Anonymous
Posted: Wed Dec 16, 2009 2:34 pm Post subject: Mild shaking of right hand third finger
--------------------------------------------------------------------------------
Why Mild shaking of right hand third finger and still no difficulty doing weight lifting,Yoga and Muay Thai exercise daily?
Is it Parkinson's Progression?
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Dr. Fernandez
Joined: 20 Jan 2007
Posts: 90
Posted: Thu Dec 17, 2009 11:09 pm Post subject:
--------------------------------------------------------------------------------
The general belief is that PD is a universally progressive illness....so, over time, patients typically get worse.
Having said that, the speed of progression varies widely between patients. in fact, just yesterday I saw a patient, who I still believe has PD, but has had minimal progression in the last 7 years. Now this is not typical and probably exceptional, but it does exists.
Your PD seems to be very slow and benign. In many ways, you should count your blessings! Happy holidays!
Yours,
_________________
Hubert H. Fernandez
Monday, December 21, 2009
can sinenetsow the progression of pd?
Posted: Sat Dec 19, 2009 5:59 pm Post subject: Post of the Week: Can sinemet slow disease progression?
Does levodopa slow the progression of Parkinson disease?
Levodopa has changed the lives of millions of Parkinson’s disease patients. Patients now live longer, and have more rewarding lives with much less and even slower progressing disability in some cases (when compared to the pre-levodopa era). The positive effects of levodopa can be felt for many years, however, levodopa is not a cure. Levodopa does not relieve all symptoms of Parkinson’s disease. Additionally, not all patients respond to levodopa with consistent results, although most respond very well. Levodopa may also have side effects—and some patients in the Parkinson’s disease population seem to be more susceptible to side effects than others---so therapy needs to be tailored to the individual.
As to whether levodopa slows disease progression in Parkinson’s disease, the jury is still out. The data are conflicting. We have a large clinical trial that showed that those on the highest dose of levodopa had the best motor function, and the slowest decline. The imaging arm of that study however revealed that the basal ganglia (the part of the brain that is sick in Parkinson’s disease) had significantly less amounts of surviving dopaminergic brain cells. We have been unable to definitively explain this discrepancy between the clinical finding and the imaging results. Most authorities believe however that levodopa does not affect disease progression, but this remains a controversial topic. More research may shed light on this controversy (Clarke 2004; Olanow 2004; Castro, Valldeoriola et al. 2005; Fahn 2005; Fahn 2006; Fahn 2006; Suchowersky, Gronseth et al. 2006; Chan, Nutt et al. 2007; Schapira 2007; LeWitt and Taylor 2008).
_________________
Hubert H. Fernandez
Does levodopa slow the progression of Parkinson disease?
Levodopa has changed the lives of millions of Parkinson’s disease patients. Patients now live longer, and have more rewarding lives with much less and even slower progressing disability in some cases (when compared to the pre-levodopa era). The positive effects of levodopa can be felt for many years, however, levodopa is not a cure. Levodopa does not relieve all symptoms of Parkinson’s disease. Additionally, not all patients respond to levodopa with consistent results, although most respond very well. Levodopa may also have side effects—and some patients in the Parkinson’s disease population seem to be more susceptible to side effects than others---so therapy needs to be tailored to the individual.
As to whether levodopa slows disease progression in Parkinson’s disease, the jury is still out. The data are conflicting. We have a large clinical trial that showed that those on the highest dose of levodopa had the best motor function, and the slowest decline. The imaging arm of that study however revealed that the basal ganglia (the part of the brain that is sick in Parkinson’s disease) had significantly less amounts of surviving dopaminergic brain cells. We have been unable to definitively explain this discrepancy between the clinical finding and the imaging results. Most authorities believe however that levodopa does not affect disease progression, but this remains a controversial topic. More research may shed light on this controversy (Clarke 2004; Olanow 2004; Castro, Valldeoriola et al. 2005; Fahn 2005; Fahn 2006; Fahn 2006; Suchowersky, Gronseth et al. 2006; Chan, Nutt et al. 2007; Schapira 2007; LeWitt and Taylor 2008).
_________________
Hubert H. Fernandez
sinemet and prevard
Anonymous
Posted: Sat Dec 05, 2009 9:44 am Post subject: sinemet and prevacid
--------------------------------------------------------------------------------
Dear Kathrynne,
Will taking Sinemet and Prevacid interfere with the absorption of the Sinemet?
If they are both supposed to be taken on an empty stomach, how does one do this?
Back to top
Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Sat Dec 05, 2009 11:46 am Post subject:
--------------------------------------------------------------------------------
.
Dear Friend,
If you are taking the prevacid once daily, try to schedule it in between Sinemet doses. For example, if you take Sinemet at 7:00 am, 11:00 am, 3:00 pm, and 7:00 pm, and have your meals at 8:00 am, 12:00 noon, and 5:00 pm, ask your prescribing doctor if you can take the Prevacid at 7:30 am. That will give the Sinemet 30 minutes to clear the stomach; then the Prevacid will have 30 minutes to clear; then at 8:00 you should be able to have your breakfast without concern.
Let me know if you have further questions, or if this did not help.
_________________
Best regards,
Kathrynne Holden, MS
Posted: Sat Dec 05, 2009 9:44 am Post subject: sinemet and prevacid
--------------------------------------------------------------------------------
Dear Kathrynne,
Will taking Sinemet and Prevacid interfere with the absorption of the Sinemet?
If they are both supposed to be taken on an empty stomach, how does one do this?
Back to top
Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Sat Dec 05, 2009 11:46 am Post subject:
--------------------------------------------------------------------------------
.
Dear Friend,
If you are taking the prevacid once daily, try to schedule it in between Sinemet doses. For example, if you take Sinemet at 7:00 am, 11:00 am, 3:00 pm, and 7:00 pm, and have your meals at 8:00 am, 12:00 noon, and 5:00 pm, ask your prescribing doctor if you can take the Prevacid at 7:30 am. That will give the Sinemet 30 minutes to clear the stomach; then the Prevacid will have 30 minutes to clear; then at 8:00 you should be able to have your breakfast without concern.
Let me know if you have further questions, or if this did not help.
_________________
Best regards,
Kathrynne Holden, MS
Monday, December 7, 2009
PD,B6, B12 and Folate What is the connection?
S
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Thu Dec 03, 2009 5:05 pm Post subject: Parkinson's, B6, B12, and Folate - What's the Connection?
--------------------------------------------------------------------------------
.
Parkinson's, B6, B12, and Folate - What's the Connection?
Kathrynne Holden, MS, RD
Copyright 2008
Ms. Holden is a registered dietitian specializing in Parkinson's
disease. She has published research, books, articles, and manuals on
nutrition and PD, including "Eat well, stay well with Parkinson's
disease."
In the past decade, there has been increasing interest among
researchers about the effects of three B vitamins - B6, B12, and folate.
We now know that deficiencies occur with greater frequency than ever
suspected previously, particularly in older adults. We also now know
that deficiencies, if not corrected, can result in irreversible damage
in some people. Some health professionals are beginning to suspect that
these three vitamins may be significant factors in Parkinson's disease.
What are B6, B12, and folate, and what do they do?
These are essential nutrients, meaning that they are vital to life.
These three vitamins work both independently and together in many of the
body's systems.
Vitamin B6 assists in making hormones, new proteins, and
neurotransmitters ("messengers" between nerve cells) for the body's use.
It also helps release stored sugar when we need it for fuel. It works
together with B12 and folate to remove homocysteine from the blood.
Homocysteine is a substance increasingly associated with a number of
diseases; more about this later.
Vitamin B12 plays a role in the synthesis of DNA, needed for formation
of new red blood cells. It takes part in the manufacture of the myelin
sheath - the protective coating that surrounds nerve cells. With B6 and
folate it removes homocysteine from the blood.
Folate, also called folacin or folic acid, is a partner with B12 in DNA
synthesis and in removal of homocysteine, and is required in many other
vital processes. Without folate, B12 would be unable to complete many of
its functions, and vice versa. Folate is the form found in foods, folic
acid is the form in dietary supplements.
How much do we need of these vitamins?
Nutrient needs are broken down by gender, age group, pregnancy, and
lactation. New guidelines have also established a Tolerable Upper Intake
Level. So, for example, while the RDA for vitamin B6 for males and
females age 19-30 years is 1.3 mg/day, the Tolerable Upper Intake Level
for both is 100 mg/day, making it easier to provide recommended amounts.
RDA* Tolerable Upper Intake Level ** +
Vitamin B6*** + 1.7 mg/day 100 mg/day (age 19 and older)
Vitamin B12 + 2.4 mcg/day Not Determined
Folate + 400 mcg/day 1000 mcg/day
* Recommended Dietary Allowance
** The Tolerable Upper Intake Level is the maximum level of daily
nutrient intake that is likely to pose no risk of adverse effects, and
represents the total intake from food, water, and supplements.
*** Adults age 51 and older
+ not applicable if pregnant or lactating
Why do deficiencies occur, and what are signs of deficiencies?
Vitamin B6. Mild deficiencies of B6 are fairly common in the U.S.,
mostly because of dietary deficiencies, but sometimes due to use of
certain medications which interfere with B6, including hydralazine,
isoniazid, MAO inhibitors, penicillamine, and theophylline. (Conversely,
large amounts of B6 can interfere with the absorption of levodopa, an
important medication for Parkinson's disease. Current use of the
combinations of carbidopa-levodopa or benserazide-levodopa offset this
interaction for the most part; but use of supplements containing more
than 15 mg of B6 can overwhelm the protective effects of the carbidopa
and benserazide.)
Good food sources of B6 include chicken, fish, eggs, nuts and seeds,
dried beans and peas, soybeans, wheat germ, bananas, avocados, and
brewer's yeast. Also, some foods, including a number of breakfast
cereals, are fortified with B6.
Signs of B6 deficiency include irritability, depression, and confusion;
sore tongue, sores or ulcers of the mouth, and ulcers of the skin at the
corners of the mouth.
Vitamin B12. The human body stores this vitamin so well that it can
take a long time to deplete, sometimes several years. Nevertheless,
there are several reasons why people sometimes do experience deficiency.
