Author Topic: May not always be a brain disease - May be different OS  (Read 14777 times)

Offline JC Spencer

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May not always be a brain disease - May be different OS
« Reply #20 on: March 13, 2012, 10:22:27 AM »
Thank you for your question. Everyone is unique and responds differently; however, some participants are experiencing remarkable mental improvement from simply using the sugar trehalose.  Other people are participating in our T/C+ six-month Pilot Survey where we match the funding.  You can receive more information at http://endowmentmed.org. You may qualify to participate in the T/C+ Pilot Survey.  Complete the Forms about that study at http://www.endowmentmed.org/content/view/1164

rocioroush

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Re: May not always be a brain disease - May be different OS
« Reply #19 on: March 13, 2012, 07:50:00 AM »
I am not able to recall everything. I am able to recall only a part of whole situation. Is it a symptom of some diseases?
Secondly what should one do to increase his memory strength.

Offline JC Spencer

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Trehalose, plant sugars and clean high pH water
« Reply #18 on: April 15, 2008, 01:53:51 PM »
You are going in the right direction.  We have researched this some and should soon be able to report our findings.  I have a capter in Expand Your Mind - Improve Your Brain that deals with pH and the importance of moving toward a body pH of 7.4 (I am encouraging 7.5).  It is interesting that my findings show that the best pH balance or soil, blood, and water appears to be 7.5.
« Last Edit: May 05, 2008, 03:42:01 PM by JC Spencer »

kendersa

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May not always be a brain disease - May be different OS
« Reply #17 on: April 15, 2008, 01:27:28 PM »
My family and I are trying to slowly cut out the bad foods in our lives.  We have printed lists of hidden names of MSG and Aspartame that we take with us when we go shopping to make sure we buy good items.  We have currently been experimenting with juicing and surprisingly it tastes good.  We are limiting the amounts of soft drinks in our diet with the hopes of completely knocking them out of our lifestyles.  And are currently researching what would be the best water purifier for our family; since we have been researching that in oxygen rich environments it is hard for disease to survive.  So far we are thinking about getting a water purification system that is alkalized ionized water because we will still get the good minerals and have a lot of oxygen still in every glass.  Anyone have any good suggestions of what they use?
« Last Edit: May 01, 2008, 10:32:42 AM by JC Spencer »

Offline JC Spencer

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Trehalose Huntington's Report - Still no spasms today
« Reply #16 on: April 15, 2008, 01:10:22 PM »
What a thrill to know those with Huntington's have seen a difference with good nutrition, good sugars, and clean water.  I pray we can see many more HD sufferers benefit and share their experiences.  Good nutrition replacing bad foods can make a life regardless of the ailment.  I had a doctor call me this morning thrilled that his wife was given two more years with him.

kendersa

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Trehalose Huntington's Report - Still no spasms today
« Reply #15 on: April 15, 2008, 09:52:20 AM »
Still great news....no spasms today....I promise I wont do this everyday but this is just such happy news for my family and I want to make sure that anyone who might benefit from this information has it made available to them to try on their own.  I know two days might not seem like much of a big deal but to someone who it petrified of having HD it makes the day.  They were having spasms in their shoulders or thighs that could last anywhere from 3 seconds to about 15 and it would drive them crazy.

I must also mention that of course they are still using plant sugars, trehalose, and noni juice along with the magnesium supplements.  I don't really know if the brand of magnesium makes any difference but the one they are using combines two excellent forms of magnesium-citrate and malate.  The other Ingredients are: Magnesium stearate (vegetable), cellulose (plant fiber), silicon dioxide (powdered silica), gelatin, and water.

My family and I are anxiously waiting to hear what the next pilot study is and what fabulous results you are going to have this time.

« Last Edit: May 06, 2008, 08:33:14 PM by JC Spencer »

Offline JC Spencer

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That is great news for Huntington's sufferers.  We will greatly appreciate reports from individuals using trehalose with or without magnesium, or any combination of trehalose, magnesium and glyconutrients or used separately.

Pass the word and let us gather reports over the next few months to lay the ground work for a Pilot Survey and Clinical Trials.

Thank you so much for this ground breaking work in Huntington's.

kendersa

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May not always be a brain disease - May be different OS
« Reply #13 on: April 14, 2008, 01:04:50 PM »
Could be great news in dealing with adding magnesium supplementation.........

