Eye Shots For Wet Macular Degeneration
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The Ignored Vitamin Cure For Macular Degeneration
*What Is Wet Macular Degeneration
*Wet Macular Degeneration Treatment Options
*Eye Shots For Wet Macular Degeneration
*New Treatments For Macular Degeneration
Macular Degeneration (Wet AMD) EYLEA improved vision in people with Wet AMD. 94% of Wet AMD patients treated with EYLEA maintained their vision at 1 year of treatment. In addition, EYLEA helped people with Wet AMD see 7 more letters on the eye chart at 1 year. Wet age-related macular degeneration (AMD) develops when abnormal blood vessels grow into the macula. These leak blood or fluid which leads to scarring of the macula and rapid loss of central vision. Wet AMD can develop very suddenly, but it can now be treated if caught quickly. Wet macular degeneration treatment consists of anti-VEGF injections into the eye. These help prevent blood vessels from forming behind the retina and leaking blood, serum, and lipids into the retina. Further, leakage causes scarring and kills macular cells. The wet form of age-related macular degeneration (wet AMD) can start suddenly. You won’t feel pain, but you might notice problems with your eyesight. At first, you may simply notice blurred. At present, there are several other FDA-approved treatments for wet age-related macular degeneration: photodynamic therapy with a drug called Visudyne and injection into the eye of other VEGF inhibitors drugs called Eylea, Macugen and Lucentis.
Posted June 20, 2019: by Bill Sardi
If you want to avert the development of a sight-robbing disease called macular degeneration you are going to have to step outside modern medicine. Eye doctors only have treatment but no prevention for this dastardly eye disease that robs senior adults of their central vision for reading, driving and watching TV.
Don’t both your eye doctor about this proposed vitamin cure for macular degeneration. Your eye doctor will demand a controlled human study before he/she prescribes a vitamin. There are no published human studies to confirm its safety and effectiveness and none are planned. So, it is unproven (but not disproven). You will just have to endure slow progressive loss of vision (dry macular degeneration) and hope you don’t develop the fast-progressive form (wet macular degeneration), which requires monthly needle injections directly into your eye(s) to avoid permanent loss of vision.
The National Eye Institute promotes a multi-nutrient formula called the AREDS formula (Age-Related Eye Disease) that barely slows the progression of this disease (you still are losing your sight). The AREDS formula does not benefit patients with early macular degeneration.
A simple vitamin cure for macular degeneration has eluded eye researchers for decades and now that the ophthalmic industry has come to rely on a multi-billion dollar income stream generated by 12 million worldwide annual needle injections of medicine (5.9 million U.S. 2016) directly into the eyes to stave off permanent loss of vision. There is little if any financial impetus to prevent or cure this disease. Would it be that modern medicine allows an eye disease to progress to precipitous loss of functional vision and then attempts to rescue vision only temporarily, requiring repeated treatment, rather than prevent the disease from occurring in the first place?
This eye disease is age-related, striking a significant portion of senior adults and robbing them of independent living in their retirement years. What is the initiating factor that brings on this devastating eye disease that robs older adults of their central vision?
The medical literature points to chronic insufficient supply of oxygen to the retina, which is (incorrectly) called ischemia (iss-keem-ee-ah), as the instigating factor in macular degeneration. This report makes a scientific argument that chronic ischemia initiates macular degeneration and is also the malevolent factor in the onset of a host of other eye disorders (glaucoma, macular edema, diabetic retinopathy, retinal vein occlusion and uveitis) as well as many non-ophthalmic maladies such as chronic obstructive pulmonary disease (COPD), dementia, angina, and Alzheimer’s disease.
Numerous researchers conclude that oxygen deprivation is the starting point for dry macular degeneration:
“Our research supports the association of ischemia with dry macular degeneration.” —British Journal Ophthalmology Aug. 2013
“All retinal nerve cells are most susceptible to ischemia.” — Annals Ophthalmology (Russian) May 2010
“Ischemia may play a central role (in macular degeneration).” — Progress in Retinal Eye Research Sept. 1999
One might say there is scientific consensus that oxygen deprivation is at the starting point for the disease.The vitamin cure for macular degeneration
This report also reveals a single nutrient, thiamine (thii-ah-meen) vitamin B1, by virtue of its ability to facilitate the transport of oxygen on hemoglobin (the red oxygen-carrying pigment in red blood cells), as the antidote to eye, nerve, heart, brain and lung disorders.
