What would be considered a healthy amount of calories per meal?


Around 2,200 calories a day is enough unless you are an athletic girl.

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Food energy is energy that animals (including human beings) derive from their food, through the process of cellular respiration, the process of joining oxygen with the molecules of food (aerobic respiration) or of reorganizing the atoms within the molecules for anaerobic respiration. Animals need a minimum intake of food energy in order to sustain their metabolism and drive their muscles. For humans, food energy typically comes from joining oxygen with carbohydrates, fats, proteins, organic acids, polyols, and ethanol present in the diet. Some diet components that provide little or no food energy, such as water, minerals, vitamins and fiber, may still be necessary to health and survival for other reasons. Ruminants are able to extract food energy from the respiration of cellulose thanks to bacteria in their rumens. In the International System of Units, energy is measured in joules (J) or its multiples; the kilojoule (kJ) is most often used for food-related quantities. An older metric system unit of energy, still widely used in food-related contexts, is the calorie; more precisely, the "food calorie", "large calorie" or kilocalorie (kcal or Cal), equal to 4.184 kilojoules. (It should not be confused with the "small calorie" (cal) that is often used in chemistry and physics, equal to 1/1000 of a food calorie.) Within the European Union, both the kilocalorie ("kcal") and kilojoule ("kJ") appear on nutrition labels. In many countries, only one of the units is displayed; in the US and Canada the unit is spelled out as "calorie" or "Calorie". Fats and ethanol have the greatest amount of food energy per mass, 38 and 30 kJ/g (9 and 7 kcal/g), respectively. Proteins and most carbohydrates have about 17 kJ/g (4 kcal/g). Carbohydrates that are not easily absorbed, such as fiber or lactose in lactose-intolerant individuals, contribute less food energy. Polyols (including sugar alcohols) and organic acids have less than 17 kJ/g (4 kcal/g). Theoretically, food energy could be measured in different ways, such as Gibbs free energy of combustion, or the amount of ATP generated by metabolizing the food. But the convention is to use the heat of the oxidation reaction, with the water substance produced being in the liquid phase. Conventional food energy is based on heats of combustion in a bomb calorimeter and corrections that take into consideration the efficiency of digestion and absorption and the production of urea and other substances in the urine. These were worked out in the late 19th century by the American chemist Wilbur Atwater. See Atwater system for more detail. Each food item has a specific metabolizable energy intake (MEI). This value can be approximated by multiplying the total amount of energy associated with a food item by 85%, which is the typical amount of energy actually obtained by a human after respiration has been completed.][ In animal nutrition where energy is a critical element of the economics of meat production, a specific metabolizable energy may be determined for each component (protein, fat, etc.) of each ingredient of the feed. Many governments require food manufacturers to label the energy content of their products, to help consumers control their energy intake. In the European Union, manufacturers of packaged food must label the nutritional energy of their products in both kilocalories and kilojoules, when required. In the United States, the equivalent mandatory labels display only "Calories", often as a substitute for the name of the quantity being measured, food energy; an additional kilojoules figure is optional and is rarely used. The energy available from the respiration of food is usually given on labels for 100 g, for a typical serving size (according to the manufacturer), and/or for the entire pack contents.][ A paper published in 2011 by the American Journal of Public Health proposed to also display the time needed to burn the food energy contained in the product by running.] [ This would indicate how much exercise would be necessary if the food would bring the person's energy intake above what is necessary for that day. The amount of food energy associated with a particular food could be measured by completely burning the dried food in a bomb calorimeter, a method known as direct calorimetry. However, the values given on food labels are not determined in this way. The reason for this is that direct calorimetry also burns the indigestible dietary fiber, and so does not allow for fecal losses (i.e. the fact that not all food eaten is actually absorbed by the body); thus direct calorimetry would give systematic overestimates of the amount of fuel that actually enters the blood through digestion. What are used instead are standardized chemical tests or an analysis of the recipe using reference tables for common ingredients to estimate the product's digestible constituents (protein, carbohydrate, fat, etc.). These results are then converted into an equivalent energy value based on the following standardized table of energy densities. However 'Energy Density' is a misleading term for it once again assumes that energy is IN the particular food, whereas it simply means that that 'high density' food needs more oxygen during respiration, leading to greater transfer of energy. All the other nutrients in food are noncaloric and are thus not counted. Recommendations in the United States are 2,700 and 2,100 kcal (11,000 and 8,800 kJ) for men and women (respectively) between 31 and 50, at a physical activity level equivalent to walking about 1.5 to 3 miles per day at 3 to 4 miles per hour on top of the light physical activity associated with typical day-to-day life, with French guidance suggesting roughly the same levels. Children, those with sedentary lifestyles, and older people require less energy; physically active people more. In Australia, because different people require different daily energy intakes there is no single recommended intake. Instead there is a series of recommendations for each age and gender group, although packaged food and fast food outlet menu labels refer to the average Australian daily energy intake of 8700 kJ (2079 kcal). According to the Food and Agriculture Organization of the United Nations, the average minimum energy requirement per person per day is about 1,800 kcal (7,500 kJ). Increased mental activity has been linked with moderately increased brain energy consumption. The human body uses the energy released by respiration for a wide range of purposes: about 20% of the energy is used for brain metabolism, and much of the rest is used for the basal metabolic requirements of other organs and tissues. In cold environments, metabolism may increase simply to produce heat to maintain body temperature. Among the diverse uses for energy, one is the production of mechanical energy by skeletal muscle to maintain posture and produce motion. The conversion efficiency of energy from respiration into mechanical (physical) power depends on the type of food and on the type of physical energy usage (e.g. which muscles are used, whether the muscle is used aerobically or anaerobically). In general, the efficiency of muscles is rather low: only 18 to 26% of the energy available from respiration is converted into mechanical energy. This low efficiency is the result of about 40% efficiency of generating ATP from the respiration of food, losses in converting energy from ATP into mechanical work inside the muscle, and mechanical losses inside the body. The latter two losses are dependent on the type of exercise and the type of muscle fibers being used (fast-twitch or slow-twitch). However, alterations in the structure of the material consumed can cause modifications in the amount of energy that can be derived from the food; i.e. caloric value depends on the surface area and volume of a food. For an overall efficiency of 20%, one watt of mechanical power is equivalent to 4.3 kcal (18 kJ) per hour. For example, a manufacturer of rowing equipment shows calories released from 'burning' food as four times the actual mechanical work, plus 300 kcal (1,300 kJ) per hour, which amounts to about 20% efficiency at 250 watts of mechanical output. It can take up to 20 hours of little physical output (e.g. walking) to "burn off" 4,000 kcal (17,000 kJ) more than a body would otherwise consume. For reference, each pound of body fat equates to approximately 3,500 calories. The differing energy density of foods (fat, alcohols, carbohydrates and proteins) lies mainly in their varying proportions of carbon, hydrogen, and oxygen atoms. This then determines the volume of oxygen needed for (aerobic) respiration, approximately 300 kj per mole of molecular oxygen that reacts. In addition, the quality of calories matters because the energy absorption rate of different foods with equal amounts of calories may vary. Some nutrients have regulatory roles effected by cell signaling, in addition to providing energy for the body. For example, leucine plays an important role in the regulation of protein metabolism and suppresses an individual's appetite. Saturated fats promote fat synthesis in the human body, while PUFAs (poly unsaturated fatty acids) inhibit fat synthesis and promote fat oxidation. Swings in body temperature – either hotter or cooler – increase the metabolic rate, thus burning more energy. Prolonged exposure to extremely warm or very cold environments increases the basal metabolic rate (BMR). People who live in these types of settings often have BMRs 5–20% higher than those in other climates. Physical activity also significantly increases body temperature, which in turn uses more energy from respiration. Glycolysis ⇄ Gluconeogenesis Glycogenolysis ⇄ Glycogenesis Pentose phosphate pathway  Fructolysis  Galactolysis Photosynthesis  Anoxygenic photosynthesis  Chemosynthesis  Carbon fixation
M: MET mt, k, c/g/r/p/y/i, f/h/s/l/o/e, a/u, n, m k, cgrp/y/i, f/h/s/l/o/e, au, n, m, epon m (A16/C10), i (k, c/g/r/p/y/i, f/h/s/o/e, a/u, n, m) M: MET mt, k, c/g/r/p/y/i, f/h/s/l/o/e, a/u, n, m k, cgrp/y/i, f/h/s/l/o/e, au, n, m, epon m (A16/C10), i (k, c/g/r/p/y/i, f/h/s/o/e, a/u, n, m) M: MET mt, k, c/g/r/p/y/i, f/h/s/l/o/e, a/u, n, m k, cgrp/y/i, f/h/s/l/o/e, au, n, m, epon m (A16/C10), i (k, c/g/r/p/y/i, f/h/s/o/e, a/u, n, m)
Negative calorie illusion
