These systems include digestion, reproduction, and growth. These hormones do not return to normal levels until the stress passes. If the stress does not pass, the nervous system continues to trigger physical reactions that can eventually lead to inflammation and damage to cells. Stress places a greater demand on the body for oxygen, energy, and nutrients.

Yet people who experience chronic stress may crave comforting foods such as highly processed snacks or sweets, which are high in fat and calories but low in nutrients. Stress can disrupt sleep by causing lighter sleep or more frequent awakenings, which leads to fatigue during the day.

The reverse may also be true that poor-quality sleep is itself a stressor. Studies have found that sleep restriction causes a significant increase in cortisol levels. A balanced diet can support a healthy immune system and the repair of damaged cells. It provides the extra energy needed to cope with stressful events.

Early research suggests that certain foods like polyunsaturated fats including omega-3 fats and vegetables may help to regulate cortisol levels. Mindful eating. Mindful eating practices counteract stress by encouraging deep breaths, making thoughtful food choices, focusing attention on the meal, and chewing food slowly and thoroughly.

This increases enjoyment of the meal and improves digestion. Mindful eating can also help us realize when we are eating not because of physiological hunger but because of psychological turbulence, which may lead us to eat more as a coping mechanism.

Regular exercise. Physical activity will help to lower blood pressure and stress hormone levels. Aerobic exercise like walking and dancing increases breathing and heart rate so that more oxygen reaches cells throughout the body.

This reduces tension in muscles, including the heart. Meditation or deep breathing techniques. Fast, shallow breathing and erratic thoughts occur in response to stress.

Therefore, take slow deep breaths to reduce muscular tension, lower the heart rate, and calm the mind. Whenever you feel stressed, breathe slowly, focusing on each in- and out-breath. Through this simple act, your parasympathetic nervous system kicks in and can help you calm down. Additionally, certain exercises like yoga and tai chi emphasize deep breathing and a focused mind.

Research has also found that meditation training may lengthen or prevent the shortening of protein structures called telomeres. Meditation practice has been associated in some studies with greater telomere activity and length in response to a reduction in anxiety, chronic stress, and cortisol levels.

Mental health counseling or other social support. Feeling alone can add to stress. It can help to talk through feelings and concerns with a trusted individual. Often, just realizing that you are not alone and that your feelings are not unusual can help lower stress.

Practicing work-life balance. Use vacation and personal time, or just set aside an hour a day. A periodic escape from the pressures of work can do wonders to reduce stress, increase productivity, and decrease the risk of physical and mental illnesses that are associated with workplace burnout.

Schedule fun activities or hobbies at least once a week. Gardening, reading, enjoying music, getting a massage, hiking in nature, and cooking a favorite recipe are examples of welcome stress relievers. Good sleep hygiene.

Stress can cause a heightened sense of alertness, which delays the onset of sleep as well as cause interrupted sleep throughout the night.

This can prevent one from entering the deeper sleep stages in which the body repairs and grows tissue and supports a healthy immune system.

The REM rapid eye movement sleep stage in particular helps with mood regulation and memory. Aim for hours of sleep a night by slowing down about 30 minutes before bedtime. Controlling stress through the other tips listed above can also improve sleep quality.

References Waxenbaum JA, Reddy V, Varacallo M. Anatomy, Autonomic Nervous System. In: StatPearls [Internet]. Treasure Island FL : StatPearls Publishing; Jan. Diet and stress.

Carbohydrates, protein, fat, vitamins and minerals are all important for energy, mental concentration, and emotional stability. A balanced diet will help you stay focused, alert, energetic, and healthy during times of stress.

However, if you live off of fast food or frequently skip meals, you are more likely to perform poorly or get sick during stressful times. Whole foods contain many substances, such as phytochemicals and fiber, which boost the immune system and maintain health.

Any discussion about eating and stress must include caffeine and sugar. Many people use high sugar foods to keep their energy up and caffeine to keep going when they need rest. Too much caffeine will contribute to poor quality sleep and add to the negative effects of stress on the body.

Sugar will satisfy you in the short term, leaves you with less energy and more hungry after an hour or two. Whole foods will provide you with energy that will last for several hours.