T slot rack. Extremely quiet, aerodynamic crossbars attach to Yakima towers to create a stylish roof rack for your vehicle. Rubber strips in T-slots push down to load carriers or accessories - no need to trim. Maintain fuel efficiency Full-length design maximizes space for carriers and accessories Versatile crossbars accommodate accessories that mount in the T-slots or clamp around the. TracRac truck bed racks are all aluminum construction which makes them both light and strong. With a Thule truck or van rack, you get a whole new world of possibilities. Offering a variety of carrying options, they have everything you need to get your through the work week to the weekend. With different adjustable, versatile and aerodynamic solutions, finding the perfect rack. FREE Shipping by Amazon. Lot 4 Each, 48’ Aluminum T Track 3/4’ by 3/8’ Slot, Accepts 1/4’ Hex Bolts, 1/4’ or 5/16’ T Bolts, Countersunk Holes Every 6’ 112134. 4.6 out of 5 stars203. Get it as soon as Thu, Jan 28. FREE Shipping by Amazon. T-Track 36’ –Double Cut Profile Universal with Predrilled Mounting Holes -Woodworking and Clamps -High Strength.
By definition, ischemia is insufficient blood flow to provide adequate oxygenation to cells. Ischemia may then lead to tissue hypoxia (hi-pox-ee-ah), reduced oxygen, or anoxia (an-ox-ee-ah), which is absence of oxygen altogether.
However, these defined terms do not encompass what actually may be happening. It may not be impaired blood flow but rather impaired transport of oxygen to tissues that induces disease. This etiology is generally not considered in research papers.
Reduced tissue oxygenation is strongly implicated in the onset of macular degeneration. Impaired oxygen delivery can emanate from a deficiency of thiamine (vitamin B1) required for cell energy and oxygen delivery on hemoglobin.
To continue, an understanding of how the retina of the human eye is organized is necessary to understand how macular degeneration gets started.
The retina is organized from back to front as follows:
Back of Eyes
The blood supply layer of the retina (choroid) is separated from the light (photo) receptors by a thin cellophane-like film called Bruch’s (Bruuks’s) membrane and a single layer thick row of cells called the retinal pigment epithelium (RPE). Calcium and fats accumulate in Bruch’s membrane with advancing age. This membrane doubles in thickness from 2.0 microns to 4.7 microns over ten decades.
It has been argued that lipid (fat) accumulation in Bruch’s membrane does impairs delivery of oxygen to the photoreceptors. However, researchers rule out that accumulation of fats in Bruch’s membrane impairs blood flow or oxygen delivery in any significant way.
A thickened Bruch’s membrane can delay oxygen to the photoreceptors. Calcification of Bruch’s membrane can impair oxygenation. A more acute example is a disease called pseudoxanthoma elasticum which is characterized by calcification throughout the body. Calcification is known to starve the photoreceptors of oxygen and induce destructive new blood vessels (aka neovascularization or angiogenesis) in cases of pseudoxanthoma elasticum.
Blood flow through the choroid is said to be the highest of any tissue in the body but oxygen extraction from hemoglobin is one of the lowest of any tissue in the body (less than 1 volume percent of oxygen). This makes a shortage of thiamine/B1 critical in normalizing oxygen delivery to the retina.
Oxygen levels are high in the barrier layer (RPE) because it is in close approximation to the oxygen-rich choroid. But further away from the choroid, oxygen levels decline to near zero at the photoreceptors in the dark. This near-zero oxygen environment must be a defensive mechanism to limit oxidation. But it also increases their vulnerability to oxygen deprivation.Human body designed to rely on thiamine/vitamin B1
It has also been documented that as a total oxygen-less state develops in tissues (ischemia/hypoxia), molecular transporters of thiamine are increased on hemoglobin, evidence the body is designed and relies upon thiamine naturally for dynamic defense against oxygen-deprivation.Sending a signal for ischemia/hypoxia without true lack of oxygen
Of interest, thiamin-deficiency can molecularly elevate a protein called hypoxia-inducing factor (HIF-1) and induce destructive new blood vessels without true oxygen deprivation, a condition called pseudo-hypoxia.