The CRON-diet (Calorie Restriction with Optimal Nutrition) is a nutrient-rich, very low calorie diet developed by Roy Walford, Lisa Walford, and Brian M. Delaney. The CRON-diet involves calorie restriction in the hope that the practice will improve health and retard aging, while still attempting to provide the recommended daily amounts of various nutrients. Other names include CR-diet, Longevity diet, and Anti-Aging Plan. Several people, including the Walfords and Delaney, founded the CR Society International to promote the CRON-diet. The CRON-diet was developed from data Walford compiled during his participation in Biosphere 2, and from Walford's decades of animal testing. Proponents of the CRON-diet believe that everyone has what they call a "set-point": a weight, specific to an individual, at which each naturally stays when they eat their usual daily diet. Proponents believe that the set-point is determined through heredity and childhood eating habits. Proponents recommend that adherents remain 10–25% under their set-point, suggesting that this is necessary for the diet to be maximally effective. A guideline that proponents use to determine an individual's set-point is to measure that person's body fat content. Proponents state that this should be 10–15% for females and 6–10% for males. Proponents suggest the use of skinfold test tools (they specifically recommend the "Fat-O-Meter"), certain digital scales, densiometry, and/or bioelectrical impedance analysis to determine the body fat content. Proponents then use the current weight and body fat content to determine the goal weight (below the set point), and plan and follow a preliminary diet until the goal weight is reached. Next, the proponent determines the level of caloric restriction they wish to implement in their regular eating pattern. Proponents recommend a goal of restricting intake by 20%. The actual daily amount eaten depends on the adherent's basal metabolic rate (BMR), although Walford has stated that he doubts the verifiability of BMR calculation tools. A common daily intake is 1800 calories per day. The Walfords propose three meals in their book, but variation is possible. Adherents can vary the number of meals they eat per day in order to fit their schedules: typically, this is achieved by combining calorie-dense and calorie-lean foods in different ways. Proponents also use "supplements", which refers to vitamin pills as well as certain high-nutrition foods (which are necessarily calorie-lean). The Walfords describe these foods as "nutrient super-chargers"; examples include kombu, brewers yeast, wheat bran, wheat germ, shiitake mushrooms, non-fat dry milk, soybeans, and tofu. These "nutrient super-chargers" are used frequently to boost meals' nutritional density. The Walfords propose that adherents eat three meals per day. They suggest that adherents cook eight meals on a specific day of the week, and then freeze these meals to use during the entire week. They refer to this process as the "Quantity-Cook-and Freeze Option", and the meals themselves as "One-a-day MegaMeals". They suggest that adherents use two "Free-Choice Recipes" for the other two courses per day. Adherents may compose their own meals. The Walfords caution that such meals must be planned exactly and contain all the required RDA nutrients. There are computer tools available to plan meals, including the official Dr. Walfords Interactive Diet Planner and the unofficial CRON-o-Meter. Books on the CRON-diet include:
Caloric restriction (CR), or calorie restriction, is a dietary regimen that is based on low calorie intake. "Low" can be defined relative to the subject's previous intake before intentionally restricting calories, or relative to an average person of similar body type. CR without malnutrition has been shown to work in a variety of species, among them yeast, fish, rodents and dogs to decelerate the biological aging process, resulting in longer maintenance of youthful health and an increase in both median and maximum lifespan. No clinical trial has been performed involving humans. Two trials have been performed involving primates, but have not demonstrated increases in median lifespan. A study of rhesus monkeys begun in 1987 by the National Institute on Aging published results in August 2012 that found evidence of health benefits, but did not demonstrate increased median lifespan. A study by the University of Wisconsin beginning in 1989 is still ongoing. Research on maximum life span in that study is still ongoing. Calorie restriction is a feature of several dietary regimens, including the Okinawa diet and the CRON-diet. Sometimes calorie restriction is called calorie restriction with adequate nutrition (or CRAN) to clarify that this is done while still keeping healthy levels of protein, vitamins and minerals while lowering calories. In 1934, Mary Crowell and Clive McCay of Cornell University observed that laboratory rats fed a severely reduced calorie diet while maintaining micronutrient levels resulted in life spans of up to twice as long as otherwise expected. These findings were explored in detail by a series of experiments with mice conducted by Roy Walford and his student Richard Weindruch. In 1986, Weindruch reported that restricting the calorie intake of laboratory mice proportionally increased their life span compared to a group of mice with a normal diet. The calorie-restricted mice also maintained youthful appearances and activity levels longer and showed delays in age-related diseases. The results of the many experiments by Walford and Weindruch were summarized in their book The Retardation of Aging and Disease by Dietary Restriction (1988) (ISBN 0-398-05496-7). The findings have since been accepted and generalized to a range of other animals. Researchers are investigating the possibility of parallel physiological links in humans. In the meantime, many people have independently adopted the practice of calorie restriction in some form. In 1989, scientists at University of Wisconsin started a study of 20 adult male rhesus monkeys; 9 of them were put on a normal diet and 11 were subjected to a 30% reduction in dietary intake. Results are being periodically published. A study at UCSF called "CRONA" was started in December 2010, and studied 28 long-term CR practitioners over a few months. The study was completed on September 20, 2011. As of August 2012 the results had not yet been published. Some research has shown CR to reduce atherosclerosis risk factors. A small study of long-term CR practitioners studied the effects of a diet with 10–25% less calorie intake than the average "Western" diet. Mean Body mass index (BMI) was 19.6 in the CR group; the matched group's mean BMI was 25.9, comparable to the BMI for middle-aged people in the US. The mean BMI in the CR group dropped from 24 (range of 19.4 to 29.6) to 19.5 (range of 16.5 to 22.8) over periods of 3–15 years. Nearly all the decrease in both BMI and cardiovascular risk factors occurred in the first year. Adjusting for age, the average total cholesterol and LDL (bad) cholesterol levels in the CR group were below those seen in all but the lowest 10% of the population. The average HDL (good) cholesterol levels were in the 85th to 90th percentile range for normal middle-aged US men. The CR group had triglyceride levels as low as the lowest 5% of Americans in their 20s. (The CR group's age range was 35–82.) Systolic and diastolic blood pressure levels in the CR group were about 100/60, a level more typical of 10-year-olds.][ Fasting plasma insulin concentration was 65% lower. Fasting plasma glucose concentration was also lower. The principal investigator in this study noted an apparent lower rate of cardiovascular aging, with arteriosclerosis progress indicators particularly slowed. The comparison group's statistics aligned approximately with the US national average on the dimensions considered. Fasting plasma insulin levels and fasting plasma glucose levels are used as tests to predict diabetes. The American CALERIE study began in 2007 and investigates the effects of a 25% reduction in caloric intake on healthy adults over a period of two years. The effect of CR on IGF-1 serum levels seen in rodents appears to only manifest in humans when protein intake is not much higher than the Recommended Dietary Allowance. A 2009 research paper compared results of a group of normal to overweight elderly people who were given no intervention, who were given fish oil, or who were placed on a CR diet: the CR subjects "were instructed to reduce caloric intake aiming at a 30% reduction relative to previous habits, over a period of 3 months". Memory tests were done at baseline and three months after the study started (in other words, just when they had actually reduced their intake to 30% of baseline). The study found that the CR group lost the most weight; this group also had an improvement in memory. The study did not show whether the memory improvement was due to weight loss or specifically due to the CR intervention. Reacting to this study, a spokesman for the British Dietetic Association said that people, particularly for those already at normal or low weight, should be "extremely careful" about attempting such a diet. She said, "There is other evidence that, far from enhancing memory, dieting or removing meals can interfere with memory and brain function." Another study found that while people who were underweight or of normal weight from midlife onward were at reduced risk of dementia, for people older than 65, those who were underweight had a higher dementia risk than normal or overweight people. Such findings are often interpreted as evidence of "reverse causation," with disease leading to weight loss late in life rather than low weight leading to disease. The long-term effects of CR on humans are still unknown. Short-term studies in humans report loss of muscle mass and strength and reduced bone mineral density. This is to be expected as part of the weight loss that accompanies CR. Beyond using lean tissue as an energy source, the presence of catabolic hormones, such as cortisol, and the lack of anabolic ones, such as insulin, disrupts protein synthesis, amino acid uptake, and immune response. People who lose weight as a result of CR but who are sedentary have a reduced capacity to perform exercise compared with those who lost similar amounts of weight from exercise alone, emphasizing the need for strength training in CR practitioners. A study of long-term CR practitioners "who had been eating a CR diet (approximately 35% less calories than controls) for an average of 6.8 ± 5.2 years (mean age 52.7 ± 10.3 years)" found that they had reduced bone mineral density at the level of hip and spine, in accordance with a previous one-year weight-loss trial, but that after initial weight loss they had achieved a stable, normal level of bone turnover and that the microarchitectural structure of their bones was healthy; the researchers concluded that "These findings suggest that markedly reduced BMD is not associated with significantly reduced bone quality in middle-aged men and women practicing long-term calorie restriction with adequate nutrition." Some specialists say that minor mineral losses can be minimized with regular physical activity and vitamin D and calcium supplements. The authors of a 2007 review of the CR literature warned that "[i]t is possible that even moderate calorie restriction may be harmful in specific patient populations, such as lean persons who have minimal amounts of body fat." CR diets typically lead to reduced body weight, and in some studies, low body weight has been associated with increased mortality, particularly in late middle-aged or elderly subjects. One of the more famous of such studies linked a body mass index (BMI) lower than 18 in women with increased mortality from noncancer, non−cardiovascular disease causes. The authors attempted to adjust for confounding factors (cigarette smoking, failure to exclude pre-existing disease); others argued that the adjustments were inadequate. While low body weight in the elderly can be caused by conditions associated with aging (such as cancer, chronic obstructive pulmonary disorder, or depression) or of the cachexia (wasting syndrome) and sarcopenia (loss