Hubbry Logo
DietingDietingMain
Open search
Dieting
Community hub
Dieting
logo
7 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Contribute something
Dieting
Dieting
Dieting
View on Wikipedia
from Wikipedia

Part of a series on
Human body weight
General concepts
Medical concepts
Measurements
Related conditions
Obesity-associated morbidity
Management of obesity
Social aspects

Dieting is the practice of eating food in a regulated way to decrease, maintain, or increase body weight, or to prevent and treat diseases such as diabetes and obesity. As weight loss depends on calorie intake, different kinds of calorie-reduced diets, such as those emphasising particular macronutrients (low-fat, low-carbohydrate, etc.), have been shown to be no more effective than one another.[1][2][3][4][5] As weight regain is common, diet success is best predicted by long-term adherence.[2][5][6] Regardless, the outcome of a diet can vary widely depending on the individual.[2][7]

The first popular diet was "Banting", named after William Banting. In his 1863 pamphlet, Letter on Corpulence, Addressed to the Public, he outlined the details of a particular low-carbohydrate, low-calorie diet that led to his own dramatic weight loss.[8]

Some guidelines recommend dieting to lose weight for people with weight-related health problems, but not for otherwise healthy people.[9][10] One survey found that almost half of all American adults attempt to lose weight through dieting, including 66.7% of obese adults and 26.5% of normal weight or underweight adults.[11] Dieters who are overweight (but not obese), who are normal weight, or who are underweight may have an increased mortality rate as a result of dieting.[9]

History

[edit]
William Banting popularized one of the first weight loss diets in the 19th century.

The word diet comes from the Greek δίαιτα (diaita), which represents a notion of a whole way healthy lifestyle including both mental and physical health, rather than a narrow weight-loss regimen.[12][13]

One of the first dietitians was the English doctor George Cheyne. He himself was tremendously overweight and would constantly eat large quantities of rich food and drink. He began a meatless diet, taking only milk and vegetables, and soon regained his health. He began publicly recommending his diet for everyone who was obese. In 1724, he wrote An Essay of Health and Long Life, in which he advises exercise and fresh air and avoiding luxury foods.[14]

The Scottish military surgeon, John Rollo, published Notes of a Diabetic Case in 1797. It described the benefits of a meat diet for those with diabetes, basing this recommendation on Matthew Dobson's discovery of glycosuria in diabetes mellitus.[15] By means of Dobson's testing procedure (for glucose in the urine) Rollo worked out a diet that had success for what is now called type 2 diabetes.[16]

The first popular diet was "Banting", named after the English undertaker William Banting. In 1863, he wrote a booklet called Letter on Corpulence, Addressed to the Public, which contained the particular plan for the diet he had successfully followed. His own diet was four meals per day, consisting of meat, greens, fruits, and dry wine. The emphasis was on avoiding sugar, sweet foods, starch, beer, milk and butter. Banting's pamphlet was popular for years to come, and would be used as a model for modern diets.[17] The pamphlet's popularity was such that the question "Do you bant?" referred to his method, and eventually to dieting in general.[18] His booklet remains in print as of 2007.[8][19]

The first weight-loss book to promote calorie counting, and the first weight-loss book to become a bestseller, was the 1918 Diet and Health: With Key to the Calories by American physician and columnist Lulu Hunt Peters.[20]

It was estimated that over 1000 weight-loss diets have been developed up to 2014.[21]

Types

[edit]
Main article: List of diets

A restricted diet is most commonly pursued by those who want to lose weight. Some people follow a diet to gain weight (such as people who are underweight or who are attempting to gain more muscle). Diets can also be used to maintain a stable body weight or to improve health.[22]

Low-fat

[edit]
Main article: Low-fat diet

Low-fat diets involve the reduction of the percentage of fat in one's diet. Calorie consumption is reduced because less fat is consumed.[23] Diets of this type include NCEP Step I and II. A meta-analysis of 16 trials of 2–12 months' duration found that low-fat diets (without intentional restriction of caloric intake) resulted in average weight loss of 3.2 kg (7.1 lb) over habitual eating.[1]

A low-fat, plant-based diet has been found to improve control of weight, blood sugar levels, and cardiovascular health.[24]

Low-carbohydrate

[edit]
This section is an excerpt from Low-carbohydrate diet.[edit]

An example of a low-carbohydrate dish, cooked kale and poached eggs

Low-carbohydrate diets restrict carbohydrate consumption relative to the average diet. Foods high in carbohydrates (e.g., sugar, bread, pasta) are limited, and replaced with foods containing a higher percentage of fat and protein (e.g., meat, poultry, fish, shellfish, eggs, cheese, nuts, and seeds), as well as low carbohydrate foods (e.g. spinach, kale, chard, collards, and other fibrous vegetables).

There is a lack of standardization of how much carbohydrate low-carbohydrate diets must have, and this has complicated research.[25] One definition, from the American Academy of Family Physicians, specifies low-carbohydrate diets as having less than 20% of calories from carbohydrates.[26]

There is no good evidence that low-carbohydrate dieting confers any particular health benefits apart from weight loss, where low-carbohydrate diets achieve outcomes similar to other diets, as weight loss is mainly determined by calorie restriction and adherence.[27]

One form of low-carbohydrate diet called the ketogenic diet was first established as a medical diet for treating epilepsy.[28] It became a popular diet for weight loss through celebrity endorsement, but there is no evidence of any distinctive benefit for this purpose and the diet carries a risk of adverse effects,[28][29] with the British Dietetic Association naming it one of the "top five worst celeb diets to avoid" in 2018.[28]

Low-calorie

[edit]
Main article: Calorie restriction

Low-calorie diets usually produce an energy deficit of 500–1,000 calories per day, which can result in a 0.5 to 1 kilogram (1.1 to 2.2 pounds) weight loss per week.[30] The National Institutes of Health reviewed 34 randomized controlled trials to determine the effectiveness of low-calorie diets. They found that these diets lowered total body mass by 8% in the short term, over 3–12 months.[1] Women doing low-calorie diets should have at least 1,000 calories per day and men should have approximately 1,200 calories per day. These caloric intake values vary depending on additional factors, such as age and weight.[1]

Very low-calorie

[edit]
Main article: Very low calorie diet

Very low calorie diets provide 200–800 calories per day, maintaining protein intake but limiting calories from both fat and carbohydrates.[31] They subject the body to starvation and produce an average loss of 1.5–2.5 kg (3.3–5.5 lb) per week.[citation needed] "2-4-6-8", a popular diet of this variety, follows a four-day cycle in which only 200 calories are consumed the first day, 400 the second day, 600 the third day, 800 the fourth day, and then totally fasting, after which the cycle repeats.[citation needed] There is some evidence that these diets results in considerable weight loss.[2] These diets are not recommended for general use and should be reserved for the management of obesity as they are associated with adverse side effects such as loss of lean muscle mass, increased risks of gout, and electrolyte imbalances. People attempting these diets must be monitored closely by a physician to prevent complications.[1]

