Background
Exhausting exercise induces muscle damage associated with high production of free radicals and pro-inflammatory mediators.
Aim
The objective of this study was to determine for the first time and simultaneously whether oral coenzyme Q10 (CoQ10) supplementation can prevent over-expression of inflammatory mediators and oxidative stress associated with strenuous exercise.
Methods
The participants were classified in two groups: CoQ10 group (CG) and placebo group (PG). The physical test consisted in a constant run (50 km) that combined several degrees of high effort (mountain run and ultra-endurance), in permanent climbing.
Results
Exercise was associated with an increase in TNF-α, IL-6, 8-hydroxy-2′-deoxyguanosine (8-OHdG), and isoprostane levels, revealing the degree of inflammation and oxidative stress induced. Oral supplementation of CoQ10 during exercise was efficient reducing oxidative stress (decreased membrane hydroperoxides, 8-OHdG and isoprostanes generation, increased catalase, and total antioxidant status), which would lead to the maintenance of the cell integrity. Data obtained also indicate that CoQ10prevents over-expression of TNF-α after exercise, together with an increase in sTNF-RII that limits the pro-inflammatory actions of TNF. Moreover, CoQ10 supplementation reduced creatinine production.
Conclusions
CoQ10 supplementation before strenuous exercise decreases the oxidative stress and modulates the inflammatory signaling, reducing the subsequent muscle damage.
Study: Coenzyme Q10 supplementation ameliorates inflammatory signaling and oxidative stress associated with strenuous exercise. EUROPEAN JOURNAL OF NUTRITION DOI: 10.1007/s00394-011-0257-
A new analysis of the Multi-Ethnic Study of Atherosclerosis (MESA) shows that changes in coronary artery calcium (CAC) (as measured by the heart scan) may lag behind changes in coronary disease risk factors.
CAC is a common measure of subclinical coronary disease, but the association between changes in coronary disease risk factors and progression of CAC is not clear. So Arguelles and colleagues analyzed data from 6800 participants of the MESA study. All participants underwent a CAC imaging test with computed tomography at baseline and either 1.6 or 3.2 years later. A quarter of the study subjects also underwent a third CAC test at an average of 4.9 years after baseline.
Reason: Individuals who come in with a very high risk-factor profile and are the most likely to be placed on medications already have a very high underlying level of pathology that could be driving that calcification process independent of declines in risk factors, including blood pressure, lipid levels, and blood glucose.
The authors analyzed if the changes in CAC over time were associated with changes in blood pressure and lipid levels. The analysis was adjusted for age, ethnicity, smoking status, family history of cardiovascular disease, total income as a marker of socioeconomic status, and previous use of hypertension, lipid, and glucose-lowering drugs.
Among men who had detectable CAC at baseline, CAC increased an average of 57 Agatston units/year. In women, CAC progressed by 39 Agatston units/year. In all patients, the risk-factor measures went up or down depending on whether they were taking antihypertensivse, statins, or other medications.
The researchers said that CAC "occurs in a time-lagged fashion" such that a longer study would have eventually seen CAC progression stop or reverse many years after the reversal in risk factors in patients taking medication. Whether risk factors such as high blood pressure and hyperlipidemia are more important to the initiation of calcification--or if they have more of a role in the progression of existing disease--is not clear yet.
I like to use CAC for a baseline before treatment or to monitor progress. I aslo require all chelation patients to get one. I have seen this time lag in my practice many times now but it took me about three years to notice it. It typically takes two to three years to see a reversal of plaque after initiating aggressive treatment. This is a very important thing to explain to patients. I typically see less calcium deposition per year the above numbers because I use combination therapy. A moderate to high risk patient in my office would typically be on some or all of the following: fish oil, Coenzyme Q10, statins, vitamin K2, vitamin D, blood pressure meds, antioxidants, superoxide dismutase, pomegranate, phosphatidylcholine, lipoic acid, vitamin C, niacin and tocotrienols. After all, the goal is to reverse plaque or stop its progression. Sometimes patients do intravenous treatments as well.
