Insulin--Could This Be the Key?

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Re: Insulin--Could This Be the Key?

Postby lyndacarol » Wed Feb 06, 2013 6:49 pm

Linda – I expect your neurologist will NOT order the insulin test for you – this kind of test is not in his area of expertise. I think your GP or an endocrinologist is more likely to order it. It is one of the least expensive blood tests.

I have not succeeded in decreasing my insulin level; there is no medication to lower the level; there is no "excess insulin therapy"; diet is the only recognized method for reducing the insulin level – nothing has worked for me. I take no MS drugs; I have used many supplements for many years with no change. I follow a very healthy diet – extremely low carb, no processed sugar, no caffeine, etc. I am now reading about anti-inflammatory diet and will try that next.
My hypothesis: excess insulin (hyperinsulinemia) plays a major role in MS, as developed in my initial post: http://www.thisisms.com/forum/general-discussion-f1/topic1878.html "Insulin – Could This Be the Key?"
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Re: Insulin--Could This Be the Key?

Postby Anonymoose » Thu Feb 21, 2013 5:52 pm

Lyndacarol,
Have you tried hibiscus tea for your insulin resistance?
http://naturalmedicinejournal.com/artic ... rticle=215
Hibiscus extract was also studied in 222 patients—some with and some without metabolic syndrome (MS).35 A total daily dose of 100 mg H. sabdariffa extract powder (HSEP) was given for 1 month to men and women, 150 without MS and 72 with MS. Participants were randomly assigned to a preventive diet, HSEP treatment or diet combined with HSEP treatment. The MS patients receiving HSEP had significantly reduced glucose, total cholesterol and LDLc and increased HDLc. A triglyceride lowering effect was seen in all groups but was only significant in the control group that was treated with diet. The triglyceride/HDL-c ratio was also significantly reduced with HSEP in the control and MS groups, indicating an improvement in insulin resistance. It has been hypothesized that the anthocyanins regulate adipocyte function, which has important implications for both preventing and treating metabolic syndrome.
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Re: Insulin--Could This Be the Key?

Postby lyndacarol » Thu Feb 21, 2013 7:01 pm

Thank you for this information, Anonymoose. I have not tried hibiscus tea, but it is on the grocery list now; I will be trying it soon. Thanks again.
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Re: Insulin--Could This Be the Key?

Postby ljelome » Fri Apr 26, 2013 4:31 am

Dear lyndacarol,
Fyi, i just got my fasting insulin level tested. It was 6.14 mikroU/mL and my fasting blood glucose was 95 mg/dL.
Would like to hear from you.
Thank u.

Regards,
Linda
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Re: Insulin--Could This Be the Key?

Postby jimmylegs » Fri Apr 26, 2013 8:18 am

hi lj, sorry to jump in on you LC but I happened to be on..

refer to general-discussion-f1/topic1878.html and you can find LC's posted optimal range for fasting insulin: (4-7)

elevated glucose could be another indicator of insufficient zinc.

posting this study b/c it ties in poor zinc status and elevated glucose:

Maternal myo-inositol, glucose, and zinc status is associated with the risk of offspring with spina bifida
http://www.researchgate.net/publication ... 053d3c.pdf

(note that elevated RBC (erythrocyte) zinc is an indicator of overall zinc deficiency).
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Re: Insulin--Could This Be the Key?

Postby lyndacarol » Fri Apr 26, 2013 10:30 am

ljelome wrote:Fyi, i just got my fasting insulin level tested. It was 6.14 mikroU/mL and my fasting blood glucose was 95 mg/dL.
Would like to hear from you.
Thank u.

Regards,
Linda


http://www.mercola.com/nutritionplan/index2.html

Factor #1: Your Insulin Level
Insulin and leptin are absolutely essential to staying alive, but the sad fact is that most of you reading this have too much, and it is pushing you towards chronic degenerative illness and increasing the rate at which you age.

Most adults have about one gallon of blood in their bodies and are quite surprised to learn that in that gallon, there is only one teaspoon of sugar! You only need one teaspoon of sugar at all times -- if that. If your blood sugar level were to rise to one tablespoon of sugar you would quickly go into a hyperglycemic coma and die.

