LifeCare Chiropractic

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Mitochondrial dysfunction

THE ROLE OF OXIDATIVE STRESS – (05-15-06)

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Developmental origins of diabetes: The role of oxidative stress

This is not the first article to look at oxidative stress/mitochondrial dysfunction as the initiating factor of insulin resistance. The basic premise is that, due to poor nutrient intake coupled w/ genetic risk factors, the mitochondria in the cell (many articles specifically look at the muscle cell) begin to function poorly and can’t provide the energy needed for that cell to function properly. Hence begins the disruption of that cell’s ability to respond positively to insulin signalling.

Read entire article here

ETIOLOGY OF INSULIN RESISTANCE – (05-29-06)

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Etiology of Insulin Resistance

While insulin resistance is probably one of my more often used soapboxes, my heart truly lies with mitochondrial dysfunction as undoubtedly this trigger that begins all chronic diseases of today’s time. That is why the approach to managing many chronic diseases is so similar–they all focus around reducing damage to the mitochondria while at the same time giving these same structures all the nutrients they need to function optimally.

With the recent study published on the mitochondrial effects of calorie restriction w/o nutrient restriction, this vaults this type of an approach to the top of the list of beneficial approaches for managing all chronic diseases.

Read entire article here

DIETARY FATTY ACIDS RISKS IN PARKINSON DISEASE – (07-18-05)

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Dietary fatty acids and the risk of Parkinson disease

While the finding that healthier fats lower the risk of Parkinson’s should be no surprise (most evidence is suggesting an inflammatory/mitochondrial dysfunction etiology for PD and Alzheimer’s and healthy fats will have an anti-inflammatory effect), the level of protection was a little surprising.

When looking at a hazard ratio, higher than 1.00 means an increased risk (a hazard ratio of 2.0 would mean a doubling of risk) and lower than 1.00 means a protective effect (.50 would mean half the risk).  The hazard ratio found was 0.68 for monounsaturated fat and 0.66 for polyunsaturated fats.

Read entire article here

MITOCHONDRIA DYSFUNCTION IS THE ROOT OF ALL EVIL – (06-20-05)

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The Pathobiology of Diabetic Complications

Well, I need to just wrap it all up right here.  For those of you who’s eyes glaze over as I talk about mitochondrial dysfunction being the root of all that is evil in today’s chronic diseases (my wife just rolls her eyes now–she stopped throwing stuff sometime last year…), turns out I wasn’t quite ready for the looney bin.
This article may be worth paying for full text access for some getting this update.  It truly begins to tie in the cause as well as the potential routes of management for diabetes.

WHAT IS A GOOD SOLID BIOMARKER FOR PARKINSON DISEASE? – (03-28-05)

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Urinary 8-hydroxydeoxyguanosine levels as a biomarker for progression of Parkinson disease

Following up on the previous article, the base problem with using a mitochondrial dysfunction/oxidative stress model is that we have not yet identified a good, solid, commercially available marker.

This article helps in that regards in suggesting that 8-OHDG, a marker of oxidative damage to DNA, may be a viable option.  Interestingly and, not surprisingly, the treatment of choice for Parkinson’s, l-dopa, did not affect 8-OHDG levels.

Read entire article here

MITOCHONDRIAL DYSFUNCTION IS THE REASON FOR SEIZURES, PD, AD, ALS – (03-28-05)

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Is the mitochondrial permeability transition a viable therapeutic target against neuronal dysfunction and death?

Any regular readers of the updates know my position on neurodegenerative disorders, and the research continues to support this position.  I do, however, wonder how long it really will be before clinicians in neurology begin to pick up on the concept that mitochondrial dysfunction the reason for seizures, PD, AD, ALS and the like.  I’m putting my money on 30 years…

Read entire article here

MITOCHONDRIAL DYSFUNCTION LEADS TO NEURODEGENERATIVE DISORDERS – (04-04-05)

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Efficacy of coenzyme Q10 in migraine prophylaxis

Almost a 50% response with taking 300 mg CoQ10 per day.  Not too shabby.  This is yet another notch in the “mitochondrial dysfunction leads to neurodegenerative disorders” belt.  The research is no longer questioning the association between altered brain behavior/pathology and oxidative stress–the research is now moving onto the deeper, more practical questions.

Read entire article here

WHAT IS A GOOD SOLID TEST TO CHECK OXIDATIVE STRESS – (04-25-05)

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Urinary 20-hydroxyeicosatetraenoic acid excretion is associated with oxidative stress in hypertensive subjects

Not to confuse anyone with long words (just how much would that be worth in Scrabble?) but it is surprising to me just how many ways we are finding to evaluate oxidative stress.  Truly this is a wonderful movement, because we are still lacking a good, overall, solid test to check for oxidative stress.

What I can see happening is a panel of several oxidative stress markers that will give a good idea of what state a patient is in.  Given that I think oxidative stress/mitochondrial dysfunction is the root of all evil, any markers we can identify to evaluate this is a good thing.

Read entire article here