La vitamine E inverse l’athérogénie et protège contre les dommages induits par les endotoxines

 De : https://articles.mercola.com/sites/articles/archive/2024/12/09/vitamin-e-atherogenesis-endotoxin-induced-damage.aspx

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Vitamin E Reverses Atherogenesis and Protects Against Endotoxin-Induced Damage

Analysis by Dr. Joseph Mercola 9 décembre 2024

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Story at-a-glance

• Vitamin E, a fat-soluble antioxidant, protects cells from damage, supports immunity and reduces cellular stress. Research shows α-tocopherol, its most active form, offers the broadest health benefits
• A study by researchers at the University of Antwerp found that α-tocopherol reverses atherogenesis, reducing arterial plaque buildup and enhancing heart function
• Another study at the University of Illinois Urbana-Champaign revealed that α-tocopherol protects against muscle weakness from endotoxin-induced inflammation
• Vitamin E also mitigates damage from excess linoleic acid (LA) and estrogen, inhibiting the oxidation of stored LA and acting as an estrogen antagonist to reduce tissue damage and metabolic disruptions
• Tips for increasing vitamin E intake and selecting high-quality supplements are included below

Vitamin E is a fat-soluble vitamin best known for its role as an antioxidant, protecting cells from damage caused by free radicals. It also boosts immune function, aids in cell signaling, promotes skin health and protects tissues from cellular stress.

Unfortunately, many people do not get enough vitamin E from their diet. Around 88.5% of Americans do not meet the recommended dietary allowance (RDA) for this micronutrient.¹

One major reason for this shortfall is the widespread reliance on processed foods, which are generally low in vitamin E and other essential nutrients. Severe vitamin E deficiency leads to troubling symptoms like muscle weakness, balance issues and even heart rhythm problems. Some also experience vision problems, dementia and liver or kidney complications.^2,3

Vitamin E exists in eight different forms — four tocopherols and four tocotrienols — with alpha-tocopherol (α-tocopherol) being the most biologically active and the primary form used and stored by the body.⁴ Recent studies^5,6 have found that α-tocopherol plays an even more impactful role in your health than previously understood.

Specifically, it's been shown to reverse atherogenesis, the process that leads to the hardening and narrowing of arteries. It also demonstrated protective action against endotoxin-induced damage.^7,8 Given these benefits, keeping your vitamin E levels in check is essential for supporting overall health.

Vitamin E Reverses Atherogenesis and Improves Cardiac Function

Mainstream media often suggests that once heart disease sets in, it's irreversible, with treatments focused on managing symptoms and slowing further plaque buildup. However, a June 2024 study published in the journal Vascular Biology⁹ challenges this view, suggesting that α-tocopherol aids in reducing atherosclerosis and boosting heart function.

Conducted by researchers at the University of Antwerp, the study involved mice that develop unstable atherosclerotic plaques similar to those seen in advanced human cases. This close resemblance to human plaque instability provided a solid basis for studying how vitamin E affects cardiovascular health.

The mice were fed a Western-style diet with either a low or high dose of α-tocopherol over 24 weeks. Throughout the study, the researchers observed for changes in plaque thickness, the size of necrotic (dead cell) cores and overall heart function. Their goal was to see if high-dose α-tocopherol could stabilize these vulnerable plaques and support heart health beyond its usual antioxidant role.

Their findings showed that high-dose α-tocopherol exhibited positive effects, specifically reducing plaque buildup and dead cell areas within the carotid arteries, which are key factors in preventing plaque ruptures that lead to strokes and heart attacks. As the authors explained:¹⁰

"[P]laque formation in the right common carotid artery (RCCA), as shown by the plaque formation index, was significantly decreased in mice treated with a high dose of α-tocopherol. Furthermore, plaque thickness in the RCCA was significantly reduced in mice treated with a high dose of α-tocopherol. In addition, a WD (Western diet) supplemented with 500 milligrams α-tocopherol per kilogram diet reduced the necrotic core area."

In addition to reducing plaque, α-tocopherol supplementation improved heart function among the high-dose group. Mice treated with high doses of vitamin E demonstrated enhanced left ventricular performance, as shown in increased measures of fractional shortening and ejection fraction, which are key indicators of effective blood pumping.

