...Five abstracts below. The abstracts are not a complete lists of issues in Parkinson's, but they represent a good starting point. My brief comments:
ONE
Notice in the first abstract that group 1 patients had 'normal' vitamin D status. They cite 21.7 ng/mL as 'normal'. Sure, okay. Healthy? NOT EVEN CLOSE. You want to be up more like 40 ng/mL or a bit higher still. in SI units i aim for the 100-140 nmol/L range. When I first started getting tested I was at 72 nmol/L and the docs said that was fine. Not true.
TWO
Osteoporosis and conditions of that kind have been linked to elevated Parathyroid Hormone (PTH). When your vitamin D3 status drops below the 70s (increasingly likely as we age), PTH goes up and the bone changes begin. Magnesium is one of the keys for utilizing vitamin D3, but potassium can't be left out of it - for more detail see abstract three.
THREE
Magnesium and potassium go hand in hand. If you have a 'refractory' or stubborn potassium deficiency, magnesium deficiency is a likely culprit. You can't just take magnesium at the same time as vitamin D3. the D3 uses it all up. you have to take some separately to make sure it's doing its other various jobs in your body. Such as making sure you can use the potassium in your food.
FOUR
You can't just do D3 and calcium and expect that to be enough for your bones. You need magnesium too. You can see in the study that there is no difference in calcium concentration between Parkinson's brains and control brains. There *is* a difference in magnesium levels - Parkinson's have less magnesium. This is important for your bones too, as described in abstract two.
By the way, in the Niagara Escarpment, the cap layer of dolostone is harder than the layer beneath, limestone. What's the difference? Dolostone has magnesium plus calcium, limestone just has calcium. (PS linking stones to bones: at one time the material in the escarpment belonged to living creatures with exoskeletons and such)
FIVE
Zinc. It is such a bottom line kind of nutrient. I have a lot of personal experience with finding and correcting zinc deficiency, with lab-measured improvements in things like vitamin D3 absorption (more than twice as effective now) and uric acid levels (jumped from 'MS average' to 'healthy control' levels). I have seen info on iron imbalance in Parkinson's and if I read more I am willing to bet that it can be connected to the finding of zinc deficiency in Parkinson's patients.
Your action items:
1) Get blood tests for vitamin D3, magnesium, and zinc. All three will come back 'normal'. Get the numbers and then work on getting your D3 over 100, your magnesium over .91, and your zinc to 18.2. I have units for all those and we can easily do the conversion if your lab uses different units than mine.
2) based on test results, i expect you will need to start taking at least 4000 IU vitamin D3 per day *for maintaining* current status. more if you need to increase your level (you will). 600mg/day albion-chelated magnesium glycinate (mine is by Carlson, and the glycinate form is KEY). 50mg/d zinc. whatever form. after a month drop to 50 every other day.
3) get follow up blood tests to assess the effects of your regimen.
If you want to be really proactive add a multivitamin/multimineral, a b-100 complex, and 1000mg/d vitamin C. I have not gotten into the research available on those - 5 abstracts is enough for now
NEUROLOGY 1997;49:1273-1278
© 1997 American Academy of Neurology
High prevalence of vitamin D deficiency and reduced bone mass in Parkinson's disease
Yoshihiro Sato, MD, Munetsugu Kikuyama, PhD and Kotaro Oizumi, MD
Abstract
Despite excessive hip fractures in patients with Parkinson's disease (PD), little is known about bone changes in these patients. We measured bone mineral density (BMD; Z scores) in PD patients and analyzed its relation to serum biochemical indices and sunlight exposure. We measured BMD in 71 patients in the second metacarpals and divided the patients into two groups according to functional independence: group 1, Hoehn and Yahr stages 1 and 2; and group 2, stages 3 to 5. In four of 20 patients in group 1 (20%), the Z scores was less than -1.0, indicating osteopenia. In 51 patients in group 2, 31 (61%) had a Z score less than -1.0.
The group 1 patients showed a normal mean serum level of 25-hydroxyvitamin D (25-OHD; 21.7 ng/ml), while most group 2 patients were in a deficiency range (group mean 8.9 ng/ml). Many group 2 patients were sunlight deprived. Both groups had elevated serum ionized calcium levels correlating positively with Hoehn and Yahr stage and markedly depressed serum 1,25-dihydroxyvitamin D(1,25-[OH]2D) concentrations, indicating that immobilization-induced hypercalcemia had inhibited 1,25-[OH]2D production. Z scores correlated positively with 25-OHD levels and negatively with parathyroid hormone concentration and Hoehn and Yahr stage. Vitamin D deficiency due to sunlight deprivation and hypercalcemia induces compensatory hyperparathyroidism, which contributes to reduced BMD in PD patients, particularly those who are functionally dependent. Low BMD increases risk of hip fractures in patients with PD but may be improved by vitamin D supplementation.
