Brain Food

We ve all heard a lot about fat, how it is bad for us, bad for our hearts, our arteries, our brains. But that s not necessarily true. Some fat in our diets is healthful. Certain fats are even essential to well-being. They energize us, satisfy hunger, and aid in maintaining cell membranes and steroid hormone production. We also know that the brain regulates almost all systems of the body to some extent. So fat can either promote good brain health—or impair it. What s important is to separate out the good fats from the bad. 

FATS THAT ARE BAD FOR BRAINS AND OTHER LIVING THINGS Saturated Fats and Trans Fats 

The molecules in saturated fats and trans fats pack together closely so they are solid not only while refrigerated, but also at room temperature. Saturated fats increase the amount of cholesterol your 

Cheese, whole milk, butter, lard, and other fatty animal products are loaded with saturated fat. Plant-based saturated fats include coconut oil, palm oil, and palm kernel oil. 

Trans fats are found mostly in baked goods, snack foods such as popcorn and potato chips, salad dressings, margarine, shortening, prepared mixes, and fried foods. A few cities like New York and Philadelphia have banned the use of 

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Phosphatidylcholine, commonly known as lecithin, is the most commonly occurring in natnre and consists of two fatty add moieties in each molecule. Phosphati-dylethanolamine, also known as cephahn, consists of an amine gronp that can be methylated to form other compounds. This is also one of the abundant phospholipids of animal, plant, and microbial origin. Phosphatidylserine, which has weakly acidic properties and is found in the brain tissues of mammals, is found in small amounts in microorganisms. Recent health claims indicate that phosphatidylserine can be used as a brain food for early Alzheimer s disease patients and for patients with cognitive dysfunctions. Lysophospholipids consist of only one fatty acid moiety attached either to sn-1 or sn-2 position in each molecule, and some of them are quite soluble in water. Lysophosphatidylchohne, lysophosphatidylserine, and lysophos-phatidylethanolamine are found in animal tissues in trace amounts, and they are mainly hydrolytic products of phospholipids. 

What your body needs for peak performance is simply a balanced diet. Eat plenty of fruits and vegetables, along with lean protein and complex carbohydrates. Foods that are high in lecithin (an amino acid), such as fish and beans, are especially good brain foods. ... 

Young, S. N., The clinical psychopharmacology of tryptophan, in Nutrition and the Brain. Food Constituents Affecting Normal and Abnormal Behavior, Vol. 7, Wurt-man, R. J. and Wurtman, J. J., Eds., Raven Press, New York, 1986, 49-88. 

Subhash MN, Padmashree TS. 1991. Effect of manganese on biogenic amine metabolism in regions of the rat brain. Food Chem Toxicol 29 579-582. 

Amaze Brain Food RTD (Unilever), Turkey - 200 ml 33.3. rg/serve... 

Gilgun-Sherki Y, Melamed E, Offen D (2006) Anti-inflammatory drugs in the treatment of neurodegenerative diseases current state. Curr Pharmaceut Des 12 3509-3519 Gomez-PiniUa F (2008) Brain foods the effects of nutrients on brain function. Nat Neurosci Rev... 

The aroma of fmit, the taste of candy, and the texture of bread are examples of flavor perception. In each case, physical and chemical stmctures ia these foods stimulate receptors ia the nose and mouth. Impulses from these receptors are then processed iato perceptions of flavor by the brain. Attention, emotion, memory, cognition, and other brain functions combine with these perceptions to cause behavior, eg, a sense of pleasure, a memory, an idea, a fantasy, a purchase. These are psychological processes and as such have all the complexities of the human mind. Flavor characterization attempts to define what causes flavor and to determine if human response to flavor can be predicted. The ways ia which simple flavor active substances, flavorants, produce perceptions are described both ia terms of the physiology, ie, transduction, and psychophysics, ie, dose-response relationships, of flavor (1,2). Progress has been made ia understanding how perceptions of simple flavorants are processed iato hedonic behavior, ie, degree of liking, or concept formation, eg, crispy or umami (savory) (3,4). However, it is unclear how complex mixtures of flavorants are perceived or what behavior they cause. Flavor characterization involves the chemical measurement of iadividual flavorants and the use of sensory tests to determine their impact on behavior. 

Mood and hedonic value associated with feeding, food intake, foraging, consummatory behaviors, and craving in addiction complex regulation by food entrainable oscillators in the brain and periphery, neuropeptides (including orexins) and biogenic amines. 

The first hormonal signal found to comply with the characteristics of both a satiety and an adiposity signal was insulin [1]. Insulin levels reflect substrate (carbohydrate) intake and stores, as they rise with blood glucose levels and fall with starvation. In addition, they may reflect the size of adipose stores, because a fatter person secretes more insulin than a lean individual in response to a given increase of blood glucose. This increased insulin secretion in obesity can be explained by the reduced insulin sensitivity of liver, muscle, and adipose tissue. Insulin is known to enter the brain, and direct administration of insulin to the brain reduces food intake. The adipostatic role of insulin is supported by the observation that mutant mice lacking the neuronal insulin receptor (NDRKO mice) develop obesity. 

Leptin is a cytokine produced and secreted by adipose tissue in proportion to the body fat content [3]. Mice and humans lacking leptin or its receptor develop a severe hyperphagia and a dramatic degree of obesity which is considerably more pronounced than that of the NDRKO mouse. Thus, leptin is the key adiposity signal in rodents and humans. Leptin secretion appears to reflect the metabolic status of the adipocyte rather than the sheer size of triglyceride deposits, and leptin levels may transiently be dissociated from total body fat. Nonetheless, over the course of a day with unrestricted food supply, plasma leptin levels reliably reflect the amount of total body fat. Local administration of leptin into the brain results in reduced food intake. The vast majority of patients with obesity have elevated serum levels of leptin. Thus, it is believed that the polygenic obesity is due to leptin resistance rather than to inadequate leptin secretion, or to a reduced blood/brain transport of the cytokine. 

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