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It's a problem
When you're filling out a new patient neurological form from Emory and it doesn't list cataplexy anywhere, that's a problem. When you see a neurologist and they have to leave the room to look up cataplexy, that's a problem.
Narcolepsy Cataplexy is a hypothalamic disease, which means it is a neurological disease. Yes, laughing and being surprised, along with stress can trigger a cataplectic attack, but it is not caused by a psychological problem, it is caused by a diseased hypothalamus.
Narcolepsy Cataplexy is a hypothalamic disease, which means it is a neurological disease. Yes, laughing and being surprised, along with stress can trigger a cataplectic attack, but it is not caused by a psychological problem, it is caused by a diseased hypothalamus.
Wednesday, September 27, 2017
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Doctor In Italy Quells Parkinson’s With Overlooked Vitamin Cure
Doctor In Italy
Quells Parkinson’s With Overlooked Vitamin Cure
By Bill Sardi
January 12, 2017
In recent weeks the
world has learned the news media creates fake news and/or completely
shuns significant news stories to match its own politically correct
agendas. So an unequivocal cure for a major brain disease goes
unreported. Shame on CNN, CBS, ABC, NBC, the BBC, Reuters,
Associated Press and the New York Times.
For a disease
considered incurable, a physician in Italy has begun to provide a
common B vitamin to successfully treat a debilitating motor-nerve
disease commonly known as Parkinson’s disease. The importance of
this startling discovery has escaped major news outlets. It should be
heralded on television and in newspapers worldwide. But it has only
been reported by an obscure European news source. [Ultima
Edizione.eu] (Be sure to click the before-and-after video tabs.)
History of vitamin
B1 and Parkinson’s
Physician James
Parkinson first described a “shaking palsy” in 1817. [Cold
Spring Harbor Perspectives in Medicine 2011] Today, 200 years later
Parkinson’s disease is still considered an incurable disease.
Parkinson’s
disease emanates from the loss of dopamine-producing cells in the
brain. Approximately 60-80% of dopamine-producing cells are damaged
before symptoms arise. Dopamine is a nerve-transmitting chemical in
the brain.
It has taken two
centuries for a vitamin-phobic medical profession to hesitantly begin
to treat Parkinson’s disease with vitamin B1 (thiamin).
Historically the
link between Parkinson’s disease and thiamin deficiency has been
agonizingly slow.
Thiamin, vitamin B1,
was the first vitamin to be discovered. Vitamin B1 was first
synthesized in 1936. [Annals New York Academy Sciences April 1962]
So dietary supplementation was possible from that point forward.
It took till 1967
for the first published report that a decline in brain dopamine
levels of pigeons was due to experimentally induced thiamin
deficiency. [International Journal Neuropharmacology July 1967]
A link between
thiamin deficiency and low dopamine levels was discussed in 1987 in
an experiment that attempted to determine why rats tend to eat mice
(muricide). Low dopamine levels induced by a shortage of thiamin in
the diet were linked to this abnormal animal behavior. [Pharmacology
Biochemistry Behavior 1987]
In 1988 researchers
noted a thiamin-deficient diet decreased dopamine concentration and
synthesis in the brain (striatum). The provision of alcohol to lab
animals also decreased dopamine levels. The brain region most
susceptible to damage (the hypothalamus) in thiamin deficient animals
is the very same region of the brain that produces dopamine. [Drug
Alcohol Dependency 1988]
In 1999 it was
observed that low levels of thiamin in the cerebrospinal fluid were
related to Parkinson’s disease. [Neuroscience Letters 1999]
In 2013 researchers
reviewed all prior published scientific reports and concluded that
thiamin plays a role in Parkinson’s disease. [CNS Neuroscience
Therapy2013]
First therapeutic
trials report
In 2013 the first
reports were published the use of high-dose thiamin among Parkinson’s
disease sufferers resulted in considerable improvement in measured
motor function (31.3% to 77.3%). Injection of high-dose thiamin was
effective in reversing symptoms. [BMJ Case Reports 2013]
Then another study
published in 2015 confirmed that injectable thiamin treatment (100 mg
twice a week) improves motor nerve function among Parkinson’s
patients. [Journal Alternative Complementary Medicine 2015]
In 2016 researchers
in Italy reported on the successful use of high-dose thiamin among
Parkinson’s patients. Notably, all of the patients had normal
blood levels of thiamin yet thiamin therapy led to significant
improvement in Parkinson’s symptoms. There were no adverse events.