Your body works very hard to prevent this by producing insulin to keep your blood sugar at the appropriate level. Any meal or snack high in grain and sugar carbohydrates typically generates a rapid rise in blood glucose. To compensate for this your pancreas secretes insulin into your bloodstream, which lowers your blood sugar to keep you from dying.

However, if you consume a diet consistently high in sugar and grains, over time your body becomes "sensitized" to insulin and requires more and more of it to get the job done. Eventually, you become insulin and leptin resistant, and then diabetic.

If you have high cholesterol, high blood pressure, type 2 diabetes, or are overweight, it is highly likely that you are eating too many grains -- yes, even unrefined whole grains -- as this is the most common culprit causing your insulin level to become abnormal.

Compounding the problem, when your insulin and leptin levels rise due to an excess of carbohydrates, they send your body a hormonal message telling it to store fat while holding on to the fat that is already there. So not only will excess carbohydrates make you overweight, they will effectively hamper your weight loss efforts too.

Your Fasting Blood Insulin Test
To find out your insulin and leptin levels, you need to get tested by your doctor. The test you need to ask for is a fasting blood insulin and leptin test, The tests are done by just about every commercial laboratory and the insulin test is relatively inexpensive.

Facts about Your Fasting Insulin Test:
o This test is profoundly useful. It's one of the least expensive tests in traditional medicine, yet it is one of the most powerful. A normal fasting blood insulin level is below 5, but ideally you'll want to be below 3.
o You can safely ignore the reference ranges from the lab as they are based on "normals" of a population that has highly-disturbed insulin levels.
o This is a great test to do BEFORE you start your program as you can use it to assess how well you are progressing in the program.
o If your level is above 5 you will want to consider significantly reducing most sugars and grains, even whole wheat grains, until you lower your level. Once you've normalized your insulin level you can reintroduce grains into your diet at a lower level to optimize your health.
o Exercise is of enormous benefit in improving the sensitivity of your insulin and leptin receptors, and to help normalize your insulin level far more quickly.
My hypothesis: excess insulin (hyperinsulinemia) plays a major role in MS, as developed in my initial post: http://www.thisisms.com/forum/general-discussion-f1/topic1878.html "Insulin – Could This Be the Key?"
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Re: Insulin--Could This Be the Key?

Postby CureOrBust » Fri Apr 26, 2013 5:37 pm

a little (ok a lot) off topic, but I think this paper supplies a lot of good science in what happens to the body (and brain) during low glucose availability (ie during fasting)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292907/pdf/jcinvest00272-0077.pdf

Brain Metabolism during Fasting
Abstract.
Catheterization of cerebral vessels in three obese patients undergoing 5-6 wk of starvation demonstrated that /8-hydroxybutyrate and acetoacetate replaced glucose as the predominant fuel for brain metabolism. A strikingly low respiratory quotient was also observed, suggesting a carboxylation mechanism as a means of disposing of some of the carbon of the consumed substrates.
...snip...
Discussion:
Finally, our subjects failed to show any
deficit on psychometric testing, and electroencephalographic tracings remained unchanged, which suggests that the keto acids did fulfill the predominant energy requirement in a satisfactory fashion.
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Re: Insulin--Could This Be the Key?

Postby CureOrBust » Fri Apr 26, 2013 5:49 pm

lyndacarol wrote:I have not succeeded in decreasing my insulin level; there is no medication to lower the level; there is no "excess insulin therapy"; diet is the only recognized method for reducing the insulin level – nothing has worked for me.
OK, sorry if the following appears antagonistic (you know I mean no aggression :wink: ), however, if you have true conviction that lowering your insulin levels would improve (if not cure your MS) have you not tried total and complete fasting? and I am not talking a single day, and yes it should be performed under medical supervision :!: .
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Re: Insulin--Could This Be the Key?

Postby CureOrBust » Fri Apr 26, 2013 10:25 pm

Reversal of Behavioral and Metabolic Abnormalities, and Insulin Resistance Syndrome, by Dietary Restriction in
Mice Deficient in Brain-Derived Neurotrophic Factor

http://endo.endojournals.org/content/144/6/2446.full.pdf
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Re: Insulin--Could This Be the Key?