of muscle mass, structure, and function), the results of a large epidemiological study published in the fall of 2011 show that among the Japanese, an association between a BMI under 21 (under 65 kg for a 1.75 m tall individual (or in imperial units, under 140 lb for a 5'-9" tall individual)) and increased mortality persists even when confounders like age, smoking, and disease are carefully controlled for. Such epidemiological studies of body weight are not about CR as used in anti-aging studies; they are not about caloric intake to begin with, as body weight is influenced by many factors other than energy intake. Moreover, "the quality of the diets consumed by the low-BMI individuals are difficult to assess, and may lack nutrients important to longevity." Typical low-calorie diets rarely provide the high nutrient intakes that are a necessary feature of an anti-aging calorie restriction diet. As well, "The lower-weight individuals in the studies are not CR because their caloric intake reflects their individual ad libitum set-points, and not a reduction from that set-point." Concerns are sometimes raised that CR can make people feel hungry all the time and may lead to obsessing about food, causing eating disorders. However, a controlled study of human CR found no increase in eating disorder symptoms or other harmful psychological effects, in line with extensive earlier research. In those who already suffer from a binge-eating disorder, calorie restriction can precipitate an episode of binge eating, but it does not seem to pose any such risk otherwise. Long-term calorie restriction at a level sufficient for slowing the aging process is generally not recommended in children, adolescents, and young adults (under the age of approximately 21), because this type of diet may interfere with natural physical growth, as has been observed in laboratory animals. In addition, mental development and physical changes to the brain take place in late adolescence and early adulthood that could be negatively affected by severe calorie restriction. Pregnant women and women trying to become pregnant are advised not to practice calorie restriction, because low BMI may result in ovulatory dysfunction (infertility), and underweight mothers are more prone to preterm delivery. It has also been noted that people losing weight on such diets risk developing cold sensitivity, menstrual irregularities, and even infertility and hormonal changes. Moreover, calorie restriction has been reported in mice to hinder their ability to fight infection, and some evidence suggests that in patients with amyotrophic lateral sclerosis, calorie restriction accelerates the onset of the disease. Excessive calorie restriction may result in starvation. A study on rhesus macaques funded by the National Institute on Aging was started in 1989 at the University of Wisconsin–Madison and is still ongoing. Monkeys were enrolled in the study at ages of between 7 and 14 years. Preliminary results published in 2000 showed lower fasting insulin and glucose levels as well as higher insulin sensitivity and LDL profiles, associated with lower risk of atherogenesis in dietary-restricted animals. Results published in 2008 showed that CR attenuated age-related sarcopenia in these primates. Results published in 2009 showed that caloric restriction in rhesus monkeys blunts aging and significantly delays the onset of age-related disorders such as cancer, diabetes, cardiovascular disease, and brain atrophy. 80% of the calorie-restricted monkeys were still alive, compared to only half of the controls. Results to date have also found a trend toward a reduced overall death rate, which has not yet reached statistical significance. An additional analysis, restricted to causes of death related to aging, did find a significant reduction in age-related deaths. However, the interpretation of this finding is uncertain, as it is hypothetically possible that the exclusion of deaths due to non-aging causes may somehow mask an involvement of CR in such deaths, although the sample size is too low to say for certain. A study published in 2011 examined the effect of stress on various brain functions in these monkeys. In the control group, stress reactivity was associated with less volume and tissue density in areas important for emotional regulation and the endocrine axis, including prefrontal cortices, hippocampus, amygdala, and hypothalamus. CR reduced these relationships. In contrast to the conclusions reached by the University of Wisconsin–Madison (WNPRC) study, a 2012 National Institute on Aging (NIA) study published in the journal Nature, concluded that a calorie restriction regimen did not improve survival outcomes whether implemented in young or older age rhesus monkeys. A key difference between the WNPRC and the NIA studies is that the monkeys in the WNPRC study were fed a more unhealthy diet. In 2006, researchers at New York's Mount Sinai School of Medicine reported results comparing the brains of 3 monkeys fed a normal diet and 3 monkeys on a CR diet for their entire lives. The normal diet group "consisted of three male Squirrel monkeys (20–27 years old), who died from congestive heart failure, liver failure or complications of intestinal bleeding, respectively; the weight at the time of death of the CON group ranged 526–866 g. The CR group consisted of 3 male Squirrel monkeys (15–20 years old) on CR diet for 14 to 18 years, who died from inanition, complications of bleeding or by complications from liver necrosis, respectively; the weight at the time of death of CR group ranged 526–813." The squirrel monkeys on a lifelong calorie-restrictive diet were less likely to develop Alzheimer's-like changes in their brains. Seventy years ago, C. M. McCay et al. discovered that reducing the amount of calories fed to rodents nearly doubled their life spans. The life extension varied for each species, but on average there was a 30–40% increase in life span in both mice and rats. CR preserves a range of structural and functional parameters in aging rodents. For example, studies in female mice have shown that estrogen receptor-alpha declines in the aging pre-optic hypothalamus. The female mice that were given a calorically restricted diet during the majority of their lives maintained higher levels of ERα in the pre-optic hypothalamus than did their non–calorically restricted counterparts. Studies in female mice have shown that both the Supraoptic nucleus (SON) and Paraventricular nucleus (PVN) lose about one-third of IGF-1R immunoreactivity with normal aging. Old calorically restricted mice lose higher numbers of IGF-1R non-immunoreactive cells while maintaining similar counts of IGF-1R immunoreactive cells in comparison to Old-Al mice. Consequently, Old-CR mice show a higher percentage of IGF-1R immunoreactive cells, reflecting increased hypothalamic sensitivity to IGF-1, in comparison to normally aging mice. Fungi models are very easy to manipulate, and many crucial steps toward the understanding of aging have been made with them. Many studies were undertaken on budding yeast and fission yeast to analyze the cellular mechanisms behind increased longevity due to calorie restriction. First, calorie restriction is often called dietary restriction because the same effects on life span can be achieved by only changing the nutrient quality without changing the amount of calories. Data from Dr Guarente, Dr Kennedy, Dr Jazwinski, Dr Kaeberlein, Dr Longo, Dr Shadel, Dr Nyström, Dr Piper, and others showed that genetic manipulations in nutrient-signaling pathways could mimic the effects of dietary restriction. In some cases, dietary restriction requires mitochondrial respiration to increase longevity (chronological aging), and in some other cases not (replicative aging). Nutrient sensing in yeast controls stress defense, mitochondrial functions, Sir2, and others. These functions are all known to regulate aging. Genes involved in these mechanisms are TOR, PKA, SCH9, MSN2/4, RIM15, SIR2, etc. Research in 2003 by Mair et al. showed that dietary restriction extends the life of fruit flies of any age, with instantaneous effects on death rates. Two years later, the same group showed that calories do not explain the extension of life span by dietary restriction in the fruit fly. Recent work on Caenorhabditis elegans has shown that restriction of glucose metabolism extends life span by primarily increasing oxidative stress to exert an ultimately increased resistance against oxidative stress, a process called (mito)hormesis. Laboratory rodents placed on a CR diet tend to exhibit increased activity levels (particularly when provided with exercise equipment) at feeding time. In one study, animals on a conventional diet "showed little activity" by early middle age, while those on CR "were observed to run around the cage and climb onto and hang from the wire cage tops throughout their life spans. In fact, the longest surviving [CR] mouse was observed hanging from the top of his cage only 3 days before he became moribund." Monkeys undergoing CR also appear more restless immediately before and after meals. Observations in some accounts of animals undergoing CR have noted an increase in stereotyped behaviors. For example, monkeys on CR have demonstrated an increase in licking, sucking, and rocking behavior. Unlike rodents with normal access to food, rats on CR exhibit longer periods of eating, higher food consumption, and hoarding of food. Studies of nonhuman primates on CR noted cooing, pacing, and intense eating. A CR regimen may also lead to increased aggressive behavior in animals. For example, rats on CR are prone to attack strangers more fiercely and are more likely to kill other rats than are controls, while monkeys have been observed to demonstrate threat displays at meal times. Even though there has been research on CR for over 70 years, the mechanism by which CR works is still not well understood. Some explanations include reduced cellular divisions, lower metabolic rates, reduced production of free radicals, reduced DNA damage and hormesis. Research has pointed toward hormesis as an explanation. Southam and Ehrlich (1943) reported that a bark extract that was known to inhibit fungal growth actually stimulated growth when given at very low concentrations. They coined the term "hormesis" to describe such beneficial actions resulting from the response of an organism to a low-intensity biological stressor. The word "hormesis" is derived from the Greek word "hormaein", which means "to excite". The (mito)hormesis hypothesis of CR proposes that the diet imposes a low-intensity biological stress on the organism, which elicits a defensive response that helps protect it against the causes of aging. In other words, CR places the organism in a defensive state so that it can survive adversity, resulting in improved health and longer life. This switch to a defensive state may be controlled by longevity genes (see below). Mitochondrial hormesis was a purely hypothetical concept until late 2007, when work by Michael Ristow's group on a small worm named Caenorhabditis elegans suggested that the restriction of glucose metabolism extends life span primarily by increasing oxidative stress to stimulate the organism into having an ultimately increased resistance to further oxidative stress. This is probably the first experimental evidence for