The concept of crash dieting is to drastically reduce calories, using a very-low-calorie diet.[32][33][34][35] Crash dieting can be highly dangerous because it can cause various kind of issues for the human body. Crash dieting can produce weight loss but without professional supervision all along, the extreme reduction in calories and potential unbalance in the diet's composition can lead to detrimental effects, including sudden death.[36]

Fasting

[edit]
Main articles: Fasting and Intermittent fasting

Fasting is the act of intentional taking a long time interval between meals. Lengthy fasting (multiple days in a week) might be dangerous due to the risk of malnutrition.[37] During prolonged fasting or very low calorie diets the reduction of blood glucose, the preferred energy source of the brain, causes the body to deplete its glycogen stores.[22] Once glycogen is depleted the body begins to fuel the brain using ketones, while also metabolizing body protein (including but not limited to skeletal muscle) to be used to synthesize sugars for use as energy by the rest of the body.[22] Most experts believe that a prolonged fast can lead to muscle wasting,[38] although some[who?] dispute this.[citation needed] The use of short-term fasting, or various forms of intermittent fasting, have been used as a form of dieting to circumvent the issues of long fasting.[39]

Intermittent fasting commonly takes the form of periodic fasting, alternate-day fasting, time-restricted feeding, and/or religious fasting.[22] It can be a form of reduced-calorie dieting but pertains entirely to when the metabolism is activated during the day for digestion. The changes to eating habits on a regular basis do not have to be severe or absolutely restrictive to see benefits to cardiovascular health, such as improved glucose metabolism, reduced inflammation, and reduced blood pressure.[40] Studies have suggested that for people in intensive care, an intermittent fasting regimen might "[preserve] energy supply to vital organs and tissues... [and] powerfully activates cell-protective and cellular repair pathways, including autophagy, mitochondrial biogenesis and antioxidant defenses, which may promote resilience to cellular stress."[41] The effects of decreased serum glucose and depleted hepatic glycogen causing the body to switch to ketogenic metabolism are similar to the effects of reduced carbohydrate-based diets.[citation needed] There is evidence demonstrating profound metabolic benefits of intermittent fasting in rodents.[22] However, evidence is lacking or contradictory in humans and requires further investigation, especially over the long-term.[22] Some evidence suggests that intermittent restriction of caloric intake has no weight-loss advantages over continuous calorie restriction plans.[42][22] For adults, fasting diets appear to be safe and tolerable, however there is a possibility that periods of fasting and hunger could lead to overeating[22] and to weight regain after the fasting period.[22] Adverse effects of fasting are often moderate and include halitosis, fatigue, weakness, and headaches.[22] Fasting diets may be harmful to children and the elderly.[22]

Exclusion Diet

[edit]

This type of diet is based on the restriction of specific foods or food groups. Examples include gluten-free, Paleo, plant-based, and Mediterranean diets.

Plant-based diets include vegetarian and vegan diets, and can range from the simple exclusion of meat products to diets that only include raw vegetables, fruits, nuts, seeds, legumes, and sprouted grains.[43] Exclusion of animal products can reduce the intake of certain nutrients, which might lead to nutritional deficiencies of protein, iron, zinc, calcium, and vitamins D and B12.[43] Therefore, long term implementation of a plant-based diet requires effective counseling and nutritional supplementation as necessary. Plant-based diets are effective for short-term treatment of overweight and obesity, likely due to the high consumption of low energy density foods.[22] However, evidence for long-term efficacy is limited.[22]

The Paleo diet includes foods that it identifies as having been available to Paleolithic peoples[44][45] including meat, nuts, eggs, some oils, fresh fruits, and vegetables.[22] Overall, it is high in protein and moderate in fats and carbohydrates. Some limited evidence suggests various health benefits and effective weight loss with this diet. However, similar to the plant-based diet, the Paleo diet has potential nutritional deficiency risks, specifically with vitamin D, calcium, and iodine.[22]

Gluten-free diets are often used for weight loss but little has been studied about the efficacy of this diet and metabolic mechanism for its effectiveness is unclear.[22]

The Mediterranean diet is characterized by high consumption of vegetables, fruits, legumes, whole-grain cereals, seafood, olive oil, and nuts. Red meat, dairy and alcohol are only recommended in moderation. Studies show that the Mediterranean diet is associated with short term as well as long term weight loss in addition to health and metabolic benefits.[22]

Detox

[edit]
Main article: Detox diet

Detox diets are promoted with unsubstantiated claims that they can eliminate "toxins" from the human body. Many of these diets use herbs or celery and other juicy low-calorie vegetables. Detox diets can include fasting or exclusion (as in juice fasting). Detox diets tend to result in short-term weight loss (because of calorie restriction), followed by weight gain.[46]

Environmentally sustainable

[edit]
See also: Environmental vegetarianism

Another kind of diet focuses not on the dieter's health effects, but on its environment. The One Blue Dot plan of the BDA[47] offers recommendations towards reducing diets' environmental impacts, by:

  1. Reducing meat to 70g per person per day.
  2. Prioritising plant proteins.
  3. Promoting fish from sustainable sources.
  4. Moderate dairy consumption.
  5. Focusing on wholegrain starchy foods.
  6. Promoting seasonal locally sourced fruits and vegetables.
  7. Reducing high fat, sugar and salty foods overconsumption.
  8. Promoting tap water and unsweetened tea/coffee as the de facto choice for healthy hydration.
  9. Reducing food waste.

Effectiveness

[edit]

Several diets are effective for short-term weight loss for obese individuals,[10][2] with diet success most predicted by adherence and little effect resulting from the type or brand of diet.[2][5][21][48][49][50] As weight maintenance depends on calorie intake,[2][3] diets emphasising certain macronutrients (low-fat, low-carbohydrate, etc.) have been shown to be no more effective than one another and no more effective than diets that maintain a typical mix of foods with smaller portions and perhaps some substitutions (e.g. low-fat milk, or less salad dressing).[51][4][52] A meta-analysis of six randomized controlled trials found no difference between low-calorie, low-carbohydrate, and low-fat diets in terms of short-term weight loss, with a 2–4 kilogram weight loss over 12–18 months in all studies.[1] Diets that severely restrict calorie intake do not lead to long term weight loss.[7] Extreme diets may, in some cases, lead to malnutrition.

