More Eye-Opening Science

What are the things that damage eyesight, and what can you do about it? Does eating carrots help? The answer to that can be a categorical yes and an undeniable no, and the real reasons for both the yes and the no, rarely get a mention.

Sugar can help, but it probably won’t get the credit it deserves anytime soon. The polyunsaturated fatty acids (PUFAs) are a big problem, but they’re likely to continue to get a free pass. Diet isn’t the only factor, but it makes more of a difference than most realise.

I’m not a medical practitioner, and I’m not here to give you any advice, but I have read plenty of good quality biological science, and if you understand how, you can put it all together in such a way as to give you some powerful insight and direction.

There are many different kinds of visual impairment or vision loss. There are refractive errors (like nearsightedness and astigmatism), cataracts and diabetic retinopathy, as well as macular degeneration and other things. Do they have anything in common? Biology seems to think they do.

Women are more likely than men to suffer from eyesight issues such as myopia or shortsightedness, and cataracts and macular degeneration tend to be issues of aging. Age and sex differences can be useful clues, but regardless, it is always important to look at the factors which impact upon metabolic function. This means a discussion about the activity of hormones and other biochemical substances, thyroid included.

“In case of thyroid pathology, visual acuity…was worse than in the control group…Myopia dominated in patients with thyroid pathology.”

“Visual field defect was detected in 71% of patients suffering of primary hypothyroidism. The most common characteristic change was the defect in the central visual field. All cases of visual field defect were cured by thyroid hormone replacement therapy.”

It doesn’t make sense to talk about the proper function of the body – from cells to tissue, including organs – without mention of the crucial role played by thyroid energy metabolism. The sensitive and potentially vulnerable nature of eye tissue, makes this subject even more relevant. In general, if you improve metabolic function, you can protect against many things that impact upon eyesight.

There is likely a far stronger connection between the progression of symptoms of the degenerative diseases like diabetes, and the gradual worsening of vision often associated with metabolic suppression, than is commonly discussed.

“Diabetic retinopathy (DR) is the most common ocular complication of diabetes, and is the leading cause of visual impairment and blindness in working-aged people…The association between T2DM and SCH (subclinical hypothyroidism) is well known…In this research, the pooled effect estimated from eight included papers demonstrated a 2.13 fold increased risk of DR in SCH patients compared with non-SCH individuals.”

Exposure to extreme or chronic stress – whether it be environmental or nutritional or something else – can promote the conditions which tend to interfere with the ability of thyroid metabolism to function optimally.

Whatever the level of stress, it must be met with the provision of enough energy to maintain proper metabolic performance. When this does not occur, for example when sugar is being restricted, the stress metabolism kicks in, and this comes with a cost.

When glycogen stores are depleted, cortisol and adrenalin rise, promoting the release of a number of stress related, inflammatory substances – such as nitric oxide (NO), serotonin and estrogen – which tend to suppress mitochondrial energy systems, and make the eyes more sensitive to stress, and susceptible to damage and degeneration.

“The visual system is one of the most energetically demanding systems in the brain. The currency of energy is ATP, which is generated most efficiently from oxidative metabolism in the mitochondria…Deficiencies in energy metabolism, such as in diabetes, mitochondrial DNA mutation, mitochondrial protein malfunction, and oxidative stress can lead to retinopathy, visual deficits, neuronal degeneration, and eventual blindness.”

“Plasma serotonin concentration was increased significantly only in the patients with proliferative DR (diabetic retinopathy), while in the rest groups this concentration was notably decreased.”

When stress is high and energy availability is insufficient, rising levels of cortisol and adrenalin encourage the release of free fatty acids into the blood, and the more polyunsaturated they are, the more they promote the stress substances.

The unstable nature of PUFA leads to lipid peroxidation, via exposure to oxidative stress, both of which have been shown to have a direct involvement in eye degeneration.

“In the eye, lipid peroxidation has been reported to play an important role in degenerative ocular diseases (age-related macular degeneration, cataract, glaucoma, diabetic retinopathy)…peroxidation of long chain polyunsaturated acids (LCPUFAs) such as arachidonic acid and docosahexaenoic acid leads to generation of LCPUFA metabolites…that may…exert pharmacological/toxicological actions in ocular tissues.”

