’s major defense cells. Think of macrophages as both first responders and messengers. They can attack and clean up unwanted material, but they also release chemical signals that help organize the larger immune response.
The researchers placed these human immune cells into laboratory dishes and exposed them to different amounts of Acemannan.
They then looked for something called interleukin-1, or IL-1.
That name sounds complicated, but the idea is simple. IL-1 is a chemical messenger produced by activated immune cells. When a monocyte or macrophage releases IL-1, it is essentially sending a signal that can help recruit and activate other parts of the immune system.
So the researchers were asking:
If we expose these immune cells to Acemannan, will they respond by producing more of this immune-system messenger?
According to the patent, the answer was yes.
The Acemannan-treated cells showed increased production of IL-1. And importantly, the response changed depending upon how much Acemannan the cells received.
The researchers also examined another substance called prostaglandin E2, or PGE2. PGE2 is another chemical messenger involved in inflammation and the regulation of immune activity.
Again, the important point for us is not memorizing the names of these molecules.
The important point is what the experiment was showing.
Acemannan was not simply sitting beside these human immune cells in a laboratory dish. The cells were responding to it.
Exposure to Acemannan changed the chemical signals being produced by these immune cells.
That makes Example 1 very different from many of the patient stories we will encounter later in the patent. Here, researchers were working directly with human cells under controlled laboratory conditions and measuring their biological response.
This experiment does not tell us that Acemannan can cure a disease, and it does not tell us what the same response would necessarily accomplish inside the human body.
What it does provide is laboratory evidence supporting a more basic idea:
Acemannan was capable of interacting with human immune cells and stimulating measurable changes in their activity.
Example 2 — Acemannan and the Activity of Macrophages (Laboratory Experiment)
Example 2 moves us into another laboratory experiment.
This time, the researchers wanted to know whether Acemannan could affect the activity of macrophages—important immune cells whose job includes finding, capturing, and consuming foreign material.
That process has a scientific name: phagocytosis.
But the idea is actually pretty simple.
Think of a macrophage as one of the immune system’s cleanup and defense cells. It surrounds unwanted material, pulls it inside, and breaks it down.
So the basic question behind this experiment was:
Could Acemannan make macrophages better at doing that job?
To find out, researchers gave Acemannan to mice. Three days later, they collected macrophages from the animals and tested those cells in the laboratory.
They gave the macrophages something they could recognize and consume—sheep red blood cells.
Then they simply measured how many of the macrophages actually took those red blood cells inside themselves.
The researchers also used comparison groups so they could see whether Acemannan was making a meaningful difference.
When the macrophages were left largely on their own, Acemannan produced only a modest increase in their ability to consume the red blood cells. In this part of the experiment, the difference was not statistically significant.
But then the researchers made the experiment more closely resemble the way the immune system normally works.
They added antibodies that recognized the sheep red blood cells.
You can think of those antibodies as putting a “this is the target” tag on the cells.
Now the results became much more noticeable.
Macrophages from the Acemannan-treated animals were significantly better than the untreated controls at interacting with and consuming these antibody-marked targets.
And when the researchers added complement—a group of immune proteins that can help antibodies mark a target and make it easier for macrophages to recognize—the response increased even further.
So what did the researchers conclude?
Their results suggested that Acemannan could enhance the activity of macrophages—particularly when those macrophages were working together with other parts of the immune system, such as antibodies and complement.
And there is something especially interesting here. The strongest result wasn’t that the macrophages simply became more aggressive on their own. The more significant effect appeared when they were working as part of a coordinated immune response—with antibodies and complement helping identify the target.
And that’s really the heart of Example 2.
Acemannan appeared to help macrophages do one of their fundamental jobs: recognize, capture, and consume targeted material.
This was a laboratory experiment involving macrophages obtained from mice. It was not a human clinical trial, and it does not demonstrate that Acemannan can prevent or cure a particular disease.
What it does provide is experimental evidence that Acemannan could influence the activity of an important part of the immune system—the macrophage.
Example 3 — Acemannan, Macrophages, and Tumor Cells (Laboratory Experiment)
Example 3 takes us into another laboratory experiment.
This time, the researchers were asking a particularly interesting question:
Could Acemannan stimulate macrophages in a way that would help them attack tumor cells?
Remember, macrophages are important immune cells. They help the body identify, capture, and destroy material that does not belong.
For this experiment, researchers used mice as the source of the macrophages. Some of the mice were given Acemannan before their macrophages were collected.
The researchers then brought those macrophages into the laboratory and placed them together with tumor cells.
The tumor cells had been given a radioactive marker.
That sounds complicated, but its purpose was actually quite simple.
The radioactive marker gave the researchers a way to measure whether the tumor cells were being damaged.
As a tumor cell was damaged and began breaking apart, some of that radioactive material would be released. By measuring how much was released, researchers could estimate how much tumor-cell destruction had occurred.
They then compared the activity of macrophages from the different groups of mice.
The results showed that macrophages stimulated by Acemannan were capable of producing measurable destruction of the tumor cells.
In other words, Acemannan wasn’t being tested here as something that directly killed the tumor cells.
Instead, the experiment was looking at something quite different:
Could Acemannan activate macrophages, and could those activated immune cells then attack tumor cells?
According to the patent, the experiment provided evidence that they could.
And that’s really the important point of Example 3.
The researchers were beginning to explore Acemannan as what scientists call a biological response modifier—something that can change the way the body’s own immune cells respond.
This was a laboratory experiment involving mouse macrophages and tumor cells grown in culture. It was not a cancer treatment study in people, and it does not demonstrate that Acemannan can treat or cure cancer.
What it does provide is evidence of a biological effect:
Macrophages stimulated by Acemannan showed an increased ability to damage tumor cells under laboratory conditions.
Example 4 — Acemannan and the Communication Between Human Immune Cells (Laboratory Experiment)
Example 4 takes us into another laboratory experiment involving the immune system.
And although the science behind this experiment gets complicated very quickly, the basic question is actually pretty simple:
Could Acemannan help human immune cells respond more strongly when they encountered something they recognized as foreign?
The researchers studied two important kinds of immune cells: monocytes and T cells.
We’ve already encountered monocytes. They are immune cells that can develop into macrophages and can also send chemical messages to other parts of the immune system.
T cells are another major part of our immune defenses. Among their many jobs, they help recognize threats and coordinate an immune response.
In this experiment, researchers placed immune cells together in laboratory cultures.
When immune cells from the same source were placed together, Acemannan did not simply cause them to become more active.
That is important.
But when the cells encountered cells from a different source—something the immune system recognized as foreign—the response increased when Acemannan was present.
And the amount of Acemannan mattered.
As the dose changed, the immune response changed with it. At the highest concentration tested, the patent reports an increase in response of about 60 percent above the baseline level.
The researchers then went one step further.
They wanted to know whether Acemannan was acting through the monocytes—the immune cells that help send instructions to T cells.
Their experiments indicated that when monocytes were exposed to Acemannan, those monocytes produced signals that increased the response of the T cells.
So rather than thinking of Acemannan as simply turning the entire immune system “on,” this experiment suggested something more specific.
Acemannan appeared to influence the communication between immune cells.
The researchers proposed that one explanation involved a chemical messenger called interleukin-1, or IL-1—the same immune signal we encountered back in Example 1.
In simple terms, Acemannan appeared to stimulate the monocytes, the monocytes sent stronger signals, and the T cells responded more strongly when presented with something foreign.
And that’s really the heart of Example 4.
This was a laboratory experiment involving human immune cells. It was not a study showing that Acemannan prevented or treated a disease in people.
What it does provide is evidence for a more basic biological effect:
Under these laboratory conditions, Acemannan enhanced the way certain human immune cells communicated and responded to a foreign target.
Example 5 — Tracking Acemannan Through the Body (Scientific Experiment)
Example 5 takes us into a different kind of scientific experiment.
This time, the researchers weren’t primarily asking what Acemannan did to an immune cell.
They wanted to answer an even more basic question:
What happens to Acemannan after it enters the body?
Does it get absorbed? Does it reach the bloodstream? How long does it remain there? And where does it eventually go?
To answer those questions, researchers needed some way to follow Acemannan through the body.
So they gave Acemannan a detectable radioactive label called carbon-14.
Think of it as putting a tiny tracking device on the Acemannan. The label allowed researchers to follow where the material went by measuring the radioactivity associated with it.
Female dogs were given the labeled Acemannan in three different ways.
Some received it directly into a vein.
Others received it by injection into the abdominal cavity.
And others received it orally.
The researchers then collected blood, urine, and fecal samples over the next 48 hours or longer. They also examined different organs and tissues.
And here’s the first important finding:
The patent reports that significant absorption occurred with all three methods—including when Acemannan was given orally.
As you would expect, putting it directly into a vein produced the highest and fastest blood levels.
Injection into the abdominal cavity came next.
Oral administration was slower.
But the researchers were able to track the labeled material after oral administration as well.
They also discovered something else they considered particularly interesting.
The labeled material remained in the body for a surprisingly long time.
Scientists describe this using the term half-life—the amount of time required for the measured level of a substance to fall by half.
Following intravenous administration, the patent reports a half-life of approximately 50 to 60 hours.
In simple terms, Acemannan—or more precisely, the radioactive material associated with the labeled Acemannan—did not simply appear and then rapidly disappear.
It persisted.
And that’s the heart of Example 5.
The researchers used radioactive labeling to track Acemannan after it was administered to animals. They reported measurable absorption by injection and by mouth, followed by a relatively long period in which the labeled material remained detectable.
Why was that important to the researchers?
Because many of the earlier experiments had shown biological effects when cells were exposed directly to Acemannan in a laboratory dish.
Example 5 was helping them address the next logical question:
Could Acemannan actually be absorbed into a living body and remain there long enough for those laboratory observations to have biological relevance?
According to the patent, these experiments provided evidence that it could.
This was an animal experiment, not a human clinical trial. And radioactive tracking tells us where labeled material travels and how long it remains detectable; it does not, by itself, prove that Acemannan will produce a particular health benefit.
But Example 5 gave the researchers an important piece of the puzzle:
Acemannan wasn’t only producing effects when placed directly onto cells in a laboratory. When administered to animals—including orally—labeled material associated with Acemannan could be absorbed, tracked through the body, and detected for an extended period of time.
Example 6 — The First Clinical Pilot Studies of Acemannan in People with HIV (Preliminary Studies on People)
Example 6 represents an important transition.
Up to this point, much of what we’ve been looking at involved cells in a laboratory or experiments with animals.
Now Acemannan was being studied in people.
The patent describes two early pilot studies involving patients infected with HIV-1—the virus responsible for AIDS.
These were preliminary studies. Their purpose was not to provide the kind of definitive evidence we would expect from a large clinical trial. Instead, researchers were taking an early look at whether Acemannan could be safely given to HIV-positive patients and whether there were signs that it might affect their condition.
One of the most important things researchers followed was the patients’ T4 cells, which today we commonly call CD4 T cells.
These cells play a central role in coordinating the immune system.
And HIV attacks these very cells.
So in a person with HIV, a falling T4 or CD4 count was an important sign that the immune system was being progressively weakened.
The researchers therefore followed these cell counts over time.
According to the patent, patients receiving Acemannan showed increases in their T4 cell counts during the observation period.
The researchers also followed other indicators of the patients’ health and immune function.
One of these was HIV core antigen—a substance associated with the virus that could be detected in the blood.
You don’t need to remember the technical name.
The basic idea was this:
If less of this viral marker could be detected over time, that might suggest a reduction in detectable viral activity.
