For the last few weeks my left (most affected side) foot has been swollen, especially after a day of sitting at a desk. Has anyone had success in dealing with such issues, post (or pre) liberation? Besides not sitting at my desk all day or taking Lasix (which will probably be prescribed, if it doesn't improve), I mean.
... Ted
Swollen foot
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fiddler
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Swollen foot
Dx SPMS in 2004. Liberated 29/04/2010.
My blog: www.my-darn-ms.blogspot.com
My blog: www.my-darn-ms.blogspot.com
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fiddler
- Family Elder
- Posts: 398
- Joined: Wed Dec 02, 2009 3:00 pm
- Location: Fredericton, Canada
- Contact:
No restenosis
I was checked out a few weeks ago, and my blood flow (in my jugulars) seems to be good, so that doesn't seem to be the issue.
...Ted
...Ted
Dx SPMS in 2004. Liberated 29/04/2010.
My blog: www.my-darn-ms.blogspot.com
My blog: www.my-darn-ms.blogspot.com
an interesting read. the peripheral edema in stage four is relevant to this discussion. vitamin b1 features strongly in the klenner protocol for MS. i have also seen zinc linked to peripheral edema (ie foot swelling due to abnormal fluid accumulation).
HTH.
*****
http://intelegen.com/nutrients/five_sta ... ciency.htm
Five Stages of Nutrient Deficiency Leading to Disease
by Richard Gerber
In 1964 Myron Brin published a classic analysis of the five stages in the development of a vitamin or nutrient deficiency. He illustrated the schema with reference to vitamin B1 (thiamin).
In the first, or preliminary stage, inadequate B1 availability due to faulty diet, malabsorption or abnormal metabolism leads to a greatly reduced urinary B1 loss.
In the second, or biochemical stage, the activity of a key enzyme—transketolase—which is activated by B1, is significantly reduced. Adding B1 to a blood sample from a person at this stage increases his or her transketolase activity.
In the third, or physiologic stage, various general symptoms develop, such as lessened appetite, insomnia, increased irritability, and malaise.
In the fourth, or clinical stage, a constellation of symptoms classically specific to B1 deficiency disease (beri-beri) develops: e.g., intermittent claudication, polyneuritis, bradycardia, peripheral edema, and ophthalmoplegia (paralysis of eye muscles).
In the fifth, or anatomical stage, histopathological changes due to cellular structural damage are seen, such as cardiac hypertrophy, degeneration of the cerebellar granule layer, and swelling of the microglia.8
Although Brin’s five-stage deficiency schema is exemplified with regard to B1, it is in principle applicable to any nutrient, as Brin himself notes. Brin’s schema is especially illuminating with regard to the RDAs, since the “just preventing failure of specific functions” and “just preventing specific deficiency signs” criteria of nutritional requirement, which is the basis of the RDA concept, are only evidenced in the fourth (clinical) and fifth (anatomical) stages of developing nutritional deficiency disease.
The first three stages, although they are objectively, empirically measurable and observable phases of a developing nutrient deficiency, do not involve either “specific deficiency symptoms” or “failure of a specific nutrient-related function.” What follows from this is quite simple. The RDA level of nutrient intake may keep most people out of the severe illness-leading-to-death fourth and fifth nutrient deficiency stages, but RDA nutrient levels cannot be presumed to be adequate to keep one out of the first three stages of “subclinical” deficiency, let alone in a more optimal, vibrant, energized state of health.
HTH.
*****
http://intelegen.com/nutrients/five_sta ... ciency.htm
Five Stages of Nutrient Deficiency Leading to Disease
by Richard Gerber
In 1964 Myron Brin published a classic analysis of the five stages in the development of a vitamin or nutrient deficiency. He illustrated the schema with reference to vitamin B1 (thiamin).
In the first, or preliminary stage, inadequate B1 availability due to faulty diet, malabsorption or abnormal metabolism leads to a greatly reduced urinary B1 loss.
In the second, or biochemical stage, the activity of a key enzyme—transketolase—which is activated by B1, is significantly reduced. Adding B1 to a blood sample from a person at this stage increases his or her transketolase activity.
In the third, or physiologic stage, various general symptoms develop, such as lessened appetite, insomnia, increased irritability, and malaise.
In the fourth, or clinical stage, a constellation of symptoms classically specific to B1 deficiency disease (beri-beri) develops: e.g., intermittent claudication, polyneuritis, bradycardia, peripheral edema, and ophthalmoplegia (paralysis of eye muscles).
In the fifth, or anatomical stage, histopathological changes due to cellular structural damage are seen, such as cardiac hypertrophy, degeneration of the cerebellar granule layer, and swelling of the microglia.8
Although Brin’s five-stage deficiency schema is exemplified with regard to B1, it is in principle applicable to any nutrient, as Brin himself notes. Brin’s schema is especially illuminating with regard to the RDAs, since the “just preventing failure of specific functions” and “just preventing specific deficiency signs” criteria of nutritional requirement, which is the basis of the RDA concept, are only evidenced in the fourth (clinical) and fifth (anatomical) stages of developing nutritional deficiency disease.
The first three stages, although they are objectively, empirically measurable and observable phases of a developing nutrient deficiency, do not involve either “specific deficiency symptoms” or “failure of a specific nutrient-related function.” What follows from this is quite simple. The RDA level of nutrient intake may keep most people out of the severe illness-leading-to-death fourth and fifth nutrient deficiency stages, but RDA nutrient levels cannot be presumed to be adequate to keep one out of the first three stages of “subclinical” deficiency, let alone in a more optimal, vibrant, energized state of health.
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