A Natural Way to View the World



I never thought a simple teaspoon of turmeric in my food could alter the way I perceive things around me. Literally! No pun intended! A recent study published in 2013 states the beneficial effects that curcumin, the main component of turmeric, has on rescuing retinal degenerations or more simply put, vision loss.

Retinal degenerations are the deterioration of the retina resulting in irreversible blindness. There are two common forms of this degenerative disease. The first one is known as Age-related muscular degeneration (AMD) and usually affects older adults and results in a loss of vision in the center of the visual field, known as the macula because of damage to the retina. The second one is known as Retinitis Pigmentosa (RP), which is the main focus of this paper. RP is an inherited degenerative eye disease, in which genetic defects cause cell death of the rod and cone photoreceptors, predominantly the rod photoreceptors.

Rods are photoreceptor cells concentrated at the outer edges of the retina and function in less intense light and are used for peripheral vision. Cones are responsible for color vision and function best in bright light. Some of the symptoms for RP include decreased vision at night or in low light, loss of peripheral vision also known as “tunnel vision,” and loss of central vision in more advanced stages of the disease (Figure 1).

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RP is commonly caused by mutations in Rhodopsin. Rhodopsin is a biological pigment in photoreceptor cells in the retina that is responsible for the first events in the perception of light. This pigment is a G-protein coupled receptor and is the most abundant protein in rod photoreceptor cells. Rhodopsin consists of a protein moiety called opsin and a covalently bound co-factor 11-cis retinal. Mutations in Rhodopsin have been classified into three different groups however this paper only focuses on the Class III mutants. Class III mutants are expressed at very low levels and remain in localized in the Endoplasmic Reticulum (ER). These mutants form the Rhodopsin chromophore poorly and cause abnormal trafficking of the protein resulting in formation of aggregates retained near the ER.

The genetic link between the P23H mutant in rhodopsin and RP has been established however the mechanism underlying photoreceptor degeneration due to this mutation is yet to be understood. Studies suggest that the negative effect exerted by the P23H mutation leads to aggregation and mislocalization of rhodopsin thereby leading to photoreceptor cell death in RP. Therefore, researchers are evaluating synthetic and natural compounds to check for their therapeutic effects in helping treat these protein aggregates. In this study researchers wanted to test whether curcumin exerts anti-protein aggregating activity in the retina and rescue photoreceptors from degeneration due to misfolded rhodopsin.

In this study the researchers wanted to test to check whether curcumin does in fact exhibit protein-aggregating properties. In order to test this they had cells expressing wild type (WT), P23H mutant rhodopsin and P23H mutant rhodopsin treated with curcumin. (Figure 2). Tags were also used to help visualize the area in which these proteins aggregate. The first image depicts the area in which Rhodopsin is localized, as shown by the green marker. In the second image the cells have been co-labeled with an ER-maker, therefore the red marks the location of the ER in this image. Lastly, the third image shows an overlay of the first two images. The green marker shows that in the WT the rhodopsin is localized to the plasma membrane. The white arrow in the P23H rhodopsin mutant marks the formation of protein aggregates localized in the ER region. The red arrow shows that the mutant aggregates were disrupted upon treatment with curcumin and resembled the WT. Thus this experiment helped conclude that curcumin helps disrupt protein aggregates as well as the distribution pattern of the mutant.

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Next the researchers wanted to test whether curcumin improved retinal morphology, so they used P23H rhodopsin mutant transgenic rats for evaluation (Figure 3).

The untreated transgenic rats, as expected, developed severe retinal degeneration. The photoreceptor outer nuclear layer (ONL) and inner nuclear layer (INL) segments were shorter and the ONL region was found to be very thin, only containing 2-3 nuclei. Whereas the transgenic rats that were treated with curcumin showed an overall improvement in retinal morphology. The photoreceptor ONL and INL were longer and ONL preserved 6-7 rows of photoreceptor nuclei. A wild-type normal rat retina was also used in this case, which served as a control and the curcumin treated rats and this control were very similar in morphology.