The patent reports that fewer patients had detectable HIV core antigen as time went on, although the authors also cautioned that this particular change was not statistically significant. In other words, they could not confidently rule out chance as the explanation.
The researchers also compared patients whom they believed had a better chance of responding with those whose condition suggested a poorer prognosis.
Both groups showed improvement in some of the measurements being followed, although the group expected to respond more favorably generally showed the stronger improvement.
So what should we take away from Example 6?
Not that Acemannan had been proven to treat HIV.
These were early pilot studies, not large, definitive controlled trials.
But researchers had now moved beyond laboratory cells and animal experiments and were administering Acemannan to actual HIV-positive patients.
And they were seeing enough measurable changes—including changes in T4 immune-cell counts—to justify continued investigation.
That makes Example 6 an important step in the story.
The question was no longer simply, “Can Acemannan affect immune cells in the laboratory?”
The question had become:
“When Acemannan is given to people whose immune systems are being damaged by HIV, can we measure changes that suggest their immune function is responding?”
According to these early pilot studies reported in the patent, the researchers believed the answer was encouraging enough to keep investigating.
Example 7 — A Phase II Human Study of Acemannan and AZT (Observational Study of People)
Example 7 takes another important step forward.
This was no longer a laboratory experiment or an early observational study.
This was a randomized, double-blind Phase II clinical study involving 47 people with HIV.
The study was conducted at Hospital St. Pierre in Brussels, Belgium, and lasted 24 weeks.
The researchers were primarily interested in two questions:
Was Acemannan safe and well tolerated?
And:
When Acemannan was used together with AZT, were there signs that it provided additional benefit?
AZT was one of the principal drugs being used against HIV at the time.
The 47 participants were divided into two broad categories.
Twenty-three were HIV-positive but had not yet developed symptoms.
Twenty-four had what was then called AIDS-related complex, or ARC. These patients were experiencing illness associated with HIV but had not necessarily progressed to what was then classified as AIDS.
The asymptomatic patients received either Acemannan or a placebo.
The patients with ARC all received AZT. Half also received Acemannan, while the other half received a placebo.
The daily Acemannan dose was 1,000 milligrams, given for 24 weeks.
Because the study was double-blind, neither the patients nor those evaluating them were supposed to know who was receiving Acemannan and who was receiving the placebo.
Thirty-three of the original 47 patients completed the entire 24-week study.
One of the first important findings involved safety.
According to the patent, none of the patients left the study because Acemannan caused side effects or was poorly tolerated.
The researchers also reported no evidence of liver or kidney toxicity associated with the treatment.
Side effects—particularly nausea—occurred more often among the patients receiving AZT. But when the researchers compared patients receiving Acemannan with those receiving placebo, they did not find a significant difference in adverse reactions.
Then came the question of whether Acemannan might provide additional benefit when combined with AZT.
The researchers looked at a measurement called the Karnofsky score.
We don’t need to make that complicated.
It is basically a way of measuring how well a person is functioning in everyday life. A higher score means the person is generally functioning better.
Among the patients receiving both AZT and Acemannan, the average score increased from 84 to 90.
Among those receiving AZT with placebo, it increased only from 81 to 83.
The difference between these groups was reported as statistically significant.
The researchers also looked at CD4 cells—the important immune cells that HIV attacks.
Among the patients receiving AZT plus Acemannan, the average CD4 count increased from 263 to 369.
Among those receiving AZT plus placebo, it increased from 145 to 252.
The patent reports that the improvement was significantly greater in the combination-treatment group.
There was another observation.
Two patients receiving AZT without Acemannan progressed to AIDS during the study—one developing Kaposi’s sarcoma and another developing esophageal candidiasis.
None of the patients receiving the combination of AZT and Acemannan did so.
However, the patent states that this difference was not statistically significant.
So what does Example 7 actually tell us?
It does not prove that Acemannan treated HIV, and it certainly does not show that Acemannan could replace antiviral medication.
But this was considerably stronger evidence than a patient testimonial.
It was a randomized, double-blind Phase II clinical study.
The study found that Acemannan was generally well tolerated over 24 weeks.
And among the symptomatic patients receiving AZT, those who also received Acemannan showed greater improvement in measures of everyday functioning and CD4 immune-cell counts than those receiving AZT with placebo.
The patent authors therefore proposed something very specific:
Not that Acemannan should replace AZT, but that it might have a role alongside AZT as an additional—or adjunct—therapy.
That is the central message of Example 7.
Example 8 — Acemannan and HIV-Infected Cells in the Laboratory (Laboratory Experiment)
Example 8 — Acemannan and HIV-Infected Cells in the Laboratory (Laboratory Experiment)
Example 8 brings us back into the laboratory.
This time, researchers wanted to answer a very direct question:
What happens when HIV-infected cells are exposed to increasing amounts of Acemannan?
Researchers used several different types of immune cells that could be infected with HIV-1.
They infected those cells with the virus and then exposed them to different concentrations of Acemannan.
Then they watched two things very carefully.
Were the infected cells surviving?
And:
How much virus was being produced?
The first important finding was that the effect of Acemannan depended upon the amount being used.
As the concentration of Acemannan increased, protection of the infected cells generally increased as well.
In one group of human blood cells, the patent reports protection ranging from 14 percent to 100 percent, depending upon the concentration of Acemannan.
In another type of HIV-infected cell, treatment with 62.5 micrograms per milliliter of Acemannan produced greater than 85 percent protection.
But the researchers weren’t only looking at whether the cells survived.
They also looked at something called cell fusion.
HIV can cause infected cells to fuse together, producing large abnormal cells. You don’t need to remember the scientific name for them. The important point is that this cell fusion is one visible sign of the damage being caused by the virus.
As the amount of Acemannan increased, this abnormal cell fusion decreased.
At concentrations above 62.5 micrograms per milliliter, the researchers reported that they could no longer detect these fused cells.
Then they looked directly at viral activity.
Again, the results changed according to the concentration of Acemannan.
In the human blood cells, concentrations of 62.5 micrograms per milliliter or greater were associated with a 95 to 100 percent reduction in detectable HIV-related RNA inside the cells.
In another HIV-infected cell line, concentrations above that level produced a greater than 60 percent reduction in virus released outside the cells.
And there was another important observation.
At the concentrations tested, the researchers reported no evidence that Acemannan itself was toxic to the cells.
So let’s strip all of that down to its simplest meaning.
The researchers infected cells with HIV and then added increasing amounts of Acemannan.
As the concentration of Acemannan increased, they generally observed:
more infected cells surviving,
less abnormal cell fusion,
and
less detectable viral activity.
This was all happening in a laboratory dish—not in patients.
So Example 8 does not demonstrate that Acemannan can treat HIV infection in the human body.
But it does demonstrate something important under these laboratory conditions:
Acemannan was associated with a measurable, concentration-dependent reduction in several signs of HIV activity and HIV-related cell damage.
And perhaps the easiest way to remember Example 8 is this:
The more Acemannan the researchers added—within the concentrations they tested—the greater the protective effect they generally observed.
Example 9 — Acemannan and AZT Working Together Against HIV in the Laboratory (Laboratory Experiment)
Example 9 continues the laboratory investigation of HIV, but this time the researchers asked a different question.
They already knew that AZT could interfere with HIV.
And they had evidence that Acemannan could also affect HIV-infected cells.
So now they wanted to know:
What happens when you put Acemannan and AZT together?
Could the combination protect HIV-infected cells better than either substance used alone?
To find out, researchers infected cells with HIV-1 and then treated them with different amounts of AZT and Acemannan.
Some cells received AZT alone.
Some received Acemannan alone.
And others received different combinations of the two.
Then the researchers measured how many of the HIV-infected cells remained alive.
And this is where the experiment became particularly interesting.
The researchers found evidence of what scientists call synergy.
Synergy simply means that two things working together produce a greater effect than you would expect from either one working alone.
One result illustrates this especially well.
At one very low concentration of AZT, the AZT by itself provided essentially no protection.
At a low concentration of Acemannan, the Acemannan by itself also provided essentially no protection.
But when those same two concentrations were combined, about 32 percent of the HIV-infected cells survived.
Neither one had protected the cells by itself at those concentrations.
Together, they did.
The researchers found another striking result at higher concentrations.
At one concentration, AZT alone provided about 65 percent protection.
Acemannan alone provided about 40 percent protection.
But when the two were combined, the researchers measured 100 percent protection of the cells under those laboratory conditions.
So why might the combination work better?
The patent offers a possible explanation.
AZT was already known to interfere with one stage of the HIV life cycle.
The researchers proposed that Acemannan might interfere with the virus at a different stage.
Think of it this way:
AZT may have been putting up one roadblock in the virus’s attempt to reproduce, while Acemannan may have been putting up another roadblock somewhere else.
One roadblock alone might slow the virus down.
But two different roadblocks working together could make it much more difficult for the virus to complete its replication process.
And that’s really the heart of Example 9.
The researchers found that Acemannan and AZT protected HIV-infected cells more effectively together than would have been expected from their effects separately.
This was a laboratory experiment involving HIV-infected cells.
It was not a clinical trial in people, and 100 percent protection of cells in a laboratory dish does not mean 100 percent protection from HIV in a human being.
But under these laboratory conditions, the researchers found evidence of a genuine synergistic interaction between Acemannan and AZT.
And that gave them another reason to investigate Acemannan not as a replacement for established HIV therapy, but as something that might potentially work alongside it.
Example 10 — Acemannan Used in Treating a Skin Ulcer (Real-world Case Report)
Example 10 describes an 83-year-old woman who had developed an ulcer along the outside of her left foot. The wound was about 25 millimeters—or roughly one inch—in diameter. It had been there for several months and had already failed to respond to several different treatments.
The treatment described in the patent used aloe-derived products prepared according to an earlier Carrington patent and was identified as Acemannan. Three times each day, the clean wound was soaked for 15 minutes with one of these preparations. The excess was then removed with sterile gauze, and another preparation was applied over the wound in an amount sufficient to keep it from drying out between dressing changes.
Importantly, the researchers didn’t rely only on someone’s impression that the wound looked better. They followed its progress with photographs and actually measured the size of the wound.
At the beginning, the wound area measured 1.24 square inches. By day 28, it had decreased to 0.51 square inches—about 59 percent healed. By day 77, the patent reports about 77 percent healing, and by day 83, just over 90 percent.
The skin defect was substantially closed after 12 weeks, and by 14 weeks—day 97—the patent reports complete closure of the wound.
This is not presented as a controlled clinical trial. It is a report involving a single patient. But what makes the example noteworthy is that the wound had persisted for several months despite previous treatments, and its subsequent closure was documented with measurements over time.
Example 11 — Acemannan Used as a Treatment for Tic Douloureux (Real-world Case Report)
Example 11 describes a 43-year-old woman suffering from tic douloureux, better known today as trigeminal neuralgia. This condition affects the trigeminal nerve in the face and can produce sudden attacks of extremely severe pain. In her case, the right side of her face was affected, and something as simple as brushing or combing her hair could trigger the pain.
She had already been treated unsuccessfully with a number of medications, including Valium, antihistamines, pain relievers, Inderal, and phenobarbital. According to the patent, she said she had not experienced a single pain-free day since the condition began.
She then began drinking one to two ounces of Acemannan daily, with an initial treatment period of three months.
Within two weeks, the patent reports that her pain had diminished significantly, and for the next few weeks she said she felt well.
Then something particularly interesting happened. She went on a two-week trip and stopped taking the Acemannan. During that interruption, her symptoms and pain returned. When she resumed taking it, the patent reports that the pain disappeared again within a few days.
