How Non-toxin-Forming Infections Cause Diseases
Many medical practitioners and scientists have always pondered over how non-toxin-forming micro-organisms cause disease. The fact is that by causing stress, these agents ramp up metabolism, to take care of the stress sequelae(threat; exertion and external damage with consequential, respective autophagy/apoptosis and inflammation; and ultimate repairs) and they use up the host's food resources, to stay alive. Additionally, microbial waste may contribute to the host's metabolic burden.
The body responds to foreign intruders, which deprive it of valuable nutrients and cause stress(damage), by fighting back with the immune system, whose function is equally highly energy-demanding. When the immune system is not strong enough, the body's effort to get rid of the microbes is futile and the adaptation acquired by these foreign agents makes them to go into a small cell-wall,'wounded', dormant state within the host cell, and this promotes prolonged low-grade inflammation.This is the scenario with parasites.
Suffice it to say that there are commensals and symbiotic microbes. While being so in the gut, other body orifices and the skin where they feed on digestive or epithelial debris, they may become parasitic(disease causing) inside the body's tissues where they rob the body of its limited food resources. In their normal habitat(gut, skin and orifices), the body has learnt to treat the commensals and symbiotic microbes as friendly and not to react to them immunologically.
So, it appears that deprivation of the body of its food resources is the prime trigger in non-toxin forming infectious diseases, since through the microbes' taking care of their own food needs, the initial infectious damage, the subsequent reactionary inflammatory/immunological damage, repairs that follow and by corollary the energy demands from these, will make the body not to function optimally. Initially, because appetite is suppressed by inflammatory mediators, free radicals and adrenaline(epinephrine), this leads to tissue breakdown(autophagy) to supply the body with the necessary food resources for energy.
The consequence of energy deprivation is body deterioration both physically and in function. Bacteria especially use up micro-nutrients(trace metals and vitamins) and the tendency is for the host to eat more food in an attempt to try and balance up the loss. This will lead to fat build-up rather since full glucose catabolism is impaired first by negative feedback mechanism and then by micro-nutrient deprivation. No amount of exercise will completely correct this deficiency. The fat build-up is visceral, in the torso, where blood flow increases in distress( long-term stress and fear, as opposed to acute flight and fight response and eustress that direct blood to the muscles, which are programmed to use more energy in exercise). Corticosteroids induce glucose resistance in the muscle where receptors may be abundant in contrast to the liver and other visceral organs.
The limbs would use up some fat in physical activity, but not the viscera. Moreover, the fat reserves are used to provide the building blocks for stress hormones, needed initially to counteract the threat by increasing energy release and supply(increasing blood pressure) but which hormones become problematic in the long run. Norepinephrine causes glucagon release that promotes gluconeogenesis which supplies glucose, taken up directly and used by the heart, muscle, liver and brain, which organs may require a little or no insulin to use the glucose. The heart, liver and may be the brain will need this in disease stress.Norepinephrine also promotes lipolysis that supplies fatty acids that the heart, liver and muscles use. In disease stress, preferentially the liver and the heart will use fatty acids. This explains the increased blood flow to the viscera in disease(infectious) stress i.e. distress. Where blood fails to go, because of sympathetic vasoconstriction, tissue degenerates. Where blood succeeds to go there is nitric oxide release that accounts for the increased blood flow.
To correct this cascade of events, the infection must be eliminated. Failing this, the micro-nutrient imbalance must be investigated and corrected in order for the body to resume its ideal physique and function. But this may have the opposite effect of feeding the parasite rather than the host.
Disease stress will stimulate the inflammatory pathways through TNF(macrophages) and leptin(fat cells), similar in structure and function to IL-6. Both macrophages and progenitor fat cells are phagocytic, the latter also delivering melanin to the keratinocytes(hair and skin). Fatty acids, leptin and TNF will directly lead to inflammation and insulin resisitance. Leptin, also found in the placenta(hyperemesis gravidarum) and other tissues, is an appetite suppressant in response to increase in the number and size of fat cells through stress response with inflammation-induced ectopic fat lay-down(unhealthy storage) in the viscera(internal organs), muscle and arteries. (Leptin resistance may be responsible for the current obesity epidemic as more palatable meals are devised and this may have as objective, to confer advantage in times of food short supplies).
Eustress hormone, testosterone(tissue build-up) and the 'distress hormones', the corticosteroids(vascular fluid retention, tissue breakdown and glucose/fat mobilization) will counteract the stressor-induced fluid redistribution and the inflammation and immunity that go with it. So initially in stress(acute, eustress) good things happen to the body like increased metabolism with increased body oxygen and nutrient use(insulin sensitivity), inflammation/immunity in the bid to avert threat and correct any ensuing damage but in the long run(chronic, distress) decompensation sets in with mitochondrial malfunction, metabolic dysfunction , impaired immunity/persistent low-grade inflammation with insulin resistance and ectopic fat lay-down.