Changes in tissues due to true lack of oxygen (hypoxia-ischemia) are identical to those produced by thiamine deficiency. This suggests many cases of wet macular degeneration may be induced by thiamin deficiency alone, without oxygen deprivation. This may also explain why some patients with wet macular degeneration do not respond to anti-growth factor injections.Dry versus wet macular degeneration
The so-called early form of macular degeneration, called the dry form, is distinguished from the wet form by leaky blood vessels (micro-hemorrhages) and oxygen deprivation so acute that new blood vessels outcrop and invade the visual center (macula) of the eyes.
There is no argument that wet-form macular degeneration is triggered by frank lack of oxygenation. In an oxygen-less environment, a growth factor (vascular endothelial growth factor or VEGF) activates the outcropping of invasive blood vessels that destroy the visual center (macula) of the eyes. Eye doctors inject anti-VEGF medications periodically (monthly) to prevent permanent loss of vision.
The less invasive dry form of this disease “can only be caused by ischemia” say researchers at Colombia University Medical Center. And certainly the absence of oxygen also triggers the more severe wet macular degeneration as well.Autonomic control of blood circulation and thiamine
More specifically, researchers note there are dysfunctional small arteries (arterioles) in the blood layer (choroid) are under the control of the autonomic nervous system (not under conscious control by the individual). Bodily functions like heart rate, respiration rate, temperature control, hunger and appetite, waste elimination, and sweating are automatically controlled in the human body.
Autonomic control goes haywire in dry form of macular degeneration. Colombia University Medical School researchers hypothesize their investigation “supports a parasympathetic (autonomic) control of the arterioles as a causative factor in reduced perfusion (passage of blood) of the area surrounding the RPE (retinal pigment epithelium).”
Not noted by these researchers is that thiamine/vitamin B1 is essential for proper control of the autonomic nervous system.Dilation of arteries by nitric oxide gas negated by lack of thiamine
Normally a transient gas called nitric oxide dilates (widens) arteries to maintain blood flow and pressure. Drugs like niacin and Viagra-like drugs that activate nitric oxide would then have application for this disease. But the production of nitric oxide is impaired due to loss of autonomic control, note researchers. Albeit, the lack of nitric oxide gas is also associated with blockage of veins (retinal vein occlusion) as de-oxygenated blood exits the retina.
Dietary nitrates, such as found in sugar beets, may increase nitric oxide and inhibit autonomic (parasympathetic) constriction of arterioles(small arteries) in the retina. Other molecules found in garlic (allicin) and grape wine (resveratrol) activate nitric oxide and improve circulation. But again, lack of thiamine limits the capacity to produce nitric oxide.
Lack of cell energy is given as another reason why insufficient amounts of nitric oxide gas are produced in certain disease states. Given that thiamine boosts cell energy (adeno-triphosphate or ATP levels) within the atomic power plants (mitochondria) of living cells, it is no surprise to learn that thiamine is a critical nutrient to enabling nitric oxide to do its job of dilating (widening) arteries to improve blood circulation and delivery of oxygen.To test the oxygen-deprivation theory of macular degeneration
In further support of the oxygen deprivation origin of macular degeneration, it is well documented that sleep apnea (stop-and-start breathing during sleep) worsens macular degeneration whereas hyperbaric oxygen treatment is efficacious in preserving or improving sight. Furthermore, in more severe oxygen deprivation (total or near-total absence of oxygen), hyperbaric oxygen rescues patients with wet macular degeneration. Untreated sleep apnea hinders the response to anti-growth factor injections into the eyes of macular degeneration patients.Thiamine/vitamin B1 theory of eye disease put to the test
Consistent with the thiamine-deficiency theory of wet-macular degeneration, it has been shown that a shortage of thiamine promotes more of a protein complex called hypoxia inducing factor (HIF1) that then triggers the production of growth factors (VEGF) that then sprout new blood vessels that destroy central vision. Therefore, thiamine supplementation would be strongly indicated to head off wet macular degeneration and needle-injections of anti-growth factors directly into the eyes. However, use of thiamine to prevent wet macular degeneration remains untried.
