Also known as multiple sclerosis (MS), it is a chronic, autoimmune, inflammatory, and neurodegenerative disease of the central nervous system (CNS). It is estimated that since 2008, 2.5 million individuals worldwide have been affected by the disease. It is commonly referred to as a disease of young adults, primarily affecting individuals between the ages of 25-35, with a higher prevalence in women. It constitutes the leading cause of disability today.
In 2008, the World Health Organization (WHO) estimated the global median prevalence of multiple sclerosis to be 30 cases per 100,000 individuals. The prevalence varies significantly in different regions: a) regions with low prevalence (approximately 5 cases per 100,000 individuals in Central Asia), b) regions with high prevalence (Australia, Canada, the United States, and Europe with more than 60 cases per 100,000 individuals).
On a global scale, the average age of onset of the disease is 29 years (range: 25th to 32nd year of age). The disease initially presents with a relapsing-remitting form characterized by unpredictable acute episodes of neurological symptoms (relapses), followed by periods of remission during which there is partial or complete recovery of deficits incurred during the relapse. However, as the disease progresses, it results in permanent neurological impairments. Approximately 75% of patients will develop clinically definite multiple sclerosis within approximately 25 years, characterized by a gradual increase in disability during relapses, followed by worsening disability.
PATHOPHYSIOLOGY
Multiple sclerosis is an inflammatory disorder in which the autoimmune response targeting myelin proteins in the CNS leads to the destruction of the myelin sheath surrounding neuronal axons. These autoimmune processes are mediated by self-reactive lymphocytes that become activated, proliferate, and mature in lymph nodes. Subsequently, these lymphocytes enter the bloodstream and cross the blood-brain barrier, causing localized inflammation, demyelination, gliosis, and axonal loss. These pathological changes, visualized as lesions in the Central Nervous System (CNS) on magnetic resonance imaging (MRI), serve as hallmarks of the disease. The tissue damage resulting from inflammation occurs in the early stages of the disease and can, to some extent, be compensated by endogenous repair mechanisms, such as remyelination and axonal remodelling.
Nevertheless, as the disease worsens, these CNS repair processes begin to fail, leading to progressive, irreversible neurodegeneration and disability.
ETIOLOGY
The destruction of the myelin sheath around axons at lesion sites can eventually result in axonal transection and disrupt nerve conduction. Repeated inflammatory episodes lead to cumulative axonal loss, which is associated with the onset of permanent disability. In the early stages of the disease, there is remyelination by oligodendrocyte progenitor cells, which produce myelin, thus contributing to a reduction in disease pathology. However, as plaque sclerosis progresses, remyelination decreases, possibly due to the depletion or inadequate production of precursor oligodendrocytes that can mature into remyelinating cells. This increased lesion burden leads to permanent tissue loss, as reflected in MRI scans.
The cumulative effect of these neurodegenerative changes is the progressive, irreversible atrophy of the brain, a common feature of all forms of multiple sclerosis. Brain volume is expected to decrease by approximately 0.5–1.35% per year. In comparison, this rate in healthy adults is around 0.1–0.4%.
SYMPTOMS
Common symptoms include motor problems such as gait and balance issues, fatigue, optic neuritis with accompanying visual disturbances, urinary and bowel problems, and pain. The course of symptoms typically consists of two main stages: sudden exacerbation episodes lasting from a few days to months, referred to as relapses, followed either by improvement in 85% of cases or gradual worsening over time without periods of recovery in 10-15% of cases, or a combination of these two scenarios. Relapses are usually unpredictable. Viral infections such as the common cold, flu, and gastroenteritis can exacerbate the condition. Stress can also trigger a crisis. Pregnancy reduces the risk of relapse, but the risk increases after childbirth.
CAUSES
The causes of multiple sclerosis are unknown. It is believed to result from a combination of environmental and infectious factors, along with genetics. Various theories have been proposed, but none have been proven. The disease is more common in regions far from the equator, particularly in Northern Europe. Reduced exposure to sunlight leading to decreased vitamin D production has been suggested as an explanation for this geographic distribution. I will discuss the role of this essential vitamin later in this article.