This results in an increase in the expression of TNF- α , a proinflammatory cytokine; monocyte chemotactic protein-1, a key chemokine; and intercellular adhesion molecule-1 ICAM Glucose administration to nondiabetic subjects also induces other acute inflammatory changes at the cellular and molecular levels for at least 3 hours 9 , 11 , with more intense and prolonged effects in individuals with obesity with impaired glucose tolerance Other proinflammatory transcription factors, such as activator protein-1 and intranuclear early growth response gene-1, are activated by the intake of glucose, resulting in an increased expression of matrix metalloproteinases 2 and 9 MMP-2 and MMP-9 , plasminogen activator inhibitor-1, and tissue factor This clearly demonstrates the induction of a prothrombotic state, in addition to the oxidative and inflammatory stress seen following the intake of glucose.

Cream saturated fat intake increases ROS generation, p47 phox expression, and plasma concentration of thiobarbituric acid-reactive species, which is an index of lipid peroxidation.

In addition, cream induces an increase in intranuclear NF- κ B binding, a decrease in I κ B α , and an increase in the expression of proinflammatory cytokines. Plasma concentrations of IL and IL increased, and cream ingestion induced an increase in intracellular lipid content in mononuclear cells MNCs 6 , In addition, cream intake results in an increase in the expression of CD68 and platelet-endothelial cell adhesion molecule PECAM in MNCs Fig.

Schematic representation of the effect of a high-fat high-calorie meal and cream intake on inflammation, insulin resistance, and atherosclerosis. It is noteworthy that the ingestion of cream induces the profound effects shown in this figure, laying the foundations of oxidative stress, inflammation, insulin resistance, and atherogenesis.

This calorie HFHC meal increases p47 phox expression and ROS generation The transcription factor NF- κ B is activated via the induction of I κ B kinase IKK and the phosphorylation of I κ B α Elevated levels of TNF- α , IL-1 β , plasma endotoxin, and Toll-like receptor TLR -4 expression and its coreceptor CD were induced.

Suppressor of cytokine signaling 3 SOCS-3 and IKK β , which with TNF- α , interfere with insulin signal transduction at the insulin receptor substrate 1 IRS-1 level, are induced after the intake of these meals 6 , TNF- α plays a key role in insulin resistance via the suppression of the autophosphorylation of the tyrosine residue of the insulin receptor and the suppression of IRS-1 phosphorylation, thus, resulting in the inhibition of insulin-stimulated glucose uptake IL-1 β is a key cytokine mediating damage to the β -cell, whereas SOCS-3 causes ubiquitylation and proteolysis of IRS-1 The habitual consumption of these meals results in caloric overload, obesity, and insulin resistance.

SOCS-3 also interferes with leptin signaling, which could result in lack of satiety and potentiate an increase in caloric intake Progressive weight gain occurs with insulin resistance, predisposing to hypertension, hypertriglyceridemia, the metabolic syndrome, and a host of systemic complications.

Increased malondialdehyde levels an index of lipid peroxidation and oxidative stress are also seen after the ingestion of HFHC meals The supraphysiologic postprandial glycemia and lipidemia that occur following the ingestion of these meals potentiate inflammatory and oxidative stress, and these are indicators of future cardiovascular events Elevated plasma concentrations of inflammatory mediators significantly increase the risk of atherosclerotic complications.

In contrast to the proinflammatory effects of HFHC meals, the intake of equicaloric meals rich in fruit and fiber do not induce an increase in ROS generation or inflammation at the cellular and molecular level 7 , 14 , Similar to our findings on macronutrient-induced inflammation, Nappo et al.

However, the study by Nappo et al. Whereas adequate production of insulin may partly account for this observation, a closer scrutiny of the carbohydrate meal ingested by these subjects revealed 4. It is quite possible then that the anti-inflammatory effect of fiber coupled with the polyphenols and antioxidants in tomatoes may have attenuated the inflammatory effect of the carbohydrate meal in the healthy subjects.

In accordance with this observation is the study by Esposito et al. It is also worth mentioning that in the study by van Oostrom et al. In fact, the polyunsaturated fatty acid PUFA linoleate was observed to inhibit the palmitate-induced IL-6 production.

Thus, as expounded above, HFHC meals are important in the pathogenesis of the proinflammatory states of insulin resistance, obesity, and type 2 diabetes. On the contrary, fiber-rich meals exert anti-inflammatory effects that can significantly suppress the inflammation caused by HFHC meals when these meals are compared HFHC intake predisposes to visceral adiposity and intrahepatic fat accumulation, creating the milieu for inflammation, which leads to insulin resistance.