“Age-related macular degeneration (AMD) is a major cause of blindness in developed countries and is closely related to oxidative stress, which leads to lipid peroxidation. Malondialdehyde (MDA) is a major byproduct of polyunsaturated fatty acid (PUFA) peroxidation. Increased levels of MDA have been reported in eyes of AMD patients.”

“… the neurosensorial tissue of the eye…extremely rich in polyunsaturated lipid…makes it especially sensitive to oxygen and/or nitrogen activated species and lipid peroxidation…In the present study, we have used…antioxidants…to ameliorate the oxidative stress that exists in the retina in diabetic patients.”

“Initial stages of cataract were characterized by the accumulation of primary LPO (free-radical-induced lipid peroxidation) products, while in the latest stages there was a prevalence of fluorescent end products of LPO…”

Excess circulating iron, especially in the presence of PUFA, is another factor involved in oxidative damage of the eyes associated with aging and the progression of diseases of degeneration.

“Iron is a potent generator of oxidative damage whose levels increase with age, potentially exacerbating age-related diseases. Several lines of evidence suggest that iron accumulation may be a factor in age-related macular degeneration.”

“…it has been known for years that iron overload is associated with retinal degeneration in the context of ocular siderosis, intraocular hemorrhage…evidence suggests that age-related macular degeneration (AMD) may also be exacerbated by retinal iron…Iron overload…can cause retinal toxicity through the generation of oxygen free radicals.”

The amount of PUFA circulating in the system is a significant factor in the creation of an inflammatory environment (potentially becoming a chronic and systemic issue), and this contributes to the vulnerability of cells and tissue, to damage arising out of interactions both with external and internal stressors.

PUFA is known to powerfully interfere with thyroid function, and inhibit digestion. When metabolism is suppressed, more opportunity is provided for bacteria to feed and multiply, to move further and further up the intestines, and to pass into the main system. This means increased circulation of endotoxin, and further release of serotonin, estrogen, NO and other inflammatory things, which then further the advancement of metabolic suppression, eventuating in damage to tissue and organs.

“Serotonin…has a multitude of more or less clearly established effects on peripheral vessels…It influences blood viscosity, platelet aggregation, and vasoconstruction and -dilatation, it enhances capillary permeability, it is the precursor of melatonin… a role for serotonin in the development of glaucoma and diabetic retinopathy might be suspected…”

As greater amounts of these substances pass through to the liver, the liver can become overloaded, reducing detoxification capability, and interfering with thyroid function. This again allows for systemic levels of endotoxin, serotonin, estrogen and NO to rise, encouraging a downward spiraling state, exposing sensitive organs like the eyes to more harm.

“The patients with type 2 diabetes had significantly higher levels of serum NOx (nitric oxide) than the nondiabetic controls. In addition, the levels in the patients with proliferative DR (diabetic retinopathy) were significantly higher than the levels in the patients with nonproliferative or no DR.”

Experimental (as well as epidemiological) evidence suggests that there is a connection between the issues of the eyes, and a variety of manifestations of thyroid dysfunction, commonly associated with increased levels of estrogen, serotonin, and the polyunsaturated fats.

“The finding that female susceptibility to axonal injury, retinal pathology, and vision loss in the setting of optic glioma reflects estrogen activation of microglia represents one of the first demonstrations of sexually dimorphic differences in human disease.”

So called hyperthyroid conditions (often the result of the same metabolically suppressed state) have been associated with macular degeneration and other forms of vision impairment.

“The data we have found suggest that Graves’ disease in children, teenagers, and adults have influence on proptosis, visual acuity, and refractive changes.”

“Overt hyperthyroidism was independently associated with an increased risk of incident AMD. Thyroxine usage in older adults was also positively associated with incidence of AMD.”

Women generally have more estrogen than men (at least young men), and this often goes hand in hand with a sluggish liver and a far greater frequency of thyroid related issues. This can probably help to explain their increased susceptibility to certain types of issues relating to eyesight.

