13-Feb-2019: Kerala takes the lead in tackling trans-fat hazard
In a first, the Health Department has drawn up an action plan to generate public awareness on the harmful effects of trans fatty acids (TFA) in commercially available food items and to encourage the local food industry to meet the current statutory limits set for TFA. The draft is expected to be finalised and released shortly.
The initiative has been launched by the department as various studies suggest that an unhealthy diet with a high TFA content is a significant factor that pushes up metabolic syndrome and the burden of its associated complications amongst Keralites.
The year-long action plan has specific components on building awareness on trans-fat amongst food business operators (FBOs) and giving them scientific sessions and training on how they can keep their food TFA-free.
Generating public awareness on the harmful effects of trans fat, especially among schoolchildren, is being given special focus so that the demand for healthier versions of their favourite foods come from the children themselves.
Clear timelines are being set as to when each of the components of the plan should be completed and when enforcement should begin.
Salt being a major contributor to hypertension and stroke, the action plan also plans to address the high salt content in processed foods, pickles, papads and condiments by encouraging manufacturers to move to low sodium options.
The food industry is willing to ditch partially hydrogenated vegetable oils (PHVOs, one of the main sources of TFA in industrially produced food) and switch to TFA-free margarine or shortening to produce baked goods. But we have to provide them alternative technologies and know-how on re-adjusting their recipes to maintain the taste and texture of their products.
The pickle industry is in agreement that good hygienic and manufacturing practices and low sodium options can reduce the salt content in their products.
The department is being supported in this initiative by Vital Strategies, the nutrition wing of the World Bank, WHO, the Food Safety and Standards Authority of India (FSSAI), and the State Food Safety wing, which will be in charge of enforcement.
An experts’ group has been constituted for the implementation of the guidelines on TFA and salt reduction.
14-Jan-2019: Bihar bans fish trade in Patna due to presence of formalin
Bihar government has banned the sale, storage and transportation of all kinds of fishes within the municipal area of Patna. The ban, initially for 15 days, was imposed after high contents of formalin, lead, mercury and cadmium were found in fish samples.
The ban has been imposed under the provisions of the Food Safety and Standards Act, 2006. The violation of the ban is punishable with imprisonment up to seven years and a fine of Rs 10 lakh.
Used for preserving fish, formalin is a carcinogenic substance, while heavy metals such as lead, mercury and cadmium affect human kidneys, bones, liver, brain and reduce immunity.
9-Feb-2018: IISc scientists identify potential early biomarker for Alzheimer’s disease
Researchers at the Centre for Neuroscience and Centre for Brain Research at the Indian Institute of Science (IISc) have now identified a key protein in the brain that is broken down early on in Alzheimer’s disease, affecting communication between nerve cells that is important for memory formation. The protein, called F-actin (fibrillar actin, a polymer of the protein G-actin), is responsible for maintaining the shape of mushroom-shaped projections called dendritic spines on the surface of a nerve cell. These spines protrude into synapses, the junctions between nerve cells, and act as docking spots for other neurons to connect and transmit signals.
The researchers found for the first time that F-actin is broken down very early on in Alzheimer’s disease, affecting the shape and number of spines, which in turn disrupts synaptic communication and leads to memory deficits.
Alzheimer’s disease is thought to affect 60-70% of the 50 million people worldwide who suffer from some form of dementia. There is currently no cure or treatment to slow down its progression. Identifying key molecules involved in the initial stages may help detect it early and develop drugs that delay its onset or slow it down, allowing patients to lead a better quality of life.
Research has shown that one of the key early events is the disruption of synapses caused by loss of, or defects in dendritic spines, which interrupts the flow of information between nerve cells. However, what causes this disruption has remained unclear.
In this study, the researchers used mice with genetically introduced genes that are mutated in familial Alzheimer’s disease (AD mice) to look at proteins involved in maintaining dendritic spine shape and number. Inside these spines, proteins called G-actins assemble to form long filaments called F-actins that control the spine’s structure. The researchers found that in AD mice as young as 1 month old, the F-actin/G-actin balance was disrupted, with more F-actin being broken down into G-actin, leading to misshapen and lost spines. By contrast, the formation of toxic protein clumps called amyloid plaques, which is one of the first clinical symptoms, is typically seen only at 7-8 months of age in AD mice.
To test if F-actin loss had any effect on behaviour, the researchers used a paradigm called contextual fear conditioning. In these experiments, mice are trained to fear a specific location or context by giving them a mild electric shock. When normal mice are placed in the same arena the next day, they freeze, remembering and anticipating the shock. AD mice as young as 2 months old, however, did not freeze as expected, indicating that they had forgotten the context.
Remarkably, when the researchers injected a chemical into AD mice that prevented F-actin from breaking down, they found that the mice were able to regain their normal fear response. “That was very striking. When we stabilized the F-actin, we were able to see the behaviour recovery,” says Reddy Kommaddi, first author and DBT Ramalingaswami Fellow at the Centre for Neuroscience.
To find out if similar effects were also happening in humans, the researchers looked at post-mortem brain tissue samples of patients with Alzheimer’s disease, who had been studied for more than a decade before their death. The samples were obtained from collaborator David Bennett at the Rush Alzheimer’s Disease Center in Chicago, USA. Just like the AD mice, these samples also showed a gradual breakdown of F-actin over time, as their symptoms — memory loss and accumulation of plaques — worsened.
Taken together, these results indicate a direct link between F-actin loss and early behavioural changes that lead to Alzheimer’s disease.
Because F-actin is a structural protein, it gives shape to all cells in the body, and is present everywhere. It could potentially become a biomarker.
The researchers are currently working on understanding what causes F-actin to break down. They found, for example, that nerve cells treated with a toxic protein called amyloid beta 42 — which eventually gives rise to the classical AD plaques — show reduced F-actin levels. The team is currently working on unravelling the molecular mechanisms involved.