Animal foods are the only source of B12, therefore people who eat few or
no animal products (meat, fish, poultry, eggs, milk) are at risk unless
they use vitamin supplements.
Another problem is that B12 in foods cannot be absorbed by the body
until it is freed from the proteins in the food; the stomach produces an
acid that removes this protein. However, with age, we produce less and
less of this stomach acid. Many older adults don't produce enough acid
to allow them to absorb B12. Further, people who have acid reflux often
use medications that reduce stomach acid, which unfortunately also
decreases absorption of B12. Vitamin B12 is one of the few nutrients
that is better absorbed in pill form than from dietary sources.
Signs of B12 deficiency include numbness or a tingling "pins and
needles" sensation, or a burning feeling; a red, sore, or burning
tongue; loss of appetite; gait abnormalities, personality changes, an
Alzheimer-like dementia, psychosis, depression, and agitation,
particularly in older adults. Other signs are megaloblastic anemia, and
elevated serum homocysteine, in people of all ages. Researchers believe
that as many as 42% of people aged 65 and older may have some degree of
B12 deficiency. Many people with PD are age 65 or older, and should be
considered at risk and tested for B12 deficiency.
Folate. Folate is available in many foods: lima beans, brewer's yeast,
orange juice, dried beans, green peas, asparagus, beets, Brussels
sprouts, broccoli, corn, spinach and other dark green leafy vegetables,
soybeans, nuts and seeds. Further, the U.S. government requires that
food manufacturers fortify processed grain products with folic acid.
Yet, deficiencies of folate are not uncommon. This could be in part
because folate is another of the few nutrients in which the synthetic
form is absorbed much better (about 40 percent better) than the natural
form.
Because of the possibility of deficiency, women, including women with
PD, who are pregnant or wish to become pregnant are advised to take
supplements of folic acid; deficiencies can result in neural tube
defects in the unborn child.
Deficiencies of folate are also being increasingly studied for a
possible role in other diseases:
. A low intake of folic acid is associated with risk for colon cancer.
Chronic constipation, experienced by many people with PD, also increases
risk for colon cancer; it is prudent for those with PD to control
constipation and to be sure the diet is adequate in folate.
. A low level of folic acid in the blood is associated with higher
levels of serum homocysteine, a substance in the blood that may
contribute to heart disease, stroke, and dementias.
. Animal studies point to a link between low levels of folic acid and
Alzheimer's disease; and people with Alzheimer's are often found to have
low levels of folic acid. Some people with PD develop an Alzheimer-type
dementia. Again, prudence dictates consumption of adequate folate.
. Another study using mice found that folic acid deficiency led to
increased levels of homocysteine and symptoms of Parkinson's disease.
Researchers speculate that homocysteine may damage DNA in the substantia
nigra, the area of the brain affected in Parkinson's disease.
. There are reports of improvement in restless leg syndrome (RLS) with
use of folate supplements; this has not as yet been studied thoroughly,
so it is too early to say whether there is a definite link. However,
people with PD often complain of RLS, and physicians should rule out the
possibility of folic acid deficiency.
Signs of folic acid deficiency include appetite loss, weight loss,
burning tongue, fatigue, weakness, shortness of breach, memory loss,
irritability, megaloblastic anemia, and increased levels of serum
homocysteine.
Should people with PD be concerned about these vitamins?
Although there are concerns, as mentioned above, that deserve further
study, it's too early to say definitely that these three vitamins are of
significance to people with PD. However, if you are over age 50 these
vitamins are of importance independently of PD. Furthermore, studies
have demonstrated that some people who use levodopa, considered the best
medication for PD, develop elevated levels of serum homocysteine, due to
the way in which the medication is metabolized. It is certainly a good
idea to ask your doctor to test levels of serum homocysteine annually,
and to check for signs of B vitamin deficiencies.
Should you take supplements?
There is growing agreement that older adults are at risk for nutrient
deficiency, whether PD is present or not, and that supplements can help.
. One study of older adults found that a multivitamin containing 100% of
the Daily Value improved low levels of several nutrients, including
vitamins B6, B12, and folate.
. A recent study in the United Kingdom suggests that folic acid intake
should be about three times that of the current recommendation for
elderly people.
. Other studies indicate that up to 10% of older adults with low-normal
levels of B12 are actually deficient and could benefit from supplements.
Because folate supplements can mask a B12 deficiency, it becomes extra
important to get enough B12 daily.
. The American Heart Association recommends a folate-rich diet to lower
homocysteine levels, and supplements of 2 mg B6, 400 mcg folic acid, and
6 mcg of B12 if dietary means are not sufficient to lower the
homocysteine.
For people with PD who use a medication that contains levodopa (such as
Sinemet, Madopar, Syndopa, Larodopa, etc.), you should be aware that
large amounts of vitamin B6 (more than 15 mg) can affect the absorption
of levodopa, by converting levodopa to dopamine in the stomach and
bloodstream. Dopamine cannot cross the blood-brain barrier, so it is
effectively blocked from its purpose.
Sinemet and Madopar contain either carbidopa or benserazide, which
"protect" the levodopa from B6; so ordinary supplements of B6 should not
be a problem for most people. However, very large amounts of B6, greater
than 15 mg (and in sensitive persons, possibly as low as 10 mg), could
overwhelm the protective effects of the carbidopa or benserazide. Such a
supplement should be taken at bedtime with a light snack, or with meals
at least two hours separately from levodopa.
In summary, older adults are acknowledged to be at increased risk for B
vitamin deficiencies. People with PD who are age 50 and over, therefore,
are at increased risk also. Whether younger people with PD should be
concerned about such deficiencies remains to be seen. A prudent and
rational approach for all those with PD is to:
. Discuss the possibility with their physicians, and to request tests
for B vitamin deficiencies
. Be aware of the signs of B vitamin deficiency
. Take a multivitamin/mineral supplement daily. Unless anemic, choose a
supplement that does not contain iron
. Take a B complex supplement if deficiencies occur; and take the
supplement separately from levodopa by at least two hours, preferably
with meals or a snack.
Knowledge is strength; awareness of dietary needs can prevent illness,
malnutrition, suffering, and hospitalization. If you have questions
about B vitamins or other nutrition or dietary needs, please visit the
National Parkinson Foundation website:
The above article may not be reproduced in any form except with
permission from the author.
References
Giovannucci, E. et al. Alcohol, low-methionine-low-folate diets, and
risk of colon cancer in men. Journal of the National Cancer Institute.
1995; volume 87: pages 265-273.
Kruman II, Kumaravel TS, Lohani A, Pedersen WA, Cutler RG, Kruman Y,
Haughey N, Lee J, Evans M, Mattson MP. Folic Acid deficiency and
homocysteine impair DNA repair in hippocampal neurons and sensitize them
to amyloid toxicity in experimental models of Alzheimer's disease. J
Neurosci 2002 Mar 1;22(5):1752-62.
Lobo A, Naso A, Arheart K, Kruger WD, Abou-Ghazala T, Alsous F, Nahlawi
M, Gupta A, Moustapha A, van Lente F, Jacobsen DW, Robinson K. Reduction
of homocysteine levels in coronary artery disease by low-dose folic acid
combined with vitamins B6 and B12. Am J Cardiol 1999 Mar 15;83(6):821-5.
Malinow, M.R. et al. Homocyst(e)ine, diet, and cardiovascular diseases:
a statement for healthcare professionals from the nutrition committee,
American Heart Association. Circulation. 1999; volume 99: pages 178-182.
Muller T, Werne B, Fowler B, Kuhn W. Nigral endothelial dysfunction,
homocysteine, and Parkinson's disease. Lancet. 1999 Jul
10;354(9173):126-7.
Muller T, Woitalla D, Hauptmann B, Fowler B, Kuhn W. Decrease of
methionine and S-adenosylmethionine and increase of homocysteine in
treated patients with Parkinson's disease.
Neurosci Lett. 2001 Jul 27;308(1):54-6.
Naurath HJ, Joosten E, Riezler R, Stabler SP, Allen RH, Lindenbaum J.
Effects of vitamin B12, folate, and vitamin B6 supplements in elderly
people with normal serum vitamin concentrations. Lancet 1995; 346:85-89.
O'Keeffe ST. Restless legs syndrome. A review. Arch Intern Med.
1996;156:243-248.
_________________
Best regards,
Kathrynne Holden, MS
--
For a Parkinson Tip of the Day visit:
http://www.nutritionucanlivewith.com/
Back to top
Anonymous
Posted: Thu Dec 03, 2009 7:49 pm Post subject:
--------------------------------------------------------------------------------
Nuts and seeds cure all ills ... ;o)
Nice detailed recap of the B Vitamins
Rich
Back to top
Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Fri Dec 04, 2009 8:51 am Post subject:
--------------------------------------------------------------------------------
.
Tut, Rich, you did not read the part about B12: "Animal foods are the only source of B12.....meat, fish, poultry, eggs, milk..."
See? dietitians aren't just about nuts and seeds.
_________________
Best regards,
Kathrynne Holden, MS
--
For a Parkinson Tip of the Day visit:
http://www.nutritionucanlivewith.com/
Back to top
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Thu Dec 03, 2009 5:05 pm Post subject: Parkinson's, B6, B12, and Folate - What's the Connection?
--------------------------------------------------------------------------------
.
Parkinson's, B6, B12, and Folate - What's the Connection?
Kathrynne Holden, MS, RD
Copyright 2008
Ms. Holden is a registered dietitian specializing in Parkinson's
disease. She has published research, books, articles, and manuals on
nutrition and PD, including "Eat well, stay well with Parkinson's
disease."
In the past decade, there has been increasing interest among
researchers about the effects of three B vitamins - B6, B12, and folate.
We now know that deficiencies occur with greater frequency than ever
suspected previously, particularly in older adults. We also now know
that deficiencies, if not corrected, can result in irreversible damage
in some people. Some health professionals are beginning to suspect that
these three vitamins may be significant factors in Parkinson's disease.
What are B6, B12, and folate, and what do they do?
These are essential nutrients, meaning that they are vital to life.
These three vitamins work both independently and together in many of the
body's systems.