GENETICS
It is not considered an inherited disease, but a series of genetic variations increase the risk. If both parents are affected, it has been statistically shown that the risk for their children is ten times greater than that of the general population. It would be more accurate to say that we still do not fully understand the genetic factors related to multiple sclerosis. In the case of identical twins, both siblings are affected in 30% of cases, whereas in non-identical twins, this occurs in 5% of cases. Specific genes associated with multiple sclerosis include variations in the HLA antigen of white blood cells. This HLA region has also been implicated in other autoimmune diseases such as type 1 diabetes and systemic lupus erythematosus. Overall, it has been estimated that HLA changes account for 20 to 60% of the genetic predisposition. Modern genetic methods, such as whole-genome association studies, have identified 12 additional genes that increase the risk of multiple sclerosis. Even microorganisms have been implicated as a cause of multiple sclerosis, as well as viruses like the Epstein-Barr virus, known as the infectious mononucleosis virus.
OTHER FACTORS
Smoking, as well as stress, are also risk factors. Work conditions, toxins, hormone intake, and certainly POOR DIET.
TREATMENT
There is no known cure. Various treatment methods aim to restore function after an episode and to prevent new episodes and disability. Like any medical treatment, drugs administered to those with multiple sclerosis have several side effects. For these reasons, many patients turn to alternative therapies.
THE ROLE of VITAMIN D
As previously mentioned, many individuals suffering from multiple sclerosis, and given that they do not observe any cure for the disease (treatments often address symptoms and are frequently unsuccessful), turn their attention and hopes to alternative therapies. Here, I will recount an incident that happened to me recently. I was invited to speak with the board of the Multiple Sclerosis Patients Association. The meeting took place at the association's offices, located at the old airport (Hassani), which was once the site of the American base in Elliniko, Greece. I spoke to them about Ganoderma, also known internationally as Reishi, and how it can assist them as a dietary supplement. I also referred them to international literature on the subject. Furthermore, I emphasized how a combination of Ganoderma, vitamin D, and Omega-3 would be highly beneficial. When I finished, a lady told me that their doctors allowed them to take some "herbs" if they wished, as long as these "do not interfere with the body's biochemistry." After a moment of surprise and astonishment, I explained that anything a person consumes, even a sip of water, a small bite of bread, or a spoonful of sweet milk, or anything else for that matter, will indeed "enter the body's biochemistry." Enzymes will be involved in its breakdown, its nutrient components will enter the bloodstream, and the rest will be eliminated through the digestive tract, among other processes. I also told them that when we ask someone about a topic, there are two possibilities: those who know about the topic and those who do not. Those who do not know would do well to say, "I don't know!" As I say in all my lectures, and I have given many in various parts of Greece on the pharmacological properties of Ganoderma, for which I have written the book "Ganoderma the Miraculous," www.ganodermathemiraculous.com, there is nothing more ethical and admirable than admitting, "I don't know." By doing so, one opens the door to knowledge and has the opportunity to learn what was previously unknown. I am not entirely sure if the aforementioned lady's suggestion was made by an actual doctor, but if it was, I consider it simply unacceptable. Hundreds of thousands of esteemed scientists around the world conduct serious studies, and numerous universities conduct research on the ancestors of pharmaceuticals, which are herbs.
These herbs have evolved and have given rise to drugs. Billions of people use various alternative treatment methods, often with significant results. Of course, this is "unpleasant" for the pharmaceutical industry, but we will not delve into that sorrow now. I want to emphasize that patients should be informed and should be allowed to decide freely. They have a say, especially as patients who have a choice in the treatment they will pursue. Ganoderma will help them, and they will see it very soon, with scientific evidence. Ganoderma contains a plethora of ingredients, from organic germanium with its maximum oxygenation of nerve cells to triterpenoids that stimulate oligodendrocytes in myelin production for remyelination.
Vitamin D, which is abundant in Ganoderma, also plays a significant role in the treatment of multiple sclerosis. Researchers from the Multiple Sclerosis Society Cambridge Centre for Myelin Repair, as well as many others in various university clinics (read more on the subject), have observed that vitamin D receptors are linked to a protein called RXR gamma receptor, known for its involvement in myelin repair. By adding vitamin D to brain stem cells where RXR proteins were present, it was observed that the rate of oligodendrocyte production, responsible for remyelination of damaged neuron axons in the central nervous system and spinal cord, increased.
Another study conducted at Johns Hopkins University confirms that vitamin D can either prevent or alleviate the symptoms of neurodegenerative diseases. This research was based on the observation that countries with minimal sunlight and, consequently, a deficiency in vitamin D, also have increased cases of multiple sclerosis. However, the fact that our country receives ample sunlight throughout the year does not reassure us. In a recent study I conducted with Harokopio University (March - May 2016), we measured vitamin D levels in 26 volunteers. Among the 26 samples, 18 had very low levels of vitamin D, 5 had low levels, and only 3 had levels that approached normal limits.
