|February 10, 2004|
|Life Extension Weekly Update Exclusive |
Carotenoids may protect against early atherosclerosis
The researchers studied 477 participants in the Los Angeles Atherosclerosis Study, a prospective study of possible causes of atherosclerosis. Subjects between the 40 and 60 years of age were enrolled from 1995 to 1996, and were followed up approximately eighteen months later. At each examination questionnaires were completed on health behaviors, and carotid intima-media thickness was measured via ultrasound to assess the presence and progression of atherosclerosis. Fasting blood samples taken at the study’s onset provided information on levels of vitamin C, carotenoids, alpha and gamma-tocopherol, and vitamin A as well as serum total cholesterol, high-density lipoprotein, and C-reactive protein (a marker of inflammation).
Adjusted analysis found that higher levels of lutein, zeaxanthin, beta-cryptoxanthin and alpha-carotene were associated with a reduction in the progression of carotid intima-media thickness over the study period. Ascorbic acid, alpha and beta-carotene and lycopene levels were significantly inversely associated with total cholesterol levels. C-reactive protein levels were inversely related to ascorbic acid levels as well as inversely related to the levels of all carotenoids with the exception of zeaxanthin.
The anti-inflammatory effect for lutein found in previous in vitro studies could be the mechanism of action for this carotenoid in helping to protect against atherosclerosis. The authors recommend randomized clinical trials to determine if the associations revealed in the current study are causal.
High vitamin A and beta-carotene serum levels have been reported to reduce fibrinogen levels in humans and animals (Green 1997). Animals fed a vitamin A-deficient diet have an impaired ability to break down fibrinogen, but when injected with vitamin A, they produce tissue plasminogen activators that break down fibrinogen, reducing the risk of clot formation.
Vitamin A is beneficial to individuals with Syndrome X and diabetes. A study involving 52 patients indicated that vitamin A enhanced insulin-mediated glucose disposal (Facchini et al. 1996a). Since beta-carotene must be converted in the body to vitamin A, an adaptation some individuals lack, diabetics may do better using vitamin A rather than beta-carotene.
It should be noted that the protection of beta-carotene is not absolute. In fact, if the individual is consuming greater amounts of alcohol, beta-carotene may actually increase the risk of intracerebral hemorrhage (Leppala et al. 2000). A blend of phytoextracts (alpha-carotene, beta-carotene, lutein, and lycopene) appears to offer more comprehensive cardiac protection than using beta-carotene.
Chloroplex contains a variety of carotenoids and other plant extracts that can protect against DNA mutation and enhance cardiovascular and ocular health. Chloroplex also contains chlorophyll, an antioxidant and DNA protectant.* In addition, chlorophyll has the ability to neutralize aflatoxins, produced by the Aspergillus flavus mold that grows on corn and peanuts. While vitamin A and beta-carotene can neutralize aflatoxins to some degree, chlorophyll is much more effective.
CoQ10 is an essential component of the respiratory cycle of the cell that takes place in the mitochondria and generates ATP, the cell’s energy currency.
Orally administered coQ10 goes directly to the mitochondria where it works to regulate the oxidation of fats and sugars into energy—an important function since the natural production of coQ10 declines with advancing age. When the body has an ample amount of coQ10 the mitochondria can work most efficiently throughout the entire body, in cells everywhere, including the most densely populated area, the heart.
As we see it: Cardiologists overlook lifesaving discovery
In particular, a study of heart attack patients showed that compared to placebo, supplementation with 120 mg a day of coenzyme Q10 reduced secondary cardiac events by 45% and significantly reduced the number of cardiac deaths. Many of these heart-attack patients were prescribed a “statin” drug to lower cholesterol levels. The major adverse effect of statin treatment was fatigue that occurred in 40.8% of the placebo group, whereas only 6.8% of the patients supplemented with coenzyme Q10 experienced fatigue.
In newly published findings over the past year, positive results were shown when coenzyme Q10 was tested against disorders including macular degeneration, Parkinson’s disease, viral myocarditis, and hereditary neurodegenerative diseases. Additional studies indicate that coenzyme Q10 deficiency is linked with disorders such as infertility and brain atrophy.
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