Low cellular levels of thiamine results in a decline in cellular energy and poor transport of oxygen to tissues, particularly in the retinal pigment epithelial cells that separate the retinal blood supply (choroid) and the photoreceptors. In a state of thiamine deficiency excess lactic acid is produced in tissues throughout the body. Patients with macular degeneration characteristically exhibit low cell energy and elevated lactic acid.What Is Wet Macular Degeneration
In 2009 vitamin B1 was heralded as a cure for uveitis, an inflammation of pigmented inner lining of the eye. But it is not known if thiamine has come into common practice in eye clinics for this malady, given modern medicine’s reluctance to embrace nutritional medicine.How laser treatment increases oxygen delivery to the retina
An explanation of how laser treatment rescues threatened vision centers on the restoration of oxygen supply to a starved retina. It has been noted that if some retinal photoreceptors are destroyed by laser light, then subsequent scars that form at the back of the eyes allow oxygen to diffuse directly to the inner retina via these laser-induced scars rather than being consumed by the energy-making compartments (mitochondria) of the photoreceptors. With adequate oxygenation, then growth factors are inhibited and destructive new blood vessel formation is halted.Oxygen deprivation and other diseases
Thiamine deficiency and consequent oxygen deprivation is linked to many other maladies.
Chronic obstructive pulmonary disease (COPD) is a serious lung disease. It takes the breath out of COPD sufferers. It is not surprising to learn that dietary intake of thiamine is lower than the Recommended Daily Allowance in over 75% of COPD patients.
Nor is it surprising to learn that the symptoms of an inherited mitochondrial disorder called Leigh Syndrome (maternally inherited) which encompasses night blindness, nerve disorders and abnormally uncoordinated movements called ataxia, are treated with thiamine.
Thiamine in its fat-soluble form (benfotiamine) is literally curing Alzheimer’s disease as evidenced in brain scans. Given that benfotiamine does not pass through the blood/brain barrier, it is obviously working indirectly (autonomic control or by increasing oxygenation before it reaches the brain?).
Dementia, a progressive decline in mental function, is actually called transient ischemic attack (TIA). Loss of autonomic control is at the core of all chronic brain disorders. Thiamine is considered a protective factor for dementia.
Nor should silent ischemia that produces no symptoms of chest pain be overlooked. Some 3 to 4 million Americans experience silent heart disease (angina).
Regardless of the lack of published evidence, any human disease that involves oxygen deprivation should be indicative of need for thiamine.Why the eyes, but not other tissues and organs, are affected
It is not difficult to understand why patients with macular degeneration may not exhibit signs or symptoms of oxygen deprivation in other organs and tissues. The human eye is particularly vulnerable to shortages of oxygen.
There are 140 million night vision (rod) cells and ~6 million color vision cells (cones) in the retina. Rods can function in remarkably ultra-low oxygen environment. In the dark the 140 million rod cells devour oxygen and virtually surround and overwhelm the far fewer cone cells, resulting in a zone of near-zero oxygen in the macula, the visual center of the eyes. The central retina has very little oxygen reserve capacity.Arsenic is the environmental toxin that induces hypoxia
An interesting environmental factor that exacerbates any oxygen-deprived tissue is arsenic, a heavy metal contaminant found in water supplies and in the widely used glyphosate herbicide, that can mimic a hypoxic effect. Arsenic can set the stage for oxygen deprivation diseases.
Few if any eye physicians would suspect arsenic toxicity in out-of-control wet macular degeneration or diabetic retinopathy. Without knowledge of their cause, many cases of eye disease that don’t respond to conventional treatment will remain unexplained. Given that glyphosate is associated with kidney disease, it is not beyond the realm of possibility that the more vulnerable retina could also be harmed by arsenic toxicity via pseudo-hypoxia. There is some scientific awareness that arsenic is related to macular degeneration.Do macular degeneration patients have beriberi?