She continued taking Acemannan daily for more than six months without another interruption. At that point, she reported that she could brush and comb her hair without triggering the pain. The patent also notes that her appearance had improved and that she said she felt better than ever before.
This is an individual patient report, not a controlled clinical trial, so it cannot by itself establish that Acemannan caused the improvement. Nevertheless, the sequence reported in the patent is noteworthy: her symptoms improved after beginning the treatment, returned when she stopped it, and improved again after she resumed it.
Example 12 — A Pilot Study of Acemannan in Inflammatory Bowel Disease (Human Clinical Study)
Example 12 moves us into a small human clinical study.
The researchers were interested in inflammatory bowel disease, or IBD.
IBD includes conditions such as Crohn’s disease and ulcerative colitis. In simple terms, these are diseases in which parts of the digestive tract become chronically inflamed.
The researchers wanted to ask a straightforward question:
What would happen if people with inflammatory bowel disease were given Acemannan?
The study involved nine patients with either Crohn’s disease or ulcerative colitis.
These were not people with mild digestive complaints. The patients had longstanding disease, and their conditions had not responded satisfactorily to conventional treatment.
The patients were given 200 milligrams of Acemannan each day.
Then the researchers followed their progress in several different ways.
First, they looked at the symptoms the patients were experiencing—things such as abdominal pain, diarrhea, blood in the stool, watery stools, and mucus.
But they didn’t stop with asking the patients how they felt.
They also looked directly inside the intestinal tract to see whether the diseased tissue appeared to be improving.
And they examined tissue samples under a microscope to look for changes in inflammation.
So the researchers were essentially looking at the disease from three different angles:
How did the patients feel?
How did the intestine actually look?
And:
What did the tissue look like under a microscope?
According to the patent, improvement was observed in all three areas.
The patients’ clinical symptoms generally improved.
Examination of the intestinal tract showed improvement in the visible signs of disease.
And microscopic examination of tissue samples showed reductions in inflammatory activity.
The patent presents the individual patient results in several different ways, allowing the researchers to compare each patient’s condition before Acemannan with that patient’s best response during treatment.
And that’s really the heart of Example 12.
This was more than someone simply saying, “I took Acemannan and I felt better.”
The researchers were looking for changes that could be observed and documented.
They measured symptoms.
They examined the intestine.
And they examined tissue under a microscope.
That makes this an exploratory clinical pilot study.
But the word pilot is important.
There were only nine patients. There was no large placebo-controlled comparison group, and a small exploratory study like this cannot establish that Acemannan was responsible for the improvements that were observed.
What it can do is provide an early signal that something interesting may be happening—and give researchers a reason to investigate further.
So, stripped down to its simplest form, Example 12 asked:
If people with difficult-to-treat inflammatory bowel disease are given Acemannan, do we see evidence of improvement—not only in their symptoms, but also in the diseased tissue itself?
According to the observations reported in the patent, the answer was encouraging.
Improvement was reported in symptoms, in the visible condition of the intestinal tract, and in the inflammation seen under the microscope.
Example 13 — Acemannan and Measles Virus in the Laboratory (Laboratory Experiment)
Example 13 takes us back into the laboratory for another antiviral experiment.
This time, the researchers were working with the measles virus.
And the question was surprisingly simple:
What happens if measles virus is exposed to Acemannan before the virus has a chance to infect a cell?
To find out, researchers took measles virus and mixed it with different concentrations of Acemannan.
They then introduced that mixture to cells that measles virus could normally infect.
The cells used in this experiment were called VERO cells.
We don’t really need to remember that name. They are simply cells commonly used by researchers for growing and studying viruses in the laboratory.
The researchers then watched to see whether the measles virus damaged the cells.
Normally, when measles virus infects these cells, the infection produces visible damage.
Scientists call this a cytopathic effect.
But again, the idea is simple:
If the virus successfully infects the cells, you can see the damage it causes.
The researchers found that the results depended upon the amount of Acemannan used.
At lower concentrations, the measles virus was still capable of producing infection.
But as the concentration of Acemannan increased, the virus’s ability to damage the cells decreased.
At 2.5 milligrams of Acemannan per milliliter, the researchers reached what the patent describes as a threshold where the usual visible signs of viral damage were no longer detected.
And at 5 milligrams per milliliter, the patent reports a complete absence of those visible signs of infection.
So let’s reduce Example 13 to its simplest form.
The researchers took measles virus.
They exposed it to Acemannan.
Then they gave that virus an opportunity to infect susceptible cells.
At sufficiently high concentrations of Acemannan, the researchers no longer observed the cell damage they normally expected from measles infection.
That led them to believe that Acemannan was somehow interfering with the virus’s ability to successfully infect the cells.
But there is an important limitation.
This experiment does not tell us that Acemannan treats measles in a person.
It doesn’t even tell us exactly how Acemannan interfered with the virus.
And these were cells growing in a laboratory dish, not a human body.
What Example 13 does provide is laboratory evidence for a much narrower conclusion:
When measles virus was exposed to sufficient concentrations of Acemannan before encountering susceptible cells, the usual visible evidence of viral infection could be prevented under these laboratory conditions.
Example 14 — Could Acemannan Stop Measles After the Cells Had Already Been Exposed? (Laboratory Experiment)
Example 14 follows directly from the measles experiment we just looked at.
In Example 13, researchers mixed measles virus with Acemannan before allowing the virus to encounter susceptible cells.
Under those conditions, sufficient concentrations of Acemannan protected the cells from infection.
So the researchers now asked the obvious next question:
What happens if we reverse the order?
What if the measles virus gets to the cells first, and Acemannan is added afterward?
Could Acemannan stop an infection that had already begun?
To find out, researchers exposed laboratory-grown cells to measles virus for different lengths of time—from just 30 minutes up to six hours.
They then washed away any virus that had not attached to the cells.
Only after that did they add Acemannan.
They used a concentration of 5 milligrams per milliliter—the same concentration that had provided complete protection when the virus was exposed to Acemannan first in the previous experiment.
Then they waited five days and examined the cells for signs of measles infection.
And this time, the result was very different.
Once the cells had already been exposed to the measles virus, adding Acemannan afterward did not significantly protect them from infection.
There were some signs of lower infection when the virus had been allowed only a short period of time—about 30 minutes to an hour—to interact with the cells.
But when the virus had more time with the cells before Acemannan was added, there was no meaningful protection.
That negative result is actually important.
Put Examples 13 and 14 together, and a clearer picture begins to emerge.
In Example 13:
Virus meets Acemannan first → cells are protected.
In Example 14:
Virus reaches the cells first → adding Acemannan afterward does not significantly protect them.
That suggests that timing mattered.
Whatever Acemannan was doing in the first experiment, the results suggest that it was much more effective when it interacted with the virus before the virus established its interaction with the cells.
And that’s really the heart of Example 14.
This was a laboratory experiment involving measles virus and cultured cells. It does not show that Acemannan can prevent or treat measles in people.
In fact, the value of this particular experiment may be what Acemannan didn’t do.
Once the cells had already been exposed to measles virus, Acemannan did not reverse the infection under these laboratory conditions.
And that helped the researchers narrow down when—and perhaps eventually how—the effect observed in the previous experiment was occurring.
Example 15 — Could Acemannan Help a Vaccine Produce a Stronger Immune Response? (Animal Experiment)
Example 15 takes us into another animal experiment.
This time, the researchers were working with young chickens and asking a very practical question:
Could Acemannan help a vaccine produce a stronger immune response?
The chickens were being vaccinated against a disease caused by something called infectious bursal disease virus, or IBDV.
The technical name isn’t especially important.
What matters is that this virus attacks part of a chicken’s immune system and can leave the animal less able to fight infection.
Vaccines were already available.
But the researchers wondered whether adding Acemannan could make a vaccine more effective at stimulating the immune system.
In other words:
Vaccine alone versus vaccine plus Acemannan—which would produce the stronger immune response?
To find out, the researchers divided young chickens into different groups.
Some received no real vaccine and served as controls.
Some received the vaccine by itself.
And some received the vaccine together with Acemannan.
The researchers then collected blood from the chickens every week.
They weren’t simply watching to see whether the chickens looked healthy.
They measured antibodies against the virus.
That’s important because antibodies gave the researchers a measurable way to determine how strongly the immune system had responded to the vaccine.
And in the first study, the difference was substantial.
Two weeks after vaccination, antibody levels began rising in the vaccinated chickens.
But the chickens that received the vaccine plus Acemannan developed a considerably stronger antibody response than those receiving the vaccine alone.
At one point, their average antibody level was approximately 3.9 times higher.
After the chickens received a second vaccination, the difference increased to approximately 4.1 times higher.
Even after antibody levels eventually began declining, they fell more slowly in the Acemannan group.
The researchers interpreted this as evidence that Acemannan was helping produce a stronger and possibly longer-lasting immune response to the vaccine.
The patent also reports that the chickens showed no discomfort or side effects from the Acemannan.
The researchers then conducted a second study with a larger number of chickens.
But this time, things didn’t go nearly as smoothly.
Some of the chickens developed unrelated health problems. There were unexpectedly small birds, problems around identification bands, tissue damage, and secondary bacterial infections.
Those problems could themselves suppress the immune system.
As a result, the researchers concluded that the second experiment had been compromised and terminated the study.
That’s important.
We shouldn’t pretend that every experiment produced clean, convincing results.
The first study produced encouraging evidence.
The second study did not provide reliable confirmation because unrelated problems interfered with the experiment.
Even so, observations from the studies led the researchers to propose that Acemannan might act as what scientists call a vaccine adjuvant.
That’s a complicated word for a simple idea.
An adjuvant helps a vaccine get the immune system’s attention.
It doesn’t replace the vaccine.
Instead, it is used with the vaccine in an effort to produce a stronger immune response.
And that’s really the heart of Example 15.
The researchers weren’t asking whether Acemannan could cure this viral disease in chickens.
They were asking:
Could Acemannan help the immune system respond more strongly to a vaccine?
In the first experiment, chickens receiving the vaccine with Acemannan developed substantially higher antibody levels than chickens receiving the vaccine alone.
The second experiment was compromised and had to be stopped.
So this was not definitive proof.
But the first study provided experimental evidence supporting a new possibility:
Acemannan might be useful as an adjuvant—something used alongside a vaccine to help strengthen the immune response.
Example 16 — Acemannan Used for Malabsorption Syndrome (Real-world Case Report)
Example 16 concerns malabsorption syndrome—a condition in which the small intestine has difficulty absorbing essential nutrients from food. The patent specifically discusses conditions such as sprue and celiac disease, where sensitivity to gluten can damage the intestinal lining and interfere with normal absorption.
The example describes a 56-year-old man suffering from chronic gluten-sensitive sprue. His condition had become serious enough that he had lost more than 40 pounds.
According to the patent, the man began taking Acemannan orally at an estimated dose of 500 to 800 milligrams per day. What followed was described as a rapid reduction in his chronic diarrhea, followed by progressive weight gain.
The patent then offers an explanation for what might have been happening. It proposes that mannose, an important component associated with Acemannan, could support the production of glycoproteins needed for the normal maturation of cells lining the small intestine. The authors suggest that improving this process could help restore the intestinal surface and, in turn, improve the absorption of nutrients.
This is important to distinguish from the patient outcome itself. The improvement in diarrhea and subsequent weight gain were observations reported in this one patient; the explanation involving glycoprotein production and intestinal-cell maturation was the mechanism proposed by the patent authors.
