Changing the Direction of Research to Solutions and/or Treatments for Neurodegenerative Diseases By Dr. Vincent Tedone M.D.
The Purpose of This Statement
The purpose of this statement is to change the direction of the current research on a number of serious debilitating diseases that are becoming more common. Unless the direction of the research is changed, many patients will be left hopeless and die horrible deaths.
Investigational Medicine – What It Is & Why It’s Necessary
I’m a medical doctor who has been involved in investigational medicine since 2007. Investigational medicine means I review all of the research that’s been done on neurodegenerative diseases and I use my knowledge of the human body and clinical experience to connect the dots between the many research studies.
Each study has its own purpose and conclusions, etc. When we put those conclusions together and connecting those dots…this reveals a new set of hypotheses that could lead to groundbreaking research in a new direction.
You can think of scientific studies as trees. Each study is a single tree…but when you put them all together, you can construct a whole forest. To cure diseases, we need to focus on the forest and not just the individual trees. This is the main difficulty and often forgotten in the world of medical research.
Brief History of Dr. Tedone’s Work With ALS
Many have watched my presentation to ALS patients in Brugos Spain. I discussed the history of my daughter Deanna and her battle with ALS, and related it to the subsequent development of the Deanna Protocol® Plan, using Deanna as my test case. Today, I’d like to present new developments in my research.
Every patient who is diagnosed with ALS has the standard CDC test protocol for Lyme disease to rule out an infection with the borrelia Bacteria. Most ALS patients test negative and are then confirmed over a 2-year period as having ALS. These patients are told they will die a horrible death and there is no cure or treatment for their disease.
If you recall hearing about the DP™ Plan, you’ll remember that it stopped the progression of Deanna’s ALS, and did the same for over 2,000 PALS. If you’ve followed our story, you’ve also read that winning the Fight (our non-profit medical research organization) funded studies that documented that the DP™ Plan also works in mice with ALS. Since then, we’ve discovered new information, which is the relationship between ALS and the borrelia bacteria.
Borrelia Bacteria Infection in Deanna
In November of 2015, Deanna developed severe meningitis. She had had tests in 2009 for the Borrelia infection, which were negative. Then in 2014 she was tested at a different laboratory [IGeneX] and these revealed the possible presence of borrelia. Then, in October of 2015 she was tested again at IGeneX. The new tests came back positive for borrelia bacteria. The very next month, she developed severe meningitis. To recap this series of events: Negative borrelia tests in 2009. Tests at IGeneX in 2014 revealed questionable results. Then positive borrelia tests at IGeneX in October of 2015, then the onset of severe meningitis one month later in November of 2015.
Knowing she was infected with borrelia, it was decided to treat her with IV antibiotics 2 Gms every 24 hours. Her pain subsided, but as time elapsed from her last dose, her pain would start to return. We increased the dose to every 12 hours and the pain went away completely and has never returned.
Borrelia Bacteria and ALS
This series of events indicated to me that it’s highly likely that Deanna’s ALS is caused by an infection with the Borrelia bacteria. The suspicion of borrelia as the causative agent for ALS has been entertained for over 20 years and ruled out by several research papers. One of the research papers stated that when ALS was treated with antibiotics the symptoms never subsided, therefore, ALS cannot be caused by Borrelia. At the surface, this conclusion seems logical…but when we examine it in more depth, we begin to see its flaws.
The problem with the conclusion above is that Borrelia forms a biofilm around its colonies and this biofilm is impervious to antibiotics…Hence antibiotics alone will not kill the bacteria. To kill Borrelia, antibiotics must be administered IN CONJUNCTION with antifungals. These break down the biofilm so then antibiotics can kill the borrelia. The research that concluded that antibiotics are not effective in ALS did not include antifungals to break down the biofilm surrounding and protecting the Borrelia.
Negative Borrelia Tests Aren’t Accurate
I mentioned before that Deanna did not test positive for borrelia until 2015. It so happens that many patients test negative for borrelia, even when they ARE infected. Why is this? Borrelia is usually NOT present in the blood circulation until very late in the disease when the Borrelia is rampant and has taken over the patient. In the beginning and middle stages of the disease, borrelia lives in the soft tissues and lymphatics…which makes it nearly impossible to detect. Borrelia can also change the configuration of the proteins on the surface of its cell membrane so antibodies cannot detect it Hence the CDC test criteria for establishing the diagnosis of a Borrelia infection are not valid. Borrelia is also mobile and can move around in the soft tissues selecting a beneficial environment and move away from cells that would attack it. Its mobility is so great it can swim in circulation against the blood flow.
