Genes are short segments of DNA deoxyribonucleic acid found in chromosomes. DNA contains the instructions for building proteins. And proteins control the structure and function of all the cells that make up your body.
Any factors that affect the mitochondrial membrane can severely impact the body's ability to aerobically respire and force it to use anaerobic respiration more, or to convert ATP to AMP, to produce energy, include some of the following: Essential Fatty To see what factors affect the EFAsnamely Omega 3 and 6 fatty acids, are a key component of cellular membranes and brain tissue, and with an insufficient intake, or excessive intake of bad saturated fats, rancid heated polyunsaturated fats or trans fats, our cellular membranes may experience inflammation and a loss of permeability essential to cellular and mitochondrial functioning.
For more information see the Nutritional page. If mitochondrial membranes are less permeable, it means that the requisite nutrients required to produce ATP are not available quickly enough, and so it has a knock-on effect in terms of ATP production in the cells of the body.
The body is not able to produce energy as efficiently. Red blood cells are not able to oxygenate as efficiently either, nor to deliver their payload of oxygen to the cells of the body. Excessive free radical oxidative damage to the mitochondrial membrane: Free radicals are produced inside the mitochondria as a byproduct of energy production and respiration.
The more energy you produce, the more free radicals you produce. The body has its own natural defence against such free radicals to prevent excessive free radical damage to the mitochondrial membranes. These are the antioxidant enzymes SOD and to a somewhat lesser extent Glutathione.
Mitochondrial function is limited in a sense by the available of SOD as without it extensive mitochondrial damage would occur with elevated respiration rates beyond the available SOD and glutathione that can be produced.
However, if levels of the rogue oxidant peroxynitrite are elevated in the mitochondria, these may destroy the SOD enzymes, resulting in an increase in Sueroxide levels produced during respiration, resulting in more free radical damage to the mitochondrial membranes.
Please see the Nitric Oxide and Peroyxnitrite Cycle page for more information on Peroxynitrite formation and damage. A deficiency in the production of either of these primary antioxidant enzymes can of course result in excessive free radical damage to the mitochondrial membranes and excessive perforation and leaking of powerful free radicals like Superoxide out of the mitochondria, causing additional knock on problems.
Damaged mitochondrial membranes are sometimes referred to as causing 'energy leaks', although this is rather a gross simplification. The mitochondrial membranes are subject to wear and tear from the residual heat-induced damage from frequent discharge of its electric polarity.
These factors are discussed in more detail in the next bullet point below. A third indicator of peroxidation of the mitochondrial membranes is F2-Alpha Isoprostane a.
It is a downstream oxidation production of membrane oxidation, specifically the Omega 6 Essential Fatty Acid EFA component of the phospholipid matrix. Isoprostanes as prostaglandin-like compounds created from the free radical attack of esterified of the Omega 6 EFA known as Arachidonic Acid ARA inside the membrane phospholipid.
ARA is particularly sensitive to peroxidation by free radicals. Isoprostanes in general are valuable markers in clinical biology as they are found in all biological fluids and tissues and are stable in vivo and ex vivo.
There are 10 times more isoprostanes in atherosclerotic plaque compared with normal vascular tissue. They are also only dependent on their production in this case free radical attack rather than metabolism or excretion without intraindividual variability.
There are many studies validating Isoprostanes as the most accurate and reliable indicator of oxidative stress in vitro and in vivo. F2-Alpha Isoprostane levels can be measured in one's urine and are a direct measurement of the extent of free radical oxidation of the mitochondrial membranes.
Please see the Oxidative Stress Tests section on the Tests page for more information. Compounds clogging up the Mitochondrial Membranes: Mitochondria are the energy furnaces of the cells of the body, and it is essential for certain types of compounds, nutrients and minerals to be able to carried enzymatically in and out of the inner and outer membrane.
If the mitochondrial membranes are clogged up, it can result in a bottleneck in the krebs cycle and thus a reduced capability to produce ATP, the energy currency of the cell.
There should not be any such 'garbage' clogging up the mitochondrial membranes. The presence of unwanted substances that can interfere with mitochondrial function contribute to a condition known as Neurotoxic Membrane Syndrome a. Please see the Inefficient Liver Function page for more information.
An article 'The Detoxx System: Detoxification of Biotoxins in Chronic Neurotoxic Syndrome' [a. Two indicators or downstream products of excessive phospho lipid peroxidation and mitochondrial membrane damageas discussed above, are the aldehyde derivates Malondialdehyde MDA and Crotonaldehyde.
Crotonaldehyde is a known irritant. According to John McLaren Howard of Acumen Laboratory, Aldehydes from lipid peroxidation when it occurs tend to accumulate in the mitochondrial membranes.
Such aldehydes, usually in the form of malondialdehyde or crotonaldehyde, can block some translocator TL sites in the inner mitochondrial membranes.
It is rare for them to accumulate to very high levels on the inner mitochondrial membranes but moderate or trace accumulation on TL sites does occur.Three Factors That Affect Your Visual Acuity From a technical standpoint, visual acuity is limited by diffraction, optical aberrations, and photoreceptor density in the eye.
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