Beriberi is the name of the disease symptoms that emanates from a frank deficiency of thiamine/vitamin B1. Oxygen deprivation due to poor transport of oxygen in thiamin-deficient individuals could theoretically produce abnormalities simultaneously throughout the body. However, certain organs and tissues ar
https://diarynote.indered.space
The Ignored Vitamin Cure For Macular Degeneration
*What Is Wet Macular Degeneration
*Wet Macular Degeneration Treatment Options
*Eye Shots For Wet Macular Degeneration
*New Treatments For Macular Degeneration
Macular Degeneration (Wet AMD) EYLEA improved vision in people with Wet AMD. 94% of Wet AMD patients treated with EYLEA maintained their vision at 1 year of treatment. In addition, EYLEA helped people with Wet AMD see 7 more letters on the eye chart at 1 year. Wet age-related macular degeneration (AMD) develops when abnormal blood vessels grow into the macula. These leak blood or fluid which leads to scarring of the macula and rapid loss of central vision. Wet AMD can develop very suddenly, but it can now be treated if caught quickly. Wet macular degeneration treatment consists of anti-VEGF injections into the eye. These help prevent blood vessels from forming behind the retina and leaking blood, serum, and lipids into the retina. Further, leakage causes scarring and kills macular cells. The wet form of age-related macular degeneration (wet AMD) can start suddenly. You won’t feel pain, but you might notice problems with your eyesight. At first, you may simply notice blurred. At present, there are several other FDA-approved treatments for wet age-related macular degeneration: photodynamic therapy with a drug called Visudyne and injection into the eye of other VEGF inhibitors drugs called Eylea, Macugen and Lucentis.
Posted June 20, 2019: by Bill Sardi
If you want to avert the development of a sight-robbing disease called macular degeneration you are going to have to step outside modern medicine. Eye doctors only have treatment but no prevention for this dastardly eye disease that robs senior adults of their central vision for reading, driving and watching TV.
Don’t both your eye doctor about this proposed vitamin cure for macular degeneration. Your eye doctor will demand a controlled human study before he/she prescribes a vitamin. There are no published human studies to confirm its safety and effectiveness and none are planned. So, it is unproven (but not disproven). You will just have to endure slow progressive loss of vision (dry macular degeneration) and hope you don’t develop the fast-progressive form (wet macular degeneration), which requires monthly needle injections directly into your eye(s) to avoid permanent loss of vision.
The National Eye Institute promotes a multi-nutrient formula called the AREDS formula (Age-Related Eye Disease) that barely slows the progression of this disease (you still are losing your sight). The AREDS formula does not benefit patients with early macular degeneration.
A simple vitamin cure for macular degeneration has eluded eye researchers for decades and now that the ophthalmic industry has come to rely on a multi-billion dollar income stream generated by 12 million worldwide annual needle injections of medicine (5.9 million U.S. 2016) directly into the eyes to stave off permanent loss of vision. There is little if any financial impetus to prevent or cure this disease. Would it be that modern medicine allows an eye disease to progress to precipitous loss of functional vision and then attempts to rescue vision only temporarily, requiring repeated treatment, rather than prevent the disease from occurring in the first place?
This eye disease is age-related, striking a significant portion of senior adults and robbing them of independent living in their retirement years. What is the initiating factor that brings on this devastating eye disease that robs older adults of their central vision?
The medical literature points to chronic insufficient supply of oxygen to the retina, which is (incorrectly) called ischemia (iss-keem-ee-ah), as the instigating factor in macular degeneration. This report makes a scientific argument that chronic ischemia initiates macular degeneration and is also the malevolent factor in the onset of a host of other eye disorders (glaucoma, macular edema, diabetic retinopathy, retinal vein occlusion and uveitis) as well as many non-ophthalmic maladies such as chronic obstructive pulmonary disease (COPD), dementia, angina, and Alzheimer’s disease.
Numerous researchers conclude that oxygen deprivation is the starting point for dry macular degeneration:
“Our research supports the association of ischemia with dry macular degeneration.” —British Journal Ophthalmology Aug. 2013
“All retinal nerve cells are most susceptible to ischemia.” — Annals Ophthalmology (Russian) May 2010
“Ischemia may play a central role (in macular degeneration).” — Progress in Retinal Eye Research Sept. 1999
One might say there is scientific consensus that oxygen deprivation is at the starting point for the disease.The vitamin cure for macular degeneration
This report also reveals a single nutrient, thiamine (thii-ah-meen) vitamin B1, by virtue of its ability to facilitate the transport of oxygen on hemoglobin (the red oxygen-carrying pigment in red blood cells), as the antidote to eye, nerve, heart, brain and lung disorders.