“Proliferation of the retinal microvascular endothelium is an integral component in the development of proliferative diabetic retinopathy (PDR), a major cause of blindness worldwide…The addition of exogenous E2 induced a significant increase in…cell proliferation…”

“…high concentrations of E2 (estradiol) in IMH (idiopathic macular hole) patients…pro-inflammatory cytokines…are known to…promote the aromatization of testosterone to E2…studies have reported that these proinflammatory cytokines were significantly higher in…proliferative diabetic retinopathy…”

Estrogen and serotonin promote NO release, and NO suppresses oxidative metabolism, exacerbating conditions closely tied to diabetes, and aggravating problems in the eyes directly connected to the progression of diabetes.

“We found that…NO levels…of the active PDR (proliferative diabetic retinopathy) group were significantly higher…NO present in the ocular tissues may play important roles in the progression of DR.”

“Increased plasma NO levels are associated with increased severity of diabetic retinopathy. For the first time, it has been demonstrated that increased plasma LPO (lipid peroxide), NO…are associated with in vivo structural changes…”

Prolactin and melatonin (closely linked to rising estrogen and serotonin) are known to rise under conditions of stress, including darkness, and some studies have found that they can promote problems with the eyes (particularly in combination with the polyunsaturated fats), including refractive errors and a susceptibility to damage from exposure to light.

“This study reports for the first time in humans that myopes exhibit higher serum Mel (melatonin) concentrations than non-myopes. This may indicate a role for light exposure and circadian rhythm in the human myopic growth mechanism…”

When metabolism is functioning well, the level of bacteria in the intestines is maintained at a minimum, keeping endotoxin at bay, and reducing secretion of the stress substances in general. Raw carrot fiber is antimicrobial, and regular consumption helps to reduce bacterial issues and clear out excess estrogen and serotonin, preventing re-absorption into the main system.

This reduces the load on the liver, improving detoxification capabilities and enabling further removal of estrogen. This means thyroid can function better, and the end result is greater protection against many of the inflammatory substances (including PUFA released from storage) which interact promoting conditions which put strain on the eyes.

Inflammation in general is closely associated with eye disease, and ongoing exposure to excessive levels of the substances of stress such as NO, which promote and are promoted by inflammatory low-metabolism conditions, seems to play a big part in the progression of damage.

“NO formed by inducible NOS (iNOS) expressed under influences of inflammatory mediators evokes neurodegeneration and cell apoptosis, leading to serious ocular diseases.”

“Inducible nitric oxide (NO) synthase (iNOS) has been implicated in the pathogenesis of endotoxin-induced uveitis (EIU)…results support the hypothesis that both inflammatory and resident ocular cells are involved in iNOS expression during EIU.”

Excessive exposure to PUFA under stress, interferes with proper blood sugar regulation, and this is made worse by dietary recommendations to increase intake of fat in general and to avoid consumption of sugar.

Sugar protects against rising levels of the stress substances (starting with cortisol and adrenalin) and sufficient glycogen stores can help to protect against free fatty acid release, and the dangers of both hyper and hypoglycemia, both of which can lead to eye issues.

“This pilot study is the first to demonstrate significant diminution of central retinal function in individuals with and without diabetes during acute hypoglycemia…long-term consequences of low glucose levels on vision. Sustained hypoglycemia has been associated with loss of vision and retinal degeneration.”

Sugar restriction – and blood sugar dysregulation resulting from exposure to PUFA and iron – also has an impact on cholesterol metabolism, interfering with the role of cholesterol in the production of the anti-aging hormones, and in the basic function of tissue and organs in general, including the eyes.

“Our study suggests a causal relationship between elevated HDL-C levels and an increased risk of advanced AMD”

“We have shown, for the first time, that oxysterols accumulate in human cataracts. Although the total amount of oxidized cholesterol in cataracts is not likely to be high it may account for much of the…damage associated with cataract formation.”

“Several lines of evidence suggest a link between age-related macular degeneration and retinal cholesterol maintenance…Collectively, our findings indicate the importance of enzymatic cholesterol metabolism for maintenance of retinal structure and function.”

There are also non-dietary ways to approach eyesight dysfunction, depending on the individual circumstances. Red light (LLLT or photobiomodulation) therapy has been shown to be powerful, as are a variety of drills which relate to nervous system function.

“In patients with AMD, LLLT significantly improved visual acuity without adverse side effects and may thus help to prevent loss of vision.”

