Hyperlipidemia prolongs ALS survival by 1 year

[eml256]

Hyperlipidemia prolongs ALS survival by 1 year
Neurology 2008

*http://www.lipidsonline.org/news/article.cfm?aid=5876

MedWire News: Hyperlipidemia is associated with a significantly lower
risk for death in patients with amyotrophic lateral sclerosis (ALS),
highlighting the caution that must be exercised when implementing
lipid-lowering interventions in these patients, claim researchers.

[Biologist]

I am wondering if Henry Lorin, author or "Alzheimer's Solved," has seen this paper. It is entirely consistent with his research on lipids (e.g., cholesterol) and Alzheimer's.

I'm also wondering how DEB is doing. We have not heard from her in some time. I'm not sure that's good news. I hope you are doing OK, DEB.

The following may be interesting for some, particularly regarding acceptable cholesterol levels. My mother was concerned about her levels now being at 325. I am not. Older people (75) need more cholesterol because they live longer with higher levels. I got both of my parents off statins some time ago, neither ever should have been on them. No heart risk factors at all. Mom now has Fibromyalgia, a classic statin effect, for Phama to treat. This is from page 172. I have included some of my comments in between his sentences to follow. Here goes:

"Lastly, let's review the main points of this section.

Eating cholesterol does not give you blood cholesterol levels high enough to cause heart disease.

(My note here: A biochemical feedback system in the body cuts off intestinal absorption of cholesterol when you have absorbed enough. When you have enough, your body does not need to spend the energy and resources to make its own. Does this mean you could take 200 mg of Lipitor a day and still have the exact amount of cholesterol levels your body wants if you eat enough eggs. No, you would not survive the Lipitor, but if you did, your cholesterol levels would be just where your body wants them to be.)

Eating carbohydrates (starches) CAN lead to blood cholesterol levels that are very high. Body fat may increase. Diabeties may develop.

(My note: This is entirely consistent with Gary Taubes' excellent book "Good Calories, Bad Calories." But if you ate right, what would that do to Pharma Profits? We would have to bail them out too, right? I Googled his name just now to see if I was spelling it right and found this link which I will read after this post, others may also be interested:

(*http://www.pbs.org/wgbh/pages/frontline/shows/diet/interviews/taubes.html)

Average, healthy cholesterol levels vary widely from person to person and between countires.

Atherosclerosis and heart attacks occur at all ranges of blood cholesterol levels.

There is evidence that shows that blood cholesterol levels must remain well over 350 mg/dl before a consistent relationship to atherosclerosis formation develops. At 500 mg/dl and above, as in cases of a rare genetic disease called familial hypercholesterolemia, heart disease will almost always occure. Below the 350 level, however, there is no definite relationship between blood cholesterol levels and atherosclerosis, except where other factors are involved."

(My comments: I theorize that a major part of familial hypercholesterolemia cases involve inadequate downward regulation of the mevalonate pathway. So there is "too much" of all products from the pathway including CoQ10 and others, which is entirely inconsequential except for the cholesterol. Therefore, lowering cholesterol with HMG CoA Reductase Inhibitors make sense for this group. For most other people, taking statins is asinine unless you also supplement dolichols, heme a, CoQ10, etc., which are also cut off by chopping down the mevalonate tree. Unfortunately, of course, those are not "supplemented" when statins are prescribed. And that turns out to be good for Pharma profits -- more disease states to treat.)

Biologist

[cjbrooksjc]

B: Interesting write-up. Thanks for the link.

Brooks

[carbuffmom]

Hi Biologist,

I am still hanging in there. I am still progressing. The weakness has spread to my right leg. I am back in PT and OT. I have continued with the supplements. The neuro put me in a trial using lithium carbbonate. Of couse, I had an adverse reaction---depression. I have come back from that and now am just praying for a cure.

Glad to hear that a lot of you are doing better. I plan to be more active on the forum. I did get a letter from State Rep. Bart Stupak that the FDA concluded there was no correlation between statins and ALS. Go figure!

Take care, DEB

[Ray Holder]

Hi Biologist

Is not the cause of familial hypercholesterol the absence, partial, or total, of the gene responsible for bringing about absorbsion of LDL cholesterol? and normally produced levels cannot be disposed of. Cholestipol, ezetimibe and similar drugs have been used to try to clear this, but seem to cause more problems than they cure.

Ray

[Biologist]

I am glad you liked it, Brooks. I did too. It is good to hear unbiased scientific voices about these issues. Wonder how many doctors would believe or even consider what Lorin says the science actually says regarding the 350 mg/dl minimum "threshold" for treatment. Many or most might angerly dismiss it. Hard to even consider the possibility that one has been badly bamboosled, damaged patients and wasted valuable and limited medical resource dollars. What a monumental mess we have!

Good to hear from you, DEB. I personally have no faith in the FDA. They are a political organization now. There are certainly some excellent scientists there, its just that they do not make the decissions and have no voice. They are threatened, punished and banished if they speak the truth. I have seen and read various accounts of this.

