Dementia is not an unevitable result of ageing. It always have a cause. Early symptoms may include poor concentration, foggy brain and some times decreased attention span. For many years early signs of dementia were ignored or labeled as mild cognitive impairment. Most of these patients unfortunately progressed to dementia and therefore the new perspective of early intervention has replaced the old conservative measure. The same is true for Parkinsons Disease.
At Pacific Medical Center of Hope we have successfully been able to manage difficult neurodegenerative disorders, and are honored to say that patients' satisfaction has been beyond expectation in every case! Most of the patients even after seeing the highest class neurology clinics in the State, they somehow find their way to here and take advantage of the services provided which includes IV treatments with Natural medicine, Gluthatione and precursors, and protocols developed by the efforts of physicians who thought out of the box, and used research based medicine in it's highest capacity to treat those devastated by the disease progression in one hand and the huge undesirable side effects of medicine prescribed by their doctors in the other hand.
Again no surprise that against our advice they usually stop taking their synthetic pills and improve just by the treatments they receive through us. All treatment modalities are strongly science based and backed up by validated medical literature, unfortunately most often; ignored or overlooked by the conventional physicians.
Most of the conventional physicians and specialists are treating the neurodegenerative disorders with currently available medications which are unfortunately very limited as far as their desirable effect, however nutrition and hormones play a huge role in the treatment of such patients and there are many many studies that support their role.
At Pacific Medical Center of Hope we have successful stories and testimonials from patients treated for Neurodegenerative Disorders including MS. Multiple Sclerosis is characterized by chronic inflammation with neuronal demyelination and scarring. Aside from trauma, MS is the most frequent cause of neurologic disability in early to middle adulthood. It is more common in females. An autoimmune etiology is suspected and susceptibility increases with the presence of the HLA-DR2 allele.
MS derived its name from the multiple scarred areas in the brain termed plaques. The acute lesion in MS is characterized by perivenular cuffing and tissue infiltration by mononuclear cells predominantly T lymphocytes and macrophages. As the lesion evolves, demyelination occurs, with macrophages and microglial cells scavenging the myelin debris. Proliferation of astrocytes lead to scar formation.
The most common initial symptoms of MS include weakness in one or more limbs, blurring of vision secondary to optic neuritis, sensory disturbances, diplopia and ataxia. CSF abnormalities include mononuclear cell pleocytosis, elevation of total Ig, and the presence of oligoclonal Ig. Evoked response testing may reveal slowed or abnormal conduction in visual, auditory, somatosensory , or motor pathways. On MRI, periventricular lesions may be found on T2 weighted MRI brain scans. However, no clinical sign or diagnostic test finding is unique for MS.
Conventional treatment may be for symptomatic management, or focused to arrest the disease with chemotherapeutic drugs, depending on the pattern of MS.
Our concept of the disease would be different in the sense that we focus in conjunction with the pathogenesis of the disorder on immune imbalance involved in etiology of the disease, for example Vit D is involved in pathogenesis and exacerbations of the disease. Also TH1/ TH2 immune response and cytokines are involved. Heavy metals and infectious diseases can also trigger the immune reaction which leads to antibody production and damage/ cross reaction with normal cells/ neurons in this case producing myelin sheath.
Management depends on the cause and we don't treat patients with MS with synthetic medicine. We put that in the hands of Neurologists and honestly with all the side effects they cause and lack of the cost effectiveness in most of the cases, patients desire to discontinue them even against out advise.
Following is a case report that we are in the process of submitting to the medical gjournal for publication and I include that here for your review. What is left unsaid here is that this case was finally diagnosed with Lyme's disease and treated accordingly. It is very interesting that neuroborreliosis mimics the MRI findings as well as clinical manifestations of MS!
A 48 year old female diagnosed with multiple sclerosis (MS) by the local neurologist based on clinical findings and MRI results with white matter changes indicating MS. Patient was refered to our clinic with chief complaint of weakness and numbness in her left foot and ankle. Physical examination revealed left foot drop and decreased sensation in left ankle and foot, unsteady gait and positive Rhomberg test. The patient’s extended disability status scale was 6.5 (Constant bilateral assistance (Cane, Crutches) required to walk about 20 meters without resting) and her fatigue severity scale was 5.2. Previous labs indicated vitamin D2 level of 20 and DHEA of 67. It is noteworthy that neurologist reported that “there was no expected clinical improvement in her current condition despite treatment”. Medical history was positive for Hoshimotos thyroiditis and MS, PSH was C section X one and family history was positive for MI, HTN and diabetes. Patient was perimenopausal and was experiencing irregular periods along with insomnia. Her medications included. daily Copaxone® injections, vitamin D3 1.25 mg/day and thyroid medication.