“…facilitation exercise sessions…were administered…to patients with ophthalmoplegia…exercises significantly improved the horizontal movement of eyes with ophthalmoplegia…”

Cooking or juicing carrots reduces their antimicrobial impact, and increases absorption of beta carotene, which many claim helps the eyes, but in actual fact can worsen thyroid related issues.

Vitamin A plays a role in healthy eye function, but in reality, beta carotene can have a powerful anti-metabolic effect, and particularly for women, can add to stress levels and potentially worsen eyesight.

Proper thyroid function is crucial for the conversion of beta carotene to Vitamin A, and so especially when carrot is juiced or cooked, the metabolism suppressive effect of excessive intake, can create the opposite result than was intended.

Some other things which might be helpful in relation to a number of eyesight issues include minocycline and various other safe antibiotics, aspirin, vitamin E, active thyroid hormone, charcoal, coconut oil, progesterone and pregnenolone, certain antihistamines and gelatin.

The Ray Peat carrot salad – sliced raw carrot, a little coconut or olive oil, salt and vinegar – can be taken regularly to improve digestion and help with the detoxification of thyroid suppressing substances, potentially protecting against visual impairment.

A diet removing the polyunsaturated fats, with sufficient protein and nutrients from milk, cheese and gelatin, and plenty of sugar from sweet ripe juicy fruits, fruit juice, honey and white sugar, can support metabolic function, adding power to any approach used to improve eyesight.

See More Here

Retinal serotonin, eye growth and myopia development in chick.

Changes of vision and refraction in patients with thyroid pathology.

Assessment of Visual Acuity, Refraction Changes, and Proptosis in Different Ages of Patients with Thyroid Diseases

Vitreous estrogen levels in patients with an idiopathic macular hole

The effect of raw carrot on serum lipids and colon function.

Antimicrobial activity of shredded carrot extracts on food-borne bacteria and yeast.

Energy metabolism of the visual system

Melatonin is a potent modulator of dopamine release in the retina.

Melatonin increases photoreceptor susceptibility to light-induced damage.

Dietary fat and risk for advanced age-related macular degeneration.

Estrogen-Induced Retinal Endothelial Cell Proliferation: Possible Involvement of Pigment Epithelium-Derived Factor and Phosphoinositide 3-Kinase/Mitogen-Activated Protein Kinase Pathways

Low-level laser therapy improves vision in a patient with retinitis pigmentosa.

Minocycline reduces proinflammatory cytokine expression, microglial activation, and caspase-3 activation in a rodent model of diabetic retinopathy.

Inhibition of Inducible Nitric Oxide Synthase Reverses the Loss of Functional Hyperemia in Diabetic Retinopathy

Abnormal vascularization in mouse retina with dysregulated retinal cholesterol homeostasis

Basal serum nitric oxide levels in patients with type 2 diabetes mellitus and different stages of retinopathy.

Relationship between Diabetic Retinopathy and Subclinical Hypothyroidism: a meta-analysis

The eye as a window to rare endocrine disorders

[Serotonin in diabetic retinopathy].

Lipid peroxidation is increased in tears from the elderly.

Redox changes precede the occurrence of oxidative stress in eyes and aorta, but not in kidneys of diabetic rats.

Agonists at the serotonin receptor (5-HT(1A)) protect the retina from severe photo-oxidative stress.

[Significance of serotonin in the pathogenesis of diabetic retinopathy and central chorioretinal dystrophy].

Association between subclinical hypothyroidism and proliferative diabetic retinopathy in type 2 diabetic patients: a case-control study.

Selective Serotonin Reuptake Inhibitor Use and Increased Risk of Cataract Surgery: A Population-Based, Case-Control Study

Therapeutic potentials of aspirin in glaucomatous optic neuropathy.

Depression and Incident Diabetic Retinopathy: A Prospective Cohort Study

Human tear serotonin levels correlate with symptoms and signs of dry eye

Low-level laser therapy improves vision in patients with age-related macular degeneration.

New facilitation exercise using the vestibulo-ocular reflex for ophthalmoplegia: preliminary report.