In addition, central adiposity increases with advancing age, and the importance of a healthy diet with the appropriate macronutrient composition, caloric restriction, and increased physical activity cannot be overemphasized Central adiposity is closely associated with metabolic syndrome, insulin resistance, type 2 diabetes, hypogonadotropic hypogonadism, and cardiovascular diseases The proinflammatory effects of macronutrients, such as HFHC meals, are more prolonged and more intense in individuals with obesity 30 , consistent with the previously established fact that the state of obesity is proinflammatory Furthermore, the redox environment of the muscle is highly sensitive to macronutrients, and it shifts to a more oxidized redox state in response to high-caloric food ingestion.

The overall cellular redox environment is modulated by the rate of mitochondrial emission of H 2 O 2 a gauge of mitochondrial function. Mitochondrial H 2 O 2 emission has been demonstrated to be acutely increased in lean subjects following a fatty meal, with substantial reductions in the ratio of reduced glutathione GSH to oxidized GSH disulfide GSSG The shift to a more oxidized redox state results in the activation of transcription factors, such as NF- κ B, which induce TNF- α with consequent interference with the insulin signal transduction at the level of IRS The expression of SOCS-3 is also increased, consistent with the induction of this gene, following the intake of a high-fat meal The binding of I κ B α to NF- κ B is normally required for the prevention of the nuclear translocation of NF- κ B.

Oxidative stress increases phosphorylation of I κ B α , leading to the dissociation of I κ B α from NF- κ B. This results in the translocation of NF- κ B into the nucleus, activating the transcription of proinflammatory genes, including TNF- α Elevated levels of TNF- α concentrations are seen in subjects with obesity 35 , and the concentrations of TNF- α in the sera and adipose tissue of subjects with obesity fall with weight loss 36 , In addition, elevations in the plasma concentrations of products of lipid peroxidation thiobarbituric acid-reactive species and 9- and hydroxyoctadecadienoic acid and protein carbonylation ortho- and meta-tyrosine are seen in those with obesity in the fasting state.

Dietary restriction leads to a reduction in their levels 30 , Increased mitochondrial biogenesis and fatty acid oxidation are initially seen in skeletal muscles following acute ingestion of HFHC foods.

Excess fat builds up in muscle tissue as intramyocellular lipid metabolites when fatty acid supply exceeds metabolic demand. The intramyocellular lipid metabolites activate protein kinase C The activation of protein kinase C subsequently results in impaired insulin signaling and decreased insulin sensitivity 40 , Reduced overall sensitivity of the body to insulin and decreased mitochondrial function in skeletal muscle are well documented in obesity and aging The state of insulin resistance further potentiates the inflammation seen in obesity and type 2 diabetes secondary to the reduced anti-inflammatory effect of insulin in these conditions.

Insulin exerts anti-inflammatory and vasodilatory actions, and this has been demonstrated at the cellular and molecular levels 42 — The infusion of a low dose of insulin decreases ROS generation by MNC.

I κ B α expression is induced, and the suppression of p47 phox expression, intranuclear NF- κ B binding, TNF- α , and IL-1 β is seen. Insulin suppressed plasma ICAM-1, monocyte chemotactic protein-1, early growth response gene-1, MMP-9, tissue factor, and plasminogen activator inhibitor-1 levels 42 , The expression of the series of TLRs TLR-1, TLR-2, TLR-4, TLR-7, TLR-9 and PU.

Furthermore, endothelial nitric oxide NO synthase and the secretion of nitric oxide NO from the endothelium occur with insulin administration Insulin is, thus, a vasodilator at the arterial, microvascular, and venous levels 48 — This action of insulin is appropriate for the distribution and uptake of macronutrients postprandially at the tissue level.

The anti-inflammatory action of insulin is relevant to postprandial inflammation, as endotoxemia and TLR-4 induction are a part of HFHC-induced inflammatory changes.

The suppression of endotoxin-induced inflammation has also been demonstrated with insulin This involves the inhibition of ROS generation, lipid peroxidation, NO generation through inducible NO synthase, and macrophage migration inhibitory factor. In addition, insulin suppresses an endotoxin-induced increase in troponin I as well unpublished observation.

