Insulin--Could This Be the Key?

If it's on your mind and it has to do with multiple sclerosis in any way, post it here.

Postby jimmylegs » Wed Dec 05, 2007 8:46 am

oh dear LC, i hear u about the tray. i have this carry-case of jars, and a giant-size weekly pill box. what a chore!

so that sounds like you are getting that bedtime magnesium separately from a D3 by a few hours? if so good, that's what i was hoping you do. :)

had any levels tested lately? i went for a barrage of tests on friday, still waiting for them to get through it all.
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On supplements

Postby lyndacarol » Wed Dec 05, 2007 5:55 pm

JL, to your question
bedtime magnesium separately from a D3 by a few hours?
, the answer is yes.

I have had no testing recently; I have had other things going on. Friday I'll have a renal CT scan looking for kidney stones or remnants. About 10 days ago I had what I'm sure was a kidney stone attack. I've NEVER had such pain!!! May you never suffer such a time!

When life settles back to normal, maybe after the holidays, I'll think about other testing.
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Postby jimmylegs » Wed Dec 05, 2007 7:07 pm

oh my, kidney stones are NO fun, i hope you recover really quickly!!!
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Fetuin A and "Insulin Activity"

Postby Shayk » Wed Jan 02, 2008 6:39 pm

Lynda Carol

I sure hope you're fully recovered by now. Happy New Year to you and everyone.

I’ve come across more info about “Fetuin A”. It's a potential disease marker for MS and guess what, among other things it regulates “insulin activity”—or so they say.

Here’s a power point presentation on the topic: Disease Activity Markers by N.R. Donelan of the MS Research Center of New York.

Here’s more info on it from the October 2007 ANA meeting (pdf file) Fetuin A is a Possible Marker of Disease Activity in MS Rammal, et al, MS Research Center of New York. (Fairly technical)

And lastly, while I haven’t learned how to link directly to the abstract itself from the Society for Neuroscience 2007 Meeting there’s more info. If you type Fetuin A and Multiple Sclerosis in the search function a link to the abstract they presented there should be accessible. As “Purkinje cells” might be important to people with MS I found this quote from that abstract interesting:
In non-plaque areas, the most notable immunostaining for Fetuin-A was seen in the Purkinje cells of the cerebellum in MS brains, a finding not seen in normal brains.

I think finding a difference between people with so called "normal" brains and people with MS and in areas outside of lesions may be noteworthy. Unfortunately, I don't have a clue as to how "fetuin A" might actually regulate the activity of insulin, but onward and upward in 2008.

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Seasonal variation

Postby lyndacarol » Wed Feb 13, 2008 5:38 pm

I have been reading my favorite book, Good Calories, Bad Calories by Gary Taubes, again. New ideas stick with me with each reading. This time: What if the following quote somehow explains the gradient observation (MS is more prevalent the farther from the equator--with some blatant exceptions!)?

I have doubted the vitamin D angle ever since I took 8000IU daily for a year with no observable changes (except continued deterioration) in MS. By the way, I continue to take 6000IU every day.

When researchers have measured seasonal variations in insulin levels in humans, they have invariably reported that insulin is highest in late fall and early winter -- twice as high, according to one 1984 study -- and lowest in late spring and early summer.


Perhaps this is tied to amount of sunlight. More insulin with less sunlight (i.e., fall and winter); less insulin with more sunlight--nearer the equator. Hmmm....
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Postby jimmylegs » Wed Feb 13, 2008 6:00 pm

will reiterate that vitamin d is not supposed to repair damage. i don't imagine it's doing any damage and i would think you are getting the appropriate things monitored over time, but if you continue to deteriorate there's also something else going on, obviously. like me, i can take d all i want but it never did anything for my b-vitamin deficiencies, it doesn't help my current zinc deficiency symptoms, and it wasn't helping my throat problems (but magnesium did) and it won't help the numbness in my hands (which turns out to be carpal tunnel syndrome). so my problems appear to be general malnutrition, i don't know what yours are but vitamin d is likely only one of many factors for many people with many different illnesses, not a cure-all for everyone.
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"...turmeric increasing levels of blood insulin."

Postby lyndacarol » Thu Oct 30, 2008 6:14 pm

Many of you will remember that I believe that excess insulin is involved in MS--initially by damaging the inside wall of the blood vessels (and thus causing the burning sensation in my feet and legs!). My insulin levels have been measured, found to be moderately high, and remain high despite my attempts for years (!) to reduce them with a VERY low-carb diet.

