This Is MS Multiple Sclerosis Knowledge & Support Community

Hi Annesse,

Would mind linking this back to your original post on protease and DNase 1 as a refresher please?

Regards

Hi Scott~Yes, I thought you are might be wondering what I was going for here. My next post will be on the connection to COPD, homocysteine and diabetes. I am trying to show the damage homocysteine can cause in all of the blood vessels, including of course the brain. Plus, the common denominators that all of these diseases share.

All of these diseases have been found to be deficient in vitamin B12. Lack of B12 will lead to elevated levels of homocysteine. All of these diseases also have elevated homocysteine. B12 is only found attached to dietary animal proteins. Protease break down proteins and studies show that protease are "essential" for the binding and transport of vitamin B12.

As an example, I could just say that I believe the white matter lesions in MS were caused by lack of B12, but who would have believed me. By showing that all of these diseases lack B12 and all of these diseases have white matter lesions, it becomes more evident that they are connected. And of course posting studies that show white matter lesions are caused by a lack of B12 doesn't hurt. Hopefully, by showing the damage homocysteine is doing to the vascular system in all of these diseases, it will be evident that homocysteine is linked to the venous insufficiency in MS.

In the following study, researchers found that those with COPD were nearly twice as likely to develop type 2 diabetes as those without COPD. The researchers suggest that inflammation may explain this association. They state, "Inflammation plays a key role in chronic obsructive pulmonary disease (COPD) and asthma. Increasing evidence points toward a role of inflammation in the pathogenesis of type 2 diabetes." Homocysteine is the powerful inflammatory component that both COPD and type 2 diabetes share.

http://www.ncbi.nlm.nih.gov/pubmed/15451919

The following study, published in the Annals of Internal Medicine, concluded that, “In this large cohort of patients with type 2 diabetes, plasma homocysteine was a strong and independent risk factor for CHD (coronary heart disease) events,” (Soinio, 2004).

Elevated Plasma Homocysteine Level Is an Independent Predictor of Coronary Heart Disease Events in Patients with Type 2 Diabetes Mellitus

Background: High plasma homocysteine level has been associated with increased risk for coronary heart disease (CHD) events in nondiabetic individuals, especially in those with previously diagnosed CHD. In persons with type 2 diabetes mellitus, the association between homocysteine level and cardiovascular disease may be stronger than that in nondiabetic individuals, but no large prospective studies have examined the relationship between homocysteine level and CHD mortality in persons with type 2 diabetes.

Objective: To investigate whether moderately elevated plasma homocysteine levels are independently related to increased incidence of fatal and nonfatal CHD events in persons with type 2 diabetes.

Setting: Finnish sample of patients with type 2 diabetes.
Patients: 462 men and 368 women who were 45 to 64 years of age at baseline.

Conclusions: In this large cohort of patients with type 2 diabetes, plasma homocysteine level was a strong and independent risk factor for CHD events.

In the following study of 65 patients with type 2 diabetes, elevated levels of homocysteine were found to be independently associated with the prevalence of peripheral neuropathy. The authors suggested that this association could be explained either by direct cytotoxic effects on nerve function, or by small vessel occlusions caused by endothelial damage. This results in a loss of blood supply to nerve fibers, a pathogenetic mechanism of peripheral neuropathy.

Relation Between Homocysteinaemia and Diabetic Neuropathy in Patients with Type 2 Diabetes Mellitus
Ambrosch, A., J. Dierkes, R. Lobmann, W. Kühne, W. König, C. Luley, H. Lehnert. 2001.
Diabet Med. 18(3):185-92.

Conclusion: The data indicate that homocysteine is independently associated with the prevalence of diabetic neuropathy in a collective of Type 2 diabetic patients. A larger, prospective study would be desirable to clarify the role of homocysteine in the pathogenesis of diabetic neuropathy.

Wow! Great information. When is your new book coming out?

Hi Monte~It is available on Amazon, but out of the sellers listed, we are the only ones that have the 2nd edition.

