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Metallothionein MT Promoter Therapy

Alzheimer’s and MT Promoter Therapy

Alzheimer’s and MT Promoter developed by Dr William Walsh Phd.

NOTES FROM 10/18/16

Notes from Dr Walsh’s presentation at the October 2016 Physician Workshop and Training Conference.

Alzheimers was named after the Doctor bearing his name. Hallmarks of this condition include

  1. Apoptosis – spontaneous death of cells at rate of 5000 times normal.
  2. Severe oxidative stress – inflammation and tissue damage.
  3. Neurofibrillary tangles – twisted fibers inside brain cells. Derived from microtubules that are responsible for transporting nutrients to nerve cells.
  4. Metal problems – initially believed to be aluminum, then brain volume, then concentration of aluminum. Theory of metal toxicity is back in favor with issues of role of copper and zinc recognized as playing a more important role.

Dr Walsh has developed an amino acid blend, called MT Promoter which is intended to improve metallothionein protein production. One such protein, ceruloplasmin is important for binding or chelating ‘free metals’. Unbound copper and other metals are free radicals that cause tissue damage. From a neurotransmitter standpoint, free copper lowers dopamine, the reward and executive thought neurotransmitter, and raises levels of norepinephrine, an excitatory neurotransmitter.  To prevent this conversion and avoid other effects of oxidative stress, we like to increase these binding proteins. In addition to MT Promoter, binding proteins level improves with improved consumption and digestive uptake of protein.  Metallothionein proteins are found in border cells of the digestive track and brain. They are believed to be a first line of defense against free radical damage.

There are believed to be two types of Alzheimer’s conditions:

  1. Genetic – runs in some families – out of 5-6 siblings, 1-3 will get this, as they get progressively older
  2. ApoE – genetically expressed proteins – Believed now that 50% of people 85+ have some amount

 

Signs and symptoms of progressive worsening condition:

  1. Early warning signs – often as early as 55-60 years old
    1. Lose interest in schedules – move away from life
    2. MCI
    3. Why recent/old – as memories formed, as sensory nerves strike outer part of brain and lay down inputs, memories are processed, info transferred to hippocampus and base of brain parts, processed/organized, then back where it came from and laid down as memory
  2. Moderate symptoms
    1. Inability to form new memories
    2. Years 4-6
    3. Often require nursing home – though may not be bothered by this
  3. Later stage
    1. Awful
    2. Complete loss of speech and response
    3. Some may have some understanding of who’s there but unable to respond

Risk Factors for Alzheimer’s

  1. Only realized in mid-50s had something to do with age
    1. Prior didn’t have long enough lifespan
  2. Many documented cases of boxers
    1. Family of well-known boxers in England – all developed
    2. Also football players – more and more cases now
  3. Education – big surprise
    1. Someone in MI developed ability to measure amyloid plaque level in alive human being – proportional to disorder in autopsies
    2. People who never went past HS, vs. college – factor of 5 difference – Even stronger if didn’t finish 8th grade
  4. Keep mind as active as possible
    1. If retired and learn new language or learn something new
  5. Sedentary FAR more likely
  6. Vascular Alzheimer’s Disease – not vascular dementia
    1. Most begins very close to blood vessels
    2. People with hypertension AND hypotension are more prone
  7. Alcohol abuse – factor 2-3
  8. Toxic metals – seen in high levels
  9. Poor nutrition
    1. Lots to do with glial cells nourishing all neurons
    2. Need nutrition to stay healthy, or neurons deteriorate and die

 

Diagnostic tests for Alzheimer’s:

  1. MMSE – common
  2. Best test – CANTAB – from Yale
    1. Like video game test – spend 45” going through the test
    2. Measures many cognitive functions, not just memory
    3. He got that to test his people pre/post
  3. Odor discrimination – entorhinal cortex is first to go
    1. Scratch and sniff, differentiate smells in multiple choice
    2. Correctly tell 10+ – very low likelihood of Alzheimer’s Disease development
    3. If 2-4, chances within 5 years much higher
    4. He gave to a good friend, who flunked the test – dad had died of Alzheimer’s Disease
      1. Had been getting affairs in order, then found out had a bad cold that day!
      2. Totally normal on retest, repeated since
    5. Direct measure
      1. Not yet FDA approved – research only

Theories:

  1. Ach
  2. Amyloid – losing favor
    1. They have gunky material in brain when they die
    2. As it grows, when it touches neuron, it dies – they thought
    3. 12-13 years ago – discovered drug to eliminate plaque from rat brains, rushed to human testing
      1. At first, so exciting. Got rid of plaques with mild-mod Alzheimer’s Disease
      2. Bad news – didn’t change trajectory of disease – still deteriorate and die
    4. Tau
      1. Makes the tangles
      2. Still leading theory
    5. Inflammation
      1. Could be this alone?
      2. Curcumin theory – India incidence of Alzheimer’s Disease in old people – 90yo – very small
        1. Curcumin very able to reduce inflammation in brain
      3. Oxidative stress
        1. Present in almost every neurodegenerative condition
      4. Toxic metal causation
        1. Persuasive Alzheimer’s Disease research on copper
      5. Could also be glial and nutrition related

ApoE isoforms:

