Cause: Uncontrolled Diabetes is the main cause for Diabetic Retinopathy. High blood sugar causes damage to retinal blood vessels which increases the pressure in blood capillaries and made them weak.

Diabetic retinopathy affects both eyes and initially shows no symptoms. In progressive stages, symptoms like swollen blood, fluid leak, abnormal new blood vessels on retina surface occurs and all these results into irreversible Vision loss.

Omega 3 & Diabetic Retinopathy: Omega-3 fatty acid is highly concentrated in retina and significantly preserved retinal function. Lack of omega 3 supplement in daily diet may cause various eye problems. Omega 3 fatty acid plays vital role against development and progression of diabetic retinopathy. In diabetic retinopathy patients, Omega 3 supplement protects against the growth of abnormal blood vessels and promotes the growth of healthy blood vessels. It reduces the inflammatory eye conditions.

Supportive studies: Studies shows that possible protective mechanism is because of an enzyme 5-lipoxygenase (5-LOX) that converted omega 3 fatty acid into an acid called 4-HDHA which slows the growth of abnormal blood vessel. Regular intake of Omega 3 slows down the progression of retinopathy severity and vision loss by approx. 40-50 %.

Studies also suggest that intake of omega-3 fatty acid by pregnant women may significantly decrease the occurrence of retinopathy of prematurity (ROP) in premature infants. It significantly supports the development of eye in fetuses.

Omega 3 fatty acid plays a vital role to maintain eye health and reduces the occurrence of diseases. 

The drug was given priority review by the FDA for this indication, a statement from Pfizer notes, and brings to 5 the number of approved indications for pregabalin in the United States; others include diabetic neuropathy, postherpetic neuralgia, fibromyalgia, and partial-onset seizures in adults with epilepsy who take 1 or more drugs for seizures.

More than 100,000 patients, or about 40% of patients with traumatic or nontraumatic spinal cord injury in the United States, develop neuropathic pain associated with the injury. “Neuropathic pain associated with spinal cord injury can be severely debilitating and may significantly hinder rehabilitation and the ability to regain function,” the statement said.

Neuropathic pain can be experienced above, at, or below the level of injury and is typically not confined to one area of the body, the statement notes. “Approximately one-third of spinal cord injury patients report below-level neuropathic pain that is severe or excruciating,” they write. It can be begin as soon as 2 weeks after the injury and persist up to 25 years.

The approval is based on results of 2 randomized, double-blind phase 3 trials comparing flexibly dosed pregabalin (150 to 600 mg/d) with placebo in 357 patients. Patients were allowed to continue other medications, including other pain medications, such as nonsteroidal anti-inflammatory drugs, opioids, and nonopioid medications. One study included only patients with traumatic spinal cord injury, and the other included about 5% of patients with nontraumatic injuries.

Studies showed pregabalin significantly reduced neuropathic pain between baseline and 12 and 16 weeks in each study, respectively, vs placebo. More patients taking pregabalin showed 30% and 50% reductions in pain than those taking placebo. For some patients, the reduction in pain was significant as soon as week 1 and continued throughout the trial, the statement notes.

The most common adverse events with pregabalin were somnolence, dizziness, dry mouth, fatigue, and peripheral edema. Antiepileptic drugs, including pregabalin, increased the risk for suicidal thoughts or behaviors. There have been postmarketing reports of angioedema and hypersensitivity with pregabalin, the release adds. Other reactions include blurred vision, weight gain, constipation, euphoric mood, balance disorder, increased appetite, and abnormal thinking (primarily difficulty with concentration and attention).

“This milestone represents an important opportunity for physicians to more effectively manage the debilitating neuropathic pain that often accompanies spinal cord injury,” said clinical study investigator Diana Cardenas, MD, MHA, professor and chair, department of rehabilitation medicine, University of Miami Miller School of Medicine and chief of service for rehabilitation medicine and medical director of Jackson Rehabilitation Hospital, Miami, Florida, in the Pfizer statement. “Given the clinical challenges of investigating neuropathic pain in this patient population, any advancements in treatment are welcome by physicians and patients alike.”

Glaucoma is an eye disorder in which internal eye pressure (Intraocular pressure-IOP) is very high. In this condition, eye has too much aqueous humor pressure either because of over production of fluid or of improper draining. This leads to damage of optic nerve results in Vision loss. This nerve acts like an electric cable with over a million wires. It is responsible for carrying images from the eye to the brain.
According to World Health Organization, Glaucoma is the second leading cause of blindness (behind cataracts).