hormesis being the reason for extended life span following CR. Although aging can be conceptualized as the accumulation of damage, the more recent determination that free radicals participate in intracellular signaling has made the categorical equation of their effects with "damage" more problematic than was commonly appreciated in the past. It was previously proposed on a hypothetical basis that free radicals may induce an endogenous response culminating in more effective adaptations that protect against exogenous radicals (and possibly other toxic compounds). Recent experimental evidence strongly suggests that this is indeed the case, and that such induction of endogenous free-radical production extends the life span of a model organism and mitohormetically exerts life-extending and health-promoting effects. Sublethal mitochondrial stress with an attendant stoichiometric augmentation of reactive oxygen species may precipitate many of the beneficial alterations in cellular physiology produced by caloric restriction. It has been recently argued that during years of famine, it may be evolutionarily desirable for an organism to avoid reproduction and to up-regulate protective and repair enzyme mechanisms to try to ensure that it is fit for reproduction in future years. This argument seems to be supported by recent work studying hormones. A study on male mice found that CR generally feminizes gene expression, and that many of the most significantly changed individual genes are involved in aging, hormone signaling, and p53-associated regulation of the cell cycle and apoptosis; it concluded that the life-extending effects of CR may arise partly from a shift toward a gene expression profile more typical of females. Prolonged severe CR lowers total serum and free testosterone while increasing SHBG concentrations in humans; these effects are independent of adiposity. Lowering of the concentration of insulin and substances related to insulin, such as insulin-like growth factor 1 and growth hormone, has been shown to up-regulate autophagy, the repair mechanism of the cell. A related hypothesis suggests that CR works by decreasing insulin levels and thereby up-regulating autophagy, but CR affects many other health indicators, and it is still undecided whether insulin is the main concern. Calorie restriction has been shown to increase DHEA in primates, but it has not been shown to increase DHEA in post-pubescent primates. The extent to which these findings apply to humans is still under investigation. Evidence suggests that the biological effects of CR are closely related to chromatin function. A study conducted by the Salk Institute for Biological Studies and published in the journal Nature in May 2007 determined that the gene PHA-4 is responsible for the longevity behind calorie restriction in roundworms, "with similar results expected in humans". Two very prominent proposed explanations of aging that have a bearing on calorie restriction are the free radical theory and the glycation theory. With high amounts of energy available, mitochondria do not operate very efficiently and generate more superoxide. With CR, energy is conserved and there is less free radical generation. A CR organism will have less fat and require less energy to support the weight, which also means that there does not need to be as much glucose in the bloodstream. Less blood glucose means less glycation of adjacent proteins and less fat to oxidize in the bloodstream to cause sticky blocks resulting in atherosclerosis. Type 2 diabetics are people with insulin insensitivity caused by long-term exposure to high blood glucose. Obesity leads to type 2 diabetes. Type 2 diabetes and uncontrolled type 1 diabetes are much like "accelerated aging", due to the above effects. There may even be a continuum between CR and the metabolic syndrome. Caloric restriction with optimal nutrition has not been tested in comparison to caloric excess with optimal nutrition. It may be that with extra calories, nutrition must be similarly increased to ratios comparable to that of calorie restriction in order to provide similar anti-aging benefits. Stated levels of calorie needs may be biased towards sedentary individuals. Calorie restriction may be nothing other than adapting the diet to the body's needs. Calorie restriction reduces production of reactive oxygen species (ROS). ROS cause several types of DNA damage including 8-hydroxy-2’-deoxyguanosine (8-OHdG). The level of 8-OHdG is often used as an indicator of the general level of oxidative damage in DNA. Sohal et al. observed that caloric restriction decreased 8-OHdG damages in the DNA of mouse, heart, skeletal muscle, brain, liver and kidney. The levels of 8-OHdG in the DNA of these organs in 15 month old mice were reduced to an average of 81% of that in the DNA of mice fed an unrestricted diet. Kaneko et al. observed that, in rats, dietary restriction retarded the onset of age-related increases in 8-OHdG in nuclear DNA of brain, heart, liver and kidney. The level of 8-OHdG in these organs of the calorie restricted rats at 30 months averaged 65% of the level in rats fed an unrestricted diet. Hamilton et al. found that dietary restriction in both mice and rats reduced the age-related levels of 8-OHdG. In rats aged 24–26 months that had been fed a calorie restricted diet, the level of 8-OHdG in heart, skeletal muscle, brain and kidney DNA was, on average, 62% of the level in rats fed an unrestricted diet. In mice, after a calorie restricted diet for 24–26 months, the level of 8-OHdG in heart, brain, liver and kidney DNA averaged 71% of the level in mice fed an unrestricted diet. Also, Wolf et al. observed that, in the rat, calorie restriction reduced 8-OHdG in the DNA of heart, skeletal muscle, brain and liver. After 24 months, the levels of 8-OHdG in these organs averaged 64% of those in the rats fed an unrestricted diet. Thus in rodents, calorie restriction slows aging, decreases ROS production and reduces the accumulation of oxidative DNA damage in multiple organs. These results link reduced oxidative DNA damage to slower aging. The consistent observation that calorie restriction reduces oxidative DNA damage lends support to the proposal of Holmes et al. that oxidative DNA damages are a prominent cause of aging. This is also discussed in detail by Bernstein et al. Work on the mechanisms of CR has given hope to the synthesizing of future drugs to increase the human life span by simulating the effects of calorie restriction. In particular, the large number of genes and pathways reported to regulate the actions of CR in model organisms represent attractive targets for developing drugs that mimic the benefits of CR without its side effects. However, MIT biologist Leonard Guarente cautioned that "(treatment) won't be a substitute for a healthy lifestyle. You'll still need to go to the gym." Sir2, or "silent information regulator 2", is a sirtuin, discovered in baker's yeast cells, that is hypothesized to suppress DNA instability. In mammals, Sir2 is known as SIRT1. David Sinclair at Harvard Medical School in Boston is a leading proponent of the view that the gene Sir2 may underlie the effect of calorie restriction in mammals by protecting cells from dying under stress. It is suggested that a low-calorie diet that requires less Nicotinamide adenine dinucleotide to metabolize may allow SIRT1 to be more active in its life-extending processes. An article in the June 2004 issue of the journal Nature showed that SIRT1 releases fat from storage cells. Attempts are being made to develop CR mimetics interventions. Resveratrol has been reported to activate Sir2/SIRT1 and extend the lifespan of yeast, nematode worms, fruit flies, and mice consuming a high-caloric diet. Resveratrol does not extend life span in normal mice. The effect of resveratrol on lifespan in C. elegans and Drosophila was reinvestigated by D. Gems and L. Partridge. They concluded that previously reported life-span increases were in fact due to natural variability in the life spans of C. elegans. A recent study found resveratrol extends the lifespan of a vertebrate fish by 59%. In the yeast, worm, and fly studies, resveratrol did not extend life span if the Sir2 gene was mutated. A 2010 study concluded that SRT1720 and resveratrol are not direct activators of SIRT1. Matt Kaeberlein and Brian Kennedy at the University of Washington believe that Sinclair's work on resveratrol is an artifact and that the Sir2 gene has no relevance to CR. They have proposed that caloric restriction increases life span by decreasing the activity of the Target of Rapamycin (TOR) kinase. Gurarente has recently published that behavior associated with caloric restriction did not occur when Sirt1 knockout mice were put on a calorie-restricted diet, the implication being that Sirt1 is necessary for mediating the effects of caloric restriction. However, the same paper also reported that the biochemical parameters thought to mediate the life span–extending effects of calorie restriction (reduced insulin, IGF-1, and fasting glucose) were no different in normal mice and mice lacking Sirt1. Whether the life span–extending effect of CR was still evident in Sirt1 knockout mice was not reported in that study. According to Sinclair's data, Sirtuins (SirT1, Sir2, ...) are behind the putative effect of calorie restriction on longevity, although some research has cast doubt on this claim. A clinical trial of the resveratrol formulation SRT501 was suspended. CR extends the life span and prevents aging. It has been found that these effects are modulated by SIRT3, a member of the sirtuins, a class of protein deacetylases. SIRT3 is mitochondrial. SIRT3-knockout mice did not live longer when calorically restricted, but wild-type mice did live longer when calorically restricted. One set of experiments shows that CR has no benefits in the housefly. The authors hypothesize that the widely purported effects of CR may be because a diet containing more calories can increase bacterial proliferation, or because the type of high-calorie diets used in past experiments have a stickiness, general composition, or texture that reduces longevity. At one time, some researchers suggested that some of the effects of CR are artifacts because the laboratory model organisms are kept on non-physiological high-calorie diets. This would mean that calorie restriction simply means mimicking the energy supply of a natural environment. However, many modern CR studies restrict the control animals by 10–20% below their ad libitum intake in order to avoid confounding by obesity. Additionally, "at least some laboratory mice under a caloric restriction regimen that maximizes longevity have been reported to cease estrous cycling. Because all existing wild mice populations must reproduce or become extinct, presumably they are eating relatively more than restricted laboratory mice during at least part of the year." A study designed to evaluate the energy intake, expenditure, and balance of mice in the wild, ad libitum–fed laboratory mice, and calorie-restricted mice concluded that "CR experiments do in fact restrict energy consumption beyond that typically experienced by mice in nature. Therefore, the retarded aging observed with CR is not due to eliminating the detrimental effects of overeating." While some tests of calorie restriction have shown increased