Nicotinamide adenine dinucleotide (NAD) is an essential aspect of existing for all living cells. NAD controls gene expression, stress responses, and DNA damage repair. The body uses NAD precursors, such as nicotinamide mononucleotide (NMN), to create NAD. There are multiple ways NAD precursors create NAD; NAD precursors create NAD via various efficient and inefficient NAD synthesis chemical transformations. Redox reactions between NAD and hydrogen generate NAD in the form of NADH. Nicotinamide adenine dinucleotide, a crucial cofactor essential to redox reactions and responsible for cellular energy metabolism, converts the food we eat into energy. NAD guides the work enzymes such as N-acyl phosphatidylethanolamine phospholipase D (NAPE-PLD) and fatty acid amide hydrolase (FAAH), do in the body. NAPE-PLD and FAAH work together to convert lipids into the ethanolamide lipid oleoylethanolamide. Research suggests that NAPE-PLD has a significant role in synthesizing OEA and absorbing fat.
OEA uses various mechanisms to act on food intake and decrease appetite. As a ligand of PPAR-α, TRPV1, and GPR119 receptors, OEA participates in regulating energy intake and expenditure and controlling weight gain. Oleoylethanolamide also exerts biological processes such as meal initiation delay, meal size reduction, and increasing intervals between meals.
OEA derives from oleic acid, a fatty acid, and is typically present in small intestine cells, neurons, astrocytes, and adipose tissues. This substance generates the feeling of satiety following food intake. Oleoylethanolamide acts on the proximal proliferator-activated receptor-α (PPAR-α). The use of laboratory animals in previous studies concluded that the activation of the PPAR-α receptor in rat intestines resulted in the rats eating a reduced amount of food. Researchers in food science and other domains conduct clinical trials to investigate these effects in humans.
Health professionals recognize obesity as a chronic low-grade inflammation condition and continue to investigate the role OEA plays in managing its symptoms. Studies suggest that in many cases, a high-fat diet, as well as low levels of NAPE-PLD in adipocytes, can induce obesity. Findings demonstrate that adipose tissue NAPE-PLD plays a part in controlling the development of fat mass. In humans, gene expression of the CB1 receptor is in the central and peripheral nervous systems, and that of CB2 typically occurs in immune cells. Through CB1 and CB2, endocannabinoids exert physiological functions in the body. Research shows the involvement of a modified endocannabinoid system tone in obesity pathogenesis. Per clinical studies, CB1 and CB2 impact inflammation and food intake. Oleoylethanolamide is an ethanolamide fatty acid that acts independently of cannabinoid pathways and doesn’t bind to cannabinoid receptors, such as CB1 and CB2. Previous reports from research studies on obesity and the impact of OEA detailed findings that OEA can activate various receptors such as PPAR-α, GPR119, and TRPV1, to regulate appetite and energy homeostasis in individuals with obesity. Recent and ongoing research investigates the role of the TRPV1 channel on insulin resistance, leptin resistance, and obesity-induced by a diet. TRPV1 studies examine the role of TRPV1 in intervening in pancreatitis pains and its potential effects on diabetes. Health and food science studies reveal that consuming unhealthy foods or adhering to a high-fat diet can negatively impact brain function. Upon consuming dietary fats, oleoylethanolamide serves as a satiety signal. To send a satiety signal, OEA engages the vagus nerve sensory fibers to reach the brain’s satiety centers. Physiology and food science studies reveal the vagus nerve’s role in obesity.
Numerous studies conclude that NAD levels decrease as we age. In some conditions, there may be an imbalance between NAD and NADH. In diabetes, for instance, there is a depletion of NAD and an overproduction of NADH. Researchers noted an association between decreased NAD levels and obesity and metabolic disorders such as fatty liver disease, diabetes, and insulin resistance. Further study into this association led researchers to conclude that altered NAD metabolism can have positive nutritional effects. Dietary fatty acids can impact food digestion in the small intestine multiple ways, including reducing the OEA-degrading activity of fatty acid amide hydrolase. Food science studies using rodents suggest that prolonged adherence to a high-fat diet can decrease OEA levels.
Increased OEA and NAD levels in the body enable people to enjoy optimum physical health. Higher NAD levels allow the body to restore cells properly. Further study of NAD and its nutritional impact suggests that high NAD levels in body tissues may prevent the development of metabolic disorders and insulin resistance. Increasing NAD metabolism can lead to extended lifespans in many organisms. As such, humans with a boost of NAD can enjoy longer, healthier, more active lives. While fast food and high-fat food consumption may be typical because of their affordability and convenience, people should consider decreasing their fat intake. By replacing high-fat foods with natural ingredients, people can do their bodies an excellent service, better than the customer service any restaurant could offer. Significant increases of OEA in the body can amplify the weight regulation effects of OEA. Caring for your cells is the first step to caring for yourself. Weight management should be about feeling good and boosting energy in addition to weight loss. Increased OEA and NAD levels can better manage the pain and inflammation associated with numerous conditions. While cocoa powder, oatmeal, and nuts are primary oleoylethanolamide sources, they contain low OEA levels. Supplements containing OEA can provide the natural boost people need to manage their food intake, weight, and physical health.