GLAUCOMA SYMPTOMS:
Glaucoma, known as “silent thief of sight” as it causes no pain and shows no symptoms in early stages and quietly causes vision loss. As no symptoms occur, the best way to diagnose this form of glaucoma is by periodic eye examination. Onset of any of symptoms like blurred vision, severe eye pain, red eyes, headache, nausea and vomiting is the warning alarm for eyes.

GLAUCOMA CAUSE:
A clear fluid flows in and out of the space at the front of the eye, nourishing nearby tissues. Glaucoma causes the fluid to pass through too slowly or to stop draining altogether. As the fluid builds up, the pressure inside the eye increases, causing damage to the optic nerve and vision loss.

RISK FACTORS:
Age: Glaucoma is more common among older people. People above 40 are 6 times more likely to get glaucoma.
Family History: The most common type of glaucoma, primary open angle glaucoma, is hereditary. Family history of glaucoma increases the risk of glaucoma four to nine times.
Indiscriminate use of Steroids: Studies indicate Steroids increase intraocular pressure. These could be in the form of Oral medications, Steroid Inhalers and Steroid Eye Drops used for long periods of time.
Injury to Eye: Injury to the eye may cause secondary open angle glaucoma. This type of glaucoma can occur immediately after the injury or years later.

CARE, NUTRITION AND SUPPLEMENTS:
Glaucoma is controlled and treated if detected in early stages. Early detection of Glaucoma save the patient form vision loss and eye damage. Glaucoma is control with Medicines (Oral and eye-drops) and Laser Surgery.

Other than Medicines and Surgery, following care, nutrition and supplements are required to keep eye healthy and free from eye problems:

1. Exercise: Regular physical activity can lower intra ocular pressure by a little bit.

2. Food & Diet: Carrots, Spinach, Green leafy vegetables, citrus fruits, blueberries, cherries, tomatoes, whole milk, egg, lean meat and seafood should be taken to keep eye healthy and full of vision. And should limit the intake of caffeine, alcohol and smoking.

3. Nutritional Supplements: There are few supplements known to improve the clinical condition of Glaucoma.

A. Alpha Lipoic Acid (ALA): Alpha Lipoic Acid (ALA) is very powerful antioxidant and this antioxidant property is helpful in improving eye conditions like glaucoma, cataract and diabetic retinopathy. Clinical studies shows that, regular intake of 150 mg of Alpha Lipoic acid improves visual acuity and colour perception by 45- 47% in glaucoma patients. ALA shows strong neuroprotective properties which significantly prevent ischemic optic nerve damage and improves fluid discharge.

Ref.: Filina AA, et al. Lipoic acid as a means of metabolic therapy of open-angle glaucoma. Vestn Oftalmol 1995; 111:6-8.

B. Omega-3 Fatty Acids: Studies show direct association between Omega 3 fatty acid and eye health. Omega 3 fatty acid is helpful in inflammatory and intraocular pressure (IOP) conditions. It is studied that with the regular consumption of Omega 3 fatty acid leads to decrease in IOP with age by increasing the aqueous outflow in glaucoma patients. Omega 3 fatty acid helps to decrease the eye inflammation by reducing the production of inflammatory cellular signaling molecules.

Ref.: 1. Cellini M, Rossi A & Moretti M. The use of polyunsaturated fatty acids in ocular hypertension. Acta ophtalmol Scand 1999;77 (suppl. 229):54-55
2. Dietary omega 3 fatty acids decrease intraocular pressure with age by increasing aqueous outflow. Invest Ophthalmol Vis Sci. 2007.

Even if it is considered top-of-the-line HGH supplements, it can still contain some negative insights from users. HGH is highest in developing adolescents and the older we get, the much less we generate. Other health improvements include an increased metabolism, weight loss and increased muscular mass, that’s why it can be therefore preferred among athletes and bodybuilders. But using a “releaser” or stimulator product, your. The HGH throughout Sytropin is natural it can be enhanced by six growth factors and eight amino acid releasers to enhance great and bad the compound and how your body reacts the idea.

Some people experienced a rise in regrowth, but no harmful effects. By like the following ingredients their own specific dosage – L-Glutamine 200 mg. All I want, but, to be able to remain younger on the lookout for somewhat added time. So you see that a persons human growth hormone may be very much a significant portion of body of a human and growth system. although it could possibly, if you’re willing to stop paying it.

