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December 9, 2004 Research Update |
James Bogash, D.C. Mesa, AZ
info@lifecarechiro.com
www.lifecarechiro.com
Differential Effects of H. pylori Eradication on Oxidative DNA Damage at the Gastroesophageal Junction and at the Gastric Antrum
This is another article in my "lone crusade to prove that H. pylori is merely an opportunistic infection and the real problem is the environment that allowed H. pylori to grow and prosper." However, this article goes even further then my lone crusade. What if, in some cases, having H. pylori present is actually PROTECTIVE? Now wouldn't that be a novel concept. I'm not quite to this extreme yet, but this article found and increase in oxidative DNA damage when H. pylori was eradicated. This would lead to an increase in the risk of cancer at the GE junction. Stay tuned... Differential Effects of Helicobacter pylori Eradication on Oxidative DNA Damage at the Gastroesophageal Junction and at the G..
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Oxidized Low-Density Lipoprotein Levels and Risk of Colorectal Cancer
I have always stood by the concept that LDL cholesterol does not do damage to us until it gets damaged. However, what if the oxidized LDL (ox-LDL or oxysterols) are merely a marker for the amount of inflammation, and that the increased oxidative stress from the increased inflammation is actually the real culprit? Here we see an increased risk of colon cancer with an increasing level of ox-LDL, with greater than a three fold increase with the higher levels. Serum Oxidized Low-Density Lipoprotein Levels and Risk of Colorectal Cancer: A Case-Control Study Nested in the Japan Collabo..
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Coenzyme Q10 Combined With Mild Hypothermia After Cardiac Arrest
We know that the area damaged with an ischemic attack, whether it is a brain attack (stroke) or a heart attack, is actually smaller than the area that ultimately gets damaged. Anything that can be done during the repurfusion stage (when blood is reintroduced back into the oxygen starved area) will shrink the amount of damage done. Magnesium has already been shown to be protective and this study adds Coenzyme Q10 to the list. This was a small study, but survival rates with CoQ10 was 68%, versus 29% in the placebo. Over twice the survival rates for a (comparitively) cheap and very safe approach. Sadly, studies like this rarely lead to approach changes in our ERs and hospitals. Were it me or my family, I would lock the door and give magnesium and CoQ10 myself. Coenzyme Q10 Combined With Mild Hypothermia After Cardiac Arrest: A Preliminary Study -- Damian et al. 110 (19): 3011 -- Circ..
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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
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A Systematic Review and Meta-analysis of Studies Comparing Readmission Rates and Mortality Rates in Patients With Heart Failure
So, with all of our new lifesaving (and expensive) drugs used to treat heart patients, it is good to know that we are extending their lives with these wonder drugs. Oops. Scratch that. We are keeping them out of the hospital, but the mortality rate remains unchanged. Isn't that a kick in the behind? It just further drives home the point that mainstream medicine does little to impact the underlying mechanisms behind chronic disease. Those mechanisms continue to detoriorate the health of the patient while masking the symptoms only. Arch Intern Med -- Abstract: A Systematic Review and Meta-analysis of Studies Comparing Readmission Rates and Mortality Rates..
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A RCT of the Health Effects of Antioxidant Vitamins and Minerals
This was a relatively simple approach to affecting long term health and at least is a little more representative of a natural approach (low doses of Vit C, E, selenium, beta carotene and zinc). This study found a very strong protective effect in men for any cause of death. This protective effect was not found in women, however. The authors suggest a reduced levels of pre-trial antioxidant status in men to explain the difference. I might add another angle--most of the women in this study were pre-menopausal. These women would generally have less iron due to loss of blood during the menstrual cycle. Iron has the capacity to be a pro-oxidant in higher levels. This may be a factor that contributed to the differences. It would be easy to check--just stratify the group into pre- and post-menopausal women. Regardless, this is a very, very cheap and simple protective mechanism for preventing chronic disease. Arch Intern Med -- Abstract: The SU.VI.MAX Study: A Randomized, Placebo-Controlled Trial of the Health Effects of Antioxidant..
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High-Dosage Vitamin E Supplementation May Increase All-Cause Mortality
My, wasn't this one a hot one for a day or so? This always brings up the question about how some of these articles manage to make it to the mainstream media when other topics much more important (like Syndrome X) remain unheard of. A couple comments. First, the end results from the study were very weakly positive. 1.04 X risk. 1.00 risk means no effect, so a .04 increase in risk is very small. Also, the "p" value is .035--this is an evaluation of how much the study results are a result of chance (p value of coin flip is 1). The lower the number the stronger the study. I prefer p values lower than .001. That being said, there's still the possiblity of a risk, which is NOTHING NEW. I've included a strong article that reviews the pro-oxidant effects of Vit E. Vit E can act as a pro-oxidant but THIS IS ABOLISHED BY CO-ANTIOXIDANTS LIKE VIT C. From a natural perspective, we don't treat supplements in a vacuum and lifestyle changes would ALWAYS be done in a package, not with just one supplement. I'm sure that taking Vit E along with Vit C and other compounds like green tea and red wine will show nothing but a strongly protective effect. Meta-Analysis: High-Dosage Vitamin E Supplementation May Increase All-Cause Mortality -- Miller et al., -- Annals of Internal..
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This reviews the pro-oxidant effects and how they are eliminated...
Prevention of Tocopherol-mediated Peroxidation in Ubiquinol-10-free Human Low Density Lipoprotein -- Bowry et al. 270 (11): 5..
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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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Neuroprotective role of melatonin in oxidative stress vulnerable brain
In doing some research on how to protect the brain from this onslaught of oxidative stress, I was somewhat surprised to find articles on the ability of melatonin to increase the enzymes responsible for quenching free radicals such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase. Live and learn, I guess. Entrez PubMed
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Genetic risk factors for statin myopathy found; coenzyme Q10, carnitine supplements might help
I will refrain from dancing around saying "I told you so." I have always noted that I felt the deaths that occurred with Baychol were most likely due to a genetic suseptability to a lower CoQ10 status. The statins are well known to inhibit the production of CoQ10 while it is lowering cholesterol. So, take a person who has a genetically diminished ability to produce CoQ10 and shut that production down. These people literally melted because one of the main protectors against oxidative stress was taken away. Recent findings have confirmed that this is indeed the pathway that these fatal reactions took. However, what continues to stump me is that researchers would suggest giving CoQ10 and L-carnitine along with the statin drugs. With literally no end to the natural approaches to lowering cholesterol, NONE of which required another natural compound to be used to protect from KILLING the patient, why even think about using statins? This mindset escapes me.