[Neural Regeneration Research2016]
Loss of sense of
smell is earliest sign
Finally, in January
of 2017 researchers noted that the sense of smell declines years
prior to the onset of Parkinson’s disease. Scented strips were
used to test scent among individuals with Parkinson’s disease.
Almost half of the individuals tested (47%) scored low on this test
and dietary thiamin was also low in these subjects.
The main finding of
the study was an association between low thiamin in the diet reported
2-8 years prior to the onset of symptoms and diagnosis. Impairment
of olfaction (sense of smell) is a characteristic and early feature
of Parkinson’s disease these researchers wrote. Involvement of
many B- family vitamins appears to be involved in the decline of
smell. Therefore, a decline in the sense of smell may serve as an
early screening tool for Parkinson’s disease. [European Journal
Clinical Nutrition Jan 2017]
Because of a change
in western diets, Dr. Derrick Lonsdale, the reigning clinical
authority on vitamin B1, says the high sugar/carbohydrate diet of
today results in a return of the scourge of beri beri. The problem
is, modern medicine observes symptoms of this nutrient deficiency
disease and treats those instead of its cause.
User's Guide to the
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Western populations
are paying a high price for poor absorption or depletion of thiamin
due to consumption of alcohol, drugs like diuretics (water pills),
refined sugar, carbohydrates, even coffee and tea. [Evidence Based
Complementary Alternative Medicine 2006]
The ordeal of
undetected thiamin deficiency is only exacerbated by the modern
paradigm of treating symptoms of disease as if they emanate from the
drug deficiency, not a nutrient deficiency.
So we now have
60,000 Americans diagnosed with Parkinson’s disease annually and 10
million worldwide living with the disease. More than 23,000 die of
Parkinson’s disease annually in the U.S. [Parkinsons Disease
Foundation]
Levodopa, the main
drug prescribed for Parkinson’s disease, costs ~$2500/year.
[Parkinson’s Disease Foundation]
As of 2014 there
were 23 medicines under development for Parkinson’s disease. Drugs
only serve as a distraction for a disease that may emanate from a
vitamin deficiency.
Thiamin deficiency
is associated with other age-related brain diseases such as
Alzheimer’s and Huntington’s disease. [The Scientist Oct 2013]
Alzheimer’s too
This author penned
an earlier report linking Alzheimer’s disease to thiamin
deficiency. [Knowledge of Health]
The earliest sign of
Alzheimer’s disease is also a decline in the sense of smell.
[Neuropsychiatric Disease Treatment 2016] That was first reported in
1974. [Acta Psychiatric Scandinavia 1974]
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The startling
problem with Alzheimer’s disease is that there is no proven cure
for this brain disease either and only 1 in 244 drugs undergoing
trials for this brain disease have achieved FDA approval.
Accumulation of beta
amyloid plaque in the brain begins up to 20 years before symptoms
occur. With so many Americans now living into their eighth, ninth
and tenth decade of life and 44% of age 75-84 adults affected, it is
too late to conduct a long-term controlled study to head off this
anticipated Alzheimer’s plague. We are going to have close to half
of the senior adult population living with Alzheimer’s memory loss
and the other half of that population taking care of them!
Rx: B vitamins
The provision of the
entire family of supplemental B vitamins, in particular thiamin (B1),
pyridoxine (B6), folic acid (B9), and cobalamin (B12) appears to be
important in the theoretical model of these diseases. Disturbed
sense of smell has been reversed with vitamin B12 supplementation.
[International Forum Allergy Rhinology 2016; Psychosomatics 2014]
The best way to
achieve this proposed prophylaxis is either a B-vitamin complex or a
multivitamin. In most instances the provision of B vitamins in these
formulas is marginal, often not exceeding the outdated Daily Value or
the Recommended Daily Allowance.