muscle tissue in the calorie-restricted test subjects, how this has occurred is unknown.][ Muscle tissue grows when stimulated, so it is possible that the calorie-restricted test animals exercised more than their companions on higher calories. The reason behind this may be that animals enter a foraging state during calorie restriction. To control for this variable, tests would need to be monitored to ensure that levels of physical activity are equal between groups. Exercise has also been shown to increase health and life span and lower the incidence of several diseases (relative to sedentary and obese controls, but not to energy-restricted sedentary controls of matching body weight). Calorie restriction comes into conflict with the high caloric needs of athletes, and may not provide them sufficient energy levels or amino acids for repair, although this is not a criticism of CR per se, since it is certainly possible to be an unhealthy athlete or an athlete destined to die at a young age due to poor diet, stresses, etc. Moreover, in experiments comparing CR to exercise, CR animals lived much longer than exercised animals. There is some evidence suggesting that the benefit of CR in rats might only be reaped in early years. A study on rats that were gradually introduced to a CR lifestyle at 18 months showed no improvement over the average life span of the ad libitum group. This view, however, is disputed by Spindler, Dhahbi, and colleagues, who showed that in late adulthood, acute CR partially or completely reversed age-related alterations of liver, brain and heart proteins, and that mice placed on CR at 19 months of age showed increases in life span. The Wisconsin rhesus monkey study showed increased survival rates and decreased diseases of aging from caloric restriction even though the study started with adult monkeys. Both animal and human research suggest that CR may be contraindicated for people with amyotrophic lateral sclerosis (ALS). Research on a transgenic mouse model of ALS demonstrates that CR may hasten the onset of death in ALS. Hamadeh et al. therefore concluded, "These results suggest that CR diet is not a protective strategy for patients with amyotrophic lateral sclerosis (ALS) and hence is contraindicated." Hamadeh et al. also note two human studies that, they indicate, show "low energy intake correlates with death in people with ALS." However, in the first study, Slowie, Paige, and Antel state, "The reduction in energy intake by ALS patients did not correlate with the proximity of death but rather was a consistent aspect of the illness." They conclude, "ALS patients have a chronically deficient intake of energy and recommended augmentation of energy intake." Previously, Pedersen and Mattson also found that in the ALS mouse model, CR "accelerates the clinical course" of the disease and had no benefits. Suggesting that a calorically dense diet may slow ALS, a ketogenic diet in the ALS mouse model has been shown to slow the progress of disease. More recently, Mattson et al. opine that the death by ALS of Roy Walford, a pioneer in CR research and its antiaging effects, may have been a result of his own practice of CR. However, as Mattson et al. acknowledge, Walford's single case is an anecdote that by itself is insufficient to establish the proposed cause-effect relation. Another objection to CR as an advisable lifestyle for humans is the claim that the physiological mechanisms that determine longevity are very complex, and that the effect would be small to negligible in our species. Studies by Dr. Mark P. Mattson, chief of the National Institute on Aging's (NIA) Laboratory of Neurosciences, and colleagues have found that intermittent fasting and calorie restriction affect the progression of diseases similar to Huntington's disease, Parkinson's disease, and Alzheimer's disease in mice (PMID 11119686). In one study, rats and mice ate a low-calorie diet or were deprived of food for 24 hours every other day. Both methods improved glucose metabolism, increased insulin sensitivity, and increased stress resistance. Researchers have long been aware that calorie restriction extends life span, but this study showed that improved glucose metabolism also protects neurons in experimental models of Parkinson's and stroke. Another NIA study found that intermittent fasting and calorie restriction delay the onset of Huntington's disease–like symptoms in mice and prolongs their lives. Huntington's disease (HD), a genetic disorder, results from neuronal degeneration in the striatum. This neurodegeneration results in difficulties with movements that include walking, speaking, eating, and swallowing. People with Huntington's also exhibit an abnormal, diabetes-like metabolism that causes them to lose weight progressively. This NIA study compared adult HD mice who ate as much as they wanted with HD mice who were kept on an intermittent fasting diet during adulthood. HD mice possess the abnormal human gene huntingtin and exhibit clinical signs of the disease, including abnormal metabolism and neurodegeneration in the striatum. The mice on the fasting program developed clinical signs of the disease about 12 days later and lived 10–15% longer than the free-fed mice. The brains of the fasting mice also showed less degeneration. Those on the fasting program also regulated their glucose levels better and did not lose weight as quickly as the other mice. Researchers found that fasting mice had higher brain-derived neurotrophic factor (BDNF) levels. BDNF protects neurons and stimulates their growth. Fasting mice also had high levels of heat-shock protein-70 (Hsp70), which increases cellular resistance to stress. Another NIA study compared intermittent fasting with cutting caloric intake. Researchers let a control group of mice eat freely (ad libitum). Another group was fed 60% of the calories that the control group consumed. A third group was fasted for 24 hours, then permitted to free-feed. The fasting mice did not cut total calories at the beginning and end of the observation period, and only slightly cut calories in between. A fourth group was fed the average daily intake of the fasting mice every day. Both the fasting mice and those on a restricted diet had significantly lower blood sugar and insulin levels than the free-fed controls. Kainic acid, a toxin that damages neurons, was injected into the dorsal hippocampus of all mice. Hippocampal damage is associated with Alzheimer's. Interestingly, the scientists found less damage in the brains of the fasting mice than in those on a restricted diet, and most damage in mice with an unrestricted diet. But the control group that ate the average daily intake of the fasting mice (~10% restriction) also showed less damage than the mice on the restricted diet. Another Mattson study in which overweight adult asthmatics followed alternate day calorie restriction (ADCR) for eight weeks showed a marked improvement in oxidative stress, inflammation, and the severity of the disease. Evidence from the medical literature suggests that ADCR in the absence of weight loss prolongs life span in humans. Intermittent fasting has also been shown to increase the resistance of neurons in the brain to excitotoxic stress.
The name calorie is used for two units of energy. Although these units are part of the metric system, they now have been superseded in the International System of Units by the joule. One small calorie is approximately 4.2 joules (one large calorie or kilocalorie is therefore approximately 4.2 kilojoules). The factors used to convert calories to joules are numerically equivalent to expressions of the specific heat capacity of water in joules per gram or per kilogram. The conversion factor depends on the definition adopted. In spite of its non-official status, the large calorie is still widely used as a unit of food energy in the US, UK and some other Western countries. The small calorie is also often used in chemistry as the method of measurement is fairly straightforward in most reactions, though the amounts involved are typically expressed in thousands as kcal, an equivalent unit to the large calorie. The calorie was first defined by Nicolas Clément in 1824 as a unit of heat, and entered French and English dictionaries between 1841 and 1867. The word comes from Latin calor meaning "heat". The energy needed to increase the temperature of a given mass of water by 1 °C depends on the atmospheric pressure and the starting temperature, and is difficult to measure precisely. Accordingly, there have been several definitions of the calorie that attempt to make the definition more precise. The pressure is usually taken to be the standard atmospheric pressure (101.325 kPa). The temperature increase is often stated to be one kelvin, which by current definitions is exactly equal to an increment of one degree Celsius. ≈  ≈  ≈  ≈  ≈ 1.16810−6 kWh ≈ 2.6241019 eV ≈  ≈ 1.162610−6 kWh ≈ 2.61241019 eV ≈  ≈ 1.16210−6 kWh ≈ 2.6101019 eV ≈  ≈ 1.16410−6 kWh ≈ 2.6151019 eV ≈  ≈ 1.163010−6 kWh ≈ 2.61321019 eV ≈  ≈ 1.163010−6 kWh ≈ 2.61321019 eV Note 1: The figure depends on the conversion factor between international joules and absolute (modern) joules. Using the mean international ohm and volt (1.00049 Ω, 1.00034 V), the international joule is about 1.00019 J, using the US international ohm and volt (1.000495 Ω, 1.000330 V) it is about 1.000165 J, giving 4.18684 J and 4.18674 J, respectively. The two definitions most common in older literature appear to be the 15 °C calorie and the thermochemical calorie. The calorie was first defined specifically to measure energy in the form of heat, especially in experimental calorimetry. In nutritional contexts, the kilojoule (kJ) is the SI unit of food energy. However, calorie and kilocalorie are still in common use. In these contexts, confusingly, the word "calorie" and "kilocalorie" refer to equivalent units (the former to the large calorie and the latter to small calories). Sometimes, in an attempt to avoid confusion, the large calorie is written as "Calorie" (with a capital "C"). This convention is not always followed, and not explained to the average person clearly. These quantities are often used for the total amount of food energy (e.g., in a meal) and for the specific energy, namely amount of energy per unit of mass (e.g. "calories per gram", "calories per serving"). Nutritional requirements or intakes are often expressed in calories per day. In scientific contexts, the term calorie almost always refers to the small calorie. Even though it is not an SI unit, it is still used in chemistry. For example, the energy released in a chemical reaction per mole of reagent is occasionally expressed in kilocalorie per mole. This use is largely due to the ease with which it can be calculated in laboratory reactions, especially in aqueous solution; a volume of reagent dissolved in water forming a solution, with concentration expressed in moles per liter (1 liter weighing 1kg), will induce a temperature change in degrees Celsius in the total volume of water solvent, and these quantities (volume, molar concentration and temperature change) can then be used to calculate kcal/mol. It is also occasionally used to specify energy quantities that relate to reaction energy, such as enthalpy of formation and the size of activation barriers. However, its use is being superseded by the SI joule unit.