A major challenge regarding weight loss and dieting relates to compliance.[2] While dieting can effectively promote weight loss in the short term, the intervention is hard to maintain over time and suppresses skeletal muscle thermogenesis. Suppressed thermogenesis accelerates weight regain once the diet stops, unless that phase is accompanied by a well-timed exercise intervention, as described by the Summermatter cycle.[53] Most diet studies do not assess long-term weight loss.[2]

Some studies have found that, on average, short-term dieting results in a "meaningful" long-term weight-loss, although limited because of gradual 1 to 2 kg/year weight regain.[10][2][6] Because people who do not participate in weight-loss programs also tend to gain weight over time, and baseline data from such "untreated" participants are typically not included in diet studies, it is possible that diets do result in lower weights in the long-term relative to people who do not diet.[2] Others have suggested that dieting is ineffective as a long-term intervention.[7] For each individual, the results will be different, with some even regaining more weight than they lost, while a few others achieve a tremendous loss, so that the "average weight loss" of a diet is not indicative of the results other dieters may achieve.[2][7] A 2001 meta-analysis of 29 American studies found that participants of structured weight-loss programs maintained an average of 23% (3 kg) of their initial weight loss after five years, representing a sustained 3.2% reduction in body mass.[6] Unfortunately, patients are generally unhappy with weight loss of <10%,[2] and reductions even as high as 10% are insufficient for changing someone with an "obese" BMI to a "normal weight" BMI.

Partly because diets do not reliably produce long-term positive health outcomes, some argue against using weight loss as a goal, preferring other measures of health such as improvements in cardiovascular biomarkers,[54][55] sometimes called a Health at Every Size (HAES) approach[56] or a "weight neutral" approach.[57]

Long term losses from dieting are best maintained with continuing professional support, long term increases in physical activity, the use of anti-obesity medications, continued use of meal replacements, and additional periods of dieting to undo weight regain.[2] The most effective approach to weight loss is an in-person, high-intensity, comprehensive lifestyle intervention: overweight or obese adults should maintain regular (at least monthly) contact with a trained interventionalist who can help them engage in exercise, monitor their body weight, and reduce their calorie consumption.[10] Even with high-intensity, comprehensive lifestyle interventions (consisting of diet, physical exercise, and bimonthly or even more frequent contact with trained interventionists), gradual weight regain of 1–2 kg/year still occurs.[10] For patients at high medical risk, bariatric surgery or medications may be warranted in addition to the lifestyle intervention, as dieting by itself may not lead to sustained weight loss.[10]

Many studies overestimate the benefits of calorie restriction because the studies confound exercise and diet (testing the effects of diet and exercise as a combined intervention, rather than the effects of diet alone).[58]

Adverse effects

[edit]

Increased mortality rate

[edit]

A number of studies have found that intentional weight loss is associated with an increase in mortality in people without weight-related health problems.[59][60][61][62] A 2009 meta-analysis of 26 studies found that "intentional weight loss had a small benefit for individuals classified as unhealthy (with obesity-related risk factors), especially unhealthy obese, but appeared to be associated with slightly increased mortality for healthy individuals, and for those who were overweight but not obese."[9]

Dietary supplements

[edit]

Due to extreme or unbalanced diets, dietary supplements are sometimes taken in an attempt to replace missing vitamins or minerals. While some supplements could be helpful for people eating an unbalanced diet (if replacing essential nutrients, for example), overdosing on any dietary supplement can cause a range of side effects depending on the supplement and dose that is taken.[63] Supplements should not replace foods that are important to a healthy diet.[63]

Eating disorders

[edit]

In an editorial for Psychological Medicine, George Hsu concludes that dieting is likely to lead to the development of an eating disorder in the presence of certain risk factors.[64] A 2006 study found that dieting and unhealthy weight-control behaviors were predictive of obesity and eating disorders five years later, with the authors recommending a "shift away from dieting and drastic weight-control measures toward the long-term implementation of healthful eating and physical activity".[65]

Mechanism

[edit]

When the body is expending more energy than it is consuming (e.g. when exercising), the body's cells rely on internally stored energy sources, such as complex carbohydrates and fats, for energy. The first source to which the body turns is glycogen (by glycogenolysis). Glycogen is a complex carbohydrate, 65% of which is stored in skeletal muscles and the remainder in the liver (totaling about 2,000 kcal in the whole body). It is created from the excess of ingested macronutrients, mainly carbohydrates. When glycogen is nearly depleted, the body begins lipolysis, the mobilization and catabolism of fat stores for energy. In this process fats, obtained from adipose tissue, or fat cells, are broken down into glycerol and fatty acids, which can be used to generate energy.[66] The primary by-products of metabolism are carbon dioxide and water; carbon dioxide is expelled through the respiratory system.

Set-Point Theory

[edit]
See also: Energy homeostasis § Imbalance

The Set-Point Theory, first introduced in 1953, postulated that each body has a preprogrammed fixed weight, with regulatory mechanisms to compensate. This theory was quickly adopted and used to explain failures in developing effective and sustained weight loss procedures. A 2019 systematic review of multiple weight change procedures, including alternate day fasting and time-restricted feeding but also exercise and overeating, found systematic "energetic errors" for all these procedures. This shows that the body cannot precisely compensate for errors in energy/calorie intake, countering the Set-Point Theory and potentially explaining both weight loss and weight gain such as obesity. This review was conducted on short-term studies, therefore such a mechanism cannot be excluded in the long term, as evidence is currently lacking on this timeframe.[67]

Methods

[edit]

Meal timing

[edit]

A meal timing schedule is known to be an important factor of any diet. Recent evidence suggest that new scheduling strategies, such as intermittent fasting or skipping meals, and strategically placed snacks before meals, may be recommendable to reduce cardiovascular risks as part of a broader lifestyle and dietary change.[68]

Food diary

[edit]

A 2008 study published in the American Journal of Preventive Medicine showed that dieters who kept a daily food diary (or diet journal), lost twice as much weight as those who did not keep a food log, suggesting that if a person records their eating, they are more aware of what they consume and therefore eat fewer calories.[69]

Water

[edit]
Main article: Weight loss effects of water

A 2009 review found limited evidence suggesting that encouraging water consumption and substituting energy-free beverages for energy-containing beverages (i.e., reducing caloric intake) may facilitate weight management. A 2009 article found that drinking 500 ml of water prior to meals for a 12-week period resulted in increased long-term weight reduction. (References given in main article.)

Society

[edit]

It is estimated that about 1 out of 3 Americans is dieting at any given time. 85% of dieters are women. Approximately sixty billion dollars are spent every year in the USA on diet products, including "diet foods", such as light sodas, gym memberships or specific regimes.[70][71] 80% of dieters start by themselves, whereas 20% see a professional or join a paid program. The typical dieter attempts 4 tries per year.[72]

Weight loss groups

[edit]

Some weight loss groups aim to make money, others work as charities. The former include Weight Watchers and Peertrainer. The latter include Overeaters Anonymous, TOPS Club and groups run by local organizations.

