Os perigosos laços da medicina com a indústria farmacêutica – Vitamina D comentado

Os perigosos laços da medicina com a indústria farmacêutica – Vitamina D comentado.

Dr. Celso Galli CoimbraOs perigosos laços da medicina com a indústria farmacêutica – Vitamina D comentado

25/12/2012 — Celso Galli Coimbra

Acrescentamos ao texto, que os pacientes podem ser vítimas das doenças e dos remédios, tanto quanto da ausência de tratamento eficaz para doenças para as quais existem terapias de alta complexidade e custo fornecidas pela indústria farmacêutica, QUANDO a eficácia do tratamento pode ser realizada a BAIXO CUSTO, tanto para paciente como para o Governo, o maior pagador do SUS.   Soma-se a este fato a ausência de prevenção à saúde, que é a providência de mais baixo custo ainda. Neste triângulo das bermudas criado pela indústria farmacêutica e aceito pela Medicina perdem-se recursos públicos, dinheiro dos pacientes e familiares, saúde e vidas.  É neste triângulo da doença e da morte que funciona os laços mercantis com a indústria de remédios e a medicina.

A subtração – no Brasil – em especial do valor preventivo e terapêutico do hormônio conhecido por Vitamina D de baixíssimo custo, é um perfeito exemplo disto. Os medicamentos de alto custo da indústria farmacêutica para as doenças autoimunes precisam de PACIENTES VÍTIMAS da ganância desenfreada e da omissão das autoridades. O desinteresse das pessoas ainda saudáveis em informar-se em tempo sobre o que ocorre neste meio médico-farmacêutico, também contribui para o desastre da saúde.

Celso Galli Coimbra

OABRS 11352

cgcoimbra@gmail.com

http://biodireitomedicina.wordpress.com/

https://www.facebook.com/celso.gallicoimbra

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————–

Repercussão internacional das discussões no Brasil sobre a validade dos critérios diagnósticos para a identificação da morte encefálica

 

Não terá uma grande e inabalável influência sobre a vida das pessoas, e sobre a percepção do valor do Maior Bem Vida, o conhecimento desse bem?

 

—————

Repercussão internacional das discussões no Brasil sobre a validade dos critérios diagnósticos para a identificação da morte encefálica

 

 

  DEPARTAMENTO DE NEUROLOGIA E NEUROCIRURGIA
Disciplina de Neurologia Experimental
 

http://www.unifesp.br/dneuro/opinioes.htm

 

Repercussão internacional das discussões no Brasil sobre a validade dos critérios diagnósticos para a identificação da morte encefálica

“é livre a expressão da atividade intelectual, artística, científica e de comunicação, independentemente de censura ou licença”

(Art.5º, inciso IX da Constituição Federal)

Cícero Galli Coimbra
Médico Neurologista e Pesquisador
Professor Adjunto do Departamento de Neurologia e Neurocirurgia
Universidade Federal de São Paulo – UNIFESP
email: coimbracg.nexp@epm.br


  1. 1.     Histórico Preliminar

http://www.unifesp.br/dneuro/opiniao1.htm

 

2. Cartas do Exterior

 

2.1 James Bernat (EUA) – Presidente da Comissão de Ética da Academia Americana de Neurologia

http://www.unifesp.br/dneuro/opiniao21.htm

 

2.2 Comissão Organizadora do 3º Simpósio Internacional sobre Coma e Morte

http://www.unifesp.br/dneuro/opiniao22.htm

 

2.3 Alan Shewmon (EUA) – Professor de Neuropediatria da UCLA

http://www.unifesp.br/dneuro/opiniao23.htm

 

2.4 Paul Byrne (EUA) – Presidente da Associação Médica Católica Norte-Americana para o biênio 1997-1998

http://www.unifesp.br/dneuro/opiniao24.htm

 

2.5 Yoshio Watanabe (Japao) – Diretor do Toyota Medical Center

http://www.unifesp.br/dneuro/opiniao25.htm

 

2.6 David Evans (Inglaterra)

http://www.unifesp.br/dneuro/opiniao26.htm

 

2.7 Johan Loibner (Áustria)

http://www.unifesp.br/dneuro/opiniao27.htm

 

3. Comentários Finais

http://www.unifesp.br/dneuro/opiniao3.htm

 


Textos

http://www.unifesp.br/dneuro/textos.htm

   Unifesp

http://www.unifesp.br/

 

Informações Cícero Galli Coimbra

 

—–

Cura do mal de Parkinson, a DP, ocorre por terapia natural

 

Cura do mal de Parkinson, a DP, ocorre por terapia natural

 

A cura com Dr. Cícero Galli Coimbra. Parkinson, Estresse emocional, depressão, doenças autoimunes e neurodegenerativas.

 

vídeo

http://www.youtube.com/watch?v=yRQkITHjZ5k&feature=player_embedded#!

 

”Terapêutica simples, não onerosa, dotada eficácia largamente superior àquelas até então disponíveis, além de não ser patenteável.”’

Prof. Dr. Cicero Galli Coimbra e Profa. Dra. Virgínia Berlanga Campos Junqueira

http://www.unifesp.br/dneuro/nexp/riboflavina/

Publicada cura do Parkinson em Revista Medica Internacional

 

Publicada cura do Parkinson em Revista Medica Internacional

 

Braz J Med Biol Res v.36 n.10 Ribeirão Preto out. 2003

doi: 10.1590/S0100-879X2003001000019

Braz J Med Biol Res, October 2003, Volume 36(10) 1409-1417

 

High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson’s disease patients

 

C.G. Coimbra1,2 and V.B.C. Junqueira3,4

1Setor de Neurologia

 

Disponivel em

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003001000019&lng=pt&nrm=iso

 

 

Natural Treatment For Parkinson’s disease from 2003

Natural Treatment For Parkinson’s disease from 2003

 

High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson’s disease patients

 

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003001000019

 

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Brazilian Journal of Medical and Biological Research

On-line version ISSN 1414-431X

Braz J Med Biol Res vol.36 no.10 Ribeirão Preto Oct. 2003

http://dx.doi.org/10.1590/S0100-879X2003001000019

Braz J Med Biol Res, October 2003, Volume 36(10) 1409-1417

High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson’s disease patients

C.G. Coimbra1,2 and V.B.C. Junqueira3,4

1Setor de Neurologia,Hospital do Servidor Público Municipal de São Paulo, São Paulo, SP, Brasil
2Departamento de Neurologia e Neurocirurgia, Universidade Federal de São Paulo, São Paulo, SP, Brasil
3Disciplina de Geriatria, Departamento de Medicina, Centro de Estudos do Envelhecimento, Universidade Federal de São Paulo, São Paulo, SP, Brasil
4VITÆ – Cromatografia Líquida em Análises Clínicas S/C Ltda., São Paulo, SP, Brasil

Abstract
Introduction
Patients and Methods
Results
Discussion
References
Acknowledgments
Correspondence and Footnotes


Abstract

Abnormal riboflavin status in the absence of a dietary deficiency was detected in 31 consecutive outpatients with Parkinson’s disease (PD), while the classical determinants of homocysteine levels (B6, folic acid, and B12) were usually within normal limits. In contrast, only 3 of 10 consecutive outpatients with dementia without previous stroke had abnormal riboflavin status. The data for 12 patients who did not complete 6 months of therapy or did not comply with the proposed treatment paradigm were excluded from analysis. Nineteen PD patients (8 males and 11 females, mean age ± SD = 66.2 ± 8.6 years; 3, 3, 2, 5, and 6 patients in Hoehn and Yahr stages I to V) received riboflavin orally (30 mg every 8 h) plus their usual symptomatic medications and all red meat was eliminated from their diet. After 1 month the riboflavin status of the patients was normalized from 106.4 ± 34.9 to 179.2 ± 23 ng/ml (N = 9). Motor capacity was measured by a modification of the scoring system of Hoehn and Yahr, which reports motor capacity as percent. All 19 patients who completed 6 months of treatment showed improved motor capacity during the first three months and most reached a plateau while 5/19 continued to improve in the 3- to 6-month interval. Their average motor capacity increased from 44 to 71% after 6 months, increasing significantly every month compared with their own pretreatment status (P < 0.001, Wilcoxon signed rank test). Discontinuation of riboflavin for several days did not impair motor capacity and yellowish urine was the only side effect observed. The data show that the proposed treatment improves the clinical condition of PD patients. Riboflavin-sensitive mechanisms involved in PD may include glutathione depletion, cumulative mitochondrial DNA mutations, disturbed mitochondrial protein complexes, and abnormal iron metabolism. More studies are required to identify the mechanisms involved.

Key words: Parkinson’s disease, Riboflavin, Flavin-adenine dinucleotide, Glutathione, Iron, Hemin


 

Introduction

During absorption of riboflavin, flavokinase phosphorylates the vitamin to yield flavin mononucleotide (FMN) that, according to the cellular requirements, is transformed into flavin-adenine dinucleotide (FAD) by FAD synthase (1,2). Progressive deficiency of riboflavin is associated with co-factor loss in a controlled manner, apparently ensuring that essential catalytic activity such as that related to aerobic metabolism is preserved (3,4).

Low riboflavin status may also result from defective absorption. In spite of an adequate dietary intake of riboflavin (FAD, vitamin B2), 10-15% of the inhabitants of London and of Florence present low activities of two riboflavin-dependent enzymes – erythrocyte glutathione reductase (EGR) and pyridoxin(pyridoxamine)-phosphate oxidase (5). The activity of both enzymes was corrected by adding their respective co-factors (FAD or FMN) to a test tube assay or by administering high doses of riboflavin (24-30 mg per day for 5-8 weeks) to the affected individuals (6). The dependency of both FMN and FAD levels on riboflavin absorption (i.e., on flavokinase activity), and the normalization of the activities of both FMN- and FAD-dependent enzymes only at a high riboflavin intake, taken together, are consistent with the expression of flavokinase isoforms with low affinity for the substrate – riboflavin (5). Anderson et al. (5) suggested that the relatively large percent of persons with altered riboflavin absorption (10-15%) may reflect the situation in the world population rather than being a feature of a particular ethnic group.

Low EGR activity may explain glutathione depletion with impaired antioxidant defense, the earliest neurochemical abnormality in Parkinson’s disease (PD), already observed in the substantia nigra before the disorder becomes clinically evident (7). Moreover, the reduced bioavailability of FMN and/or FAD may also explain the impaired oxidative metabolism of PD patients (8-10).

The first objective of the present study was to determine the status of riboflavin in PD patients. The second was to evaluate the specificity of the alterations of riboflavin status for PD by measuring the levels of vitamin B2 and of other determinants of homocystinemia (vitamins B6, B12, and folic acid) in PD patients and comparing them with those of individuals with dementia (11-13). Third, we also determined the effect of normalization of riboflavin status on the motor capacity of PD patients. Part of the data reported here, obtained during the first 3 months of treatment, were reported at the 6th International Conference on Parkinson’s and Alzheimer’s Diseases (14).


 

Patients and Methods

This study was approved by the Ethics Committee for Clinical Research of the Hospital do Servidor Público Municipal de São Paulo (HSPM) and informed consent was obtained from all participants or persons responsible for them.

The diagnosis of sporadic PD was made according to current criteria (15) with special care taken to exclude confounding disorders, particularly in the early stages of the disease.

Vitamin and homocysteine determinations were performed on 31 sporadic PD patients (67.5 ± 9.3 years old, 13 males and 18 females): 3, 3, 3, 8, and 14 patients were assigned, early in the morning, to stages I to V of Hoehn and Yahr (16), respectively.

Ten individuals (77.5 ± 8.8 years old, 5 males and 5 females) with dementia without stroke (DwoSt) and a low Mini-Mental score (13) were used as the control group for blood chemistry. They had no history of stroke or evidence for ischemic lesions of the brain by CT or NMRI and had been consecutively attended in the Neurology Clinic of HSPM.

Blood samples were obtained after a 10- to 12-h fast for serum assays of vitamin B12 by electrochemiluminescence immunoassay (11820753 Roche Diagnostics GmbH, Mannheim, Germany) and of homocysteine by HPLC (17). Heparinized plasma was assayed for FAD (18), vitamin B6 (19), and folic acid (20)by HPLC, as well as for the determination of the EGR-activation coefficient (EGR-AC) (21) in red blood cell lysates (22).

