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Mitochondrial dysfunction

Powerhouse Vitamin Plays Role in Alzheimer’s Dementia Diagnosis

March 7, 2013 by James Bogash

As far as I’m concerned, the medical dementia research strongly points to an oxidative stress/mitochondrial dysfunction model of neurodegenerative disorders like Alzheimer’s dementia and Parkinson’s disease.  The idea that we really don’t have any idea what causes it is just not true.

The likely reason why mainstream medicine hasn’t accepted this model is because it puts much  of the responsibility smack dab in the middle of the patient’s lap.  Genetics play a role, but it’s likely a small one.  Lifestyle is key to both preventing and causing Alzheimer’s dementia.

Pivotal in prevention is protecting my favorite organelle, the mitochondria.  This little factory within each of our cells generate energy in the form of ATP.  (Are we dredging up bad memories from high school biology yet?)  Since brain cells require extremely high amounts of energy, the mitochondria are critical for your brain cells to function correctly.  Not enough energy in the brain cells and they begin to break down and, when things get bad enough, your brain cells commit suicide (a process called apoptosis).

Too many suicidal cells in the neocortex or hippocampal regions of your brain and you begin to develop what we call Alzheimer’s dementia.  Unfortunately, by the time symptoms are noticed, the condition has been progressing for decades and a very large chunk of the brain cells in this region are already dead.

So how can we protect our brain from this suicidal pathway?

In two ways.

The first is to stop abusing the mitochondria in our brain cells.  The list of items that damage our brain is quite long, but should not drop any jaws.  Here are a few of the more dangerous risks:

  • Stress
  • Chemicals in our environment
  • Prediabetes and diabetes

After you’ve cleaned up the mess, the next thing to focus on is aspects of lifestyle that are well know to protect the brain.  The general recommendations that I promote for all chronic diseases remains the same and can be found by clicking here.  Besides lifestyle, there are numerous supplements that have some pretty good support for protecting the brain.  These include:

  1. Vitamin D
  2. Choline
  3. Magnesium threonate

However, there is another strong player.  Vitamin E.

And not your normal, run of the mill, cheap vitamin E supplement.  Vitamin E is actually a combination of 8 different forms–4 tocopherols and 4 tocotrienols.  Nature provides us with these multiple forms of tocopherols and tocotrienols.  Any good supplemental form of vitamin E is going to have a this mix of all 8 forms. Giving high levels of just one form of vitamin E can actually drive down levels of other forms of vitamin E in the bloodstream.

Vitamin E, as a blend of all 8 forms, is very protective to our body, especially the heart and blood vessels.  And if you protect your blood vessels, you’re protecting your brain.

But just how protective is it??

You might want to sit down for this one, or if you’re driving, pull over (actually…you shouldn’t really be driving trying to read this anyway..).

Diagnosing Alzheimer’s using a MRI alone is not without its problems and faults.  Currently, it is not used as a sole measure to make the diagnosis.  In this particular study, researchers looked at what happened when they added blood levels of these 8 vitamin E forms to an MRI for differentiating Alzheimer’s dementia from cognitive impairment from normal brains.  Here’s what they found:

  • MRI and plasma vitamin E measures increased accuracy to 98.2% for differentiating Alzheimer’s dementia from normal brains.
  • For  telling mild cognitive impairment from normal brains, the accuracy was 90.7%.
  • In addition, also identified 85% of individuals with cognitive loss who converted to Alzheimer’s dementia at 1 year follow-up (Tweet this).

Basically, the serum levels of the vitamin E family made the MRI diagnosis far more powerful, especially when it came to predicting who was going to progress to full blown Alzheimer’s dementia.  Isn’t your brain worth a little vitamin E?  Plan on spending $15-20 / month.  Do NOT buy the cheap forms with only alpha tocopherol–it may make things worse.

Filed Under: Alzheimer's, Parkinson's, Vitamin E Tagged With: Alzheimer's Disease, Alzheimers dementia, Causes Alzheimer's, Cognitive Disorders, dementia, Dementia And Parkinson's, Dementia Diagnosis, Dementia Research, Dementia Support, Mild Cognitive Impairment, Mitochondrial dysfunction, neurodegenerative disorders, Research Dementia, tocotrienol

ROLE OF MITOCHONDRIAL DYSFUNCTION IN INSULIN RESISTANCE – (05-29-03)

November 15, 2012 by James Bogash

Mitochondrial dysfunction in elderly: possible role in insulin resistance.

This is an interesting concept and would lead to some additional intervention for lower insulin resistance in an elderly population. Mitochondrial support with supplements such as coenzyme Q10, carnitine and malic acid may be warranted in this situation. This would, of course, be on top of lifestyle changes, resistance training, chromium and essential fatty acids to affect the insulin resistance.

Entrez-PubMed –

Read entire article here

Filed Under: Insulin Tagged With: lower insulin resistance, malic acid, Mitochondrial dysfunction

DYSFUNCTION AND STRESS CAUSE OF EPILEPTIC SEIZURES – (12-09-04)

October 14, 2012 by James Bogash

MITOCHONDRIAL DYSFUNCTION AND OXIDATIVE STRESS: CAUSE AND CONSEQUENCE OF EPILEPTIC SEIZURES

Regular readers of the Updates know that I feel oxidative stress and subsequent oxidative stress (or vice versa) is an underlying mechanism for many chronic conditions.

The research supporting the link between mitochondrial dysfunction and seizures is getting stronger, and yet most physicians (neurologists included) are blissfully unaware and still say diet and vitamins have no impact on seizures. That statement alone proves they have not cracked a medical journal in at least the past year.