These organizations' customs and practices differ widely. Some groups are modelled on twelve-step programs, while others are quite informal. Some groups advocate certain prepared foods or special menus, while others train dieters to make healthy choices from restaurant menus and while grocery-shopping and cooking.[citation needed]

Attending group meetings for weight reduction programmes rather than receiving one-on-one support may increase the likelihood that obese people will lose weight. Those who participated in groups had more treatment time and were more likely to lose enough weight to improve their health. Study authors suggested that one explanation for the difference is that group participants spent more time with the clinician (or whoever delivered the programme) than those receiving one-on-one support.[73][74]

See also

[edit]

References

[edit]

Further reading

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Dieting

View on Grokipedia
from Grokipedia

Dieting is the intentional restriction of caloric intake or modification of dietary composition aimed primarily at reducing body weight or improving metabolic health. First popularized in the 1860s by , a British undertaker who achieved substantial through a low-carbohydrate regimen emphasizing protein and fats while avoiding sugars and starches, the practice has since encompassed a range of approaches including low-fat, low-calorie, and macronutrient-specific strategies. Empirical studies confirm that dieting induces short-term weight loss via energy deficits, with various protocols yielding comparable results when adherence is maintained, but long-term outcomes reveal high relapse rates, as metabolic adaptations reduce resting energy expenditure and behavioral factors undermine sustainability. Controversies center on macronutrient emphases, with recent evidence favoring lower-carbohydrate diets for superior , glycemic control, and cardiovascular risk reduction over historically promoted low-fat models, highlighting limitations in prior consensus driven by incomplete data. Despite these challenges, even modest, sustained weight reductions of 5% or more correlate with improved health markers such as and insulin sensitivity, underscoring dieting's potential when integrated with lifestyle modifications rather than transient restriction.

Overview and Definitions

Core Principles and Goals

The primary goal of dieting is to induce a reduction in body and overall weight by establishing a negative energy balance, wherein caloric intake falls below total energy expenditure over time. This principle derives from the as governed by the first law of , which applies to human physiology: excess energy intake leads to storage as , while a deficit mobilizes stored for fuel, resulting in measurable weight of approximately 1 pound per 3,500 kcal deficit. Empirical from controlled trials confirm that sustained deficits of 500–1,000 kcal daily yield 0.5–1 kg weekly without compromising essential metabolic functions, provided protein intake remains adequate to preserve lean . Key principles emphasize selecting whole, unprocessed foods rich in protein, , and micronutrients to promote and metabolic efficiency during restriction, rather than relying solely on caloric counting, which often proves unsustainable. Diets incorporating these elements—such as moderate reduction or high intake—enhance adherence by mitigating signals driven by glycemic fluctuations, with meta-analyses showing superior short-term outcomes compared to unrestricted low-fat approaches. Prevention of regain forms a foundational goal, as regain rates exceed 80% within five years post-diet in observational cohorts; thus, principles prioritize gradual loss (no more than 1–2% body weight monthly) to minimize adaptive , wherein declines disproportionately to lost mass. While weight loss predominates, dieting pursues ancillary objectives including improved insulin sensitivity, lowered inflammation, and reduced cardiovascular risk factors, as evidenced by interventions yielding 5–10% body weight reduction correlating with 20–30% drops in HbA1c and LDL cholesterol independent of specific macronutrient ratios. These outcomes underscore dieting's role in reversing obesity-related pathologies, though benefits accrue primarily through fat mobilization rather than caloric restriction alone, with long-term viability hinging on behavioral integration over pharmacological or surgical alternatives.

Distinction from Lifestyle Changes

Dieting generally involves intentional, temporary restrictions on calorie intake or specific food groups to induce short-term weight loss, often through structured regimens like low-calorie or elimination diets. In contrast, lifestyle changes prioritize sustainable, holistic shifts in eating habits, physical activity levels, and behavioral patterns, such as incorporating regular exercise and balanced nutrition without rigid timelines or eliminations, aiming for enduring weight management and overall metabolic health. This distinction arises from the causal reality that acute energy deficits in dieting trigger adaptive physiological responses, including reduced metabolic rate and increased hunger signaling, which facilitate weight regain upon cessation, whereas gradual habit formation in lifestyle approaches aligns with long-term energy balance without such rebound effects. Empirical data underscore the divergence in outcomes: a of 29 long-term studies found that more than 50% of lost weight is typically regained within two years, rising to over 80% by five years, largely due to the impermanence of restrictive dieting protocols. Conversely, interventions emphasizing lifestyle modification—combining diet, exercise, and behavior —demonstrate superior maintenance rates, with sustained adoption linked to up to 8.9 years of additional in modeling studies of dietary pattern shifts toward evidence-based guidelines. Qualitative analyses of successful long-term weight maintainers highlight strategies like consistent and flexible eating, which mitigate the cycling associated with repeated dieting attempts, where physiological counter-regulation preserves energy stores and promotes regain. While short-term dieting can achieve initial losses effectively through energy restriction, its reliance on willpower-intensive deprivation often undermines adherence, as evidenced by estimates that only about 20% of individuals maintain significant loss beyond a year. Lifestyle changes, by fostering in habits via repeated exposure and environmental cues, better counteract metabolic adaptations like set-point defense, though both require ongoing vigilance against modern obesogenic environments. Peer-reviewed evidence consistently favors the latter for causal durability in preventing obesity-related comorbidities, prioritizing empirical over transient results.

Historical Context

Early Practices and Cultural Origins

The concept of dieting for weight management originated in ancient medical traditions, where excess body fat was recognized as a health risk primarily among elites, often linked to sedentary lifestyles and overconsumption of calorie-dense foods. In ancient India, texts like the Charaka Samhita (circa 300 BCE) and Sushruta Samhita (circa 600 BCE) described sthaulya (obesity) as a disorder arising from impaired digestion (agni), overindulgence in sweet and fatty substances, and lack of physical activity, recommending treatments such as vigorous exercise, light barley-based diets, fasting, and herbal preparations like honey and medohara (fat-reducing) drugs to restore metabolic balance. Similarly, in ancient China, legendary emperor Shen Nong (circa 2695 BCE) is associated with using green tea to mitigate obesity among nobility accustomed to heavy feasting, though empirical evidence for widespread practice remains anecdotal. In the , dieting emerged as part of a holistic diaita (regimen of life) emphasizing moderation for physical and , with viewed as a humoral imbalance favoring moist and phlegmatic conditions. (circa 460–370 BCE), often called the father of medicine, advised corpulent individuals to engage in hard labor or exercise before meals—such as walking or running on an empty —followed by sparse intake of lean foods and diluted wine, while avoiding to prevent sudden death and other ailments linked to fatness. Spartan culture (circa 900–800 BCE) institutionalized anti- measures through mandatory physical training and communal meals designed to promote lean physiques, banning luxurious foods that fostered fat accumulation. (circa 570–495 BCE) further advocated dietary restraint and to curb gluttony, influencing later philosophical views on self-control. Later Greco-Roman physicians built on these foundations; (2nd century CE) prescribed exercise, , , and purgatives like vinegar-induced to reduce excess flesh, while Caelius Aurelianus (5th century CE) stressed and caloric restriction. These practices prioritized causal mechanisms—such as expending through labor to offset intake—over mere , reflecting empirical observations of obesity's rarity in labor-intensive societies but its prevalence in affluent, inactive groups.