A food questionnaire covered the weekly dietary habits of all PD and DwoSt patients from 5 years prior to the onset of PD until the appearance of spontaneous changes associated with the onset of chewing and/or swallowing impairment or until the medical interview in the absence of these impairments. The questionnaire also evaluated the adequacy of daily vitamin intake.

All PD patients received 30 mg riboflavin orally at about 8-h intervals (90 mg/day) and their usual symptomatic medications. This dosage was used to avoid decreased absorption associated with higher doses or shorter intervals between administrations. Due to the renal excretion of riboflavin (3), the treatment was only initiated after confirmation of normal blood levels of creatinine (0.5-1.4 mg/dl). Because the PD patients had a higher consumption of red meat (beef and pork) than sex-matched controls (19 healthy non-consanguineous relatives or neighbors of similar age recruited for controlling the dietary habits), all PD patients were required to eliminate all red meat from their diets. The symptomatic drugs for PD in use included L-DOPA with carbidopa (200/50 mg tablets), L-DOPA with benserazide hydrochloride (200/50 mg tablets), biperiden (2 or 4 mg tablets), amantadine hydrochloride (100 mg tablets), selegiline (5 mg tablets), and pramipexole (0.25 or 1.0 mg tablets) taken alone or in diverse combinations. The treatment paradigm with symptomatic drugs for PD for each patient when the study began was maintained.

The motor capacities of the 19 PD patients who complied with the proposed treatment for 6 months by early August 2003 were rated monthly according to a motor function scale (Table 1), and compared with their own pretreatment values. The scale was based on that of Hoehn and Yahr (16) and new categories were added in order to detect subtle changes in the patients’ motor capacity. In addition, the presence or absence of responses to symptomatic drugs for PD is also used for more accurate characterization of the residual motor capacity of PD patients (for instance, compare the descriptions corresponding to 0 and 15% of motor capacity, Table 1). Although there are no direct validation studies of this rating system, the different levels of motor capacity in Table 1 represent a simple increase in the number of components within stages I to V of the widely employed Hoehn and Yahr system (16).

After the first month of treatment, compliance with the dietary directions and vitamin intake was determined in all patients, and the fasting plasma levels of FAD and EGR-AC values were re-evaluated in 9 of them approximately 9-12 h after the latest riboflavin dose.

The blood chemistry data obtained from both groups were compared statistically by the Student t-test and the motor function data were analyzed statistically by the Wilcoxon signed rank test, with the level of significance set at P < 0.05.


 

Results

Diversified food intake, including daily ingestion of milk, which is particularly rich in vitamin B2, was confirmed in all patients, with PD patients frequently declaring a strong preference for red meat. The content of the daily family meals was usually adapted to meet the high demand for red meat of most PD patients. In contrast, all 10 DwoSt patients passively accepted the family diet. The estimated red meat consumption prior to the onset of impaired chewing/swallowing by 19 PD patients (8 males and 11 females, mean age ± SD = 66.2 ± 8.6 years) at lunch and dinner within a 7-day period was significantly higher (mean consumption = 2,044 ± 1,439 g/week, range = 0-5,100 g/week) than that of their 19 diet controls (8 males and 11 females, all healthy individuals of similar social and cultural background, recruited among non-consanguineous relatives and neighbors of PD patients of similar age; mean age = 64.6 ± 11.3 years, mean consumption = 789 ± 509 g/week, range = 150-1800 g/week; P < 0.01, Mann-Whitney U-test). The calorie intake did not differ significantly between the two groups.

The basal plasma concentrations of FAD of the PD patients (100.9 ± 22 ng/ml) were significantly lower than those observed in the patients with DwoSt (128.8 ± 25.6 ng/ml, P < 0.01, Student t-test) while other determinants of homocysteine levels (pyridoxine, folic acid, and methylcobalamin) were usually within normal limits, and did not differ significantly between the two groups (Table 2). The PD group also had significantly higher EGR-AC levels than DwoSt patients (1.43 ± 0.26 vs 1.20 ± 0.11, respectively, P < 0.01, Student t-test).

It is important to point out that all 31 PD patients (including 3 newly diagnosed individuals not on symptomatic drugs for PD) but only 3 of 10 DwoSt patients had low plasma riboflavin levels. Normalization of the plasma concentrations of riboflavin and EGR-AC values was confirmed after 1 month of treatment (from 106.4 ± 34.9 to 179.2 ± 23.0 ng/ml, and from 1.40 ± 0.25 to 1.11 ± 0.08, N = 9, respectively).

About 10 to 15 days after the beginning of high-dose riboflavin treatment, PD patients often reported better (progressively less interrupted) sleep at night, improved reasoning, higher motivation, and reduced depression. Their family members usually started noticing motor improvements after 20 days of treatment, but in some cases of advanced disability the patient was able to change body position in bed at night as early as on the third day of treatment.

By the time of writing this report in August 2003, 19 PD patients (respectively, 3, 3, 2, 5, and 6 patients initially rated as stages I to V of Hoehn and Yahr (16)) had completed 6 months of treatment with riboflavin administration and dietary red meat elimination. The data in Figure 1A show that all of them improved their motor capacity during the first 3 months and most reached a plateau, while 5/19 continued to improve in the 3- to 6-month interval. Figure 1B shows that the average motor capacity for these 19 patients increased from 44 to 71%. Their motor capacity increased significantly during the first month and every month for the next 5 months of treatment compared with their own pretreatment status, demonstrating a progressive and marked improvement (P < 0.001, Wilcoxon signed rank test). The rate of motor recovery was higher in the first 3 months than in the last 3 months of treatment. No patient on high doses of riboflavin reported adverse effects.

Because they could stand and walk with improved (although still altered) balance by 2 months of treatment, two male patients (initially in stage V (16) with associated dementia and hallucinations) started striking imaginary persons and/or often attempted to leave home unaccompanied, reacting aggressively against the relative who tried to stop them. These episodes of agitation and aggressiveness were observed less often by the end of the third month of riboflavin treatment and disappeared thereafter, but caused transient concern and distress among their family members who initially regarded them as signs of neurological worsening.

Three patients (2 individuals initially in stage II and 1 in stage I of Hoehn and Yahr (16)) reached 100% motor capacity within the first 3 months of treatment (Figure 1A). Four patients had run out of riboflavin tablets for up to 7 days between two consecutive clinical appointments, but sustained the benefit already achieved by then.

Twelve of 31 patients initially assessed for riboflavin status who either did not complete 6 months of therapy or did not comply with the proposed treatment paradigm were excluded from statistical analysis.


 

Figure 1. Motor capacity of patients with Parkinson’s disease who received 30 mg riboflavin/8 h, orally (240 mg/day) and abstained from dietary red meat for 6 months. Motor capacity was evaluated monthly for each patient by a modification of the method of Hoehn and Yahr (16) to provide a score in percent (Table 1). A, Individual data for the evolution of motor capacity of 19 patients for 0 to 3 and 3 to 6 months of treatment. *P < 0.001 for values at 3 months (month 0) compared with those before treatment; **P < 0.05 for values at 6 months compared with those obtained at 3 months (Wilcoxon signed rank test). B, The height of the columns indicates the mean motor capacity values (see Table 1) after the indicated periods of treatment. When compared with their own basal levels (month 0), highly significant and progressively higher differences were observed for each consecutive month of treatment. *P < 0.001 (Wilcoxon signed rank test).

View larger version of this image (29 K GIF file)]


 

Discussion

This study demonstrated a progressive and marked improvement of motor capacity in consecutively evaluated patients with sporadic PD who started with below normal laboratory indexes of riboflavin and who eliminated red meat from their diets while receiving high multiple daily doses of riboflavin over a period of 6 months while taking their usual symptomatic medications. The mean motor capacity of a group of 19 PD patients showed a progressive 50% recovery over a period of only 3 months – a most surprisingly high and fast improvement, considering that about 60% of nigral neurons have already been lost at the onset of manifestations of PD (15).

The initial riboflavin status was low in all 31 consecutively evaluated PD individuals, and significantly lower in PD patients compared with those with another neurodegenerative disease also associated with hyperhomocystinemia (DwoSt), suggesting that abnormal riboflavin status may be a specific feature of PD rather than a minor metabolic contributor to the degeneration of nigral neurons. Taken together with the rapid and profound neurological improvement associated with normalization of riboflavin status, this observation suggests that altered riboflavin status may be a cause of neurodegeneration in PD.

Although urinary excretion of riboflavin peaks within 1-2 h and returns to baseline within 5-6 h after a large oral dose (3), the benefit achieved did not vanish in four PD patients over a therapeutic interval of up to 7 days. This observation suggests the occurrence of steady plastic changes rather than a pharmacological effect of high-dose riboflavin treatment to account for the improved motor capacity shown in Figure 1. The steady build-up of the motor recovery observed during the first 3 months of treatment suggests that this treatment paradigm may inactivate fundamental neurodegenerative mechanisms (e.g., glutathione depletion, considered to be an early key event in the pathogenesis of PD (23,24)), possibly allowing regenerative plastic phenomena to occur.

The importance of the elimination of dietary red meat for the results reported here is not known. The content of vitamin B2 in meat in general is considerable (about 0.2 mg/100 g), and diverse cooking procedures cause only minor (7-18%) loss of this micronutrient (25). The daily requirement for individuals above the age of 14 years is £1.3 mg/day. Therefore, if the PD patients had a normal absorptive capacity for vitamin B2, their large ingestion of red meat (up to 700 g/day), associated with milk, rice and beans, fruits and vegetables, should have provided a normal riboflavin status. In contrast, 31 consecutive PD patients had laboratory evidence for riboflavin deficiency (Table 2) suggesting that patients with sporadic PD belong to the subset of the general population (10-15%) (3) that may express a flavokinase with low affinity for vitamin B2, leading to a decreased absorption.

However, the digestion of red meat releases hemin, a highly diffusible toxin that, when not properly inactivated, increases intracellular iron concentrations and enhances hydroxyl radical production (Fenton reaction). Most of the absorbed hemin is destroyed by the enzyme heme oxygenase (HO) in the digestive tract and liver (26). Because HO is oxidized during the catabolization of hemin to biliverdin, the HO molecules must be reduced through the coordinated activity of the flavoenzyme cytochrome P450 reductase for continued hemin inactivation (Figure 2) (27). Cytochrome P450 reductase is particularly sensitive to riboflavin deficiency because it requires both FMN and FAD as prosthetic groups (28). It is possible that individuals with decreased absorption of vitamin B2 may not completely inactivate high dietary levels of hemin, allowing this neurotoxic compound to reach the brain cells. Consistently, the staining for HO-1 isozyme is increased in astrocytes and reacts with neuronal Lewy bodies in the nigra of PD patients, suggesting that its overexpression may contribute to the pathological iron deposition and mitochondrial damage in PD (29). By binding glutathione (30) hemin may further decrease glutathione levels in the brains of PD patients through a direct mechanism.

Because humans lack efficient iron excretory mechanisms, iron excess is dealt with by increasing the synthesis of the iron-storage protein ferritin (31). Disturbed systemic (32) and brain (33) iron metabolism has been reported in PD, suggesting that a selective decrease in the levels of ferritin may result in an increase in intracellular free iron, thereby enhancing free radical production (34). Indeed, vitamin B2 deficiency in rodents is associated with low circulating iron concentrations, increased iron turnover and excretion into the intestinal lumen, which may occur in response to impaired ferritin synthesis (35,36). Therefore, the consistent finding of an abnormal riboflavin status in PD, as reported here, may help to explain the disturbed iron metabolism found in PD patients, with the underlying mechanisms possibly involving impaired hemin catabolism and reduced ferritin synthesis. Interestingly, the highest world prevalence of PD is found among the inhabitants of Buenos Aires (37), where the consumption of red meat is traditionally high. Similarly, the identification of high dietary animal fat as a risk factor for PD (37) may actually reflect a role of high dietary hemin in PD pathology.

Moreover, because FAD is required in the two alternative pathways of deoxynucleotide synthesis (2), DNA repair and replication are expected to be disturbed upon decreased bioavailability of riboflavin, and abnormal riboflavin status may also explain the cumulative mitochondrial DNA mutations reported in PD (38).