A meal replacement is a drink, bar, soup, etc. intended as a substitute for a solid food meal, usually with controlled quantities of calories and nutrients for purposes of weight loss. Some drinks are in the form of a health shake. Medically prescribed meal replacement drinks, which include required vitamins and minerals, include Optifast and HMR. Bodybuilders sometimes use meal replacements, not formulated for weight loss, to save food preparation time when they are eating 5 to 6 meals a day. In the European Union weight-reduction meal replacements intended either to supplement ("Meal replacement for weight control") or to replace totally ("Total diet replacement for weight control") normal meals are regulated as to their energy content, the nutrients they must provide, and information and advice on packaging by COMMISSION DIRECTIVE 96/8/EC of 26 February 1996 on foods intended for use in energy-restricted diets for weight reduction. For example, a meal replacement must provide between 200 and 400 food calories of energy, of which not more than 30% from fat, and not less than specified amounts for various vitamins and minerals. Labelling information is prescribed, and packaging must provide information such as a statement that the product should not be used for more than three weeks without medical advice. This protects users of meal replacements without other food from inadvertent malnutrition. In the United States, the term "meal replacement is not defined in federal Food and Drug Administration regulations, but generally refers to a calorie-controlled, prepackaged product in the form of a bar or beverage (ready to drink or powder), that replaces a regular meal. Meal-replacement products usually provide 200 to 250 calories per serving, are fortified with more than 20 vitamins and minerals at “good” or “excellent source” levels and often bear nutrient content claims, such as percent fat free and reduced sugar." Meal replacement products can be regulated as conventional/functional foods.
Dietary fiber, dietary fibre, or sometimes roughage and ruffage is the indigestible portion of food derived from plants. There are two main components: Dietary fibers can act by changing the nature of the contents of the gastrointestinal tract and by changing how other nutrients and chemicals are absorbed. Some types of soluble fiber absorb water to become a gelatinous, viscous substance and is fermented by bacteria in the digestive tract. Some types of insoluble fiber have bulking action and are not fermented. Lignin, a major dietary insoluble fiber source, may alter the rate and metabolism of soluble fibers. Other types of insoluble fiber, notably resistant starch, are fully fermented. Chemically, dietary fiber consists of non-starch polysaccharides such as arabinoxylans, cellulose, and many other plant components such as resistant starch, resistant dextrins, inulin, lignin, waxes, chitins, pectins, beta-glucans, and oligosaccharides. A novel position has been adopted by the US Department of Agriculture to include functional fibers as isolated fiber sources that may be included in the diet. The term "fiber" is something of a misnomer, since many types of so-called dietary fiber are not actually fibrous. Food sources of dietary fiber are often divided according to whether they provide (predominantly) soluble or insoluble fiber. Plant foods contain both types of fiber in varying degrees, according to the plant's characteristics. Advantages of consuming fiber are the production of healthful compounds during the fermentation of soluble fiber, and insoluble fiber's ability (via its passive hygroscopic properties) to increase bulk, soften stool, and shorten transit time through the intestinal tract. Disadvantages of a diet high in fiber is the potential for significant intestinal gas production and bloating. Constipation can occur if insufficient fluid is consumed with a high-fiber diet. Originally, fiber was defined to be the components of plants that resist human digestive enzymes, a definition that includes lignin and polysaccharides. The definition was later changed to also include resistant starches, along with inulin and other oligosaccharides. Official definition of dietary fiber differs a little among different institutions:
Dietary fiber is most found in vegetables and fruit. The exact amount of fiber contained in the food can be seen in the following table of expected fiber in USDA food groups/subgroups Dietary fiber is found in plants. While all plants contain some fiber, plants with high fiber concentrations are generally the most practical source. Fiber-rich plants can be eaten directly. Or, alternatively, they can be used to make supplements and fiber-rich processed foods. The Academy of Nutrition and Dietetics (AND), formerly the American Dietetic Association, recommends consuming a variety of fiber-rich foods. Some plants contain significant amounts of soluble and insoluble fiber. For example plums and prunes have a thick skin covering a juicy pulp. The skin is a source of insoluble fiber, whereas soluble fiber is in the pulp. Also, grapes have a fair amount of fiber in them. The root of the konjac plant, or glucomannan, produces results similar to fiber and may also be used to relieve constipation. Glucomannan is sold in various forms, and while safe in some forms, it can be unsafe in others, possibly leading to throat or intestinal blockage. Soluble fiber is found in varying quantities in all plant foods, including: Sources of insoluble fiber include: These are a few example forms of fiber that have been sold as supplements or food additives. These may be marketed to consumers for nutritional purposes, treatment of various gastrointestinal disorders, and for such possible health benefits as lowering cholesterol levels, reducing risk of colon cancer, and losing weight. Soluble fiber supplements may be beneficial for alleviating symptoms of irritable bowel syndrome, such as diarrhea and/or constipation and abdominal discomfort. Prebiotic soluble fiber products, like those containing inulin or oligosaccharides, may contribute to relief from inflammatory bowel disease, as in Crohn's disease, ulcerative colitis, and Clostridium difficile, due in part to the short-chain fatty acids produced with subsequent anti-inflammatory actions upon the bowel. Fiber supplements may be effective in an overall dietary plan for managing irritable bowel syndrome by modification of food choices. The insoluble fiber, resistant starch from high amylose corn, has been used as a supplement and may contribute to improving insulin sensitivity and glycemic management as well as promoting regularity and possibly relief of diarrhea. One preliminary finding indicates that resistant corn starch may reduce symptoms of ulcerative colitis. Chemically defined as oligosaccharides occurring naturally in most plants, inulins have nutritional value as carbohydrates, or more specifically as fructans, a polymer of the natural plant sugar, fructose. Inulin is typically extracted by manufacturers from enriched plant sources such as chicory roots or Jerusalem artichokes for use in prepared foods. Subtly sweet, it can be used to replace sugar, fat, and flour, is often used to improve the flow and mixing qualities of powdered nutritional supplements, and has significant potential health value as a prebiotic fermentable fiber. Inulin is advantageous because it contains 25–30% the food energy of sugar or other carbohydrates and 10–15% the food energy of fat. As a prebiotic fermentable fiber, its metabolism by gut flora yields short-chain fatty acids (see below) which increase absorption of calcium, magnesium, and iron, resulting from upregulation of mineral-transporting genes and their membrane transport proteins within the colon wall. Among other potential beneficial effects noted above, inulin promotes an increase in the mass and health of intestinal Lactobacillus and Bifidobacterium populations. Vegetable gum fiber supplements are relatively new to the market. Often sold as a powder, vegetable gum fibers dissolve easily with no aftertaste. In preliminary clinical trials, they have proven effective for the treatment of irritable bowel syndrome. Examples of vegetable gum fibers are guar gum and acacia Senegal gum. Dietary fibers have three primary mechanisms: bulking, viscosity and fermentation. Dietary fibers can change the nature of the contents of the gastrointestinal tract, and to change how other nutrients and chemicals are absorbed through bulking and viscosity. Some types of soluble fibers bind to bile acids in the small intestine, making them less likely to enter the body; this in turn lowers cholesterol levels in the blood. Viscous soluble fibers may also attenuate the absorption of sugar, reduce sugar response after eating, normalize blood lipid levels and, once fermented in the colon, produce short-chain fatty acids as byproducts with wide-ranging physiological activities (discussion below). Insoluble fiber is associated with reduced diabetes risk, but the mechanism by which this occurs is unknown. One type of insoluble dietary fiber, resistant starch has been shown to directly increase insulin sensitivity in healthy people, in type 2 diabetics, and in individuals with insulin resistance, possibly contributing to reduced risk of type 2 diabetes. Not yet formally proposed as an essential macro-nutrient, dietary fiber is nevertheless regarded as important for the diet, with regulatory authorities in many developed countries recommending increases in fiber intake. Dietary fiber has distinct physicochemical properties. Most semi-solid foods, fiber and fat are a combination of gel matrices which are hydrated or collapsed with microstructural elements, globules, solutions or encapsulating walls. Fresh fruit and vegetables are cellular materials. A slowly eaten meal will enter the absorptive phase of the gastrointestinal tract more slowly than a rapidly eaten meal of similar composition. Many of the differences between low and high glycemic foods would disappear if a meal was eaten slowly. The chemical and physico-chemical nature (lipid, protein, carbohydrate) of the meal will also influence the gastric emptying of the food multiphase system. Fatty foods and hypertonic solutions empty slowly. The movement of food, i.e., chyme, along the gastrointestinal tract is typical of flow in a disperse system. As chyme moves along the