Moreover, a reduction in cardiac mass in the high-dose group points to a protective effect against cardiac hypertrophy, a condition that progresses to heart failure if left unchecked. Interestingly, the study found an unexpected increase in markers of lipid peroxidation, including oxidized LDL (oxLDL) and malondialdehyde, in the group receiving a high dose.

This effect suggests that, at higher doses, vitamin E contributes to oxidative stress instead of reducing it. These findings show that while vitamin E has clear benefits for reducing plaque and improving heart function, its effects vary on dosage. Taking the appropriate dose is important to reap its benefits and avoid any downsides.¹¹

Vitamin E Deficiency Linked to Endotoxin-Induced Muscle Weakness

A deficiency in α-tocopherol has also been linked to various neurological disorders, including spinocerebellar ataxia, peripheral neuropathy and myopathy. Additionally, people and animals with low vitamin E levels have reduced antibody production, weakened T cell function and increased cytokine levels, which are indicators of inflammation.¹²

To further investigate how vitamin E affects muscle strength under inflammatory conditions, researchers at the University of Illinois Urbana-Champaign used lipopolysaccharide (LPS) to mimic inflammation.¹³ LPS is a highly virulent form of endotoxin that's produced by pathogenic bacteria. It causes inflammation if it crosses your compromised gut barrier into systemic circulation.

In the study,¹⁴ animal models with and without vitamin E deficiency were exposed to LPS. The researchers measured their muscle strength before and after exposure to assess the impact of inflammation. Their findings showed that those with lower vitamin E levels experienced a significantly greater decline in muscle strength compared to those with adequate vitamin E.

The researchers also measured interleukin-6 (IL-6) levels, an inflammatory marker that rises as part of the body's response to stressors like infection. Both groups showed increased IL-6 levels after LPS exposure, confirming that inflammation was activated in all subjects.

However, despite similar IL-6 increases, muscle weakness was more severe in vitamin E-deficient subjects, indicating that a deficiency doesn't necessarily increase inflammation, but it does intensify its physical effects on muscles. These findings underscore the importance of maintaining adequate vitamin E levels, not only for protecting muscle function but also for mitigating the effects of endotoxin-induced inflammation.

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Vitamin E Mitigates the Effect of Linoleic Acid and Estrogen

Beyond reversing atherogenesis and protecting against endotoxin damage, another important benefit of vitamin E is its ability to keep the linoleic acid (LA) stored in your tissues from being oxidized into toxic by-products. This is particularly significant since most people have LA stores up to 10 times higher than normal levels, contributing to the rise in chronic diseases.

Taking vitamin E regularly until you get your LA down to healthy levels is beneficial, especially since this takes up to six years for most people. During this time, vitamin E will inhibit most of the damage done by LA.

Moreover, vitamin E counteracts the effects of excess estrogen. High levels of estrogen have striking similarities to the effects of excess LA, both causing metabolic disruptions and other health problems.

Both LA and estrogen raise calcium influx into cells, which then boosts nitric oxide and superoxide inside those cells. When these combine, they almost instantaneously form peroxynitrite, a highly reactive nitrogen compound that causes pervasive damage to your tissues.

LA and estrogen also promote a process in your body called lipolysis, where fats are released from fat cells into the bloodstream. This increases LA oxidation, which is precisely what you want to avoid — vitamin E neutralizes this harmful effect. Ideally, LA should stay in the fat cells until it's safely metabolized by peroxisomes.

Vitamin E also directly inhibits aromatase, the enzyme that converts male hormones like testosterone and DHEA into estrogens. Even better, it acts as an estrogen antagonist, blocking estrogen from binding to receptors and therefore reducing the damage caused by high estrogen levels. It functions similarly to tamoxifen, the drug used to treat estrogen receptor-positive breast cancers.

Boost Your Vitamin E Intake Through Your Diet

While the studies above focused on the benefits of vitamin E supplementation, remember that supplements should complement a healthy diet, not replace it — and they're only necessary if you have specific deficiencies. Vitamin E is easily incorporated into your diet through certain foods, so before turning to supplements, consider adding more vitamin E-rich options.