Vitamin B6 assists in making hormones, new proteins, and
neurotransmitters ("messengers" between nerve cells) for the body's use.
It also helps release stored sugar when we need it for fuel. It works
together with B12 and folate to remove homocysteine from the blood.
Homocysteine is a substance increasingly associated with a number of
diseases; more about this later.
Vitamin B12 plays a role in the synthesis of DNA, needed for formation
of new red blood cells. It takes part in the manufacture of the myelin
sheath - the protective coating that surrounds nerve cells. With B6 and
folate it removes homocysteine from the blood.
Folate, also called folacin or folic acid, is a partner with B12 in DNA
synthesis and in removal of homocysteine, and is required in many other
vital processes. Without folate, B12 would be unable to complete many of
its functions, and vice versa. Folate is the form found in foods, folic
acid is the form in dietary supplements.
How much do we need of these vitamins?
Nutrient needs are broken down by gender, age group, pregnancy, and
lactation. New guidelines have also established a Tolerable Upper Intake
Level. So, for example, while the RDA for vitamin B6 for males and
females age 19-30 years is 1.3 mg/day, the Tolerable Upper Intake Level
for both is 100 mg/day, making it easier to provide recommended amounts.
RDA* Tolerable Upper Intake Level ** +
Vitamin B6*** + 1.7 mg/day 100 mg/day (age 19 and older)
Vitamin B12 + 2.4 mcg/day Not Determined
Folate + 400 mcg/day 1000 mcg/day
* Recommended Dietary Allowance
** The Tolerable Upper Intake Level is the maximum level of daily
nutrient intake that is likely to pose no risk of adverse effects, and
represents the total intake from food, water, and supplements.
*** Adults age 51 and older
+ not applicable if pregnant or lactating
Why do deficiencies occur, and what are signs of deficiencies?
Vitamin B6. Mild deficiencies of B6 are fairly common in the U.S.,
mostly because of dietary deficiencies, but sometimes due to use of
certain medications which interfere with B6, including hydralazine,
isoniazid, MAO inhibitors, penicillamine, and theophylline. (Conversely,
large amounts of B6 can interfere with the absorption of levodopa, an
important medication for Parkinson's disease. Current use of the
combinations of carbidopa-levodopa or benserazide-levodopa offset this
interaction for the most part; but use of supplements containing more
than 15 mg of B6 can overwhelm the protective effects of the carbidopa
and benserazide.)
Good food sources of B6 include chicken, fish, eggs, nuts and seeds,
dried beans and peas, soybeans, wheat germ, bananas, avocados, and
brewer's yeast. Also, some foods, including a number of breakfast
cereals, are fortified with B6.
Signs of B6 deficiency include irritability, depression, and confusion;
sore tongue, sores or ulcers of the mouth, and ulcers of the skin at the
corners of the mouth.
Vitamin B12. The human body stores this vitamin so well that it can
take a long time to deplete, sometimes several years. Nevertheless,
there are several reasons why people sometimes do experience deficiency.
Animal foods are the only source of B12, therefore people who eat few or
no animal products (meat, fish, poultry, eggs, milk) are at risk unless
they use vitamin supplements.
Another problem is that B12 in foods cannot be absorbed by the body
until it is freed from the proteins in the food; the stomach produces an
acid that removes this protein. However, with age, we produce less and
less of this stomach acid. Many older adults don't produce enough acid
to allow them to absorb B12. Further, people who have acid reflux often
use medications that reduce stomach acid, which unfortunately also
decreases absorption of B12. Vitamin B12 is one of the few nutrients
that is better absorbed in pill form than from dietary sources.
Signs of B12 deficiency include numbness or a tingling "pins and
needles" sensation, or a burning feeling; a red, sore, or burning
tongue; loss of appetite; gait abnormalities, personality changes, an
Alzheimer-like dementia, psychosis, depression, and agitation,
particularly in older adults. Other signs are megaloblastic anemia, and
elevated serum homocysteine, in people of all ages. Researchers believe
that as many as 42% of people aged 65 and older may have some degree of
B12 deficiency. Many people with PD are age 65 or older, and should be
considered at risk and tested for B12 deficiency.
Folate. Folate is available in many foods: lima beans, brewer's yeast,
orange juice, dried beans, green peas, asparagus, beets, Brussels
sprouts, broccoli, corn, spinach and other dark green leafy vegetables,
soybeans, nuts and seeds. Further, the U.S. government requires that
food manufacturers fortify processed grain products with folic acid.
Yet, deficiencies of folate are not uncommon. This could be in part
because folate is another of the few nutrients in which the synthetic
form is absorbed much better (about 40 percent better) than the natural
form.
Because of the possibility of deficiency, women, including women with
PD, who are pregnant or wish to become pregnant are advised to take
supplements of folic acid; deficiencies can result in neural tube
defects in the unborn child.
Deficiencies of folate are also being increasingly studied for a
possible role in other diseases:
. A low intake of folic acid is associated with risk for colon cancer.
Chronic constipation, experienced by many people with PD, also increases
risk for colon cancer; it is prudent for those with PD to control
constipation and to be sure the diet is adequate in folate.
. A low level of folic acid in the blood is associated with higher
levels of serum homocysteine, a substance in the blood that may
contribute to heart disease, stroke, and dementias.
. Animal studies point to a link between low levels of folic acid and
Alzheimer's disease; and people with Alzheimer's are often found to have
low levels of folic acid. Some people with PD develop an Alzheimer-type
dementia. Again, prudence dictates consumption of adequate folate.
. Another study using mice found that folic acid deficiency led to
increased levels of homocysteine and symptoms of Parkinson's disease.
Researchers speculate that homocysteine may damage DNA in the substantia
nigra, the area of the brain affected in Parkinson's disease.
. There are reports of improvement in restless leg syndrome (RLS) with
use of folate supplements; this has not as yet been studied thoroughly,
so it is too early to say whether there is a definite link. However,
people with PD often complain of RLS, and physicians should rule out the
possibility of folic acid deficiency.
Signs of folic acid deficiency include appetite loss, weight loss,
burning tongue, fatigue, weakness, shortness of breach, memory loss,
irritability, megaloblastic anemia, and increased levels of serum
homocysteine.
Should people with PD be concerned about these vitamins?
Although there are concerns, as mentioned above, that deserve further
study, it's too early to say definitely that these three vitamins are of
significance to people with PD. However, if you are over age 50 these
vitamins are of importance independently of PD. Furthermore, studies
have demonstrated that some people who use levodopa, considered the best
medication for PD, develop elevated levels of serum homocysteine, due to
the way in which the medication is metabolized. It is certainly a good
idea to ask your doctor to test levels of serum homocysteine annually,
and to check for signs of B vitamin deficiencies.
Should you take supplements?
There is growing agreement that older adults are at risk for nutrient
deficiency, whether PD is present or not, and that supplements can help.
. One study of older adults found that a multivitamin containing 100% of
the Daily Value improved low levels of several nutrients, including
vitamins B6, B12, and folate.
. A recent study in the United Kingdom suggests that folic acid intake
should be about three times that of the current recommendation for
elderly people.
. Other studies indicate that up to 10% of older adults with low-normal
levels of B12 are actually deficient and could benefit from supplements.
Because folate supplements can mask a B12 deficiency, it becomes extra
important to get enough B12 daily.
. The American Heart Association recommends a folate-rich diet to lower
homocysteine levels, and supplements of 2 mg B6, 400 mcg folic acid, and
6 mcg of B12 if dietary means are not sufficient to lower the
homocysteine.
For people with PD who use a medication that contains levodopa (such as
Sinemet, Madopar, Syndopa, Larodopa, etc.), you should be aware that
large amounts of vitamin B6 (more than 15 mg) can affect the absorption
of levodopa, by converting levodopa to dopamine in the stomach and
bloodstream. Dopamine cannot cross the blood-brain barrier, so it is
effectively blocked from its purpose.
Sinemet and Madopar contain either carbidopa or benserazide, which
"protect" the levodopa from B6; so ordinary supplements of B6 should not
be a problem for most people. However, very large amounts of B6, greater
than 15 mg (and in sensitive persons, possibly as low as 10 mg), could
overwhelm the protective effects of the carbidopa or benserazide. Such a
supplement should be taken at bedtime with a light snack, or with meals
at least two hours separately from levodopa.
In summary, older adults are acknowledged to be at increased risk for B
vitamin deficiencies. People with PD who are age 50 and over, therefore,
are at increased risk also. Whether younger people with PD should be
concerned about such deficiencies remains to be seen. A prudent and
rational approach for all those with PD is to:
. Discuss the possibility with their physicians, and to request tests
for B vitamin deficiencies
. Be aware of the signs of B vitamin deficiency
. Take a multivitamin/mineral supplement daily. Unless anemic, choose a
supplement that does not contain iron
. Take a B complex supplement if deficiencies occur; and take the
supplement separately from levodopa by at least two hours, preferably
with meals or a snack.
Knowledge is strength; awareness of dietary needs can prevent illness,
malnutrition, suffering, and hospitalization. If you have questions
about B vitamins or other nutrition or dietary needs, please visit the
National Parkinson Foundation website:
The above article may not be reproduced in any form except with
permission from the author.
References
Giovannucci, E. et al. Alcohol, low-methionine-low-folate diets, and
risk of colon cancer in men. Journal of the National Cancer Institute.
1995; volume 87: pages 265-273.
Kruman II, Kumaravel TS, Lohani A, Pedersen WA, Cutler RG, Kruman Y,
Haughey N, Lee J, Evans M, Mattson MP. Folic Acid deficiency and
homocysteine impair DNA repair in hippocampal neurons and sensitize them
to amyloid toxicity in experimental models of Alzheimer's disease. J
Neurosci 2002 Mar 1;22(5):1752-62.
Lobo A, Naso A, Arheart K, Kruger WD, Abou-Ghazala T, Alsous F, Nahlawi
M, Gupta A, Moustapha A, van Lente F, Jacobsen DW, Robinson K. Reduction
of homocysteine levels in coronary artery disease by low-dose folic acid
combined with vitamins B6 and B12. Am J Cardiol 1999 Mar 15;83(6):821-5.