Misconceptions About Borrelia
There are misconceptions regarding how borrelia is transmitted and I’d like to dispel them. The common perception is that borrelia is only transmitted by ticks. The reality is that borrelia can also be transmitted by bed bugs, mosquitoes, sand fleas and other vectors. Another misconception is that borrelia is endemic because ticks that cause Lyme disease are primarily found in New England, and other limited regions. We are now learning that borrelia infections are much more wide spread than previously thought and it is highly likely that they also cause other neurodegenerative diseases.
It is important to understand the flaws in the research on ALS and its connection to Borrelia. The cause of the false negatives in borrelia tests can shed new light on the Borrelia connection to ALS and inspire groundbreaking research.
Another extremely important point is this: A person could have been in contact with borrelia and have it inside them, but not show signs of infection for many years. Why is this? It all relates to the human biome.
The human body is made up of human cells and bacteria that are essential to its chemistry and physiology. When a foreign bacterium enters the body, the normal flora and bacteria secrete a hormone that activates the immune system to attack this foreign bacterium. Therefore, when a body has the borrelia bacteria, the body’s immune system keeps the Borrelia under control and the body remains a-symptomatic. This is why a patient can live with these bacteria for many years and show no or limited signs of infection. This is also the reason why epidemiological studies have little value here. The Borrelia bacterium begins to produce symptoms when the body’s immune system is compromised or the growth of the Borrelia enhanced. There are several factors that can compromise the immune system, such as severe stress, pregnancy, exposure to toxins, and other events. There are also substances that can enhance the growth of Borrelia. One such substance is aluminum but I’m sure there are others yet to be determined.
I have developed a great respect for borrelia. It is extremely difficult to detect and protects itself very well. Patients with Lyme disease caused by borrelia, and usually accompanied by co-infections, are known to have relapses after being treated with antibiotics. Doctor Eva Sapi has shown that when the borrelia is confronted with an antibiotic, it breaks down into small globules of DNA and becomes dormant. Once the antibiotic is stopped, it becomes active again and the disease recurs. She has also shown that herbal chemicals kill the borrelia.
Treating Deanna’s Borrelia Infection
Following Deanna’s episode of severe meningitis in 2015, Deanna was on IV antibiotics for almost a year. I added to this an antifungal when she left the hospital because the infectious disease Doctor did not accept the fact that a biofilm could protect the borrelia. I then learned of Dr. Sapi’s work comparing treatment with herbal chemicals to treatment with antibiotics. That is when I switched Deanna to Herbal chemicals with the Cowden Support Program from Nutramedix. Deanna has been on the herbal protocol for about a year and we now believe the borrelia is suppressed. We are treating her co-infections by using different herbs.
Borrelia’s Energy Cycle
It is interesting to note a few other facts about borrelia. Borrelia can only metabolize glucose. It does not have a high-powered energy cycle [TCA] based on ATP production like other organisms. It reproduces once a week and needs the high-powered energy cycle do so. This is why it enters host cells and co-opts the cell’s energy cycle, starving the cell of energy and causing it to die. This fact indicates why the DP™ Plan kept Deanna’s disease from progressing. The basis for the DP™ Plan is to add energy to cells to keep them alive.
Why Borrelia Infections Don’t Look The Same In All Patients
There are many different species and strains of borrelia plus combinations with other infecting agents, and this diversity accounts for the predilection by the infecting agents of one cell over another. This, in turn, explains the diverse clinical pictures we see in neurodegenerative diseases. The disease will look different, clinically, depending on which specific cells the borrelia infects and which genus, species or strain of borrelia that is present. This is further complicated by co-infections with other bacteria, parasites and viruses injected by the vector into the host or Patient along with borrelia.
Autoimmune Diseases & How Research Should Change
I would also like to bring your attention to autoimmune diseases. Among the common diseases that are classified as autoimmune are ALS, Parkinson’s, MS, Alzheimer’s, fibromyalgia, CFS [chronic fatigue syndrome], and probably others. We don’t know what causes these diseases, but they all have classical areas of involvement with classic symptoms and an activated immune system.
What is astounding is that we all agree that cells die in these diseases due to lack of energy…but there is zero research, except for that funded by our nonprofit foundation [WFND], on metabolic solutions for these diseases to enhance energy production in the cells to keep them alive. There is also no research to improve our capacity to detect the possible cause of the activation of the immune system.
