Insulin--Could This Be the Key?

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lyndacarol
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"...turmeric increasing levels of blood insulin."

Post by lyndacarol »

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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Post by Terry »

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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Post by gibbledygook »

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]
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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

Post by lyndacarol »

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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Post by DIM »

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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Post by cheerleader »

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.
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Re: Growth factor is a component of insulin

Post by CureOrBust »

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?

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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

Post by lyndacarol »

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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Post by cheerleader »

I thought IGF-1 was the "signaling factor" for insulin's cellular transmission and that it's different from insulin.... but I could be wrong.

Folks have tried to use IGF-1 to repair myelin before, but it's hard to get it past the BBB, so they used a virus as a transport mechanism in Lynda's study mentioned above. And the IGF-1 didn't do anything.

Here's a study from the Netherlands where they injected IGF into MSers..notice it states IGF is a growth factor that "should" provide signals to repair MS lesions....but it didn't.

Insulin-like growth factor (IGF)-1 is a growth factor that should provide the appropriate signals to promote repair of MS lesions, because it acts as a survival factor for cells of the oligodendrocyte lineage and stimulates myelin synthesis. In a pilot study on MS patients, no detectable remyelinating effects in the CNS were observed following subcutaneous administration of IGF-1. A number of reasons might explain a lack of beneficial effects: a) it is unlikely that subcutaneous administration of IGF-1 provides sufficient passage across the blood-brain-barrier and into the CNS, b) the biological actions of IGF-1 are tightly regulated by several insulin-like growth factor binding proteins (IGFBPs), which become upregulated in the demyelinated lesions and may prevent access of IGF-1 to its receptor, c) IGF-1 not only acts on oligodendrocytes, but also stimulates the proliferation of astrocytes, which form the glial scar that impedes repair processes.
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Re: To answer Cure

Post by CureOrBust »

lyndacarol wrote:Growth factor is a component of insulin.
That does not make it the same. Many people have warm milk to help them sleep, and others have warm milk in their coffee, but a coffee is very different to a glass of warm milk.
lyndacarol wrote:They are in essence the same thing.
With diabetics injecting insulin every day, why are there studies on the effects of specific IGF-1? I think its because they are very different, and I have yet to read any scientific study saying they are in effect the same. I explicitly read effects for IGF-1, that are not suggested for "plain old" insulin. and I have also read how IGF-1 is different to the other IGF's (ie IGF-2, IGF-3 etc)
lyndacarol wrote:If there are cells or substances that IGF (Insulin Growth Factor) will bind to, the growth factor in insulin will do the same.
But IGF-1 will bind to components that insulin will not.
lyndacarol wrote:I do not believe the growth factor should act any differently if it is pure and concentrated from how it acts when in insulin.
but all the studies treat IGF-1 very differently to insulin, and I have yet to read the exact same effects for insulin, that are seen with IGF-1. A pure and concentrated component of something is not the same as what it is derived from. :?
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Post by DIM »

IGF isn't the same as insulin, the first promotes myelination the second (from what have read) does the opossite!
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One effect of IGF-1

Post by lyndacarol »

I do not mean to usurp a book recommendation from Sharon (Shayk); but I think The MS Solution: How I Solved the Puzzle of My Multiple Sclerosis by Kathryn R. Simpson, M.S. has important information for us--including about insulin, which is also a hormone. I import a post here from another forum because of this insulin connection:

"Sharon (Shayk) is absolutuly right when she said, Quote:
I've been reading more about thryoid issues lately and I do think it wouldn't hurt to ask your GP about it again. End quote.
This is something I intend to do after reading the book The MS Solution by Kathryn R. Simpson.

Overall, the book has good ideas, especially about checking hormone and vitamin/mineral levels. I take exception to her statement on IGF-1 on pages 141-142. Quote:
Growth hormone production is highest at puberty and declines progressively after age 21. Made in your pituitary, it stimulates bone and organ growth. It causes increased production and release of a substance called insulin-like growth factor 1 (IGF-1), which travels to target tissues such as bones, organs, and muscles to trigger growth and repair. It has also been shown to promote growth of myelin and nerves. End quote.


I prefer to believe the research reported in the recent Winter 08-09 issue of Momentum, publication of the NMSS (I am generally skeptical of this group and its projects), which addressed this idea with the following:

"The growth factor IGF-1 had shown some success in promoting myelin formation, so a Society-funded team led by Stephane Genoud, PhD (The Salk Institute, La Jolla, Calif.), injected it into mice with EAE. The injections actually WORSENED the disease. (Journal of Neuroimmunology 2005; 168:40-5) Such failures are important to pinpoint before they affect people with MS in clinical trials."

Here is the abstract of the work mentioned:

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

It's another one of those areas that deserves more examination!"

I felt these ideas needed to be with this forum--even if repeating the abstract, so I can find them again easily. I lose things so often! How do you folks keep track of things here?!!!
Last edited by lyndacarol on Sun Oct 25, 2009 11:57 am, edited 1 time in total.
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Post by jimmylegs »

LC you probably have known this forever but you can filter the search by individual posts instead of topic and it's waaaay easier to find your own stuff. still a touch confusing when you start getting into the results but yea.
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Still trying to reduce insulin level

Post by lyndacarol »

I am still trying to reduce my insulin level, so I found the episode of "60 Minutes" shown on Sunday, May 24, 2009, especially interesting because of this comment at the end of the segment on resveratrol:
Convinced that they were on the right path, they fast-tracked the drug into human trials on people with untreated diabetes. The results were impressive: it significantly lowered glucose and insulin levels, without the patients changing their diet or taking any other drugs.
To view or read the entire segment see:http://www.cbsnews.com/stories/2009/01/ ... 2082.shtml
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