So, once again, this is not a controlled clinical trial and cannot establish that Acemannan caused the patient’s improvement. But the patent records a noteworthy case: a man who had lost more than 40 pounds from chronic gluten-sensitive sprue experienced a rapid reduction in diarrhea followed by progressive weight gain after beginning daily oral Acemannan.
Example 17 — Acemannan and Multiple Sclerosis (Real-world Case Report)
Example 17 describes a 36-year-old woman who had suffered from multiple sclerosis for more than six years. Her disease had progressed to the point that she had been bedridden for four months.
She was treated with steroids, and afterward she regained enough mobility to walk inside her home with the help of a walker. She still required a wheelchair whenever she traveled outside the home. According to the patent, her physician warned that without additional chemotherapy—including treatment with Cytoxan—she was expected to become bedridden again within six months.
The patient chose instead to discontinue all of her prescribed therapy and began taking approximately 500 milligrams of oral Acemannan each day.
The patent reports that her voice progressively became stronger and that other symptoms improved. After six months, she reported that her neurologist had told her that plaques previously seen using NMR imaging—an earlier term for what we now commonly call MRI—had regressed.
The patent further reports that she continued to experience remission of symptoms associated with her multiple sclerosis.
This is an individual patient report, not a controlled clinical trial. The reported regression of the plaques was also based on what the patient said her neurologist had told her rather than imaging data presented in the example itself. So this example cannot establish that Acemannan caused her improvement. Nevertheless, the case was significant enough to the patent authors that they specifically documented the patient’s improvement after beginning daily oral Acemannan.
Example 18 — Acemannan and a Virus Affecting Mushrooms (Plant Experiment)
Example 18 takes us in a completely different direction.
This time, the researchers weren’t studying people, animals, or human immune cells.
They were studying mushrooms.
Commercial mushroom growers faced a serious problem from something called LaFrance virus. Infection could damage mushroom crops and create significant losses for growers.
So the researchers asked a straightforward question:
Could Acemannan interfere with this viral infection?
To find out, they deliberately used mushroom-growing material that had been infected with LaFrance virus.
They then mixed different amounts of Acemannan into the compost where the mushrooms would grow.
Some of the growing material received very little Acemannan.
Other groups received progressively larger amounts.
The mushrooms were then allowed to grow under controlled conditions and were harvested over several weeks.
But the researchers weren’t simply looking at the mushrooms and asking whether they appeared healthier.
They actually looked for genetic material associated with the virus.
The technical term used in the patent is double-stranded viral RNA, or dsRNA.
We don’t need to make that complicated.
Think of it simply as a laboratory marker that allowed the researchers to look for evidence of the virus.
When the researchers analyzed the mushrooms, they found less of this viral RNA in mushrooms grown in compost containing certain concentrations of Acemannan than in mushrooms grown without Acemannan.
The patent reports this reduction with Acemannan concentrations ranging from 0.01 percent up to 1 percent.
So let’s reduce Example 18 to its simplest form.
The researchers started with mushroom-growing material infected with a virus.
They added different amounts of Acemannan.
They grew the mushrooms.
And then they looked for evidence of the virus.
The mushrooms grown with certain concentrations of Acemannan showed less detectable viral RNA than the untreated controls.
And that’s really the heart of Example 18.
This experiment doesn’t tell us that Acemannan can treat viral infections in people.
Mushrooms are obviously very different from humans.
But that’s also what makes the example interesting.
The researchers were investigating whether the antiviral effects they had been exploring with Acemannan might extend beyond one particular virus or one particular biological system.
Under the conditions of this experiment, Acemannan was associated with a reduction in a laboratory marker of LaFrance virus infection in mushrooms.
So Example 18 gives us another piece of experimental evidence—but in an entirely different biological setting:
Acemannan was added to virus-infected mushroom-growing material, and the mushrooms that developed in certain Acemannan-treated groups showed less detectable viral RNA than the untreated controls.
Example 19 — Acemannan Used for Chronic Fatigue Syndrome (Real-world Case Report)
Example 19 describes two individuals suffering from what the patent identified as chronic fatigue syndrome.
The first was a 41-year-old woman who had experienced severely debilitating chronic fatigue syndrome for two years. The patent also reports that she had elevated Epstein-Barr virus titers.
She began taking 800 milligrams of Acemannan orally each day. After six months, she reported complete relief from the lethargy she had been experiencing.
She then remained symptom-free for three months and decided to stop taking the Acemannan. Following that interruption, her tiredness and fatigue gradually began to return. According to the patent, when she resumed taking Acemannan, her symptoms were rapidly alleviated again.
The second case involved the sister of a physician. She had experienced chronic fatigue syndrome for an extended period and also had elevated Epstein-Barr antibodies. The patent reports that she had undergone multiple clinical evaluations and treatment regimens without improvement.
She then began taking 800 milligrams of Acemannan daily. She reported significant improvement, followed by elimination of her symptoms after approximately two to three months of Acemannan use.
These are individual patient reports, not controlled clinical trials, and they cannot establish that Acemannan caused the reported improvements. Nevertheless, the first case contains a particularly noteworthy sequence: symptoms improved while taking Acemannan, gradually returned after Acemannan was discontinued, and improved again when Acemannan was resumed. The second patient similarly reported substantial improvement after beginning daily Acemannan following previous treatments that had not helped.
Example 20 — Acemannan Combined with Radiation and Chemotherapy for a Malignant Tumor (Real-world Case Report)
Example 20 describes a 41-year-old patient identified as W. H., who went to a medical center suffering from severe chest pain.
Initial X-rays revealed what appeared to be a large mass in the chest, possibly involving the blood vessels, so the patient was transferred to a cardiovascular center for further evaluation.
There, physicians determined that the mass was extensive. It stretched from the lower neck all the way to the diaphragm, grew between the lungs, and involved the base of the heart.
A biopsy identified the mass as a malignant embryonic sinus tract tumor.
Treatment was then begun using approximately 500 milligrams of oral Acemannan each day in combination with radiation and chemotherapy.
The patent reports a remarkable long-term outcome. Six years after treatment, the patient had a normal chest X-ray and was living a normal, active life.
The authors also report that their review of the medical literature found 20 cases of this type of tumor, with all 20 patients dying within nine to twelve months of diagnosis.
This is an individual patient report and does not allow us to determine what contribution Acemannan made to the outcome. Radiation and chemotherapy were being administered at the same time and therefore cannot be separated from the result.
Nevertheless, the reason this example stands out is clear: the patent describes an extremely serious and extensive malignant tumor, treatment that combined conventional cancer therapy with daily oral Acemannan, and a patient who was reported to be alive, active, and showing a normal chest X-ray six years later.
Example 21 — Acemannan Combined with Chemotherapy in a Patient with Liver Tumors (Real-world Case Report)
Example 21 describes a patient identified as M.A., who sought medical attention because his abdomen had become so enlarged that he could no longer zip his pants or fasten his belt.
CAT scans performed in April 1988 revealed an extremely serious condition. More than 20 tumor masses, some measuring as much as 10 centimeters in diameter, had largely replaced the patient’s liver. The tumors extended as far as the urinary bladder.
According to the patent, the patient was given a life expectancy of only four to six weeks.
At the time, he was already taking 800 milligrams of oral Acemannan each day for HIV-1 infection. Doctors then began a multi-drug chemotherapy regimen, while the daily Acemannan was continued.
The patent reports that the patient experienced minimal side effects and toxicity of the kind normally associated with cancer chemotherapy.
Three months later, a CAT scan showed an estimated 60 percent reduction in tumor mass. At six months, the estimated reduction had reached 85 percent. By 12 months, only minimal tumor remained.
And at 24 months, the patent reports that only small scars and what was described as questionable tumor mass remained in the liver. His clinical laboratory results were normal, and at the time the example was written, the patient was reported to be doing well.
This is an individual patient report, not a controlled clinical trial, and Acemannan was not used by itself. The patient was receiving multi-drug chemotherapy at the same time, so this example cannot tell us how much, if anything, Acemannan contributed to the reduction in his tumors.
What the patent does document is an extraordinary clinical course: a patient with more than 20 liver tumors and a reported life expectancy of only four to six weeks received multi-drug chemotherapy while continuing 800 milligrams of Acemannan daily. Over the following two years, the patent reports a dramatic reduction in tumor mass, with only small scars and questionable remaining tumor visible at 24 months.
Example 22 — Acemannan Treatment of Skin Tumors Associated With HIV (Real-world Case Report)
Example 22 describes two patients with skin lesions associated with Kaposi’s sarcoma, a type of cancer that was frequently seen in people with HIV and AIDS.
The first patient, identified as S.G., had two black, raised lesions on his arm that had previously been confirmed by biopsy as Kaposi’s sarcoma. Similar lesions were present elsewhere on his body, but those were initially left untreated, providing an informal comparison.
An Acemannan gel containing five percent DMSO was applied directly to the two lesions on his arm.
The patient was reexamined weekly. According to the patent, the treated lesions progressively became flatter and lost their dark pigmentation. After 60 days of treatment, only flat, scarred areas remained.
The patent reports that other lesions on this same patient were subsequently treated in the same way and produced similar results.
The second patient, identified as T.P.D., had a raised, pigmented lesion on his ankle characteristic of Kaposi’s sarcoma. In this case, however, another treatment was used first. The lesion was injected beneath the skin with one cubic centimeter of recombinant alpha interferon.
Within three days, the patent reports improvement in both the size and pigmentation of the lesion.
Acemannan gel was then applied topically using a bandage. By the end of one week, the patent reports that there was no visible evidence of the lesion, with no scarring or change in pigmentation.
These are individual patient reports, not controlled clinical trials. And the second case is particularly important to interpret cautiously because interferon was administered before the Acemannan gel, making it impossible to determine what contribution Acemannan made to the disappearance of that lesion.
Still, the first case is noteworthy because Acemannan was applied directly to two biopsy-confirmed Kaposi’s sarcoma lesions while similar lesions elsewhere on the patient’s body were initially left untreated. The patent reports progressive flattening and loss of pigmentation in the treated lesions, with only flat, scarred areas remaining after 60 days.
Example 23 — Acemannan Treatment of Premalignant Skin Lesions (Real-world Case Report)
Example 23 describes a physician identified as W.B. who had numerous solar keratoses on areas of his skin that had received significant sun exposure.
Solar keratoses are rough, scaly areas of sun-damaged skin that can have a premalignant appearance—meaning that while they are not necessarily cancer, some can potentially progress toward skin cancer.
According to the patent, Acemannan gel was applied to these lesions every night for two weeks.
After those two weeks, the patent reports that the scales, crusts, and irregular areas of skin that had appeared premalignant were removed.
The authors then add that they had observed a similar response in many other mature patients.
This is a very brief clinical observation rather than a controlled clinical study. The example does not tell us how many lesions were treated, provide measurements of their size, report biopsy results before and after treatment, or give us long-term follow-up to determine whether the lesions returned.
So this example cannot establish that Acemannan prevented skin cancer or permanently eliminated premalignant tissue. What the patent does report is straightforward: a physician with numerous sun-related keratoses applied Acemannan gel nightly, and after two weeks the scales, crusts, and visible skin irregularities associated with those lesions had disappeared.
Example 24 — Acemannan Treatment of Severe Swelling Associated With Cancer Surgery (Real-world Case Report)
Example 24 describes a 32-year-old man with a primary tumor of the pharynx—the area of the throat behind the mouth and nasal cavity.
He had already undergone an unsuccessful attempt to surgically remove the tumor, along with radical neck surgery, radiation, and chemotherapy.