In these diseases, we have evidence that the body’s immune system is activated, but we cannot detect an etiological agent or cause of this activation…so the common claim is “the body is attacking itself.” Then, we spend vast sums of money to find a pharmaceutical agent to cure or suppress these immune responses or correct the damage without even knowing what caused the response and hence the disease. Perhaps we should be spending money to look for the CAUSE of the disease.
Research Done on ALS
To further make my case to change the direction of the research on neurodegenerative diseases, I will use the example of the research that has been done on ALS.
PALS develop protein tangles in their brain given various designations such as TAU, TDP-43, Ubiquitin and others. Researchers use very sophisticated equipment to investigate and monitor these tangles in vitro and hypothesize that they are the cause of ALS or they spread ALS, when in reality, in my opinion these tangles are actually debris from dead cells.
Then, there are the clinical trials such as using stem cells to treat PALS. I have been monitoring this research since 2009 and, in every case, when patients improve initially; their condition gets worse again over time. We know that the cells are being killed by something in their environment, so why would we not realize that whatever is killing these cells would also kill the new cells that grow during stem cell treatments? If we’re going to put new cells into a toxic environment, why not find a way to make the environment non-toxic before exposing new cells to the same fate – death?
Another example is a clinical trial called NPOO1. A PALS in France informed me that the substance used in this clinical trial is Sodium chlorite, which is a disinfectant. She took it and was able to get up and walk. It is a highly toxic substance and cannot be taken for a prolonged period. When she stopped taking it, her condition worsened rapidly. Common sense tells us that if using a disinfectant that kills bacteria improved her condition, ALS could very likely be caused by bacteria!
My investigation into the research has brought me in contact with very reputable physicians, who have anecdotal and serology evidence that borrelia and other bacteria are the causative agents in the autoimmune diseases ALS, MS, Parkinson’s, and Alzheimer’s. I realize that this evidence is certainly not conclusive. However, when people are dying terrible deaths this evidence should at least suffice to direct further research to improve detection of the presumed infecting agent and to determine a treatment. When people are dying, sitting back and claiming “the body is attacking itself” is not a sufficient conclusion.
There are several physiological and biochemical facts that need to be mentioned here to reveal how all the pieces fit together and how the borrelia bacteria may also be involved in concussions and CTE [chronic traumatic encephalopathy]. Studies from the Weismann institute in Israel, by Dr. Vivian Teichberg, revealed that extracellular glutamate is toxic to contiguous cells. We documented this in our research by placing glutamate in a petri dish with human nerve cells. The microtubules that run down the axon and carry the nerve impulses became tortuous and crooked. Then, we added the DP™ Plan and the tubules straightened out.
Why did this happen? The ratio of glutamate inside the cell to outside the cell is in a normal case 10,000 to 1. There is a normal physiological process that lowers the glutamate in the extracellular space to maintain this physiological ratio. The glutamate is moved out of the extracellular space into circulation on a gradient basis. It is then transformed into glutamine and eliminated by the kidneys.
So, when too much glutamate is outside the cell, it is toxic. When it’s inside the cell, it is the primary excitatory neurotransmitter. Research has been done for over 20 years to block glutamate receptors based on the assumption that there is excess glutamate in ALS. However, the existence of excess glutamate in the body is not the problem.
The problem is that the ratio of glutamate outside the cell to inside the cell is incorrect. When cells degenerate and die, glutamate is spilled out and displaced into the environment surrounding the contiguous cells. This changes the intracellular and extracellular ratio and kills contiguous cells and causes the disease to spread.
What happens when there is a traumatic brain injury? The cell membrane ruptures and micro blood vessels are torn, causing bleeding into the extra cellular space. In concussions, some people develop CTE others do not. Why? Could it be that the person that develops CTE has had contact with the borrelia bacterium? Interestingly enough, autopsies of people with CTE reveal amyloid plaque in the brain. Amyloid plaque is also found in Alzheimer’s disease.
Dr. Alan MacDonald, a forensic pathologist, has cultured borrelia from the amyloid plaque in AD. Dr. Miklossy has independently corroborated his work. Dr. Sapi has produced protein tangles TDP -43 and Tau by adding borrelia to human nerve cells. She is seeking funding to demonstrate the formation in vitro of amyloid plaque when borrelia is added to human nerve cells.