A family member of mine.......has been having tremors and muscle spasms every single day for the past 4 months...mostly on the tops of the shoulders and and the tops of their thighs and yesterday was the first day that they did not have any...not one single spasm....they started the supplementation on Saturday with 6 magnesium pills (at 200 mg each one) 2 with each meal and Sunday continued with this and reported NO muscle spasms.  And as we speak, today still nothing.  They have not yet been tested for HD but because it runs in the family it could be because they are starting to show symptoms of HD already or possibly from stress from other family members having it....either way...a very welcomed relief in dealing with spasms.

its seems very interesting to me that symptoms of magnesium deficiency are quite similar to the physical symptoms of HD........and since magnesium is so depleted in patients with HD and used so extensively with HD for the NMDA glutamate receptor and as an antioxidant to deal with free radicals,wouldn't it be so great if adding magnesium could help deal with the physical aspects of HD

I have been trying to figure out if rats have a high amount of magnesium usually in their little bodies.  If they did, could that possibly be why scientists have not been able to replicate the physical symptoms of HD in them?  It would be so great if that really was the answer-a simple magnesium deficiency to negate the tremors, large gait, and muscle spasms that persist uncontrollably with those who have HD.  It would be so nice to just give my family extra magnesium to help be able to control their own bodies.

« Last Edit: May 01, 2008, 10:32:19 AM by JC Spencer »

Offline JC Spencer

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Short, powerful, well rounded lesson on magnesium by The Franklin Institute
« Reply #12 on: April 12, 2008, 09:09:03 PM »
Here is a short but powerful lesson on the importance of magnesium in the brain published by The Franklin Institute:

Proper brain function depends on a constant supply of biochemical energy. When magnesium is chronically deficient or depleted, then brain metabolism and power suffer.

Several factors contribute to the lack of magnesium in our diet. To begin with, a big part of American diets (fats, meats, dairy products) are low in magnesium. This mineral is often depleted in our soils. Processing or cooking further reduce its levels in food, and not all of the magnesium we consume is absorbed.
 
The Top Six Reasons Your Brain Needs Magnesium

#1 Your brain needs magnesium to build the protective myelin sheaths that insulate the nerve fibers which network your nervous system.

#2 Magnesium activates a key enzyme in cell membranes that controls the balance of sodium and potassium. This is absolutely essential to the electrical activity of nerve cells, as well as to the very existence of a cell. If its sodium-potassium ratio got too far out of balance, the cell would burst.

#3 Magnesium activates glutamine synthetase, an enzyme responsible for converting waste ammonia - an extremely toxic byproduct of normal protein metabolism - into urea for proper disposal. The ability to focus and pay attention can be compromised by even small increases in brain ammonia.

#4 Magnesium activates almost all the key enzymes needed for your neurons to produce energy from glucose, in the form of ATP molecules. Magnesium is also necessary for the stable storage of ATP, so it won't spontaneously break down and waste its energy as heat.

#5 Of the 300+ different enzymes in the human body that require magnesium to function, a great many are crucial to cerebral metabolism and cognitive function. In the cerebrospinal fluid that bathes the brain and spinal cord, magnesium is present in higher concentrations than in the blood plasma.

#6 Magnesium is needed to activate the enzyme (D6D) that converts dietary fatty acids into DHA, the most abundant fatty acid in brain cell membranes. Deficiencies in DHA have been associated with numerous neurological disorders - from attention-deficits to Alzheimer's disease.

Factors in Magnesium Loss

Many factors increase magnesium loss from the body, particularly stress - including physical stress from intense exercise. Normal daily loss through urine is from 100 to 300 mg. Of all the drugs known to deplete magnesium, alcohol is the most notorious.

An extreme case of alcohol-induced magnesium deficiency is delirium tremens (the d.t.'s), a life-threatening emergency. It is characterized by sweating, shaking, confusion, hallucinations, seizures, agitation, and disturbances of memory. Emergency room treatment for the d.t.'s includes injections of magnesium sulfate.

Low Magnesium and Increased Stress

Do noises sound excessively loud? Do lights seem too bright? Are your emotional reactions exaggerated? These may be signs of a magnesium deficiency.

Along with vitamin B1, magnesium supports the reparative process that neurons need to offset the stress from the continual firing of the electrical impulse.

Low levels of magnesium may cause nerves to fire too easily, even from minor stimuli. Because stress affects the kidneys' ability to recycle magnesium, hypersensitivity can continue to escalate. The brain may even be too stimulated to sleep.

