Recipes for Kids in Urdu for Desserts for Dinner for Chicken with Ground Beef In Hindi for Cakes : Low Fat Recipes Recipes for Kids in Urdu for Desserts for Dinner for Chicken with Ground Beef In Hindi for Cakes for Cookies Photos

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A low-fat diet is one that restricts fat and often saturated fat and cholesterol as well. Low-fat diets are intended to reduce diseases such as heart disease and obesity. Reducing fat in the diet can make it easier to cut calories. Fat provides nine calories per gram while carbohydrates and protein each provide four calories per gram, so choosing low-fat foods makes it possible to eat a larger volume of food for the same number of calories. The Institute of Medicine recommends limiting fat intake to 35% of total calories to help prevent obesity and to help control saturated fat intake.
Evidence Reducing total fat intake leads to reductions in caloric intake, resulting in weight loss or less weight gain.[2] The overall benefit is small but beneficial.[3] With respect to weight loss low-fat diets do not appear to differ from other diets that also reduce overall calories.
Low-fat diets have been promoted for the prevention of heart disease. Lowering fat intake from 35-40% of total calories to 15-20% of total calories has been shown to decrease total and LDL cholesterol by 10 to 20%; however, most of this decrease is due to a reduction in saturate fat intake.[6] Saturated fat has been shown to raise total and LDL cholesterol in a large number of studies and has also been correlated with a higher risk of heart disease.[8] Furthermore, a high-fat diet can contain "unacceptably high" amounts of saturated fat, even if saturated fats from animal products and tropical oils are avoided. This is because all fats contain some saturated fatty acids. For example, if a person chose fats with only 20% saturated fatty acids, setting fat intake at 35% of total calories would mean that 7% of calories would come from saturated fat. For this reason, the Institute of Medicine recommends consuming no more than 35% of calories from fat.
While low-fat diets lower total and LDL cholesterol, a sudden increase in carbohydrate has been "consistently" shown to raise triglycerides.[6] Increasing the carbohydrate content of the diet gradually has been shown to prevent hypertriglyceridemia.[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. Caloric restriction 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.The long-term effects of moderate CR with adequate intake of nutrients on humans are unknown.
Two main lifespan studies have been performed involving nonhuman primates (rhesus monkeys). One, begun in 1987 by the National Institute on Aging, published interim results in August 2012 indicating that CR confers health benefits in these animals, but did not demonstrate increased median lifespan. A second study by the University of Wisconsin beginning in 1989 issued preliminary lifespan results in 2009,and final results in 2014.[6] It found that CR primates were only 36.4% as likely to die from age-related causes when compared with control animals, and had only 56.2% the rate of death from any cause.Severe or extreme CR may result in serious deleterious effects, as it has been shown in the “Minnesota Starvation Experiment”.[7] This study was conducted during World War II on a group of lean men, who restricted their calorie intake by 45% for 6 months.[7] As expected, this severe degree of CR resulted in many positive metabolic adaptations (e.g. decreased body fat, blood pressure, improved lipid profile, low serum T3 concentration, and decreased resting heart rate and whole-body resting energy expenditure), but also caused a wide range of negative effects, such as anemia, lower extremity edema, muscle wasting, weakness, neurological deficits, dizziness, irritability, lethargy, and depression.
Musculoskeletal losses Short-term studies in humans report loss of muscle mass and strength and reduced bone mineral density.
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. Low BMI, high mortality[edit]
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.[10] The authors attempted to adjust for confounding factors (cigarette smoking, failure to exclude pre-existing disease); others argued that the adjustments were inadequate.[11]
"epidemiologists from the ACS (American Cancer Society), American Heart Association, Harvard School of Public Health, and other organizations raised specific methodologic questions about the recent Centers for Disease Control and Prevention (CDC) study and presented analyses of other data sets. The main concern ... is that it did not adequately account for weight loss from serious illnesses such as cancer and heart disease ... [and] failed to account adequately for the effect of smoking on weight ... As a result, the Flegal study underestimated the risks from obesity and overestimated the risks of leanness."[12]
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).[13]
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."[2] Typical low-calorie diets rarely provide the high nutrient intakes that are a necessary feature of an anti-aging calorie restriction diet.[14][15][16] 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."[2]
Triggering eating disorders[edit]
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.[17]
Young or pregnant[edit]
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.[18] 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.[18]
Miscellaneous concerns It has also been noted that people losing weight on such diets risk developing cold sensitivity, menstrual irregularities, and even infertility and hormonal changes.[19]
MechanismsEven though there has been research on CR for over 70 years, the mechanism by which CR works is still not well understood.[1] Some explanations include reduced cellular divisions, lower metabolic rates, reduced production of free radicals,[20] reduced DNA damage[21][22] and hormesis.[23]
Hormesis
Main article: 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).[24]
Mitochondrial hormesisMitochondrial 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.[25] 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).[26] 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.EvolutionIt 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.[30] 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.[31] Prolonged severe CR lowers total serum and free testosterone while increasing SHBG concentrations in humans; these effects are independent of adiposity.
See also: Insulin § Physiological effects
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.[33] A related hypothesis suggests that CR works by decreasing insulin levels and thereby up-regulating autophagy,[33][34] but CR affects many other health indicators, and it is still undecided whether insulin is the main concern.[35] 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.Chromatin and PHA-Evidence suggests that the biological effects of CR are closely related to chromatin function.[38] 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".
Free radicals and glycation[edit]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. 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.
Reduced DNA damage[edit]Main article: DNA damage theory of aging
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.[41] 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.[42] 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.[43] 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.[22] This is also discussed in detail by Bernstein et al.Caloric restriction mimeticsMain article: Caloric restriction mimetic
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.[46][47][48] 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.[50] 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.[51] 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.
Sirtuins
Attempts are being made to develop drugs that act as CR mimetics, and much of that work has focused on a class of proteins called sirtuins.[53] Resveratrol has been reported to activate SIRT1 and extend the lifespan of yeast,[54] nematode worms, fruit flies,[55] vertebrate fish,[56] and mice consuming a high-caloric diet.[57] However, resveratrol does not extend life span in normal mice[58] and the effect of resveratrol on lifespan in nematodes and fruit flies has been disputed.[59]
There are studies that indicate that resveratrol may not function through SIRT1[60][61] but may work through other targets.[62][63] A clinical trial of the resveratrol formulation SRT501 was suspended.[64]
There is some evidence from mice that caloric restriction may be mediated through SIRT3[65] or SIRT6.

Low Fat RecipesRecipes for Kids in Urdu for Desserts for Dinner for Chicken with Ground Beef In Hindi for Cakes for Cookies Photos