By January 1984, his condition had become extremely serious. According to the patent, both his larynx and esophagus had become completely blocked, leaving him in severe, unmanageable pain. His lymphatic system was also obstructed, producing massive edema—or fluid-related swelling. His head had swollen to approximately twice its normal size, and the swelling had become so severe that his facial features could no longer be distinguished.
At this point, he was being kept alive through a feeding tube placed into his stomach and a tracheotomy that allowed him to breathe.
Acemannan gel was then applied generously over his entire head, neck, and shoulders every eight hours.
By the third day, the patent reports that the swelling was noticeably reduced. By the tenth day, the excess tissue fluid was reported to be gone.
Then, between days 14 and 16, additional changes occurred. Soft, fluid-filled areas developed around the base of his neck, along the angles of his jaw, and behind his ears. The skin opened, and dead tissue began draining from areas where the tumor had previously been hard, infiltrative, and nodular.
The patent also reports that the patient began coughing up masses of gray-white degenerating tumor tissue. This was accompanied by massive bleeding, requiring multiple blood transfusions.
Over time, however, the patient reportedly regained abilities he had lost. He gradually became able to speak again, eat soup, and breathe through his mouth and nose.
This is an individual patient report, not a controlled clinical trial. The patient had also previously undergone surgery, radiation, and chemotherapy, and the example does not provide the kind of comparison or testing that would allow us to determine exactly what role Acemannan played in what followed.
What the patent does document is a striking sequence of events: a critically ill cancer patient with massive swelling began receiving topical Acemannan; the swelling was noticeably reduced within three days and reportedly gone by day ten; this was followed by drainage of dead tissue and what the patent described as degenerating tumor tissue; and the patient eventually regained some of his ability to speak, eat, and breathe normally.
Example 25 — Acemannan Combined with Chemotherapy Following Rectal Cancer Surgery (Real-world Case Report)
Example 25 describes a patient identified as C.M. who had adenocarcinoma—a type of cancer—in the lower portion of the rectum.
The cancer was treated surgically by removing the affected portion of the rectum and surrounding tissue. The patent also reports that the cancer had spread to a lymph node in the mesentery, the tissue that supports and connects the intestines within the abdomen.
Following surgery, the patient declined radiation therapy but chose to receive weekly intravenous treatments with 5-fluorouracil, commonly called 5-FU, a chemotherapy drug.
At the same time, the patient took 800 milligrams of oral Acemannan each day.
The patent specifically notes that during this treatment the patient did not experience the mouth ulcers, severe fatigue, nausea, or vomiting that can be associated with 5-FU chemotherapy.
The patient was subsequently evaluated extensively using isotope scans and computerized tomography—or CAT scans.
At 24 months following surgery, the patent reports that no adenocarcinoma could be detected and that the patient continued to be normal.
This is an individual patient report, not a controlled clinical trial, and several important factors were involved. The cancer had been surgically removed, and the patient was also receiving weekly 5-FU chemotherapy. Therefore, this example cannot tell us whether Acemannan contributed to the absence of detectable cancer or to the patient’s apparent tolerance of chemotherapy.
What the patent documents is that a patient with rectal cancer that had spread to a lymph node underwent surgery and then received weekly 5-FU chemotherapy while taking 800 milligrams of Acemannan daily. The patent reports that the patient avoided several side effects commonly associated with 5-FU and, at 24 months after surgery, had no detectable adenocarcinoma.
Example 26 — Acemannan Combined with Multi-Drug Chemotherapy (Real-world Case Report)
Example 26 describes two cancer patients who received Acemannan along with conventional chemotherapy.
The first patient, identified as H.H., had adenocarcinoma of the colon and underwent surgery to remove the cancer.
After surgery, however, there were signs suggesting that cancer was still present or progressing. The patient’s CEA level—a blood marker that can be used to follow certain cancers—was rising, tumor nodules were detected, and a CAT scan showed a nodule in the liver.
Treatment was then begun using 800 milligrams of oral Acemannan each day along with weekly intravenous chemotherapy consisting of 500 milligrams of 5-fluorouracil, commonly called 5-FU, and 50 milligrams of dacarbazine.
According to the patent, the tumors progressively decreased in size, and the patient’s CEA levels also declined. The patent further reports that there was no evidence of side effects or biochemical or blood-related toxicity during the treatment.
The second case involved a 66-year-old man identified as V.G. He had undergone complete removal of a lung because of squamous-cell cancer originating in the bronchial passages. Despite the surgery, the cancer had spread to his bones and liver.
His condition was serious enough that his alkaline phosphatase and other liver-enzyme levels were more than three times the upper limit of normal.
He was treated weekly with 500 milligrams of intravenous 5-FU and 50 milligrams of dacarbazine while also taking 800 milligrams of oral Acemannan each day.
After one month, the patent reports that his alkaline phosphatase and liver-enzyme levels had fallen to approximately half of their pretreatment levels. His general condition was also reported to have improved.
These are individual patient reports, not controlled clinical trials. And in both cases, Acemannan was administered alongside established chemotherapy drugs. Therefore, these cases cannot tell us how much, if anything, Acemannan contributed to the reported tumor reduction, changes in laboratory values, or improvement in the patients’ conditions.
What the patent documents is that two patients with serious cancers received multi-drug chemotherapy together with daily oral Acemannan. In the first patient, tumor size and CEA levels progressively declined without reported biochemical or blood-related toxicity. In the second, substantially elevated liver-enzyme levels fell by approximately half after one month, accompanied by an improvement in his general condition.
Example 27 — Acemannan Combined with Chemotherapy and Hormone Therapy for Prostate Cancer (Real-world Case Report)
Example 27 describes a 72-year-old man identified as J.R. who had metastatic adenocarcinoma of the prostate—meaning that his prostate cancer had spread beyond its original location.
He had already undergone surgery and radiation therapy, but two blood markers used to follow prostate cancer were continuing to rise. These were acid phosphatase, or PAP, and prostate-specific antigen, better known as PSA.
The patient was then started on a treatment regimen that included 800 milligrams of oral Acemannan each day, along with 500 milligrams of 5-fluorouracil, or 5-FU, and 50 milligrams of another chemotherapy drug.
Following the beginning of this combination treatment, the patent reports that the previous rise in his tumor markers leveled off. PAP reached a high of 15 units, while PSA reached 186.
An anti-hormonal drug called Eulexin was then added to the treatment regimen. Eulexin, also known as flutamide, works by blocking the effects of male hormones that can stimulate the growth of prostate cancer.
After Eulexin was added, the patent reports a substantial decline in both tumor markers. Within 60 days, PAP had fallen from 15 to 3, while PSA had fallen from 186 to 15.
The patent also reports that this response occurred without toxicity or side effects at any stage and that the patient continued to be monitored while the complete treatment regimen was continued.
This is an individual patient report, not a controlled clinical trial, and several treatments were being used together. Acemannan was combined with chemotherapy, and the major decline in the tumor markers occurred after anti-hormonal therapy was added. Therefore, this example cannot tell us what contribution Acemannan made to the patient’s response.
What the patent does document is that a man with metastatic prostate cancer and rising tumor markers began a combination treatment that included daily oral Acemannan and chemotherapy. His previously rising tumor markers leveled off. After anti-hormonal therapy was added, those markers then fell dramatically over the following 60 days, with no toxicity or side effects reported during the treatment.
Example 28 — Acemannan Treatment of Venomous Snake Bites (Real-world Case Report)
Example 28 describes an unusual report involving Acemannan gel that was sent to Swangi Province in southern China.
Two cases of the gel were provided to the Red Cross for use on burns, bed sores, ulcers caused by poor circulation, and diabetic skin ulcers.
Approximately one year later, the head of the Red Cross wrote back reporting that the Acemannan gel had been useful for these conditions. But he also reported something unexpected.
According to the patent, he said that Acemannan gel was the best treatment they had ever used for water-snake bites—a relatively common problem among people working manually in the rice paddies.
The patent explains that these snake bites could become infected and sometimes failed to respond to antibiotics. The resulting loss of blood flow to the surrounding soft tissue could lead to tissue death and considerable loss of skin and muscle.
The treatment involved covering the wounds with Acemannan gel and an occlusive dressing—a covering designed to keep the wound protected and the gel in contact with the injured tissue.
According to the report, this treatment eliminated otherwise difficult-to-manage infections and appeared to help restore circulation through the small blood vessels surrounding the injured area.
The patent further reports that this helped preserve fingers and toes, as well as muscle, nerves, and other soft tissue that might otherwise have been lost.
This example should be understood for what it is. It is not a controlled clinical trial, and the patent does not provide the number of snake-bite patients treated, measurements of their wounds, the species of snake involved, or a comparison group receiving another treatment.
Instead, this is a field report communicated to the patent authors by the head of a Red Cross organization in southern China.
What makes the example noteworthy is the reported experience itself: Acemannan gel had originally been supplied for several types of difficult wounds, but the Red Cross subsequently reported that they had also found it particularly useful in treating serious water-snake bites, where infection, loss of circulation, and destruction of surrounding tissue were major concerns.
Example 29 — Acemannan and Aging Fibroblasts (Real-world Case Report)
Example 29 moves away from individual patient reports and into the laboratory.
Researchers obtained fibroblasts from a 60-year-old man. Fibroblasts are cells that help produce collagen and maintain the structural framework of tissues such as the skin.
When these aging fibroblast cells were treated with Acemannan, the researchers observed changes in their appearance and behavior.
According to the patent, when the fibroblasts were maintained for longer periods in a culture medium containing Acemannan at a concentration of one milligram per milliliter, the cells began displaying biochemical and physical characteristics resembling those of neonatal—or very young—cells.
The patent authors interpreted these changes as evidence suggesting a reversal of certain features associated with cellular aging.
The example then describes a separate observation from 1989. A physician examined facial skin tissue obtained during surgery for skin cancer at Duke University. Acemannan gel had been applied after the surgery.
According to the patent, examination of the tissue showed an unusual breakdown and removal of damaged collagen fibers, along with rapid formation of young collagen fibers by enlarged fibroblasts. The authors described this as rapid remodeling of the aged skin tissue.
The example also describes another observation made by the same physician in 1990 involving dogs that had received Acemannan. Their thymus glands were reported to be two to six times larger than those of untreated control dogs.
Under the microscope, the thymus glands from the Acemannan-treated dogs contained increased numbers of cells and showed signs of increased thymocyte activity. The patent also reports increased numbers of T-lymphocytes and what are called nurse cells, which the authors interpreted as evidence of increased T-cell activity.
Putting these observations together, the patent authors proposed that stimulation of fibroblast activity and thymus activity by Acemannan might help restore function in tissues whose activity had declined with age.
It is important, however, not to interpret this example as evidence that Acemannan reverses human aging. The fibroblast experiment was performed on human cells in a laboratory, while some of the additional observations came from tissue specimens and animals.
What Example 29 reports is something more specific and still intriguing: aging human fibroblasts exposed to Acemannan in laboratory culture began displaying characteristics that the patent authors described as resembling those of much younger cells.
Example 30 — Acemannan and Cholesterol Levels (Animal and Human Study)
Example 30 describes an interesting finding that appeared first in an animal safety study and then again in a human study.
The original purpose wasn’t simply to see whether Acemannan could lower cholesterol.
Researchers were conducting a 91-day toxicity study in male dogs to evaluate the safety of Acemannan.
The dogs received a relatively large amount—855 milligrams of Acemannan per kilogram of body weight each day.
During that study, researchers noticed something unexpected:
The dogs experienced a statistically significant reduction in their blood cholesterol levels.
That observation raised an obvious question.
Would anything similar happen in people?
The patent then describes a study involving 24 healthy male volunteers.