T slot rack. Extremely quiet, aerodynamic crossbars attach to Yakima towers to create a stylish roof rack for your vehicle. Rubber strips in T-slots push down to load carriers or accessories - no need to trim. Maintain fuel efficiency Full-length design maximizes space for carriers and accessories Versatile crossbars accommodate accessories that mount in the T-slots or clamp around the. TracRac truck bed racks are all aluminum construction which makes them both light and strong. With a Thule truck or van rack, you get a whole new world of possibilities. Offering a variety of carrying options, they have everything you need to get your through the work week to the weekend. With different adjustable, versatile and aerodynamic solutions, finding the perfect rack. FREE Shipping by Amazon. Lot 4 Each, 48’ Aluminum T Track 3/4’ by 3/8’ Slot, Accepts 1/4’ Hex Bolts, 1/4’ or 5/16’ T Bolts, Countersunk Holes Every 6’ 112134. 4.6 out of 5 stars203. Get it as soon as Thu, Jan 28. FREE Shipping by Amazon. T-Track 36’ –Double Cut Profile Universal with Predrilled Mounting Holes -Woodworking and Clamps -High Strength.
By definition, ischemia is insufficient blood flow to provide adequate oxygenation to cells. Ischemia may then lead to tissue hypoxia (hi-pox-ee-ah), reduced oxygen, or anoxia (an-ox-ee-ah), which is absence of oxygen altogether.
However, these defined terms do not encompass what actually may be happening. It may not be impaired blood flow but rather impaired transport of oxygen to tissues that induces disease. This etiology is generally not considered in research papers.
Reduced tissue oxygenation is strongly implicated in the onset of macular degeneration. Impaired oxygen delivery can emanate from a deficiency of thiamine (vitamin B1) required for cell energy and oxygen delivery on hemoglobin.
To continue, an understanding of how the retina of the human eye is organized is necessary to understand how macular degeneration gets started.
The retina is organized from back to front as follows:
Back of Eyes
The blood supply layer of the retina (choroid) is separated from the light (photo) receptors by a thin cellophane-like film called Bruch’s (Bruuks’s) membrane and a single layer thick row of cells called the retinal pigment epithelium (RPE). Calcium and fats accumulate in Bruch’s membrane with advancing age. This membrane doubles in thickness from 2.0 microns to 4.7 microns over ten decades.
It has been argued that lipid (fat) accumulation in Bruch’s membrane does impairs delivery of oxygen to the photoreceptors. However, researchers rule out that accumulation of fats in Bruch’s membrane impairs blood flow or oxygen delivery in any significant way.
A thickened Bruch’s membrane can delay oxygen to the photoreceptors. Calcification of Bruch’s membrane can impair oxygenation. A more acute example is a disease called pseudoxanthoma elasticum which is characterized by calcification throughout the body. Calcification is known to starve the photoreceptors of oxygen and induce destructive new blood vessels (aka neovascularization or angiogenesis) in cases of pseudoxanthoma elasticum.
Blood flow through the choroid is said to be the highest of any tissue in the body but oxygen extraction from hemoglobin is one of the lowest of any tissue in the body (less than 1 volume percent of oxygen). This makes a shortage of thiamine/B1 critical in normalizing oxygen delivery to the retina.
Oxygen levels are high in the barrier layer (RPE) because it is in close approximation to the oxygen-rich choroid. But further away from the choroid, oxygen levels decline to near zero at the photoreceptors in the dark. This near-zero oxygen environment must be a defensive mechanism to limit oxidation. But it also increases their vulnerability to oxygen deprivation.Human body designed to rely on thiamine/vitamin B1
It has also been documented that as a total oxygen-less state develops in tissues (ischemia/hypoxia), molecular transporters of thiamine are increased on hemoglobin, evidence the body is designed and relies upon thiamine naturally for dynamic defense against oxygen-deprivation.Sending a signal for ischemia/hypoxia without true lack of oxygen
Of interest, thiamin-deficiency can molecularly elevate a protein called hypoxia-inducing factor (HIF-1) and induce destructive new blood vessels without true oxygen deprivation, a condition called pseudo-hypoxia.
