This Is MS Multiple Sclerosis Knowledge & Support Community

On March 28, 2007 Reuters reported "Type 2 diabetes may raise Parkinson's risk: study"

You'll have to find it on their website, http://today.reuters.com

"All rights reserved" etc.

Insulin keeps popping up all over. This concerns a study done by Dr. Gang Hu et al. at the National Public Health Institute in Helsinki (Hello, finn?).

You can substitute "Hyperinsulinemia" for "Type 2 diabetes." People are confused by the name similarity, but Type 1 and Type 2 are two completely different things: Type 1--the body produces NO insulin; Type 2--the insulin produced is ineffective, and is usually produced in excess.

Interesting study! Thanks for sharing it, lyndacarol.

Btw, here's its abstract.

-finn

Lynda Carol--a couple of abstracts for you to ponder.

You wrote:

You can substitute "Hyperinsulinemia" for "Type 2 diabetes."

Here's a studyabout DHEA that suggests it has the potential to reduce fasting plasma insulin levels in some women.

Fasting plasma insulin and glucagon were lower with DHEA.....
suggesting that DHEA replacement could have a potential impact in preventing type 2 diabetes.

Now I know you'd never consider taking DHEA without having your DHEA level checked first to determine if it is in fact low and if it is, what dose the physician might recommend to bring it into the normal range.

And, here's a study that highlights some neuroprotective properties of one of the "diabetes" drugs, pioglitazone, that is in trial for MS (I think). This study was in spinal cord injury.

Thiazolidinedione class of peroxisome proliferator-activated receptor gamma agonists prevents neuronal damage, motor dysfunction, myelin loss, neuropathic pain, and inflammation after spinal cord injury in adult rats

Both pioglitazone and rosiglitazone... significantly decreased the lesion size (by 57 to 68%, p < 0.05), motor neuron loss (by 3- to 10-fold, p < 0.05), myelin loss (by 66 to 75%, p < 0.05), astrogliosis (by 46 to 61%, p < 0.05), and microglial activation (by 59 to 78%, p < 0.05) after SCI.

You just never know what will turn up.

Sharon

I need more time to think on the DHEA post. It is intriguing!

To the pioglitazone (commercial drug: Actos)--Yes, there is a study of it and MS being conducted by Dr. Douglas Feinstein of the University of Illinois at Chicago. He learned of one woman whose MS improved greatly while taking the drug.

On that basis, I asked to try Actos and did for a couple months. I saw no changes and stopped. Since that time I have read about another in that same family of Thiazolidinediones, Rezulin (active ingredient is Troglitazone).

This drug is metabolized in the liver and requires a healthy liver detoxification system. It is contra-indicated for pregnant or breast feeding women. It may render oral contraceptives ineffective.

This drug received fast-track approval by the FDA; it was tied to at least 33 deaths; it has now been recalled from the American marketplace because of its link to liver cancer. Rezulin has been removed from the British market.

If I had known this, I would not have tried Actos. Now, maybe Actos is safer--I don't know. One must always consider the risk vs. benefit.

I still think that insulin is the villain; I am still using diet to try to bring down my insulin level (There must be SOMETHING to Ivy Larson's experience with The Gold Coast Cure!), but no luck yet. At least it is safe and VERY healthy!

I admit that this thread has gotten unmanageably large and I no longer know what I have posted here. I have used it to work my way through my thoughts.

Perhaps I have already posted this information. If so, I apologize for repeating; if not, I encourage you to read (or even print the 20+ pages of) the transcript of Dr. Ron Rosedale's talk: http://bodye.com/insulin1.htm

"Insulin and Its Metabolic Effects"

presented at Designs for Health's BoulderFest in August 1999 Seminar.

It appears on more than 50 other sites on the Internet. Given my belief in hyperinsulinemia's involvement in MS, I think this could be very important in tying together diet, hormones, HPA axis, magnesium....LOTS of our suspicions.

In the past several months there have been questions about the precise conditions for the fasting serum insulin test. The most recent (and complete) information I have comes from the book, Protein Power by Michael Eades, M.D. and Mary Dan Eades, M.D. (page 53-54):

Serum Insulin
The handling of this test is very important. The specimen should be kept frozen and the test completed within 24 hours of the blood draw. Be sure that the test is performed by a national reference laboratory, such as Smith-Kline, Roche Biomedical, or Nichols, or by a research laboratory accustomed to doing this test. Results can vary widely -- even from the same specimen -- if it's not handled properly. Remember that even though most laboratories will set values of over 25 to 30 as abnormally high, the "normal" samples include many people with insulin resistance who have not yet developed diabetes. General clinical evaluation of insulin levels as a marker for disease is still in its infancy. In our clinic, as in many research settings, we use the fasting insulin normal values of healthy young people as the standard against which we should measure ourselves. If your insulin reading is over 10 mU/ml you can consider yourself to have developed some degree of insulin resistance. The more over 10 your reading, the greater your disturbance. With 10 as the upper end of normal, a reading of 25 would mean that it's taking 2 1/2 times the normal amount of insulin to control blood sugar at its current level. A reading of 48 would mean it's taking over 4 1/2 times more insulin to keep blood sugar at its current level. If your insulin reading is high, repeat the test at eight weeks and at eight-week intervals thereafter during your intervention regimen until normal.