Malinow, M.R. et al. Homocyst(e)ine, diet, and cardiovascular diseases:
a statement for healthcare professionals from the nutrition committee,
American Heart Association. Circulation. 1999; volume 99: pages 178-182.
Muller T, Werne B, Fowler B, Kuhn W. Nigral endothelial dysfunction,
homocysteine, and Parkinson's disease. Lancet. 1999 Jul
10;354(9173):126-7.
Muller T, Woitalla D, Hauptmann B, Fowler B, Kuhn W. Decrease of
methionine and S-adenosylmethionine and increase of homocysteine in
treated patients with Parkinson's disease.
Neurosci Lett. 2001 Jul 27;308(1):54-6.
Naurath HJ, Joosten E, Riezler R, Stabler SP, Allen RH, Lindenbaum J.
Effects of vitamin B12, folate, and vitamin B6 supplements in elderly
people with normal serum vitamin concentrations. Lancet 1995; 346:85-89.
O'Keeffe ST. Restless legs syndrome. A review. Arch Intern Med.
1996;156:243-248.
_________________
Best regards,
Kathrynne Holden, MS
--
For a Parkinson Tip of the Day visit:
http://www.nutritionucanlivewith.com/
Back to top
Anonymous
Posted: Thu Dec 03, 2009 7:49 pm Post subject:
--------------------------------------------------------------------------------
Nuts and seeds cure all ills ... ;o)
Nice detailed recap of the B Vitamins
Rich
Back to top
Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Fri Dec 04, 2009 8:51 am Post subject:
--------------------------------------------------------------------------------
.
Tut, Rich, you did not read the part about B12: "Animal foods are the only source of B12.....meat, fish, poultry, eggs, milk..."
See? dietitians aren't just about nuts and seeds.
_________________
Best regards,
Kathrynne Holden, MS
--
For a Parkinson Tip of the Day visit:
http://www.nutritionucanlivewith.com/
Back to top
Forced exercises
MDS 2009: Forced Exercise Provides Benefit Similar to Levodopa in Parkinson's Disease
June 15, 2009 (Paris, France) - Patients with Parkinson's disease (PD) who exercise on a stationary tandem bicycle with a healthy partner during a single 40-minute session experience a 35% improvement in motor function and increased brain activation similar to that found with levodopa treatment, new research shows.
The study, by researchers at the Cleveland Clinic in Ohio, found that maintaining a steady rate of 80 to 90 revolutions per minute (rpm) on the bicycle not only improved function in lower extremities but also in upper extremities.
The improvement was dramatic and similar to that achieved by levodopa therapy, said 1 of the researchers, Jay L. Alberts, PhD, from the Center for Neurological Restoration at the Lerner Research Institute, in Cleveland.
"It looks like there are global effects in terms of the improvement in motor function," he told Medscape Neurology. "It suggests to us that maybe we're changing central motor function or maybe we're actually changing brain function through something very noninvasive."
The study was presented during the Movement Disorder Society's 13th International Congress of Parkinson's Disease and Movement Disorders.
A previous published study by this Cleveland research group found that the same forced exercise intervention administered 3 times a week for 8 weeks provided a similar 35% improvement in motor function.
"Couple these new findings with our longer-term data, and for us it's very encouraging," said Dr. Alberts. "Maybe if we can alter brain function, we can potentially alter the course and potentially slow the progression of this disease."
Tandem Exercise
For the study, researchers selected 11 male and female patients ranging in age from mid 50s to early 70s who had mild to moderate PD but no cardiac concerns. They tested these patients under 3 random conditions: not on medication, on medication (levodopa), and not on medication but completion of the forced-exercise intervention.
When on a stationary bicycle, PD patients normally pedal at a sustained rate of about 40 to 60 rpm. In this intervention, however, the patients sat on the back of a tandem bicycle while a healthy young adult trainer occupied the front seat and regulated the pedaling rate, ensuring that it remained between 80 to 90 rpm for 40 minutes.
Researchers monitored each patient's heart rate and made sure it stayed within 60% to 80% of his or her age-determined target range.
Patients also performed a force-tracking task and a bilateral finger-tapping task to demonstrate their level of control and coordination. Similar grasping tasks are necessary to perform daily activities such as buttoning a shirt or tying shoe laces, said Dr. Alberts.
The researchers found that the forced exercise and the levodopa produced similar significant reductions in Unified Parkinson's Disease Rating Scale (UPDRS III) motor scores, 35% with exercise and 38% with levodopa. Data from functional magnetic resonance imaging (fMRI) showed increased activation in the supplementary motor area (SMA) and primary motor cortex (M1) regions of the brain in response to both interventions.
"In terms of the fMRI data, we found that there was an increase in the level of cortical activation in the 2 motor areas - the SMA and the primary motor cortex - and this increase in activation looks very similar to the increase you see when you administer L-dopa," said Dr. Alberts.
For the force-tracking task and bilateral finger tapping, motor performance was 35% better following forced exercise compared with no exercise.
"Overdriving" Central Nervous System
These findings suggest that the exercise and the drug treatment elicit the same underlying mechanisms that provide similar symptomatic relief from PD symptoms, said Dr. Alberts.
The researchers surmise that the exercise may facilitate central motor control processes in Parkinson's patients. "For lack of a better word, we may be 'overdriving' the central nervous system by providing an increase in the quantity and quality of sensory information provided to the patient," said Dr. Alberts.
He added that this type of intervention could also be carried out on a treadmill, but it may be riskier and less practical than on a tandem bike. "We can't increase someone's walking rate 30% without having them in a harness and even then, I think you'll find that their feet would be dragging."
The next step in this line of research, he said, is to develop a motor-assisted cycle that will allow patients to do this type of exercise at home.
Many Beneficial Effects
Asked for a comment, Kapil D Sethi, MD, professor of neurology and director of the movement disorders program at the Medical College of Georgia, in Augusta, said the research highlights additional benefits of exercise. "Exercise has many beneficial effects both physical and psychological," he told Medscape Neurology. "There is evidence in the animal models and now in humans that exercise may have beneficial effects in PD. The exact mechanism is unclear, and the exact paradigm is unknown."
Mark Hallett, MD, from the National Institute of Neurological Disorders and Stroke, in Bethesda, Maryland, added in a press release that the finding of similarities between exercise and drug treatment "is certainly interesting and may indicate that exercise, in the short term, causes dopa release."
Dr. Alberts has no disclosures. Dr. Sethi is a member of the editorial advisory board for Medscape Neurology. He has disclosed he has served as an advisor or consultant to and received grants for clinical research from Boehringer Ingelheim Pharmaceuticals, Schering-Plough, GlaxoSmithKline, Allergan, Novartis Pharmaceuticals, and Solvay. He owns stock, stock options, or bonds in and has received grants for educational activities from Pfizer and Elan Pharmaceuticals.
Movement Disorder Society's 13th International Congress of Parkinson's Disease and Movement Disorders: Abstract LB-13. Presented June 10, 2009.
June 15, 2009 (Paris, France) - Patients with Parkinson's disease (PD) who exercise on a stationary tandem bicycle with a healthy partner during a single 40-minute session experience a 35% improvement in motor function and increased brain activation similar to that found with levodopa treatment, new research shows.
The study, by researchers at the Cleveland Clinic in Ohio, found that maintaining a steady rate of 80 to 90 revolutions per minute (rpm) on the bicycle not only improved function in lower extremities but also in upper extremities.
The improvement was dramatic and similar to that achieved by levodopa therapy, said 1 of the researchers, Jay L. Alberts, PhD, from the Center for Neurological Restoration at the Lerner Research Institute, in Cleveland.
"It looks like there are global effects in terms of the improvement in motor function," he told Medscape Neurology. "It suggests to us that maybe we're changing central motor function or maybe we're actually changing brain function through something very noninvasive."
The study was presented during the Movement Disorder Society's 13th International Congress of Parkinson's Disease and Movement Disorders.
A previous published study by this Cleveland research group found that the same forced exercise intervention administered 3 times a week for 8 weeks provided a similar 35% improvement in motor function.
"Couple these new findings with our longer-term data, and for us it's very encouraging," said Dr. Alberts. "Maybe if we can alter brain function, we can potentially alter the course and potentially slow the progression of this disease."
Tandem Exercise
For the study, researchers selected 11 male and female patients ranging in age from mid 50s to early 70s who had mild to moderate PD but no cardiac concerns. They tested these patients under 3 random conditions: not on medication, on medication (levodopa), and not on medication but completion of the forced-exercise intervention.
When on a stationary bicycle, PD patients normally pedal at a sustained rate of about 40 to 60 rpm. In this intervention, however, the patients sat on the back of a tandem bicycle while a healthy young adult trainer occupied the front seat and regulated the pedaling rate, ensuring that it remained between 80 to 90 rpm for 40 minutes.
Researchers monitored each patient's heart rate and made sure it stayed within 60% to 80% of his or her age-determined target range.
Patients also performed a force-tracking task and a bilateral finger-tapping task to demonstrate their level of control and coordination. Similar grasping tasks are necessary to perform daily activities such as buttoning a shirt or tying shoe laces, said Dr. Alberts.
The researchers found that the forced exercise and the levodopa produced similar significant reductions in Unified Parkinson's Disease Rating Scale (UPDRS III) motor scores, 35% with exercise and 38% with levodopa. Data from functional magnetic resonance imaging (fMRI) showed increased activation in the supplementary motor area (SMA) and primary motor cortex (M1) regions of the brain in response to both interventions.
"In terms of the fMRI data, we found that there was an increase in the level of cortical activation in the 2 motor areas - the SMA and the primary motor cortex - and this increase in activation looks very similar to the increase you see when you administer L-dopa," said Dr. Alberts.
For the force-tracking task and bilateral finger tapping, motor performance was 35% better following forced exercise compared with no exercise.
"Overdriving" Central Nervous System
These findings suggest that the exercise and the drug treatment elicit the same underlying mechanisms that provide similar symptomatic relief from PD symptoms, said Dr. Alberts.