Investigations: The patient underwent a full laboratory studies. Post challenge testing with dimercaptosuccinic acid for urine heavy metals produced essentially normal results, except for mild elevation in lead levels. Hematology revealed CBC, Met 15, thyroid stimulating hormone and thyroid panel all within normal limits. Thrombopoetin was increased to 305 and anti thyroglobulin antibody was 150 indicating Hoshimotos thyroiditis. Metabolic studies indicated high methyl malonate (methylation cofactor marker) indicating the need for vitamin B12, increased alpha keto –B- methyl valerate and low 5 hydroxy indole acetate (neurotransmitter metabolism marker), and high ethyl malonate (fatty acid metabolism) indicating the need for carnitine and vitamin B2. Saliva testing indicated increased morning cortisol (31.7 nM).
Targeted Metabolic Treatments: Based on the testing discussed above, a supplement regimen along with IV treatments for nutritional deficiencies and metabolic abnormalities was initiated. The regimen included “Neuroprotect-Hope”. This product contains N-acetyl-cysteine (NAC), acetyl-L-carnitine, thiamine, niacin, riboflavin (vitamin B2), vitamins B6 and B12, folic acid and grape seed extract. NAC is used to facilitate detoxification and carnitine along with the B vitamins were administered based on the above lab reports. Patient also received IV treatments with vitamin C, H2O2, amino acids and DMSO.
Response to Treatment: The patient was monitored during weekly clinic visits. Dramatic improvement was observed 8 weeks following initiation of treatment with the above regimen. After 4 weeks of treatment, the patient’s foot drop, numbness and her ability to walk showed improvement; she stopped using the cane was reported to be independently ambulating without aid or rest for about 100 meters. The initial Expanded Disability Status Scale of 6.5 improved to 5.5. The patient stopped using Copaxone® against our advice and continued improving clinically.
Discussion: Vitamin B12 is a key nutrient factor supporting myelin formation. Acquired B12 deficiency and inborn errors in its metabolism are recognized causes of CNS demyelination, so its deficiency in MS would be expected to contribute to progression. Early studies of B12 status in MS produced conflicting results, but improved testing techniques confirmed B12 levels that were lower in the CSF of MS patients, if not always lower in the serum. For more than 30 years, clinicians have been reporting consistent clinical improvement of MS symptoms following B12 injections. Many integrative physicians routinely prescribe intramuscular injections of B complex with B12 and folic acid to their MS patients, reportedly with improvement. Immune-suppressive steroids or cyclophosphamide can produce comparable results, but with severe adverse side effects.
Studies in mice indicate that antioxidants such as grape seed extract may block the progression of MS. Grape seed extract is the primary commercial source of a group of powerful antioxidants known as oligomeric proanthocyanidins (OPCs), also generically called pycnogenol, a class of flavonoids. Laboratory studies have indicated OPCs are much more effective than vitamin C and vitamin E in neutralizing free oxygen radicals, which contribute to organ degeneration and aging in humans. The primary sources of OPCs are pine bark extract and grape seed extract.
L-carnitine increases mitochondrial producion of ATP and plays an important role in lipid metabolism and energy production. It is important for mitochondrial function and the transport of fatty acids into the mitochondria for beta-oxidation and energy production. In one study patients affected with MS with low serum carnitine levels were given 3-6 g/day of L-carnitine for three months. After three months, serum carnitine levels had returned to normal, and 63% of the patients reported an improvement in fatigue. N-acetyl-carnitine is a more bioavailable form than L-carnitine.
In animal studies NAC has been indicated to play an important role in controlling the inflammation associated with neurodegenerative process in MS, and encephalitis by increasing interleukin IL-10. These observations indicate that NAC treatment may be of therapeutic value in MS against the inflammatory disease process associated with the infiltration of activated mononuclear cells into the CNS.
