EFFECT OF TEA ON GLAUCOMA

 

A study has been performed by Wu et al, to evaluate the association between the consumption of coffee, tea, or soft drinks, and glaucoma.

The study is based on the participants of the 2005–2006 National Health and Nutrition Examination Survey (NHANES), conducted in the USA.

The authors reported that individuals who consumed at least one cup of hot tea daily had 74% decreased odds of having glaucoma compared with those who did not consume hot tea (adjusted OR=0.26, 95%CI 0.09 to 0.72, P=0.004 for trend).

No significant associations were found between the consumption of coffee, iced tea, decaffeinated tea, and soft drinks, and glaucoma risk.

Caffeine has been postulated to increase glaucoma risk by promoting increases in intraocular pressure (IOP) and homocysteine levels in the body.

Caffeine transiently increases IOP ranging from 1-2 mmHg within one hour of ingestion. However, other studies have shown that drinking non-caffeinated fluids ranging from 250-1000 mL also increases IOP, indicating that the fluid overload could be the cause of the rise in the IOP and not due to the effect of caffeine alone.

Tea contains phytochemicals and flavonoids, which have been observed to have anti-inflammatory, anticarcinogenic, antioxidant, and neuroprotective properties, which help in the prevention of cardiovascular disease, cancer, and diabetes.

Flavonoids have been shown to inhibit the vascular endothelial growth factor receptor and potentially prevent neovascular glaucoma, fibrotic scar tissue formation after glaucoma surgery, and neurodegeneration. They may also play a protective role by promoting vasodilation.

Caffeinated teas have been found to have greater antioxidant capacity compared with decaffeinated teas, which may explain why decaffeinated tea consumption was not correlated with decreased glaucoma risk.

Compared with tea, coffee contains more caffeine and a different profile of polyphenols comprising fewer flavonoids but more hydroxycinnamic acids, which may explain why tea is better at modulating the risk of glaucoma.

REFERENCE:

Wu CM, Wu AM, Tseng VL, Yu F, Coleman AL. Frequency of a diagnosis of glaucoma in individuals who consume coffee, tea and/or soft drinks. Br J Ophthalmol. 2018 Aug;102(8):1127-1133. doi: 10.1136/bjophthalmol-2017-310924. Epub 2017 Dec 14. PMID: 29242183.

ALLVAR GULLSTRAND. The only ophthalmologist to win a Nobel Prize

 

Since awarding the first Nobel Prize in 1901, the only practicing ophthalmologist to be conferred this honor has been Allvar Gullstrand. He received the Nobel Prize in Physiology or Medicine in 1911. 

Gullstrand applied principles of physical mathematics to the study of optical images and the refraction of light in the eye, for which he was awarded the Nobel Prize. While conferring the award, King Gustav V of Sweden announced that Gullstrand was being awarded for his works concerning the dioptrics of the eye. An interesting anecdote regarding his Nobel Prize is that he is one of the few people to decline this prestigious honor. He was also being considered for the Nobel Prize in Physics; however, he rejected that award in favor of the award in Physiology or Medicine.

Gullstrand is credited with many seminal achievements, the most significant being the invention of the slitlamp. He combined a slit with a microscope made by the Zeiss Optical Works in Germany, creating the instrument that is used by all ophthalmologists today. Reacting to the development, the President of the International Congress of Ophthalmology held in Washington, DC, in 1922, De Schweinitz jokingly said, that medicine now has a "gentleman with the lamp," a male counterpart to nursing's Florence Nightingale, the lady with the lamp.

He also invented the reflex-less ophthalmoscope which avoided the light reflexes usually occurring from the cornea when using the ophthalmoscope.

Gullstrand also made the eponymous schematic eye that includes the lens curvature, the distance between the lens and the cornea, and the refractive indexes of all components (Gullstrand schematic eye).

Gullstrand was born on 5th June 1862, in Landskrona, Sweden. He completed a study of mathematics at Jonkoping in 1880 and then started studying Medicine in Uppsala. Initially, he had considered studying engineering, but his physician father persuaded him to study medicine by hiring him as a medical assistant for the summer. In 1885, Gullstrand left for Vienna to learn ophthalmoscopy, otoscopy, and laryngoscopy. After a year in Vienna, he returned to continue his medical studies in Stockholm, where he graduated in 1888. His thesis was titled ‘A Contribution to the Theory of Astigmatism’, laying the foundation for his future work.