American Journal of Clinical Nutrition, Vol. 69, No. 4, 727-736, April 1999
© 1999 American Society for Clinical Nutrition
Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women
Katherine L Tucker, Marian T Hannan, Honglei Chen, L Adrienne Cupples, Peter WF Wilson and Douglas P Kiel
ABSTRACT
Background: Osteoporosis and related fractures will be growing public health problems as the population ages. It is therefore of great importance to identify modifiable risk factors.
Objective: We investigated associations between dietary components contributing to an alkaline environment (dietary potassium, magnesium, and fruit and vegetables) and bone mineral density (BMD) in elderly subjects.
Design: Dietary intake measures were associated with both cross-sectional (baseline) and 4-y longitudinal change in BMD among surviving members of the original cohort of the Framingham Heart Study. Dietary and supplement intakes were assessed by food-frequency questionnaire, and BMD was measured at 3 hip sites and 1 forearm site.
Results: Greater potassium intake was significantly associated with greater BMD at all 4 sites for men and at 3 sites for women (P < 0.05). Magnesium intake was associated with greater BMD at one hip site for both men and women and in the forearm for men. Fruit and vegetable intake was associated with BMD at 3 sites for men and 2 for women. Greater intakes of potassium and magnesium were also each associated with less decline in BMD at 2 hip sites, and greater fruit and vegetable intake was associated with less decline at 1 hip site, in men. There were no significant associations between baseline diet and subsequent bone loss in women.
Conclusion: These results support the hypothesis that alkaline-producing dietary components, specifically,
potassium, magnesium, and fruit and vegetables, contribute to maintenance of BMD.
Arch Intern Med. 1992 Jan;152(1):40-5.
Refractory potassium repletion. A consequence of magnesium deficiency.
Whang R, Whang DD, Ryan MP.
Abstract
Experimental and clinical observations support the view that
uncorrected magnesium (Mg) deficiency impairs repletion of cellular potassium (K). This is consistent with the observed close association between K and Mg depletion. Concomitant Mg deficiency in K-depleted patients ranges from 38% to 42%. Refractory K repletion due to unrecognized concurrent Mg deficiency can be clinically perplexing. Refractory K repletion as a consequence of Mg deficiency may be operative in patients with congestive failure, digitalis toxicity, cisplatin therapy, and in patients receiving potent loop diuretics. Therefore, we recommend that: (1) serum Mg be routinely assessed in any patients in whom serum electrolytes are necessary for clinical management and (2) until serum Mg is routinely performed consideration should be given to
treating hypokalemic patients with both Mg as well as K to avoid the problem of refractory K repletion due to coexisting Mg deficiency.
(note: calling it refractory potassium repletion is a bit confusing. They mean refractory depletion or deficiency)
Neurotoxicology. 1992 Fall;13(3):593-600.
Calcium, magnesium and aluminum concentrations in Parkinson's disease.
Yasui M, Kihira T, Ota K.
Abstract
Concentrations of calcium (Ca) and aluminum (Al) were measured by neutron activation analysis and that of magnesium (Mg) by inductively coupled plasma emission spectrometry in 26 regions of Parkinson's disease (PD) and control brains. Ca concentration was unchanged in all anatomic subregions of PD brains compared with control brains.
Mg concentration was lower in cortex, white matter, basal ganglia and brain stem of PD brains compared to control brains (p < 0.01). Al concentration in the substantia nigra, caudate nucleus and globus pallidus was higher in PD brains compared to controls (p < 0.05) and significantly higher in gray matter and the basal ganglia (p < 0.01). These studies are consistent with other observations linking high concentrations of Al and low levels of Mg in the pathogenesis of CNS degeneration and PD.
J Altern Complement Med. 1999 Feb;5(1):57-64.
Evidence of functional zinc deficiency in Parkinson's disease.
Forsleff L, Schauss AG, Bier ID, Stuart S.
Abstract
One of the primary areas of investigation in the pathophysiology of Parkinson's disease (PD) is the loss of the dopamine-producing cells in the melanized neurons of the substantia nigra, believed to be caused by oxidative stress resulting from excessive free radical activity. The cuprozinc enzyme, superoxide dismutase (SODCu2Zn2), catalyzes the dismutation of superoxide anions to hydrogen peroxide plus oxygen, and is normally found in high concentrations in the substantia nigra where it protects neurons by scavenging free radicals. Zinc supplementation has been shown to significantly increase SODCu2Zn2 in vitro. A novel oral zinc tally test (ZTT) used in the assessment of zinc status was administered to 100 PD patients and 25 controls.
Patients with PD showed a significantly decreased zinc status as compared to controls (p < 0.001). Significance was also established for 3 self-reported health-related variables thought to be related to zinc status: vision problems, olfactory loss, and taste loss (p < 0.05). Relative risks for patients with PD for these variables were 1.51, 1.56, and 1.33, respectively. Zinc status as measured by the ZTT is negatively correlated with PD status. PD status is positively correlated with self-reported vision problems, and olfactory and taste loss. Further study of the role of zinc in the development and treatment of PD is warranted.