The researchers surmise that the exercise may facilitate central motor control processes in Parkinson's patients. "For lack of a better word, we may be 'overdriving' the central nervous system by providing an increase in the quantity and quality of sensory information provided to the patient," said Dr. Alberts.
He added that this type of intervention could also be carried out on a treadmill, but it may be riskier and less practical than on a tandem bike. "We can't increase someone's walking rate 30% without having them in a harness and even then, I think you'll find that their feet would be dragging."
The next step in this line of research, he said, is to develop a motor-assisted cycle that will allow patients to do this type of exercise at home.
Many Beneficial Effects
Asked for a comment, Kapil D Sethi, MD, professor of neurology and director of the movement disorders program at the Medical College of Georgia, in Augusta, said the research highlights additional benefits of exercise. "Exercise has many beneficial effects both physical and psychological," he told Medscape Neurology. "There is evidence in the animal models and now in humans that exercise may have beneficial effects in PD. The exact mechanism is unclear, and the exact paradigm is unknown."
Mark Hallett, MD, from the National Institute of Neurological Disorders and Stroke, in Bethesda, Maryland, added in a press release that the finding of similarities between exercise and drug treatment "is certainly interesting and may indicate that exercise, in the short term, causes dopa release."
Dr. Alberts has no disclosures. Dr. Sethi is a member of the editorial advisory board for Medscape Neurology. He has disclosed he has served as an advisor or consultant to and received grants for clinical research from Boehringer Ingelheim Pharmaceuticals, Schering-Plough, GlaxoSmithKline, Allergan, Novartis Pharmaceuticals, and Solvay. He owns stock, stock options, or bonds in and has received grants for educational activities from Pfizer and Elan Pharmaceuticals.
Movement Disorder Society's 13th International Congress of Parkinson's Disease and Movement Disorders: Abstract LB-13. Presented June 10, 2009.
Saturday, December 5, 2009
Low blood pressure and PD
Posted: Fri Dec 04, 2009 4:19 am Post subject: Low blood pressure
--------------------------------------------------------------------------------
Dear Doctor,
I have different low blood pressure at time either sit and stand.
I feel slightly dizziness and nearly losing my balance.
My Blood test:
*RBC* 4.3 X10 12/L (below normal level Male 4.5-
Haemoglobin 13.7 g/dL,PCV 40 %
MCVC 32 pg,MCH 91 fl,MCHC 35 g/dL,
*Platelets* 141 X10 9/L, (below normal 150-400 ),
WBC 6.2 X10/9L,Neutrophils 70 %,
Lymphocytes 28 %, Monocytes 1,below normal 2-10
Eosinophils 1 ,Baspphils 0
My medication:
Sinemet regular 1, Sinemet CR 3, Requip 6 mg,Jumex 10mg Plavix 75mg, Zantac 300 mg daily
Xatral XL 10mg, Stilnox 5 mg, Xanax 0.25 mg,Seroquel 12.5 mg
Lexapro 5mg *nightly*
I had T.I.A 2008, gastrointestinal disorder and insomina, bladder dysfunction.
Kindly advise
Back to top
Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Fri Dec 04, 2009 9:03 am Post subject:
--------------------------------------------------------------------------------
.
Dear Friend,
I am not a doctor, rather a nutritionist, and I recommend you address your question to “Ask the Doctor” on the Discussion Corner. However, I can make some comments:
Certainly your lab tests are somewhat low with regard to iron, and anemia can cause dizziness, and lightheadedness.
However, Requip can also cause dizziness as a side effect; Jumex (selegiline) can cause both dizziness and hypotension (low blood pressure, especially when changing position, such as rising, or lying down).
Further, PD itself can, in some people, cause hypotension.
If the dizziness is due to hypotension, one possible course of action is to add salt to the diet and drink plenty of water. This increases blood volume and helps to correct the blood pressure. However, this must only be done under the care of your doctor, because the dizziness might be due to some other cause. And the addition of salt is potentially harmful in some cases, such as for persons with congestive heart failure.
I believe the doctors on “Ask the Doctor” can provide much better help than I, and I would also discuss this with your own neurologist and/or primary care physician. You might need an adjustment in your medication regime.
_________________
Best regards,
Kathrynne Holden, MS
--------------------------------------------------------------------------------
Dear Doctor,
I have different low blood pressure at time either sit and stand.
I feel slightly dizziness and nearly losing my balance.
My Blood test:
*RBC* 4.3 X10 12/L (below normal level Male 4.5-
Haemoglobin 13.7 g/dL,PCV 40 %
MCVC 32 pg,MCH 91 fl,MCHC 35 g/dL,
*Platelets* 141 X10 9/L, (below normal 150-400 ),
WBC 6.2 X10/9L,Neutrophils 70 %,
Lymphocytes 28 %, Monocytes 1,below normal 2-10
Eosinophils 1 ,Baspphils 0
My medication:
Sinemet regular 1, Sinemet CR 3, Requip 6 mg,Jumex 10mg Plavix 75mg, Zantac 300 mg daily
Xatral XL 10mg, Stilnox 5 mg, Xanax 0.25 mg,Seroquel 12.5 mg
Lexapro 5mg *nightly*
I had T.I.A 2008, gastrointestinal disorder and insomina, bladder dysfunction.
Kindly advise
Back to top
Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Fri Dec 04, 2009 9:03 am Post subject:
--------------------------------------------------------------------------------
.
Dear Friend,
I am not a doctor, rather a nutritionist, and I recommend you address your question to “Ask the Doctor” on the Discussion Corner. However, I can make some comments:
Certainly your lab tests are somewhat low with regard to iron, and anemia can cause dizziness, and lightheadedness.
However, Requip can also cause dizziness as a side effect; Jumex (selegiline) can cause both dizziness and hypotension (low blood pressure, especially when changing position, such as rising, or lying down).
Further, PD itself can, in some people, cause hypotension.
If the dizziness is due to hypotension, one possible course of action is to add salt to the diet and drink plenty of water. This increases blood volume and helps to correct the blood pressure. However, this must only be done under the care of your doctor, because the dizziness might be due to some other cause. And the addition of salt is potentially harmful in some cases, such as for persons with congestive heart failure.
I believe the doctors on “Ask the Doctor” can provide much better help than I, and I would also discuss this with your own neurologist and/or primary care physician. You might need an adjustment in your medication regime.
_________________
Best regards,
Kathrynne Holden, MS
Low blood pressure
Anonymous
PostPosted: Fri Dec 04, 2009 10:09 am Post subject: Low blood pressure Reply with quote
Dear Doctor,
My low blood pressure measurement varies from each time either sitting and standing
I feel slightly dizziness and nearly losing my balance.
My Blood test:
*RBC* 4.3 X10 12/L (below normal Male 4.5-6.5)
Haemoglobin 13.7 g/dL,PCV 40 %
MCVC 32 pg,MCH 91 fl,MCHC 35 g/dL,
*Platelets* 141 X10 9/L, (below normal 150-400 ),
WBC 6.2 X10/9L,Neutrophils 70 %,
Lymphocytes 28 %, Monocytes 1,below normal 2-10
Eosinophils 1 ,Baspphils 0
My medication:
Sinemet regular 1, Sinemet CR 3, Requip 6 mg,Jumex 10mg Plavix 75mg, Zantac 300 mg daily
Xatral XL 10mg, Stilnox 5 mg, Xanax 0.25 mg,Seroquel 12.5 mg
Lexapro 5mg *nightly*
I had T.I.A 2008, gastrointestinal disorder and insomina, bladder dysfunction.
Kindly advise
Back to top
Dr. Okun
Joined: 19 Jan 2007
Posts: 251
Location: University of Florida
PostPosted: Fri Dec 04, 2009 3:56 pm Post subject: Reply with quote
If it is low blood pressure and dizziness:
Ask your doc about getting rid of dopamine agonists, hydrating (6-8 glasses of water a day), stiockings, and in some cases midodrine or florinef.
_________________
Michael S. Okun, M.D.
PostPosted: Fri Dec 04, 2009 10:09 am Post subject: Low blood pressure Reply with quote
Dear Doctor,
My low blood pressure measurement varies from each time either sitting and standing
I feel slightly dizziness and nearly losing my balance.
My Blood test:
*RBC* 4.3 X10 12/L (below normal Male 4.5-6.5)
Haemoglobin 13.7 g/dL,PCV 40 %
MCVC 32 pg,MCH 91 fl,MCHC 35 g/dL,
*Platelets* 141 X10 9/L, (below normal 150-400 ),
WBC 6.2 X10/9L,Neutrophils 70 %,
Lymphocytes 28 %, Monocytes 1,below normal 2-10
Eosinophils 1 ,Baspphils 0
My medication:
Sinemet regular 1, Sinemet CR 3, Requip 6 mg,Jumex 10mg Plavix 75mg, Zantac 300 mg daily
Xatral XL 10mg, Stilnox 5 mg, Xanax 0.25 mg,Seroquel 12.5 mg
Lexapro 5mg *nightly*
I had T.I.A 2008, gastrointestinal disorder and insomina, bladder dysfunction.
Kindly advise
Back to top
Dr. Okun
Joined: 19 Jan 2007
Posts: 251
Location: University of Florida
PostPosted: Fri Dec 04, 2009 3:56 pm Post subject: Reply with quote
If it is low blood pressure and dizziness:
Ask your doc about getting rid of dopamine agonists, hydrating (6-8 glasses of water a day), stiockings, and in some cases midodrine or florinef.
_________________
Michael S. Okun, M.D.
Wednesday, December 2, 2009
swallowing
Singing is the therapy that help your swallowing.
Speaking and swallowing use many muscles and nerves in common, much as those of the lower
face, lips, tongue, voice box, and throat. The nerves and muscles of these structures are often
affected by the Parkinson's disease process. The speech and swallowing problems of Parkinson's
mirror other movement problems associated with the disease.
http://www.npfocc.org/uploads/swallowingproblems.pdf
2 people marked this post as helpful.
Speaking and swallowing use many muscles and nerves in common, much as those of the lower
face, lips, tongue, voice box, and throat. The nerves and muscles of these structures are often
affected by the Parkinson's disease process. The speech and swallowing problems of Parkinson's
mirror other movement problems associated with the disease.
http://www.npfocc.org/uploads/swallowingproblems.pdf
2 people marked this post as helpful.