Therefore, in our country, a significant portion of the population has very low vitamin D levels. This happens for two reasons. Firstly, in order to produce vitamin D in our bodies, sunlight exposure is essential. Fifteen to twenty minutes per day is sufficient to meet this requirement. During the summer in our country, this is achievable, although not without the well-known risks that can threaten our health (e.g., malignant melanoma due to excessive sun exposure). However, during the winter, many people neglect this. Additionally, poor diet choices made by most of us, often without taking supplements into account, are considered essential since the raw materials we use to prepare our daily meals are of unacceptable quality. I should also mention that after the initial laboratory measurements of the 26 volunteers (all women), they were given a special diet based on mushrooms, which are known to contain large quantities of vitamin D. After 2 months, an increase in vitamin D levels in the volunteers' serum was observed, ranging from 18% to 82%. ***
Α FEW WORDS ABOUT VITAMIN D
Vitamin D is a steroid hormone that plays a crucial role in the intestinal absorption of calcium and the regulation of calcium-phosphorus homeostasis. It assists in maintaining normal calcium and phosphorus levels within the body. Its role extends to the formation and maintenance of strong and healthy bones, as well as supporting neuromuscular function. Furthermore, it has significant implications for nearly all cells of the immune system. Vitamin D deficiency has been linked to a wide range of diseases, including heart disease, hypertension, diabetes, and cancer.
Vitamin D is a fat-soluble vitamin synthesized in the skin upon exposure to ultraviolet radiation. However, sun exposure can be influenced by factors such as season, time of day, geographic location, skin type, sunscreen use, and age. Less than 10% of our vitamin D comes from dietary sources, primarily when supplemented through dietary supplements.
Certain foods are rich in vitamin D, including salmon, mackerel, herring, sardines, and tuna, dairy products, egg yolks, beef liver, and notably, mushrooms. It is worth noting that a recent study found that taking vitamin D with orange juice could result in up to five times higher serum levels compared to taking it with milk.
Daily exposure to sunlight for a few minutes can cover the body's daily vitamin D requirements. Exposure for 15-20 minutes in sunlight between 10 a.m. and 2 p.m., without sunscreen, three times a week, is adequate to provide the necessary vitamin D to our bodies. During this time, the body can produce 10,000 to 20,000 international units (IU) of vitamin D. However, many people do not get sufficient sun exposure during the winter months.
Therefore, it is essential to measure vitamin D levels in the body, through a test called total vitamin D [25(OH)D], to prevent deficiency-related health issues. Low vitamin D levels can result from inadequate sunlight, dietary deficiency, poor vitamin absorption, or disorders in liver sterol metabolism. It is not recommended to measure 1,25-dihydroxyvitamin D levels to detect vitamin D deficiency, as these levels can be misleadingly normal in individuals with significant vitamin deficiency.
Obesity, among other serious health problems, has been shown to cause vitamin D deficiency. Recent studies have indicated that every 10% increase in Body Mass Index (BMI) leads to a 4% further decrease in available vitamin D in the body.
Individuals who should undergo vitamin D level testing include those with suspected deficiency (e.g., individuals with persistent, non-specific musculoskeletal pain, rickets, osteomalacia, osteoporosis, chronic kidney disease, liver insufficiency, malabsorption syndromes, hyperparathyroidism). Additionally, pregnant or breastfeeding women, elderly adults with a history of non-traumatic fractures, obese individuals, homebound individuals, and infants breastfeeding from mothers with vitamin D deficiency should be tested. Also, individuals taking medications associated with reduced vitamin D levels, such as antiepileptics, glucocorticoids, antifungals, and cholestyramine, as well as ALL patients with multiple sclerosis.
Normal vitamin D values in ng/ml
STATUS RANGE OF VALUES
Deficiency < 11.0 Insufficiency 11.0 – 29.0 Sufficiency 30.0 – 100 Toxicity > 100
Gerassimos Tsiolis, PhD in Biochemistry
University of Bologna, Italy
NOTES
** According to existing data, it has been observed that 33% of individuals tested at Quest Diagnostics laboratories in the USA had vitamin D insufficiency, while 60% had either deficient or suboptimal levels. In our country, despite the abundant sunshine for 300 days a year, the vast majority of women and many men have vitamin D insufficiency.
***Data from a study conducted by the medical laboratories "In Vitro" , in collaboration with the Charokopio University of Athens.