Plants produce vitamin E naturally, and some of the highest levels are found in plant oils. While some health authorities recommend vegetable oils, seeds and nuts as good sources, they're actually terrible because of their high LA content. Beans, another food rich in vitamin E, are also problematic to some people due to their high lectin content.

Good natural vitamin E sources that do not have negative effects on your health include fresh fruits and vegetables, such as spinach, pumpkin, asparagus, red bell peppers, tomatoes, kiwi and mango. Grass fed ruminants, such as beef or bison, are also excellent sources. A single serving provides enough vitamin E to help counteract oxidative stress, especially in a low-LA diet.

However, due to high LA levels in the modern Western diet, most people need supplements to get enough vitamin E to counteract oxidative stress. To check if you might benefit from a vitamin E supplement, try using a nutrient tracker like Cronometer. It's the most accurate one on the market as it avoids crowd-sourced data inaccuracies, and it's also available free of charge.

Vitamin E supplementation doesn't have to be lifelong — especially if you're working to reduce LA intake. By keeping LA intake below 5 grams a day for about three years, you may find you don't need regular supplements anymore, or only occasionally. If you do happen to eat a high-LA meal, taking a vitamin E capsule afterward helps protect you from that exposure.

Once your LA levels become low, you'll only need about 2 milligrams (mg) of vitamin E per gram of LA. With a recommended LA intake of 5 grams or less per day, this works out to about 10 mg of vitamin E, which is a very low dose. Since vitamin E is fat-soluble, it stays in your fat tissues for a while, providing lasting benefits.

What to Look for in a Vitamin E Supplement

When it comes to vitamin E supplements, many options on the market are synthetic, and you want to steer clear of those. Research has shown that synthetic vitamin E has opposite effects to natural vitamin E, sometimes even increasing certain health risks rather than reducing them. This is why it's important to make sure you're selecting a natural form.

Synthetic vitamin E is labeled as alpha-tocopherol acetate. The word "acetate" indicates that it's synthetic. Another key detail to check is the isomer type, which refers to the orientation of the vitamin's molecular structure. Many synthetic supplements are "racemic," containing both left-handed (L) and right-handed (D) isomers, but only the D isomer is beneficial to your body. The L isomer doesn't contribute to your health.

Synthetic versions often contain 50% of the ineffective L isomer, and they may use an ester form of vitamin E that only offers about half the potency of natural vitamin E. Altogether, this means that some synthetic supplements are up to 75% less effective than their natural counterparts.

So, the first step in identifying healthy good vitamin E supplements is to make sure you're getting real vitamin E and not synthetic. What you're looking for is "d-alpha-tocopherol" on the label, which indicates the pure D form that your body can use, rather than "dl-alpha-tocopherol," which indicates a synthetic form.

There are also other vitamin E isomers, and you want the complete spectrum of tocotrienols, specifically the beta, gamma and delta types of vitamin E, in the effective D isomer. These variations work together for a broader range of benefits. Taking high doses of alpha-tocopherol alone depletes the other forms in your body. This is true whether you're taking a natural or a synthetic one.

So, for a balanced intake, I recommend looking for a food-based supplement with all eight forms of vitamin E. Make sure to choose a supplement that's free from soy, soybean oil and genetically engineered (GE) ingredients. Common GE ingredients in supplements often come from corn, soy or cottonseed, so choosing a clean, natural source ensures you're getting the highest quality possible.

Avoid supplements that don't meet these criteria or much higher doses of vitamin E, as more is not necessarily better and can be highly counterproductive. For best absorption, it's ideal to take vitamin E with a healthy fat source, like coconut oil, since vitamin E is fat-soluble. Studies show that without fat, your body may only absorb about 10% of the vitamin E in a supplement.¹⁵

- Sources and References

• ¹ USA Today, April 1, 2023
• ² StatPearls [Internet]. Vitamin E Deficiency
• ³ Oregon State University, Vitamin E
• ⁴ NIH ODS, Vitamin E
• ^{5, 7, 9, 10, 11} Vasc Biol. 2024 Jun 3;6(1):e240002
• ^{6, 8, 12, 13, 14} The Journal of Nutrition. Volume 154, Issue 2, February 2024, Pages 498-504
• ¹⁵ Science Daily, October 7, 2015