gastrointestinal tract, polymer flow and diffusion becomes important. Following a meal, the stomach and upper gastrointestinal contents consist of Micelles are colloid-sized clusters of molecules which form in conditions as those above, similar to the critical micelle concentration of detergents. In the upper gastrointestinal tract, these detergents consist of bile acids and di- and monoacyl glycerols which solubilize triacylglycerols and cholesterol. Two mechanisms bring nutrients into contact with the epithelium: The multiple physical phases in the intestinal tract slow the rate of absorption compared to that of the suspension solvent alone. Adding viscous polysaccharides to carbohydrate meals can reduce post-prandial blood glucose concentrations. Wheat and maize but not oats modify glucose absorption, the rate being dependent upon the particle size. The reduction in absorption rate with guar gum may be due to the increased resistance by viscous solutions to the convective flows created by intestinal contractions. Dietary fiber interacts with pancreatic and enteric enzymes and their substrates. Human pancreatic enzyme activity is reduced when incubated with most fiber sources. Fiber may affect amylase activity and hence the rate of hydrolysis of starch. The more viscous polysaccharides extend the mouth-to-cecum transit time; guar, tragacanth and pectin being slower than wheat bran. The colon may be regarded as two organs, The presence of bacteria in the colon produces an ‘organ’ of intense, mainly reductive, metabolic activity, whereas the liver is oxidative. The substrates utilized by the cecal have either passed along the entire intestine or are biliary excretion products . The effects of dietary fiber in the colon are on Enlargement of the cecum is a common finding when some dietary fibers are fed and this is now believed to be normal physiological adjustment. Such an increase may be due to a number of factors, prolonged cecal residence of the fiber, increased bacterial mass, or increased bacterial end-products. Some non-absorbed carbohydrates, e.g. pectin, gum arabic, oligosaccharides and resistant starch, are fermented to short-chain fatty acids (chiefly acetic, propionic and n-butyric), and carbon dioxide, hydrogen and methane. The cecal fermentation of 40–50 g of complex polysaccharides will yield 400–500 mmol total short-chain fatty acids, 240–300 mmol acetate, and 80–100 mmol of both propionate and butyrate. Almost all of these short-chain fatty acids will be absorbed from the colon. This means that fecal short-chain fatty acid estimations do not reflect cecal and colonic fermentation, only the efficiency of absorption, the ability of the fiber residue to sequestrate short-chain fatty acids, and the continued fermentation of fiber around the colon, which presumably will continue until the substrate is exhausted. The production of short-chain fatty acids has several possible actions on the gut mucosa. All of the short-chain fatty acids are readily absorbed by the colonic mucosa, but only acetic acid reaches the systemic circulation in appreciable amounts. Butyric acid appears to be used as a fuel by the colonic mucosa as the preferred energy source for colonic cells. Dietary fiber may act on each phase of ingestion, digestion, absorption and excretion to affect cholesterol metabolism, such as the following: An important action of some fibers is to reduce the reabsorption of bile acids in the ileum and hence the amount and type of bile acid and fats reaching the colon. A reduction in the reabsorption of bile acid from the ileum has several direct effects. The fibers that are most effective in influencing sterol metabolism (e.g. pectin) are fermented in the colon. It is therefore unlikely that the reduction in body cholesterol is due to adsorption to this fermented fiber in the colon. Feces consist of plasticine-like material, made up of water, bacteria, lipids, sterols, mucus and fiber. Water is distributed in the colon in three ways: Fecal weight is dictated by: Wheat bran is minimally fermented and binds water and when added to the diet increases fecal weight in a predictable linear manner and decreases intestinal transit time. The particle size of the fiber is all-important, coarse wheat bran being more effective than fine wheat bran. The greater the water-holding capacity of the bran, the greater the effect on fecal weight. For most healthy individuals, an increase in wet fecal weight, depending on the particle size of the bran, is generally of the order of 3–5 g/g fiber. The fermentation of some fibers results in an increase in the bacterial content and possibly fecal weight. Other fibers, e.g. pectin, are fermented and have no effect on stool weight. Research has shown that fiber may benefit health in several different ways. Lignin and probably related materials that are resistant to enzymatic degradation, diminish the nutritional value of foods. Color coding of table entries: Fiber does not bind to minerals and vitamins and therefore does not restrict their absorption, but rather evidence exists that fermentable fiber sources improve absorption of minerals, especially calcium. Some plant foods can reduce the absorption of minerals and vitamins like calcium, zinc, vitamin C, and magnesium, but this is caused by the presence of phytate (which is also thought to have important health benefits), not by fiber. An experiment designed with a large sample and conducted by NIH-AARP Diet and Health Study studied the correlation between fiber intake and colorectal cancer. The analytic cohort consisted of 291 988 men and 197 623 women aged 50–71 y. Diet was assessed with a self-administered food-frequency qustionnaire at baseline in 1995-1996; 2974 incident colorectal cancer cases were identified during 5 y of follow-up. The result was that total fiber intake was not associated with colorectal cancer. But on the other hand, the analyses of fiber from different food sources showed that fiber from grains was associated with a lower risk of colorectal cancer. Although many researchers believe that dietary fiber intake reduces risk of colon cancer, one study conducted by researchers at the Harvard School of Medicine of over 88,000 women did not show a statistically significant relationship between higher fiber consumption and lower rates of colorectal cancer or adenomas. Similarly, a 2010 study of 58,279 men found no relationship between dietary fiber and colorectal cancer. Dietary fiber has many functions in diet, one of which may be to aid in energy intake control and reduced risk for development of obesity. The role of dietary fiber in energy intake regulation and obesity development is related to its unique physical and chemical properties that aid in early signals of satiation and enhanced or prolonged signals of satiety. Early signals of satiation may be induced through cephalic- and gastric-phase responses related to the bulking effects of dietary fiber on energy density and palatability, whereas the viscosity-producing effects of certain fibers may enhance satiety through intestinal-phase events related to modified gastrointestinal function and subsequent delay in fat absorption. In general, fiber-rich diets, whether achieved through fiber supplementation or incorporation of high fiber foods into meals, have a reduced energy density compared with high fat diets. This is related to fiber’s ability to add bulk and weight to the diet. However, the subsequent effect of fiber on food intake has been more variable because in some cases, food intake at a test meal was reduced, in other cases, it was not. Although much of the discrepancy in results may be ascribed to differences among studies, different responses related to gender and body weight status (i.e., obese vs. normal weight) may also be responsible. With regard to gender, work in our][ laboratory indicates that women may be more sensitive to dietary manipulation with fiber than men, which is consistent with a previous report by Burley et al. (1993). Moreover, we][ have found that the subjective satiety response to dietary manipulation in men and women is supported by differences in the CCK response, suggesting that signals for satiety differ between genders (Burton-Freeman et al. 1998 and personal communication). The relationship of body weight status and fiber effect on energy intake suggests that obese individuals may be more likely to reduce food intake (Evans and Miller 1975, Porikos and Hagamen 1986) with dietary fiber inclusion. Current recommendations from the United States National Academy of Sciences, Institute of Medicine, suggest that adults should consume 20–35 grams of dietary fiber per day, but the average American's daily intake of dietary fiber is only 12–18 grams. The AND (Academy of Nutrition and Dietetics, previously ADA) recommends a minimum of 20–35 g/day for a healthy adult depending on calorie intake (e.g., a 2000 Cal/8400 kJ diet should include 25 g of fiber per day). The AND's recommendation for children is that intake should equal age in years plus 5 g/day (e.g., a 4 year old should consume 9 g/day). No guidelines have yet been established for the elderly or very ill. Patients with current constipation, vomiting, and abdominal pain should see a physician. Certain bulking agents are not commonly recommended with the prescription of opioids because the slow transit time mixed with larger stools may lead to severe constipation, pain, or obstruction. The British Nutrition Foundation has recommended a minimum fiber intake of 18 g/day for healthy adults. On average, North Americans consume less than 50% of the dietary fiber levels recommended for good health. In the preferred food choices of today's youth, this value may be as low as 20%, a factor considered by experts as contributing to the obesity levels seen in many developed countries. The actual fiber intake gaps of different age groups of Americans are shown in the graph from USDA: Recognizing the growing scientific evidence for physiological benefits of increased fiber intake, regulatory agencies such as the Food and Drug Administration (FDA) of the United States have given approvals to food products making health claims for fiber. In clinical trials to date, these fiber sources were shown to significantly reduce blood cholesterol levels, an important factor for general cardiovascular health, and to lower risk of onset for some types of