Recap of Borreila Disease Process
So now that I’ve explained some of the research and the clinical picture, I’d like to recap the disease process that I discussed earlier. First, the patient is bitten by a borrelia vector (a tick, mosquito, bed bug or another vector). Less than 40% have a cutaneous reaction at the bite site. At first, the patient is not symptomatic because the normal flora and the body’s immune system keep the borrelia in check and, because of this, not enough cells are being killed to cause any noticeable changes in the patient. A person can live for years without any manifestation of a borrelia infection.
Then, there is a concomitant factor, which either lowers the body’s immune system or enhances the growth of the borrelia (again, this could be stress, toxins or some other factor). The borrelia enters cells to reproduce, co-opts the cells’ energy systems, and ultimately kills the cells as the borrelia multiply. The patient begins to show symptoms, the borrelia overcome the normal flora in the body, and the borrelia take over the host (the patient), ultimately causing the body’s systems to fail. With that process in mind, I’d like to discuss some probable factors that interfere with the body’s ability to fight borrelia infections.
There are very high instances of ALS in populations that have been exposed to certain substances and these substances could very well be the concomitant factors that inhibit the body’s immune response to borrelia or enhance the growth of the borrelia. We have increased incidence of ALS with diesel fuel truck drivers, sports in which concussions occur, Gulf War veterans, those in contact with certain organic substances, those in contact with asbestos, and also those in contact with heavy metals. (My daughter living in a house with Chinese dry wall that had heavy metal in it, and those same metals in the drywall were found in her body]. People with mercury fillings have an increased incidence of ALS and, perhaps, some patients vaccinated with vaccines that contain a mercury derivative thimerosal.
It is interesting to note that autistic children have inflammatory cells in their brain. They usually do not present with a functional deficit until age 2. The Phylum spirochete, as we know from Syphilis, crosses the placenta. Could Borrelia, a spirochete, also cross the placenta? Could it be that the neonate gets the Borrelia from the asymptomatic mother then the mercury in the vaccines it receives in the first 15 mos. of life enhances the growth of the Borrelia which then causes brain damage? This would explain the late onset of autistic symptoms at age 2. This is only a hypothesis but it is certainly worthy of investigation. It has been estimated that in the future 50 % of children will be autistic.
Other Neurodegenerative Diseases Linked to Bacteria
Environmental factors aside, let’s not forget that other neurodegenerative diseases besides ALS have been linked to the spirochete bacteria as well. As I mentioned, the same spirochetes found in gum disease have been found in amyloid plaque in the brains of deceased Alzheimer’s patients…with an overwhelming frequency. There is also an increased incidence of ALS in people who live near bodies of water that contain algae and hence the Cyano bacteria that produce the neurotoxin BMAA.
Dr. Alfred Miller, graduate of Harvard medical school and a Mayo trained rheumatologist, and now retired has notified me of positive tests for Borrelia in Multiple Sclerosis. Dr. David Martz, an internist and infectious disease specialist now retired has had patients with ALS as well as Parkinson’s disease who have tested positive for Borrelia.
Changing the Narrative
My purpose is to change the narrative concerning Lyme disease and the Borrelia bacteria. Lyme disease is only one manifestation of a borrelia infection. Other manifestations are very likely ALS, MS, Parkinson’s, Alzheimer’s, fibromyalgia, CFS, CTE, possibly autism and who knows what else. We need to concentrate on the borrelia bacteria, how to detect it, what factors enhance its growth, and what is the most efficacious method of treatment.
There is obviously a great deal of research that needs to be done in a new direction. Unfortunately, it is not research that has much commercial appeal.
Suggestions for Those With Neurodegenerative Diseases
What I can suggest, to those unfortunate enough to have these diseases is the following:
First, help to keep the nerve cells alive with metabolic substances that give them the energy they need to stay alive. This is what the DP™ Plan provides.
Second, kill the bacteria with antibiotics and antifungals in the first 3 mos. of the infection before the Borrelia is ensconced in the soft tissues. Later in the disease kill the Borrelia with herbal chemicals. The Cowden Support Program has been effective. Based on the work of Eva Sapi Ph.D. and my daughter’s response, I believe that the herbs are more effective than antibiotics…mainly because the current antibiotics in use are probably more effective in killing normal flora bacteria than they are at killing the Borrelia. Also b/c antibiotics probably don’t eradicate the Borrelia and they are revived when the AB are stopped.