These men received different amounts of oral Acemannan, ranging from 400 to 3,200 milligrams per day.
Researchers measured their cholesterol levels before and after the study.
At the beginning, the group’s average cholesterol level was 189 milligrams per deciliter.
By the end, the average had fallen to 174.
That’s an average decrease of 15 points.
The researchers then analyzed the results statistically to determine whether the change might simply have occurred by chance.
According to the patent, their analysis indicated a greater than 98 percent probability that the reduction was not due to chance variation.
And there was another observation that caught their attention.
Seven of the 24 participants experienced a cholesterol decrease of more than 20 points in only six days.
The subjects were living under controlled conditions during the study.
Because some of these reductions occurred so quickly, the patent authors argued that it would be difficult to explain the change simply as the result of the participants improving their diets.
And that’s really the heart of Example 30.
Researchers first noticed a statistically significant reduction in cholesterol during an animal toxicity study.
Then a similar pattern appeared among 24 healthy male volunteers taking oral Acemannan.
This was not a large clinical trial designed to prove that Acemannan is a cholesterol-lowering treatment. And the example does not give us the kind of detailed cholesterol information we would expect from a modern cardiovascular study—such as separate LDL, HDL, and triglyceride results.
So we should not turn this observation into a claim that Acemannan has been proven to treat high cholesterol or prevent cardiovascular disease.
What the patent actually documents is narrower, but still interesting:
During studies involving both animals and humans, researchers observed statistically significant reductions in total blood cholesterol associated with Acemannan.
In the 24 human volunteers, the average cholesterol level fell from 189 to 174, while seven participants experienced decreases of more than 20 points within six days.
Example 31 — Acemannan and Injuries Caused by Plants (Real-world Case Report)
Example 31 describes two competition hunters who traveled to Africa carrying a supply of Acemannan that had originally been intended for veterinary use.
After experiencing an episode of diarrhea during the trip, the two hunters decided to begin taking the Acemannan themselves. They took approximately 800 milligrams each day.
According to the patent, the hunters reported experiencing less diarrhea than other members of their hunting party.
But another observation caught their attention.
While traveling through the African bush, the hunters encountered numerous briars that produced cuts and scratches on their arms and legs.
The two men reported that while taking Acemannan, these cuts and scratches seemed to heal virtually overnight. They said that the wounds did not develop the redness or inflammation they might normally have expected.
By the time the hunters returned to the United States, the patent reports that all of their abrasions had completely healed.
The experience of other members of the hunting party was reportedly quite different. Some developed serious infections in their cuts and abrasions and later required treatment from their physicians with both systemic and topical antibiotics.
In contrast, the two hunters taking Acemannan reportedly developed no infections and were left with no scarring.
This is an anecdotal field observation, not a controlled clinical study. We are not told how many other hunters were injured, whether their wounds were comparable, or what other factors might have influenced the differences in healing.
So this example cannot establish that Acemannan caused the rapid healing or prevented infection.
What the patent records is an interesting observation: two hunters taking 800 milligrams of Acemannan daily experienced numerous cuts and scratches from briars while traveling in Africa. They reported that their injuries healed unusually quickly, without redness, infection, or scarring, while some other members of the hunting party reportedly developed infections serious enough to require antibiotic treatment.
Example 32 — Acemannan and Allergic Reactions to Plants (Real-world Case Report)
Example 32 describes the use of Acemannan for inflammatory reactions caused by plant allergens.
The first case involved a person identified as H.R.M., who had a family history of seasonal hay fever and experienced symptoms every year.
These symptoms included itching, burning, congestion, and watering of the mucous membranes. The swelling inside the nasal passages also produced sinus headaches.
Beginning in 1988, the individual took 800 milligrams of oral Acemannan each day for five days.
According to the patent, this treatment virtually eliminated the person’s hay fever symptoms, including the sinus headaches associated with the swollen nasal tissue.
The following year, in 1989, Acemannan was used in a different way. Instead of taking it orally, Acemannan gel was applied directly to the mucous membranes of the eyes and nasal passages. It was applied at bedtime and then every eight hours afterward.
The patent reports that this topical application produced a similar beneficial effect.
The example then extends the observation to another type of plant reaction—poison ivy.
According to the patent, similar results had been observed when Acemannan was applied topically to poison ivy lesions in both humans and animals. The authors report that both the severity of the lesions and the amount of time required for them to heal were significantly reduced.
This is not presented as a controlled clinical trial. In the hay fever portion, the patent describes the experience of a single individual, and it does not provide objective allergy testing, symptom scores, or a comparison with a placebo or conventional allergy treatment.
Likewise, the poison ivy portion does not tell us how many humans or animals were treated or provide the underlying measurements.
So this example cannot establish that Acemannan was responsible for these improvements. What the patent reports is that one person with recurring seasonal hay fever experienced substantial relief after both oral and topical Acemannan, and that the authors had observed similar benefits when topical Acemannan was used on poison ivy lesions.
Example 33 — Acemannan and Hypersensitivity to Chemicals (Real-world Case Report)
Example 33 describes a professional painter identified as T.R. who was experiencing serious respiratory problems associated with the chemicals he encountered at work.
According to the patent, vapors from the paints and solvents he worked with were triggering wheezing and bronchitis. The problem had become severe enough that he was on the verge of giving up his profession.
He then began taking 800 milligrams of oral Acemannan each day.
After five days, the patent reports that his symptoms were relieved.
The painter then continued taking 800 milligrams of Acemannan before going to work each day. According to the patent, he was able to continue working as a professional painter while following this routine.
This is a single-person report, not a controlled clinical trial. The example does not provide lung-function testing, measurements of his chemical exposure, information about other treatments he may have been using, or a comparison with periods when he was not taking Acemannan.
So this example cannot establish that Acemannan prevented or treated respiratory reactions caused by chemical exposure.
What the patent records is a straightforward observation: a professional painter whose wheezing and bronchitis had become serious enough that he was considering leaving his profession began taking 800 milligrams of Acemannan daily. His symptoms were reported to have improved within five days, and he continued taking Acemannan before work each day while remaining able to continue painting.
Example 34 — Acemannan and Longstanding Asthma (Real-world Case Report)
Example 34 describes a 76-year-old man identified as T.T. who had lived with asthma for 72 years—essentially since early childhood.
Interestingly, he did not begin taking Acemannan specifically to treat his asthma. He was taking 800 milligrams of Acemannan each day for an unrelated condition.
After approximately one year, the patient told his attending physician that he had not needed to use his aerosolized bronchodilator for more than a year. In fact, a significant amount of medication was still left in the unit.
That was particularly noteworthy because his wife reported that, for the previous 15 years, he had typically gone through about two bronchodilator units every month. Before that, he had used a hand-held aerosolizer for approximately 50 years to manage his chronic asthma.
According to the patent, the patient continued taking 800 milligrams of Acemannan daily and was no longer experiencing wheezing or chronic bronchitis.
This is an individual patient report, not a controlled clinical trial. The example does not provide lung-function testing, medical records documenting the change in bronchodilator use, information about other medications or treatments, or a comparison group.
So this example cannot establish that Acemannan caused the improvement in his asthma.
What makes the report noteworthy is the patient’s history. According to the patent, this was a 76-year-old man who had suffered from asthma for 72 years and had depended heavily on inhaled medication for decades. After beginning daily Acemannan for an unrelated reason, he reported going for more than a year without using his bronchodilator and was subsequently reported to be free of wheezing and chronic bronchitis.
Example 35 — Acemannan and Symptoms Associated With Cystic Fibrosis (Real-world Case Report)
Example 35 is a very brief report involving a college-age woman who had what the patent describes as a six-month history of cystic fibrosis syndrome.
She began taking 800 milligrams of oral Acemannan each day.
According to the patent, within two weeks of beginning Acemannan, she reported an abrupt return of her energy.
And that is essentially the entire case as presented in the patent.
No additional information is provided about her diagnosis, the severity of her condition, other symptoms she may have been experiencing, medications or treatments she was receiving, or what happened beyond those first two weeks.
There are also no laboratory measurements, lung-function tests, or other objective clinical findings reported in this example.
So this individual report cannot establish that Acemannan treated cystic fibrosis or that Acemannan was responsible for the improvement she experienced.
What the patent records is much more limited: a college-age woman with a six-month history of what the authors called cystic fibrosis syndrome began taking 800 milligrams of Acemannan daily and reported an abrupt return of energy within two weeks.
Example 36 — Acemannan and Cytomegalovirus Infection in an HIV-Positive Patient (Real-world Case Report)
Example 36 describes a 27-year-old man identified as M.M. who was HIV-1 positive.
For approximately two months, he had been experiencing persistent pain beneath his breastbone that had not been relieved by medications.
Doctors performed an esophagoscopy—an examination of the esophagus—and discovered an erosion in the lining of the lower portion of his esophagus.
A biopsy was then taken from the affected tissue. According to the patent, microscopic examination and special staining of the biopsy revealed cytomegalovirus, commonly called CMV, within the epithelial cells lining the esophagus.
The patient was then given 1,000 milligrams of oral Acemannan in the form of a lozenge.
According to the patent, after three days of Acemannan treatment, all of his symptoms had disappeared.
And that is essentially the entire case as reported in the patent.
The example does not tell us whether another esophagoscopy or biopsy was performed afterward to determine whether the CMV infection itself had disappeared. It reports the elimination of the patient’s symptoms, not laboratory confirmation that the virus had been eliminated.
This is also a single-patient report, not a controlled clinical trial, so it cannot establish that Acemannan caused the improvement.
What makes the case noteworthy is the sequence the patent records: an HIV-positive man had experienced persistent chest pain for two months despite medication; examination and biopsy identified an erosion of the esophagus containing CMV; he was then given oral Acemannan; and within three days, the patent reports that all of his symptoms had disappeared.
Example 37 — Acemannan Following an Episode of Rheumatic Fever (Real-world Case Report)
Example 37 describes a 25-year-old woman identified as S.M. who developed a number of serious inflammatory symptoms following an episode of rheumatic fever caused by a streptococcal throat infection.
Her symptoms came on suddenly and included arthritis, inflammation of the tendons, and swelling of the joints. Laboratory testing also showed abnormalities in her white blood cell count and an elevated sedimentation rate—a blood test commonly used as an indicator of inflammation.
Another blood test, known as an ASO titer, was markedly elevated. This test can provide evidence of a recent streptococcal infection.
The patent also notes an interesting family history. Her sisters and mother had experienced severe and repeated episodes of acute rheumatic fever, with some of those episodes leaving them incapacitated for as long as a year.
The patient began taking 800 milligrams of oral Acemannan each day.
According to the patent, by the sixth week of treatment, her sedimentation rate and white blood cell count had returned to normal, and all of her clinical symptoms had disappeared.
By eight weeks, she had improved enough to return to a manual-labor job that required a high degree of dexterity.
This is an individual patient report, not a controlled clinical trial. The example does not provide a comparison group, and it does not give us enough information about other treatments she may have received or the natural course her illness might otherwise have taken. Therefore, it cannot establish that Acemannan caused her recovery.
What the patent records is a notable clinical course: a 25-year-old woman developed significant inflammatory symptoms following post-streptococcal rheumatic fever and began taking 800 milligrams of Acemannan daily. By six weeks, the patent reports that her laboratory abnormalities had returned to normal and her clinical symptoms were gone. And by eight weeks, she had returned to physically demanding work requiring considerable manual dexterity.
Example 38 — Acemannan and Autoimmune Disease (Real-world Case Report)
Example 38 describes a 21-year-old woman identified as E.M. who had suffered for more than two years from progressively worsening blood abnormalities.