What factors be considered before medication?
I am newly diagnosed with Parkinson’s disease, what factors are considered by my doctor when starting me on a medication?
You ask a very important question. Several factors require consideration when initiating symptomatic drug therapy in Parkinson’s disease. The choice of pharmacotherapy depends on the patient’s age, degree of disability, and cognitive status, as well as the impact of dosing, possible impact on the patient’s employment, domestic responsibilities, and lifestyle. Potential drug side effects must also be considered. Thus there are a lot of factors to consider!
The patient’s age is an important factor in predicting how well certain medications might be tolerated, as the risk of developing dyskinesia and motor fluctuations, especially with levodopa use, increases with earlier/younger onset Parkinson’s disease (most especially those who get it before 50 to 60 years old). Dopamine agonists, which delay the risk of dyskinesia and end-of-dose wearing off, may be offered as a first-line treatment option for younger patients. However, in older patients (which in our field means greater than 70 years old), the dopamine agonists have a higher risk for producing psychiatric and cognitive side effects. In addition, dopamine agonists have a complicated initial titration schedule before a therapeutic dose can be achieved. They require multiple dosing throughout the day, making the use of these agents challenging for many patients but especially so for patients 70 and older, who may be on several therapies for other conditions. Morover, the elderly patient is less likely to develop motor fluctuations and dyskinesias compared to the younger patient. Thus, in the currently published treatment algorithm, it is suggested that for the older patient, levodopa may be a better choice as initial first-line therapy compared to dopamine agonists.
The good news is that recent data suggest that an alternative option for initial monotherapy for early PD patients is rasagiline, a selective monoamine oxidase type B (MAO-B) inhibitor that offers effective control of symptoms and appears to be have a much lower incidence of the dopaminergic side effects seen with dopamine agonists and levodopa.
In one large placebo-controlled, multi-center clinical trial, after 5 years of levodopa use and as Parkinson’s disease progressed, about 50% of patients who were given levodopa from the onset developed motor complications compared to only 20% of patients who were first started on dopamine agonists for their early symptoms. However, the traditional view that treatment of Parkinson’s disease should begin only when symptoms become functionally significant has been challenged by some recent studies suggesting that initiation of treatment at the time of diagnosis results in better clinical outcome later in the course of the disease.
The patient’s perception of their level of disability and its impact on their lifestyle is also a driver of initial choice of therapy. Patients at the early stage whose major presenting symptom is tremor and who have minimal slowness or stiffness may respond to drugs such as anticholinergic agents or amantadine before their symptoms worsen. Rasagiline, selegiline, dopamine agonists or levodopa may be added as the disease progresses.
The potential of therapies to produce untoward side effects based upon the patient age and comorbid conditions is another important factor in choosing initial Parkinson’s disease therapy. As mentioned, dopamine agonists are not a good first choice in older patients due to concerns of leg swelling, cognitive impairment, and hallucinations. In patients in whom excessive sleepiness and drowsiness may affect daily activities, dopamine agonist use may also not be appropriate.
Yours,
_________________
Hubert H. Fernandez
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View user's profile Send private message
Anonymous
PostPosted: Tue Nov 17, 2009 8:43 am Post subject: Reply with quote
Good recap ... thanks!
Rich
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Dr. Fernandez
Joined: 20 Jan 2007
Posts: 90
PostPosted: Thu Nov 19, 2009 7:37 pm Post subject: Reply with quote
You are welcome!
_________________
Hubert H. Fernandez
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View user's profile Send private message
Anonymous
PostPosted: Sat Nov 21, 2009 11:01 am Post subject: Reply with quote
Let me pull out a small portion of your post that is very important - the fact that motor complications occurred more often with the patients on sinemet than on the dopamine agonists after five years.
For those just beginning therapy you must realize that many of these motor complications can be very very minimal. I for example will have movement of my feet first thing in the morning when my sinemet hits my brain. The movement is minimal and causes no problems. No the dopamine agonists did not cause a problem like this but they caused me to faint at least 15 times a day. I did not change because I was afraid to take dopamine.
My point is - don't be afraid to try sinemet (dopamine). It really does work amazingly well (it stopped ALL my PD problems from drooling to freezing to tremor) and the side effects can be controlled one way or another by adjusting dosage and adding or subtracting other things. If the dopamine agonists work for you - GREAT. But if they don't - DON'T WAIT. Get on sinemet. I lost three years of my life because I waited too long to get on dopamine because of the older articles that said that taking it caused the disease to progress faster. From what I understand this is no longer thought to be true.
Good luck all!
Back to top
Dr. Fernandez
Joined: 20 Jan 2007
Posts: 90
PostPosted: Sat Nov 21, 2009 5:46 pm Post subject: Reply with quote
Thank you for your comments!
_________________
Hubert H. Fernandez
You ask a very important question. Several factors require consideration when initiating symptomatic drug therapy in Parkinson’s disease. The choice of pharmacotherapy depends on the patient’s age, degree of disability, and cognitive status, as well as the impact of dosing, possible impact on the patient’s employment, domestic responsibilities, and lifestyle. Potential drug side effects must also be considered. Thus there are a lot of factors to consider!
The patient’s age is an important factor in predicting how well certain medications might be tolerated, as the risk of developing dyskinesia and motor fluctuations, especially with levodopa use, increases with earlier/younger onset Parkinson’s disease (most especially those who get it before 50 to 60 years old). Dopamine agonists, which delay the risk of dyskinesia and end-of-dose wearing off, may be offered as a first-line treatment option for younger patients. However, in older patients (which in our field means greater than 70 years old), the dopamine agonists have a higher risk for producing psychiatric and cognitive side effects. In addition, dopamine agonists have a complicated initial titration schedule before a therapeutic dose can be achieved. They require multiple dosing throughout the day, making the use of these agents challenging for many patients but especially so for patients 70 and older, who may be on several therapies for other conditions. Morover, the elderly patient is less likely to develop motor fluctuations and dyskinesias compared to the younger patient. Thus, in the currently published treatment algorithm, it is suggested that for the older patient, levodopa may be a better choice as initial first-line therapy compared to dopamine agonists.
The good news is that recent data suggest that an alternative option for initial monotherapy for early PD patients is rasagiline, a selective monoamine oxidase type B (MAO-B) inhibitor that offers effective control of symptoms and appears to be have a much lower incidence of the dopaminergic side effects seen with dopamine agonists and levodopa.
In one large placebo-controlled, multi-center clinical trial, after 5 years of levodopa use and as Parkinson’s disease progressed, about 50% of patients who were given levodopa from the onset developed motor complications compared to only 20% of patients who were first started on dopamine agonists for their early symptoms. However, the traditional view that treatment of Parkinson’s disease should begin only when symptoms become functionally significant has been challenged by some recent studies suggesting that initiation of treatment at the time of diagnosis results in better clinical outcome later in the course of the disease.
The patient’s perception of their level of disability and its impact on their lifestyle is also a driver of initial choice of therapy. Patients at the early stage whose major presenting symptom is tremor and who have minimal slowness or stiffness may respond to drugs such as anticholinergic agents or amantadine before their symptoms worsen. Rasagiline, selegiline, dopamine agonists or levodopa may be added as the disease progresses.
The potential of therapies to produce untoward side effects based upon the patient age and comorbid conditions is another important factor in choosing initial Parkinson’s disease therapy. As mentioned, dopamine agonists are not a good first choice in older patients due to concerns of leg swelling, cognitive impairment, and hallucinations. In patients in whom excessive sleepiness and drowsiness may affect daily activities, dopamine agonist use may also not be appropriate.
Yours,
_________________
Hubert H. Fernandez
Back to top
View user's profile Send private message
Anonymous
PostPosted: Tue Nov 17, 2009 8:43 am Post subject: Reply with quote
Good recap ... thanks!
Rich
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Dr. Fernandez
Joined: 20 Jan 2007
Posts: 90
PostPosted: Thu Nov 19, 2009 7:37 pm Post subject: Reply with quote
You are welcome!
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Hubert H. Fernandez
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Anonymous
PostPosted: Sat Nov 21, 2009 11:01 am Post subject: Reply with quote
Let me pull out a small portion of your post that is very important - the fact that motor complications occurred more often with the patients on sinemet than on the dopamine agonists after five years.
For those just beginning therapy you must realize that many of these motor complications can be very very minimal. I for example will have movement of my feet first thing in the morning when my sinemet hits my brain. The movement is minimal and causes no problems. No the dopamine agonists did not cause a problem like this but they caused me to faint at least 15 times a day. I did not change because I was afraid to take dopamine.
My point is - don't be afraid to try sinemet (dopamine). It really does work amazingly well (it stopped ALL my PD problems from drooling to freezing to tremor) and the side effects can be controlled one way or another by adjusting dosage and adding or subtracting other things. If the dopamine agonists work for you - GREAT. But if they don't - DON'T WAIT. Get on sinemet. I lost three years of my life because I waited too long to get on dopamine because of the older articles that said that taking it caused the disease to progress faster. From what I understand this is no longer thought to be true.
Good luck all!
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Dr. Fernandez
Joined: 20 Jan 2007
Posts: 90
PostPosted: Sat Nov 21, 2009 5:46 pm Post subject: Reply with quote
Thank you for your comments!
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Hubert H. Fernandez
Amanatadine
Amanatadine initially was an antiviral medication against influenza, but its main use now is as a type of pain reliever as it inhibits something called an NMDA receptor.
The NMDA receptor is a nervous system receptor that can bind to aspartate (or more specifically to N-methyl-D-aspartate) or glutamate to create chronic pain. Even worse, when glutamate or aspartate binds to this receptor, a stimulus that is normally not painful actually becomes painful.
By coincidence it was found to help the symptoms of Parkinson's disease. It may be used alone or in combination with levodopa or dopamine agonists. Amantadine reduces symptoms of fatigue, tremor and bradykinesia.