Most who have neurodegenerative diseases have functional deficits. Once treatment has suppressed the borrelia to a point where the body’s immune system is able to keep the borrelia bacteria under control, then it will be time to implant stem cells or nerve growth factors into patients with the goal of forming new nerve cells to help patients regain lost function.
This is my plan for the way forward in finding a solution to ALS in specific and neurodegenerative diseases in general…until further research can document a better way forward.
Dear WFND Subscribers:
There is anecdotal and laboratory evidence that ALS, MS, and perhaps some Alzheimer disease are caused by the Borrelia bacteria.
Medical science has a difficult time detecting the Borrelia bacteria. This has been documented by many people with ALS (pALS) initially testing negative for a Borrelia infection to rule out Lyme disease, but then testing positive in late stages of their disease.
There is a host response to the Borrelia bacteria which is a lowering of natural killer (NK) lymphocytes in response to the Borrelia infection.
Who should be tested?
If an individual has a neurological deficit or cognitive impairment of unknown cause, testing for NK lymphocytes will indicate contact with the Borrelia infection, and can be used to justify treatment for the Borrelia infection. This approach is much more acceptable than watching and waiting while the individual continues a downhill spiral.
Where can I be tested?
After many unanticipated delays the scientists at University of South Florida (USF) are moving forward with the experiment to determine the efficacy of the Deanna Protocol® Plan when combined with glutamic oxaloacetate transaminase (GOT). The experiment is being performed in steps using SOD1-G93A mice.
The next step is to collect the first of weekly biometric and behavioral data and separate the mice into experimental groups. The experiment includes four treatment groups: standard diet (SD); SD + Deanna Protocol® Plan (DP); SD +GOT + oxaloacetate (OX); SD + DP + GOT + OX.
Mice will be humanely euthanaized when disease progression, as determined by the USF veterinarians, is causing undue suffering. Tissues (muscles, brain and other organs) will be collected, processed and analyzed to see what effects the various treatments had. Once results are evaluated and available, an additional update will be shared on the website.
What were the delays?
Please continue reading for more details from the lab regarding the experiment. Results of the experiment will be shared in an additional blog post.
Dr. Tedone's Response to Dr. Bedlack's Criticism of Deanna Protocol® Plan on ALS Untangled Webinar on April 3, 2016
Responding to Dr. Bedlack’s Criticism of the Deanna Protocol® Plan
The webinar hosted by Dr. Bedlack for ALS Untangled criticized the Deanna Protocol® Plan. One criticism states that documentation of the DP™ Plan is faulty because it only reported on those patients who did well and did not include many other patients and, therefore, the data was biased. He is absolutely correct.
Regardless of the aforementioned bias, the fact that there are individuals who are improving and stabilizing for years (and some indefinitely) while following the DP™ Plan means that it delivers results better than those of any pharmaceutical ALS treatments on the market today. This is a fact that cannot be negated by lack of data on those who did not see improvements while on the DP™ Plan.
Regarding the bias in the data collection, Bedlack failed to mention that it is impossible to gather unbiased data because large amounts of data are nearly impossible to collect, given the limited number of PALS in any one geographic area. Winning the Fight has attempted to remedy this problem and has succeeded somewhat, but we have a ways to go. We began asking PALS to periodically record their ALSFRS scores on our website and, as a result, roughly 2,000 PALS have registered on our personal database. Those who have reported their scores have reported that they have declined less than the average amount and some have not declined at all.
In our PLOS ONE peer reviewed research paper in another sample, we reported on 40 out of 41 patients. One patient passed away. The success rate in this group was 70% with ALSFRS scores lower than the average. What happened to the PALS that did not respond? We don’t know.
Methodology vs. Common Sense
This is a situation where experts accept methodology over common sense, which is correct in most cases. However, in cases in which patients suffer from aggressive illnesses that will kill them in two to five years, common sense must reign supreme if it leads to a better outcome for patients. If the DP™ Plan yields better results than any other solution on the market, does it really make sense to say that nobody should use it because the methodology is imperfect? If we agree to this school of thought, what we’re really saying is that PALS should choose a definite and horrible death over an imperfect methodology that can improve their quality of life and extend their lives. Would you rather die a horrible death than accept imperfection?
Deanna Protocol® Plan vs. Pharmaceutical ALS Treatments
Neuroscientists have been trying to find a treatment to keep ALS patients alive for over 100 years, and patients continue to die within two to five years of diagnosis. The medical research community has spent many billions of dollars in this endeavor and watched tens of thousands of patients die horrible deaths. What result has this yielded? The greatest success in the ALS research community so far is a chemical called Riluzole, which extends life for 2 months and can damage the liver. Contrast the above with an over-the-counter, natural, non-harmful, metabolic solution that laboratory studies have proven effective in mice and anecdotal evidence has proven effective in humans.