20th-Century Shifts and Commercialization

In the early , dieting shifted toward scientific quantification with the popularization of calorie counting as a primary mechanism for weight control. Lulu Hunt Peters, one of the first women in the United States to earn a medical doctorate, published Diet and Health: With Key to the Calories in 1918, which became the first bestselling diet book and introduced widespread awareness of restricting caloric intake to achieve . This approach reframed food consumption as a measurable energy input, influencing cookbooks, public advice columns, and personal regimens, particularly amid emphases on rational self-discipline and efficiency. Commercialization accelerated in the and , driven by cultural ideals of slenderness promoted through media and , especially targeting women via the flapper aesthetic and Hollywood imagery. Pharmaceutical interventions emerged, with extracts used off-label for since the late and amphetamine-based drugs like Benzedrine prescribed for weight suppression by the , reflecting a demand for pharmacological shortcuts amid rising consumer culture. companies marketed cigarettes, such as , as appetite suppressants in the "Reach for a Lucky instead of a sweet" campaigns of the , blending dieting with emerging products despite later evidence of risks. Post-World War II abundance and increasing obesity prevalence fueled the mass-market diet industry, with organized programs and branded products proliferating. Weight Watchers, founded in 1963 by after informal group meetings for mutual accountability, incorporated as a that year and expanded rapidly through franchised meetings emphasizing behavioral support and portion control, achieving significant revenue growth by the 1980s. This era saw the rise of shakes, prepackaged foods, and diet books as commercial staples, transforming dieting from personal efforts into a multibillion-dollar sector by the late , often prioritizing short-term appeal over sustained empirical validation of efficacy.

Modern Era and Public Health Campaigns

In the late 20th century, U.S. public health authorities responded to rising concerns over by issuing formal dietary guidelines, beginning with the 1980 , which advised avoiding excessive , , and while increasing intake of starchy, fiber-rich foods. This marked a shift toward population-wide recommendations emphasizing reduced overall consumption to approximately 30% of calories, influenced by observational studies linking dietary to heart disease, though subsequent analyses have questioned the causal evidence due to confounding factors like sugar intake and variables. The 1992 USDA Food Guide Pyramid institutionalized these principles, positioning 6-11 daily servings of grains at the base—predominantly refined carbohydrates—while relegating fats and oils to the apex as "use sparingly." This visual tool, intended to simplify , spurred widespread adoption of low-fat processed foods by the , often compensated with added sugars and refined carbs to maintain , contributing to increased caloric density without addressing mechanisms. Critics, including analyses of metabolic trial data, argue the pyramid's carbohydrate emphasis exacerbated and weight gain by prioritizing energy-dense, low-nutrient staples over protein and healthy fats, which better regulate hunger hormones like and . Concurrent with these guidelines, adult prevalence in the U.S. tripled from about 13% in the early to over 40% by the 2010s, as tracked by CDC and Nutrition Examination Surveys, undermining claims of efficacy for broad low-fat messaging. campaigns, such as the WHO's global prevention efforts starting in the 1990s and U.S. initiatives like the CDC's 2009 community strategies for and promotion, focused on environmental changes like reducing portion sizes and increasing intake but often retained calorie-restriction paradigms without robust evidence for long-term adherence or metabolic adaptation countermeasures. Evaluations indicate limited population-level impact, with critiques highlighting overreliance on correlational and underappreciation of hormonal drivers of , such as chronic from high-glycemic loads. By the 2010s, revisions like the shift to in 2011 attempted corrections by de-emphasizing grains and promoting half-plate fruits/vegetables, yet institutional inertia—rooted in entrenched low-fat orthodoxy from mid-century cohort studies—delayed broader acknowledgment of low-carbohydrate approaches' superior short-term outcomes in randomized trials. Campaigns such as Michelle Obama's Let's Move! (launched 2010) targeted through reforms and exercise, achieving modest reductions in sugary drink consumption but failing to reverse overall trends, as evidenced by persistent rises in severe rates to 9.2% among adults by 2017-2018. These efforts underscore a pattern where strategies, while data-informed on aggregate risks, have historically undervalued individualized metabolic responses and overemphasized simplistic behavioral nudges amid environmental obesogens like ultra-processed foods.

Biological Foundations

Energy Balance and Thermodynamics

The principle of energy balance in human physiology is governed by the first law of thermodynamics, which states that energy cannot be created or destroyed in a ; thus, changes in body energy stores equal the difference between energy intake (primarily from ) and expenditure (including , , thermic effect of food, and adaptive thermogenesis). In the context of dieting, sustained requires a balance, where expenditure exceeds intake, prompting the oxidation of stored triglycerides in to provide approximately 9 kcal per gram of fat mobilized, though this process also involves water and lean mass losses that complicate net calculations. Empirical models, such as those derived from studies, confirm that a deficit of roughly 7,700 kcal corresponds to one of body fat loss under controlled conditions, but real-world applications deviate due to incomplete accounting for fecal energy loss and variable storage efficiency. Thermodynamic considerations extend beyond simple intake-expenditure arithmetic, as the second law introduces inefficiencies in energy conversion; for instance, converting dietary carbohydrates to stored fat dissipates more heat than storing dietary fat directly, implying that macronutrient composition influences the effective energy surplus or deficit beyond nominal caloric values. This has led to debates over whether equating "a calorie is a calorie" oversimplifies obesity causation, with some analyses arguing it neglects pathway-specific thermodynamic costs that affect partitioning of energy into fat versus lean tissue. Nonetheless, longitudinal trials consistently demonstrate that negative energy balance, regardless of dietary composition, drives short-term fat loss, as validated by controlled feeding studies where energy deficits of 20-30% of total expenditure yield 0.5-1 kg weekly reductions initially. A key biological complication arises from metabolic adaptation during prolonged deficits: resting energy expenditure declines disproportionately to lost metabolically active mass (e.g., by 10-15% beyond predictions after 10% body weight loss), driven by reduced activity, thyroid downregulation, and efficiency changes, thereby attenuating the rate of further loss and contributing to weight plateaus observed in 80-90% of dieters within 6-12 months. This adaptation, quantified in overfeeding and underfeeding experiments, underscores that while mandates a deficit for loss, physiological feedback resists it, often requiring escalating behavioral efforts to maintain balance, as signals from increase concurrently. Such dynamics explain why dynamic models of balance, incorporating time-dependent expenditure adjustments, better predict outcomes than static caloric prescriptions.