She had pancytopenia, meaning that several major types of blood cells were abnormally low. She was anemic, had a low white blood cell count, and had a dangerously low number of platelets, the blood cells needed for normal clotting.
According to the patent, she had already been treated unsuccessfully at eight major medical centers in the United States, and a bone marrow transplant had been proposed as the next step.
When she was first examined, she was experiencing bruising, small areas of bleeding beneath the skin called petechiae, and significant fatigue.
Her laboratory results reflected the seriousness of her condition. Her hemoglobin was only 6.1 grams per deciliter. Her platelet count was between 20,000 and 25,000, and her total white blood cell count was only 1,500.
The patent also reports that a specialty clinical pathology laboratory had detected an antibody directed against her own white blood cells, providing evidence of an autoimmune component to her condition.
She was then given 800 milligrams of oral Acemannan each day for 60 days.
During those first two months, the patent reports only minor improvement in her laboratory values and minimal improvement in her fatigue.
At that point, a hematologist became involved and treated her with low-dose prednisone and horse antithymocyte globulin, a treatment designed to suppress certain immune cells. The patent notes that prednisone had previously been ineffective for her.
By October 1988, her blood counts had improved substantially. Her hemoglobin had risen to more than 10, her white blood cell count had increased to 3,500, and her platelet count had risen to 60,000.
Then, in the middle of 1989, she resumed taking 800 milligrams of oral Acemannan each day and continued it for six months.
By January 1990, the patent reports that her hemoglobin had reached 12.7, her platelet count had increased to 120,000, and her white blood cell count had risen to 5,200.
At the time the example was written, the patent reports that she was taking no medication and was attending graduate school while working as a professional dancer and choreographer.
This is an individual patient report, not a controlled clinical trial, and the treatment history makes interpretation especially important. Acemannan alone produced only minor laboratory improvement during the initial 60 days. More substantial improvement occurred after prednisone and horse antithymocyte globulin were introduced. Acemannan was later resumed, and further improvement was reported.
Therefore, this example cannot tell us how much of the patient’s recovery was attributable to Acemannan, the other treatments, the combination of treatments, or other factors.
What the patent does document is a remarkable clinical course: a young woman with severe and longstanding abnormalities involving all three major blood-cell lines, who had reportedly failed treatment at eight major medical centers and was facing a possible bone marrow transplant, experienced substantial improvement over time and was eventually reported to be medication-free and functioning at a high level.
Example 39 — Acemannan and Systemic Lupus Erythematosus (Real-world Case Report)
Example 39 describes a patient with systemic lupus erythematosus, commonly known as lupus.
Lupus is an autoimmune disease in which the immune system mistakenly attacks the body’s own tissues, potentially producing inflammation and symptoms involving different parts of the body.
According to the patent, the patient was treated by a physician in New York with 800 milligrams of oral Acemannan each day.
After eight weeks of Acemannan therapy, the physician reported that all of the patient’s symptoms had diminished and that laboratory values had markedly improved.
The patient continued taking Acemannan, and the patent reports that the continuing treatment appeared to control the symptoms associated with the patient’s condition.
And that is essentially the entire case as presented in the patent.
We are not given the patient’s age or sex, how long the patient had suffered from lupus, which symptoms were present, what the laboratory abnormalities were, or what other medications or treatments the patient may have been receiving.
This is also an individual physician report, not a controlled clinical trial. So it cannot establish that Acemannan caused the improvement or that Acemannan is an effective treatment for systemic lupus erythematosus.
What the patent records is more limited: a patient with systemic lupus erythematosus was given 800 milligrams of oral Acemannan daily, and after eight weeks the treating physician reported diminished symptoms and markedly improved laboratory values. Continued Acemannan use was reported to appear to control the patient’s symptoms.
Example 40 — Acemannan and Acute Rheumatoid Arthritis (Real-world Case Report)
Example 40 describes a physician’s experience with a series of patients suffering from acute rheumatoid arthritis.
Rheumatoid arthritis is an autoimmune disease in which the immune system attacks the joints, producing inflammation, swelling, stiffness, and pain.
According to the patent, these patients had elevated RA latex levels, a laboratory test used at the time in evaluating rheumatoid arthritis. They also had elevated sedimentation rates, a blood test that can indicate the presence of inflammation in the body.
The patients were given 800 milligrams of oral Acemannan each day.
After six to eight weeks, the physician reported that the patients’ symptoms had been significantly reduced and that their clinical laboratory values had markedly improved.
And that is essentially the entire report presented in Example 40.
The patent does not tell us how many patients were included in this series. It also does not provide their ages, individual symptoms, starting or ending laboratory values, other medications they may have been taking, or how long they had suffered from rheumatoid arthritis.
There was also no control group described.
So while the patent uses the word “significantly” to describe the reduction in symptoms, it does not provide the underlying data or statistical analysis that would allow us to evaluate that statement independently.
What the patent records is more limited: a physician reported treating a series of patients with acute rheumatoid arthritis who had elevated laboratory markers associated with the disease and inflammation. After six to eight weeks of taking 800 milligrams of Acemannan daily, the patients were reported to have substantially reduced symptoms and markedly improved clinical laboratory values.
Example 41 — Acemannan and Chronic Rheumatoid Arthritis (Real-world Case Report)
Example 41 describes a 65-year-old woman identified as B.L.H. who had suffered from chronic rheumatoid arthritis for 20 years.
Her disease had resulted in deformed joints, nodules beneath the skin, nodules involving the tendons, and persistent chronic pain.
When she was evaluated in the fall of 1988, she had already undergone numerous treatments, including gold injections, but according to the patent, these treatments had provided little benefit.
She was then advised to begin taking 800 milligrams of oral Acemannan each day.
Importantly, the patent reports that she experienced no benefit during the first six months.
By the middle of 1989, another issue had developed. The patient reported experiencing diarrhea if she took Acemannan more often than twice a week. Despite this, she also reported that her arthritis symptoms were beginning to improve.
Over time, she became able to tolerate 800 milligrams of Acemannan three times per week, and the patent reports that her rheumatoid arthritis symptoms noticeably improved.
By January 1990, the patient said that the preceding six months had been the best six months she had experienced in the previous 15 years.
According to the patent, both the effort required to perform her everyday activities and the pain associated with those activities had been markedly reduced.
This is an individual patient report, not a controlled clinical trial. The patent does not provide objective measurements of joint function, laboratory values, X-rays, or a comparison group. It also does not give us a complete account of any other treatments she may have been receiving during this period.
There was also an apparent side effect worth noting: taking Acemannan more frequently than twice weekly initially produced diarrhea.
So this example cannot establish that Acemannan caused the patient’s improvement.
What the patent records is a more complicated and therefore interesting course: a woman with a 20-year history of severe chronic rheumatoid arthritis began taking Acemannan after numerous previous treatments had provided little benefit. She reported no improvement for the first six months. Later, despite having to reduce the frequency because of diarrhea, her arthritis symptoms began to improve. Eventually, while tolerating 800 milligrams three times per week, she reported markedly less pain and difficulty with everyday activities—and described those six months as the best she had experienced in 15 years.
Example 42 — Acemannan and Depression and Anxiety (Real-world Case Report)
Example 42 describes a psychologist’s experience with patients suffering from severe depression and anxiety.
According to the patent, these patients had been under long-term observation and had failed to respond adequately to psychotherapy and antidepressant medications.
The psychologist then gave the patients 800 milligrams of oral Acemannan each day.
By the end of the first week, he reported observing that the patients’ emotions had become more stable. He also described what he considered a remarkable improvement in their attitudes—the first such improvement he had observed during the time these patients had been under his long-term care.
And that is essentially the entire report presented in Example 42.
The patent does not tell us how many patients were involved, which forms of depression or anxiety they had, how long they had been treated, which antidepressant medications they had received, or whether those medications and psychotherapy were continued while Acemannan was being taken.
It also provides no standardized depression or anxiety scores, laboratory measurements, control group, or long-term follow-up.
So this report cannot establish that Acemannan caused the changes the psychologist observed or that Acemannan is an effective treatment for depression or anxiety.
What the patent records is much more limited: a psychologist gave 800 milligrams of oral Acemannan each day to patients with severe depression and anxiety who had previously failed to respond to psychotherapy and antidepressant drugs. By the end of one week, he reported greater emotional stability and a remarkable improvement in attitude that he had not previously observed during his long-term care of these patients.
Example 43 — Acemannan and Feline Leukemia (Animal Study)
Example 43 takes us into a veterinary study involving cats with feline leukemia virus, commonly called FeLV.
Feline leukemia is caused by a retrovirus that can severely damage a cat’s immune system and produce a variety of serious health problems.
The cats in this study were already described as having end-stage disease.
So the researchers were dealing with very sick animals.
The study included 45 cats.
Each cat received an injection of Acemannan into the abdominal cavity once a week for six weeks.
The researchers didn’t simply give the injections and rely on someone’s impression of what happened.
The cats were examined every week during treatment.
Laboratory tests were also performed at the beginning of the study, again during the study, and at the end.
After the six weekly Acemannan treatments were completed, the cats were observed for another six weeks.
And what happened?
According to the patent, 67 percent of the cats improved during the study.
That’s approximately two out of every three cats.
The patent also tells us something about the cats that did not respond.
Among those nonresponding animals, the average survival time was less than 28 days.
And that’s really the heart of Example 43.
Researchers took 45 cats with advanced feline leukemia virus disease, treated them with Acemannan once a week for six weeks, monitored them with physical examinations and laboratory testing, and then continued observing them for another six weeks.
The patent reports that 67 percent improved during the study.
This was more than a testimonial involving one pet owner saying that a cat seemed better.
It was a veterinary study involving a defined group of 45 animals that were followed over time.
But there are also important limitations.
The example does not describe an untreated control group for comparison. It does not tell us here exactly how “improvement” was defined for each cat, and it does not demonstrate that Acemannan eliminated the feline leukemia virus.
So we should not turn the result into a stronger claim than the patent supports.
What Example 43 actually documents is this:
Among 45 cats with end-stage feline leukemia virus disease that received six weekly Acemannan injections, the patent reports that 67 percent improved during the study, while the cats that did not respond had an average survival time of less than 28 days.
Example 44 — Acemannan Combined with Antifungal Treatment in HIV Patients (Real-world Case Report)
Example 44 describes three patients with HIV-1 who developed recurring and often painful lesions in the mouth.
The patent reports that these patients developed hairy leukoplakia, yeast-related plaques, oral ulcers, or some combination of these conditions. In some cases, the lesions were extensive and painful.
The patients had been treated with ketoconazole, an antifungal medication. According to the patent, ketoconazole had improved the condition in some of the patients, while others had not responded.
Acemannan was then added to their treatment at a dose of 800 milligrams orally each day.
Within one week of adding Acemannan, the patients reported that the lesions involving the skin and mucous membranes had disappeared.
The patent further reports that taking Acemannan together with ketoconazole for three to five days cleared an outbreak for periods ranging from several weeks to several months.
Continued use of Acemannan was also reported to either eliminate or reduce subsequent outbreaks of these infections.
This report involves only three patients and was not a controlled clinical trial. The patients were also receiving ketoconazole, so the example cannot determine how much of the reported improvement was attributable to Acemannan, the antifungal medication, or the combination of the two.
The patent also does not provide laboratory cultures or other testing demonstrating that the underlying infectious organisms had been eliminated.