You can't imagine my surprise when I read on page 262 of the November 2008 issue of Better Homes and Gardens magazine:
Numerous studies in Asia have demonstrated that compounds in turmeric can lead to a decrease in blood glucose, while increasing levels of blood insulin.

I have been taking turmeric for decades! I am stopping it today! I never saw any improvements while taking it; with the insulin hypothesis, it may have been just the WRONG thing!

Can anyone help me find these "numerous studies in Asia" which have info on turmeric and blood insulin?
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Postby Terry » Thu Oct 30, 2008 6:33 pm

Wow, LC,
One of my worst fears...that I will take something that actually makes this worse!
Hope someone finds the articles for you.
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Postby gibbledygook » Fri Oct 31, 2008 1:51 am

Here's something that says it's good for diabetes:
1: Endocrinology. 2008 Jul;149(7):3549-58. Epub 2008 Apr 10. Links
Dietary curcumin significantly improves obesity-associated inflammation and diabetes in mouse models of diabesity.Weisberg SP, Leibel R, Tortoriello DV.
Russ Berrie Medical Science Pavilion, Diabetes and Endocrinology Research Center, Columbia University Medical Center, 1150 St. Nicholas Avenue, New York, NY 10032, USA.

Obesity is a major risk factor for the development of type 2 diabetes, and both conditions are now recognized to possess significant inflammatory components underlying their pathophysiologies. We tested the hypothesis that the plant polyphenolic compound curcumin, which is known to exert potent antiinflammatory and antioxidant effects, would ameliorate diabetes and inflammation in murine models of insulin-resistant obesity. We found that dietary curcumin admixture ameliorated diabetes in high-fat diet-induced obese and leptin-deficient ob/ob male C57BL/6J mice as determined by glucose and insulin tolerance testing and hemoglobin A1c percentages. Curcumin treatment also significantly reduced macrophage infiltration of white adipose tissue, increased adipose tissue adiponectin production, and decreased hepatic nuclear factor-kappaB activity, hepatomegaly, and markers of hepatic inflammation. We therefore conclude that orally ingested curcumin reverses many of the inflammatory and metabolic derangements associated with obesity and improves glycemic control in mouse models of type 2 diabetes. This or related compounds warrant further investigation as novel adjunctive therapies for type 2 diabetes in man.

PMID: 18403477 [PubMed - indexed for MEDLINE]
link

and here it increases insulin in plasma of db/db mice. Is that non-diabetic or diabetic?!
1: Mol Nutr Food Res. 2008 Sep;52(9):995-1004. Links
Effect of curcumin supplementation on blood glucose, plasma insulin, and glucose homeostasis related enzyme activities in diabetic db/db mice.Seo KI, Choi MS, Jung UJ, Kim HJ, Yeo J, Jeon SM, Lee MK.
Department of Food and Nutrition, Sunchon National University, Jeonnam, Republic of Korea.

We investigated the effect of curcumin on insulin resistance and glucose homeostasis in male C57BL/KsJ-db/db mice and their age-matched lean non-diabetic db/+ mice. Both db/+ and db/db mice were fed with or without curcumin (0.02%, wt/wt) for 6 wks. Curcumin significantly lowered blood glucose and HbA 1c levels, and it suppressed body weight loss in db/db mice. Curcumin improved homeostasis model assessment of insulin resistance and glucose tolerance, and elevated the plasma insulin level in db/db mice. Hepatic glucokinase activity was significantly higher in the curcumin-supplemented db/db group than in the db/db group, whereas glucose-6-phosphatase and phosphoenolpyruvate carboxykinase activities were significantly lower. In db/db mice, curcumin significantly lowered the hepatic activities of fatty acid synthase, beta-oxidation, 3-hydroxy-3-methylglutaryl coenzyme reductase, and acyl-CoA: cholesterol acyltransferase. Curcumin significantly lowered plasma free fatty acid, cholesterol, and triglyceride concentrations and increased the hepatic glycogen and skeletal muscle lipoprotein lipase in db/db mice. Curcumin normalized erythrocyte and hepatic antioxidant enzyme activities (superoxide dismutase, catalase, gluthathione peroxidase) in db/db mice that resulted in a significant reduction in lipid peroxidation. However, curcumin showed no effect on the blood glucose, plasma insulin, and glucose regulating enzyme activities in db/+ mice. These results suggest that curcumin seemed to be a potential glucose-lowering agent and antioxidant in type 2 diabetic db/db mice, but had no affect in non-diabetic db/+ mice.