The present results with 19 PD patients who showed a significant improvement in motor function after treatment with riboflavin and the elimination of red meat from the diet suggest that an abnormal riboflavin status, possibly due to flavokinase deficiency, may be an essential requirement for triggering and sustaining the degeneration of dopaminergic neurons in PD. As a result of the reduced B2 bioavailability, ATP production is selectively preserved, while the less critical FAD- or FMN-dependent metabolic pathways are impaired (4). Consequently, free iron concentrations in the cytosol increase as a result of impaired ferritin synthesis and/or reduced hemin catabolism associated with hydrogen peroxide accumulation due to glutathione depletion, thereby triggering the Fenton reaction and ultimately leading to the selective formation of the potent neurotoxin 6(OH)DA in dopaminergic neurons.

Current concepts about the cause of sporadic PD suggest an inherited predisposition to environmental or endogenous toxic agents (39), and the data presented and reviewed here suggest that flavokinase deficiency should be considered in future research as a promising candidate to account for this inherited predisposition, while dietary factors such as red meat consumption may largely account for the environmental/endogenous toxicity. The administration of high doses of riboflavin combined or not with red meat elimination may be an effective therapeutic paradigm addressing the determinants of PD, capable of providing regression to earlier clinical stages, or even to the nonsymptomatic state without symptomatic drugs for PD (at least in some cases), rather than only disease stabilization or partial symptomatic relief.

Although the relentless progression of PD clearly contrasts with the results of the treatment paradigm reported here, a larger and more prolonged study is certainly required to document the steadiness and the full extent of the ongoing recovery. A scientifically desirable blinded clinical trial with a placebo would necessarily leave known riboflavin-deficient patients untreated for a long period of time, when their neurological disability may progress as a consequence of sustained loss of nigral neurons, possibly rendering the ultimate response to delayed normalization of their riboflavin levels less complete. Therefore, the need for controlled trials should be weighed ethically considering the contrast of the natural history of PD (progress of motor disability to death despite an increase in the efficacy of symptomatic drugs for PD treatment) with the outcome of the vitamin B2 treatment observed in larger and more prolonged studies without controls.


Figure 2. Dependency of hemin catabolism on riboflavin bioavailability. The elimination of hemin requires cyclic reduction of heme oxygenase by flavoprotein cytochrome P450 reductase that, in turn, utilizes both flavin mononucleotide (FMN) and flavin-adenine dinucleotide (FAD) as prosthetic groups. Average or increased red meat consumption may overload the capacity of this chain of reactions already compromised by impaired intestinal absorption of riboflavin (with decreased FMN and FAD synthesis), leading to increased hemin (iron) delivery to the CNS and increased utilization of riboflavin for hemin inactivation. Modified from Figure 1, box 21-1, page 783 of Ref. 2.

[View larger version of this image (17 K GIF file)]


 

References

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9. Mytilineou C, Werner P, Molinari S, Di Rocco A, Cohen G & Yahr MD (1994). Impaired oxidative decarboxylation of pyruvate in fibroblasts from patients with Parkinson’s disease. Journal of Neural Transmission. Parkinson’s Disease and Dementia Section, 8: 223-228.        [ Links ]

10. Mizuno Y, Matuda S, Yoshino H, Mori H, Hattori N & Ikebe S (1994). An immunohistochemical study on alpha-ketoglutarate dehydrogenase complex in Parkinson’s disease. Annals of Neurology, 35: 204-210.        [ Links ]

11. Hustad S, Ueland PM, Vollset SE, Zhang Y, Bjørke-Monsen AL & Schneede J (2000). Riboflavin as a determinant of plasma total homocysteine: effect modification by the methylenetetrahydrofolate reductase C677T polymorphism. Clinical Chemistry, 46: 1065-1071.        [ Links ]

12. Diaz-Arrastia R (2000). Homocysteine and neurologic disease. Archives of Neurology, 57: 1422-1427.        [ Links ]

13. Crum RM, Anthony JC, Bassett SS & Folstein MF (1993). Population-based norms for the Mini-Mental State Examination by age and educational level. Journal of the American Medical Association, 269: 2386-2391.        [ Links ]

14. Coimbra CG & JunqueiraVBC (2003). Altered riboflavin metabolism in Parkinson’s disease: Pathophysiologic and therapeutic implications. 6th International Conference AD/PD. Alzheimer’s and Parkinson’s disease: new perspectives, Seville, Spain, May 8-12. Book of Abstracts, 96.        [ Links ]

15. Fahn S & Przedborski S (2000). Parkinsonism. In: Rowland LP (Editor), Merrit’s Neurology. Lippincott Williams & Wilkins, Philadelphia, PA, USA.        [ Links ]

16. Hoehn MM & Yahr MD (1967). Parkinsonism: onset, progression and mortality. Neurology, 17: 427-442.        [ Links ]

17. Pfeiffer CM, Huff DL & Gunter EW (1999). Rapid and accurate HPLC assay for plasma total homocysteine and cysteine in a clinical laboratory setting. Clinical Chemistry, 45: 290-292.        [ Links ]

18. Speek AJ, van Schaik F, Schrijver J & Schreurs WH (1982). Determination of the B2 vitamer flavin-adenine dinucleotide in whole blood by high-performance liquid chromatography with fluorometric detection. Journal of Chromatography, 228: 311-316.        [ Links ]

19. Sharma SK & Dakshinamurti K (1992). Determination of vitamin B6 vitamers and pyridoxic acid in biological samples. Journal of Chromatography, 578: 45-51.        [ Links ]

20. Kelly P, McPartlin J & Scott J (1996). A combined high-performance liquid chromatographic-microbiological assay for serum folic acid. Analytical Biochemistry, 238: 179-183.        [ Links ]

21. Sauberlich HE, Judd JH, Nichoalds GE, Broquist HP & Darby WJ (1972). Application of the erythrocyte glutathione reductase assay in evaluating riboflavin nutritional status in a high school student population. American Journal of Clinical Nutrition, 25: 756-762.        [ Links ]

22. Beutler E (1975). The preparation of red cells for assay. In: Beutler E (Editor), Red Cell Metabolism. A Manual of Biochemical Methods. 2nd edn. Grune and Straton, New York.        [ Links ]

23. Jenner P, Dexter DT, Sian J, Shapira AHV & Marsden CD (1992). Oxidative stress as a cause of nigral cell death in Parkinson’s disease and incidental Lewy body disease. Annals of Neurology, 32: S82-S87.        [ Links ]

24. Schulz JB, Lindenau J, Seyfried J & Dichgans J (2000). Glutathione, oxidative stress and neurodegeneration. European Journal of Biochemistry, 267: 4904-4911.        [ Links ]

25. Pinheiro-Sant’ana HM, Stringueta PC & Penteado MDVC (1999). Stability of B-vitamins in meats prepared by foodservice. 2. Riboflavin. Foodservice Research International, 11: 53-67.        [ Links ]

26. Brown EB, Hwang Y-F, Nichol S & Ternberg J (1968). Absorption of radioiron-labeled hemoglobin by dogs. Journal of Laboratory and Clinical Medicine, 72: 58-64.        [ Links ]

27. Ryter SW & Tyrrel RM (2000). The heme synthesis and degradation pathways: role in oxidant sensitivity. Heme oxygenase has both pro- and antioxidant properties. Free Radical Biology and Medicine, 28: 289-309.        [ Links ]

28. Wang M, Roberts DL, Paschke R, Shea TM, Masters BSS & Kim J-JP (1997). Three-dimensional structure of NADPH-cytochrome P450 reductase: Prototype for FMN- and FAD-containing enzymes. Proceedings of National Academy of Sciences, USA, 94: 8411-8416.        [ Links ]

29. Shipper HM (2000). Heme oxygenase-1: role in brain aging and neurodegeneration. Experimental Gerontology, 35: 821-830.        [ Links ]

30. Sahini VE, Dumitrescu M, Volanschi E, Birla L & Diaconu C (1966). Spectral interferometrical study of the interaction of hemin with glutathione. Biophysical Chemistry, 58: 245-253.        [ Links ]

31. Casey JL, Hentze MW, Koeller DM, Caughman SW, Rouault TA & Klausner RD (1988). Iron-responsive elements: regulatory RNA sequences that control mRNA levels and translation. Science, 240: 924-928.        [ Links ]

32. Logroscino G, Marder K, Graziano J, Freyer G, Slavkovich V, LoIacono N, Cote L & Mayeux R (1997). Altered systemic iron metabolism in Parkinson’s disease. Neurology, 49: 714-717.        [ Links ]

33. Dexter DT, Carayon A, Vidailhet M, Ruberg M, Agid F, Agid Y, Lees AJ, Wells FR, Jenner P & Marsden CD (1990). Decreased ferritin levels in brain in Parkinson’s disease. Journal of Neurochemistry, 55: 16-20.        [ Links ]

34. Mann VM, Cooper JM, Daniel SE, Srai K, Jenner P, Marsden CD & Schapira AH (1994). Complex I, iron, and ferritin in Parkinson’s disease substantia nigra. Annals of Neurology, 36: 876-881.        [ Links ]

35. Adelekan DA & Thurnham DI (1986). A longitudinal study of the effect of riboflavin status on aspects of iron storage in the liver of growing rats. British Journal of Nutrition, 56: 171-179.        [ Links ]

36. Powers HJ, Weaver LT, Austin S, Wright AJ & Fairweather-Tait SJ (1991). Riboflavin deficiency in the rat: effects on iron utilization and loss. British Journal of Nutrition, 65: 487-496.        [ Links ]

37. Tanner CM, Goldman SM & Ross GW (2002). Etiology of Parkinson’s disease. In: Jankovik JJ & Tolosa E (Editors), Parkinson’s Disease and Movement Disorders. Lippincott Williams & Wilkins, Philadelphia, PA, USA.        [ Links ]

38. Di Monte DA (1991). Mitochondrial DNA and Parkinson’s disease. Neurology, 41: 38-42.        [ Links ]

39. Jenner P, Shapira AH & Marsden CD (1992). New insights into the cause of Parkinson’s disease. Neurology, 42: 2241-2250.        [ Links ]


Acknowledgments

The authors are grateful to Mr. Terence O’Reilly (Novartis, Basel, Switzerland) for his suggestions about statistical analysis.


Correspondence and Footnotes

Address for correspondence: C.G. Coimbra, UNIFESP, Rua Pedro de Toledo, 781, 7º andar, 04039-032 São Paulo, SP, Brasil. Fax: +55-11-5539-3123. E-mail: coimbracg.nexp@epm.br

Publication supported by FAPESP. Received August 13, 2003. Accepted August 27, 2003.

 Brazilian Journal of Medical and Biological Research

Av. Bandeirantes, 3900
14049-900 Ribeirão Preto SP Brazil
Tel. / Fax: +55 16 3633-3825

bjournal@fmrp.usp.br

High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson’s disease patients. C.G. Coimbra and V.B.C. Junqueira. Brazilian Journal of Medical and Biological Research, 36 (10): 1409, 2003.

Figure 1. Motor capacity of patients with Parkinson’s disease who received 30 mg riboflavin/8 h, orally (240 mg/day) and abstained from dietary red meat for 6 months. Motor capacity was evaluated monthly for each patient by a modification of the method of Hoehn and Yahr (16) to provide a score in percent (Table 1). A, Individual data for the evolution of motor capacity of 19 patients for 0 to 3 and 3 to 6 months of treatment. *P < 0.001 for values at 3 months (month 0) compared with those before treatment; **P < 0.05 for values at 6 months compared with those obtained at 3 months (Wilcoxon signed rank test). B, The height of the columns indicates the mean motor capacity values (see Table 1) after the indicated periods of treatment. When compared with their own basal levels (month 0), highly significant and progressively higher differences were observed for each consecutive month of treatment. *P < 0.001 (Wilcoxon signed rank test).

High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson’s disease patients. C.G. Coimbra and V.B.C. Junqueira. Brazilian Journal of Medical and Biological Research, 36 (10): 1409, 2003.