Ray, I have little specific knowledge about FH and its etiology. It is on my list to explore in coming months. What you write is probably just right. High powered microscopes would even be able to visually detect the presence or absence of LDL receptors on the cell surface, and genetic analysis would be able to show differences in the individual genomes for coding of LDL receptors, it would seem to me. It is also possible that the issue is the appropriate intallation of existing cellular LDL receptors withing the cell membrane when needed. In other words, the proteins themselves might exist, they are just not appropriately expressed in the membrane at appropriate times. I recently learned of this concept of the same LDL receptors being put in position in the membrane and then being stored inside the cell when not needed. If they simply have no receptors at all, that would be very interesting in understanding how they compensate for the loss. Cholesterol would have to all come from (i.e., be manufactored in) the cell itself with no (or inadequate) access to systemic delivery from the blood. At the same time, HMG CoA Reductase Inhibitors, to my current knowledge, also work inside the cell -- and therefore that molecule (e.g., a statin) must cross the membrane barrier to prevent production there. On the other hand, it might just be that the entry of the inhibitor is through the same receptor; no receptors, no entry, and therefore the cell can survive with adequate cholesterol, a vital constituent of cells. Thanks for posting the info.

BTW, I use my left calf muscle to determine when I need more carnitine. When if hurts, it's time for more. Carnitine qualifies as the MVP find of the decade in my book.

Harley, you have no doubt as to the efficacy of NADH. For those who may question whether it is biologically active or not (regardless of whether it is helpful or not for that individual), I have an experiment they can perform. Drink a cup of coffee on an empty stomach, take a sublingual 20 mg dose, and wait 30 minutes. It made a believer out of me. In my case, this was way too much. I felt odd. But it let me know that the stuff is real and the idea is to get the dosage right. I am now working on the dosage issue and believe that NADH may be a valuable part of my regime. The five mg range is probably right. I will stick with the sublingual. My spell checker is down, so forgive the typos.

Biologist

[Brian C.]

Hmm. I tried 10mg sublingual NADH for a while with no noticeable effect. I'm now swallowing 20mg chlorophyll-coated NADH but still no effect.

Should I be adding coffee?
My Natrol Maximum Strength packaging boasts "Caffeine Free!"


Brian.

[Biologist]

Brian, I could never be sure swallowing the coated table did anything for me. Using two sublingual Nutraceutical Science Institute pills at 10 mg each on an empty stomach and with a cup of strong coffee made me feel like I had too much adrenaline in my system. The "fight or flight" syndrome. BTW, that system is getting better for me since two years ago, but a flash of anger or fear use to backfire and make me less able to deal with the situation. It made me weak and shakey rather than energized. It was an overload situation. That was a bit like the sensation I had with the experiment. I may try it again before long too make sure it was real. I have done it twice with similar results. Be sure that you let the table completely disolve and do NOT swallow any of it. It must all diffuse into your mouth membranes Spelling warning is still in effect for my posts...

Biologist

[Biologist]

Brian, the coffee was happenstance the first time. The second time, weeks later, I did it on purpose to see if I could replicate the "experiment." You probably should try it with coffee just to see if you can detect an effect. Why it may make the difference, I am not sure.

Biologist

[Brian C.]

Hmm, I love coffee but I have become extraordinarily sensitive to caffeine finding that one medium americano drunk around 10:30 am keeps me awake that night! I have to ask for decaf :(

I think I shall next try TWO sublingual 10mg lozenges and steer clear of the coffee.


Brian.

[Biologist]

And I may give your cafeine diet a try. Interesting!

I have never been a very good sleeper, but have drank full strength coffee all my life -- including as a kid. I think I was the only kid at boyscout camp that was allowed to drink it and that would have been at 11 years old where I was an old hand at it by that time. I may have been a bit hyperactive and it was believed to be a cure. I think my parents believed it was because they encouraged it (probably as recommended to them from doctors -- and probably good advice). And I have also been a substandard sleeper since as long as I can remember. So I will try it. I was sleeping a bit better when I was forced to give it up for months two years ago. It made me feel real weird at the height of my acute statin/doxycycline trauma. The withdrawal was probably nothing compared to what I was going through at the time. (On my agenda now, among other things, is to get the word out about that combination -- along with heavy aerobic exercise during that time period.)

I was never a heavy smoker, but a regular one for years (which helped justify my being placed on statins). The nicotine may have served some similar purpose. It is a muscle relaxer at the same time being a central nervous system stimulant -- a very unique combination of drug actions for a single molecule. I no longer smoke at all, but am still addicted to nicotine and get it by other means. But here's the point: when I completely quit smoking about four years ago, my long-standing case of post nasal drip just evaporated. The smoking was the cause period. I had suspected it in prior years, but not enough to quit cigarettes completely long enough to realize that that was the problem. So, who knows, you may have found the answer for some of my sleeping issues. Ambien has too many side effects, so I do not use it any more. After the withdrawal from caffeine, I may sleep better. May try that before long. Thanks for the idea.

Biologist

[Brian C.]

Hope it works for you Biologist and without unpleasant withdrawal symptoms.


Brian.