I find much valuable information even in this, my second reading of this book, and I recommend it to all you. I have begun to follow their regimen more faithfully in an attempt to lower my insulin levels. Wish me luck!!!

Both type 1 and 2 diabetes mellitus (T1DM and T2DM) have marked defect in glucose utilization.
For the brain it is a badly negative situation, because brain restoration/healing heavily depends on glucose, but glucose must be utilized, means, enter the cell, only then it will work.
Even insulin pump used for fast blood glucose correction in some T1DM patients couldn't control this defect of glucose utilization, not even speaking of T2DM correction with other kind of drugs which is even more inadequate.

Stay skinny, eat proper food, don't drink alcohol, and exercise in moderation - all that will reduce your chances for T2DM remarkably.
In a case if you have T1DM - try to control it as much as you can, it would be a tough life for you (with lot of restrictions and obligatory things to do), but it worse it.

Kind regards,
Tony

TJ--Please explain to me how your statement:
"For the brain it is a badly negative situation, because brain restoration/healing heavily depends on glucose, but glucose must be utilized, means, enter the cell, only then it will work." fits with Dr. Rosedale's comment: "Your brain will burn sugar, though it doesn't have to, by burning by-products of fat metabolism called ketones. That is what it has to burn when you fast for any length of time. It has been shown that if your brain was really good at burning ketones from fat that you can get enough sugar from eating 100 percent fat.

You can make a little bit of sugar out of the glycerol molecule of fat. Take two glycerol molecules and you have a molecule of glucose. Two triglycerides will give you a molecule of glucose. The brain can actually exist without a whole lot of sugar, contrary to popular belief."

The statements seem completely opposite--brain depends on glucose; brain uses ketones or the glycerol molecule of fat (Especially his last sentence.).

Please understand that I am not a scientist.

It is nothing wrong with not being a scientist , don’t even worry about that.

Please don’t take Dr. Rosedale seriously; he is from ‘snake oil’ guys.
If MD could say the statement like this: “Blood vessels constrict, glucose and insulin can't get to the tissues…” - stay away.
Let me explain the situation with glucose and the brain in this way.
Brain cells are highly specialized cells. Because of their narrow high specialization they lack (relatively) some components or chemical machinery to do things which are possible for more simple cells.
Extreme vulnerability of brain cells, esp. neurons, is a part of the deal; the price of being so high specialized. There is no way for brain cell to use ketones or modify fat for energetic purpose. Ketones are highly toxic and cause the brain tissue damage, irreversible by the way.
Among brain cells, only astrocytes have some reasonable storage of energy (glycogen) as some kind of energetic ‘back-up’ (for 15 min. max), but it mostly used for catastrophic events, but for second-to-second brain maintenance. Other cells used glucose only from constantly running supply, and if the supply interrupts, then start of their structural changes begins within couple of minutes (!). Turnover of glucose is so fast that there is no even time for converting fat (on site, if it would be even possible) to usable glucose.
Brain loves glucose, it tolerates it well up to 1000 (!), in vitro of course, the point is: more (usable) glucose – faster recovering brain.

Kind regards,
Tony

Given my focus on hyperinsulinemia, I was especially drawn to the line, "increase blood insulin in response to glucose."

From Fats that Heal Fats that Kill by Udo Erasmus (pages 111-112):

"A Silver Spring, Maryland researcher (Mary Enig, Trans-Fatty Acids in the Food Supply: a comprehensive report covering 60 years of research, 1993) has researched, followed, and summarized others' research on the effects of trans-fatty acids for many years. Research from Harvard (Willet, 1994) and other institutions show that besides interfering with EFA functions, raising total cholesterol and lowering the 'good' HDL, inhibiting conversions of EFAs to their derivatives, and worsening essential fatty acid deficiency, trans-fatty acids also:
- raise Lp(a), a strong risk factor in human atherosclerosis;
- lower the efficiency of B cell response and increase proliferation of T cells (B and T cells are involved in immune funtions);
- decrease testosterone and increase abnormal sperm (in animals);
- interfere with pregnancy;
- correlate with low birth weight in humans;
- lower the quality of breast milk and decrease volume of cream;
- increase blood insulin in response to glucose;
- decrease insulin response (undesirable for diabetics);
- alter the activities of a liver enzyme system that metabolizes carcinogens and toxins (mixed function oxidase cytochromes P-448/450);
- alter membrane transport and fluidity;
- alter the size, number, and fatty acid composition of adipose (fat) cells;
- increase peroxisomal activity; and
- interact with fish oil and tissue w3s.
Since trans-fatty acids have detrimental effects on our cardiovascular system, immune system, reproductive system, energy metabolism, fat and essential fatty acid metabolism, liver function, and cell membranes, we should consider margarines, shortenings, shortening oils, and partially hydrogenated vegetable oils to be harmful to human health!"