Figure 2. Dependency of hemin catabolism on riboflavin bioavailability. The elimination of hemin requires cyclic reduction of heme oxygenase by flavoprotein cytochrome P450 reductase that, in turn, utilizes both flavin mononucleotide (FMN) and flavin-adenine dinucleotide (FAD) as prosthetic groups. Average or increased red meat consumption may overload the capacity of this chain of reactions already compromised by impaired intestinal absorption of riboflavin (with decreased FMN and FAD synthesis), leading to increased hemin (iron) delivery to the CNS and increased utilization of riboflavin for hemin inactivation. Modified from Figure 1, box 21-1, page 783 of Ref. 2.

High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson’s disease patients. C.G. Coimbra and V.B.C. Junqueira. Brazilian Journal of Medical and Biological Research, 36 (10): 1409, 2003.

Figure 2. Dependency of hemin catabolism on riboflavin bioavailability. The elimination of hemin requires cyclic reduction of heme oxygenase by flavoprotein cytochrome P450 reductase that, in turn, utilizes both flavin mononucleotide (FMN) and flavin-adenine dinucleotide (FAD) as prosthetic groups. Average or increased red meat consumption may overload the capacity of this chain of reactions already compromised by impaired intestinal absorption of riboflavin (with decreased FMN and FAD synthesis), leading to increased hemin (iron) delivery to the CNS and increased utilization of riboflavin for hemin inactivation. Modified from Figure 1, box 21-1, page 783 of Ref. 2.

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Vitamina D: A Desinformação Médica e o Direito à Informação do Cidadão

Vitamina D: A Desinformação Médica e o Direito à Informação do Cidadão

20/06/2012 — Celso Galli Coimbra

__

O assunto Vitamina D e a necessidade de sua informação à população continua contrariando interesses estranhos à saúde do paciente dentro da Medicina & da Indústria Farmacêutica.

Afinal, pergunta-se: prevenir e/ou curar doenças que trazem imensos lucros interessa à Indústria Farmacêutica?  Claro que não. Doença dá lucro!

No Brasil, os médicos que comparecem a programas “jornalísticos” propondo-se a contrariar colegas seus ausentes – sem contrapontos válidos do ponto de vista jornalístico – como garotos propaganda de interesses da Indústria Farmacêutica, para levantar dúvidas levianas ao falar de forma meramente postulatória e, assim, sem indicar fonte de conhecimento, sobre assunto que tem milhões de publicações científicas na comunidade médica internacional, devem cumprir a obrigação de não desinformar a população naquilo que diz respeito à sua saúde. Esta é uma garantia constitucional da cidadania no Brasil.  

Ou, então, cumprirem a outra obrigação médica:  estar bem informado sobre o que declaram em público a respeito de conhecimento médico que tem o mais consistente fundamento bibliográfico científico internacional.  O cumprimento destas condutas dizem respeito aos direitos de cidadania garantidos na Constituição Federal brasileira.

Não pensem eles que eventual apoio de órgãos de classe profissionais, isenta-os de responsabildades graves daí decorrentes, especialmente frente ao concreto do prejuízo individual de saúde posteriormente configurado.

__

O vídeo referido na reportagem dominical de 27.05.12  da Folha está no endereço:

Vitamina D – Por uma outra terapia (Vitamin D – For an alternative therapy)

 

Vitamina D pode revolucionar o tratamento da esclerose múltipla

 

Taxas baixas de vitamina D na maioria da população preocupam especialistas

 

Pediatras dobram recomendação de consumo diário de vitamina D

 

Doses diárias de Sol – nos horários certos e com os devidos cuidados

 __

“(…) cerca de 70% da população mundial apresenta taxas inadequadas de vitamina D, substância que, dentro do corpo, trabalha como um hormônio. O fenômeno da insuficiência não poupa nem países tropicais, como o Brasil, e a defasagem tende a ser maior nas grandes cidades, já que, dentro de casa, no carro ou no escritório, as pessoas acabam fugindo do sol. De acordo com o endocrinologista Geraldo Santana, do Instituto Mineiro de Endocrinologia, “a deficiência de vitamina D é um achado frequente e também preocupante devido à importante ação da substância no organismo.”

Celso Galli Coimbra
OABRS 11352

cgcoimbra@gmail.com 

Em 19.06.2012

Fonte

http://biodireitomedicina.wordpress.com/2012/06/20/vitamina-d-a-desinformacao-medica-e-o-direito-a-informacao-do-cidadao/

__

-30.039254 -51.216930

Referencias Médico-Científicas Sobre Tratamento, Cura e Prevenção, doenças neurodegenerativas e autoimunes. Vitamina D.

 

Vitamina D pode revolucionar o tratamento da esclerose múltipla*

http://biodireitomedicina.wordpress.com/category/doencas-autoimunes/

 

POR UM NOVO PARADIGMA DE CONDUTA E TRATAMENTO

http://www.institutodeautoimunidade.org.br/novo-paradigma.html

 

Por Dr. Cícero Galli Coimbra

Médico Internista e Neurologista

Professor Associado Livre-Docente da Universidade Federal de São Paulo

Presidente do Instituto de Investigação e Tratamento de Autoimunidade

 

O vídeo referido na reportagem dominical de 27.05.12  da Folha está no endereço:

Vitamina D – Por uma outra terapia (Vitamin D – For an alternative therapy)

 

http://biodireitomedicina.wordpress.com/2012/05/28/folha-de-sao-paulo-terapia-polemica-usa-vitamina-d-em-doses-altas-contra-esclerose-multipla/

 

Vitamina D pode revolucionar o tratamento da esclerose múltipla

http://biodireitomedicina.wordpress.com/2010/08/03/vitamina-d-pode-revolucionar-o-tratamento-da-esclerose-multipla/

 —

 

Taxas baixas de vitamina D na maioria da população preocupam especialistas

http://biodireitomedicina.wordpress.com/2012/06/18/taxas-baixas-de-vitamina-d-na-maioria-da-populacao-preocupam-especialistas/

  

Pediatras dobram recomendação de consumo diário de vitamina D

http://biodireitomedicina.wordpress.com/2012/06/17/pediatras-dobram-recomendacao-de-consumo-diario-de-vitamina-d/

 

 

Doses diárias de Sol – nos horários certos e com os devidos cuidados

http://biodireitomedicina.wordpress.com/2012/06/12/doses-diarias-de-sol-nos-horarios-certos-e-com-os-devidos-cuidados/

 

“(…) cerca de 70% da população mundial apresenta taxas inadequadas de vitamina D, substância que, dentro do corpo, trabalha como um hormônio. O fenômeno da insuficiência não poupa nem países tropicais, como o Brasil, e a defasagem tende a ser maior nas grandes cidades, já que, dentro de casa, no carro ou no escritório, as pessoas acabam fugindo do sol. De acordo com o endocrinologista Geraldo Santana, do Instituto Mineiro de Endocrinologia, “a deficiência de vitamina D é um achado frequente e também preocupante devido à importante ação da substância no organismo.”

Celso Galli Coimbra
OABRS 11352

cgcoimbra@gmail.com 

Em 19.06.2012

__

 Vitamina D: A Desinformação Médica e o Direito à Informação do Cidadão

http://biodireitomedicina.wordpress.com/2012/06/20/vitamina-d-a-desinformacao-medica-e-o-direito-a-informacao-do-cidadao/

 

Vitamina D pode combater males que mais matam pessoas no mundo

http://biodireitomedicina.wordpress.com/2010/03/20/vitamina-d-pode-combater-males-que-mais-matam-pessoas-no-mundo/

 

Informações médicas sobre a prevenção e tratamento de doenças neurodegenerativas e autoimunes, Parkinson, Alzheimer, Lupus, Psoríase, Vitiligo, como depressão

 http://biodireitomedicina.wordpress.com/2011/03/23/informacoes-medicas-sobre-a-prevencao-e-tratamento-de-doencas-neurodegenerativas-e-auto-imunes-como-parkinson-alzheimer-lupus-psoriase-vitiligo-depressao/

 

Vitamina D é importantíssima para a saúde

”Estudos realizados no Brasil e no exterior apontam a importância da substância na prevenção e no tratamento do câncer, diabetes e de doenças neurológicas, cardiovasculares e até degenerativas, como a esclerose múltipla.”

http://biodireitomedicina.wordpress.com/2009/09/22/vitamina-d-e-importantissima-para-a-saude/

A importância da colina para a regeneração neuronal

http://biodireitomedicina.wordpress.com/2009/09/18/a-volta-triunfal-do-ovo/

“A colina é especialmente importante na gravidez. “Vários estudos já mostraram que ela é tão ou mais importante do que o ácido fólico durante a gestação”

Antes inimigo da saúde cardiovascular, o alimento agora está liberado pelos médicos

O tratamento com vitamina D deve ser feito com indicação por médico atualizado

http://biodireitomedicina.wordpress.com/2012/06/22/o-tratamento-com-vitamina-d/

Taxas baixas de vitamina D na maioria da população preocupam especialistas

http://biodireitomedicina.wordpress.com/2012/06/18/taxas-baixas-de-vitamina-d-na-maioria-da-populacao-preocupam-especialistas/

Solução que vem do sol – com os devidos cuidados

http://biodireitomedicina.wordpress.com/2012/06/12/solucao-que-vem-do-sol-com-os-devidos-cuidados/

11 de junho de 2012

“A vitamina D, que precisa dos raios solares para ser sintetizada no corpo, é a base de uma alternativa revolucionária para tratar doenças autoimunes”

Informações médicas sobre a prevenção e tratamento de doenças neurodegenerativas e autoimunes, como Parkinson, Alzheimer, Lupus, Psoríase, Vitiligo, depressão

Entrevista em TV com o Dr. Cícero Galli Coimbra, professor neurologista da Universidade Federal de São Paulo – Unifesp.

http://biodireitomedicina.wordpress.com/2011/03/23/informacoes-medicas-sobre-a-prevencao-e-tratamento-de-doencas-neurodegenerativas-e-auto-imunes-como-parkinson-alzheimer-lupus-psoriase-vitiligo-depressao/

 

Vitamina D pode revolucionar o tratamento da esclerose múltipla

http://biodireitomedicina.wordpress.com/2010/08/03/vitamina-d-pode-revolucionar-o-tratamento-da-esclerose-multipla/

Sobre este assunto, assista: Vitamina D – por uma outra terapia

http://biodireitomedicina.wordpress.com/2012/04/12/vitamina-d-por-uma-outra-terapia/

http://biodireitomedicina.wordpress.com/2011/03/23/informacoes-medicas-sobre-a-prevencao-e-tratamento-de-doencas-neurodegenerativas-e-auto-imunes-como-parkinson-alzheimer-lupus-psoriase-vitiligo-depressao/ 

—-

Vitamina D pode combater males que mais matam pessoas no mundo

http://biodireitomedicina.wordpress.com/2010/03/20/vitamina-d-pode-combater-males-que-mais-matam-pessoas-no-mundo/

 

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A vida humana se inicia na fertilização do óvulo com o espermatozóide

 A vida humana se inicia na fertilização do óvulo com o espermatozóide

Tradução livre: Cultura da Vida – http://culturadavida.blogspot.com

“O desenvolvimento do embrião começa no estágio 1 quando o espermatozóide fertiliza óvulo e juntos se tornam um zigoto” (Marjorie England, professor da Faculdade de Medicina de Ciências Clínicas, Universidade de Leicester, Reino Unido). [1]

“O desenvolvimento humano começa depois da união dos gametas masculino e feminino, durante um processo conhecido como fertilização (concepção). Fertilização é uma seqüência de eventos que começa com o contato de um espermatozóide com um óvulo em seqüência e termina com a fusão de seus núcleos e a união de seus cromossomos formando uma nova célula. Este óvulo fertilizado, conhecido como zigoto, é uma grande célula diplóide que é o começo, o primórdio de um ser humano” (Keith L. Moore, premiado professor emérito e catedrático da divisão de anatomia da Faculdade de Medicina da Universidade de Toronto, Canadá). [2]

“Embrião: um organismo no estágio inicial de desenvolvimento; em um homem, a partir da concepção até o fim do segundo mês no útero” (Ida G. Dox, autora sênior de inúmeros livros de referência para médicos e cientistas, premiada, trabalhou na Escola de Medicina da Universidade de GeorgeTown). [3]

