Top Ten Reasons To Take Inosine

Sunday, April 20th, 2008

Inosine Helps Repair DNAHave you heard the news?

A simple OTC (over-the-counter) dietary supplement may hold the key to slowing or even preventing the onset of Parkinson’s and other neurodegenerative diseases.

Parkinson’s is a devastating movement disorder that progresses as dopamine-producing neurons in the brain slowly die. In a recent study however, Parkinson’s patients with the highest uric acid levels, were the least likely to require prescription medication. No small feat when it comes to Parkinson’s disease.

But what does uric acid have to do with inosine?

Inosine is smack-dab in the middle of the metabolic pathway for the conversion of dietary purines (meat, nutritional yeast, certain vegetables) to uric acid. Supplemental inosine increases blood and cerebral spinal fluid levels of uric acid. While excess uric acid can cause gout in certain susceptible individuals, urate†, the physiologic form of uric acid is nothing but good news.

Here’s why:

1. Urate, (uric acid at normal blood pH) is a powerful antioxidant with more potency than vitamin C.
In fact, uric acid may very well represent a vitamin C substitute since humans are unable to synthesize ascorbic acid (vitamin C).

2. Intravenous inosine has neuroprotective and neuroregenerative properties. In fact, inosine is currently being investigated for the treatment of spinal cord injuries.

3. Inosine has anti-inflammatory and immunomodulating properties. You’ll remember that neuroinflammation is the hallmark of most neurodegenerative disorders.

4. Inosine reverses endothelial cell dysfunction. Endothelial cells line our blood vessels and regulate blood flow. Endothelial cell dysfunction is common in diabetics and people with heart disease and the metabolic syndrome. Overly reactive blood vessels will constrict when they should relax contributing to heart attack and stroke.

5. Because of it’s unique chemical structure, inosine possesses anti-arrhythmic (arrhythmia prevention) properties. Think atrial fibrillation, supraventricular tachycardia etc.

6. Inosine readily enters both cardiac and skeletal muscle ramping up ATP production and increasing the transfer of oxygen from red blood cells to heart and skeletal muscle.

7. One recent study concluded that: “inosine should be considered as a potential preventative therapy in humans susceptible to developing Type 1 diabetes and as a possible antirejection therapy for transplant recipients”.

8. In another study, inosine prevented the onset of colitis in an experimental form of the disease.

9. When mice were exposed to gamma radiation, inosine prevented oxidative damage to their DNA and dramatically decreased free-radical production.

10. Inosine protects against multiple environmental toxins such as chlorinated solvents, fluorocarbons and methylene chloride poisoning in particular.

†The Michael J. Fox Foundation announced a $5.6-million award to drive a Phase 2 clinical trial to investigate the potential of inosine — a naturally occurring chemical that gives rise to urate in the body — to slow or stop the progression of Parkinson’s disease.

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Your Waist Size NOW, Predicts Brain-Wasting Later: Here’s Why

Monday, April 14th, 2008

An Epidemic Of Abdominal ObesityThe power to predict disease is - well - powerful. And nothing is more powerful in scientific circles than a carefully constructed, decades long, longitudinal study.

In case you haven’t noticed, approximately fifty percent of adult Americans have abdominal obesity. “Abdominal” or “visceral” obesity is defined as a waist circumference greater than 102 cm for men (40 in.) and 88 cm (35 in.) for women. Your “viscera” (internal organs) now double as a convenient “dumping-ground” for fat. No surprise then, that researchers in Northern California were easily able to recruit 6,583 “apple-shaped”, middle-aged, men and women. Thirty-six years later, a whopping sixteen percent (1053 people) had developed dementia.

Apparently abdominal obesity at 40, doubles or triples your risk for dementia in your 70’s.

To put it into perspective, every-other vibrant, active, middle-aged person with belly fat that you see today, will reach retirement and be rewarded with difficulty remembering their own name.

But what is it about belly fat that ultimately leaves our brains battered and bewildered?

When fat is progressively packed around internal organs it literally takes on a life of it’s own. Adipocyte (fat cell) signaling becomes so strong that it becomes the dominant “endocrine” or hormone secreting organ in the body. Over time, insulin levels rise. Soon after, persistently elevated blood-sugars increase production of a very dangerous by-product of glucose metabolism known as Advanced Glycosylated End-products (AGE’s).

