Beneficial Nutrients

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Alpha DMX and Arterial Disease

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More on the benefits of folic acid

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Alpha DMX is formulated to boost the intake of nutrients that have a demonstrated benefit in preventing and/or reducing the negative consequences of arterial disease. The key strategies are

1. To increase beneficial mineral intake: calcium, magnesium, potassium, zinc, chromium

2. To increase folic acid intake to 400 micrograms per day.

3. To increase intake of Biotin, Vitamin B12 and Pyridoxine.

4. To supply all other vitamin and mineral nutrients at the RDA level or higher.

5. To supply free form amino acids that have in addition to nutrient function, physiological roles such as stimulating growth hormone secretion, increased neurotransmitter synthesis and protection of the digestive tract lining.

We have  increased the folic acid content of DMX to 400 micrograms per 30 gram. Several benefits are proposed for increased intake of folic acid:   reducing heart attacks, preventing strokes and protecting against the development of dementia.

High Nutrient Density

There are specific nutrients that contribute to the resolution of arterial disease and diabetes 2 . Deficiencies of chromium, biotin and zinc have been associated with glucose intolerance and need to be supplemented.  Deficiencies of folic acids, pyridoxine and Vitamin B12 are associated with increased risk of strokes, heart attacks and Alzheimer’s dementia; these vitamins must be supplemented at a generous level well above RDAs. All these nutrients have been included in the Alpha Nutrition series of elemental formulas.

I

Trobia et al  found zinc to be beneficial in diabetes prone rats. They stated: “Data indicate that dietary treatment of diabetes-prone BB Wistar rats with zinc appears to be an effective approach for delaying or preventing the onset of diabetes in genetically predisposed rodents. This finding may suggest further experimental studies regarding dietary means for preservation of pancreatic function. “

i] Donald Mock, M.D., Ph.D., Professor
Departments of Biochemistry and Molecular Biology and Pediatrics University of Arkansas for Medical Sciences 04/08/2002    Copyright 2000 by The Linus Pauling Institute

[ii] Tobia MH; Zdanowicz MM; Wingertzahn MA; McHeffey Atkinson B; Slonim AE; Wapnir RA. The role of dietary zinc in modifying the onset and severity of spontaneous diabetes in the BB Wistar rat. Mol Genet Metab, 1998 Mar, 63:3, 205-13

Increased Folic Acid

Abstracts from the Medical Literature

Dietary intake of folate and risk of stroke in US men and women: NHANES I Epidemiologic Follow-up Study. National Health and Nutrition Examination Survey.

 Stroke 2002 May;33(5):1183-9; discussion 1183-9    (ISSN: 1524-4628)

Bazzano LA; He J; Ogden LG; Loria C; Vupputuri S; Myers L; Whelton PK
Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, La 70112, USA.

BACKGROUND AND PURPOSE: Few population-based studies have examined the relationship between dietary intake of folate and risk of stroke and cardiovascular disease (CVD). This study examines the association between dietary intake of folate and the subsequent risk of stroke and CVD. METHODS: Study participants included 9764 US men and women aged 25 to 74 years who participated in the National Health and Nutrition Examination Survey I Epidemiologic Follow-up Study (NHEFS) and were free of CVD at baseline. Dietary intake of folate was assessed at baseline using a 24-hour dietary recall and calculated using ESHA software. Incidence data for stroke and CVD were obtained from medical records and death certificates. RESULTS: Over an average of 19 years of follow-up, 926 incident stroke events and 3758 incident CVD events were documented. The relative risk (RR) was 0.79 (95% confidence interval [CI], 0.63 to 0.99, P=0.03 for trend) for incident stroke events and 0.86 (95% CI: 0.78 to 0.95, P<0.001 for trend) for incident CVD events in the highest quartile of dietary folate intake (median, 405.0 microg/day) compared with those in the lowest quartile (median, 99.0 microg/day), after adjustment for established cardiovascular risk factors and dietary factors. CONCLUSIONS: Our findings indicate an inverse relationship between dietary intake of folate and subsequent risk of stroke and CVD. Increasing dietary intake of folate from food sources may be an important approach to the prevention of CVD in the US population.

