LifeCare Chiropractic

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DNA

HIGH USAGE OF SUCRALOSE MAY LEAD TO DNA DAMAGE – (11-03-03)

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Comet assay w/ mouse organs: results with 39 currently used food additives

Sucralose in this study showed DNA damage. Now, in total, many other studies have not shown this finding with sucralose.

I do bring this study up to demonstrate that we do not yet know enough about this compound for me to recommend it to patients. For now I recommend avoiding it (and most likely this recommendation will stay…) just as with aspartame. The concern is that this sweetener is being used in more and more foods.

Recently heard a commercial for “no sugar added” Ovaltine or something like that. Well–the “no sugar added” was a codeword for sucralose (Splenda). Remember that anytime we try to come up with a compound to avoid the lifestyle changes that we know we need to make (olestra, aspartame, “carb blockers”…) the results are usually less than perfect.

Entrez-PubMed.

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INTAKE OF FRUITS AND VEGETABLES TO LOWER BETA CELL DYSFUNCTION – (01-05-04)

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Superoxide-mediated activation of uncoupling protein 2 causes pancreatic beta cell dysfunction

In English, this article links the progression of Type 2 diabetes to oxidative stress (superoxide is a free radical that causes damage to cellular membranes as well as DNA). Increased intake of fruits and veggies and antioxidants should be part of every regimine to lower risk and/or progression of type 3 DM. JCI — Abstracts: Krauss et al. 112 (12): 1831 –

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

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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 ..

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REACTIVE OXYGEN SPECIES ASSOCIATED WITH DIABETIC DAMAGES – (02-17-03)

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Are Oxidative Stress-Activated Signaling Pathways Mediators of Insulin Resistance and ß-Cell Dysfunction?

This article finds that reactive oxygen species (i.e. free radicals) are a result of elevated glucose levels, and these ROS than damage DNA, proteins and lipids. This damage than starts a snowball effect killing off beta cells of the pancreas and leading to the damage we associate with diabetes. This would suggest that antioxidant supplementation (N-acetylcysteine, Vit E, Vit C, CoQ10…) would be important nutrients for any patient with impaired glucose tolerance or diabetes.

Diabetes — Abstracts: Evans et al. 52 (1): 1

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OXIDATIVE STRESS IN OBESITY EFFECTS METABOLIC SYNDROME – (12-29-04)

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INCREASED OXIDATIVE STRESS IN OBESITY AND ITS IMPACT ON METABOLIC SYNDROME

I’m really not making this stuff up. Remember that the mitochondria are our cell’s source of energy production. In the process of creating ATP for energy, free electrons (termed free radicals) are formed that, by themselves, create damage to DNA, cellular machinery and cell membranes. In addition, free radicals participate in other reactions with compounds like nitric oxide that produce incredibly damaging compounds.

This problem is further worsened by the fact that the DNA of the mitochondria (remember that mitochondria has its own DNA separate from the cell’s DNA) is very close to these damaging compounds and the repair mechanisms of the mitochondria are nowhere near as good as the cell’s ability to repair its DNA. Luckily, the cell has many compounds that protect against free radicals–glutathione, melatonin, Vit C, Vit E, alpha lipoic acid….. But, what if the mitochondria was producing so many free radicals that the protective compounds couldn’t keep up? Or if the person’s diet was producing low levels of these protective compounds? The end result is in too much damage to the mitochondria and ultimately the cell.

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VITAMIN D INTAKE FROM TANNING AND BONE DENSITY – (12-15-04)

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TANNING IS ASSOCIATED WITH OPTIMAL VITAMIN D STATUS (SERUM 25-HYDROXYVITAMIN D CONCENTRATION) AND HIGHER BONE MINERAL DENSITY

As I’ve said before, sunlight has gotten a bad rap over the past ten years or so, and yet moderate sunlight exposure has tremendous protective benefits from the increase in Vit D production. The term “vitamin” for D is actually misleading…vitamins help enzymes do their job by acting as co-factors. Hormones, on the other hand, affect the well a cell expresses it’s DNA. Vitamin D acts as a hormone and every cell in the body has a receptor for this compound, with an incredibly long list of beneficial effects.

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STRESS EFFECTS THE LENGTH OF TELOMERES OF DNA – (12-15-04)

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ACCELERATED TELOMERE SHORTENING IN RESPONSE TO LIFE STRESS

This one definately falls into the category of “wow.” Telomeres are portions at the end of our DNA that get shorter with each cell division. As these telomeres get shorter, the life span of the organism gets shorter and shorter as well.

So, in this study, stress was shown to shorten telomere length. So, if it wasn’t bad enough that stress indirectly increases your risk of many (if not most) chronic diseases, we now find that it directly shortens lifespan as well!!

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EXCESSIVE OXIDATIVE DAMAGE EFFECTS TISSUES AND IMMUNE SYSTEM – (12-04-06)

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Oxidatively modified autoantigens in autoimmune diseases

Only recently have we begun to change our views on autoimmune conditions. We used to view these conditions as a dysfunction of the immune system–it was attacking our own body and we needed to suppress the immune system to control the disease state. However, once we started taking a much closer look, we started to realize that the immune system was actually performing exactly as it was supposed to.

The problem is that there is excessive oxidative damage to the tissues and the immune system is working to remove this oxidatively damaged tissue. Oxidatively damaged DNA in lupus, oxidatively damaged Type 2 collagen in RA, etc… This can drastically impact the way these conditions need to be treated, and the best method of treatment HAS to include lifestyle modifications to lower overall oxidative stress and inflammation.

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