Raise a glass!

December 29, 2010 at 5:16pm

This year, my New Year's  resolution is going to be to get enough

WATER!

H2O!

agua!

For those who might have missed the note on hypovolemia (loss of blood volume and dehydration) and CCSVI--read the last post on Flow and CCSVI.

Jeff and I have been consciously drinking a bit more water than we normally would, since Dr. Dake recommended hydration after angioplasty.   Nothing crazy, because too much isn't good either.  But we're getting closer to the recommended amount.

Here's a wonderful calculator to help you figure out how much daily water you need.  There are nine questions based on your weight, activity level, climate and more.

http://nutrition.about.com/library/blwatercalculator.htm

According to the calculator, with my body weight, amount of daily exercise and climate, I need 91 ounces of water a day.  That's a lot!  Jeff needs 109 ounces.  We're getting there.

So, will you join us in raising a glass of water to toast the new year?

To your health,  L'chaim!

Joan

Hydration, your Heart and Blood Flow

December 26, 2010 at 2:12pm

Did you know that when you are not drinking enough water, you are straining your heart and vascular system, and depriving your brain of good blood flow?

Dehydration causes strain on your heart. The amount of blood circulating through your body, or blood volume, decreases when you are dehydrated. To compensate, your heart beats faster, increasing your heart rate and causing you to feel palpitations. link

When we do not get enough hydration from water, our blood volume decreases. Water is essential for our vascular system.

Hypovolemia means low blood volume. This condition can be very serious and can be due to blood loss from injury.  It can also happen in a body that is dehydrated or inactive, or not functioning well. Hypovolemia occurs often to the elderly and disabled.

Low blood volume can cause orthostatic hypotension. This is when there isn't enough blood getting to the brain when you change position from lying down to upright. This can lead to dizziness, confusion and falls, and often happens in the elderly. But it can happen in people with MS, too. Orthostatic hypotension is well-documented in MS and has been a mystery for researchers.

For many women, pregnancy offers a time of blessed relief of MS symptoms. This has lead to studies of hormones and MS, and a clinical trial of estrogen in MS patients. But looking at pregnancy from the vascular paradigm, what else can we learn?

When women are pregnant, their blood volume increases dramatically. This sends blood pumping throughout the body.

Perhaps the most striking maternal physiologic alteration occurring during pregnancy is the increase in the blood volume. The magnitude of the increases varies according to the size of woman, the number of pregnancies she has had, the number of infants she has delivered, and whether there is one or multiple fetuses.The increases in blood volume progress until term;the average increase in volume at term is 45-50%. The increase is needed for extra blood flow to the uterus, extra metabolic needs of fetus, and increased perfusion of others organs, especially kidneys. Extra volume also compensate for maternal blood loss during delivery. 
link

After delivery is the time during which many women report having exacerbations in their MS, or a return of MS symptoms. Yes, hormone levels are fluctuating, but so are blood volume levels. Pondering this fact has lead me to do more reading on blood volume, and I am finding some interesting things to consider.

Thinking about blood volume in terms of CCSVI treatment and restenosis of veins has been very interesting to me. If angioplasty is returning good, open routes of flow, but the body is not able to compensate by providing adequate blood volume, then these opened vessels will not have the necessary pressure to remain opened. And the areas of prior stenosis might re-collapse, just like an old garden hose with low flow.

I hope to bring this avenue of discussion to the doctors. Perhaps aftercare needs to include additional hydration, salt intake, maybe even intravenous fluids--all to keep blood levels adequate. Inactivity and remaining in the supine position increase hypovolemia--therefore, movement, exercise and upright activities would encourage blood flow and blood volume. Something to think about as we move forward with CCSVI research in 2011.

With wishes for good flow in the New Year!

Joan 

Ischemia, MMPs and Myelin loss

December 16, 2010 at 10:47am

Continuing the exploration of the "auto-immune" reaction of the body in situations of slow blood flow, oxidative stress and lowered oxygen levels in the brain--we learn that  myelin breakdown is not unique to MS.  It happens in dementia, Alzheimer's, ischemic stroke, carbon monoxide poisoning and cerebrovascular disease.   

There is recent research on myelin loss in ischemia. 

This paper studies how matrix metalloproteinases (MMPs) are involved in this process--

MMPs:   A member of a group of enzymes that can break down proteins, such as collagen, that are normally found in the spaces between cells in tissues.   Matrix metalloproteinases are involved in wound healing, angiogenesis, and tumor cell metastasis.

In MS---

Multiple MMPs are elevated in human neurologic diseases.  In the setting of MS, it has been shown that serum MMP-9 levels are increased in patients with clinically isolated syndrome (CIS) compared with normal control subjects and are further elevated in patients with clinically definite MS (CDMS) compared with patients with CIS.   In addition, serum MMP levels increase markedly between onset of neurologic symptoms and development of CDMS, whereas levels remain unchanged in subjects with CIS who do not develop CDMS. Other studies have documented elevations of MMP-9 and other MMPs in the serum, CSF, and brain of patients with MS compared with controls.

http://www.direct-ms.org/pdf/ImmunologyMS/Yong%20Exper%20models%20neurodegen%20Neurology%2007.pdf

In Ischemia--

Divergent role for MMP-2 in myelin breakdown and oligodendrocyte death following transient global ischemia.

Walker EJ, Rosenberg GA.

Departments of Neurology, Neurosciences, and Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico, USA.

Abstract

Transient global ischemia causes delayed white matter injury to the brain with oligodendrocyte (OLG) death and myelin breakdown. There is increasing evidence that hypoxia may be involved in several diseases of the white matter, including multiple sclerosis, vascular dementia, and ischemia.

Matrix metalloproteinases (MMPs) are increased in rat and mouse models of hypoxic hypoperfusion and have been associated with OLG death. However, whether the MMPs act on myelin or OLGs remains unresolved. We hypothesized that delayed expression of MMPs caused OLG death and myelin breakdown. To test the hypothesis, adult mice underwent hypoxic hypoperfusion with transient bilateral occlusion of the carotid arteries. After 3 days of reperfusion, ischemic white matter had increased reactivity of astrocytes and microglia, MMP-2 localization in astrocytes, and increased protein expression and activity of MMP-2. In addition, there was a significant loss of myelin basic protein (MBP) by Western blot and caspase-3- mediated OLG death. Treatment with the broad-spectrum MMP inhibitor, BB-94, significantly decreased astrocyte reactivity and MMP-2 activity. More importantly, it reduced MBP breakdown. However, MMP inhibition had no effect on OLG loss. Our results implicate MMPs released by reactive astrocytes in delayed myelin degradation, while OLG death occurs by an MMP-independent mechanism. We propose that MMP-mediated myelin loss is important in hypoxic injury to the white matter.

http://www.ncbi.nlm.nih.gov/pubmed/19830840