Grape-derived compounds may promote resilience against depression

Scientists from the Icahn School of Medicine at Mount Sinai describe an extensive analysis of novel grape-derived compounds, dihydrocaffeic acid (DHCA) and malvidin-3'-O-glucoside (Mal-gluc), which might be developed as therapeutic agents for the treatment of depression. The study results indicate that these natural compounds may attenuate depression by targeting newly discovered underlying mechanisms of the disease.

Conventional pharmacological treatments are estimated to produce temporary remission in less than 50 percent of patients, and they are often associated with severe adverse effects. Thus, there is an urgent need for a wider spectrum of novel therapeutics.

Depression is associated with a multitude of pathological processes, including inflammation of the peripheral immune system, a set of biological structures and processes in the lymph nodes and other tissues that protect against disease and abnormalities involving synapses, the structures that permit neurons to pass an electrical or chemical signal to other neurons.

However, currently available antidepressants are largely restricted to targeting the systems that regulate serotonin, dopamine, and other related neurotransmitters, and these treatments do not specifically address inflammation and synaptic maladaptations that are now known to be associated with MDD.

Previous research has found that grape-derived polyphenols have some efficacy in modulating aspects of depression, yet the mechanisms of action had largely remained unknown until now. The new study, led by Giulio Maria Pasinetti, PhD, Saunders Professor of Neurology, and a team of investigators from the Center for Integrative Molecular Neuroresilience at the Icahn School of Medicine at Mount Sinai, found that a bioactive dietary polyphenol preparation-a combination of three grape-derived polyphenol products, including a select Concord grape juice, a select grape seed extract, and trans-resveratrol was effective in promoting resilience against stress-induced depression in mice.

Specifically, researchers found that DHCA and Mal-gluc can promote resilience in mouse models of depression by modulating inflammation and synaptic plasticity, respectively. DHCA reduces interleukin 6 (IL-6), a pro-inflammatory substance secreted by T cells and macrophages to stimulate immune response, by epigenetically modulating the non-coding sequence of the IL-6 gene. Mal-gluc modulates histone acetylation of the Rac1 gene and allows transcription activators to access the DNA for increased transcription in the brain, which influences the expression of genes responsible for synaptic plasticity.

Researchers also demonstrated that DHCA/Mal-gluc treatment was effective in attenuating depression-like phenotypes in a mouse model of increased systemic inflammation induced by transplantation of cells from the bone marrow of stress-susceptible mice. The research shows that combination treatment with the two compounds can promote resilience against stress-mediated depression-like phenotypes by modulating systemic inflammatory responses and brain synaptic plasticity in a mouse model of depression.

The Mount Sinai study provides novel preclinical evidence supporting the targeting of multiple key disease mechanisms through DNA epigenetic modification for the treatment of depression. This study strongly supports the need to test and identify novel compounds that target alternative pathologic mechanisms, such as inflammation and synaptic maladaptation, for individuals who are resistant to currently available treatment.

Using combination treatment of DHCA and Mal-gluc to simultaneously inhibit peripheral inflammation and modulate synaptic plasticity in the brain works synergistically to optimize resilience against chronic stress-induced depression-like phenotypes. The discovery of these new, natural grape-derived polyphenol compounds targeting cellular and molecular pathways associated with inflammation may provide an effective way to treat a subset of people with depression and anxiety, a condition that affects so many people.
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Generic analysis for depression therapy

The failure of drugs such as SSRIs, used to treat depression, can be a result of genetic variations in patients. Variations within the gene that encodes the CYP2C19 enzyme results in extreme differences in the levels of escitalopram achieved. Prescribing the dose of escitalopram based on a patient's specific genetic constitution would greatly improve therapeutic outcomes.

Pharmaceutical treatment of depression commonly makes use of selective serotonin reuptake inhibitors (SSRIs) of which escitalopram is the most frequently administered clinically. However, escitalopram therapy is currently limited by the fact that some patients do not respond well to the drug, while others develop adverse reactions requiring discontinuation of treatment.

In order to individualise drug therapy, researchers are attempting to establish genetic biomarkers that can predict an individual's response to drugs. In a recent study, it was discovered that variation in the gene encoding the enzyme responsible for escitalopram metabolism (CYP2C19) is very important in this respect.