What Example 44 does record is a noteworthy clinical observation: three HIV-1 patients with extensive and sometimes painful oral lesions had experienced either incomplete improvement or no response to antifungal treatment. After 800 milligrams of oral Acemannan was added to their therapy, the patients reported elimination of the lesions within one week, with continued Acemannan use reportedly eliminating or reducing later outbreaks.
Example 45 — Acemannan Combined with Treatment for Pneumocystis Pneumonia (Real-world Case Report)
Example 45 describes an HIV-1 patient who was already taking 800 milligrams of oral Acemannan each day.
The patient was admitted to a Veterans hospital in Arkansas after developing Pneumocystis carinii pneumonia, commonly called PCP—an opportunistic lung infection that was particularly serious in people with HIV and AIDS.
According to the patent, the diagnosis was consistent with the patient’s chest X-ray and was confirmed through examination of sputum from the lungs.
The patent notes that, based on the experience of this Veterans hospital, HIV-1 patients with PCP typically required two weeks or longer to respond to treatment—if they responded at all.
This patient was treated for one week with aerosolized pentamidine, a medication delivered directly into the lungs, while his daily Acemannan treatment was continued.
According to the patent, the patient responded during that one week of treatment and was discharged from the hospital symptom-free.
And that is essentially the entire case as presented in the patent.
This is an individual patient report, not a controlled clinical trial. More importantly, Acemannan was not being used by itself to treat the pneumonia. The patient received aerosolized pentamidine, an established treatment for Pneumocystis pneumonia, while continuing Acemannan.
Therefore, this example cannot tell us whether Acemannan contributed to the patient’s relatively rapid improvement or, if it did, how much of a contribution it made.
What the patent records is more limited but still noteworthy: an HIV-1 patient already taking 800 milligrams of Acemannan daily developed confirmed Pneumocystis pneumonia. He was treated with aerosolized pentamidine while continuing Acemannan and, after one week, was reported to have responded to treatment and was discharged from the hospital symptom-free.
Example 46 — Acemannan Combined with Antibiotic Treatment for Cryptosporidiosis (Real-world Case Report)
Example 46 describes an HIV-1 patient who was suffering from chronic diarrhea and weight loss.
Testing of the patient’s stool revealed the characteristic acid-fast spores associated with cryptosporidiosis, providing evidence that this parasitic infection was responsible for the intestinal illness.
The patient was then treated with a combination of 800 milligrams of oral Acemannan each day and 250 milligrams of rifabutin four times a day.
This combination treatment was continued for two weeks.
According to the patent, after those two weeks the patient was free of diarrhea and had begun gaining weight.
And that is essentially the entire case as presented in the patent.
This is an individual patient report, not a controlled clinical trial. More importantly, Acemannan was not administered by itself. The patient was receiving rifabutin at the same time, so the example cannot determine whether Acemannan contributed to the improvement or how much of the response was attributable to either component of the combination.
The patent also does not report follow-up stool testing showing whether the Cryptosporidium infection itself had been eliminated. What it reports is the clinical outcome—the diarrhea resolved and the patient gained weight.
So the central observation in Example 46 is straightforward: an HIV-1 patient with chronic diarrhea, weight loss, and stool findings diagnostic of cryptosporidiosis received Acemannan together with rifabutin for two weeks. At the end of that period, the patent reports that the patient was free of diarrhea and gaining weight.
Example 47 — Acemannan Combined with Treatment for Tuberculosis in an HIV-Positive Patient (Real-world Case Report)
Example 47 describes an HIV-1 positive patient identified as S.G. who was experiencing progressive weight loss and a persistent low-grade fever for which doctors had not initially identified a cause.
Further examination revealed enlarged lymph nodes deep within the abdomen, behind the abdominal cavity. Biopsies were taken from this mass, and cultures eventually revealed human tuberculosis.
At the time the tuberculosis was discovered, the patient had already been taking 800 milligrams of oral Acemannan each day.
Doctors then began antituberculosis treatment using three medications: 300 milligrams of isoniazid per day, 600 milligrams of rifampin per day, and 1,000 milligrams of ethambutol per day. The patient’s daily Acemannan use was continued.
According to the patent, the patient’s fever disappeared within 24 hours after the antituberculosis therapy was begun.
Within ten days, the patient had also begun gaining weight.
And that is essentially the entire case as presented in the patent.
This is an individual patient report, not a controlled clinical trial. More importantly, the rapid improvement occurred after three established antituberculosis medications were introduced. The patient had already been taking Acemannan before the tuberculosis was diagnosed.
Therefore, this example cannot tell us whether Acemannan contributed to the patient’s improvement or whether the response was primarily the result of the antituberculosis drugs.
What the patent records is a straightforward clinical sequence: an HIV-positive patient who was already taking 800 milligrams of Acemannan daily developed progressive weight loss and a persistent low-grade fever. Tuberculosis was eventually identified through biopsy and culture. After three antituberculosis drugs were added to his treatment, his fever disappeared within 24 hours and he began gaining weight within ten days.
Example 48 — Acemannan Combined with Treatment for Mycobacterium Avium Infection in HIV Patients (Real-world Case Report)
Example 48 describes an HIV-1 patient who was suffering from continuous diarrhea.
Testing eventually identified the cause through both microscopic examination and culture as an infection with Mycobacterium avium, or MAI as it was identified in the patent. This type of infection can become particularly serious in people whose immune systems have been severely weakened by HIV.
The patent states that, at the time, no treatment was known to be effective against the infection. However, an antibiotic identified as ansamycin was provided by the Centers for Disease Control.
The patient was then treated with 250 milligrams of ansamycin four times each day, together with 800 milligrams of oral Acemannan daily.
According to the patent, the patient’s continuous diarrhea stopped in less than one week.
Before treatment, the patient had been losing three to four pounds every week. Within two weeks of beginning the combination therapy, the patent reports that the patient had begun gaining weight instead.
The patient’s fatigue and general weakness also decreased.
The example then describes a second HIV-1 patient, identified as C.C., who also had Mycobacterium avium infection confirmed by biopsy and culture.
The patent reports that this patient experienced a similarly rapid improvement after taking oral Acemannan. Importantly, it also states that follow-up cultures became negative.
This is not a controlled clinical trial, and the first patient was receiving both Acemannan and an antibiotic at the same time. Therefore, we cannot determine how much of the improvement was attributable to Acemannan, the antibiotic, or the combination of the two.
The second patient’s report is even more limited because the patent provides very little information about the treatment regimen or the timing of the response.
What Example 48 does document is an interesting clinical observation: two HIV-positive patients with laboratory-confirmed Mycobacterium avium infection experienced rapid improvement during treatment that included Acemannan. In the first patient, persistent diarrhea stopped in less than a week, weight loss reversed within two weeks, and fatigue and weakness decreased. In the second patient, the patent reports a similarly rapid improvement along with follow-up cultures that became negative.
Example 49 — Acemannan Combined with Multidrug Chemotherapy for Metastatic Breast Cancer (Real-world Case Report)
Example 49 describes a 38-year-old woman identified as J.F. who had undergone a mastectomy five years earlier for ductal carcinoma of the breast.
By the time described in this example, however, her cancer had become widely metastatic.
The cancer had spread throughout the lining of her abdominal cavity, producing a severe accumulation of fluid known as ascites. The swelling was so extensive that the patent describes her as appearing pregnant.
CAT scans also showed a tumor in her liver and multiple areas where cancer had spread to her bones and was destroying bone tissue.
The patient had delayed beginning chemotherapy, and according to the patent, her life expectancy at this point was estimated at only four to six months.
She was instructed to begin taking 800 milligrams of oral Acemannan each day and to begin the multidrug chemotherapy recommended by her oncologist.
The proposed chemotherapy included Adriamycin, cyclophosphamide, mitomycin-C, and 5-fluorouracil, commonly called 5-FU. The treatment she actually received included weekly intravenous cisplatin in combination with Adriamycin and other chemotherapy agents.
According to the patent, the only side effects she experienced were hair loss and fatigue on the day the chemotherapy was administered.
Subsequent examinations reportedly showed several striking changes.
Areas of bone that had been damaged by metastatic cancer showed evidence of new bone formation. The accumulation of fluid in her abdomen disappeared. Masses that previously could be felt within the abdomen were no longer detectable by examination. The liver mass disappeared, and the patient began gaining weight.
This is an individual patient report, not a controlled clinical trial. And Acemannan was clearly not being used by itself. The patient was receiving intensive multidrug chemotherapy, including cisplatin and Adriamycin, while taking Acemannan.
Therefore, this example cannot tell us what contribution, if any, Acemannan made to the reported cancer response or to the patient’s apparent tolerance of chemotherapy.
What the patent documents is nevertheless a remarkable clinical course: a 38-year-old woman with widely metastatic breast cancer and an estimated life expectancy of only four to six months began multidrug chemotherapy while taking 800 milligrams of Acemannan daily. Subsequent examinations reportedly showed disappearance of the abdominal fluid, palpable abdominal masses, and liver mass, along with new bone formation in areas previously damaged by metastatic disease and an accompanying gain in body weight.
Example 50 — Acemannan and Chronic Athlete’s Foot (Real-world Case Report)
Example 50 describes a 40-year-old physician who had suffered periodically from chronic athlete’s foot for more than 20 years.
He had itching, cracked, and burning areas of skin between and around the base of his toes.
The physician applied Acemannan gel directly to the affected areas.
According to the patent, in less than one week he experienced significant healing and improvement. Based on his own experience treating his chronic athlete’s foot over more than two decades, the physician reported that Acemannan was the most effective treatment he had used.
The patent goes on to say that other patients had reported similar improvement.
It also notes an interesting additional observation. Some people who were taking Acemannan for entirely different conditions reported that their athlete’s foot lesions improved as well.
And that is essentially the entire report presented in Example 50.
This is not a controlled clinical trial. The primary case is the personal experience of a single physician, and the patent does not identify the fungal organism through laboratory testing, provide measurements of the lesions, describe previous antifungal treatments in detail, or give long-term follow-up showing whether the condition returned.
Likewise, although the patent mentions similar improvement in other patients, it does not tell us how many patients were involved or provide their individual results.
So this example cannot establish that Acemannan is an effective treatment for athlete’s foot or other fungal infections.
What the patent records is more limited: a physician with a more than 20-year history of recurring athlete’s foot applied Acemannan gel to itching, cracked, and burning lesions around his toes. In less than a week, he reported healing and improvement and described Acemannan as the most effective treatment he had personally used for the condition. The patent also reports that similar improvement had been observed by other patients.
Example 51 — Acemannan and a Fire-Coral Sting (Real-world Case Report)
Example 51 describes a 40-year-old woman who injured her knee on fire coral while scuba diving.
The resulting skin lesions covered approximately nine square centimeters—an area a little larger than one square inch.
The patent explains that the usual course following this type of fire-coral injury involves intense inflammation for approximately eight hours, followed by delayed healing of the skin wound that can continue for about 14 days.
Acemannan gel was applied directly to the woman’s injured knee.
According to the patent, after eight days of applying Acemannan gel, the wound had completely healed and the resulting scarring was barely detectable.
And that is essentially the entire case as presented in Example 51.
The patent does not tell us how frequently the gel was applied, whether the woman received any other treatment, how the wound was evaluated during those eight days, or how the expected 14-day healing period was established.
This is also a single-person report without a control or comparison group. Therefore, it cannot establish that Acemannan caused the wound to heal more rapidly or reduced the amount of scarring.
What the patent records is a straightforward observation: a woman suffered a fire-coral injury to her knee involving approximately nine square centimeters of skin. Acemannan gel was applied to the wound for eight days, after which the patent reports complete healing with barely detectable scarring.