  1. Small protein, linear
  2. Cysteine is great antioxidant
  3. When replaced progressively by arginine, raises risk
  4. Most people with Apoe4 don’t get it – 40-45%
  5. 40% of Alzheimer’s Disease have neither

FDA approved:

  1. Can improve symptoms 6-12 months (actually 4-6 in practice)
  2. Does not stop progress
  3. Enables dying brain to function a bit better – just what’s left works better

Case for Metallothionein:

  1. As much as anything else in brain, protective of metals
  2. If don’t have above-average levels of these metals, highly unlikely to form plaques
  3. Fresh brains with and w/o Alzheimer’s Disease – those who died OF Alzheimer’s Disease had less than 1/3 of normal conc
  4. Very intriguing

MT Promoter for Alzheimers:

  1. He had already developed for autism
  2. Formulation of 22 nutrients that promote synth and fxn of MT
    1. They looked at over 900 studies to see which nutrients promote expression of Alzheimer’s Disease, and which promoted function of brain once expressed
    2. They found by taking it themselves that there ARE side effects if low in Zn
    3. Zn is a metal-regulating element actually on DNA – tends to promote expression of MT
    4. But, it gets expressed without Zn (naked molecule) which immediately grabs Zn, dropping blood level, and causing irritability
  3. Zn loading followed by MTP
    1. Do this till plasma zinc reaches 100 mcg/dL
  4. Aimed at overcoming brain oxidative stress and inflammation, and repair of the BBB
    1. Prevents bad stuff from coming in

MT Promoter for Alzheimer’s Disease:

  1. Unproven until RCTs confirm efficacy
  2. Very promising results
  3. Don’t give to anyone without good quality of life – don’t preserve them in state of misery, so NOT advanced
  4. Have to have caretaker
foods high in methionine

Good Foods During Pregnancy

 We are all either undermethylators, overmethylators or normal methylators.

Many persons with depression are under or over methylators. Depressed women during pregnancy are frequently undermethylators. The good news is, there are many foods that provide to reverse the deficiency and lift depression. 

This published study in the Psych Congress Journal suggests that women who have maternal depression and are undermethylated, often give birth to children who experience depression due to their own ensuing condition of .

Whole blood histamine test is a lab that indicates methylation status. An excellent natural therapy may be methionine or SAMe supplements or foods that are high in methionine. If you have high blood histamines you may be undermethylated. Persons with seasonal allergies are frequently undermethylated. I recommend you get your levels tested before indulging in high methionine foods because your depression may in fact be associated with overmethylation, which requires an opposite approach, to lower methionine.

In consideration of the the study below, know your methylation status, particularly if you are depressed, and to combat during pregnancy, eat foods high in methionine and or take supplements. It won’t just make the mother feel better, but improves chance child won’t end up with depression.

Maternal Depression Linked to Methylation Changes in Offspring

by Will Boggs MD, Psych Congress

By Will Boggs MD

Maternal depression is associated with widespread changes in DNA methylation in their offspring that may persist into adulthood, researchers from Canada report.

“These data further demonstrate the potential long-term consequences of maternal depression for the health of future generations and the importance of mental health and social support of mothers and would be mothers for the physical health of newborn and children,” Dr. Moshe Szyf from McGill University in Montreal, Quebec, told Reuters Health by email. “What is remarkable is that the mental state of a mother causes changes in DNA methylation in the newborns in the immune system, not just the brain.”

Maternal mood disorders and stress during pregnancy can result in attention learning deficits during childhood and mood disorders during adulthood for their offspring. Evidence suggests these consequences may be mediated by modifications of DNA methylation levels.

Dr. Szyf’s team investigated possible associations between maternal depression and DNA methylation changes in T lymphocytes from neonatal cord blood and in hippocampal brain tissues from adults with or without histories of maternal depression.

Offspring of depressed mothers, however, showed significant differences in DNA methylation from those of nondepressed mothers in 145 T lymphocyte CG sites. Most (75.5%) were hypomethylated in the maternal depression group compared with the control group.

“One of the main surprises was that we found a larger effect of maternal depression on the babies’ DNA methylation than the maternal DNA methylation,” Dr. Szyf said. “The second surprise was that it seems that the effect is a consequence of lifelong depression rather than depression only around the pregnancy period.”

“For healthy babies to develop into healthy adults it is important to have healthy mothers,” Dr. Szyf said. “And this involves not only physical and metabolic health but also mental and social wellbeing. This hopefully will be an important pillar in prenatal care as well as public policy relating to preconception health.”

“The consequences of maternal depression might suggest using epigenetic interventions for prevention and reversal of the impacts of maternal depression on the offspring,” Dr. Szyf added. “One clinical potential of the data is the possibility of developing biomarkers of maternal depression that might serve as predictors of lifelong health risks and guide early interventions.”

Dr. Joanne Ryan from University of Melbourne’s Murdoch Childrens Research Institute, Australia, who recently reviewed and depressive disorders, told Reuters Health by email, “An important next step in this research is to determine whether these methylation differences and associated with health outcomes in the infants/children. Maternal depression during pregnancy has been associated with long-term negative outcomes in the child — the data from this study should be used to determine whether such effects can be mediated by differential DNA methylation.”

To find out more about good foods during pregnancy to help with low methionine, we checked with our favorite food resource.

http://nutritiondata.self.com/

foods.high.in.methionine