Decreased Rate of Coronary Restenosis after Lowering of Plasma Homocysteine Levels.

Guido Schnyder, M.D., Marco Roffi, M.D., Riccardo Pin, M.D., Yvonne Flammer, M.D., Helmut Lange, M.D., Franz R. Eberli, M.D., Bernhard Meier, M.D., Zoltan G. Turi, M.D., and Otto M. Hess, M.D.

NEJM Volume 345:1593-1600    November 29, 2001 Number 22

Background:We have previously demonstrated an association between elevated total plasma homocysteine levels and restenosis after percutaneous coronary angioplasty. We designed this study to evaluate the effect of lowering plasma homocysteine levels on restenosis after coronary angioplasty. Methods A combination of folic acid (1 mg), vitamin B12 (400 µg), and pyridoxine (10 mg) — referred to as folate treatment — or placebo was administered to 205 patients (mean [±SD] age, 61±11 years) for six months after successful coronary angioplasty in a prospective, double-blind, randomized trial. The primary end point was restenosis within six months as assessed by quantitative coronary angiography. The secondary end point was a composite of major adverse cardiac events.

Results Base-line characteristics and initial angiographic results after coronary angioplasty were similar in the two study groups. Folate treatment significantly lowered plasma homocysteine levels from 11.1±4.3 to 7.2±2.4 µmol per liter (P<0.001). At follow-up, the minimal luminal diameter was significantly larger in the group assigned to folate treatment (1.72±0.76 vs. 1.45±0.88 mm, P=0.02), and the degree of stenosis was less severe (39.9±20.3 percent vs. 48.2±28.3 percent, P=0.01). The rate of restenosis was significantly lower in patients assigned to folate treatment (19.6 percent vs. 37.6 percent, P=0.01), as was the need for revascularization of the target lesion (10.8 percent vs. 22.3 percent, P=0.047).

Conclusions Treatment with a combination of folic acid, vitamin B12, and pyridoxine significantly reduces homocysteine levels and decreases the rate of restenosis and the need for revascularization of the target lesion after coronary angioplasty. This inexpensive treatment, which has minimal side effects, should be considered as adjunctive therapy for patients undergoing coronary angioplasty.

 

Plasma Homocysteine as a Risk Factor for Dementia and Alzheimer's Disease

Sudha Seshadri, M.D., Alexa Beiser, Ph.D., Jacob Selhub, Ph.D., Paul F. Jacques, Sc.D., Irwin H. Rosenberg, M.D., Ralph B. D'Agostino, Ph.D., Peter W.F. Wilson, M.D., and Philip A. Wolf, M.D.

NEJM Volume 346:476-483 February 14, 2002 Number 7

ABSTRACT

Background In cross-sectional studies, elevated plasma homocysteine levels have been associated with poor cognition and dementia. Studies of newly diagnosed dementia are required in order to establish whether the elevated homocysteine levels precede the onset of dementia or result from dementia-related nutritional and vitamin deficiencies.

Methods A total of 1092 subjects without dementia (667 women and 425 men; mean age, 76 years) from the Framingham Study constituted our study sample. We examined the relation of the plasma total homocysteine level measured at base line and that measured eight years earlier to the risk of newly diagnosed dementia on follow-up. We used multivariable proportional-hazards regression to adjust for age, sex, apolipoprotein E genotype, vascular risk factors other than homocysteine, and plasma levels of folate and vitamins B12 and B6.

Results Over a median follow-up period of eight years, dementia developed in 111 subjects, including 83 given a diagnosis of Alzheimer's disease. The multivariable-adjusted relative risk of dementia was 1.4 (95 percent confidence interval, 1.1 to 1.9) for each increase of 1 SD in the log-transformed homocysteine value either at base line or eight years earlier. The relative risk of Alzheimer's disease was 1.8 (95 percent confidence interval, 1.3 to 2.5) per increase of 1 SD at base line and 1.6 (95 percent confidence interval, 1.2 to 2.1) per increase of 1 SD eight years before base line. With a plasma homocysteine level greater than 14 µmol per liter, the risk of Alzheimer's disease nearly doubled.

Conclusions An increased plasma homocysteine level is a strong, independent risk factor for the development of dementia and Alzheimer's

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