Conclusion: It is important to examine patients with multiple sclerosis thoroughly for any signs of inflammation which may lead to myelin damage and neurodegeneration. The case described above suggest the need for future research in the area of nutritional intervention in patients with neurodegenerative disorders. In one study, 12 percent of affected patients with MS experienced malabsorption of vitamin B12. Metabolic testing indicated that nutritional interventions can improve the clinical and laboratory findings in this population.
Although future studies are required to elucidate the quantitative effect of nutritional supplements on subjective symptoms, this case strongly suggests that intervention with dietary supplements may result in positive, objectively measurable outcomes.
References
1. Hauser SL, Goodkin DE. Multiple Sclerosis and other demyelinating diseases. In: Harrison‘s Principles of Internal Medicine. 2409-2419.
2. Lovblad K, Ramelli G, et al. Retardation of myelination due to dietary vitamin B12 deficiency: cranial MRI findings. Pediatr Radiol 1997 Feb 27(2):155-158 1997.
3. Gupta JK, Ingegno AP, Cook AW, et al. Multiple sclerosis and malabsorption. Am J Gastroenterol 1977;68:560-565.
4. Reynolds EH. Multiple sclerosis and vitamin B12 metabolism. J Neuroimmunol 1992;40:225-230. Kira J, Tobimatsu S, Goto I. Vitamin B12 metabolism and massive-dose methyl vitamin B12 therapy in Japanese patients with multiple sclerosis. Intern Med (Tokyo) 1994;33:82-86.
5. Preuss, H., et al. 2000. Effects of niacin-bound chromium and grape seed proanthocyanidin extract on the lipid profile of hypercholesterolemic subjects: A pilot study. J.Med, 31, 227–246.
6. Antioxidants in multiple sclerosis: do they have a role in therapy? Carlson NG, Rose JW.GRECC, VASLCHCS, Department of Neurobiology and Anatomy, University of Utah, Salt Lake City, Utah, USA.
7. Immunopharmacol Immunotoxicol. 2009;31(1):13-29.Antioxidant therapy in multiple sclerosis. Mirshafiey A, Mohsenzadegan M. Department of Immunology, Tehran University of Medical Sciences, Iran. mirshafiey@tums.ac.ir8. The role of oxidative stress in the pathogenesis of multiple sclerosis: the need for effective antioxidant therapy. Gilgun-Sherki Y, Melamed E, Offen D.
Laboratory of Neurosciences, Felsenstein Medical Research Center, The Sackler School of Medicine, Tel Aviv University, Petach Tikva 49100, Israel.
9. L-carnitine supplementation for multiple sclerosis-related fatigue. Townsend Letter: The Examiner of Alternative Medicine Article date: January 1, 2007 Gaby, Alan R.
10. Zh Nevrol Psikhiatr Im S S Korsakova. 2002;Suppl:72-5. New approaches to antioxidant therapy in multiple sclerosis, Odinak MM, Bisaga GN, Zarubina IV.
11. J Autoimmune Dis. 2005; 2: 4.
Published online 2005 May 3. doi: 10.1186/1740-2557-2-4.
PMCID: PMC1097751
N-acetyl-L-cysteine ameliorates the inflammatory disease process in experimental autoimmune encephalomyelitis in Lewis rats
Low Free Testosterone Levels Linked to Alzheimer’s Disease in Older Men Older men with lower levels of free, or unbound, estosterone circulating in their bloodstreams could be at higher risk of developing Alzheimer’s disease (AD) than their peers, according to new research by NIH and National Center for Complementary and Alternative Medicine published in Neurology magazine, Jan 27, 2004
Pregnenolone and Memory:
Our knowledge of pregnenolone and its “family members,” the neurohormones, is at an exciting early stage. What we know is that these powerful molecules exert rapid and profound effects on vital brain structures, intimately affecting how we think, learn, and remember. It’s fair to say that studies of pregnenolone and other neurosteroids are changing the way we think about steroids and the actions of hormones in general.
Animal studies and early human trials show promising results of supplementation with this exceptionally versatile natural substance. Furthermore, dozens of new trials that are now in progress will surely shed even more light in the future on how pregnenolone can help protect and promote healthy brain function.