Magnesium Leaves During Fight or Flight Response

In preparation for "fight or flight," one of the actions of stress hormones is to take magnesium out of muscle cells and replace it with calcium.

This gives muscles their needed rigidity to defend against a foe. But, this magnesium does not necessarily re-enter the muscle cells once the stress is over.

250 References Found Magnesium Deficiency and Stress are Related

A 1994 review of more than 250 references found magnesium deficiency and stress are related. In the authors' words: "When magnesium (Mg) deficiency exists, stress paradoxically increases risk of cardiovascular damage including hypertension, cerebrovascular and coronary constriction. . . . Dietary imbalances such as high intakes of fat and/or calcium (Ca) can intensify Mg inadequacy, especially under conditions of stress...Thus, stress, whether physical (i.e. exertion, heat, cold, trauma, burns), or emotional (i.e. pain, anxiety, excitement, or depression) and dyspnea [breathing difficulties] as in asthma increases need for Mg."29

Foods Containing Magnesium

Magnesium is found in many foods, but usually in small amounts. A single food will not meet your daily magnesium needs. A variety of fruits, vegetables, and grains can supply your magnesium requirements as well as make for a more delectable menu.

Water can also provide magnesium, although
'hard water" has more magnesium than "soft water".

Check the Recommended Dietary Allowance (RDA) and Table of Food Sources of Magnesium for more information.

The Recommended Dietary Allowance of Magnesium 

The Recommended Dietary Allowance (RDA) is the average daily dietary intake level that is sufficient to meet the nutrient requirements of nearly all (97-98 percent) individuals in each life-stage and gender group.30, 31

Life Stage Men Women
Ages 14 - 18 410 mg 360 mg
Ages 19 - 30 400 mg 310 mg
Ages 31 + 420 mg 320 mg

Table of Food Sources of Magnesium30, 31

Food Milligrams
100 percent Bran, 2 Tbs 44
Almonds, dry roasted, 1 oz 86
Avocado, California, 1/2 med 35
Avocado, Florida, 1/2 med 103
Banana, raw, 1 medium 34
Bran flakes, 1/2 c 60
Bread, whole wheat, 1 slice 24
Broccoli, chopped, boiled, 1/2 c 19
Cashews, dry roasted, 1 oz 73
Cereal, shredded wheat, 2 rectangular biscuits 80
Chocolate bar, 1.45 oz 45
Hummus, 2 Tbs 20
Kiwi fruit, raw, 1 med 23
Nuts, mixed, dry roasted, 1 oz 66
Peanut butter, 2 Tbs. 50
Peanuts, dry roasted, 1 oz 50
Potato, baked w/ skin, 1 med 55
Potato, baked w/out skin, 1 med 40
Raisins, golden seedless, 1/2 c packed 28
Seeds, pumpkin, 1/2 oz 75
Shrimp, mixed species, raw, 3 oz (12 large) 29
Soybeans, cooked, 1/2 c 54
Spinach, cooked, 1/2 c 65
Spinach, raw, 1 c 24
Tahini, 2 Tbs 28
Vegetarian baked beans, 1/2 c 40
Wheatgerm, toasted, 1 oz 90

Sources of Good Magnesium Supplements

Many nutritionists believe the optimum intake of magnesium - especially when stress is a factor - should be two to three times higher than what Americans are typically getting from their diet. Supplements are the easiest way to increase magnesium intake.

Some forms of magnesium that are well-absorbed and well-utilized include magnesium ascorbate, aspartate, citrate, glycinate, succinate, and taurinate. Forms not so well absorbed are magnesium oxide and carbonate.
« Last Edit: May 06, 2008, 08:35:47 PM by JC Spencer »

Offline JC Spencer

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The importance of magnesium in the brain
« Reply #11 on: April 12, 2008, 08:57:36 PM »
According to Rosemary Fisher, magnesium is quite necessary for brain function. In Food and Nutrition Research (October, 1995), a publication of the U.S. Department of Agriculture in Greenbelt, Md., it was reported that magnesium is the fourth most abundant element in the brain. A low level of magnesium overexcites the brain's neurons and results in less coherence. Good natural sources of magnesium are defatted soy flour, whole grains, wheat bran, and nuts.
« Last Edit: May 05, 2008, 11:34:14 PM by JC Spencer »

kendersa

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May not always be a brain disease - May be different OS
« Reply #10 on: April 10, 2008, 10:06:59 AM »
We have started my brother on magnesium (non-synthetic) supplements.......have yet to find out how much he is actually supposed to take.....so I figured we would double the recommended usage.  I have read that it would probably take about 6 months for his magnesium levels to become normal so we shall see on the results month by month.  I have also debated on how to check and see if his magnesium levels are actually rising since I have read that your body can register normal levels of magnesium when in fact your brain's level of magnesium might be quite low.  Any help would be greatly appreciated 8)  If anyone knows a great brand on magnesium supplements I would love to hear!