That way, you might be keeping yourself completely informed and could be certain you’re getting the easiest product an individual. More importantly it can be a superbly legal approach to obtain HGH. Since treatments itself utilizes synthetic compounds which will cause serious unwanted side effects and complications to astonishingly, you might be putting yourself any serious risk if you take HGH injections. Pills and sprays are wonderful choices to injections, and so they offer numerous advantages. The higher regarding human growth hormone can improve heart function, boost metabolism, strengthen the defense mechanisms, reduce body fat, stabilize blood sugar and increase energy.

CoQ10: Every day, you chew a supplement that contains 60mg of coenzyme Q10, or CoQ10, an antioxidant that helps maintain the soft tissues in your body-including your gums. Some early research suggests that taking CoQ10 can even help shrink the pockets caused by gum disease.

Calcium: Calcium, a mineral found in your jawbone. If you don’t get enough calcium, your jaw weakens, loosening your teeth. Men and women from ages 19 to 49 need 1,000mg of calcium, daily, while those over 50, require 1,200mg. A cup of milk or yogurt packs about 300mg and an ounce of most cheeses has around 200mg.

Vitamin D: To absorb calcium, your body needs vitamin D. According to the WHO recommendation, a full third of Indians don’t get enough. You must follow the recommendation and get at least 400IU daily. Milk has about 100IU per cup and a 3-ounce serving of fattier fish, like salmon or mackerel, contains about 300IU. If you don’t drink milk or eat fish, you could probably use a supplement of 400 IU daily.

Vitamin C: There’s one more super-important nutrient for your teeth: Vitamin C. It’s a building block for collagen, which helps keep your teeth attached to your gums. A study in the Journal of Periodontology found that men and women who consumed less than 60mg of vitamin C daily were 150 percent more likely to have gum disease than people who took in at least 180mg. Fruit and veggies are the major sources of vitamin C (One orange alone has 60mg). You get enough C in your diet, but if you don’t, consider taking a supplement.

Omega-3 fatty acids: Studies shows that “People with low intake (of DHA) had an approximately 1.5 times higher incidence rate ratio of periodontal disease progression”. Regular intake of Omega-3 supplements is helpful in the treatment of periodontal disease and other gum diseases. Its anti-inflammatory effects effectively reduce the chances of gum inflammation, weak gum and teeth.

Probiotics & Prebiotics: Probiotics are potential therapy for maintaining oral health. It is used to reduce dental caries and periodontal diseases. Probiotics significantly maintains healthy balance of the bacteria flora in the mouth. Microbial growth promotes serious tooth decay and bad breath. Daily intake of probiotics in early childhood may result in less dental carries. Probiotics suppress the odor-producing bacteria, resulting in a decrease in the foul smelling gases arising in the mouth. It also helps to reduce the gum inflammation and plague formation caused by microbial growth. Prebiotics give the probiotics to exert their influence by aiding and boosting immunity.

Tip: AVOID FIZZY SUPPLEMENTS

Don’t buy the chewable Vitamin-C tablets or any kind of supplement that fizzes when you dissolve it in water. Chewable and fizzy vitamins lower the pH in your mouth and erode your tooth enamel big time. In fact, a recent study from the University of Helsinki found that fizzy supplements, including those containing calcium, caused teeth to lose minerals. The worst offenders were the fizzy vitamin-C supplements-they corroded the teeth so much that the layer below the enamel was exposed.

A healthy smile can help you look years younger. Just think about your diet, and weigh your need for six favorite supplements.

Although some foods, such as milk and orange juice, are fortified with vitamin D, studies have shown that many individuals still consume low amounts of this nutrient or have insufficient vitamin D serum levels. This may in part be related to changing dietary patterns in this United States, such as low consumption of milk and foods rich in vitamin D (eg, salmon, eel, tuna, and mackerel). Since most biologically active vitamin D comes from skin exposure to sunlight, the increased widespread use of broad-spectrum, high sun-protection-factor sunscreens in recent years may also contribute to the rise in vitamin D deficiency.

Several guidelines have been issued by national organizations that recommend varying amounts of vitamin D intake. Perhaps the most current, authoritative consensus report has been issued by the Institute of Medicine. This guideline recommends a daily dietary allowance of vitamin D of 600-800 IU/day for most patients. However, increased amounts are necessary for treating insufficiency and deficiency. Although much attention has been given to vitamin D intake, most consensus statements do not delineate the differences between the 2 major oral formulations: vitamin D₂ (ergocalciferol) and vitamin D₃ (cholecalciferol).