In 1891, Gullstrand became a lecturer of ophthalmology at the Karolinska Institute in Stockholm. Gullstrand was a professor at the University of Uppsala from 1894 to 1927. He was part of the Nobel Committee for Physics from 1911 to 1929, serving as chairman from 1923 to 1929. In 1913, he was elected the first president of the Swedish Ophthalmological Society.

In 1885, he married Signe Christine Breitholtz, with whom he had a daughter, Esther Gisela. However, the girl died from diphtheria when she was less than 3 years old.

While serving on the Nobel Committee, Gullstrand wrote two harsh opinions against Einstein’s theory of relativity. As a result, Einstein was denied the Nobel Prize in 1921 and 1922 for his Theory of Relativity. It was only in 1921 that Einstein got the award for his services to Theoretical Physics, and especially for his discovery of the law of the photoelectric effect.

Apart from the Nobel Prize, Gullstrand received the prestigious Graefe Medal of the Deutsche Ophthalmologische Gesellschaft in 1927.

Gullstrand died in 1930 following a cerebral hemorrhage.

ALI IBN ISA AL-KAHHAL

 

Ali ibn Isa al-Kahhal was one of the most influential and celebrated medieval Arab ophthalmologists. He is famous as “The Oculist”, denoting his name (Al-kahhal). He was also known as Jesu Oculist (Isa= Jesus; Kahhal= Oculist), the Latin translation of his name.

Belonging to Baghdad, Iraq, he was born in the year 940 AD, and passed away in 1010.

His most significant contribution to ophthalmology is the highly acclaimed book “Tadhkirat al-kahhalin”. It is translated to English under the title “Memorandum of the Oculists”. It is regarded as the most comprehensive book of Arabian ophthalmology to survive the medieval ages. During its time it was the standard reference book of ophthalmology.

https://www.loc.gov/resource/gdcwdl.wdl_17604/?st=gallery

The book is apparently based on the writings of Hunayn ibn Ishaq, Galen, and other authors. The book contains details and illustrations of the anatomy of the eye. It is a comprehensive treatise describing almost 130 diseases and treatments related to ophthalmological conditions.

Ibn Isa is credited with the first description of the anatomy of the optic chiasm and brain, symptoms of Vogt-Koyanagi-Harada syndrome, and also the first to record a case of temporal arteritis.

He described many surgical techniques in his book. His treatment for epiphora was based on the stage of the disease. In the early stages, he suggested the use of astringent materials like ammonia salt, burned copper, or lid paste. While, in the chronic stages he described a hook dissection with a feathered quill.

At the end of his book, he listed 143 medications and their effects on the eye in alphabetical order. Ali had a great sense of humanity, and during cataract operations, he said, “When the cataract needle has entered the interior of the eyeball, then address the patient with kind words to quiet the fears.

Ali ibn Isa al-Kahhal shall be remembered for setting a broad foundation of ophthalmology for future generations.

TRANS-LAMINA CRIBROSA PRESSURE DIFFERENCE

 

The lamina cribrosa (LC) is a mechanical barrier between the intraocular compartment, having high pressure, and the intra-orbital space, which has comparatively lower pressure.

In the orbital part of the optic nerve sheath, the dynamics and composition of the cerebrospinal fluid (CSF) are different from the intracranial CSF.

The pressure difference between the intraocular pressure (IOP) and intracerebral pressure (ICP) at the level of the LC is called trans-lamina cribrosa pressure difference (TLCPD). This pressure difference has an important role in the development of cupping seen in glaucoma patients.

The difference between IOP and retrolaminar tissue pressure, divided by the thickness of the LC forms the translamina cribrosa pressure gradient.

The LC is apparently thinner in glaucoma patients compared to normal controls. In NTG patients the ICP is significantly lower than in normal individuals. These features contribute to the increase in the TLCPD and promote glaucomatous cupping.

It is also found that fluctuations in the IOP lead to repeated shear and strain at the level of the LC, increasing the cupping.