Hormonal and Metabolic Regulation

Caloric restriction during dieting induces profound hormonal shifts that favor energy conservation and appetite stimulation, counteracting sustained weight loss. , an adipocyte-derived hormone signaling satiety to the , declines proportionally with fat mass reduction, persisting even after one year of maintenance in studies of obese individuals who lost 10-20% body weight, thereby diminishing suppression of hunger and increasing drive to restore fat stores. Concurrently, , a gastric orexigenic hormone, rises post-weight loss, enhancing appetite and food intake; this elevation correlates with greater weight regain risk, as baseline ghrelin levels inversely predict long-term success in dieters. Insulin sensitivity often improves initially with fat loss, but chronic caloric deficits lower circulating insulin, which in turn reduces anabolic signaling and promotes while adapting the body toward a thriftier metabolic state. , particularly (T3), decrease during restriction, contributing to lowered independent of changes; animal and human data show T3 reductions of 20-30% in prolonged deficits, slowing energy expenditure. (GH) and (DHEA-S) also fall, impairing muscle preservation and further attenuating metabolic rate. Metabolic manifests as a disproportionate drop in resting expenditure (REE), exceeding predictions based on fat-free loss alone, observed in up to 15-20% reductions beyond expected in clinical trials of low-energy diets. This , evident after 10-15% weight , delays goal achievement by 2-3 months in modeling studies of women and associates with inferior fat reduction in obesity interventions. Exercise combined with restriction mitigates some REE decline compared to diet alone, preserving fat-free and insulin dynamics more effectively in randomized comparisons. elevations from dieting stress may exacerbate central fat retention, though links this more to psychological strain than restriction per se, with chronic highs promoting visceral adiposity via receptors. These regulatory mechanisms, rooted in evolutionary survival responses to , explain the biological resistance to reversal, with hormonal persistence documented up to six years post-loss in longitudinal cohorts. Variability in adaptation—modulated by , , and initial body weight—underlies individual differences in dieting outcomes, underscoring the need for strategies addressing both behavioral and physiological drivers.

Set-Point and Adaptive Responses

The set-point theory posits that the body maintains body weight around a preferred level through homeostatic feedback mechanisms that resist changes, particularly reductions in adiposity, by altering and expenditure to defend a genetically influenced target weight. These mechanisms evolved to promote during periods of , prioritizing storage and conservation over facile depletion. Empirical observations, such as the tendency for weight regain following intentional loss, support the existence of active biological regulation, though the theory relies on inductive patterns rather than direct causal proof of a rigid "set point." Caloric restriction triggers adaptive responses, including metabolic adaptation, where resting metabolic rate (RMR) declines beyond predictions based on lost fat-free mass, a phenomenon termed adaptive thermogenesis. Metabolic adaptation typically starts after 2–3 weeks of caloric restriction, manifesting in both lean and obese individuals and creating a physiological barrier to sustained weight reduction by reducing daily energy needs by 100–500 kcal or more, depending on the degree of deficit; its severity is usually 10–20% below predicted RMR, varying by genetics, age, and sex, and is strongest with >10–15% weight loss. For instance, participants in "The Biggest Loser" study exhibited approximately 500 kcal/day slower metabolism six years post-intervention. Systematic reviews of controlled studies confirm adaptive thermogenesis occurs after negative energy balance, with inpatient trials showing early adaptations predicting poorer weight loss outcomes over 6 weeks of 50% caloric restriction. Accompanying changes involve reduced non-exercise activity (NEAT) and heightened orexigenic signaling, amplifying via shifts in hormones like and , though precise quantification varies across studies. In low-energy-deficit protocols, such as those yielding 10–15% body , metabolic adaptation averages 50–150 kcal/day below expected, correlating with diminished reduction and increased regain risk. Higher-protein diets may partially mitigate this by preserving RMR during phases post-loss. Debate persists on adaptation's magnitude and causality in regain; while reductions in RMR are verifiable, some analyses attribute apparent effects to measurement artifacts or incomplete stabilization post-loss, with no direct longitudinal link to inevitable failure in all cases. Critics argue for a "settling point" model, where environmental and behavioral factors modulate the regulated range rather than enforcing a fixed defense, emphasizing that sustained habits can shift effective over time. Nonetheless, these responses underscore why short-term dieting success rarely translates to permanence without counter-strategies like gradual deficits or exercise to offset efficiency losses.

Types of Diets

Macronutrient Manipulation Diets

Macronutrient manipulation diets adjust the proportions of carbohydrates, proteins, and fats consumed, often while creating a , to influence intake, , metabolic responses, and changes. These approaches operate on the premise that macronutrient ratios can affect hunger signals, , and substrate utilization beyond simple counting, though empirical data indicate that total balance remains the primary driver of weight outcomes. Common variants include low-carbohydrate, high-protein, and low-fat regimens, each emphasizing different macros to exploit physiological responses such as reduced insulin secretion in low-carb plans or enhanced muscle retention in high-protein ones. Low-carbohydrate diets typically limit intake to under 130 grams per day, with ketogenic variants restricting to 20-50 grams to induce , shifting toward oxidation and production for . Systematic reviews show these diets produce greater short-term than low-fat alternatives, averaging 1-2 kg more over 6-12 months, attributed to initial depletion—which releases bound water (approximately 3-4 grams per gram of glycogen) and induces diuresis—and natriuresis from reduced insulin levels, leading to temporarily increased urination, alongside suppression via elevated free fatty acids and ketones. This effect is transient, resolving after initial adaptation, with sustained fat loss not causing ongoing elevated urine volume. A 2022 of randomized trials confirmed low-carb diets improve metabolic markers like triglycerides and HDL more effectively than low-fat diets in the first year. However, long-term adherence challenges limit sustained benefits, with weight regain common upon reintroducing carbohydrates. High-protein diets elevate intake to 25-30% of calories (1.2-1.6 g/kg body weight), promoting through amino acid-induced release and preserving lean mass during caloric restriction via reduced . Clinical trials demonstrate that higher protein consumption during energy deficit enhances loss while minimizing muscle , with one review of interventions showing 0.5-1 kg greater reduction compared to standard-protein diets over 12 weeks. Mechanisms include increased diet-induced (20-30% of protein calories vs. 5-10% for carbs/fats) and hormonal shifts favoring mobilization. These diets often combine with resistance training for optimal outcomes, as evidenced by studies in adults achieving 1-2% higher lean mass retention. Low-fat diets restrict to under 30% of calories, substituting with carbohydrates to leverage fat's high caloric (9 kcal/g vs. 4 kcal/g for carbs/protein) and lower per , though very low-fat versions like the Ornish program limit to 10% while emphasizing plant-based foods. Randomized comparisons, such as a 2005 trial of Atkins (low-carb), Ornish (very low-fat), Zone, and LEARN diets, found modest across groups (2-4 kg at one year) but low adherence rates below 50%, with Ornish yielding smaller LDL reductions initially that waned over time. Meta-analyses indicate low-fat diets achieve comparable long-term to low-carb when calories are equated, but inferior short-term results due to higher glycemic loads potentially exacerbating hunger.
Diet TypeTypical Macro Ratio (% calories: Carb/Protein/Fat)Key MechanismShort-Term Weight Loss Edge (vs. Balanced)
Low-Carb/Ketogenic5-10/20/70-80, reduced insulin+1-2 kg at 6-12 months
High-Protein40-50/25-30/25-30, thermogenesis+0.5-1 kg fat loss at 12 weeks
Low-Fat (e.g., Ornish)70-80/15-20/<10-30Calorie dilution via low-density foodsEquivalent long-term, less short-term
Overall, while macronutrient shifts can facilitate initial adherence and metabolic adaptations, evidence from controlled trials underscores that differences in weight loss primarily stem from caloric intake rather than inherent metabolic advantages, with individual variability in insulin sensitivity influencing responses.

