Obesity and birth control pills raise MS risk

Two new studies will be presented at the American Academy of Neurology's 66th Annual meeting in Philadelphia during April 26-May 3.
These studies shed more light on the vascular connection to MS.

One study looked at the connection between obesity and MS risk--

For the obesity study, BMI was calculated for 210 people with MS and 210 people of the same age and sex who did not have MS at ages 15 and 20 and at the time of the study. The study found that people who are obese at age 20 are twice as likely to later develop MS as people who are not obese.

This study is one of many recent studies finding the connection of higher BMI, obesity and increased risk of developing MS.  The researchers posit that higher levels of the hormone leptin may be promoting an inflammatory response.  They never once mention the cardiovascular connection of the heart and the brain.

Here is Dr. Ronald Cohen from the University of Florida on the relationship of obesity to brain health.  He discusses the link of increased BMI to reduced cerebral blood flow, reduced gray matter volume and increased white matter abnormalities.

When we looked at brain volume and gray matter volume specifically, we found that in this cohort of people without comorbid conditons, but with a range of BMI, what we found was increased BMI was related to reduced cortical or gray matter volume, suggestng that there are actual relationships between obesity and structural brain changes. Subsequent findings from other studies that were conducted along the way, just looking strictly at obese populations, indicated relationships between other markers as well. White matter hyperintensities were increased in people with morbid obesity, but even among people who were overweight or mildly obese, there were some relationships between white matter abnormalites.

This became even clearer when we used diffusion tensor imaging, a method by which we can measure the coherense of white matter. ... Those types of findings suggested that coherence of white matter decreased as a function of BMI as well. When we look at blood flow in the brain (this was from a study of heart failure and the relationship of obesity) what we find is that obesity and cerebral blood flow are negatively correlated and together relate to cognitive problems among people with heart failure. So that was another finding that links obesity with cerebral blood flow or another marker.
https://psychiatry.ufl.edu/files/2011/12/Cohen.Newsletter.Final_.pdf

The other study looked at the connection between birth control pill use and MS--

For the birth control hormone study, researchers identified 305 women who had been diagnosed with MS or its precursor, clinically isolated syndrome, during a three-year period from the membership of Kaiser Permanente Southern California and who had been members for at least three years before the MS symptoms began. Then they compared them to 3,050 women who did not have MS.

A total of 29 percent of the women with MS and 24 percent of those without MS had used hormonal contraceptives for at least three months in the three years before symptoms began. The majority used estrogen/progestin combinations.

Women who had used hormonal contraceptives were 35 percent more likely to develop MS than those who did not use them. Those who had used the contraceptives but had stopped at least one month before symptoms started were 50 percent more likely to develop MS.
http://www.eurekalert.org/pub_releases/2014-02/aaon-dob021214.php

It is scientific fact that obese women and women who take birth control pills have an increased risk of cardiovascular disease, stroke and venous thrombosis.  And obese women on birth control pills have an even higher risk--due to the increase of hypercoagulating factors in their blood.  Both of these factors create endothelial dysfunction.  Both of these factors reduce cerebral blood flow.

We evaluated the risk of thrombosis due to overweight and obesity using data from a large population based case-control study. Four hundred and fifty-four consecutive patients with a first episode of objectively diagnosed thrombosis from three Anticoagulation Clinics in the Netherlands were enrolled in a case-control study. Controls were matched on age and sex to patients and were introduced by the patients. All patients completed a standard questionnaire and interview, with weight and height measured under standard conditions. 

The associations of obesity with clotting factor levels were studied to investigate possible mechanisms. Obesity (BMI >/=30 kg/m(2)) increased the risk of thrombosis twofold (CI95: 1.5 to 3.4), adjusted for age and sex. Obese individuals had higher levels of factor VIII and factor IX, but not of fibrinogen. The effect on risk of obesity was not changed after adjustment for coagulation factors levels (fibrinogen, F VIII, F IX, D-dimer). The relative risk estimates were similar in different age groups and in both sexes, indicating a larger absolute effect in older age groups. 

Evaluation of the combined effect of obesity and oral contraceptive pills among women aged 15-45 revealed that oral contraceptives further increased the effect of obesity on the risk of thrombosis, leading to 10-fold increased risk amongst women with a BMI greater than 25 kg/m(2) who used oral contraceptives. Obesity is a risk factor for deep vein thrombosis. Among women with a BMI greater than 25 kg/m(2) the synergistic effect with oral contraceptives should be considered when prescribing these.

http://www.ncbi.nlm.nih.gov/pubmed/12624633

Obesity and birth control pills both affect the blood.  They increase the risk of clots, due to hypercoagulation.   They slow cerebral blood flow and increase white matter abnormalities. This is a vascular connection worth exploring!