Vitamin D is produced cutaneously and converted to active metabolites in the liver and kidney. On exposure to ultraviolet irradiation, provitamin D₃ (7-dehydrocholesterol) in the skin is converted to previtamin D₃, which is then isomerized to more stable vitamin D₃ via a thermally induced transformation. Vitamin D₃, whether cutaneously formed or obtained in the diet as cholecalciferol, is subsequently hydroxylated in the liver to 25-hydroxyvitamin D. This is the major circulating form of vitamin D that is assayed to detect deficiency. 25-hydroxyvitamin D is hydroxylated again in the kidney to form 1,25-dihydroxyvitamin D₃, the major biologically active form of vitamin D, also known as calcitriol.Thus, in the setting of severe renal impairment, formulations of calcitriol are preferred over ergocalciferol and cholecalciferol because the terminal hydroxylation occurs in the kidney.

Regarding the manufacturing of oral vitamin D formulations, ergocalciferol is made from ultraviolet irradiation of ergosterol in yeast. Cholecalciferol is made from irradiation of 7-dehydrocholesterol from lanolin and the chemical conversion of cholesterol. Traditionally, oral formulations of vitamin D₂ and D₃ have long been regarded as equivalent in their clinical activity. However, studies indicate that ergocalciferol (vitamin D₂) is much less potent and has a shorter duration of action than cholecalciferol.

Historically, ergocalciferol has been used instead of cholecalciferol for severe vitamin D deficiency. This is out of convention, or perhaps because high-dose ergocalciferol is more widely available in doses of up to 50,000 IU per softgel capsule from multiple manufacturers. Although this dose of cholecalciferol is available from at least 1 manufacturer, it is often challenging to find in retail outlets. Based on this author’s experience, and verified by others, it is often difficult to raise 25-hydroxyvitamin D levels with ergocalciferol in patients with severe vitamin D deficiency.

Armas and colleaguesadministered single oral doses of 50,000 IU of the respective vitamin D preparations to 20 healthy male volunteers, and followed the time course of 25-hydroxyvitamin D levels over a period of 28 days. A pharmacokinetic analysis was also done. Both ergocalciferol and cholecalciferol produced similar initial increases in serum levels of 25-hydroxyvitamin D over the first 3 days, indicating equivalent absorption. However, levels continued to increase with cholecalciferol and peaked at day 14, whereas levels decreased rapidly with ergocalciferol and were no different from baseline at day 14. The investigators concluded that ergocalciferol potency is less than 30% of that of cholecalciferol and that it has a markedly shorter duration of action.

This study is consistent with other single, high-dose studies that indicate the mean time to peak concentration of ergocalciferol to be about 3 days compared with 14 days for cholecalciferol. A review by Houghton and Viethestimated that cholecalciferol is more than 3 times as effective as ergocalciferol in elevating 25-hydroxyvitamin D and maintaining those levels for a longer time. These authors also note that cholecalciferol metabolites have superior affinity for vitamin D-binding proteins in plasma, relative to ergocalciferol.

In conclusion, ergocalciferol (vitamin D₂) and cholecalciferol (vitamin D₃) are not bioequivalent and should not be considered interchangeable. Although few head-to-head trials exist, based on pharmacokinetic studies and limited clinical evidence, cholecalciferol is preferred over ergocalciferol. Because of its shorter half-life and decreased potency, this is especially relevant in the setting of severe deficiency, where high-dose ergocalciferol is often only given once weekly. Health professionals should encourage use of cholecalciferol over ergocalciferol in all patients without severe renal failure, either as a general supplement or as a treatment for vitamin D deficiency.

What form of vitamin D is recommended in chronic kidney disease?

Vitamin D is produced endogenously in the skin and converted to active metabolites in the liver and kidney. Upon exposure to ultraviolet irradiation, provitamin D3 (7-dehydrocholesterol) in the skin is converted to previtamin D3, which is then isomerized to vitamin D3 (cholecalciferol). Vitamin D3, whether cutaneously formed or obtained in the diet as cholecalciferol, is subsequently hydroxylated in the liver to 25-hydroxyvitamin D (25-OH VD). This is the major circulating form of vitamin D that is assayed to detect deficiency.