PMID: 18398869 [PubMed - in process]
link

db/db is diabetic:
1: Kidney Int. 2008 Oct 29. [Epub ahead of print]
Inhibition of C-jun N-terminal kinase improves insulin sensitivity but worsens albuminuria in experimental diabetes.Ijaz A, Tejada T, Catanuto P, Xia X, Elliot SJ, Lenz O, Jauregui A, Saenz MO, Molano RD, Pileggi A, Ricordi C, Fornoni A.
[1] 1Division of Nephrology and Hypertension, University of Miami Miller School of Medicine, Miami, Florida, USA [2] 2Diabetes Research Institute, University of Miami Miller School of Medicine, Miami, Florida, USA.

C-jun N-terminal kinase (JNK) regulates both the development of insulin resistance and inflammation. Podocytes of the widely used db/db mouse model of diabetic nephropathy lose their ability to respond to insulin as albuminuria develops, in comparison to control db/+ mice. Here we tested whether JNK inhibition or its gene deletion would prevent albuminuria in experimental diabetes. Phosphorylated/total JNK was significantly increased in vivo in glomeruli of db/db compared to db/+ mice. Treatment of podocytes isolated from these two strains of mice with tumor necrosis factor-alpha caused greater phosphorylation of JNK in those obtained from diabetic animals. When db/db mice were treated with a cell-permeable TAT-JNK inhibitor peptide, their insulin sensitivity and glycemia significantly improved compared to controls. We induced diabetes in JNK1 knockout mice with streptozotocin and found that they had significantly better insulin sensitivity compared to diabetic wild-type or JNK2 knockout mice. Albuminuria was, however, worse in all mice treated with the JNK inhibitor and in diabetic JNK2 knockout mice compared to controls. Nephrin expression was also reduced in JNK inhibitor-treated mice compared to controls. A similar degree of mesangial expansion was found in all diabetic mice. Our study shows that targeting JNK to improve systemic insulin sensitivity does not necessarily prevent diabetic nephropathy.Kidney International advance online publication, 29 October 2008; doi:10.1038/ki.2008.559.

PMID: 18971923 [PubMed - as supplied by publisher]
link

I must say that curcumin has helped me in high dosages. I could FEEL the positive reduction in inflammation when I started taking it in high dose just after my last relapse so I find it hard to believe it is bad for MS.

LyndaCarol, I must say I am beginning to wonder about insulin too particularly because of the kidney link. I believe the kidney, the endothelium and adrenal system are all interlinked. Perhaps connected to insulin.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Growth factor is a component of insulin

Postby lyndacarol » Sun Nov 16, 2008 9:28 am

There has been a commonly accepted notion that insulin growth factor (and, therefore, insulin) increases myelination. This idea was expressed in the winter 2008 issue of Momentum that arrived yesterday.

The article (pg. 67) went on to say on the second page,"...team led by Stephane Genoud, PhD (The Salk Institute, LaJolla, Calif.), injected it [growth factor IGF-1] into mice with EAE. The injections actually worsened the disease."

Here is the abstract of that work:

1: J Neuroimmunol. 2005 Nov;168(1-2):40-5. Epub 2005 Aug 24. Links
Targeted expression of IGF-1 in the central nervous system fails to protect mice from experimental autoimmune encephalomyelitis.Genoud S, Maricic I, Kumar V, Gage FH.
Laboratory of Genetics, The Salk Institute, 10010 N Torrey Pines Rd, La Jolla, CA 92037, USA.

Insulin-like growth factor 1 (IGF-1) has been identified as a critical molecule in the induction of myelination in the central nervous system (CNS). Systemic injection of IGF-1 has been shown to have a varied and transiently protective effect on the clinical course of experimental autoimmune encephalomyelitis (EAE). Since systemic IGF-1 can also modulate peripheral immune lymphocytes, we examined whether a sustained and local delivery of IGF-1 into the spinal cord would have any influence on the chronic course of EAE in C57/BL6 mice. The capability of adeno-associated virus (AAV) to be retrogradely transported efficiently from muscle to motor neurons of the spinal cord was used to overcome the difficulty routinely encountered when attempting chronic delivery of molecules into the CNS. We demonstrate that AAV-mediated delivery of IGF-1 in CNS did not have any beneficial effect on the clinical course of EAE. Injection of AAV-IGF1 after induction of the disease worsened the clinical symptoms. Furthermore, CNS expression of IGF-1 did not affect the pathogenic anti-MOG T cell response, as examined by proliferation and cytokine secretion. Thus, enhanced expression of IGF-1 in the CNS during inflammation does not have a significant effect on myelination. These data have important implications for the potential use of IGF-1 in the treatment of multiple sclerosis.