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The ONL and INL regions of the photoreceptor cells were also tested to see how thick these layers were. Again it was found that in the curcumin treated rats these regions were significantly thicker than the rats not treated with curcumin. These regions play an important role, as the ONL contains the light detecting portion of the eye and contains nuclear bodies such as rods and cones and the INL contains numbers of closely packed cells which help send electrical signals to our brains when light is detected. Since the ONL region was found to be significantly thicker in the curcumin treated mutants the numbers of photoreceptor cells, rods and cones, also showed a great increase. Thus, these results were able to show that curcumin does in fact have an impact on improving the retinal morphology of P23H rhodopsin mutants. This study is able to provide evidence to support the therapeutic potential of curcumin. In future studies, administration of curcumin in combination with other therapies may be more effective in treating diseases at a faster rate!

Unlike other synthetic compounds, which provide an instant fix, natural compounds like Turmeric need to be taken consistently over long periods of time to be most effective. I never would have imagined that adding just a pinch of this compound would truly help spice up my life as well as provide a myriad of other benefits at the same time. However folks! Don’t be too generous with the Turmeric; add a pinch not a dash, for it makes all the difference in making sure you don’t turn yellow!

Turmeric: Nature’s Pharmacy


Through all my years of growing up there was no ailment that could not be cured by the ingredients in my mother’s pantry. Stomach-ache or nausea? A piece of ginger or half a teaspoon of Ajwain seeds provided quick relief. Eyelid swollen due to a stye? Black pepper ground to a paste with water would be guaranteed to clear that up.

The one spice or herb that I have used everyday for multiple reasons is Turmeric. Not called the King of spices for nothing, Turmeric (also known as Haldi or Indian Saffron) is a staple in every South Asian household.  This spice is a rhizomatous perennial plant belonging to the ginger family Zingiberaceae, native to tropical South Asia. Turmeric has a slightly bitter taste and can be purchased in either a powder form or the underground rhizome of the plant can be boiled, dried and ground as shown in Figure 1.


Curcumin, which comes from the herb Curcuma longma, is thought to be the primary pharmacological agent in turmeric. While curcumin is best known as one of the ingredients used to make curry, it also gives mustard its bright yellow color. Curcumin is a lipoplilic polyphenol and hence is insoluble in water, but readily soluble in organic solvents. The polyphenolic natural product, curcumin, exhibits therapeutic activity against several diseases, which is mainly attributed to its chemical structure.

This spice is a diferuloly methane molecule and includes two ferulic acid residues joined by a methylene bridge. The three most important functional groups of this compound is the aromatic methoxy phenolic group, the beta-diketo moiety and the seven-carbon methylene linker (Figure 2). The unique chemical, physical and biological properties of this spice can be attributed to these different functional groups. The methoxy phenolic group and the methylenic hydrogen are responsible for the antioxidant activity of curcumin. The beta-diketone moiety can covalently interact with proteins and can form chelates with transition metals helping to reduce metal induced toxicity.


Curcumin has been extensively used in Ayurveda (Indian system of Medicine) for centuries and has a wide variety of uses. It has been found to soothe a sick stomach, ease achy arthritis, as a pesticide to keep off pesky ants and insects, to keep your scalp dandruff free, to fight off the fat, enliven bland food, and make a variety of delicious dishes, to name just a few. Recently, I have started to research the workings of this magical herb and more specifically its medicinal uses and to my surprise, found that one major property that modern medicine is still not very aware of is the herbs potential efficacy in the treatment of Alzheimer’s Disease (AD).

AD is a neurodegenerative disease which occurs as a result of a continuous loss of neuron structure and function in the temporoparietal and frontal cortex regions of the brain. This damage to the neurons is permanent and cannot be repaired with any current treatments, since the biological target of the disease is unknown.  The medications available for patients diagnosed with AD only serve as remedies to address some symptomatic relief. Researchers that have obtained information from postmortem studies in brains of patients that had AD to study the possible causes for this disease. They were able to observe that the shrinking brains had many plaques and tangles concentrated with iron and copper ions. The plaques are clusters of beta-amyloid proteins that surround dead neurons and the tangles are neurons, which coil due to a lack of the tau protein. There is evidence to suggest that the inflammation, aggregation and decreased elimination of the amyloid beta-protein (Aß) are critical events in the pathogenesis of AD, and therefore treatment development has focused on these processes.

