Tuesday, March 11, 2008

vitamin supplements and Parkinson's Disease

Posted: Mon Mar 10, 2008 1:05 am Post subject: Vitamin supplements and Parkinson Disease

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Dear Doctor,

There are some vitamin supplements not suitable for people who have a stroke to take:-

Boron, Chromium, Copper, Magnesium,Manganese,Molybdenum,,Selenium, and Zinic
.
Please kindly enlighten the matter soonest.

Thanks

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Dr. Fernandez



Joined: 20 Jan 2007
Posts: 90

Posted: Mon Mar 10, 2008 11:50 pm Post subject:

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None of these are contraindicated in PD.

If manganese is injested in high quanitities, however, it is known to cause parkinsonism.

High copper content in the liver and brain (but usually due to an enzyme abnormality, not due to heavy injestion) can be the result of an rare inherited parkinson-like disorder (Wilson's disease).

Yours,
_________________
Hubert H. Fernandez


Dear Mr. Teo,

Sorry about your illness.
Stroke is shares risk factors with coronary disease such as dyslipidemias, hypertension, diabetes, obesity, nutritional deficiency and high homocysteine, etc. These risk factors can be prevented and modified by dietary intervention (sodium restriction), supplement (especially vitamin B group ,folic acid ,vitamin E, magnesium , calcium and fish oil), life style modification such as exercise regularly, stop smoking which is you already done. Chromium is function as an insulin cofactor, mean help to reduce diabetes risk. About Selenium, low selenium intake is suspected to increase the risk of coronary heart disease. The other mineral that you have mentioned : Boron, Molybdenum, Manganese, Copper and Zinc have controlled blood levels and so far do not have any medical report about these mineral are increasing the risk of stroke but if you have that report please send them to me.
Best Regards and Please take care,
Kridakorn Watcharachotpimai M.D., ABAAM.
,


From: teo teo [mailto: teokimhoe@yahoo.com ] Sent: Monday, March 10, 2008 11:22 AMTo: Kridakorn WatcharachotpimaiSubject: Re: hormone report

Dear Dr. Kridakorn,

Just to inform you that I had a minor stroke last week and now recovery to normal..
I was told that some of my add-life prescription are not suitable for stroke patient.

They are Boron, Chromium, Copper, Magnesium,Manganese,Molybdenum,,Selenium, and Zinic
.
Please kindly enlighten the matter soonest.

Best regards

Yours faithfully,
TEOKIMHOO
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Dear Mr. Teo,

This is a journal about Manganese and Parkinson disease. Usually we get high exposure if we work in some industry such as steel industry not from a diet or supplements.
Willson’s disease is an abnormallity in copper metabolism which is a rare genetic disease . Your copper level in blood is in low –normal.

Best Regards and Take care,

Kridakorn Watcharachotpimai M.D., ABAAM

J Neuropathol Exp Neurol. 2007 Aug;66(8):675-82. Links
The neuropathology of manganese-induced Parkinsonism.
Perl DP, Olanow CW.
Department of Pathology, Mount Sinai School of Medicine, New York , NY 10029-6574 , USA . daniel.perl@mssm.edu
Manganese is an essential trace metal that is widely used in industry, particularly in the manufacture of steel. Exposure to high levels of manganese can cause neurotoxicity with the development of a form of parkinsonism known as manganism. It has recently been hypothesized that manganese exposure might also cause or accelerate the development of Parkinson disease (PD). This article is a review of the pathologic studies that have been reported in patients with manganism and in primates experimentally intoxicated with manganese. They demonstrate a consistent pattern characterized by damage to the globus pallidus (particularly the internal segment) with sparing of the substantia nigra pars compacta and the absence of Lewy bodies. This finding contrasts with what is seen in PD, in which there is preferential degeneration of dopamine neurons in the substantia nigra pars compacta coupled with Lewy bodies and preservation of the pallidum. These pathologic findings do not support the notion that manganese causes PD but rather argues that manganese-induced parkinsonism and PD are distinct and separate disease entities.

