Riboflavin / Parkinson's / diet

Quoted message said:

Subject: Riboflavin / Parkinson's / diet From: [email hidden] (doe) Date: 9/23/2003 2:27 AM
Mountain Daylight Time Message-id: <[email hidden]>

Braz J Med Biol Res. 2003 Oct;36(10):1409-17. Epub 2003 Sep 16. Links

High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor
functions in Parkinson's disease patients.

Coimbra CG, Junqueira VB.

Setor de Neurologia, Hospital do Servidor P blico Municipal de S o Paulo, S o Paulo, SP, Brasil.

Abnormal riboflavin status in the absence of a dietary deficiency was detected in 31 consecutive
outpatients with Parkinson's disease (PD), while the classical determinants of homocysteine levels
(B6, folic acid, and B12) were usually within normal limits. In contrast, only 3 of 10 consecutive
outpatients with dementia without previous stroke had abnormal riboflavin status. The data for 12
patients who did not complete 6 months of therapy or did not comply with the proposed treatment
paradigm were excluded from analysis. Nineteen PD patients (8 males and 11 females, mean age SD =
66.2 8.6 years; 3, 3, 2, 5, and 6 patients in Hoehn and Yahr stages I to V) received riboflavin
orally (30 mg every 8 h) plus their usual symptomatic medications and all red meat was eliminated
from their diet. After 1 month the riboflavin status of the patients was normalized from 106.4 34.9
to 179.2 23 ng/ml (N = 9). Motor capacity was measured by a modification of the scoring system of
Hoehn and Yahr, which reports motor capacity as percent. All 19 patients who completed 6 months of
treatment showed improved motor capacity during the first three months and most reached a plateau
while 5/19 continued to improve in the 3- to 6-month interval. Their average motor capacity
increased from 44 to 71% after 6 months, increasing significantly every month compared with their
own pretreatment status (P < 0.001, Wilcoxon signed rank test). Discontinuation of riboflavin for
several days did not impair motor capacity and yellowish urine was the only side effect observed.
The data show that the proposed treatment improves the clinical condition of PD patients.
Riboflavin-sensitive mechanisms involved in PD may include glutathione depletion, cumulative
mitochondrial DNA mutations, disturbed mitochondrial protein complexes, and abnormal iron
metabolism. More studies are required to identify the mechanisms involved.

PMID: 14502375 [PubMed - in process]

--------------------------------------------------------------------------

In case anyone didn't know .. riboflavin is an .. iron .. binder ..

Who loves ya. Tom Jesus Was A Vegetarian! jesuswasavegetarian.7h.comjesuswasavegetarian.7h.comOpen ↗ Man Is A Herbivore!
pages.ivillage.commanisaherbivoreOpen ↗ DEAD PEOPLE WALKING
pages.ivillage.comdeadpeoplewalkingOpen ↗

[email hidden] (doe) wrote in message

Quoted message said:

In case anyone didn't know .. riboflavin is an .. iron .. binder ..

Doe, Thank you for the abstract. Although I didn't check your above claim, I did read the entire
study (available free on Medline) and nowhere in the study is there any suggestion that iron is the
cause for low riboflavin in PD patients. Participants PD patients were put on meatless diet for the
following reason (quotes): (From the Methods section) "Because the PD patients had a higher
consumption of red meat (beef

relatives or neighbors of similar age recruited for controlling the dietary habits), all PD patients
were required to eliminate all red meat from their diets."

(And then in the discussion section) "The importance of the elimination of dietary red meat for the
results reported here is not known. The content of vitamin B2 in meat in general is considerable
(about 0.2 mg/100 g), and diverse cooking procedures cause only minor (7-18%) loss of this
micronutrient (25). The daily requirement for individuals above the age of 14 years is £1.3 mg/day.
Therefore, if the PD patients had a normal absorptive capacity for vitamin B2, their large ingestion
of red meat (up to 700
g/day), associated with milk, rice and beans, fruits and vegetables, should have provided a normal
riboflavin status. In contrast, 31 consecutive PD patients had laboratory evidence for riboflavin
deficiency (Table 2) suggesting that patients with sporadic PD belong to the subset of the general
population (10-15%) (3) that may express a flavokinase with low affinity for vitamin B2, leading
to a decreased absorption."

