| + + + Parkinsons disease Clinical Study: 3 of 5 using NADH - Life's Energy Source |
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PARKINSON'S
(pg 3 of 5)ACTUAL CLINICAL STUDY: . . . continued from the previous page A New Therapeutic Approach for Treating PARKINSON'S DISEASE MATERIALS AND METHODS: NADH (synonyms: Beta-NADH, Reduced DPN, Beta DPNH) was obtained from Boehringer Mannheim. 12.5 mg of NADH were dissolved in 100 ml 0.9 percent sterile sodium chloride, buffered, pH 7.6, filtered through a 0.22 micron Millipore filter and intravenously infused in 30 minutes. NADH solutions were prepared always fresh immediately prior to use. One group of patients received NADH infusion every other day. The other group of patients obtained 5 mg NADH orally in the form of capsules. Treatment was given every other day for 14 days. The disability score was determined before the first NADH treatment and after the last NADH treatment which was in most cases 14 days from the beginning of the therapy. RESULTS:
When the 415 patients receiving NADH intravenously were compared with those 470 persons getting the oral form of NADH the mean value of improvement in disability after i.v. applied NADH was 20.6 % after orally applied NADH 19.8 % (Table 1). These findings indicate that the oral form of NADH shows a beneficial clinical effect comparable to that of the iv. applied NADH not only in the mean value but also in the maximum value. The maximum improvement of i.v. applied NADH was 55 %, the maximum of orally applied NADH 60 %. The motoric ability improved considerably in these patients, in particular the walking, pushing, posture and speech as well as mimic. After withdrawal of NADH from the usual medication, a worsening of the patients disability was observed in between 2 - 3 weeks. This indicated the improvement of the symptoms to be caused by the NADH applied. In order to substantiate whether NADH is able to stimulate L-DOPA biosynthesis we tested this substance in tissue culture. When neuroblastoma cells were incubated with NADH a dosage dependent increase in dopamine production was observed. In the presence of 200 micro-grams NADH a four fold increase in dopamine production was observed. This stimulation was independent from the tyrosine supplied exogenously indicating that the substrate tyrosine is not the limiting factor but the enzyme or the coenzyme, respectively. The stimulation of dopamine production increased with the number of cells. In the presence of 200 micro-grams of NADH/ ml 20 million cells yielded 12 nano-grams of dopamine/ ml, 40 million cells 44 nano-grams dopamine/ml and 60 million cells 72 nano-grams despectively. |
| Variable | N | Mean | SEM | SD | Min. | Max. | Median |
| Disability NADH iv |
415 | 58.6 | 0.8 | 16.5 | 15 | 90 | 80 |
| Improve- ment NADH iv |
415 | 20.6 | 0.8 | 12.6 | -15 | 55 | 20 |
| Disability NADH oral. |
470 | 56.5 | 1.0 | 18.9 | 15 | 85 | 80 |
| Improve- ment NADH oral |
470 | 19.8 | 0.8 | 12.4 | -10 | 60 | 20 |
| When TH activity was measured directly after
NADH had been added to the culture medium, a 75 % increase could be observed. This finding
indicates that NADH is able to stimulate TH activity directly. A positive correlation
between duration of the disease and disability before treatment appears to be most
plausible. According to this one might expect that both high age and long duration of the disease coincide with a marked improvement. However, a refined statistical analysis ends up with the contrary, meaning that a negative correlation between age and improvement of the treatment as well between duration of the disease and improvement after treatment is obtained. For an accurate assessment of the real relationship between these variables (disability before treatment, age, duration of disease and improvement) it is necessary to subtract the effects of the variable disability before treatment. The results of this calculation show that in general younger patients and patients with a shorter duration of disease respectively have a better chance to gain a marked improvement than older patients and patients with a longer duration of the disease. . . . continued on the next page |
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