One of the causes of Parkinson’s disease is over in oxidative damage and low in antioxidant. Some mineral such as Copper, Selenium and manganese are an important part in antioxidant enzyme production ( SOD or superoxide dismutase) which is a protective mechanism. Our brain is very sensitive to free radicals especially you need to take sinemet that help increase energy production for brain cell which mean these will increase free radical production as well. So we need to balance your antioxidant and control oxidative stress. Next visit for antiaging program, I would suggest you to do a comprehensive anti-aging programe which included the tests for oxidative damage, total antioxidant capacity ( not only the levels in the blood) and risks of health disease. Other mineral such as Boron is importance for bone mineral density. Nutrients in supplement have a more benefit than i have told you here, included energy production, memory, immunity etc.
Best Regards,
Kridakorn Watcharachotpimai M.D.,ABAAM.
Nutr Neurosci. 2002 Dec;5(6):363-74. Links
Selenium intake, mood and other aspects of psychological functioning.
Benton D.
Department of Psychology, University of Wales Swansea , Swansea SA2 8PP, Wales , UK . d.benton@swansea.ac.uk
Selenium is an essential trace element although the level of selenium in food items reflects the soil in which they were grown and thus varies markedly between different parts of the world. The metabolism of selenium by the brain differs from other organs in that at times of deficiency the brain retains selenium to a greater extent. The preferential retention of selenium in the brain suggests that it plays important functions. To date mood is the clearest example of an aspect of psychological functioning that is modified by selenium intake. Five studies have reported that a low selenium intake was associated with poorer mood. The underlying mechanism is unclear although a response to supplementation was found with doses greater than those needed to produce maximal activity of the selenoprotein glutathione peroxidase. Although the functions of many selenoproteins are unknown some play important roles in anti-oxidant mechanisms. As there are suggestions that oxidative injury plays a role in normal aging, schizophrenia, Parkinson's and Alzheimer's disease, the possible role of selenium is considered. Although there is evidence that supplementation with anti-oxidant vitamins shown some promise with Alzheimer's patients, and in preventing the development of tardive dyskinesia in schizophrenics taking neuroleptics
Nutr Neurosci. 2002 Oct;5(5):291-309. Links
Role of oxidative stress and antioxidants in neurodegenerative diseases.
Rao AV, Balachandran B.
Department of Nutritional Sciences, University of Toronto , Ont. , Canada . v.rao@utoronto.ca
Neurodegenerative diseases (NDD) are a group of illness with diverse clinical importance and etiologies. NDD include motor neuron disease such as amyotrophic lateral sclerosis (ALS), cerebellar disorders, Parkinson's disease (PD), Huntington's disease (HD), cortical destructive Alzheimer's disease (AD) and Schizophrenia. Numerous epidemiological and experimental studies provide many risk factors such as advanced age, genetic defects, abnormalities of antioxidant enzymes, excitotoxicity, cytoskeletal abnormalities, autoimmunity, mineral deficiencies, oxidative stress, metabolic toxicity, hypertension and other vascular disorders. Growing body of evidence implicates free radical toxicity, radical induced mutations and oxidative enzyme impairment and mitochondrial dysfunction due to congenital genetic defects in clinical manifestations of NDD. Accumulation of oxidative damage in neurons either primarily or secondarily may account for the increased incidence of NDD such as AD, ALS and stroke in aged populations. The molecular mechanisms of neuronal degeneration remain largely unknown and effective therapies are not currently available. Recent interest has focused on antioxidants such as carotenoids and in particular lycopene, a potent antioxidant in tomatoes and tomato products, flavonoids and vitamins as potentially useful agents in the management of human NDD. The pathobiology of neurodegenerative disorders with emphasis on genetic origin and its correlation with oxidative stress of neurodegenerative disorders will be reviewed and the reasons as to why brain constitutes a vulnerable site of oxidative damage will be discussed. The article will also discuss the potential free radical scavenger, mechanism of antioxidant action of lycopene and the need for the use of antioxidants in the prevention of NDD.
J Physiol Anthropol. 2008 Jan;27(1):7-10. Links
The relationship between bone density and the physical performance of ambulatory patients with Parkinson's disease.
Kamide N, Fukuda M, Miura H.
School of Allied Health Sciences, Kitasato University, 1-15-1 Kitasato, Sagamihara , Kanagawa , Japan . naokami@kitasato-u.ac,jp
Compared to the general population, Parkinson's disease (PD) patients have a higher risk of hip fracture and secondary osteoporosis. In the general population, it is known that physical performance is related to bone density. However, the relationship between bone density and physical performance in ambulatory PD patients has not been studied. This study investigated the relationship between bone density and physical performance in ambulatory PD patients. Fourteen ambulatory PD patients (9 men and 5 women; mean age, 67.3+/-7.7 years; Hoehn & Yahr stages 1-3) were enrolled. Bone density of the right calcaneus was assessed using a speed of sound (SOS) ultrasound measurement device. Disease severity was categorized using the Japanese Unified Parkinson Disease Rating Scale (UPDRS). Furthermore, to assess physical performance, lower extremity strength, 10 m gait time, and body sway were measured. Since SOS is strongly affected by age and gender, it was standardized by the patient's age and gender, and the t-score was calculated with the use of SOS. Significant correlations were found between the t-score and UPDRS,lower extremity strength, and 10 m gait time. When the 4 parts of the UPDRS were analyzed separately, only the correlation between part IV and the t-score was not significant. The findings of this study suggest that higher disease severity and weaker lower extremity physical performance decreased bone density in ambulatory PD patients. Therefore, in order to prevent hip fractures in ambulatory PD patients, assessing the UPDRS and lower extremity physical performance may be clinically useful.


Dr. OkunJoined: 19 Jan 2007Posts: 251Location: University of Florida
Posted: Thu Mar 13, 2008 8:24 pm Post subject:

None of these vitamins have an evidence based record in PD so I cannot advise you. I have not seen a tremendous improvement with these sorts of regimens in my patients. I recommend a multivitamin for patients who are interested._________________Michael S. Okun, M.D.


Dear Mr Teo I do not routinely recommend vitamins and other chemical substances (such as selenium, copper, etc) to my patients as there is no direct evidence that they help in PD. Dr Chew Nee Kong, Kuala Lumpur

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