« Last Edit: May 01, 2008, 10:31:50 AM by JC Spencer »

Offline JC Spencer

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Standford University report on glutamate and HD
« Reply #9 on: April 09, 2008, 03:46:57 PM »
Stanford University report on glutamate and Huntington's disease (HD)

"Scientists have found that certain glutamate receptors in the nerve cells of patients with HD tend to be oversensitive to glutamate. For some patients with HD, glutamate can act as an excitotoxin, even if its levels are not particularly high. Treatments that attempt to inhibit glutamate activity therefore may have some therapeutic potential."

-- (HOPES: Huntington's Outreach Project for Education, at Stanford, 8/30/2005: http://www.stanford.edu/group/hopes/treatmts/antiglut/l0.html)

"The lowered amount of energy available in the nerve cells of patients with HD is thought to cause NMDA receptors to be oversensitive to glutamate. Therefore, normal physiological levels of glutamate can cause overexcitation of the NMDA receptor, leading to the influx of calcium ions into the cell. Excess calcium ion entry can lead to cell death through a combination of events."

-- (HOPES: Huntington's Outreach Project for Education, at Stanford, 12/3/2004: http://www.stanford.edu/group/hopes/treatmts/antiglut/l2.html)

"Huntington's disease is associated with both problems in energy metabolism and glutamate toxicity....

"Energy metabolism is the process by which cells produce energy. Normally, cells prefer a form of energy metabolism called aerobic respiration due to its efficiency and high-energy yield. The altered huntingtin protein in people with HD is believed to interfere with aerobic respiration, resulting in the inability of HD cells to perform aerobic respiration efficiently. Instead, HD cells must resort to anaerobic respiration, another form of energy metabolism that is less efficient. This impairment in energy metabolism results in various negative effects that eventually lead to cell death....

"One of the effects of the impairment in energy metabolism in HD cells is an increased sensitivity to glutamate. Glutamate is one of the major neurotransmitters in the nervous system, used to transmit messages from nerve cell to another.  Increased activation of receptors that receive glutamate has been observed in people with HD. Increased glutamate activity, in turn, has been associated with nerve cell death."

-- (HOPES: Huntington's Outreach Project for Education, at Stanford, 12/3/2004: http://www.stanford.edu/group/hopes/treatmts/antiglut/l3.html)
« Last Edit: May 06, 2008, 08:36:28 PM by JC Spencer »

Offline JC Spencer

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HD Study in mice shows response was not due to excessive glutamate
« Reply #8 on: April 09, 2008, 03:35:50 PM »
Age-Dependent Biphasic Changes in Ischemic Sensitivity in the Striatum of Huntington's Disease R6/2 Transgenic Mice by Gloria J. Klapstein and Michael S. Levine
Mental Retardation Research Center, The David Geffen School of Medicine, University of California, Los Angeles, California

ABSTRACT 
 
We used the oxygen/glucose deprivation (OGD) model of ischemia in corticostriatal brain slices to test the hypothesis that metabolic deficiencies in R6/2 transgenic Huntington's disease (HD) mice will impair their recovery from an ischemic challenge. Corticostriatal extracellular field excitatory postsynaptic potentials (fEPSPs) were evoked in transgenic and wild-type (WT) mice in three age groups: 3-4 wk, before the overt behavioral phenotype develops; 5-9 wk, as overt behavioral symptoms begin; and 10-15 wk when symptoms were most severe. OGD for 8 min completely and reversibly inhibited fEPSPs. Although responses of 3-4 wk WTs showed a tolerance to ischemia and recovered rapidly, ischemic sensitivity developed progressively; at 5-9 and 10-15 wk, responses recovered more slowly from OGD. In contrast, although 3-4 wk R6/2 transgenic fEPSPs showed significantly more ischemic sensitivity than their WT counterparts, the R6/2 fEPSPs maintained a relative tolerance to ischemia at 5-9 and 10-15 wk. As a result, a "crossover" point occurred, roughly coinciding with the development of the overt behavioral phenotype (5-9 wk), after which time R6/2 fEPSPs were significantly more resistant to ischemia than WT responses. The increased ischemic sensitivity in 3-4 wk R6/2 responses was not due to excessive glutamate release during OGD as it persisted in the presence of the glutamate receptor antagonist kynurenic acid (1 mM). Although the mechanism for development of ischemic resistance in R6/2 transgenics remains unknown, it correlates with metabolic and biochemical changes described in this model and in HD patients.
« Last Edit: May 06, 2008, 08:38:08 PM by JC Spencer »