Thanks to Leonard, most everyone here is aware of the association between MS and diabetes. One aspect of diabetes we would still need to explain is insulin resistance.

Insulin resistance is a fundamental aspect of type 2 diabetes. When cells become resistant to insulin, the pancreas responds by producing more insulin. If the pancreas can't produce enough insulin, or the resistance goes up, then blood sugar levels will rise and diabetes will result. We have previously discussed the fact that insulin is made from amino acids that come from the break down of dietary proteins. If even one amino acid is missing, the body will not be able to produce insulin. Therefore, the inability to properly digest proteins would lead to a lack of insulin. The inability to digest proteins would also lead to a lack of vitamin B12, which has been discovered in diabetes. The lack of vitamin B12 would then lead to elevated levels of homocysteine. And finally, homocysteine will lead to insulin resistance, as the following study shows.

http://care.diabetesjournals.org/content/24/8/1403.full

Homocysteine is also associated with narrowing of the arteries or stenosis. Here is some information from Life Extension Magazine.

Another study published in Lancet came to the same conclusion after studying 107 middle-aged British men who participated in a 2-year investigation. The authors concluded that "these findings suggest that homocysteine is a strong and independent risk factor for stroke." It has even been reported that the level of homocysteine in blood correlates with the thickness of arteries. And it was reported in the Journal of Nutrition that men with levels of homocysteine above 14 µmol/L had a greater than 50% chance of stenosis in an extracranial carotid artery, whereas men with levels below 9.1 µmol/L only had a 27% incidence of stenosis. (The data for women were slightly different. Women with levels of homocysteine greater than 14.3 µmol/L had a 39% chance of having carotid artery stenosis: below 9.1 µmol/L, their chances were about even with men.

Here is an additional study that confirms the association between homocysteine and extracranial carotid-artery stenosis.

http://www.ncbi.nlm.nih.gov/pubmed/7816063

If you were a Rat I could recommend to you something that would be real good!!

Pterostilbene

Diabetes

'Similar to what has been discovered with the drug metformin, pterostilbene has been shown to lower blood glucose levels in rats by as much as 56 percent, while simultaneously raising insulin and hemoglobin levels to near normal levels.[10]"

http://en.wikipedia.org/wiki/Pterostilbene

http://www.vitaminshoppe.com/store/en/b ... ku=JF-7342


jackD

Heat intolerance would be another symptom we would need to account for. We have shown that nitric oxide is being dysregulated due to a lack of vitamin B12. Homocysteine also interferes with nitric oxide. Here is some information from our book on the connection to nitric oxide and heat intolerance.

"Nitric Oxide may also play a role in the intolerance to heat that many autoimmune patients suffer with. In a study published in Neurology, researchers from the Netherlands and Russia monitored 10 people with multiple sclerosis that had heat induced fatigue (Beenakker, 2001). The patients were cooled with special clothing and a sharp decrease in levels of fatigue was reported. But, the researchers noted, inner body temperatures did not drop during the experiment. This was to be expected they said, considering the body’s mechanisms for keeping core temperatures stable.

Instead, they pointed to nitric oxide levels, which dropped in the patients who had been cooled. The following study showed that nitric oxide does indeed play a role in the control of body temperature.

Nitric Oxide and Body Temperature Control
Gerstberger, R. 1999. News Physiol Sci 14(1):30-6.
Abstract: Pharmacological studies of thermoregulatory effector and neuronal responses indicate that nitric oxide (NO) may have differential roles in the control of body temperature and during fever. Histochemical analysis of site-specific changes in NO synthase activity in defined states of thermal stimulation appears a promising approach to unravel the underlying hypothalamic neuronal cytoarchitecture.

Hi Annesse,

Have you looked at Taurine? I'd be most interested in the impact on Glycosis and nuclear receptors.