Time-Restricted and Intermittent Approaches

Time-restricted eating (TRE) involves confining caloric intake to a specific daily window, typically 8-12 hours, with fasting for the remainder, such as the common 16:8 protocol where eating occurs between noon and 8 p.m.. This approach aligns food consumption with circadian rhythms, potentially enhancing metabolic efficiency without mandating precise calorie counting. Intermittent fasting (IF) encompasses TRE but extends to periodic full or partial fasts, including alternate-day fasting (ADF), where calories are restricted to 500-600 on fasting days alternating with ad libitum eating, and the 5:2 method, limiting intake to 500-600 calories on two non-consecutive days per week while eating normally otherwise. These strategies gained prominence in the 2010s through proponents like Valter Longo and Jason Fung, emphasizing hormonal adaptations over sustained caloric deficits. Randomized controlled trials (RCTs) demonstrate that TRE induces modest weight loss, averaging 2-5% of body weight over 8-12 weeks in overweight adults, primarily through spontaneous reductions in overall energy intake rather than unique metabolic shifts. A 2023 meta-analysis of 19 RCTs found TRE with calorie restriction yielded greater reductions in body weight (-1.40 kg), fat mass, and waist circumference compared to calorie restriction alone, though effects diminished without explicit caloric limits. In type 2 diabetes patients, a 6-month RCT showed TRE achieving -3.6% weight loss versus -1.8% with daily calorie restriction, alongside improved glycemic control, suggesting potential adjunctive value in specific populations. However, isocaloric comparisons often reveal no superiority, as a 2022 NEJM trial reported equivalent fat loss between TRE and standard dieting in obese adults. For broader IF protocols, meta-analyses indicate small to trivial weight reductions, comparable to continuous calorie restriction, with ADF and 5:2 yielding 3-8% loss over 3-12 months but high dropout rates due to hunger and adherence challenges. A 2024 network meta-analysis confirmed IF variants like TRE and ADF produce similar short-term fat mass decreases to daily restriction, without preserving lean mass better in most cases. Long-term data remain sparse, with regain common post-intervention, mirroring other diets, and no evidence of sustained metabolic advantages independent of calorie deficits. While some studies report cardiometabolic benefits like lowered insulin resistance, these correlate with weight loss magnitude rather than fasting timing. Critics note that self-reported adherence inflates efficacy in non-supervised settings, and benefits may stem from behavioral simplicity rather than physiological novelty.

Elimination and Specialized Diets

Elimination diets involve systematically removing suspected food triggers, such as common allergens or irritants like gluten, dairy, soy, eggs, nuts, and additives, for a period typically lasting 2-6 weeks, followed by gradual reintroduction to identify intolerances. These approaches aim primarily to alleviate symptoms from sensitivities rather than achieve weight loss, though proponents claim they can indirectly support fat reduction by reducing inflammation or improving that hinders adherence to calorie deficits. A 2016 study of overweight patients with confirmed food intolerances via IgG testing found that an elimination diet tailored to those results led to significant reductions in body weight (mean 5.2 kg over 4 weeks) and fat mass, outperforming standard low-calorie diets in non-responders, suggesting utility when underlying intolerances impede metabolic responses. However, broader evidence indicates elimination diets are not designed or proven for sustainable weight management in the general population, as restrictive removal of food groups risks nutrient deficiencies without addressing energy balance fundamentals, and experts caution against their use solely for pounds lost due to potential malnutrition. Specialized diets extend elimination principles by permanently excluding broad categories deemed incompatible with human physiology or modern processing, often drawing on evolutionary or biochemical rationales. The gluten-free diet, for instance, eliminates wheat, barley, and rye proteins despite lacking evidence of benefit for non-celiac individuals seeking weight loss; a 2012 review concluded no published data support fat reduction from gluten avoidance in those without celiac disease or sensitivity, with many gluten-free products higher in calories and sugars, potentially promoting gain. Similarly, the low-FODMAP diet restricts fermentable oligosaccharides, disaccharides, monosaccharides, and polyols to manage irritable bowel syndrome symptoms but is not intended for obesity, though its exclusion of high-calorie triggers like certain fruits, grains, and legumes can incidentally lower intake; clinical guidance emphasizes monitoring to prevent unintended deficits in fiber or energy. Paleolithic diets, which eliminate grains, legumes, dairy, refined sugars, and processed oils in favor of meats, fish, vegetables, fruits, and nuts mimicking pre-agricultural eating, show modest short-term efficacy in meta-analyses. A 2019 review of randomized trials reported significant weight reductions (mean 3-5 kg over 3-6 months) and waist circumference decreases compared to controls, attributed to higher protein and fiber satiety reducing overall calories, though effects wane without sustained adherence and do not surpass balanced deficits long-term. The carnivore diet, an extreme variant confining intake to animal products only, lacks robust peer-reviewed trials but features self-reported weight loss in surveys, with 93% of adherents citing it as a primary motivator; mechanisms likely stem from zero-carbohydrate ketosis suppressing appetite, yet potential risks include micronutrient shortfalls (e.g., vitamin C, fiber) and elevated LDL cholesterol, underscoring the need for medical oversight absent causal evidence of superiority over less restrictive plans. Overall, these diets' weight outcomes hinge on caloric restriction rather than unique mechanisms, with limited comparative data revealing no consistent edge over standard interventions, and adherence challenges mirroring broader dieting patterns.