Moreover, the authors propose a different explanation altogether in the introduction section::
"During absorption of riboflavin, flavokinase phosphorylates the vitamin to yield flavin
mononucleotide (FMN) that, according to the cellular requirements, is transformed into
flavin-adenine dinucleotide (FAD) by FAD synthase (1,2). Progressive deficiency of riboflavin is
associated with co-factor loss in a controlled manner, apparently ensuring that essential catalytic
activity such as that related to aerobic metabolism is preserved (3,4). Low riboflavin status may
also result from defective absorption. In spite of an adequate dietary intake of riboflavin (FAD,
vitamin B2), 10-15% of the inhabitants of London and of Florence present low activities of two
riboflavin-dependent enzymes - erythrocyte glutathione reductase (EGR) and
pyridoxin(pyridoxamine)-phosphate oxidase (5). The activity of both enzymes was corrected by adding
their respective co-factors (FAD or FMN) to a test tube assay or by administering high doses of
riboflavin (24-30 mg per day for 5-8 weeks) to the affected individuals (6). The dependency of both
FMN and FAD levels on riboflavin absorption (i.e., on flavokinase activity), and the normalization
of the activities of both FMN- and FAD-dependent enzymes only at a high riboflavin intake, taken
together, are consistent with the expression of flavokinase isoforms with low affinity for the
substrate - riboflavin (5). Anderson et al. (5) suggested that the relatively large percent of
persons with altered riboflavin absorption (10-15%) may reflect the situation in the world
population rather than being a feature of a particular ethnic group. Low EGR activity may explain
glutathione depletion with impaired antioxidant defense, the earliest neurochemical abnormality in
Parkinson's disease (PD), already observed in the substantia nigra before the disorder becomes
clinically evident (7). Moreover, the reduced bioavailability of FMN and/or FAD may also explain the
impaired oxidative metabolism of PD patients (8-10)."

Ericam2 said:

for Parkinson's you need calcium.

DUH??? Parkinson's was brought about by SOMETHING you were doing or USING that HIT your BRAIN
STEM! Many items do same..but recently, from researching over 65 million NEW cases since
1991...have been linked to ASPARTAME..the KILLER sugar substitute put into Soda Pop...and NOW
appearing elsewhere such as in DANNON Yogurt products. ( fruit blends) One lousy teaspoon of ANY
medium using this killer will KILL and ANIMAL ( cats and dogs) within minutes..SPASMS leading to
an horrible DEATH. "Fibro-Mialgia" is another "gift" from same! (YET MONSANTO LIVES ON!!) I
cannot for the life of me see WHY the STAT's have NOT been collected by a bunch of SMART LAWYERS
and an horrendous CLASS ACTION SUIT FILED??! Better yet the GOV'T coming DOWN on them for
releasing a MURDEROUS TERROR into the public Arena?? HAH..FAT CHANCE??

I have "SLAMMED" DANNON products on the WWW. as awell as in Newspapers and E-mails. If enough
VICTIMS start to raise a ruckus...perhaps MONSANT MAY ( not likely) STOP the MFGR of same??? It
is one of the MANY HORRORS of the NEW AGE??

BTW..CALCIUM is the KEY Mineral that keeps all of us alive...coupled with equal parts of
Magnesium and Phosphorus...The entire cartilagenous system live better. (Not to mention the
MOST important chemistry in the DNA of the body PLUS catalization of GLUCOSE, the STUFF of ALL
Cartilagenous parts including Muscles. A "LACK" of Calcium in needed amounts also DRIVES ALL
CANCERS!! Get the PIX??? B-0b1