“Para o homem o termo embrião é usualmente restringido ao período de desenvolvimento desde a fertilização até o fim da oitava semana da gravidez” (William J. Larsen, PhD, Professor do Departamento de Biologia Celular, Neurologia e Anatomia, membro do Programa de Graduação em Desenvolvimento Biológico do Colégio de Medicina da Universidade de Cincinnati). [4]

“O desenvolvimento de um ser humano começa com a fertilização, processo pelo qual duas células altamente especializadas, o espermatozóide do homem e o óvulo da mulher, se unem para dar existência a um novo organismo, o zigoto” (Dr. Jan Langman, MD. Ph.D., professor de anatomia da Universidade da Virgínia). [5]

“Embrião: o desenvolvimento individual, entre a união das células germinativas e a conclusão dos órgãos que caracterizam seu corpo quando se torna um organismo separado… No momento em que a célula do espermatozóide do macho humano encontra o óvulo da fêmea e a união resulta num óvulo fertilizado (zigoto), uma nova vida começa… O termo embrião engloba inúmeros estágios do desenvolvimento inicial, da concepção até a nona ou décima semana de vida” (Van Nostrand’s Scientific Encyclopedia). [6]

“O desenvolvimento de um ser humano começa com a fertilização, processo pelo qual o espermatozóide do homem e o óvulo da mulher se unem para dar existência a um novo organismo, o zigoto” (Thomas W. Sadler, Ph.D., Departamento de Biologia Celular e Anatomia da Universidade da Carolina do Norte). [7]

“A questão veio sobre o que é um embrião, quando o embrião existe, quando ele ocorre. Eu penso, como você sabe, que, no desenvolvimento, vida é um continuum… Mas penso que uma das definições usuais que nos surgiu, especialmente da Alemanha, tem sido o estágio pelo qual esses dois núcleos (do espermatozóide e do óvulo) se unem e as membranas entre eles se chocam” (Jonathan Van Blerkon, Ph.D., pioneiro dos procedimentos de fertilização in vitro, professor de desenvolvimento molecular, celular da Universidade de Colorado, reconhecido mundialmente como o preeminente expert na fisiologia do óvulo e do espermatozóide). [8]

“Zigoto. Essa célula, formada pela união de um óvulo e um espermatozóide, é o início de um ser humano. A expressão comum “óvulo fertilizado” refere-se ao zigoto” (Keith L. Moore, premiado professor emérito e catedrático da divisão de anatomia da Faculdade de Medicina da Universidade de Toronto, Canadá; Dr. T..V.N. Persaud é professor de Anatomia e Chefe do Departamento de Anatomia, professor de Pediatria e Saúde Infantil, Universidade de Manitoba, Winnipeg, Manitoba, Canadá. Em 1991, recebeu o prêmio mais importante no campo da Anatomia, do Canadá, o J.C.B. Grant Award, da Associação Canadense de Anatomistas). [9]

“Embora a vida seja um processo contínuo, a fertilização é um terreno crítico porque, sob várias circunstâncias ordinárias, um novo organismo humano, geneticamente distinto, é por isso mesmo formado… A combinação dos 23 cromossomos presentes em cada pró-núcleo resulta nos 46 cromossomos do zigoto. Dessa forma o número do diplóide é restaurado e o genoma embrionário é formado. O embrião agora existe como uma unidade genética” (Dr. Ronan O’Rahilly, professor emérito de Anatomia e Neurologia Humana na Universidade da Califórnia). [10]

“Quase todos os animais maiores iniciam suas vidas de uma única célula: o óvulo fertilizado (zigoto)… O momento da fertilização representa o ponto inicial na história de uma vida, ou ontogenia, de um indivíduo” (Bruce M. Carlson, M.D, Ph.D., pesquisador professor emérito da Escola Médica de Desenvolvimento Biológico e Celular). [11]

“Deixe-me contar um segredo. O termo pré-embrião tem sido defendido energicamente por promotores da fertilização in vitro por razões que são políticas, não científicas. O novo termo é usado para sustentar a ilusão de que haveria algo profundamente diferente entre o que não-médicos biólogos ainda chamam de “embrião de seis dias de idade” e o que todo mundo chama de “embrião de dezesseis dias de idade”. O termo pré-embrião é usado em arenas políticas – onde as decisões são tomadas para permitir que o embrião mais novo (agora chamado de pré-embrião) possa ser pesquisado – bem como em certos consultórios médicos, onde pode ser utilizado para aliviar eventuais preocupações morais expostas por pacientes de fertilização in vitro. “Não se preocupe”, pode dizer um médico, “o que estamos congelando ou manipulando são apenas pré-embriões. Eles não se tornarão verdadeiros embriões humanos até que os coloquemos de volta no seu corpo” (Lee M. Silver, professor da célebre Universidade de Princeton no Departamento de Biologia Molecular e da Woodrow Wilson School of Public and International Affairs). [12]

[1] [England, Marjorie A. Life Before Birth. 2nd ed. England: Mosby-Wolfe, 1996, p.31]
[2] [Moore, Keith L. Essentials of Human Embryology. Toronto: B.C. Decker Inc, 1988, p.2]
[3] [Dox, Ida G. et al. The Harper Collins Illustrated Medical Dictionary. New York: Harper Perennial, 1993, p. 146]
[4] [Walters, William and Singer, Peter (eds.).. Test-Tube Babies. Melbourne: Oxford University Press, 1982, p. 160]
[5] [Langman, Jan. Medical Embryology. 3rd edition. Baltimore: Williams and Wilkins, 1975, p. 3]
[6] [Considine, Douglas (ed.). Van Nostrand’s Scientific Encyclopedia. 5th edition. New York: Van Nostrand Reinhold Company, 1976, p. 943]
[7] [Sadler, T.W. Langman’s Medical Embryology. 7th edition. Baltimore: Williams & Wilkins 1995, p. 3]
[8] [Jonathan Van Blerkom of University of Colorado, expert witness on human embryology before the NIH Human Embryo Research Panel — Panel Transcript, February 2, 1994, p. 63]
[9] [Moore, Keith L. and Persaud, T.V.N. Before We Are Born: Essentials of Embryology and Birth Defects. 4th edition. Philadelphia: W.B. Saunders Company, 1993, p. 1]
[10] [O’Rahilly, Ronan and Müller, Fabiola. Human Embryology & Teratology. 2nd edition. New York: Wiley-Liss, 1996, pp. 8, 29. This textbook lists “pre-embryo” among “discarded and replaced terms” in modern embryology, describing it as “ill-defined and inaccurate” (p. 12}]
[11] [Carlson, Bruce M. Patten’s Foundations of Embryology. 6th edition. New York: McGraw-Hill, 1996, p. 3]
[12] [Silver, Lee M. Remaking Eden: Cloning and Beyond in a Brave New World. New York: Avon Books, 1997, p. 39]

http://culturadavida.blogspot.com/2008/03/quando-comea-vida-humana.html  ‘

Postado por Cultura da Vida

A Cura e prevenção ocorrem por terapia natural. Suplementação de vitaminas, dieta alimentar

Vitamina D – Sem Censura – Dr. Cicero Galli Coimbra e Daniel Cunha em junho de 2012

http://www.youtube.com/watch?v=cIwIWim4hNM&list=UU5grjCGNi25VAR8J0eVuxVQ&index=4&feature=plcp

As células-tronco de embriões nunca foram necessárias para “curar”. Esta foi a grande mentira milionária de uma Medicina meramente comercial, industria farmaceutica e laboratórios multinacionais e clínicas – inclusive abortistas.

por Cristiane Rozicki

Os tecidos de fetos ou embrioes são usados em várias indústrias, desde as cosméticas, passando pelas de plásticas, até de medicamentos e transplantes, as injeções de células-tronco.

 

Solo le pido a Dios
Que el dolor no me sea indiferente.

 

A Cura e prevenção ocorrem por terapia  natural. Suplementação de vitaminas, dieta alimentar. O estado metabólico, depressão, alimentação e outros dados relativos á neurodegeneração.

 

 

  1. Durante muito tempo, na história da e.m., ouviu-se teses de que era doença geneticamente transmissível, ou que a esclerose múltipla poderia ser causada por um vírus, ou, ainda, que o vírus que levava ao desenvolvimento da esclerose múltipla estaria relacionado e advinha de epidemias tais como o sarampo e a catapora, ambas graves e infecciosas. Muitas dúvidas sem respostas que causavam verdadeiro estresse emocional aos doentes, uma aflição, por não se saber o que pensar e nem como agir.

  1. Alguns médicos até advertiam da necessidade do uso de vitaminas do complexo B, e outra medicação cara, valores altos em dinheiro.

  1. A esclerose múltipla é doença antiga, fim de 1800 ou início de 1900 quando surgiu notícia. Eram projetadas vacinas, um tema recente. Em mais ou menos 1995, uma vacina com células de porcos, assim como também existiu a idéia (que foi colocada em prática) de que pessoas com males do sistema nervoso central deveriam passar por terapias com choques elétricos (médicos nazistas também trabalharam com eletricidade). Já se viu de tudo. Choques elétricos foi passagem familiar. E, por fim, até a teoria de um tumor no encéfalo. Apenas na dec. de 90 surgiu a ressonância magnética. Com o diagnóstico de esclerose múltipla pararam de investir na idéia de que o mal neurológico era meramente psicológico. Mas, depois disso tudo, vingou a idéia de doença auto-imune. Daí os imunosupressores, interferon e rebif.

  1. Sofrimento emocional. Agonia mental que dizem deve-se disciplinar para não atingir o físico. Disciplinar o sofrimento parece impossível realizar. Claro que o físico acaba sendo atingido.

  1. Alimentação passou a ser difícil. Desde 1990 era possível perceber como alguns alimentos proporcionavam mal-estares tais como cansaço, fadiga, diminuição da mobilidade e alergias aparentes na pele. O pior era a carne vermelha, açúcar, adoçantes, bebidas artificiais, álcool, frituras e gorduras de origem animal e agora até o café.

  1. No entanto, desde 2003 com certeza,  já se sabe que doenças neurodegenerativas, e.m., assim como o mal de Parkinson, não são doenças transmissíveis e não são causadas por vírus. Na verdade, trata-se de algo simples e de fácil solução. A neurodegeneração é  resultado de distúrbio metabólico.

  1. Há meio de prevenir a degeneração do sistema nervoso central: basta exame de dosagem de vitaminas do complexo B no sangue, a Riboflavina, por exemplo – no caso da doença de Parkinson, e a eliminação de outros fatores desencadeantes das doenças: evitar o desgaste emocional e eliminar da dieta alimentar a carne vermelha.

Referencias:

Dieta livre de carne e rica em vitamina B2.

COIMBRA, CÍCERO GALLI.  Phd., Médico Neurologista e Professor Livre-Docente. Departamento de Neurologia e Neurocirurgia – Universidade Federal de São Paulo – Unifesp/EPM.

Dieta livre de carne e rica em vitamina B2 pode regredir Parkinson. Neurologia – Jornal da Paulista – ano 16 – n. 179 – Maio/2003.
http://www.unifesp.br/comunicacao/jpta/ed179/pesquisa4.htm

“Dieta livre de carne e rica em vitamina B2 pode regredir Parkinson. Estudo revela que portadores da doença apresentam deficiência da vitamina e ingerem muita carne vermelha; nova dieta fez com que a recuperação média motora dos pacientes saltasse de 44% para 70% em apenas três meses de tratamento”.

A “[…] situação fundamental é a mesma: a existência de um distúrbio metabólico evidente e corrigível, capaz de explicar os eventos fisiopatológicos conhecidos, e cuja correção pode deter a progressão da doença (interrompendo a continuidade da morte neuronal crônica, recuperando células neuronais já afetadas pelo processo neurodegenerativo – mas que não atingiram ainda o ponto de irreversibilidade), promover a recuperação total em casos de início recente, ou ao menos parcial das deficiências neurológicas nos casos mais avançados (minimizando seqüelas permanentes) e impedir a morte […]”.