A subsequent hydroxylation of 25-OH VD occurs in the kidney to form 1,25-dihydroxyvitamin D, the major biologically active form of vitamin D, also known as calcitriol.Thus, in the setting of severe chronic kidney disease (CKD), formulations of calcitriol may be preferred over vitamin D2 and D3 to treat deficiency because the terminal hydroxylation occurs in the kidney.

In the setting of CKD it is important to estimate glomerular filtration rate (GFR) and to determine serum 25-OH VD, calcium, phosphorous, and intact PTH levels when choosing the most optimal regimen. Supplementation of vitamin D plays a major role in the prevention of secondary hyperparathyroidism in patients with CKD. According to clinical practice guidelines from the National Kidney Foundation, the preferred form of supplementation is guided by serum 25-OH VD levels, stage of kidney failure, and presence or absence of secondary hyperparathyroidism. Before and during supplementation, both serum calcium and phosphorous levels should be drawn every 3 months. If levels of these minerals rise, vitamin D supplementation may need to be withheld or the dosage modified.

In the presence of secondary hyperparathyroidism, which usually begins in stage 3 or 4 of CKD (GFR 30-59 mL/min and 15-29 mL/min, respectively), the preferred agent for supplementation is an activated vitamin D sterol (eg, calcitriol or paricalcitol). Supplementation should begin when serum levels of 25-OH VD fall below 30 ng/mL. The vitamin D sterol dose depends on the serum levels of 25-OH VD, PTH, calcium, and phosphorus. Likewise, in stage 5 of CKD (GFR < 15 mL/min and patients treated with hemodialysis or peritoneal dialysis), an activated vitamin D sterol is also preferred in lieu of vitamin D2 or D3.

However, in the absence of secondary hyperparathyroidism, as is often the case in patients with GFR > 60 mL/min or only mild renal impairment, either oral vitamin D2 or D3 can be used. Studies indicate that vitamin D2 (ergocalciferol) is much less potent and has a shorter duration of action than D3 (cholecalciferol) and that vitamin D3 more effectively raises 25-OH VD levels. Thus, cholecalciferol is preferred in patients with normal or mild renal impairment (GFR > 60 mL/min) with a normal intact PTH level.

The dihydroxy bile acid, ursodeoxycholic acid (UDCA), has been in widespread clinical use in the Western world since the mid 1980s, when it was initially used for gallstone dissolution [1,2] and subsequently for the treatment of chronic cholestatic liver diseases. Many clinical trials of UDCA in a variety of cholestatic disorders established biochemical and clinical improvements, and most importantly showed a significant prolongation of transplant-free survival after four years of treatment with UDCA in patients with primary biliary cirrhosis. Despite its clinical efficacy, the precise mechanism(s) by which UDCA improves liver function during cholestasis is still a matter of debate. It was initially considered that the choleretic effect of UDCA, coupled with its ability to cause a marked shift in the composition of the bile acid pool towards hydrophilicity, accounted for its mechanism of action. In recent years, however, it has become evident that UDCA and its conjugated derivatives are capable of exerting direct effects at the cellular, subcellular, and molecular levels by stabilising cell membranes, affecting signal transduction pathways, and regulating immune responses. In addition, we have shown that UDCA plays a unique role in modulating the apoptotic threshold in both hepatic and non-hepatic cells. The purpose of this article is to examine the mechanism(s) by which UDCA prevents apoptotic cell death associated with cholestasis. In addition, we will also review a potentially novel and, heretofore, unrecognised role of UDCA as a therapeutic agent in the treatment of non-liver diseases associated with increased levels of apoptosis as a pathogenesis of the disorder.

A: adequate studies in pregnant women have not demonstrated a risk to the foetus in the first trimester of pregnancy and there is no evidence of risk in later trimesters.

B: animal studies have not demonstrated a risk to the foetus but there are no adequate studies in pregnant women or, animal studies have shown an adverse effect, but adequate studies in pregnant women have not demonstrated a risk to the foetus during the first trimester of pregnancy and there is no evidence of risk in later trimesters.

C: animal studies have shown an adverse effect on the foetus but, there are no adequate studies in humans; the benefits from the use of the drug in pregnant women may be acceptable despite its potential risks or there are no animal reproduction studies and no adequate studies in humans.

D: there is evidence of human foetal risk, but the potential benefits from the use of the drug in pregnant women may be acceptable despite its potential risks.

X: studies in animals or humans demonstrate fetal abnormalities or adverse reaction reports indicate evidence of foetal risk; the risk of use in a pregnant woman clearly outweighs any possible benefit.