High TLCPD causes altered axonal transport, structural changes in the LC, and ischemia.

Therefore, it can be concluded that altered TLCPD plays an important role, singly or in combination with other factors, in the development and progression of glaucomatous optic nerve degeneration.

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MOTOR VEHICLE ACCIDENTS and GLAUCOMA

 

Glaucoma is a condition characterized by deterioration in the patient’s quality of life, relative to the progression of the disease. Some studies have reported that glaucoma patients are at increased risk of motor vehicle accidents (MVA).

A study has shown that drivers with severe binocular field loss, as determined by a screening test administered 40° nasally and 60° temporally at motor vehicle licensing offices, are approximately two times more likely to be involved in a crash than those with no field loss. [1]

There is a conventional notion in clinical practice that the eye with better function dictates visual performance. However, a study by McGwin et al. has shown that the worse eye’s visual field characteristics were significantly associated with crash involvement, whereas those of the better eye were not. [2]

The study evaluated the association between visual field defects in the central 24° field and the risk of MVAs among patients, 55 years or older, with glaucoma. The control set included glaucoma patients who were never involved in an MVA. For each patient, an Advanced Glaucoma Intervention Study (AGIS) score was calculated on automated visual fields collected with the 24-2 or 30-2 programs.

Each eye was studied separately. When compared with individuals with no VF defects, in the case of the better-seeing eye of the patient having severe VF defects (scores 12-20) there was an increased risk of an MVA (odds ratio [OR] 3.2, 95% CI 0.9–10.4), although the association was not statistically significant. Moderate (6–11) or minor field defects (1–5) in the better eye were not associated with the risk of involvement in a crash.

However, when studying the worse eye of the patient, patients with moderate or severe field defects were at significantly increased risk of an MVA (OR 3.6, 95% CI 1.4–9.4 and OR 4.4, 95% CI 1.6–12.4, respectively) compared with those with no defects. However, minor field defects in the worse eye did not increase the risk of an MVA (OR 1.3, 95% CI 0.5–3.4).

The study concluded that patients with glaucoma who have moderate or severe visual field impairment in the central 24° radius field in the worse-functioning eye are at increased risk of involvement in a vehicle crash.

REFERENCE:

[1] Johnson CA, Keltner JL. Incidence of visual field loss in 20,000 eyes and its relationship to driving performance. Arch Ophthalmol. 1983;101:371–375.

[2] McGwin G Jr, Xie A, Mays A, Joiner W, DeCarlo DK, Hall TA, Owsley C. Visual field defects and the risk of motor vehicle collisions among patients with glaucoma. Invest Ophthalmol Vis Sci. 2005 Dec;46(12):4437-41. doi: 10.1167/iovs.05-0750. PMID: 16303931.

IMMUNE MECHANISM MEDIATED GOA

 

Glaucoma is commonly associated with raised intraocular pressure (IOP). However, it is known that some patients develop/progress glaucomatous neurodegeneration in the absence of raised IOP. This has led to various non-pressure-mediated theories, such as vascular, biochemical, and inflammatory, responsible for glaucomatous optic atrophy (GOA).

Another possibility is that pathophysiological stress, such as that induced by elevated IOP, triggers secondary immune or autoimmune responses, leading to retinal ganglion cell (RGC) and axon damage even after the initial insult is gone.

The evidence for an autoimmune component in glaucomatous neurodegeneration includes the presence of a wide range of serum auto-antibodies particularly those against heat shock proteins (HSPs) and retinal deposits of immunoglobulins in glaucoma patients and animal models of glaucoma.

Experimental studies report inoculation of rats with human HSP27 and HSP60 induces an optic neuropathy that resembles glaucomatous neural damage, and elevated IOP has been reported to induce expression of HSPs in the retina, particularly RGCs.

 Therefore, there is a possibility of an association between IOP elevation, HSP upregulation, and induction of anti-HSP autoimmune responses in glaucoma.

It is also thought that the anti-HSP immune responses are induced originally by bacterial HSPs, and are reactivated by host HSPs during glaucoma. The facts that glaucoma patients exhibit increased titers of antibodies against Helicobacter pylori and that immunization with HSPs in rats induces glaucomatous neural damage are in line with this possibility.