Changes in tissues due to true lack of oxygen (hypoxia-ischemia) are identical to those produced by thiamine deficiency. This suggests many cases of wet macular degeneration may be induced by thiamin deficiency alone, without oxygen deprivation. This may also explain why some patients with wet macular degeneration do not respond to anti-growth factor injections.Dry versus wet macular degeneration
The so-called early form of macular degeneration, called the dry form, is distinguished from the wet form by leaky blood vessels (micro-hemorrhages) and oxygen deprivation so acute that new blood vessels outcrop and invade the visual center (macula) of the eyes.
There is no argument that wet-form macular degeneration is triggered by frank lack of oxygenation. In an oxygen-less environment, a growth factor (vascular endothelial growth factor or VEGF) activates the outcropping of invasive blood vessels that destroy the visual center (macula) of the eyes. Eye doctors inject anti-VEGF medications periodically (monthly) to prevent permanent loss of vision.
The less invasive dry form of this disease “can only be caused by ischemia” say researchers at Colombia University Medical Center. And certainly the absence of oxygen also triggers the more severe wet macular degeneration as well.Autonomic control of blood circulation and thiamine
More specifically, researchers note there are dysfunctional small arteries (arterioles) in the blood layer (choroid) are under the control of the autonomic nervous system (not under conscious control by the individual). Bodily functions like heart rate, respiration rate, temperature control, hunger and appetite, waste elimination, and sweating are automatically controlled in the human body.
Autonomic control goes haywire in dry form of macular degeneration. Colombia University Medical School researchers hypothesize their investigation “supports a parasympathetic (autonomic) control of the arterioles as a causative factor in reduced perfusion (passage of blood) of the area surrounding the RPE (retinal pigment epithelium).”
Not noted by these researchers is that thiamine/vitamin B1 is essential for proper control of the autonomic nervous system.Dilation of arteries by nitric oxide gas negated by lack of thiamine
Normally a transient gas called nitric oxide dilates (widens) arteries to maintain blood flow and pressure. Drugs like niacin and Viagra-like drugs that activate nitric oxide would then have application for this disease. But the production of nitric oxide is impaired due to loss of autonomic control, note researchers. Albeit, the lack of nitric oxide gas is also associated with blockage of veins (retinal vein occlusion) as de-oxygenated blood exits the retina.
Dietary nitrates, such as found in sugar beets, may increase nitric oxide and inhibit autonomic (parasympathetic) constriction of arterioles(small arteries) in the retina. Other molecules found in garlic (allicin) and grape wine (resveratrol) activate nitric oxide and improve circulation. But again, lack of thiamine limits the capacity to produce nitric oxide.
Lack of cell energy is given as another reason why insufficient amounts of nitric oxide gas are produced in certain disease states. Given that thiamine boosts cell energy (adeno-triphosphate or ATP levels) within the atomic power plants (mitochondria) of living cells, it is no surprise to learn that thiamine is a critical nutrient to enabling nitric oxide to do its job of dilating (widening) arteries to improve blood circulation and delivery of oxygen.To test the oxygen-deprivation theory of macular degeneration
In further support of the oxygen deprivation origin of macular degeneration, it is well documented that sleep apnea (stop-and-start breathing during sleep) worsens macular degeneration whereas hyperbaric oxygen treatment is efficacious in preserving or improving sight. Furthermore, in more severe oxygen deprivation (total or near-total absence of oxygen), hyperbaric oxygen rescues patients with wet macular degeneration. Untreated sleep apnea hinders the response to anti-growth factor injections into the eyes of macular degeneration patients.Thiamine/vitamin B1 theory of eye disease put to the test
Consistent with the thiamine-deficiency theory of wet-macular degeneration, it has been shown that a shortage of thiamine promotes more of a protein complex called hypoxia inducing factor (HIF1) that then triggers the production of growth factors (VEGF) that then sprout new blood vessels that destroy central vision. Therefore, thiamine supplementation would be strongly indicated to head off wet macular degeneration and needle-injections of anti-growth factors directly into the eyes. However, use of thiamine to prevent wet macular degeneration remains untried.