Malondialdehyde induces autophagy dysfunction and VEGF secretion in the retinal pigment epithelium in age-related macular degeneration.

Cholesterol oxides accumulate in human cataracts.

Effects of hypophysectomy, pituitary gland homogenates and transplants, and prolactin on photoreceptor destruction.

Impaired cholesterol efflux in senescent macrophages promotes age-related macular degeneration

Serotonin (5-HT) and the rat’s eye. Some pilot studies.

Estrogen activation of microglia underlies the sexually dimorphic differences in Nf1 optic glioma–induced retinal pathology

Hypoglycemia leads to age-related loss of vision

Photobiomodulation for the treatment of retinal diseases: a review

[Oxidative stress in a model of experimental diabetic retinopathy: the utility of peroxinytrite scavengers].

Lipid peroxidation: pathophysiological and pharmacological implications in the eye

Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis

Low-level light therapy of the eye and brain

Expression of Lipid Peroxidation Markers in the Tear Film and Ocular Surface of Patients with Non-Sjogren Syndrome: Potential Biomarkers for Dry Eye Disease.

Vitamin D Status and Early Age-Related Macular Degeneration in Postmenopausal Women

Lipids and lipid peroxidation products in the pathogenesis of age-related macular degeneration.

Cholesterol and age-related macular degeneration: is there a link?

Unusual manifestations in primary hypothyroidism.

Lipid peroxidation in proliferative vitreoretinopathies

Acute Hypoglycemia Decreases Central Retinal Function in the Human Eye

Iron toxicity as a potential factor in AMD.

Aspirin and age-related macular degeneration: positives versus negatives

Diabetes, Cardiovascular Morbidity, and Risk of Age-Related Macular Degeneration in a Primary Care Population

Toxic optic neuropathy after concomitant use of melatonin, zoloft, and a high-protein diet.

Accumulation of lipid peroxidation products in human cataracts.

The increase in lipid peroxidation in diabetic rat lens can be reversed by oral sorbinil

The Effect of Hypothyroidism on Color Contrast Sensitivity: A Prospective Study

Possible involvement of nitric oxide in the progression of diabetic retinopathy.

Metabolic physiology in age related macular degeneration.

Expression of inducible nitric oxide synthase in the eye from endotoxin-induced uveitis rats.

Myopes have significantly higher serum melatonin concentrations than non-myopes.

HDL-cholesterol levels and risk of age-related macular degeneration: a multiethnic genetic study using Mendelian randomization

Diabetes mellitus and early age-related macular degeneration.

Iron and age-related macular degeneration.

An overview of thyroid eye disease

Review: effects of nitric oxide on eye diseases and their treatment.

Suppression of retinal neovascularization by the iNOS inhibitor aminoguanidine in mice of oxygen-induced retinopathy.

Involvement of inducible nitric oxide synthase in cataract formation in Shumiya cataract rat (SCR).

Refractive change in thyroid eye disease (a neglected clinical sign)

Methylene blue protects primary rat retinal ganglion cells from cellular senescence.

Mitochondrial Dysfunction in Retinal Diseases

Thyroid Dysfunction and Ten-Year Incidence of Age-Related Macular Degeneration.

Cortisol in diabetic retinopathy.

Nitric oxide and oxidative stress is associated with severity of diabetic retinopathy and retinal structural alterations.

Photobiomodulation reduces drusen volume and improves visual acuity and contrast sensitivity in dry age-related macular degeneration.

Inducible Nitric Oxide Synthase Mediates Retinal Apoptosis in Ischemic Proliferative Retinopathy

Hypothyroidism Presenting as Psychosis: Myxedema Madness Revisited

A suggested association between hypothyroidism and age-related macular degeneration.

Relation between plasma nitric oxide levels and diabetic retinopathy.

Methylene blue prevents neurodegeneration caused by rotenone in the retina.

Iron induced oxidative damage as a potential factor in age-related macular degeneration: the Cogan Lecture.

Vasoactive factors and diabetic retinopathy: vascular endothelial growth factor, cycoloxygenase-2 and nitric oxide.

Nitric oxide: ocular blood flow, glaucoma, and diabetic retinopathy.

#endotoxicnation
#sugarfeedsthyroid
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Image: goldentar.deviantart.com

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