Postby lyndacarol » Sat Apr 27, 2013 1:40 pm

EXCELLENT information, CureOrBust! The first supports the idea I have read elsewhere: ketone bodies are a perfectly acceptable fuel source for the brain; in fact, I have read ketone bodies are the preferential fuel source for the brain.


CureOrBust wrote:
lyndacarol wrote:I have not succeeded in decreasing my insulin level; there is no medication to lower the level; there is no "excess insulin therapy"; diet is the only recognized method for reducing the insulin level – nothing has worked for me.
OK, sorry if the following appears antagonistic (you know I mean no aggression :wink: ), however, if you have true conviction that lowering your insulin levels would improve (if not cure your MS) have you not tried total and complete fasting? and I am not talking a single day, and yes it should be performed under medical supervision :!: .


AND, for those who may not understand the supportive relationship that CureOrBust and I have, I know that no aggression is intended by the question here. My answer? I have tried complete fasting (having only green tea or water) for a maximum of three days. It is NOT easy – I felt a little dizzy on the third day (because my physician told me that it takes three days to reduce insulin production). Despite your admonition, I did not inform my physician. I returned to regular eating immediately – possibly undoing any long-term improvement in my insulin level. I plan to try it again, but will progress to a ketogenic diet after fasting.

The recent documentary, "Eat, Fast and Live Longer", mentioned Mark Mattson, one of the authors of the Endocrinology Journal article you posted – thank you. I believe his work with insulin resistance syndrome/dietary restriction is extremely important! It spurs me on to try this approach more diligently.
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Re: Insulin--Could This Be the Key?

Postby CureOrBust » Sat Apr 27, 2013 7:02 pm

The documentary, "Eat, Fast and Live Longer" and a lot of the articles appear to attempt to reduce IGF-1 (Insulin like Growth Factor). One of the things that is hard to reconcile, is that I am sure I have read numerous articles that say IGF-1 is good for MS. How do you reconcile this contradiction?

eg: The insulin-like growth factor system in multiple sclerosis.
Abstract wrote:Multiple sclerosis (MS) is a chronic disorder of the central nervous system characterized by inflammation, demyelination, and axonal degeneration. Present therapeutic strategies for MS reduce inflammation and its destructive consequences, but are not effective in the progressive phase of the disease. There is a need for neuroprotective and restorative therapies in MS. Insulin-like growth factor-1 (IGF-1) is of considerable interest because it is not only a potent neuroprotective trophic factor but also a survival factor for cells of the oligodendrocyte lineage and possesses a potent myelinogenic capacity. However, the IGF system is complex and includes not only IGF-1 and IGF-2 and their receptors but also modulating IGF-binding proteins (IGFBPs), of which six have been identified. This chapter provides an overview of the role of the IGF system in the pathophysiology of MS, relevant findings in preclinical models, and discusses the possible use of IGF-1 as a therapeutic agent for MS.


IGF-1 May Give Hope to MS
Recent laboratory experiments on IGF-1 have demonstrated a stimulation of the protective sheath around nerves known as the myelin sheath. In degenerative diseases like multiple sclerosis and ALS or Lou Gehrig’s disease, damage around the sheath stops signals from being transmitted between the brain and nerves.

IGF-1 has been found to regrow these sheaths according to the University of Michigan scientists. Although several growth factors are currently being studied, IGF-1 appears to be most effective at inducing the growth of the sheath and preventing neuronal cell death according to chief researcher Hsin-Lin Cheng. Michigan scientists presented the first results from their experiments with IGF-1 at a conference in New Orleans. The scientists said they removed nerve cells called dorsal root nerves from newborn rats and grew them in a dish. They found that if they stimulated the conditions of diabetes in the dish and then applied the IGF-1 it helped the nerves remain normal.

Tests with IGF-1 are now underway on 40 people with neuropathy at the Mayo Clinic in Rochester, Minnesota. According to these researchers, IGF-1 may provide a new treatment for a whole group of diseases that have not heretofore been treatable.

Sure, the last one is from a whole website promoting IGF-1 :confused:
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Re: Insulin--Could This Be the Key?