 Individuals with a variant of the gene promoting increased enzyme expression had blood levels of escitalopram too low to impact the depression symptoms, whereas patients with a defective CYP2C19 gene reached drug levels which were too high. Overall, one third of the study participants achieved escitalopram blood levels that were either too high or too low. The researchers found that 30 per cent of the patients carrying gene variants causing excessive or inadequate enzyme levels switched to other drugs within one year, in contrast with only 10 to 12 per cent of patients carrying the common gene.

The study shows that genotyping of CYP2C19 could be of considerable clinical value in individualising doses of escitalopram so that a better all-round antidepressive effect could be achieved for the patients. CYP2C19 is involved in the metabolism of many different SSRIs, the finding is also applicable to other types of antidepressants.
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Depression damages the heart

Depressed heart disease patients may die suddenly because post-coronary artery disease depression can leads to untimely death. This shows that their is
a link between depression, heart disease, and increased risks of death.

Coronary artery disease patients don't live as long as expected. But the life expectancy can be increased with better therapies, surgeries and treatment.

Depression is the strongest risk factor for dying, compared to any other risk factors like age, heart failure, diabetes, high blood pressure and kidney failure.

Hormonal changes and electrofunctioning changes which affect the heart's functioning during depression can cause sudden death.

Depressed people are prone to over eating, smoking and drinking. This can increase the risk of heart attack and sudden death. They have reduced levels of serotonin released in their brain which may affect their heart.

There are normal emotional reactions to having a heart attack, emotions like
anxiety, sadness and anger. These are normal for some people, but long-term anxiety and sadness can leads to depression.
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How to break sugar addiction

Insomnia, regular breakouts, craving for sweet and exhausted taste buds may be an indicator that you are suffering from a sugar addiction.

 Sugar addiction can leads to overweight and obesity. Excessive sugar consumption in different forms destroys body systems generally.

Acne is an indication that there is too much sugar in the diet, damage to the skin proteins, collagen and elastin, leading to premature wrinkles and aging.

Change in taste bud; taste buds are addicted to sweet foods and may not want any food that is not sweet.

Diet high in sugar can increase cancer growth; tumors used sugar as energy to mutate and spread across the body.

Bacteria in the mouth feeds on sugars which creates harmful acids causing tooth decay, destroy tooth enamel and form hole in the tooth.

The pancreas releases insulin to transfer glucose to the cell's after consuming sugar, the higher the sugar peak, the more extreme the sugar dip that will follow.

Sugar interrupts the supply of important neurotransmitter precursors through the blood-brain barrier - and particularly ones that help produce serotonin and dopamine, which influence mood.

Excess sugar consumption decrease the amount of good cholesterol in the bloodstream and increase the amount of bad cholesterol in the body, leading to heart disease.

The liver struggles to process excessive amounts of sugar. The unprocessed sugars are converted to fat calls, which are distributed throughout the body. It can leads to obesity.

Too much sugar in the body can cause bacteria to move from the colon to the small intestine, proliferate on the foods digesting in the small intestine and cause bloating, acid reflux, gas and abdominal cramping.

Sugar can be remove from the body by replacing process foods with whole foods and by replacing all processed drinks with water.
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Dangers of high fat diet in pregnancy

High-fat diet during pregnancy affects the development of the brain and endocrine system of fetus. Unhealthy diet during pregnancy can increase the risk of mental health disorders like anxiety and depression in children.

 Fetuses exposed to a high-fat diet will have greater cases of anxiety, high fat exposure impaired the development of neurons containing serotonin, a neurotransmitter that's critical in developing brains.

High fat diet in pregnancy contributes to neuropsychiatric disorders like attention deficit hyperactivity disorder ADHD spectrum disorders, bipolar
disorder, depression, eating disorders, schizophrenia, anxiety and depression in children.
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Chocolate boots brain power

Chocolate is made from cocoa butter and sugar, there are different types of chocolate, some of them are: milk, sweet, dark, brown and white chocolate.

Cocoa contains flavonoids that have anti-inflammatory and antioxidants that control insulin resistance.

Tryptophan in chocolate is used by brain to produce serotonin and phenylethylalanine that encourages feeling of happiness, attraction and excitement.

Valeric acid in chocolate reduces stress and pain, theobromine also relieve throaty tickle.

Eating chocolate improves memory, aids concentration, prevents high blood pressure and  protects the skin.