cancer. Soluble (fermentable) fiber sources gaining FDA approval are: Other examples of fermentable fiber sources (from plant foods or biotechnology) used in functional foods and supplements include inulin, resistant dextrins, fructans, xanthan gum, cellulose, guar gum, fructooligosaccharides (FOS), and oligo- or polysaccharides. Consistent intake of fermentable fiber through foods like berries and other fresh fruit, vegetables, whole grains, seeds, and nuts is now known to reduce risk of some of the world’s most prevalent diseases—obesity, diabetes, high blood cholesterol, cardiovascular disease, and numerous gastrointestinal disorders. In this last category are constipation, inflammatory bowel disease, ulcerative colitis, hemorrhoids, Crohn's disease, diverticulitis, and colon cancer—all disorders of the intestinal tract where fermentable fiber can provide healthful benefits. Insufficient fiber in the diet can complicate defecation. Low-fiber feces are dehydrated and hardened, making them difficult to evacuate—defining constipation and possibly leading to development of hemorrhoids or anal fissures. In June 2007, the British Nutrition Foundation issued a statement to define dietary fiber more concisely and list the potential health benefits established to date: ‘Dietary fibre’ has been used as a collective term for a complex mixture of substances with different chemical and physical properties which exert different types of physiological effects. The use of certain analytical methods to quantify dietary fiber by nature of its indigestibility results in many other indigestible components being isolated along with the carbohydrate components of dietary fiber. These components include resistant starches and oligosaccharides along with other substances that exist within the plant cell structure and contribute to the material that passes through the digestive tract. Such components are likely to have physiological effects. Yet, some differentiation has to be made between these indigestible plant components and other partially digested material, such as protein, that appears in the large bowel. Thus, it is better to classify fiber as a group of compounds with different physiological characteristics, rather than to be constrained by defining it chemically. Diets naturally high in fiber can be considered to bring about several main physiological consequences: Fiber contributes less energy (measured in Calories or kilojoules) than sugars and starches because it cannot be fully absorbed by the body. Sugars and starches provide 4 Calories per gram, and the human body has specific enzymes to break them down into glucose, fructose, and galactose, which can then be absorbed by the body. The human body lacks enzymes to break down fiber. Insoluble fiber does not change inside the body, so the body cannot absorb it and nutritionists say that it contributes 0 Calories per gram. Soluble fiber is partially fermented, with the degree of fermentability varying with the type of fiber, and contributes some energy when broken down and absorbed by the body. Dietitians have not reached a consensus on how much energy is actually absorbed, but some approximate around 2 Calories (8.36 joules) per gram of soluble fiber. Regardless of the type of fiber, the body absorbs fewer than 4 Calories (16.7 kilojoules) per gram of fiber, which can create inconsistencies for actual product nutrition labels. In some countries, fiber is not listed on nutrition labels, and is considered 0 Calories/gram when the food's total Calories are computed. In other countries all fiber must be listed, and is considered 4 Calories per gram when the food's total Calories are computed (because chemically fiber is a type of carbohydrate and other carbohydrates contribute 4 Calories per gram). In the US, soluble fiber must be counted as 4 Calories per gram, but insoluble fiber may be (and usually is) treated as 0 Calories per gram and not mentioned on the label. The American Association of Cereal Chemists has defined soluble fiber this way: "the edible parts of plants or similar carbohydrates resistant to digestion and absorption in the human small intestine with complete or partial fermentation in the large intestine." In this definition: As an example of fermentation, shorter-chain carbohydrates (a type of fiber found in legumes) cannot be digested, but are changed via fermentation in the colon into short-chain fatty acids and gases (which are typically expelled as flatulence). According to a 2002 journal article, fibers compounds with partial or low fermentability include: fiber compounds with high fermentability include: When soluble fiber is fermented, short-chain fatty acids (SCFA) are produced. SCFAs are involved in numerous physiological processes promoting health, including: SCFAs that are absorbed by the colonic mucosa pass through the colonic wall into the portal circulation (supplying the liver), and the liver transports them into the general circulatory system. Overall, SCFAs affect major regulatory systems, such as blood glucose and lipid levels, the colonic environment, and intestinal immune functions. The major SCFAs in humans are butyrate, propionate, and acetate, where butyrate is the major energy source for colonocytes, propionate is destined for uptake by the liver, and acetate enters the peripheral circulation to be metabolized by peripheral tissues. The FDA allows producers of foods containing 1.7g per serving of psyllium husk soluble fiber or 0.75g of oat or barley soluble fiber as beta-glucans to claim that reduced risk of heart disease can result from their regular consumption. The FDA statement template for making this claim is: Soluble fiber from foods such as [name of soluble fiber source, and, if desired, name of food product], as part of a diet low in saturated fat and cholesterol, may reduce the risk of heart disease. A serving of [name of food product] supplies __ grams of the [necessary daily dietary intake for the benefit] soluble fiber from [name of soluble fiber source] necessary per day to have this effect. Eligible sources of soluble fiber providing beta-glucan include: The allowed label may state that diets low in saturated fat and cholesterol and that include soluble fiber from certain of the above foods "may" or "might" reduce the risk of heart disease. As discussed in FDA regulation 21 CFR 101.81, the daily dietary intake levels of soluble fiber from sources listed above associated with reduced risk of coronary heart disease are: Soluble fiber from consuming grains is included in other allowed health claims for lowering risk of some types of cancer and heart disease by consuming fruit and vegetables (21 CFR 101.76, 101.77, and 101.78). A study of 388,000 adults ages 50 to 71 for nine years found that the highest consumers of fiber were 22% less likely to die over this period. In addition to lower risk of death from heart disease, adequate consumption of fiber-containing foods, especially grains, was also associated with reduced incidence of infectious and respiratory illnesses, and, particularly among males, reduced risk of cancer-related death.

Food energy is energy that animals (including humans) derive from their food, through the process of cellular respiration, the process of joining oxygen with the molecules of food (aerobic respiration) or of reorganizing the atoms within the molecules for anaerobic respiration.

Humans and other animals need a minimum intake of food energy to sustain their metabolism and drive their muscles. Foods are composed chiefly of carbohydrates, fats, proteins, water, vitamins, and minerals. Carbohydrates, fats, proteins, and water represent virtually all the weight of food, with vitamins and minerals making up only a small percentage of the weight. Carbohydrates, fats, and proteins comprise ninety percent of the dry weight of foods. Food energy is derived from carbohydrates, fats and proteins as well as organic acids, polyols, and ethanol present in the diet. Some diet components that provide little or no food energy, such as water, minerals, vitamins and fiber, may still be necessary to health and survival for other reasons. Water contains very stable chemical bonds and so cannot be oxidized to provide energy. Vitamins and minerals are present in very small amounts (in milli- or micrograms) and also cannot be used for energy. Fiber, a type of carbohydrate, cannot be completely digested by the human body. Ruminants can extract food energy from the respiration of cellulose thanks to bacteria in their rumens.

The Small Plate Movement is a combined effort by academia, government, media, and industry to help American families lose weight and feel healthier by simply reducing the size of their dinnerware. The Movement was announced in San Diego on October 27, 2008 at the American Public Health Association conference.

Recent studies in medical, nutrition, and marketing journals have illustrated how people serve themselves in proportion to the size plate that they have been given. That is, while 3 ounces of pasta on a 10-inch plate looks like a sizable portion, the same amount on a 12-inch plate looks comparatively much smaller, as can be seen in this. [Missing image?]

The freshman 15 is an expression commonly used in the United States that refers to an amount (somewhat arbitrarily set at 15 pounds) of weight often gained during a student's first year at college. In Australia and New Zealand it is sometimes referred to as First Year Fatties, Fresher Spread, or Fresher Five, the latter referring to a five-kilogram gain.

The purported causes of this weight gain are increased alcohol intake and the consumption of fat and carbohydrate-rich cafeteria-style food and fast food in university dormitories. Many dining halls in American universities are all-you-can-eat style and offer copious dessert choices. In addition, lack of sleep may lead to overeating and weight gain, because it lowers the level of leptin. Other causes include malnutrition, stress, and decreased levels of exercise. All of these factors can affect each person in a different way. Studies confirm many of these causes. Colleges and universities have recently been cracking down on this common problem and are trying to educate people on how to prevent it. This problem has grown so much that students are focusing on how to stop the freshman 15 before it happens.

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