A study conducted by Garcia-Alloza  et al. in the department of Neurology at the Alzheimer’s Disease Research Lab in Massachusetts, used transgenic mice to show symptoms of AD. They demonstrated that curcumin has potentially important biological effects in increasing the elimination of Aß and preventing Aß from aggregating into plaques. Curcumin is highly hydrophobic and can readily pass through the blood-brain barrier and bind to Aß plaques. This spice is a natural flurochrome therefore it has been shown to naturally label these plaques in transgenic mice models. The Aß plaques of the transgenic mice were imaged before and seven days following curcumin treatment. The individual plaques were then measured and compared to the control mice, not subjected to curcumin treatment. The results showed that the control treated mice did not undergo any changes. However as shown in Figure 3, Aß protein aggregation was significantly inhibited with increasing doses of curcumin. The white arrows on the image depict reduced or disappeared plaques after a seven day treatment with curcumin. Thus this research is able to provide evidence to support that curcumin can be a viable treatment in reducing the size and number of plaques in patients with AD.


Inflammation is also a key factor in chronic and degenerative diseases like AD. In order to relieve pain Non-Steroidal Anti-inflammatory Drugs (NSAID) are used. NSAID’s are COX-2 inhibitors. By inhibiting COX-2 enzymes these NSAID’s prevent the formation of prostagladins, which act as messenger molecules in the process of inflammation. It is believed that curcumin acts like an NSAID, inhibiting COX-2, but delivers far superior anti-inflammatory activity than most drugs. To prove whether this belief was fact or fiction researchers Yang et al. sought to test whether curcumin was more effective than other NSAID’s at inhibiting Aß aggregation. Curcumin, Naproxen and Ibuprofen were tested at varying levels of doses, 0-8 μm and 0-32 μm respectively. Figure 4 showed that only high concentrations of Naproxen and Ibuprofen were able to inhibit Aß aggregation. The results also showed that curcumin was more effective in reducing the Aß aggregation over a low dose range. Thus these researchers provided some evidence to support that curcumin is the better aggregation inhibitor.


Turmeric so timelessly interwoven with the origins of ancient civilizations challenges the belief held by traditional drug companies. Most believe the effects of Turmeric are an old wives tale; hopefully researchers were able to bust that myth and shed light on the relevant uses of Turmeric in the treatment of neurodegenerative diseases like AD. The day is not far of when Turmeric, the traditional herb will eventually find its niche in modern medicine as nature provides an elegant bimolecular architecture of complexity from which synthetic analogues and derivatives can be modeled after.


Garcia-Alloza, M., Borrelli, L. A., Rozkalne, A., Hyman, B. T. and Bacskai, B. J. (2007), Curcumin labels amyloid pathology in vivo, disrupts existing plaques, and partially restores distorted neurites in an Alzheimer mouse model. Journal of Neurochemistry, 102: 1095–1104. doi: 10.1111/j.1471-4159.2007.04613.x

Yang, Fusheng, et al. “Curcumin inhibits formation of amyloid β oligomers and fibrils, binds plaques, and reduces amyloid in vivo.” Journal of Biological Chemistry 280.7 (2005): 5892-5901.

Mask your Face

Midterms got you down? Try to stay relaxed and make your very own Turmeric face mask!

Its simple:
Ingredients- Flour, Turmeric, Milk, Honey

1) 2 tablespoons of flour

2) 1 teaspoon of Turmeric

3) 3 tablespoons of milk

4) A few drops of honey

5) Mix all these ingredients together to make a paste

6) Apply this paste to your face and let it dry for 20 minutes

7) Gently scrub your face with lukewarm water and apply your favourite moisturizer

This will have your skin glowing in no time!