In a study performed by Chen et al, microbeads (MB) were injected in the anterior chamber to increase IOP in one study population of mice. The control group was injected with saline.

The retina in the MB group showed infiltrating T-cells at 2 weeks after MB injection. The T-cells were scattered throughout the retina without apparent clustering or preference to any specific quadrant. The number of T cells then declined by 4 weeks.

During the infiltrative period, the glaucomatous retina also showed CD4+, but not CD8+, T cells in the ganglion cell layer (GCL), CD11b+ microglia, and macrophages.

The RGC and axon loss continued up to 8 weeks after MB injection, the longest time point that the mice were monitored. These results show that a transient elevation of IOP induces T cell infiltration into the retina and a prolonged period of retinal neurodegeneration, even after the IOP has returned to the normal level.

The study demonstrated that:

(1) a transient elevation of IOP is sufficient to induce CD4+ T-cell infiltration into the retina;

(2) T-cell responses are essential in the development of progressive GOA following IOP elevation;

(3) both bacterial and human HSPs are target antigens of these T cells; and 

(4) HSP-specific CD4+ T-cell responses and glaucomatous neurodegeneration are both abolished in mice raised in the absence of commensal microbial flora (germ-free (GF) mice), supporting a mechanism of bacteria-sensitized T-cell responses underlying the pathogenesis of glaucoma.

These observations identify a sequence of events that contribute to progressive GOA, implicating immune mechanisms, possibly in response to commensal flora.

REFERENCE:

Chen H, Cho KS, Vu THK, Shen CH, Kaur M, Chen G, Mathew R, McHam ML, Fazelat A, Lashkari K, Au NPB, Tse JKY, Li Y, Yu H, Yang L, Stein-Streilein J, Ma CHE, Woolf CJ, Whary MT, Jager MJ, Fox JG, Chen J, Chen DF. Commensal microflora-induced T cell responses mediate progressive neurodegeneration in glaucoma. Nat Commun. 2018 Aug 10;9(1):3209. doi: 10.1038/s41467-018-05681-9. 

ELEVATED GD15 IN GLAUCOMA

 

Dysregulated levels of growth/differentiation factor-15 (GDF15), a divergent member of the transforming growth factor-beta (TGF-β) superfamily, are associated with the pathology of various diseases. GDF15 is often induced under stress and with aging. The human trabecular meshwork cells express and secrete GDF15, suggesting its plausible role in regulating IOP.

In a study performed by Maddala and colleagues at Duke University, USA, the serum and aqueous humor (AH) levels of GD15 were compared between glaucoma and non-glaucomatous, cataract populations.

The GDF15 levels in AH and serum samples from primary open-angle glaucoma (POAG) patients were significantly elevated (p < 0.001 and p < 0.011, respectively) by > 9-fold and 1.5-fold, respectively, compared to the respective samples derived from non-glaucoma (cataract) patients. This held true for mild, moderate, and severe glaucoma patients.

AH GDF15 levels were significantly (p < 0.001) elevated in both male (by 11.6-fold) and female (by 5.4-fold) POAG patients compared to cataract patients.

For the serum GD15 levels, although there was an increase (median values: 2228.0 pg/mL, n = 19) in male POAG patients compared to male cataract patients (1850.0 pg/mL, n = 19), the difference did not achieve statistical significance (p < 0.148). Serum GDF15 levels in female POAG patients (n = 22), however, were significantly (p < 0.015) elevated (by 64%) compared to female cataract patients (n = 13).

This study reveals a significant and marked elevation of GDF15 levels in the AH of POAG patients compared to non-glaucoma cataract control patients. This may suggest a role of inflammation in the causation of glaucoma.

REFERENCE:

Maddala, R.; Ho, L.T.Y.; Karnam, S.; Navarro, I.; Osterwald, A.; Stinnett, S.S.; Ullmer, C.; Vann, R.R.; Challa, P.; Rao, P.V. Elevated Levels of Growth/Differentiation Factor-15 in the Aqueous Humor and Serum of Glaucoma Patients. J. Clin. Med. 2022, 11, 744. https://doi.org/ 10.3390/jcm11030744