PMID: 16120466 [PubMed - indexed for MEDLINE]



I think further research in this area will find increased insulin actually decreases myelin! (Of course I would, wouldn't I?)
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Postby DIM » Sun Nov 16, 2008 10:03 am

Lynda since my wife diagnosed with MS we try to have our dinner early at 7-8am and she never eats carbohydrates hours before sleep - only proteins and vegetables - carbs tend to decrease IGF and reduce remyelination.
This is known years ago and from what I know GABA (gamma aminobutyric acid) a non essential amino acid when taken at high doses, say 2gr before sleep increases myelination and improves sleep.
This is good even for healthy people also as reduces cell aging.
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Postby cheerleader » Sun Nov 16, 2008 10:21 am

Morning Lynda Carol...
We're inside today, avoiding breathing the smokey, particulate air!
In my research on endothelial dysfunction, I've read about insulin and insulin resistance quite a bit. There is a vicious cycle that begins with autoimmune diseases, where nitric oxide is increased to allow for glucose uptake. NO becomes imbalanced with endothelial growth factor which decreases blood flow and leads to vascular problems, and in MS- a break in the blood/brain barrier.

I truly believe that addressing healing at the level of the endothelium is an answer to halting this cycle. Here's one of many studies which links insulin sensitivity to endothelial dysfunction.

"Metabolic actions of insulin to promote glucose disposal are augmented by vascular actions of insulin in endothelium to stimulate production of the vasodilator nitric oxide (NO). Indeed, NO-dependent increases in blood flow to skeletal muscle account for 25% to 40% of the increase in glucose uptake in response to insulin stimulation.

Metabolic insulin resistance is characterized by pathway-specific impairment in phosphatidylinositol 3-kinase-dependent signaling, which in endothelium may cause imbalance between production of NO and secretion of endothelin-1, leading to decreased blood flow, which worsens insulin resistance. Therapeutic interventions in animal models and human studies have demonstrated that improving endothelial function ameliorates insulin resistance, whereas improving insulin sensitivity ameliorates endothelial dysfunction. Taken together, cellular, physiological, clinical, and epidemiological studies strongly support a reciprocal relationship between endothelial dysfunction and insulin resistance that helps to link cardiovascular and metabolic diseases."
http://www.ncbi.nlm.nih.gov/pubmed/16618833

You are so right about diet and insulin resistance, LC! Although I also believe vit. D, antioxidants, proteolytic enzymes and natural vasodilators also need to be part of the equation. Thanks for keeping the insulin dialogue going.
AC
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dx dual jugular vein stenosis (CCSVI) 4/09
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Re: Growth factor is a component of insulin

Postby CureOrBust » Mon Nov 17, 2008 3:02 am

lyndacarol wrote:... insulin growth factor (and, therefore, insulin) increases myelination...
Isn't that a stretch? I remember looking for the link previously, and didn't find any text that made the same connection / leap between the two. I think the Wiki says IGF-1 can bind to some similar things insulin can (nice and general when you don't know what your talking about :) ), but not that insulin acts in anyway like IGF?
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Re: Insulin--Could this be the key?

Postby NHE » Mon Nov 17, 2008 6:01 am

The capability of adeno-associated virus (AAV) to be retrogradely transported efficiently from muscle to motor neurons of the spinal cord was used to overcome the difficulty routinely encountered when attempting chronic delivery of molecules into the CNS.

This just strikes me as odd. These researchers injected a virus into the CNS to carry IGF-1 into the CNS so that they could study a CNS demyelinating disease. I haven't looked at the full paper yet but I hope that their control group had the virus alone and showed no ill effects. Otherwise, without such a control, the results would be inconclusive.

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To answer Cure

Postby lyndacarol » Mon Nov 17, 2008 5:28 pm

I don't know how to answer you, Cure. Growth factor is a component of insulin. They are in essence the same thing. If there are cells or substances that IGF (Insulin Growth Factor) will bind to, the growth factor in insulin will do the same. I do not believe the growth factor should act any differently if it is pure and concentrated from how it acts when in insulin.
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