In obese and diabetic patients, insulin suppresses the expression and plasma concentrations of high-mobility group box-1, which functions as a proinflammatory cytokine when secreted by damaged cells through its binding to the advanced glycation end-product receptor 51 — Insulin also suppresses proinflammatory serine kinases, which interfere with insulin signaling via serine phosphorylation of IRS-1, and insulin decreases plasma free fatty acid concentration and lipolysis, thus, potentially increasing insulin sensitivity 52 , Insulin regulates the distribution, uptake, and storage of macronutrients postprandially and also modulates postprandial oxidative and inflammatory stress.

However, the magnitude of postprandial oxidative and inflammatory stress and endotoxemia, generated after the intake of HFHC meals, overwhelms the suppressive action of insulin Therefore, the prolonged, excessive consumption of the wrong choice of macronutrients would eventually result in insulin resistance.

The typical Western diet is rich in refined carbohydrates, saturated fat, and animal protein. Increased production of a highly atherogenic compound, trimethylamine- N -oxide, is seen with these diets rich in animal products, especially red meats 55 , Healthy dietary habits coupled with the partial substitution of starchy foods and red meats with foods high in plant protein and unsaturated fat are associated with positive cardiometabolic outcomes 57 , Strategies to deal with the rising prevalence of obesity and its attending complications would involve disciplined lifestyle interventions, such as the choice of appropriate foods Fig.

Inflammatory and noninflammatory foods 7 , 59 , Diets high in polyphenols and flavonoids abundant in several fruits, vegetables, and legumes are anti-inflammatory and thus, potentially anti-atherogenic 59 , 61 — Fresh orange juice consumption has been demonstrated to be noninflammatory on its own and to be anti-inflammatory when consumed with an HFHC meal.

In spite of its caloric content being entirely a result of glucose, fructose, and sucrose, orange juice is noninflammatory, largely because of its two major flavonoids: naringenin and hesperidin.

These flavonoids probably also contribute to the ability of orange juice to inhibit ROS generation, NF- κ B binding, proinflammatory cytokine expression, endotoxemia, and TLR-4 expression, induced by an HFHC meal Fig. A combination of resveratrol with muscadyne grape extracts has also been shown to inhibit oxidative and inflammatory stress induced by the HFHC meal.

This combination, in addition, prevented the fall in the antioxidant-enhancing transcription factor, Nrf-2, and suppressed the increase in its inhibitor, Keap-1, which is induced by HFHC meals. Nrf-2 acts through antioxidant response elements and modulates the expression of key antioxidant enzymes NQO-1, HO-1, and GSTP A fall in the expression of key antioxidant enzymes NQO-1, HO-1, and GSTP-1, observed after an HFHC meal, was also prevented by the combination of resveratrol and muscadyne grapes Most recently, the addition of fiber to the HFHC meal was comprehensively shown not only to prevent oxidative stress and inflammation but also to increase insulinogenesis after the meal and reduce the glycemic increase Dietary fiber also reduces endotoxemia and the induction of TLR-4 and TLR-2, the receptors for endotoxin and gram-positive bacterial products, respectively.

Fiber induces reductions in the expression of proinflammatory cytokines, such as TNF- α and IL-1 β , which significantly increase following an HFHC meal 7 , Whereas TNF- α interferes with insulin signaling, IL-1 β is toxic to the β -cell.

The induction of SOCS-3, the mediator of insulin resistance, was also prevented by the addition of fiber. Thus, energy-dense foods should be substituted with foods rich in fiber, such as fruits, vegetables, legumes, whole grains, etc.

The benefits of fiber-rich foods have been clearly demonstrated in relation to prevention of type 2 diabetes and atherosclerosis. There are additional secondary effects of fiber supplementation.

The fermentation of fiber generates short-chain fatty acids SCFAs , such as acetate, butyrate, and propionate, which have immense beneficial effects on inflammation-mediated processes and metabolic risk factors Fig.

The SCFAs activate free fatty acid receptors FFARs , which are mainly expressed in intestinal L cells. Acetate and propionate primarily activate FFAR2, whereas FFAR3 is more often activated by propionate and butyrate The release of glucagon-like peptide 1 GLP-1 and peptide YY PYY is stimulated by FFAR2 and FFAR3, and this leads to improved insulin secretion.

GLP-1 and PYY expression is decreased in diet-related conditions, such as type 2 diabetes A study demonstrated the effects of targeted delivery of propionate to the colon via the daily administration of 10 g inulin-propionate ester which results in a 2.