Inflammation and Memory:
Presence of Metabolic syndrome and Diabetes can relate to Alzheimers Disease
Presence of chemical toxicity and heavy metals are correlated with Alzheimers Disease through inflammatory process
Homocysteine and folate as risk factors for dementia and Alzheimer disease
Elevated plasma homocystein concentrations and low serum folate concentrations are independent predictors of the development of dementia and AD. Am J Clin Nutr 2005;82:636–43
Environmental Exposure/ Lead:
Occupational lead exposure may have long-term effects and dramatically increase the risk of developing Alzheimer's disease in later years, according to research presented during the American Academy of Neurology's 52nd Annual Meeting in San Diego, CA, April 29 -- May 6, 2000. People who have worked in jobs with high levels of lead exposure are up to 3.4 times more likely to develop Alzheimer's disease. Scientists believe that Lead exposure remains a major public concern because of its adverse effects on brain development and health in general, even with low exposure levels,There are studies suggesting that we also need to be concerned because of very long-lasting changes to the nervous system that may increase the risk for Alzheimer's disease.
One study compared the occupational histories of 185 people with Alzheimer's disease to 303 people without Alzheimer's. Utilizing hazard lists developed by the National Occupational Exposure Survey, researchers estimated the probability of toxic exposure to a variety of agents used in each occupation. That occupation exposure was then multiplied by the number of years a person worked at a job to determine lifetime exposure.
In addition to lead, researchers examined exposure to aluminum, copper, iron, mercury, zinc and solvents (a group of chemicals including paint thinners, cleaning fluids and benzene). Although previous studies have raised concerns about possible relationships between Alzheimer's and many of these metals, including aluminum and solvents, only lead exposure was found to increase the risk of Alzheimer's. The researchers believe that these concerns may have been due to the unrecognized effect of lead as many occupations involve multiple exposures to numerous potentially toxic materials.
Although lead has long been known to be toxic -- and is believed to have affected the brains of some of the rulers of the Roman Empire, thereby causing its downfall -- its long-term damages are difficult to measure, and thus, the extent of its negative effects have been largely overlooked. In the workplace, people are most often exposed to lead by either breathing lead dust, which is considered to be the most toxic, or by direct skin contact. Activities that can expose workers to lead are 1) smelting or casting lead; 2) removing lead coatings (welding, brazing, cutting, sanding or blasting old paints); 3) heating, machining or spraying lead products, and 4) making lead products (lead–acid battery manufacturing, lead glazing pottery making, cable production, ammunition manufacture, production of lead pipe, cable shielding, electronic components, paint and ink manufacture).
Earlier studies have shown that education has a protective effect against Alzheimer's. As people with less education are more likely to work in blue-collar jobs where there is a greater chance of toxic exposure than white-collar jobs, the researchers statistically adjusted for participants' education levels.
Scientists beilieve that public health efforts have been successful in removing lead from sources, such as gasoline and lead-soldered food and drink cans, However, we need to remain vigilant about other sources of lead in the home and in the work place, including decaying old paint, contaminated soil or drinking water, hobbies and occupational exposure.
Parkinson Disease and Alzheimers Disease and Anti oxidants:
Alzheimers and Parkinson disease has relation with antioxidants, specifically Gluthatione. GSH is the most abundant cellular non-protein thiol, serves as an important antioxidant, and has been proposed to be important in the protection of cerebrum from oxidative damage. GSH has been reported to be decreased in cerebrum of aging rodents and humans, and alterations in GSH metabolism have been described in diseased regions of brain from AD patients. Alterations in peripheral GSH metabolism have also been described in patients with mild cognitive impairment and AD. PMID: 15857408
In one study it was shown that the concentration of glutathione was decreased in red blood cells from male Alzheimer’s disease patients compared with age- and gender-matched controls. PMID: 15693022
It has been observed that Alzheimer's patients show an increased level of plasma TBARS, which indicates a higher free radical oxidation of plasma unsaturated phospholipids, and an increased oxidation of red blood cells glutathione, which indicates oxidative stress in peripheral cells. This latter, glutathione oxidation, was found to correlate statistically with the cognitive status of the patients. PMID: 15051321
Above evidence point into the significance and importance of considering integrative approach to patients with Neurodegenerative disorders. What we consider our expertise.
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