The beneficial effects of exercise will be limited in the infectious disease state and in inflammation. Aging is promoted by these conditions.
Dr. Oliver Verbe Birnso M.D.
The body responds to foreign intruders, which deprive it of valuable nutrients and cause stress(damage), by fighting back with the immune system, whose function is equally highly energy-demanding. When the immune system is not strong enough, the body's effort to get rid of the microbes is futile and the adaptation acquired by these foreign agents makes them to go into a small cell-wall,'wounded', dormant state within the host cell, and this promotes prolonged low-grade inflammation.This is the scenario with parasites.
Suffice it to say that there are commensals and symbiotic microbes. While being so in the gut, other body orifices and the skin where they feed on digestive or epithelial debris, they may become parasitic(disease causing) inside the body's tissues where they rob the body of its limited food resources. In their normal habitat(gut, skin and orifices), the body has learnt to treat the commensals and symbiotic microbes as friendly and not to react to them immunologically.
So, it appears that deprivation of the body of its food resources is the prime trigger in non-toxin forming infectious diseases, since through the microbes' taking care of their own food needs, the initial infectious damage, the subsequent reactionary inflammatory/immunological damage, repairs that follow and by corollary the energy demands from these, will make the body not to function optimally. Initially, because appetite is suppressed by inflammatory mediators, free radicals and adrenaline(epinephrine), this leads to tissue breakdown(autophagy) to supply the body with the necessary food resources for energy.
The consequence of energy deprivation is body deterioration both physically and in function. Bacteria especially use up micro-nutrients(trace metals and vitamins) and the tendency is for the host to eat more food in an attempt to try and balance up the loss. This will lead to fat build-up rather since full glucose catabolism is impaired first by negative feedback mechanism and then by micro-nutrient deprivation. No amount of exercise will completely correct this deficiency. The fat build-up is visceral, in the torso, where blood flow increases in distress( long-term stress and fear, as opposed to acute flight and fight response and eustress that direct blood to the muscles, which are programmed to use more energy in exercise). Corticosteroids induce glucose resistance in the muscle where receptors may be abundant in contrast to the liver and other visceral organs.
The limbs would use up some fat in physical activity, but not the viscera. Moreover, the fat reserves are used to provide the building blocks for stress hormones, needed initially to counteract the threat by increasing energy release and supply(increasing blood pressure) but which hormones become problematic in the long run. Norepinephrine causes glucagon release that promotes gluconeogenesis which supplies glucose, taken up directly and used by the heart, muscle, liver and brain, which organs may require a little or no insulin to use the glucose. The heart, liver and may be the brain will need this in disease stress.Norepinephrine also promotes lipolysis that supplies fatty acids that the heart, liver and muscles use. In disease stress, preferentially the liver and the heart will use fatty acids. This explains the increased blood flow to the viscera in disease(infectious) stress i.e. distress. Where blood fails to go, because of sympathetic vasoconstriction, tissue degenerates. Where blood succeeds to go there is nitric oxide release that accounts for the increased blood flow.
To correct this cascade of events, the infection must be eliminated. Failing this, the micro-nutrient imbalance must be investigated and corrected in order for the body to resume its ideal physique and function. But this may have the opposite effect of feeding the parasite rather than the host.
Disease stress will stimulate the inflammatory pathways through TNF(macrophages) and leptin(fat cells), similar in structure and function to IL-6. Both macrophages and progenitor fat cells are phagocytic, the latter also delivering melanin to the keratinocytes(hair and skin). Fatty acids, leptin and TNF will directly lead to inflammation and insulin resisitance. Leptin, also found in the placenta(hyperemesis gravidarum) and other tissues, is an appetite suppressant in response to increase in the number and size of fat cells through stress response with inflammation-induced ectopic fat lay-down(unhealthy storage) in the viscera(internal organs), muscle and arteries. (Leptin resistance may be responsible for the current obesity epidemic as more palatable meals are devised and this may have as objective, to confer advantage in times of food short supplies).
Eustress hormone, testosterone(tissue build-up) and the 'distress hormones', the corticosteroids(vascular fluid retention, tissue breakdown and glucose/fat mobilization) will counteract the stressor-induced fluid redistribution and the inflammation and immunity that go with it. So initially in stress(acute, eustress) good things happen to the body like increased metabolism with increased body oxygen and nutrient use(insulin sensitivity), inflammation/immunity in the bid to avert threat and correct any ensuing damage but in the long run(chronic, distress) decompensation sets in with mitochondrial malfunction, metabolic dysfunction , impaired immunity/persistent low-grade inflammation with insulin resistance and ectopic fat lay-down.
The beneficial effects of exercise will be limited in the infectious disease state and in inflammation. Aging is promoted by these conditions.
Dr. Oliver Verbe Birnso M.D.
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