A progressive fall
off in the absorption of these B vitamins due to a decline in
secretion of stomach acid with advancing age, or in the case of
thiamin the blockage of absorption by drugs, antacids, alcohol, sugar
and carbohydrates and even presumably healthy beverages like tea and
coffee, serve as sufficient evidence doses of B vitamins need to be
updated in most multivitamins if a universal attempt is to be made to
head off Parkinson’s and Alzheimer’s disease epidemic.
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David Brownstein MD
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Because of poor
absorption of water-soluble forms of B1, vitamin B1 in fat-soluble
form (Benfotiamine) is the preferred form in dietary supplements but
is generally not provided in B-complex or multivitamins. [Clinical
Therapeutics Oct 2016; International Journal Clinical Pharmacology
Therapeutics 1998] Fat- soluble benfotiamine is about almost 6 times
more biologically available than water-soluble thiamin hydrochloride,
the common form used in dietary supplements. [Journal Clinical
Pharmacology 2014]
Furthermore, gut
bacteria has now been shown to regulate movement disorders like
Parkinson’s disease in laboratory mice and represents a risk
factor. [Cell2016; World Journal Gastroenterology 2015] Ditto for
Alzheimer’s disease. [Science China/Life Science 2016]
Multivitamins need to incorporate ingredients that promote healthy
gut bacteria.
As for the doctor in
Italy who has reported on the successful use of thiamin/vitamin B1
for Parkinson’s disease symptoms we can only say bravo and wonder
when the Nobel Prize committee will take notice.
A newly available
multivitamin that incorporates amply dosed B-vitamins in forms that
maximize absorption and other ingredients that beneficially modify
gut bacteria has been formulated by this author. [MolecularMulti]
Medications for Cataplexy
Medications
for improving cataplexy
Cataplexy occurs
in about half of all people with narcolepsy. Among those who have it,
some may have only one or two episodes in their whole lives, while
others can have 10 or 20 episodes each day. Thus, the decision
whether to treat cataplexy with a medication depends on how much
impact the cataplexy has on an individual’s life and the expected
risks of the medications.
Medications
can produce a 90% reduction in cataplexy, and in some patients
eliminate it entirely. As cataplexy can have a major impact on social
interactions, and sometimes safety, treatment can substantially
improve quality of life.
Most
of the time, hypnagogic
hallucinations and sleep
paralysisdo
not require treatment with medications. However, these symptoms often
improve with the medications that reduce cataplexy.
-
Antidepressants. Antidepressant medications have been used for decades to reduce cataplexy. As there have been no large clinical studies examining the effects of these medications on cataplexy, guidelines on their use are mainly based on the clinical experience of narcolepsy specialists.13
-
The rationale for using antidepressants is that these medications strongly suppress rapid-eye-movement (REM) sleep, and cataplexy is probably the occurrence of REM sleep paralysis during wakefulness. Antidepressants mainly suppress cataplexy by increasing levels of norepinephrine and serotonin in the brain.
-
Venlafaxine (Effexor) is one of the most commonly used medications for reducing cataplexy because the dosing is convenient, side effects are uncommon, and it is often very effective. Venlafaxine increases brain levels of both norepinephrine and serotonin.
-
Fluoxetine (Prozac) is also generally well tolerated and long lasting. It increases brain levels of serotonin and may be slightly less effective than venlafaxine in reducing cataplexy.
-
Clomipramine (Anafranil) and protriptyline (Vivactil) are very potent in suppressing cataplexy, but they can produce dry mouth, constipation, and other bothersome side effects. Thus, one or the other is often used as an add-on medication for additional cataplexy control. For example, some patients may take venlafaxine as their daily medication for reducing cataplexy, and also take a low dose of clomipramine just before a party for additional protection. People with heart problems, seizures, or glaucoma should not take clomipramine or protriptyline.
-
Sudden discontinuation of any of these antidepressant medications can produce rebound cataplexy: severe cataplexy that can last several hours. If someone wishes to stop one of these medications, the dose should be gradually reduce
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