Offline JC Spencer

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More infor on magnesium and HD
« Reply #7 on: April 09, 2008, 02:50:50 PM »
While we are having good reports from those using trehalose, has anyone had experience with additional magnesium?  Here is an abstract from a HD workshop.

The Electrophysiological Phenotype of HD: Impact of the NMDA Receptor Prepared by Marina Chicurel, Ph.D.

Abstract

Several studies have implicated alterations in the responses of excitatory receptors, particularly NMDA receptors, in the pathology of Huntington's disease (HD). Yet the chain of events that link these disruptions to HD's primary mutation on the one hand, and to clinical symptoms, on the other, remains unclear. Workshop participants made progress towards generating an integrated view of HD pathology and identifying new directions for future study by analyzing recent results generated by a variety of approaches. They discussed several receptor abnormalities and their potential relationships, including alterations in NMDA receptor's sensitivity to magnesium, abnormal receptor phosphorylation, disruption of postsynaptic density scaffolds, aberrant IP3 signaling, and altered receptor trafficking. They also underscored the need to understand the function of wildtype huntingtin, given that loss-of-function effects seem to be important  in HD pathology. To explain the selective vulnerability of striatal neurons, participants noted their unique complement of NMDA receptor subunits - identifying the NR2B subunit as a potentially key determinant of susceptibility - as well as potassium channel subtypes, dopamine receptors and phosphatases. Of particular interest was the convergence of several lines of evidence on dopamine modulation as an important player in HD pathology.
« Last Edit: May 06, 2008, 08:39:45 PM by JC Spencer »

Offline JC Spencer

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That is a great question.
« Reply #6 on: April 09, 2008, 02:40:16 PM »
Has anyone had first hand experience with additional magnesium with HD?  Here is an abstract from a paper on the subject.  The bottom line is that proper nutrientiton is important and the nutrient that is most needed is that one that will effect change the quickest.  We will continue to research this area and will appreciate comments from others.

EXCITATORY AMINO ACID NEUROTRANSMISSION. PATHWAYS FOR METABOLISM, STORAGE AND REUPTAKE OF GLUTAMATE IN BRAIN  by Monica Palmada and Josep Joan Centelles

Departament de Bioqu�mica i Biologia Molecular, Facultat de Qu�mica, Universitat de Barcelona, Mart� i Franqu�s, 1, 08028-Barcelona, Spain

ABSTRACT

In the nervous system, glutamate is an excitatory aminoacid which at higher concentrations has been implicated in a number of disorders. Glutamate is stored in presynaptic vesicles and is released by calcium-dependent exocytosis. After its action on ionotropic receptors (iGluR, related to ionic channels) or metabotropic receptors (mGluR, related to metabolic formation of second messengers), glutamate can be removed from the synaptic cleft through two processes: re-uptake back into pre-synaptic terminals or diffusion out of synaptic cleft for uptake by glial cells. This is achieved by glutamate transporters. In pre-synaptic terminals, glutamate is packed into the specialized secretory vesicles by means of a specific vesicular transporter. The level of glutamate available for neurosecretion is regulated by the vesicular transport activity. In order to achieve a proper concentration of the neurotransmitter in synaptic vesicles, glutamate must be synthesized. Glutamine is obtained in astroglial cells from the glutamate reuptaken, and as it has no neurotransmitter activity, it is the metabolite which regenerates glutamate in neurones (glutamate-glutamine cycle). Moreover, glutamate is also obtained from glucose by an intermediate of TCA cycle. In this paper we want to introduce some aspects of glutamate biosynthesis and release: glutamate receptors, neurotransmitter uptake by the glutamate transporters and neurotransmitter inactivation and new formation by metabolism.

« Last Edit: May 05, 2008, 11:12:18 AM by JC Spencer »