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Could a Deficiency of LA in Cardiolipin Be Caused by an Excess of LA?

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Could an excess of the omega-6 fatty acid linoleic acid in the diet and in adipose tissue create the paradoxical situation in which linoleic acid (LA) is lacking in the phospholipids needed to form mitochondrial cardiolipin? That would mean reduced mitochondrial function and increased oxidative stress, which we observe in animal models fed very high-fat diets. We have already encountered a similar situation with omega-3 fats. Take a look. The percentage of omega-3 phospholipids in cell membranes initially increases sharply but then declines as the consumption of more plant-derived omega-3 and omega-6 fats increases. This phenomenon is explained by changes in the activity of the enzymes that elongate and desaturate plant fats into the long-chain fatty acids EPA and DHA, which are found primarily in fish oil. The same enzymes also elongate and desaturate linoleic acid (LA) into arachidonic acid (ARA), whose concentration is maintained relatively stable. Thus, a higher intake of LA mean...
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Is Fat Burning Really Dangerous?

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Recently, Georgi Dinkov commented on an interesting study on his blog, which shows that uncontrolled fat burning could damage mitochondria. Let's take a closer look at this study, considering all the facts known so far. Should we be afraid of fats or not? We must first show the position of the study authors. Quote "Unrestrained fatty acid oxidation triggers heart failure in mice via cardiolipin loss and mitochondrial dysfunction" "Collectively, these results indicate that although FAO is essential for cardiac energy production, therapeutic strategies aimed at stimulating cardiac FAO may be detrimental rather than beneficial in heart failure." Unquote So, can promoting fat burning really be harmful? Well, we already know that promoting fat burning without overeating extends the life of mice . Cells need fat burning to improve resilience . So the scientists' statement about the dangers of promoting fat burning is contradictory to these findings,  so something...
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Was Conjugated LA from Dairy Products Missing in Prehistoric Times?

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We have already discussed conjugated linoleic acids (CLA) here several times. Unlike ordinary linoleic acid (C18:2n-6), CLA are also C18:2 fatty acids, but they differ in the spacing of the double bonds along the carbon chain—they are closer together. They can also have different combinations of trans and cis double bonds. What they have in common is that they are less stable than linoleic acid and are more susceptible to peroxidation . They are therefore better sensors of oxidative stress. They more accurately reflect the state of metabolism and respond more sensitively to metabolic disturbances, breaking down more readily into various signaling molecules. The most common source of CLA in our diet is milk fat. However, our bodies can also produce CLA from trans-vaccenic acid (TVA) , which is also present in milk. There are animal studies showing that as little as 1% of calories from CLA in mice completely eliminates arterial plaque and restores fat metabolism , protects the liver , a...
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Eyes, as W.H. Bates saw them?

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After more than ten years since I first became acquainted with the work of Dr. Bates, I am finally returning to the issue of the eyes, which actually started my interest in how the mechanisms in the human body work. At the end of 2012, I put away my glasses, which I had worn almost constantly until then. Since childhood, I have had excellent vision in my right eye, but my left eye is amblyopic. I wore the glasses so that my left eye would not turn off completely, so that the strongly blurred image in the left eye would be at least as large as in the right eye. In fact, I had seen very well all my life, but a few years before that, my eyesight began to deteriorate. I also had eye inflammation almost every year. During one of these, my diopters and astigmatism in both eyes suddenly changed. I was very surprised by this and even more surprised that the ophthalmologists didn't care at all, they would simply prescribe you different diopters and that would be the end of it. Then my diopt...
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What Is Lipofuscin and How To Avoid Its Production?

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As the organism and its cells age, a substance called lipofuscin accumulates in the cell cytosol. It is a yellowish-brown metabolic waste (pigment) formed by oxidized fats and proteins. It is commonly called the “pigment of aging” because it gradually accumulates in cells (especially in neurons, heart muscle, liver and retina) and its amount naturally increases with age. It is not a homogeneous compound, it is probably a mixture of intertwined and interconnected chains that exhibit fluorescence. This fluorescence when stimulated by near-UV radiation is not always the same, it varies depending on the place of origin, composition and age from green to blue. The literature tells us that it is actually unprocessed cellular waste. Normally, these substances would be removed by the formation of lysosomes, organelles where unusable substances are digested and broken down into reusable material or waste. Lipofuscin is the remnant of dysfunctional lysosomes, so it shows a state where the decomp...
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Are High Blood Glucose Levels Harmful, Even Without Aldehydes?

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The effort to lower blood glucose levels seems obvious, the reason is simple. High glucose levels cause oxidative stress and damage to body organs (eyes, blood vessels, kidneys, etc.). This leads many people to promote and apply low-carb and ketogenic diets. But is it really glucose that causes it? After all, it is the most common fuel for obtaining energy so that cells can function at all. Isn't that strange? Moreover, the cell can easily defend itself against overload by means of insulin resistance. So why doesn't it work? Is it really glucose that is harmful to the body? So let's take a closer look. If you are reading this blog, I think you already know where the core of the problem is. Yes, it is the activation of an enzyme that is supposed to serve only in emergency situations, otherwise it should be deactivated. It is the enzyme aldose reductase (AR, AKR1B1). It is present in the liver, vascular endothelium, cornea, etc. It is the first enzyme of the so-called polyol ...
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