When diabetic patients undergo HbA1c testing, whether they know it or not, they are having their advanced glycosylated end-products measured. Levels greater than 6.1 are considered abnormal and require treatment. AGE’s are found within the plaque and neurofibrillary tangles of specially stained brain tissue of Alzheimer’s patients and directly contribute to neuronal damage.

These same autopsy studies suggest that damage occurs long before the symptoms of dementia arise.

So here’s what to do if you’re 40 and find yourself in that other 50 percent category:

1. Determine your waist circumference by wrapping a tape measure midway between the top or your pelvis and the bottom of your ribs (between the bony parts in other words)

2. Ask your doctor to measure a fasting blood-sugar (fasting means nothing to eat - not even juice - after midnight of the night before)

3. Levels greater than 109 mg/dl require further evaluation with HbA1c testing

4. Exercise, exercise, exercise (all the crunches in the world will not remove this fat - neither will liposuction)

5. If you have a low HDL (good) cholesterol and elevated triglycerides, consider having Apo-E testing performed as well

I’m here to help - so feel free to leave a comment if you have a [fat] burning question!

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Fatal Familial Insomnia: No Sleep And Then You Die

Friday, April 11th, 2008

Sominex Won\'t HelpOk, relax! You DON’T have this. Only forty maybe fifty families world-wide are affected by this rare, I mean really rare, autosomal dominant genetic disorder. Genes inherited in an autosomal dominant fashion mean that offspring have a 50/50 chance of chance of being stricken with the disease. With Fatal Familial Insomnia (FFI), once the genetic switch has been flipped (usually at midlife) there is no turning back, no cure and no treatment. Sleepless night inexorably follows sleepless night. Finally, five to nine months later the afflicted lapse into an irreversible coma and die - sweet release. Sedatives, sleeping pills only make it worse and hasten the inevitable. Sominex just doesn’t cut it.

So why bother. Why waste valuable research money on such an incredibly rare disease anyway?Because FFI is one of a handful of prion-mediated diseases. Prions are proteinaceous infectious particles lacking nucleic acid. Generally speaking prions break all the rules regarding biological life forms as we know it. Nevertheless, they exist and native forms are found naturally in the brains of all mammals. A mutant prion however will replicate unchecked, decimating the brain in process. The end result is a brain filled with holes, sponge-like (spongiform) and demented.

Other prion-mediated diseases you may have heard of include:

Bovine-Spongiform Encephalopathy (Mad Cow)
Creutzfeld-Jakob Disease
v-CJD (variant Creutzfeld-Jakob Disease)
Scrapie

All of the prion-mediated diseases are characterized by a rapid onset of dementia and death. Cows get it (Mad Cow), sheep get it (Scrapie), we get it, (CJD, FFI).

Still, all of the above are exceedingly rare diseases and soon new high-tech, silicon nano-sensors that change vibrational frequency when prions bind will be available to detect Mad Cow disease before it shows up at the local meat market.

As it turns out, understanding how rogue prions cause disease may be the key to understanding all neurodegenerative disorders.

Cholesterol metabolism within the brain is carefully regulated and with very good reason. Cholesterol synthesis exerts exquisite control over cell membrane function and cell signaling (cell-to-cell communication). When prions are allowed to replicate unchecked, cell membrane function suffers and as a result the enzyme phospholipase A2 becomes hyperactive. Activated phospholipase A2 triggers a flood of inflammatory mediators with the conversion of arachidonic acid to leukotrienes.

Bingo, presto (stir and mix over a life-time) add massive amounts of damage due to neuroinflammation and you have the makings of Alzheimer’s disease, Parkinson’s disease, Multiple Sclerosis and a whole host of other dementias and neurodegenerative disorders.

Don’t let all of this keep you awake at night though! Here (finally I know), is the take-home message…

Get your cholesterol checked. Ask for a VAP test to measure all the parameters of cholesterol synthesis. Ask your doctor to measure a simple bio-marker for inflammation called hs-CRP and with your doctor’s permission, take 81 mg of aspirin a day. Feast daily on antioxidant and polyphenol-rich foods , sleep tight, manage your stress, and when the silicon-based nano-sensors become available, I’ll let you know.

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