A substantial release of gut PYY and GLP-1 from human colonic cells was seen with propionate administration. Acute ingestion of 10 g inulin-propionate ester increased postprandial plasma concentrations of PYY and GLP-1 significantly. Long-term administration of propionate over 24 weeks resulted in considerable reductions in intra-abdominal adipose tissue, intrahepatocellular lipid content, and weight gain.

It also prevented the deterioration in insulin sensitivity observed in the inulin-control group. Some of the metabolic benefits derived from SCFAs are also a result of their role in the control of energy homeostasis.

Butyrate and propionate activate intestinal gluconeogenesis gene expression, thus regulating energy homeostasis. The activation of FFAR3 by the SCFAs, such as propionate, also promotes sympathetic activity, and this enhances energy expenditure Schematic representation of some of the effects of dietary fiber, Western diet, and bariatric surgery on oxidative and inflammatory stress.

GLP1, glucagon-like peptide 1; PPAR γ, peroxisome proliferator-activated receptor γ; PYY, peptide YY. TMAO, trimethylamine- N -oxide.

A diet high in n -6 PUFAs, which is found in abundance in plant oils, seeds, and nuts, has also been shown to decrease abdominal fat, intrahepatic fat accumulation, and peripheral insulin resistance, decreasing cardiometabolic risk factors when compared with a diet high in saturated fatty acids 58 Table 1.

A Summary of the Cardiometabolic Outcomes of Different Dietary Interventions. Abbreviations: HDL-C, high-density lipoprotein cholesterol; HOMA-IR, homeostatic model assessment for insulin resistance. Caloric restriction is crucial to sustain an ideal weight, as prolonged overconsumption of food stored as excess fat can result in obesity Furthermore, adults progressively gain weight through middle age 67 ; hence, caloric restriction is essential to maintain energy balance to compensate for this effect.

The decrease of total energy intake by avoidance of energy-dense foods from highly refined carbohydrates and fatty meals from fast foods, a reduction in total alcohol intake, and an increase in water intake has been shown to help in weight maintenance Calorie-restricted diets help achieve weight loss, with improvements seen in inflammatory and oxidative stress, insulin sensitivity, glucose and lipid metabolism, blood pressure, and cardiac function 28 , 38 , 75 Table 1.

A reversal of these effects occurred following cessation of caloric restriction, with ROS generation noted to exceed the initial baseline value before commencement of the dietary restriction. A similar observation was noted in normal subjects following restriction of macronutrient intake, which was achieved by a and hour fast.

Clearly, therefore, macronutrient intake is a major modulator of oxidative stress and inflammation. Interestingly, evolving evidence suggests that Sirtuin 1 SIRT1 , a mammalian nicotinamide adenine dinucleotide dependent deacetylase enzyme, is required for some of the key metabolic alterations seen with caloric restrictions.

Increments in cellular and tissue expression of SIRT1 in mice studies following dietary restriction have been documented, with SIRT1 protecting against high-fat diet-induced inflammation and obesity Activation of SIRT1 in some mammals is shown to substantially increase mitochondrial biogenesis in skeletal muscle and brown adipose tissue with a resultant increase in energy expenditure and protection against diet-induced weight gain This is consistent with the observation that decreased SIRT1 transcription is seen in the visceral adipose tissue of morbidly patients with obesity who have severe hepatic steatosis It is also of interest that compounds, such as resveratrol, have been shown to activate SIRT1 in mice 79 , protecting against diet-induced metabolic disorders.

However, pivotal human studies are needed in this growing field. Bariatric surgery has numerous cardiometabolic benefits. Clinically apparent resolution of insulin resistance and type 2 diabetes is seen following procedures, such as Roux-en-Y gastric bypass, even before substantial weight loss occurs.

This is partly attributable to the marked reductions in caloric intake 81 , coupled with the reductions in mediators of oxidative and inflammatory stress.

Thus, there is a reduction in ROS generation, proinflammatory cytokines, endotoxemia, and the expression of TLR-4 and SOCS-3 These changes contribute to improved insulin signalin and thus, a reduction in insulin resistance.

An interesting contribution from the data obtained from bariatric surgery is the reversal of complications related to morbid obesity and the underlying mechanisms. A recent study has also shown that the expression of genes and factors related to bronchial asthma is increased in the morbidly obese and that following bariatric surgery and weight loss, there is a reduction in asthma-related factors and genes This is consistent with the clinical observation that there is an increase in the prevalence of asthma in such patients and that following weight loss, there is a substantial reduction in respiratory symptoms.