Low cellular levels of thiamine results in a decline in cellular energy and poor transport of oxygen to tissues, particularly in the retinal pigment epithelial cells that separate the retinal blood supply (choroid) and the photoreceptors. In a state of thiamine deficiency excess lactic acid is produced in tissues throughout the body. Patients with macular degeneration characteristically exhibit low cell energy and elevated lactic acid.What Is Wet Macular Degeneration
In 2009 vitamin B1 was heralded as a cure for uveitis, an inflammation of pigmented inner lining of the eye. But it is not known if thiamine has come into common practice in eye clinics for this malady, given modern medicine’s reluctance to embrace nutritional medicine.How laser treatment increases oxygen delivery to the retina
An explanation of how laser treatment rescues threatened vision centers on the restoration of oxygen supply to a starved retina. It has been noted that if some retinal photoreceptors are destroyed by laser light, then subsequent scars that form at the back of the eyes allow oxygen to diffuse directly to the inner retina via these laser-induced scars rather than being consumed by the energy-making compartments (mitochondria) of the photoreceptors. With adequate oxygenation, then growth factors are inhibited and destructive new blood vessel formation is halted.Oxygen deprivation and other diseases
Thiamine deficiency and consequent oxygen deprivation is linked to many other maladies.
Chronic obstructive pulmonary disease (COPD) is a serious lung disease. It takes the breath out of COPD sufferers. It is not surprising to learn that dietary intake of thiamine is lower than the Recommended Daily Allowance in over 75% of COPD patients.
Nor is it surprising to learn that the symptoms of an inherited mitochondrial disorder called Leigh Syndrome (maternally inherited) which encompasses night blindness, nerve disorders and abnormally uncoordinated movements called ataxia, are treated with thiamine.
Thiamine in its fat-soluble form (benfotiamine) is literally curing Alzheimer’s disease as evidenced in brain scans. Given that benfotiamine does not pass through the blood/brain barrier, it is obviously working indirectly (autonomic control or by increasing oxygenation before it reaches the brain?).
Dementia, a progressive decline in mental function, is actually called transient ischemic attack (TIA). Loss of autonomic control is at the core of all chronic brain disorders. Thiamine is considered a protective factor for dementia.
Nor should silent ischemia that produces no symptoms of chest pain be overlooked. Some 3 to 4 million Americans experience silent heart disease (angina).
Regardless of the lack of published evidence, any human disease that involves oxygen deprivation should be indicative of need for thiamine.Why the eyes, but not other tissues and organs, are affected
It is not difficult to understand why patients with macular degeneration may not exhibit signs or symptoms of oxygen deprivation in other organs and tissues. The human eye is particularly vulnerable to shortages of oxygen.
There are 140 million night vision (rod) cells and ~6 million color vision cells (cones) in the retina. Rods can function in remarkably ultra-low oxygen environment. In the dark the 140 million rod cells devour oxygen and virtually surround and overwhelm the far fewer cone cells, resulting in a zone of near-zero oxygen in the macula, the visual center of the eyes. The central retina has very little oxygen reserve capacity.Arsenic is the environmental toxin that induces hypoxia
An interesting environmental factor that exacerbates any oxygen-deprived tissue is arsenic, a heavy metal contaminant found in water supplies and in the widely used glyphosate herbicide, that can mimic a hypoxic effect. Arsenic can set the stage for oxygen deprivation diseases.
Few if any eye physicians would suspect arsenic toxicity in out-of-control wet macular degeneration or diabetic retinopathy. Without knowledge of their cause, many cases of eye disease that don’t respond to conventional treatment will remain unexplained. Given that glyphosate is associated with kidney disease, it is not beyond the realm of possibility that the more vulnerable retina could also be harmed by arsenic toxicity via pseudo-hypoxia. There is some scientific awareness that arsenic is related to macular degeneration.Do macular degeneration patients have beriberi?
Beriberi is the name of the disease symptoms that emanates from a frank deficiency of thiamine/vitamin B1. Oxygen deprivation due to poor transport of oxygen in thiamin-deficient individuals could theoretically produce abnormalities simultaneously throughout the body. However, certain organs and tissues ar
https://diarynote.indered.space
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