Postby CureOrBust » Sat Apr 27, 2013 7:15 pm

PS If you search in google with the following, it should come up with the whole 58 min video on some "Vimeo" site as the first hit.

Google Search

The thing that really caught my attention was the interview with Mark Matteson, at around 46:35 to 46:53, where Mark Matteson's research (on mice) found that the fasting mice developed new neuron growth. :mrgreen:

[edit: may be due to it being based on http://www.google.com.AU]
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Re: Insulin--Could This Be the Key?

Postby NHE » Sun Apr 28, 2013 12:05 am

Your Google search didn't work for some reason. However, you can watch the video on PBS's site.

http://video.pbs.org/video/2363162206
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Re: Insulin--Could This Be the Key?

Postby lyndacarol » Sun Apr 28, 2013 10:39 am

CureOrBust wrote:The documentary, "Eat, Fast and Live Longer" and a lot of the articles appear to attempt to reduce IGF-1 (Insulin like Growth Factor). One of the things that is hard to reconcile, is that I am sure I have read numerous articles that say IGF-1 is good for MS. How do you reconcile this contradiction?

eg: The insulin-like growth factor system in multiple sclerosis.
Abstract wrote:Multiple sclerosis (MS) is a chronic disorder of the central nervous system characterized by inflammation, demyelination, and axonal degeneration. Present therapeutic strategies for MS reduce inflammation and its destructive consequences, but are not effective in the progressive phase of the disease. There is a need for neuroprotective and restorative therapies in MS. Insulin-like growth factor-1 (IGF-1) is of considerable interest because it is not only a potent neuroprotective trophic factor but also a survival factor for cells of the oligodendrocyte lineage and possesses a potent myelinogenic capacity. However, the IGF system is complex and includes not only IGF-1 and IGF-2 and their receptors but also modulating IGF-binding proteins (IGFBPs), of which six have been identified. This chapter provides an overview of the role of the IGF system in the pathophysiology of MS, relevant findings in preclinical models, and discusses the possible use of IGF-1 as a therapeutic agent for MS.


IGF-1 May Give Hope to MS
Recent laboratory experiments on IGF-1 have demonstrated a stimulation of the protective sheath around nerves known as the myelin sheath. In degenerative diseases like multiple sclerosis and ALS or Lou Gehrig’s disease, damage around the sheath stops signals from being transmitted between the brain and nerves.

IGF-1 has been found to regrow these sheaths according to the University of Michigan scientists. Although several growth factors are currently being studied, IGF-1 appears to be most effective at inducing the growth of the sheath and preventing neuronal cell death according to chief researcher Hsin-Lin Cheng. Michigan scientists presented the first results from their experiments with IGF-1 at a conference in New Orleans. The scientists said they removed nerve cells called dorsal root nerves from newborn rats and grew them in a dish. They found that if they stimulated the conditions of diabetes in the dish and then applied the IGF-1 it helped the nerves remain normal.

Tests with IGF-1 are now underway on 40 people with neuropathy at the Mayo Clinic in Rochester, Minnesota. According to these researchers, IGF-1 may provide a new treatment for a whole group of diseases that have not heretofore been treatable.

Sure, the last one is from a whole website promoting IGF-1 :confused:


I cannot reconcile the contradiction, but I can't discount this article in Momentum magazine (NMSS application). It belongs here for its mention that IGF-1 actually worsened MS:

This idea was expressed (page 67) in the Winter 08-09 issue of the MS Society publication named Momentum; it does refer to earlier "success in promoting myelin formation." Of course, that poor mouse! BUT which abstract fits people?…

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]

_________________

Fundamentally, I think the IGF-1 IS worsening people's MS. Does anyone have the results of the Mayo Clinic test of IGF-1 mentioned above: "Tests with IGF-1 are now underway on 40 people with neuropathy at the Mayo Clinic in Rochester, Minnesota."?
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Re: Insulin--Could This Be the Key?

Postby PointsNorth » Sun Apr 28, 2013 11:26 am

I've found that when I've missed a meal I get symptom improvement. I would like to try the feed/fast cycle. Maybe fast on Monday-Wed-Fri and feed the rest of the week?

Thx for the links NHE and lynda.
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