Regards

Hi Scott1~No, sorry. I have made some additional connections though. I have been making posts on a cancer forum about the connection to autoimmune disease and cancer. Here is a link. http://www.cancerforums.net/threads/234 ... ne-Disease

One of the new connections I have made to MS, autoimmune disease and cancer is the Kynurenine Pathway.
The majority of dietary tryptophan is oxidized through the kynurenine pathway. Due to elevated tumor necrosis factor, tryptophan is being rapidly degraded and producing toxic metabolites, such as indoleamine 2,3 dioxygenase (IDO) and quinolinic acid.

Here is what the authors of the study entitled "Involvement of kynurenine pathway in neuroinflammation and diabetes" say about these metabolites.
"There is accumulating evidence that the excitotoxin quinolinic acid is involved in the neurotoxicity associated with several inflammatory brain diseases such as Alzheimer's disease, Parkinson's disease, motor neuron diseases, multiple sclerosis and major psychiatric disorders. We also recently found that the kynurenine pathway is dysregulated in diabetes."

In the study entitled "Possible roles of excess tryptophan metabolites in cancer" the researchers stated that these metabolites,"produced bladder cancer when implanted in the bladder."

In the study entitled "Indoleamine 2,3 dioxygenase and quinolinic acid immunoreativity in Alzheimer's disease hippocampus" the researchers state, "This acid kills nerve cells in the brain, leading to brain dysfunction and ultimately death." The researchers found that all of the brains of Alzheimer's patients showed quinolinic acid neurotoxicity."


Here is a study that shows the kynurenine pathway is also involved in MS.

http://onlinelibrary.wiley.com/doi/10.1 ... x/abstract

I really need to revive this thread. I strongly believe that I am suffering from B12 malabsorption.

Brief History
Crohn's Disease since late 80's
Resection of terminal ileum '91
B12 shots every 5-6 weeks until
MS diagnosis in 2003- B12 shots every 3-4 weeks for the next 5years
SPMS diagnosis 2010
Needing more often until present when I now take every 2-3 days.

My serum B12 levels are off the charts, but I have dramatic increase in fatigue if I fail to take. My gasterenterologist thinks I'm nuts . . . .

I had a Schilling's Test 6-7 years ago but it came back negative. I've since read that this test has fallen out of favour. I understand that the methylmonic acid test is the standard now. I hope Annesse is around to comment! If indeed I have malabsorption issues, I wonder how my problem might be solved.

Annesse wrote:Hi Monte~It is available on Amazon, but out of the sellers listed, we are the only ones that have the 2nd edition.

Thanks to Leonard, most everyone here is aware of the association between MS and diabetes. One aspect of diabetes we would still need to explain is insulin resistance.

Insulin resistance is a fundamental aspect of type 2 diabetes. When cells become resistant to insulin, the pancreas responds by producing more insulin. If the pancreas can't produce enough insulin, or the resistance goes up, then blood sugar levels will rise and diabetes will result. We have previously discussed the fact that insulin is made from amino acids that come from the break down of dietary proteins. If even one amino acid is missing, the body will not be able to produce insulin. Therefore, the inability to properly digest proteins would lead to a lack of insulin. The inability to digest proteins would also lead to a lack of vitamin B12, which has been discovered in diabetes. The lack of vitamin B12 would then lead to elevated levels of homocysteine. And finally, homocysteine will lead to insulin resistance, as the following study shows.

http://care.diabetesjournals.org/content/24/8/1403.full

This thread is not without its merits; contains good links..
I am convinced that the cause of the distorted metabolism is in the gut, and that a healthy gut flora will restore metabolic control..
The type 2 diabetes relationship would suggest that type 2 diabetes medication could be of use for us..
I am convinced it is of use..
see also the last 4-5 pages of http://www.thisisms.com/forum/general-d ... 15188.html

I'm drowning in great info! Could someone direct me to a link for Annesse's book? Also, I invite people to comment on my above post.

Thanks, PN

Hi PN,

Can you convert your brief history into a long history? In particular, can tell us how you medicate if you do and what other test results you have. Annesse, Jimmy Legs and others, including me, will all have different perspectives so the more we know the better the discuusion will be.

Regards

Lets keep this thread alive. Where is Annesse ?