Disponível em: http://www.unifesp.br/dneuro/nexp/riboflavina/c.htm

Parkinson – riboflavin and the elimination of dietary red meat promote the recovery

Abstract:
“Abnormal riboflavin status in the absence of a dietary deficiency was detected in 31 consecutive outpatients with Parkinson’s disease (PD), while the classical determinants of homocysteine levels (B6, folic acid, and B12)… received riboflavin orally (30 mg)”.
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003001000019&lng=pt&nrm=iso
Brazilian Journal of Medical and Biological Research
ISSN 0100-879X. COIMBRA e JUNQUEIRA.

How a 52-year-old Parkinson’s Disease Sufferer and Naturopath Banished all the Frustrating Symptoms of this Cruel Condition from his Body.  Naturally!

John Coleman’s Video

disponível em

http://www.parkinsonsrecoveryprogram.com/parkinsonsrecoveryprogram.html

O texto fala sobre o fim do estresse, a mudança de alimentação, e nutrientes, mudança total do estilo de vida, para a recuperação da doença. A neurodegeneração tratada é Parkinson. Stop Parkin and Start Living. A página tem 2 vídeos.

http://www.parkinsonsrecovery.com/startliving/

From: Robert Rodgers, Ph.D.
Sent: Friday, July 11, 2008 8:16 PM
Subject: Vitamin and Mineral Deficiencies in the Body

Parkinsons Recovery
Vitamin and Mineral Deficiencies in the Body

There is a compelling reason why you may not be
feeling as energetic as you would prefer. That reason
simply put is that your body is not getting the nutrition that it needs to be fully functional.

Why is this the case, particularly if you are the kind
of person who eats healthy food? We do not get some of the vitamins and minerals our bodies need
to function well from the food we eat.

Production systems for food have changed dramatically over the last several decades. Processing of food strips out some of the minerals and vitamines our body needs the most. What our body needs to function well is not necessarily available in the food sold at grocery stores. Let me give you a few examples.

The first is Vitamin D3. Vitamin D3 is actually what you get when you get sunshine. The effects of sunshine last about 2-3 months. In the wintertime – particularly for those of us that live in the Northwest –  we can easily get depressed.

The reason is that our bodies are deficient in the vitamin created by sunshine. Under such circumstances our body needs more Vitamin D3 which (as it turns out) is actually available at pharmacies.

A second common deficiency in food is Iodine (or salt). Interestingly enough, foods don’t have enough Iodine in order for our bodies to perform their basic tasks. Deborah and I are currently taking supplement of Iodoral which is an Iodine Potassium supplement.

Third, we know that a reason why people are often fatigued is because of an overall deficiency in minerals and specifically magnesium. Many diseases are actually related to mineral or vitamin deficiencies. Health food stores have a variety of mineral and vitamin supplements to evaluate for potential use.

Consider the possibility of testing your body to assess any deficiencies that might exist in your body. After getting the results, make it a point to work with your doctor to bolster up your deficiencies so that your body can return to full health and wellness.”

 

Robert Rodgers, Ph.D.
Parkinsons Recovery
© 2008 Parkinsons Recovery
Zero Point Healers, 7722 Cooper Point Rd NW, Olympia, WA 98502, USA
http://www.aweber.com/z/r/?rMxMTCwstCxMjCycrGzstGa0jCyMLMwMbA

 

  1. Distúrbios Metabólicos, Estresse Emocional, Nutrientes. Neurogénese. A evolução da doença degenerativa sem os cuidados necessários pode fazer uma realidade assustadora em poucos anos de vida.

A Ciência e a medicina sabem que o corpo humano cria todos os dias neurônios e células-tronco. É verdade, acontece a neurogênese. A neurogenese permite a juventude e regeneração sonhadas. De um modo muito natural, a preservação do corpo humano e do cérebro acontecem. Os artigos são científicos e médicos, e estes trabalhos estão à livre disposição de qualquer leitor da internet, pode-se ver.

8.1. VIVA SAÚDE.  O estresse e o mal de Parkinson
Um novíssimo estudo aponta que a tensão emocional influencia no desenvolvimento dessa doença neurológica, que afeta os movimentos e causa tremores no corpo

http://revistavivasaude.uol.com.br/Edicoes/11/artigo5894-1.asp

8.2. A fadiga pode ser agravada não apenas pelo curso da Esclerose Múltipla propriamente, mas pela depressão, ingestão de alimentos pesados, elevação de temperatura. A depressão pode conduzir você ao afastamento de atividades recompensantes e conduzi-lo a escassos contatos sociais com amigos, levando-o a reduzir suas atividades físicas e seu bem estar.

Esclerose Múltipla – Karla Adryana Diniz Meireles

Em: http://www.geocities.com/doug_unesp/esclero.htm

8.3. ASPECTO NUTRICIONAL: SUPLEMENTO ALIMENTAR. Sítio canadense de e.m. – DIRIGIR-MS Estratégias ES.

Sítio canadense de e.m.
Fatores nutricionais e esclerose múltipla.
Nutritional Factors and Multiple Sclerosis
http://www.direct-ms.org/

GENERAL INFORMATION FOR EVALUATING SUPPLEMENTS

National MS Society | Brochure: Vitamins
http://www.nationalmssociety.org/Brochures-Vitamins.asp

Brochures

Vitamins, Minerals, and Herbs in MS
An Introduction
by Allen Bowling, MD, PhD
and Thomas Stewart, JD, PA-C

INTRODUCTION

This booklet focuses on the use of popular vitamins, minerals, and herbs by people with multiple sclerosis (MS). The use of these supplements is one form of complementary and alternative medicine, which we’ll call CAM.

CAM is difficult to define, in part because its contours continually shift. One definition describes CAM as therapies that are not commonly taught at U.S. medical schools nor commonly available at U.S. hospitals. Almost by definition, then, this booklet explores controversial and incompletely studied treatments.

Accordingly, this booklet is not intended to be a primary source for understanding the standard, evidence-based, treatment of multiple sclerosis. Rather, it is intended for those who already use, or at least understand, the benefits of mainstream medical interventions. Over the last decade, medications have been developed that modify or slow down MS. The majority of people with MS should be using one of these medications under the supervision of a physician with expertise in treating MS.

Despite these medications, MS remains a chronic disease that is sometimes relatively benign, but sometimes frighteningly unpredictable. For this and other reasons, many people with MS use some forms of CAM therapy. Most, but not all of them, use CAM therapies in addition to, rather than instead of, medical treatments. That means that CAM therapies are usually used in a complementary, rather than an alternative, manner. Taking dietary supplements is one of the most popular CAM treatments.

Most treatments, including the ones listed in this booklet, have risks associated with them. This booklet will identify some of the risks associated with selected vitamins, minerals, and herbal supplements in MS. However, because of a lack of well-conducted scientific studies and the enormous variation in individual clinical situations, not all risks can be identified. Readers should always discuss their personal situation with their physician before using any CAM therapy.

In “General Information for Evaluating Supplements” below, we provide some basic information that relates to supplements generally, and, in “Specific Information about Select Vitamins, Minerals, and Herbs” below, we offer more detailed information relating to some of the most commonly used vitamins, herbs, and minerals.

For additional information on supplements and other forms of CAM, see the section on references below. The information presented here was developed through the Complementary and Alternative Medicine Program of the Rocky Mountain MS Center, in Englewood, Colorado.

GENERAL INFORMATION FOR
EVALUATING SUPPLEMENTS

To weigh the pros and cons of dietary supplements fairly requires a basic understanding of the role of the immune system in MS. Thoughtful supplementation also requires an understanding of evidence about safety and effectiveness, dosing issues, and the law relating to supplements.

In MS, the immune system actively damages myelin, the protective covering of nerves in the brain and spinal cord—the central nervous system. Most treatments for MS involve the attempt to down-regulate the immune system. All supplements should be considered in light of their potential effects on the immune system.

The details of the immune system are very complex, but in general it may be best to assume that in MS, immune stimulation may be dangerous and immune down-regulation may be beneficial. Accordingly, supplements that are supposed to “boost” or “improve” immune function may be the worst choice for people with MS.

Unfortunately, the immune effects of many supplements are poorly understood. Often the use of supplements requires users to make reasonable inferences based on limited evidence. However, inferences may seem reasonable and still be mistaken.

Often what is used to support the use of supplements is simply a story, sometimes called “anecdotal evidence”. This is the least reliable of all the various kinds of evidence. Particularly in MS, where symptoms come and go unpredictably, improvement in symptoms may appear to be related to the use of supplements, when it is not.

The best evidence is generally obtained from carefully controlled trials among a large group of people with MS. Another source of evidence is animal studies. These studies can be helpful, but may also be misleading. Evidence can also be obtained from experiments done in laboratories. Again, these studies are helpful, but can’t be considered definitive in any way.

Dose is always a critical factor in any medication, and more is not always better. Supplements may have different effects depending on the size of the dose that is taken. While a small amount of certain supplements may be useful, larger amounts may be dangerous. Proper dose should always be considered before beginning supplementation. And therein lies a current difficulty.

The Dietary Supplement Health and Education Act of 1994 (DSHEA) has important implications for users of supplements. Unlike some other countries, the U.S. federal government does not regulate supplements as it does drugs. Under DSHEA, sellers of supplements are not required to meet rigorous quality standards or to prove the effectiveness of their products. This means it is not easy to be certain of the amount of active ingredient in many herbal supplements. Users of any supplements should exercise caution regarding marketing information from the seller.

SPECIFIC INFORMATION ABOUT SELECT
VITAMINS, MINERALS, AND HERBS

The number of available vitamins, minerals, and herbs is too great to catalogue here. This booklet reviews only a few vitamins, minerals, and herbs that are most popular with people with MS.

Vitamins
Vitamins are chemicals without caloric content that are necessary for health. With the exception of vitamin D, we must obtain them from dietary sources.

The Food and Nutrition Board of the National Academy of Sciences has established a recommended daily allowance (RDA) or adequate intake (AI) for vitamins. In general, the RDA used in this text refers to the guidelines established for those who are 19-50 years old, without considering other factors, such as breast-feeding and pregnancy. The RDA or AI represents the minimum amount for each vitamin that we should obtain from our diet on a daily basis. On that point, there is little disagreement.

On the other hand, the question of whether larger doses of vitamins are beneficial is controversial. Vitamins do not function in isolation from one another, but rather work in careful balance. Accordingly, a high concentration of one vitamin might cause a relative deficiency of another.

Dietary sources of vitamins, such as fruits and vegetables, appear to be preferable to vitamin supplements. Perhaps this is because fruits and vegetables contain vitamins in useful proportions, as well as fiber, minerals, and other unidentified chemicals found in plants that together play a role in good nutrition and disease prevention.

Vitamins that are of particular relevance to people with MS are vitamin D, the antioxidant vitamins, and vitamin B12. A description of each follows.

Vitamin D
Vitamin D is a hormone, or chemical messenger, in the body. Dietary sources of vitamin D include fish and fortified foods, such as dairy products and breakfast cereals.
Vitamin D is produced in the skin in response to sunlight, but this production is limited by geographic location, skin pigmentation, and season. Some researchers have studied populations and suggested that there is a correlation between low vitamin D levels and MS.

Scientific studies indicate that vitamin D alters immune function in a way that may be desirable in MS. In addition, a handful of studies using an animal model of MS provide further support for the idea that vitamin D plays a protective role in MS.

One recent, large-scale study involving nurses suggested that those who had highter vitamin D intakes, in the form of multivitamin supplements, may have had a reduced risk of developing MS. However, this study did not determine whether vitamin D can have a positive impact on the course or severity of MS in people who already have the disease. Further research is necessary to clarify these findings.

A much better understood role for vitamin D among people with MS relates to its part in maintaining bone density. There is increasing awareness that low bone density (osteoporosis) may be under-diagnosed in many people, including those with MS. Importantly, many people with MS have risk factors for developing osteoporosis:

  • female gender

  • decreased physical activity

  • decreased exposure to sunlight

  • frequent treatment with steroids

People with MS who have these risk factors may wish to consider having bone density tests and taking supplements of vitamin D and calcium (see page 19). Recommended intake of vitamin D is 200 to 600 IU daily. Doses greater than 2,000 IU daily may cause toxic effects, and should not be used unless prescribed by a physician.