Vitamin D deficiency is traditionally associated with bone and muscle weakness, but in recent years a number of studies have shown that low levels of the vitamin may predispose the body to high blood pressure, congestive heart failure, and chronic blood vessel inflammation leading the increased risk of heart attack.. It also alters hormone levels to increase insulin resistance, which raises the risk of diabetes. Several large studies have shown that people with low vitamin D levels were twice as likely to have a heart attack, stroke, or other heart-related event during follow-up, compared with those with higher vitamin D levels.
In a review article published in the Journal of the American College of Cardiology, researchers surveyed recent studies on the link between vitamin D deficiency and heart disease to come up with practical advice on screening and treatment.
They concluded that vitamin D deficiency is much more common than previously thought, affecting up to half of adults and apparently healthy children in the U.S.
Researchers say higher rates of vitamin D deficiency may be due in part to people spending more time indoors and efforts to minimize sun exposure through the use of sunscreens. Sunscreen with a sun protection factor (SPF) of 15 blocks approximately 99% of vitamin D synthesis by the skin. An hour in the sun without sunblock at the beach in mid summer will cause the skin to produce about 10,000 iu of vitamin D.
We are outside less than we used to be, and older adults and people who are overweight or obese are less efficient at making vitamin D in response to sunlight. A little bit of sunshine is a good thing, but the use of sunscreen to guard against skin cancer is still a good idea for prolonged sun exposure.
Vitamin D levels can be measured with a blood test that looks at a specific form of vitamin D called 25-hydroxy vitamin D (25(OH)D). Vitamin D deficiency is defined as a blood 25(OH)D level below 20 ng/dL. Normal levels are considered to be above 30 ng/dL. Optimal evels are between 50 and 80ng/dL.
Research studies have indicated that carriers of specific 9p21 gene variants have increased risk of: 1) a heart attack before the age of 60 in women and 50 in men, 2) an abdominal aortic aneurysm‡, and 3) blocked coronary arteries or a heart attack at any age. ‡ While the recommended treatment to combat this risk has been to focus on other risk factors, such as losing weight or addressing high blood pressure, new research shows that your diet may play a role in reducing this risk.
In a recent study published in PLoS Medicine it was discovered that the risk of heart attack, and heart disease in general, associated with the 9p21 variants appeared to significantly decrease with consumption of a diet high in fruits and vegetables. In particular, for study participants who carried the 9p21 genetic risk variants and ate a diet high in raw fruits and vegetables, their risk of a heart attack or heart disease was the same as those without the risk variant. This means, that although your genes may increase your risk of heart disease, you can do something about it by changing your diet.
What this means for you.
If you have had a 9p21 genotype test and your results indicate that you are a carrier of an “at risk” gene variant (your test results will have red in them); think about how you can increase your intake of fruits and vegetables
Low serum testosterone is associated with increased adiposity, an adverse metabolic risk profile, and atherosclerosis. However, few prospective studies have demonstrated a protective link between endogenous testosterone and CV events. Polymorphisms in the SHBG gene are associated with risk of type 2 diabetes, but few studies have addressed SHBG as a predictor of CV events.
Results
During a median 5-year follow-up, 485 CV events occurred. Both total testosterone and SHBG levels were inversely associated with the risk of CV events (trend over quartiles: p = 0.009 and p = 0.012, respectively). Men in the highest quartile of testosterone (≥550 ng/dl) had a lower risk of CV events compared with men in the 3 lower quartiles (hazard ratio: 0.70, 95% confidence interval: 0.56 to 0.88). This association remained after adjustment for traditional CV risk factors and was not materially changed in analyses excluding men with known CV disease at baseline (hazard ratio: 0.71, 95% confidence interval: 0.53 to 0.95). In models that included both testosterone and SHBG, testosterone but not SHBG predicted CV risk.
Conclusion
High serum testosterone predicted a reduced 5-year risk of CV events in elderly men.
Study: Journal of the American College of Cardiology, Volume 58, Issue 16, 11 October 2011, Pages 1674-1681
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