I was taking 2 Sinemet CR and 1 Sinemet 25/100, 12 Requip (2 mg) daily in the year of 2006 and to my surprise when added 3 Amantadine (100mg ) it caused reddish mottling on few part of my body and legs which was sideeffect of Amantadine and I apply Antiseptic cream to stop itchiness. I had stopped the medicine.
In general sideeffects of this medication may cause stomach upset, nausea, drowsiness, constipation, headache, dizziness, anxiety, or purplish-red blotchy spots on the skin during the first few days as your body adjusts to the medication. If these symptoms persist or become severe, inform your doctor promptly. Notify your doctor if you develop: slurred speech, shortness of breath, swelling of the ankles/feet, unusual fatigue, vision disturbances, difficulty urinating, skin rash, mental/mood changes (sometimes severe, including rare thoughts of suicide), muscle stiffness, uncontrolled muscle movements, unusual sweating, fast heartbeat, unexplained fever. If you notice other effects not listed above, contact your doctor or pharmacist.
The NMDA receptor is a nervous system receptor that can bind to aspartate (or more specifically to N-methyl-D-aspartate) or glutamate to create chronic pain. Even worse, when glutamate or aspartate binds to this receptor, a stimulus that is normally not painful actually becomes painful.
By coincidence it was found to help the symptoms of Parkinson's disease. It may be used alone or in combination with levodopa or dopamine agonists. Amantadine reduces symptoms of fatigue, tremor and bradykinesia.
I was taking 2 Sinemet CR and 1 Sinemet 25/100, 12 Requip (2 mg) daily in the year of 2006 and to my surprise when added 3 Amantadine (100mg ) it caused reddish mottling on few part of my body and legs which was sideeffect of Amantadine and I apply Antiseptic cream to stop itchiness. I had stopped the medicine.
In general sideeffects of this medication may cause stomach upset, nausea, drowsiness, constipation, headache, dizziness, anxiety, or purplish-red blotchy spots on the skin during the first few days as your body adjusts to the medication. If these symptoms persist or become severe, inform your doctor promptly. Notify your doctor if you develop: slurred speech, shortness of breath, swelling of the ankles/feet, unusual fatigue, vision disturbances, difficulty urinating, skin rash, mental/mood changes (sometimes severe, including rare thoughts of suicide), muscle stiffness, uncontrolled muscle movements, unusual sweating, fast heartbeat, unexplained fever. If you notice other effects not listed above, contact your doctor or pharmacist.
Double vision
Double vision in Parkinson’s is often caused by problems in moving the eyes and, in particular, by
problems of tracking. ‘Tracking’ refers to the eyes moving in alignment from side to side, for
example moving across a page when reading. Impaired co-ordination and fatigue of the muscles
that move the eyeballs can mean that the eyeballs do not move together in alignment. This can
cause double vision.
The problem of double vision is usually improved by anti-Parkinson’s medication. Resting the eyes
when double vision occurs is wise and should provide relief.
There can be other causes of double vision that are unrelated to Parkinson’s. If the problem persists,
consult an ophthalmologist (doctor who specialises in the care of the eyes).
problems of tracking. ‘Tracking’ refers to the eyes moving in alignment from side to side, for
example moving across a page when reading. Impaired co-ordination and fatigue of the muscles
that move the eyeballs can mean that the eyeballs do not move together in alignment. This can
cause double vision.
The problem of double vision is usually improved by anti-Parkinson’s medication. Resting the eyes
when double vision occurs is wise and should provide relief.
There can be other causes of double vision that are unrelated to Parkinson’s. If the problem persists,
consult an ophthalmologist (doctor who specialises in the care of the eyes).
Any medication that blocks dopamine in the body can cause Parkinson's symptoms.
Any medication that blocks dopamine in the body can cause Parkinson's symptoms.
By Louis Neipris, M.D., Staff Writer, myOptumHealth
You may have heard of Parkinson's disease (PD), a movement disorder. Someone with it may have characteristic signs, such as a pill-rolling tremor in the fingers or a hunched forward posture. You may recognize someone with this disease from the faltering, tiny steps they take when they walk or by their rigidly emotionless face.
The cause of Parkinson's disease is mostly unknown. Some people develop Parkinson's-like symptoms after treatment with certain medications. This is called drug-induced parkinsonism (DIP) or secondary parkinsonism. Certain medications can also worsen symptoms in someone who already has Parkinson's disease.
Any medication that blocks dopamine in the body can cause Parkinson's symptoms. Dopamine is a brain chemical that helps control movement. Common dopamine-blocking drugs are antipsychotics. They are used to treat certain mental illnesses or severe nausea. Less commonly, certain types of calcium channel blockers cause drug-induced parkinsonism. These drugs may be used to treat chest pain and high blood pressure, or irregular heart rate.
Other types of medications that may cause drug-induced parkinsonism are:
* Some antidepressants
* Certain anti-nausea drugs
* Some drugs used to treat vertigo
* Certain drugs used to treat epilepsy
* Some anti-arrhythmics (used to treat irregular heart rhythm)
Not all drugs in these classes will cause symptoms of parkinsonism.
What's the difference?
Drug-induced parkinsonism usually develops on both sides of the body, while typical Parkinson's disease does not. Also, drug-induced parkinsonism usually does not progress like typical Parkinson's.
Unlike Parkinson's, drug-induced symptoms usually go away after the drug is stopped. It may take several months, though, for the symptoms to completely stop. If the symptoms remain, then it is possible that the drug may have "unmasked" underlying Parkinson's disease.
Who is at risk?
* Female: Women are twice as much at risk as men.
* Elderly: Older people are more likely to be on multiple medications or to have underlying Parkinson's disease.
* Those with a family history of Parkinson's disease.
* People with AIDS.
What to do to prevent drug-induced parkinsonism?
The most common drugs linked to this condition are two used to treat schizophrenia or psychotic symptoms of dementia. They are haloperidol (Haldol) and perphenazine (Trilafon). Ask your doctor about parkinsonism if you or a loved one is concerned about a drug, especially these two drugs.
In general:
* Make sure you or a loved one are on the lowest effective dose.
* If you already have Parkinson's disease, then tell your doctor if the symptoms appear to be getting worse since starting the drug.
* Never stop taking a drug on your own. Talk to your doctor about any concerns.
SOURCES:
* Parkinson's Disease Society. Drug-induced parkinsonism.
* Albin RL. Parkinson's disease: background, diagnosis, and initial management. Clinics in Geriatric Medicine. 2006;22(4):735-751.
* Alvarez MV, Evidente VG. Understanding drug-induced parkinsonism Separating pearls from oysters. Neurology. 2008;70(8):e32-e34.
.
http://www.wrex.com/Global/story.asp?S=10707421
.
_________________
Best regards,
Kathrynne Holden, MS
--
For a Parkinson Tip of the Day visit:
http://www.nutritionucanlivewith.com/
By Louis Neipris, M.D., Staff Writer, myOptumHealth
You may have heard of Parkinson's disease (PD), a movement disorder. Someone with it may have characteristic signs, such as a pill-rolling tremor in the fingers or a hunched forward posture. You may recognize someone with this disease from the faltering, tiny steps they take when they walk or by their rigidly emotionless face.
The cause of Parkinson's disease is mostly unknown. Some people develop Parkinson's-like symptoms after treatment with certain medications. This is called drug-induced parkinsonism (DIP) or secondary parkinsonism. Certain medications can also worsen symptoms in someone who already has Parkinson's disease.
Any medication that blocks dopamine in the body can cause Parkinson's symptoms. Dopamine is a brain chemical that helps control movement. Common dopamine-blocking drugs are antipsychotics. They are used to treat certain mental illnesses or severe nausea. Less commonly, certain types of calcium channel blockers cause drug-induced parkinsonism. These drugs may be used to treat chest pain and high blood pressure, or irregular heart rate.
Other types of medications that may cause drug-induced parkinsonism are:
* Some antidepressants
* Certain anti-nausea drugs
* Some drugs used to treat vertigo
* Certain drugs used to treat epilepsy
* Some anti-arrhythmics (used to treat irregular heart rhythm)
Not all drugs in these classes will cause symptoms of parkinsonism.
What's the difference?
Drug-induced parkinsonism usually develops on both sides of the body, while typical Parkinson's disease does not. Also, drug-induced parkinsonism usually does not progress like typical Parkinson's.
Unlike Parkinson's, drug-induced symptoms usually go away after the drug is stopped. It may take several months, though, for the symptoms to completely stop. If the symptoms remain, then it is possible that the drug may have "unmasked" underlying Parkinson's disease.
Who is at risk?
* Female: Women are twice as much at risk as men.
* Elderly: Older people are more likely to be on multiple medications or to have underlying Parkinson's disease.
* Those with a family history of Parkinson's disease.
* People with AIDS.
What to do to prevent drug-induced parkinsonism?
The most common drugs linked to this condition are two used to treat schizophrenia or psychotic symptoms of dementia. They are haloperidol (Haldol) and perphenazine (Trilafon). Ask your doctor about parkinsonism if you or a loved one is concerned about a drug, especially these two drugs.
In general:
* Make sure you or a loved one are on the lowest effective dose.
* If you already have Parkinson's disease, then tell your doctor if the symptoms appear to be getting worse since starting the drug.
* Never stop taking a drug on your own. Talk to your doctor about any concerns.
SOURCES:
* Parkinson's Disease Society. Drug-induced parkinsonism.
* Albin RL. Parkinson's disease: background, diagnosis, and initial management. Clinics in Geriatric Medicine. 2006;22(4):735-751.
* Alvarez MV, Evidente VG. Understanding drug-induced parkinsonism Separating pearls from oysters. Neurology. 2008;70(8):e32-e34.
.
http://www.wrex.com/Global/story.asp?S=10707421
.
_________________
Best regards,
Kathrynne Holden, MS
--
For a Parkinson Tip of the Day visit:
http://www.nutritionucanlivewith.com/
Singing is helpful for PD
Anonymous
Posted: Tue Nov 24, 2009 6:09 pm Post subject: Singing is helpful for parkinson's patients
--------------------------------------------------------------------------------
There are few articles touch on singing as a therapy that could help parkinson's patients mobility, speech, facial masked without mile and expression, soft voice,depression, anxiety breathing and etc. Singing is part of therapy to relief the motor and non motor symptoms of PD.
http://www.nwpf.org/News.aspx?Item=2578
TEOKIMHOE
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Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Thu Nov 26, 2009 10:45 am Post subject:
--------------------------------------------------------------------------------
.