 

 

The Antioxidant Vitamins
A free radical, also called an oxidant, is a molecule that contains an unpaired electron. The unpaired electron is highly unstable and generally allows the molecule to react with other nearby substances. The antioxidant vitamins include vitamin A (or its safer form, beta-carotene), vitamin C, and vitamin E. As the name implies, antioxidants tend to decrease the damage caused by oxidants or free radicals. Antioxidant vitamins are generally available in fruits and vegetables.

Preliminary evidence suggests that the damage caused by free radicals may be involved in the disease process in MS. A few studies using an animal model of MS suggest that antioxidants may even be therapeutic. But the value of these animal studies is limited. There are no well-documented published studies of people with MS that show a clinical benefit related to antioxidant supplements.

The safety of taking antioxidants for people with MS has not been established either. One small, five-week study indicates that antioxidants are safe for people with MS, but the study is too small and short to be conclusive.

There is an important theoretical risk to consider. Antioxidant vitamins stimulate the immune system in laboratory experiments and in some groups of people. In MS, where an overactive immune system appears to be part of the disease process, stimulation may be dangerous.

In summary, there is limited evidence suggesting that antioxidants may be beneficial, and there is also some evidence suggesting potential harm.

The most reasonable course may be for people to obtain antioxidants by eating 2-4 servings of fruits and 3-4 servings of vegetables every day. If antioxidant supplements are used, it may be best to use them in moderation.

 

 

 

 

Specific Issues Regarding the Antioxidant Vitamins

  • Vitamin A and Pregnancy—Vitamin A is necessary for vision and promotes normal growth and differentiation of cells in the body. Vitamin A is fat soluble, and is found in liver, eggs, and cod liver oil.

Fat soluble vitamins are stored in the body and high levels may accumulate over time. The RDA for women and men is 2,300 and 3,000 IU per day, respectively. In general, people should avoid doses in excess of 10,000 IU per day. Some studies have concluded that vitamin A in amounts greater than 10,000 IU may produce birth defects. Pregnant women taking cod liver oil (which contains vitamin A) must use caution to ensure that they are not consuming excessive amounts. In general, pregnant women should obtain vitamin A in the form of beta-carotene found in fruits and vegetables.

  • Vitamin C and Urinary Tract Infections—Vitamin C, also known as ascorbic acid, plays a role in building and maintaining body tissues. Vitamin C is readily available in foods such as citrus fruits and tomatoes. The RDA for this vitamin is 90 milligrams for men and 75 milligrams for women under normal circumstances. The RDA for smokers is an additional 35 milligrams.

For a variety of reasons, people with MS tend to be at an increased risk for urinary tract infections. Some people supplement with vitamin C to reduce that risk. The theory in support of that practice is that vitamin C supplementation can acidify the urine, thereby creating a challenge to infection-causing bacteria. However, the weight of evidence suggests that vitamin C does not acidify urine. There is more evidence to support the use of cranberry (see below) to prevent urinary tract infections than there is for vitamin C.

Whether a higher intake of vitamin C is beneficial is controversial. The proper dose of vitamin C (and all other vitamins) for people with MS is unresolved. Some authorities believe that daily doses greater than 1,000 milligrams may cause diarrhea or kidney damage.

  • Vitamin E and Polyunsaturated Fatty Acids (PUFAs)—Vitamin E prevents oxidative damage to cell membranes or linings and can be obtained from vegetable oils, fruits, vegetables, nuts, and meat. The RDA for vitamin E is 22.5 IU for both men and women.

The body’s requirements for vitamin E increase as the intake of polyunsaturated fats (PUFAs) in the diet increases. This is relevant to MS because some people increase their consumption of PUFAs in the hope that PUFAs are beneficial in MS.

In general, the additional amount of vitamin E needed in diets that are high in PUFAs is quite low: approximately 0.6 to 0.9 additional IU of vitamin E is needed for each additional gram of PUFA. This means that a person consuming 25-30 grams of PUFAs daily needs 15-27 IU of vitamin E daily.

Daily vitamin E doses greater than 1000 IU should be avoided. Consuming substantially lower doses of vitamin E (in the range of 100 IU or less) may be preferable in light of the unresolved questions about the immune effects of vitamin E in people with MS.

 

 

Vitamin B12
Vitamin B12 is found in eggs, meat, poultry, shellfish, and dairy products. The RDA for vitamin B12 is 2.4 micrograms/day for both men and women. Also known as cobalamin, vitamin B12 is required for the production of red blood cells and for proper function of the nervous system.
In fact, a severe vitamin B12 deficiency produces neurological symptoms similar to those seen in people with MS.

A variety of observations have suggested that there may be a relationship between B12 levels and MS. For example, people with MS have low levels of vitamin B12 in their blood more frequently than the general population. Some have unusually large red blood cells. This can sometimes be caused by low vitamin B12.

For all people with MS to supplement with vitamin B12 on the basis of these associations would be a mistake. However, B12 deficiency can be evaluated through a blood test. People with low levels should consider vitamin B12 supplementation. For other people with MS, there is no evidence that vitamin B12 either improves neurological symptoms or favorably alters the course of the disease.

Minerals
Minerals are elements widely distributed in nature that perform diverse and critical roles in human health and disease. The potential roles of selenium, calcium, and zinc are considered here.

S
e

Selenium
Selenium is a mineral that has antioxidant effects. For a brief review of the relevance of antioxidants in MS, see the section on antioxidant vitamins on page 12. As with the other antioxidants, it is difficult to determine the exact effect that selenium has on people with MS. Good sources of selenium include seafood, legumes, whole grains, low-fat meats, and dairy products.

Some studies indicate that selenium levels may be lower in people with MS than in the general population. Partly based on that observation, some have speculated that increased amounts of selenium might have beneficial effects in people with MS.

However, in a study using laboratory animals, selenium supplementation worsened an MS-like disease. In one five-week human study, selenium supplementation seemed to be safe. However, that study was too short and involved too few people to reliably assure safety. Furthermore, selenium may increase the immune response, which may be undesirable in people who have MS.

For adults over the age of 19 the RDA of selenium is 55 micrograms. Until more information is available, it may be best for people with MS to obtain selenium from foods or to use selenium supplements only in moderation. Toxic effects may occur with daily doses greater than 200 micrograms.

 

C
a

Calcium
Important in the formation of teeth and bone and in the regulation of many body processes, calcium is the most abundant mineral in the human body. Good food sources for calcium include dairy products, eggs, and green leafy vegetables.

An old hypothesis about the cause of MS connected it to calcium intake. Based on the studies of populations, the incidence of MS appeared linked to high intake of milk during childhood followed by a large or sudden reduction in milk drinking during adolescence. Very little evidence supports this hypothesis.

On the other hand, calcium is a critically important supplement for those who are at risk for very thin bones, or osteoporosis. As indicated in the section on vitamin D above, many people with MS have risk factors for osteoporosis.

People between the ages of 19 and 50 should consume 1,000 mg of calcium in the diet. Daily doses greater than 2,500 milligrams should be avoided.

 

Z
n

Zinc
Zinc is a mineral that plays a role in many different processes in the body. The results of limited studies of MS and zinc are unclear.
Some studies indicate that zinc levels are low in people with MS. Other studies indicate that zinc levels are high in MS, that zinc may activate the immune system, and that zinc supplementation may worsen an animal model of MS.

The RDA for zinc is 11 mg for men and 8 mg for women. Given the uncertainties about zinc and MS, it would seem preferable for people with MS to avoid doses of zinc in excess of the RDA.

Herbs
The word herb generally refers to a plant, or part of a plant, used for medicinal purposes. Herbs, like drugs, interact with the cells of the body and can sometimes produce changes in body processes. The changes produced by both herbs and drugs may be beneficial, but they may also be harmful.

To minimize the risk of harmful side effects, herbs should only be used with caution. Herb users should be aware of proper dosing, potential side effects, and potential drug-herb and herb-herb interactions. It is important to recognize that there are many unknown aspects to herbs. Specifically, herbs contain many different chemicals. Their effects on the body, on different diseases (such as MS), and on drugs have not been fully determined. In addition, the quality and composition of herbal preparations currently marketed in the United States are extremely variable.

The six herbs described below are among those commonly considered to have potential relevance to people with MS.

Ginkgo Biloba
Ginkgo comes from one of the oldest tree species and has been used in China for medicinal purposes for thousands of years. There is some limited evidence to support ginkgo’s ability to improve cognitive function among older people with mild to moderate dementia. There is no evidence that it improves memory or concentration in healthy adults or people with MS.

Ginkgo is an antioxidant (the function of antioxidants is discussed above). It also inhibits a substance known as platelet activating factor (PAF). By inhibiting PAF, ginkgo can cause a decrease in the activity of certain immune cells. These activities provide theoretical support for the use of ginkgo to treat MS.

Ginkgo has been studied in both the animal model of MS and in people with MS. In the animal model, ginkgo decreased disease activity. Two studies have been done in people. One suggested a benefit, but the larger of the two trials suggested no benefit. In that study, ginkgo was used to treat exacerbations, or attacks, of MS. The study did not consider whether ginkgo might have a role in preventing attacks or in improving MS-related cognitive dysfunction.

Few serious side effects with ginkgo supplementation are known. Ginkgo may inhibit blood clotting and therefore should be avoided by people with bleeding disorders, those who take blood-thinning medications, and those who plan elective surgery. In all cases, regular ginkgo use should be reported to all health-care providers.

 

 

Echinacea
Echinacea, an extremely popular herb, is a flowering plant native to North America and a member of the daisy (Asteraceae) family.
Of the three species available, the best studied is echinacea purpurea.

Echinacea is generally used to treat the common cold. Some studies suggest that it may be helpful for decreasing the duration and symptoms of the common cold. But many studies of echinacea have been criticized by scientists for being poorly designed and performed. No definitive conclusion can be drawn regarding the efficacy of echinacea to treat colds.

Because viral respiratory infections may be linked to exacerbations or acute attacks of MS, treating colds with echinacea is an appealing strategy. The problem is that echinacea may stimulate the immune system. This is a theoretical risk for people with MS because their immune systems are already inappropriately stimulated. No study has been done to investigate this theoretical risk in people with MS.

 

 

St. John’s Wort
St. John’s wort is a yellow flower that grows in many parts of the world. It is generally used as an antidepressant. Many studies indicate that St. John’s wort indeed has antidepressant effects. However, the claim was not supported by data from the first large-scale multicenter clinical trial of St. John’s wort versus an inert placebo or Zoloft. This trial, conducted by the National Institute of Mental Health, National Center for Complementary and Alternative Medicine, and the federal Office of Dietary Supplements, was completed in 2002. It concluded that St. John’s wort is not effective in treating major depression of moderate severity. The NIMH and cosponsors are now planning to study the herb in people with mild depression.

St. John’s wort is generally well tolerated and no reported study has identified effects on the immune system that could be concerning to people with MS.

Interaction with other medications is one important risk of using this herb. St. John’s wort appears to alter the body’s metabolism of certain drugs, which may include birth control pills and drugs commonly used to treat heart disease, seizures, certain cancers, and depression. Medications taken by people with MS that could possibly be affected by St. John’s wort include amitriptyline (Elavil), nortriptyline (Pamelor), carbamazepine (Tegretol), phenobarbital, phenytoin (Dilantin) and primidone (Mysoline).

There is a relatively high incidence of depression among people with MS. It is important to recognize that depression should not be self-diagnosed or self-treated. If you think that you may be a candidate for treatment with St. John’s wort, you should first seek a professional evaluation. St. John’s wort is not suitable for anyone with severe depression.

 

 

Valerian
The unpleasant-smelling root of a flower called valerian is sometimes used as a sleep aid. (It is also sometimes used in root beer!) People with MS may have difficulty sleeping, and difficulties with sleep may contribute to MS-related fatigue. Thus, a sleep aid may be very useful to some people with MS.

A few well-designed trials not involving people with MS show that valerian can decrease the amount of time required to fall asleep without residual feelings in the morning. Valerian is usually well tolerated. However, its immune effects have not been studied.

People with fatigue should consider the possibility that their fatigue may worsen when they take valerian as it may have a lingering sedating effect. Also, valerian may increase the sedating effects of prescription medications such as diazepam (Valium), baclofen (Lioresal), and tizanidine (Zanaflex).