The ALS association and other organizations focused on ALS research do much to benefit the ALS population. They provide services, provide assisted technology, raise awareness, and more. Despite the good these organizations do, they do a disservice to patients by overlooking the DP™ Plan, a solution that many PALS say helps. Is it a Cure? No, but it is better than nothing...which is what the medical community currently offers.
We believe that the DP™ Plan can be improved with research, but funding is necessary to continue this research. Rather than continue to waste so much money on chemicals that have little basis for their benefit to PALS, why not divert some money for research to help current PALS. Why not contribute to helping preserve their ability to function, lead more comfortable lives, and live longer lives? Ask the PALS using the DP™ Plan. Most will support the idea.
Vincent M Tedone M.D., F.A.A.O.S.
AIRED: December 28, 2015– 11 am PST
TITLE: “The Deanna Protocol®: Hope For ALS and other Neurological Conditions”
SPECIAL GUEST: Dr. Vincent Tedone
AUDIO REPLAY/DOWNLOAD: http://answersforthefamily.com/the-deanna-protocol-hope-for-als-and-other-neurological-conditions-dr-vincent-tedone/
Dr. T. and Deanna discuss the development of the protocol with reporter Gina Pitisci. When Dr. Vincent Tedone’s daughter was diagnosed with ALS in 2007, he told her she would beat the disease. Deanna Tedone Gage was an attorney, recently married and starting her life when she learned her diagnosis at age 30. "Without my father, I would not be sitting here talking to you today,” she said. “He not only provided a method to keep me alive, but he also gave fuel to my positive attitude." Doctors gave her little hope. But she and her father decided to create their own. That’s how the Deanna Protocol® was born.
"All traditional research currently in progress is based on finding a pharmaceutical drug to cure ALS. Meanwhile, metabolic researchers at Winning the Fight believe they have found an additional supplement that might provide a therapy that can stop the disease in its tracks."
Amyotrophic Lateral Sclerosis (ALS), also known as Lou Gehrig’s disease, is a neurodegenerative disorder of motor neurons causing progressive muscle weakness, paralysis, and eventual death from respiratory failure. There is currently no cure or effective treatment for ALS. Besides motor neuron degeneration, ALS is associated with impaired energy metabolism, which is pathophysiologically linked to mitochondrial dysfunction and glutamate excitotoxicity. The Deanna Protocol (DP) is a metabolic therapy that has been reported to alleviate symptoms in patients with ALS. In this study we hypothesized that alternative fuels in the form of TCA cycle intermediates, specifically arginine-alpha-ketoglutarate (AAKG), the main ingredient of the DP, and the ketogenic diet (KD), would increase motor function and survival in a mouse model of ALS (SOD1-G93A). ALS mice were fed standard rodent diet (SD), KD, or either diets containing a metabolic therapy of the primary ingredients of the DP consisting of AAKG, gamma-aminobutyric acid, Coenzyme Q10, and medium chain triglyceride high in caprylic triglyceride. Assessment of ALS-like pathology was performed using a pre-defined criteria for neurological score, accelerated rotarod test, paw grip endurance test, and grip strength test. Blood glucose, blood beta-hydroxybutyrate, and body weight were also monitored. SD+DP-fed mice exhibited improved neurological score from age 116 to 136 days compared to control mice. KD-fed mice exhibited better motor performance on all motor function tests at 15 and 16 weeks of age compared to controls. SD+DP and KD+DP therapies significantly extended survival time of SOD1-G93A mice by 7.5% (p = 0.001) and 4.2% (p = 0.006), respectively. Sixty-three percent of mice in the KD+DP and 72.7% of the SD+DP group lived past 125 days, while only 9% of the control animals survived past that point. Targeting energy metabolism with metabolic therapy produces a therapeutic effect in ALS mice which may prolong survival and quality of life in ALS patients.
People and families affected by ALS are finally seeing a glimmer of hope. The deadly illness, also known as Lou Gehrig's disease, destroys nerve cells and muscle control. There is currently no cure. However, a new treatment has been shown to slow and even stop its progression.
*The mouse studies referenced in this video are now finished. Research concluded that the Deanna Protocol® is effective.