Thanks for posting this, it's an excellent article!
.
_________________
Best regards,
Kathrynne Holden, MS
--
For a Parkinson Tip of the Day visit:
http://www.nutritionucanlivewith.com/
Posted: Tue Nov 24, 2009 6:09 pm Post subject: Singing is helpful for parkinson's patients
--------------------------------------------------------------------------------
There are few articles touch on singing as a therapy that could help parkinson's patients mobility, speech, facial masked without mile and expression, soft voice,depression, anxiety breathing and etc. Singing is part of therapy to relief the motor and non motor symptoms of PD.
http://www.nwpf.org/News.aspx?Item=2578
TEOKIMHOE
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Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Thu Nov 26, 2009 10:45 am Post subject:
--------------------------------------------------------------------------------
.
Thanks for posting this, it's an excellent article!
.
_________________
Best regards,
Kathrynne Holden, MS
--
For a Parkinson Tip of the Day visit:
http://www.nutritionucanlivewith.com/
When to medicate?
Anonymous
Posted: Sun Nov 29, 2009 2:12 pm Post subject: when to medicate
--------------------------------------------------------------------------------
Dear Kathrynne,
What to do when you have an invitation for Thanksgiving dinner at the time you are supposed to take one of your meds?
Are the pills more effective when taken with th e meal at the correct hour, or waiting for two hours after the meal, whicb will throw off your pill schedule for the whole day.
And all of this for "quality of life".
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Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Mon Nov 30, 2009 11:46 am Post subject:
--------------------------------------------------------------------------------
.
Dear Friend,
This is a very good question, and it’s difficult to give a perfect answer. I am assuming you refer to use of levodopa. If you take the levodopa at the correct hour and that coincides with the start of the meal, it will not have time to be absorbed and enter the bloodstream ahead of the meal. If, however, you take levodopa right after a meal, the proteins in the food are likely to block its absorption. Either way, your PD symptoms will not be well controlled.
Two hours is normally enough time for the stomach to clear a meal; but if the meal is high in fat, that will slow clearance by as much as an hour or more. A large meal also takes longer to clear. And, many folks with PD have gastroparesis (slowed stomach emptying), which means the meal takes much longer to empty from the stomach. So, two hours is not a guarantee.
The very best solution generally, if it is possible for you, would be to reschedule your day’s medications, starting about 30 to 60 minutes earlier than usual. That would allow you to take the levodopa about 30 minutes ahead of the Thanksgiving dinner, and allow them to be absorbed ahead of the food.
For example, if you normally take levodopa at 8:00 am, 12:00, 4:00, and 8:00 pm, and dinner is scheduled for 4:00 pm, you might take your first levodopa at 7:30 am, 11:30, 3:30 (then have dinner at 4:00), and at 7:30 pm. Taking it at 3:30 should allow the levodopa to clear the stomach and enter the bloodstream before the start of the meal. Hopefully, this will improve quality of life, which I know is of concern for folks with PD.
If you have further questions, or if I didn’t explain this well enough, let me know and I’ll try again.
.
_________________
Best regards,
Kathrynne Holden, MS
--
For a Parkinson Tip of the Day visit:
http://www.nutritionucanlivewith.com/
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Anonymous
Posted: Tue Dec 01, 2009 7:13 am Post subject: when to medicate
--------------------------------------------------------------------------------
thank you for y our prompt reply.
My problem i s that I must take my medication every 3 hrs.
And what do I do if it takes longerto finish a course?
Thank y ou so much for being there for us.
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Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Tue Dec 01, 2009 11:24 am Post subject:
--------------------------------------------------------------------------------
.
Dear Friend,
Thanksgiving is a problem when scheduling levodopa, for sure, for one thing because it usually lasts a good deal longer than most meals. And that makes it even more difficult to take medications on time.
I would try to work with your host/hostess ahead of time, explaining the times that you will need to take levodopa, and the importance of taking them about 30 minutes before the meal. Also, try to reschedule your levodopa for that day – for example, if you take your medications at 7:00 am, 10:00 am, 1:00 pm, 4:00 pm, and 7:00 pm, and dinner is scheduled for 4:00, try to re-schedule yourself for that day – take your first levodopa at 6:30 am, then 9:30, 12:30, 3:30. Have dinner at 4:00. Perhaps your hostess can see that you are able to complete your meal by 5:00. Then by 6:30 you will need to take your next medication. You may need to stretch the time to 7:00 pm, because if the meal is large, it may take longer than usual to clear your stomach.
It does bring up a couple of points to my mind, however.
1) Do you use Stalevo? It extends the effective time of levodopa, and might allow you to take your medications less often
2) If you already do take Stalevo (or cannot tolerate the Comtan component) you might discuss occasional use of “liquid Sinemet” with your neurologist. It does not last as long as regular Sinemet, but it is absorbed much faster and can be taken closer to meals.
3) Is it possible that you might have gastroparesis (slowed stomach emptying)? This is fairly common among folks with PD. Food stays in the stomach much longer than normal, and the medications taken while the stomach is full of food cannot clear the stomach to reach the bloodstream. PD symptoms thus are not well controlled, and the physician may prescribe more frequent doses. If you have not yet done so, I would ask your primary care physician about the possibility of gastroparesis, because if present, there are ways of eating that can help, and also some medications that can speed stomach emptying.
I hope this helps, but if not, let me know.
_________________
Best regards,
Kathrynne Holden, MS
--
For a Parkinson Tip of the Day visit:
http://www.nutritionucanlivewith.com/
Posted: Sun Nov 29, 2009 2:12 pm Post subject: when to medicate
--------------------------------------------------------------------------------
Dear Kathrynne,
What to do when you have an invitation for Thanksgiving dinner at the time you are supposed to take one of your meds?
Are the pills more effective when taken with th e meal at the correct hour, or waiting for two hours after the meal, whicb will throw off your pill schedule for the whole day.
And all of this for "quality of life".
Back to top
Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Mon Nov 30, 2009 11:46 am Post subject:
--------------------------------------------------------------------------------
.
Dear Friend,
This is a very good question, and it’s difficult to give a perfect answer. I am assuming you refer to use of levodopa. If you take the levodopa at the correct hour and that coincides with the start of the meal, it will not have time to be absorbed and enter the bloodstream ahead of the meal. If, however, you take levodopa right after a meal, the proteins in the food are likely to block its absorption. Either way, your PD symptoms will not be well controlled.
Two hours is normally enough time for the stomach to clear a meal; but if the meal is high in fat, that will slow clearance by as much as an hour or more. A large meal also takes longer to clear. And, many folks with PD have gastroparesis (slowed stomach emptying), which means the meal takes much longer to empty from the stomach. So, two hours is not a guarantee.
The very best solution generally, if it is possible for you, would be to reschedule your day’s medications, starting about 30 to 60 minutes earlier than usual. That would allow you to take the levodopa about 30 minutes ahead of the Thanksgiving dinner, and allow them to be absorbed ahead of the food.
For example, if you normally take levodopa at 8:00 am, 12:00, 4:00, and 8:00 pm, and dinner is scheduled for 4:00 pm, you might take your first levodopa at 7:30 am, 11:30, 3:30 (then have dinner at 4:00), and at 7:30 pm. Taking it at 3:30 should allow the levodopa to clear the stomach and enter the bloodstream before the start of the meal. Hopefully, this will improve quality of life, which I know is of concern for folks with PD.
If you have further questions, or if I didn’t explain this well enough, let me know and I’ll try again.
.
_________________
Best regards,
Kathrynne Holden, MS
--
For a Parkinson Tip of the Day visit:
http://www.nutritionucanlivewith.com/
Back to top
Anonymous
Posted: Tue Dec 01, 2009 7:13 am Post subject: when to medicate
--------------------------------------------------------------------------------
thank you for y our prompt reply.
My problem i s that I must take my medication every 3 hrs.
And what do I do if it takes longerto finish a course?
Thank y ou so much for being there for us.
Back to top
Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Tue Dec 01, 2009 11:24 am Post subject:
--------------------------------------------------------------------------------
.
Dear Friend,
Thanksgiving is a problem when scheduling levodopa, for sure, for one thing because it usually lasts a good deal longer than most meals. And that makes it even more difficult to take medications on time.
I would try to work with your host/hostess ahead of time, explaining the times that you will need to take levodopa, and the importance of taking them about 30 minutes before the meal. Also, try to reschedule your levodopa for that day – for example, if you take your medications at 7:00 am, 10:00 am, 1:00 pm, 4:00 pm, and 7:00 pm, and dinner is scheduled for 4:00, try to re-schedule yourself for that day – take your first levodopa at 6:30 am, then 9:30, 12:30, 3:30. Have dinner at 4:00. Perhaps your hostess can see that you are able to complete your meal by 5:00. Then by 6:30 you will need to take your next medication. You may need to stretch the time to 7:00 pm, because if the meal is large, it may take longer than usual to clear your stomach.
It does bring up a couple of points to my mind, however.
1) Do you use Stalevo? It extends the effective time of levodopa, and might allow you to take your medications less often
2) If you already do take Stalevo (or cannot tolerate the Comtan component) you might discuss occasional use of “liquid Sinemet” with your neurologist. It does not last as long as regular Sinemet, but it is absorbed much faster and can be taken closer to meals.
3) Is it possible that you might have gastroparesis (slowed stomach emptying)? This is fairly common among folks with PD. Food stays in the stomach much longer than normal, and the medications taken while the stomach is full of food cannot clear the stomach to reach the bloodstream. PD symptoms thus are not well controlled, and the physician may prescribe more frequent doses. If you have not yet done so, I would ask your primary care physician about the possibility of gastroparesis, because if present, there are ways of eating that can help, and also some medications that can speed stomach emptying.
I hope this helps, but if not, let me know.
_________________
Best regards,
Kathrynne Holden, MS
--
For a Parkinson Tip of the Day visit:
http://www.nutritionucanlivewith.com/
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