 

 

Asian Ginseng
Asian ginseng, also known as Panax ginseng, has been used for centuries by the Chinese for its supposed ability to enhance physical performance and resistance to stress and aging. The evidence in support of these vague claims is not very strong. One clinical study supported the use of ginseng to enhance quality of life, and another study showed an improvement in the speed of mathematical computations among college students. But other studies have failed to find benefits.

An herb that increases energy and strength would be of great use to people with MS who sometimes suffer from debilitating fatigue. Although some evidence suggests ginseng might be safe in people with MS, other experiments raise the possibility that ginseng may stimulate the immune system in ways that may be detrimental to people with MS. In short, there is too little evidence to conclude whether ginseng is safe for people with MS or not, and nothing to indicate that it improves energy or strength.

 

 

Cranberry
Cranberry is grown in bogs in North America for juice, jelly, and seasonal decorations. Many people use the ripe fruit from this plant to prevent or treat urinary tract infections.

Evidence suggests that cranberries prevent bacteria from sticking to the cells that line the urinary tract. This unique action of cranberry is attributed to two compounds, fructose (a type of sugar), and another chemical known as proanthrocyanidin. Recently published preliminary evidence suggests that cranberry may also kill bacteria directly.

Cranberry has very few side effects. Therefore, using cranberry tablets or juice to prevent urinary tract infections is probably reasonable. Increased fluid intake and improved hygiene may also be helpful preventive measures.

Cranberries should never be used to treat existing urinary tract infections. Urinary tract infections can have serious consequences for people with MS. Urinary tract infections require immediate antibiotic treatment from a physician to get them under control quickly.


CONCLUSION

People with MS and other chronic diseases often consider using complementary and alternative medicine (CAM). Doing all that one can to live well with MS is reasonable, but the use of CAM implies that people accept important responsibilities as well.

Nowhere in this booklet do we recommend any particular treatment. Rather, the pros and cons for each are described as well as space and available data permit. As with most CAM treatments, the evidence regarding dietary supplements is inconclusive. The lack of better evidence is frustrating. Nevertheless, an inquiry into CAM can also be rewarding.
It may help restore a sense of control and hope to people who are struggling with an unpredictable disease. Hope and a good quality of life are tightly linked, and both should be cultivated.

We hope this booklet provides enough useful and specific information to allow more informed decision-making about the supplements we described. Just as importantly, we hope that it provides a framework for thoughtful consideration of other CAM treatments not discussed here.

REFERENCES

Web sites

  • The National MS Society offers local referrals, education programs, counseling, self-help groups, and other booklets and brochures on MS.

  • Regularly updated information focused on CAM and MS is available on an interactive Web site at www.ms-cam.org. This site is managed by the Rocky Mountain MS Center.

Non-technical books
There are many non-technical books on CAM. One book that specifically deals with CAM and MS is:

  • Bowling A.C. Alternative Medicine and Multiple Sclerosis. New York: Demos Medical Publishing, 2001. Web site: www.demosmedpub.com. Tel: 800-532-8663.

Other non-technical books with objective general information on dietary supplements and CAM are:

  • Dillard J., Ziporyn T. Alternative Medicine for Dummies. Foster City, CA: IDG Books Worldwide, Inc., 1998.

  • Steven Foster and Varro E. Tyler, PhD, Tyler’s Honest Herbal: A Sensible Guide to the Use of Herbs and Related Remedies. Binghamton, NY: Haworth Press. Web site: www.haworthpressinc.com. Tel: 800-HAWORTH.

Note: The above-mentioned books may be available for loan at your local chapter of the National MS Society, or at your public library.

Technical References
Detailed technical references include:

  • 2004 Physicians’ Desk Reference for Nonprescription Drugs and Dietary Supplements, Thomson Healthcare, NJ. Web site: www.pdrbookstore.com; Tel: 800-232-7379.

  • Physicians’ Desk Reference for Herbal Medicines, Second Edition, Thomson Healthcare, NJ. Web site: www.pdrbookstore.com; Tel: 800-232-7379.

  • Bowling, A., Stewart, T. Current complementary and alternative therapies for multiple sclerosis. Current Treatment Options in Neurology, 5:55-68, 2003.

  • Ernst, E., Pittler, M.H., Stevinson, C., White, A. The Desktop Guide to Complementary and Alternative Medicine: An Evidence-Based Approach. London: Mosby, 2001.

  • Fetrow, C., Avila, J. The Professional’s Handbook of Complementary and Alternative Medicines. Springhouse, PA: Springhouse Corp., 2003.

  • Fragakis, A.S. The Health Professional’s Guide to Popular Dietary Supplements. Chicago, IL: The American Dietetic Association, 2003.

  • Jellin J.M., Batz F., Hitchens K., et al. Natural Medicines Comprehensive Database. Stockton, CA: Therapeutic Research Faculty, 2002.

Sources of information on health fraud

  • National Council Against Health Fraud, 119 Foster Street, Peabody, MA 01960. Tel: 978-532-9383. Web site: ncahf.org.

  • Quackwatch. Web site: www.quackwatch.com.

Federal government sources

  • Federal Trade Commission, Consumer Response Center, 600 Pennsylvania Avenue, NW, Washington, DC 20580. Tel: 877-FTC-HELP (877-382-4357). Web site: www.ftc.gov. Investigates false advertising.

  • Food and Drug Administration, 5600 Fishers Lane, Rockville, MD 20857. Tel: 888-463-6332. Web site: www.fda.gov. In 1988, the FDA established the National Health Fraud Unit to fight medical fraud. This unit helps coordinate federal, state, and local regulatory actions against fraudulent products and practices.

  • National Center for Complementary and Alternative Medicine Clearinghouse, P.O. Box 7923, Gaithersburg, MD 20898-7923. Tel: 888-644-6226. TTY: 866-464-3615. Web site: nccam.nih.gov. E-mail: info@nccam.nih.gov.

  • U.S. Postal Inspection Service, 475 L’Enfant Plaza, SW, Washington, DC 20260-2100. Tel: 202-268-4267. Web site: www.usps.gov/postalinspectors. Monitors products purchased by mail.

 

 

 

 

For additional information

Putting the Brakes on MS (Society brochure)

Complementary and Alternative Medicine

Managing MS Through Rehabilitation (Society brochure)

 

 

 

Allen Bowling, MD, PhD, is the Director of the Complementary and Alternative Medicine Program at the Rocky Mountain MS Center, and Clinical Assistant Professor of Neurology at the University of Colorado Health Sciences Center.

Thomas Stewart, JD, PA-C, is a certified physician assistant and is the Associate Director of the Complementary and Alternative Medicine Program at the Rocky Mountain MS Center.

Cover photograph by Bill Stanton.

This publication is supported by contributions to the National Multiple Sclerosis Society from its members and friends.

Reviewed by members of the Client Education Committee of the National Multiple Sclerosis Society’s Medical Advisory Board.

 

 

 

Copyright © 2004 National Multiple Sclerosis Society

 

8.4. Defesas Celulares e a vitamina do Sol. Scientific American, edição 67 – Dezembro 2007. Cientistas reconhecem que a vitamina D faz mais que contribuir para o fortalecimento dos ossos. Mas a maioria das pessoas não a obtém em quantidades satisfatórias. Essa deficiência estaria contribuindo para o avanço de doenças mais graves.

http://www2.uol.com.br/sciam/reportagens/defesas_celulares_e_a_vitamina_do_sol.html

8.5. Mistérios do Cérebro – A relação com os alimentos. http://globoreporter.globo.com/Globoreporter/0,19125,VGC0-2703-14904-3,00.html
Fim de um mito
Globo Repórter em 2006 – Foi falado sobre os beneficios do ovo, gema crua e clara cozida. A gema do ovo tem colina. Consumir mais fFrutas, verduras e ovo.

 

8.6. A neurogenese é inibida pelo processo emocional depressivo.

Adult neurogenesis is the production of new neurons in areas of the adult brain including the subventricular zone (SVZ) and subgranular zone (SGZ) of the hippocampus [28]. This formation of new neurons plays a number of physiological roles including damaged neuron replacement[29], [30], memory formation [31], [32] and response to stress [33]. Moreover, some reports have recently shown that neurogenesis is involved in depression [34], [35]. disponível em

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2270335

8.7. As 5 FORMAS DE PROTEGER SEU CÉREBRO.
Dr. Cicero Galli Coimbra, M.D., Ph.D. Laboratory for Brain Ischemia Research, Head Department of Neurology and Neurosurgery Federal University of São Paulo. Escola Paulista de Medcina.

Viva Saúde

http://revistavivasaude.uol.com.br/edicoes/23/artigo15542-1.asp

“Manter a saúde mental é mais fácil do que muita gente imagina. As pesquisas dos últimos 10 anos apontam ser possível, sim, estimular a formação de novos neurônios (o que até 1998 a ciência considerava impossível!) e, conseqüentemente, afastar os riscos de doenças como Parkinson e mal de Alzheimer.”

8.8. Estimulando a natureza do ser humano com ambiente e alimentação natural, equilibrando e suprindo as deficiências de nutrientes, suplementos e vitaminas, os neurônios podem regenerar o corpo. Na dec. de 2000 os cientistas da neurologia descobriram que o processo de degeneração é desencadeado por abalo e estresse emocional. Daí verificaram que existe no sangue deficiência de nutrientes.

Jornal da Paulista

Estudo revela que portadores da doença apresentam deficiência da vitamina.

http://www.unifesp.br/comunicacao/jpta/ed179/pesquisa4.htm

Estudo comprova que carne vermelha prejudica pacientes com Mal de Parkinson – vídeo Globo

http://video.globo.com/Videos/Player/Noticias/0,,GIM839564-7823-ESTUDO+COMPROVA+QUE+CARNE+VERMELHA+PREJUDICA+PACIENTES+COM+MAL+DE+PARKINSON,00.html

 

O remédio da serenidade

Quinta-Feira , 19 de Junho de 2008

 

http://jornalhoje.globo.com/JHoje/0,19125,VJS0-3076-20080619-324034,00.html

A evolução da doença degenerativa sem os cuidados necessários pode fazer uma realidade assustadora em poucos anos de vida.

 

From: Robert Rodgers, Ph.D.

robert@parkinsonsrecovery.com

Sent: Thursday, July 10, 2008 11:46 AM

Subject: Natural versus Artificial Remedies

Parkinsons Recovery


The Difference Between a Natural and Artificial Treatment


People we work with are often perplexed by what constitutes a “natural therapy” for Parkinson’s. The fundamental question is this:

“How do I know the difference between a ‘natural treatment’  and an ‘artificial treatment”?

That is to say, how do I know whether or not what I am currently doing to treat my Parkinson’s is what my body needs and wants? As it turns out the answer is deceptively simple:  Your body knows what it needs.

John Coleman ND, MANPA, MBTAV.

Mudança do estilo de vida é necessaria. As informações provam isso. Os dados são científicos e médicos, e estes trabalhos estão
à livre disposição de qualquer leitor da internet.

Estas informações, especificamente sobre alimentação natural associada aos  suplementos (e excluir fumo, bebida alcoólica, frituras, artificiais, gordura animal, doçuras, alimentos cozidos em altas temperaturas – quanto mais cru, mais saudável e preserva as vitaminas do alimento) combinados com o fim da tristeza e estresse emocional, mudança do estilo de vida e das escolhas pessoais, correspondem à única maneira de evitar a neurodegeneração.

A ciência e a medicina sabem que o corpo humano cria todos os dias neurônios e células-tronco. É verdade, acontece a neurogênese. A neurogenese permite a juventude e regeneração sonhadas. De um modo muito natural, a preservação do corpo humano e do cérebro acontecem.

  1. 9.    A necessidade de cuidados especiais.

 

Indisposições, doenças do Sistema Nervoso Central exigem a permanência de CUIDADOS ESPECIAIS apropriados para cada quadro de diagnóstico e sintomatologia, para a conservação da vida e saúde das pessoas, manutenção e melhora da qualidade de vida das mesmas.Na esclerose múltipla, HÁ TERAPIAS INDISPENSÁVEIS para serem efetivadas permanentemente. Tal tratamento começa pela AÇÃO PREVENTIVA.

 

 

São Jose, 1º de setembro de

2008.

Cristiane Rozicki

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