There is another well-known condition that is increased in obese women and women on birth control pills.  Idiopathic intracranial hypertension--
This condition occurs when cerebrospinal fluid pressure becomes increased in the brain.  This can cause headaches, visual problems, and tinnitus.  It affects cerebral perfusion, and is related to hyper coagulation.
http://www.ncbi.nlm.nih.gov/pubmed/12878984

And some researchers have found connections in patients with both demyelination and IIH-

Three patients with IIH and MS
http://content.lib.utah.edu/cdm/ref/collection/jno/id/81
One patient with MS and IIH
https://www.webmedcentral.com/article_view/2544
IIH and transverse myelitis
http://journals.lww.com/jneuro-ophthalmology/Fulltext/2004/12000/Intracranial_Hypertension_Associated_With.14.aspx
IIH and inflammatory demylinating polyneuropathy
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC504474/

MS researchers need to remove their blinders and consider how cardiovascular health is affecting the brain.  Why does smoking worsen MS and increase progression?  Why does exercise improve MS progression and symptoms?  Why is obesity linked to MS susceptibility?  Why do transfats worsen MS?   All of these environmental factors are linked to endothelial dysfunction.   If researchers continue to focus on the immune system exclusively, they miss an incredible opportunity in understanding the complete aetiology of this disease.  

Surely, if lay people can see this connection--it should be obvious to them.
Joan

What's blood got to do with it?

Nov. 27, 2012  10:17 AM

NIH researchers find that fibrinogen appears to be "the trigger" which begins neurodegeneration in MS.

http://www.nih.gov/news/health/nov2012/ninds-27.htm

Researchers are honing in on fibrinogen as a mediator in vascular disease, and they are also finding a link in MS.

Fibrinogen is always present in the blood.  The normal range is 200 - 400 milligrams per deciliter (mg/dL).

Fibrinogen is a protein which is made in our livers.  It's the signaling protein for fibrin, which allows our blood to clot.  When people develop venous ulcers on their legs, due to chronic venous insufficiency, it's fibrinogen that leaks from the veins and creates a build up of fibrin, depleting the tissue of oxygen and allowing those hallmark ulcers to form.  This is called a "fibrin cuff."  It's fibrinogen which initiates the coagulation cascade and causes our blood to thicken, as a response to low oxygen levels.

Dr. Zamboni was the first to suggest that MS lesions looked a lot like venous ulcers because of the fibrin cuffs found in both sites of injury.  

 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1633548/

And researchers have noted that fibin deposition comes FIRST, before demyelination.

Here is some recent research on this connection:

Compromised vasculature in the nervous tissue is a pathogenic manifestation apparent in traumatic injuries, such as spinal cord, optic nerve, and sciatic nerve injury, as well as in central nervous system (CNS) diseases with autoimmune characteristics, such as multiple sclerosis (MS) (7). 

Blood-brain barrier (BBB) disruption precedes clinical symptoms in MS patients (8), and fibrin is deposited in the lesions (9, 10), apparently before cerebral tissue injury and demyelination (11). Fibrin deposition also coincides with areas of demyelination (12), as well as with areas of axonal damage.

http://www.pnas.org/content/101/17/6698.full

CCSVI treatment: a lifetime commitment

May 31, 2010 at 8:01am

I think there is a disconnect happening in the MS community approaching CCSVI treatment, and it's worrisome. There is a sense that someone can be treated with venoplasty for CCSVI, come home, and be done with their problem. This couldn't be further from the truth--and I just want to put out another warning.

I've written about Jeff's multiple visits to Stanford for follow-up (three times, now) as well as his working with his GP and neurologist to keep tabs on his blood numbers and other symptoms. There is a need for patients to stay local and work with doctors in their area, which I sadly realize is just not possible for all. But it goes beyond this.

Patients need to look at lifestyle, medical regimen, diet and exercise-- as if they were recovering heart attack or stroke patients. Just as a heart patient is sent home after angioplasty and stenting with a new low fat diet, exercise regimen, blood thinning regimen and program for healthy living, CCSVI patients have to consider the same factors. Heart patients have ongoing relationships with their cardiovascular doctors--it should be the same with CCSVI.

We've seen patients' blood numbers return to hypercoagulated states after they decide to discontinue blood thinning regimens on their own. Patients have no access to medical follow-up after returning home, no blood monitoring or after care. And this scares me.

Please--if you are traveling to another country, at the very least have a relationship with a local doctor BEFORE you leave. Someone who can check your blood numbers (INR and PT testing-which measure coagulation), listen to your heart, monitor blood pressure and your veins, watch your rehabilitation and look out for complications (like clotting). It can be another vascular doctor, your GP or your neurologist. But make sure you have this in place before you go anywhere. And if you can stay close to home, PLEASE try to do this first.

So much has happened in the year since Jeff's first procedure. He has stayed on his supplements, exercise and lifestyle program, he is keeping those veins flowing, but it hasn't been a breeze.  This isn't a one time deal. It is a lifetime commitment to a new vascular reality. OK?

More than anything, I hope for treatment for all MS patients suffering with CCSVI--but I want you all to have follow-up care, too.

Joan