Here’s the scenario I envision…picture the state of a neuron with poor cellular health. Mitochondria under oxidative stress unable to produce sufficient ATP or too much free radical damage to its own DNA (with poorer repair mechanisms than cellular DNA). We lose ATP in the cell or even loss of the number of mitochondria within the neuron. Couple this with poor quality fats in the cellular membrane and it is not hard to envision a state where the neuron may spontaneously depolarize–the capacitance of the cellular membrane is much reduced and just can’t hold a charge. Seizure activity results. ScienceDirect – Free Radical Biology and Medicine : Mitochondrial dysfunction and oxidative stress: cause and consequence of ..

Read entire article here

Filed Under: Oxidative Stress, Seizures / Epilepsy Tagged With: DNA, Mitochondrial dysfunction, oxidative stress, seizures / epilepsy

MITOCHONDRIAL DYSFUNCTION LEAD TO PARKINSON’S DISEASE – (12-09-04)

October 14, 2012 by James Bogash

XENOBIOTIC METABOLISM IN PARKINSON’S DISEASE

I would have to say that we have PD pretty close to wrapped up. There has been strong evidence of mitochondrial dysfunction leading to loss of dopaminergic neurons leading to the symptoms of PD. Once that is understood, all the protective factors and the contributing factors really make sense.

This study found a very, very strong difference in the ability to detoxify between PD patients and controls. Along the sulfation pathway, only 30% of PD patients were able to sulfate greater than 5% of a dose of acetominophen–that leaves 95% unsulfated and able to increase oxidative stress and mitochondrial dysfunction. Controls? 84% were able to detoxify greater than 5%. So, a reduced ability to detoxify leads to increased oxidative stress from damaging toxins; increased oxidative stress leads to greater burden on the mitochondria and greater potential for damage. Xenobiotic metabolism in Parkinson’s disease — Steventon et al. 39 (7): 883 — Neurology –

Read entire article here

Filed Under: Parkinson's Tagged With: acetominophen, dopaminergic neurons, Mitochondrial dysfunction, oxidative stress, Parkinson's disease, Xenobiotic

MELATONIN USAGE MAY AID NEURODEGENRATIVE DISORDERS – (12-29-04)

October 8, 2012 by James Bogash

Pro-oxidant activity of aluminum in the rat hippocampus: gene expression of antioxidant enzymes after melatonin administration

Maybe I’m just looking, but it seems like there’s been an awful lot of research on melatonin lately. I had previously just considered melatonin as a sleep aid, and did not consider it as an antioxidant. However, with the current literature supporting an oxidative stress/mitochondrial dysfunction etiology for seizures, Alzheimer’s, Parkinson’s and other neurodegenerative disorders, I have begun to look at melatonin in a much different light with great therapeutic potential.

Read entire article here

Filed Under: Alzheimer's, Parkinson's, Seizures / Epilepsy Tagged With: Alzheimer's, Etiology, hippocampus, melatonin, Mitochondrial dysfunction, Parkinson's, seizures / epilepsy

OXIDATIVE STRESS RELATED TO TREATMENT OF MACROANGIOPATHY – (12-29-04)

October 8, 2012 by James Bogash

PREVENTION AND TREATMENT OF MACROANGIOPATHY: FOCUSING ON OXIDATIVE STRESS.

My wife thinks I’m a little overboard on this whole oxidative stress/mitochondrial dysfunction kick, but the research is really heading towards this physiological problem being a major contributor to many (if not all?) chronic diseases. Here we see alpha-lipoic acid protecting the blood vessels of type 2 diabetics by an antioxidant mechanism.

Read entire article here

Filed Under: Oxidative Stress Tagged With: alpha lipoic acid, macroangiopathy, Mitochondrial dysfunction, oxidative stress, type 2 diabetics

REDUCED MITOCHONDRIAL DYSFUNCTION IN PATIENTS WITH INSULIN RESISTANCE – (01-09-06)

August 16, 2012 by James Bogash

Reduced mitochondrial density and increased IRS-1 serine phosphorylation in muscle of insulin-resistant offspring of type 2 diabetic parents

I’ve continued to say that mitochondrial dysfunction is the root of all evil, and have yet to see any studies that convince me otherwise. This article finds that mitochondrial function is reduced by 60% IN THE CHILDREN of patients with insulin resistance. If this just isn’t the scariest thing that we can envision for successive generations, then I’d be hiding under the desk if something contained worse news. The children of insulin resistant patients are 60% less efficient at using energy, resulting in fat accumulation in their cells. If we do not get on the bandwagon against insulin resistance soon, several generations of our children will be paying the price in chronic diseases.

Read entire article here

Filed Under: Diabetes (Type 2) Tagged With: insulin resistance, Mitochondrial dysfunction, phosphorylation, type 2 diabetic

MITOCHONDRIAL DYSFUNCTION AND MIGRAINE – (05-15-06)

August 7, 2012 by James Bogash

Mitochondrial dysfunction and migraine: evidence and hypotheses

Ok–so some still consider it a hypothesis. But once I get my book together (titled: Mitchondrial Dysfunction as the Root of All That is Evil in Chronic Diseases) everyone will consider it fact. This model fits very well into migraine but leaves a big gaping problem. Mitochondrial dysfunction can create a very large variety of problems (see title for future book, above…) and I have yet to have a migraine patient come into my office that has been treated w/ anything other than meds. If this model turns out to be correct, then we are grossly mismanaging our migraine patients by not addressing the problem. Rather, we are medicating to get rid of the symptoms.

Read entire article here

Filed Under: Migraine Tagged With: hypotheses, migraine, Mitochondrial dysfunction

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