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Beneficial
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More on the benefits of folic acid Order Book of Brain without starter pack options
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Alpha BMX contains specific nutrients that contribute to the prevention and resolution of brain disorders. For example, deficiencies of folic acid, 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 Alpha BMX at therapeutic levels. Alpha BMX is formulated to boost the intake of all nutrients that have a demonstrated benefit in preventing and/or reducing brain disease. The key strategies are 1. To increase beneficial mineral intake: calcium, magnesium, potassium, and zinc 2. To increase folic acid intake to 800 micrograms per day. 3. To increase intake of thiamine, niacinamide, Vitamin B12 and pyridoxine. 4. To supply all other vitamin and mineral nutrients at the RDA level or higher. 5. To reduce or replace problematic proteins by supplying free-form l-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. One of the therapeutic secrets of Alpha ENF, Alpha PMX, Alpha BMX and Alpha DMX is the avoidance of proteins or peptides. Proteins are the most reactive molecules in food allergic disease. Staple foods such as milk, eggs, wheat, corn, soy and meat contain proteins that frequently cause immune responses and are the basic problem in delayed patterns of food allergy. Prominent allergist-immunologists such as Brennerman, Gerrard, Knicker, Hill, Brostoff and numerous others have made conspicuous efforts to elucidate the delayed forms of food allergy which involve the most profound immune mechanisms. Delayed reactions begin in the gastrointestinal tract mucosa and spread inward to any body tissue if food proteins enter the circulation and interact with the circulating immune system. Incoming food protein/antigens tend to form immune complexes, and can injury target organs by triggering inflammatory responses in a variety of ways. The brain is a target organ and negative effects range from episodic disturbances in brain function to permanent brain damage. Food proteins have metabolic costs that can be avoided by replacing protein with precisely selected amino acids. For example, patients with reduced kidney or liver function are required to restrict protein, since their ability to handle the nitrogen waste of oxidized amino acids is limited. In liver disease, reduced ability to synthesize urea leads to ammonia accumulation. Ammonia is neurotoxic and contributes to the syndrome of brain dysfunction in liver failure, hepatic encephalopathy. Patients with reduced kidney or liver function are required to restrict protein, since their ability to handle the nitrogen waste of oxidized amino acids is limited. Fluctuating levels of ammonia influences brain cell function; they should be considered whenever brain function is abnormal. Some children are born with metabolic abnormalities in the handling of amino acids and ammonia. They often present with malfunctioning brains. The use of elemental nutrient formulas such as Alpha BMX is useful in reducing or eliminating proteins from the diet. The formulas provide a precise intake of amino acids in a well balanced mixture – impossible to achieve with food. Increased Folic Acid We have increased the folic acid content of BMX from 120 micrograms per 30 gram serving to 800 micrograms. The increased intake of folic acid has significant benefit in reducing heart attacks, preventing strokes and protecting against the development of dementia. Sample 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 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. Plasma Homocysteine as a Risk Factor for Dementia and Alzheimer's Disease NEJM Volume 346:476-483 February 14, 2002 Number 7 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 According to a press report from the US National Institute of Aging: [i] “Mouse experiments suggest that folic acid could play an essential role in protecting the brain against the ravages of Alzheimer’s disease and other neurodegenerative disorders, according to scientists at the National Institute on Aging. One animal study [ii] the underlying biochemical mechanisms were investigated: People with high blood levels of homocysteine have nearly twice the risk of developing the disease. [iii] “The NIA team counted neurons in the hippocampus, a brain region critical for learning and memory that is destroyed as plaques accumulate during Alzheimer’s disease (AD). The investigators found a decreased number of neurons in the mice fed the folic acid deficient diet. The scientists also discovered that mice with low amounts of dietary folic acid had elevated levels of homocysteine, an amino acid, in the blood and brain. They suspect that increased levels of homocysteine in the brain caused damage to the DNA of nerve cells in the hippocampus. In transgenic mice fed an adequate amount of folate, nerve cells in this brain region were able to repair damage to their DNA. But in the transgenic mice fed a folate-deficient diet, nerve cells were unable to repair this DNA damage… These new findings establish a possible cause-effect relationship between elevated homocysteine levels and degeneration of nerve cells involved in learning and memory in a mouse model of Alzheimer's disease,” said Mark Mattson, Ph.D., chief of the NIA’s Laboratory of Neurosciences and the study’s principal investigator. “ Parkinson's disease occurs when certain nerve cells die or become impaired and can no longer produce dopamine. Without it, individuals can develop tremor or trembling in hands, arms, legs, jaw, and face; rigidity or stiffness of the limbs and trunk; bradykinesia, or slowness of movement; and postural instability or impaired balance and coordination. Patients may also have difficulty walking, talking, or completing other simple tasks. Parkinson's is not usually inherited; the incidence of the disease increases with age, with an average onset at about 60 years. It afflicts about 50,000 Americans annually.” In another NIA report, [iv] mouse experiments suggested that folic acid deficiency could increase the brain’s susceptibility to Parkinson’s disease. Investigators fed one group of mice a diet that included folate, while a second group was fed a diet lacking this vitamin. They then gave the mice MPTP, a chemical that can cause Parkinson-like symptoms. In the mice fed folate, MPTP caused only mild symptoms of disease. But mice fed the folate-deficient diet developed severe Parkinson’s symptoms. Mice with low amounts of dietary folic acid had elevated levels of homocysteine in the blood and brain. ..homocysteine in the brain may damage the DNA of nerve cells in the substantia nigra, a brain system that produces dopamine. Loss of dopamine activity causes the symptoms of PD. In mice fed adequate amounts of folate, dopamine-producing nerve cells were able to repair damaged DNA and counteract the adverse effects of homocysteine. However, similar nerve cells in folate-deficient mice could not repair extensive DNA damage. As a result, these cells died. People who have Parkinson’s disease often have low levels of folic acid in their blood… based on this study, Dr. Mattson speculates that consuming adequate amounts of folic acid—either in the diet or by supplementation—could help protect the aging brain against Parkinson’s and other neurodegenerative diseases”
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