Mary Enig, the expert on diets and fats, was behind the push to get trans fats out of the food system. She has for years recommended that we eat unprocessed coconut oil, butter and olive oil.

Big companies have been playing a game with the FDA for years so that they could buy time in getting the hydrogenated fats out of their products.

Even now if you look at the ingredients on the side panels of food, it may show no trans fats, but further down in the list of ingredients, partially hydrogenated oil will show up. The per serving ratio can be made so low that the trans fats are below the 1g level and then the companies don't have to declare it in the fat count.

The FDA knows that these fats are artery blockers and killers, but did not until the past few years come up with guidelines to get the fats out of the system and I believe that Mary Enig was the one that made it happen

Why the FDA stalls on getting these killers out of the system is any one's guess.

gwa

gwa wrote:The per serving ratio can be made so low that the trans fats are below the 1g level and then the companies don't have to declare it in the fat count.

It was my understanding that trans fat had to be below 0.5 g per serving in order to be counted as "0" g on the label. Please see this link for more information.

As a result of this ruling, I have noticed a general trend where the "serving size" has shrunk. On one box of crackers it was about 4 crackers that made up one serving. I think that very few people actually eat just 4 crackers at a time...

NHE

NHE,

You are right about the 0.5g count. I should have looked the figure up instead of trying to remember the accurate number.

The serving size is definitely shrinking. It must be easier to shrink the size than to remove the trans fats.

gwa

This is a good day for thinking. Although I have posted this analogy in another thread, it seems to fit here, too:

"My own analogy of MS is like being locked in a room lined with shelves filled with boxes of keys. The key to the door and freedom is in one of those boxes! But researchers have been looking in the wrong box for 60 years (the one labeled "autoimmune" or "neurology.")

My own opinion is that they need to be looking in the box labeled "neuro-endocrine." HOW do we get them to try keys from a different box???"

Now today, when reconsidering my situation, I have more questions: My first neurological tests showed no evidence of MS--my first three MRIs reported NO lesions (In fact, my first neuro said categorically that I did not have MS. Doctors at the Mayo Clinic in Rochester, MN, said the same.); the visual evoked responses were normal; the first EMG was normal. But the abnormal sensations were there! Why were the doctors looking in the "neurology box?"

The paresthesia in my legs and feet could be the same experienced by diabetics, couldn't it? Those with peripheral vascular disease (PVD), specifically peripheral artery disease (PAD), have the same sensations, I believe. In fact, PAD involves various aneurysms (someone mentioned that on this site), even leg weakness, and other symptoms shared by MS.

Insulin damages the lining of blood vessels (endothelium); it also thickens smooth muscles (these surround the blood vessels, bladder, too). Couldn't these effects be responsible for MS difficulties? In my case, it seems logical that the source of my problem is closer to the "vascular box," or the "muscular problem box," or even the "insulin (endocrinology) box!!!" Has anyone had these checked and ruled out?

This would seem to explain why diet improves MS for many--diets that are reducing glucose in the blood stream, and consequently the insulin level, that is.

And a newpaper article reported just this week that scientists have found a genetic basis for the condition of "jimmy legs" (a term that came from a Seinfeld episode--news to me, since I have not watched the TV program Seinfeld!). Has anyone ever looked at excess insulin as a cause of that???

So many questions and no answers--such frustration!!

Although I first mentioned Good Calories, Bad Calories by Gary Taubes in the Reading Nook, it has become my favorite book and I think it has relevance to many conditions and to many hypotheses held at this site.

I think it will be the most important book concerning health to be published in the last century!

Of course, I think the author's chapters on insulin have direct bearing on the insulin hypothesis for MS, although he never mentioned that disease.

The book is obviously well-researched and well-written. It is filled with information! It gives new insight into how research has been done and how results which contradict the preconceptions of the researcher often have been ignored.

I was especially interested in the details of the 1928 experiment when Vilhjalmur Stefansson and Karsten Anderson lived with the Inuit to settle the meat diet controversy. They lived exclusively on meat and fat--NO carbohydrates. "The Inuit considered vegetables and fruit not proper human food." (p. 320)

Please recall that carbohydrates convert to glucose and thus stimulate insulin secretion. Also please recall that MS has been nonexistent among the Eskimos and this has contradicted the generally accepted conventional wisdom of the "north-south gradient."