Most recently, it has also been shown that bariatric surgery leads to a decrease in vasoconstrictors and an increase in vasodilators, thus contributing to a fall in blood pressure. Bariatric surgery also leads to a fall in neprilysin, which increases the risk of congestive heart failure in these patients Whereas a single meal may not induce changes in these genes, it is possible that persistent intake of HFHC meals may lead to an increased expression of these genes, in addition to the proinflammatory genes known to increase following such meals.

The restructuring of the gut following bariatric surgery also leads to changes in gut microbiota, with a resultant increase in the microbial production of the SCFAs Fig.

This may also contribute to reduced adiposity, weight loss, increased insulin sensitivity, and several other beneficial cardiometabolic effects Macronutrient intake has important implications for health.

A fast food-based Western diet is clearly associated with oxidative and inflammatory stress. These lead to insulin resistance and obesity, with increased atherogenicity and cardiovascular risk factors.

These risks can be avoided by the restriction of caloric intake and the choice of an appropriate diet, including fiber-rich meals, such as fresh fruits and vegetables. Disclosure Summary: P.

has received research support from National Institutes of Health, Juvenile Diabetes Research Foundation, American Diabetes Association, Novo Nordisk, Bristol Meyer Squibb, AbbVie Pharmaceuticals, Astra Zeneca, and Boehringer Ingelheim Pharmaceuticals.

has received honoraria from Eli Lilly, Novartis, GlaxoSmithKline, Merck, Novo Nordisk, Takeda, and Sanofi-Adventis. The remaining authors have nothing to disclose. Data Availability: All data generated or analyzed during this study are included in this published article or in the data repositories listed in References.

A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, — a systematic analysis for the Global Burden of Disease Study [published corrections appear in Lancet. Google Scholar. Holt SH , Miller JC , Petocz P , Farmakalidis E.

A satiety index of common foods. Eur J Clin Nutr. Bellissimo N , Akhavan T. Effect of macronutrient composition on short-term food intake and weight loss. Having a fried chicken breakfast sandwich, but you should try to have it once maybe twice a week, rather than for every breakfast.

Even "healthy" foods in large quantities can be unhealthy. For example, "Green Smoothies" contain large amounts of oxalates that can cause build-up and lead to kidney stones when consumed in large quantities.

Additionally, it is crucial to notice that common misconception states that eating in moderation means eating less. This IS NOT what this means. Eating "everything in moderation" means that you can have a little bit of anything, even "unhealthy" foods, but while making sure you are meeting all nutritional goals necessary for your body to stay healthy 5.

Please remember not to eat less than you need, but to make sure you are not overeating any food. Macronutrients Marcos are the three nutrients that make up much of the human diet. They are Carbohydrates, Fats, and Proteins. Despite what many people say, we need all these nutrients to support a healthy life!

These macronutrients are made up of micronutrients vitamins, minerals, etc. that our bodies need to function at their highest level. Many people track their eating habits by maintaining a balance between these macros 6. Looking at your food intake this way might help you find a balance of nutrients that can help you feel like your best self.

These ratios help many people maintain moderation and meet their necessary micronutrients in a day. Remember, everyone's body performs better with different proportions of macros, so reach out to the nutritionist at Texas Tech to learn more!

One last note on macros: it's essential to know that not all macros are created equal! An example of this would be salmon and fried chicken wings. This is because different micronutrients make up the macros that are protein in fat. For example, there are saturated fats and unsaturated fats, unsaturated being healthier because your body can break them down easier.

However, in moderation, chicken wings might be just what your body wants on a given day. You know yourself the best! We provided you with a basic understanding of what nutrients offer benefit to your body to help you begin your healthy eating journey.

RISE wants all students to live the happiest, healthiest lives possible here at Texas Tech and beyond, so hopefully these tips can help you do just that!

Many people use high sugar foods to keep their energy up and caffeine to keep going when they need rest. Too much caffeine will contribute to poor quality sleep and add to the negative effects of stress on the body.

Sugar will satisfy you in the short term, leaves you with less energy and more hungry after an hour or two. Whole foods will provide you with energy that will last for several hours. UHC Home About Toggle child menu Expand. Well-Being Resources Toggle child menu Expand.