Empirical Evidence on Effectiveness

Short-Term Weight Loss Outcomes

Short-term weight loss outcomes from dieting interventions, defined as the initial 3 to 6 months, consistently demonstrate reductions of 5% to 9% of initial body weight across various approaches emphasizing caloric restriction.01483-6/abstract) A systematic review and meta-analysis of 80 randomized controlled trials involving reduced-energy diets, with or without exercise or pharmacotherapy, reported average losses of 5 to 8.5 kg during this period, equivalent to 5% to 9% of baseline weight, with very-low-energy diets achieving up to 16% loss by 3 months before tapering. These results hold irrespective of macronutrient composition, as evidenced by a head-to-head trial of low-fat, low-carbohydrate, and other diets, where participants lost an average of 6 kg (7% of initial weight) at 6 months across groups. The primary mechanism is a sustained energy deficit, leading to initial rapid depletion of glycogen stores—which releases bound water, causing temporary diuresis (increased urination)—and natriuresis from reduced insulin levels, resulting in associated water weight loss (often 1-2 kg in the first week), followed by fat mobilization; sustained fat loss does not typically cause ongoing increased urination. Intermittent fasting variants, such as alternate-day fasting or time-restricted eating, yield comparable short-term losses of 3% to 8% body weight, without superiority over continuous caloric restriction in randomized trials. Multicomponent interventions combining diet with physical activity further support these outcomes, with a meta-analysis of 14 short-term randomized controlled trials showing statistically significant weight reductions in adults with overweight or obesity. Individual variability exists, influenced by adherence, baseline metabolic factors, and intervention intensity, but even control groups in obesity trials exhibit modest losses of approximately 1-2 kg over similar durations due to heightened awareness or incidental changes. Primary care-based programs have documented average 6.5% losses (7 kg) at 6 months, accompanied by improvements in waist circumference and blood pressure, underscoring the feasibility of short-term caloric deficit strategies. However, these gains often plateau by month 6 as metabolic adaptations, such as reduced resting energy expenditure, emerge.

Long-Term Maintenance Challenges

A systematic review and meta-analysis of 29 U.S. studies on long-term weight-loss maintenance, published in 2001, found that while initial weight loss varied by diet type, sustained maintenance beyond one year was limited, with very-low-energy diets showing modestly better retention than hypoenergetic balanced diets, yet overall regain predominated in most cohorts. Subsequent analyses confirm this pattern: a 2022 systematic review and meta-analysis of low-calorie diet interventions reported that only about 25% of participants maintained significant weight loss long-term, with the majority regaining 50% or more of lost weight within 2-5 years post-intervention. Large-scale trials underscore these difficulties. In the Look AHEAD study, a randomized trial of 5,145 overweight or obese adults with type 2 diabetes, the intensive lifestyle intervention group achieved an average 8.6% body weight reduction at one year through calorie restriction and exercise, but this declined to 4.7% by year eight despite continued group sessions and support, reflecting gradual regain in the cohort. Two years after the intervention's termination in 2012, participants regained an average of 2.2 kg, erasing much of the sustained loss and highlighting the fragility of maintenance without indefinite oversight. Physiological mechanisms exacerbate these challenges. Weight loss induces adaptive reductions in resting energy expenditure—often exceeding predictions based solely on lost fat mass—and alterations in hunger hormones like ghrelin and leptin, promoting regain through increased appetite and energy conservation, as detailed in a 2025 review of post-loss physiology. Behavioral lapses compound this: adherence to calorie tracking and physical activity declines over time, with systematic reviews identifying inconsistent self-monitoring and environmental cues (e.g., food availability) as key relapse triggers. Data from successful outliers, such as the National Weight Control Registry (NWCR), which tracks over 10,000 individuals maintaining at least 13.6 kg loss for one year or longer (average 5.7 years), indicate that maintainers expend over 1,000 kcal weekly in physical activity (often exceeding 2,000 kcal) and adhere to structured eating patterns, yet these represent a self-selected minority amid broader failure rates. A 2023 analysis of behavioral weight management programs estimated that partial regain occurs in 80-90% of completers within four years, driven by the sustained effort required to counteract biological drives. Thus, long-term success demands perpetual vigilance, rendering it attainable for few without pharmacological or surgical adjuncts.

Comparative Studies Across Diet Types

Comparative randomized controlled trials and meta-analyses have consistently demonstrated that various diet types achieve similar weight loss outcomes when total energy intake is restricted, with differences primarily attributable to adherence rather than macronutrient composition or timing. A 2018 randomized trial involving 609 overweight adults (DIETFITS study) compared healthy low-fat diets (emphasizing whole grains, fruits, and vegetables) against healthy low-carbohydrate diets (focusing on vegetables, nuts, and lean proteins), finding no significant difference in 12-month weight change: median losses of 5.3 kg in the low-fat group and 6.0 kg in the low-carbohydrate group, despite genotype or insulin secretion patterns not predicting success. Similarly, a 2020 network meta-analysis of 121 randomized trials encompassing over 21,000 participants showed that low-fat, low-carbohydrate, and balanced macronutrient diets yielded modest weight reductions of 2-5 kg over six months, alongside cardiovascular risk improvements, but with no single approach superior across metrics like BMI or waist circumference. These findings underscore that sustained caloric deficits, rather than specific ratios, drive short-term efficacy, though individual preferences influence compliance. For macronutrient-manipulating diets, low-carbohydrate and ketogenic approaches often produce greater initial weight loss due to reduced appetite and water/glycogen depletion, but long-term results converge with low-fat alternatives. A 2022 Cochrane systematic review of 61 trials (n=4,555) concluded there is likely little to no difference in weight reduction between low-carbohydrate diets (≤130 g/day carbs) and balanced-carbohydrate diets up to two years, with mean differences under 1 kg and no sustained advantages in cardiovascular risk factors like LDL cholesterol or blood pressure. In contrast, a 2020 meta-analysis of 48 studies reported low-carbohydrate diets achieving 1-2 kg more weight loss than low-fat diets at 6-12 months, attributed to higher protein satiety, though this edge diminished beyond one year as adherence waned. Ketogenic diets (typically <50 g/day carbs) exhibit rapid short-term losses of up to 4.5 kg in the first weeks, per a 2023 umbrella review of meta-analyses, but a 2024 network meta-analysis of dietary interventions found ketogenic, Mediterranean, and low-fat diets similarly effective for body weight reduction in overweight adults over 6-12 months, with ketogenic showing modest benefits in triglyceride lowering but potential LDL elevations in susceptible individuals. Time-restricted and intermittent fasting regimens compare favorably to continuous calorie restriction in short-term trials but lack superiority in metabolic or weight maintenance outcomes. A 2024 systematic review and meta-analysis of 18 trials (n=1,228) found intermittent fasting (e.g., 5:2 or alternate-day protocols) led to slightly greater short-term body weight reductions (mean difference 0.9-1.5 kg) than continuous restriction when isocaloric, possibly via enhanced fat oxidation, yet no differences in insulin sensitivity or lean mass preservation. However, a contemporaneous meta-analysis of 10 studies concluded isocaloric intermittent fasting is not superior to daily calorie restriction for health markers in adults, with both yielding 5-8% body weight loss over 3-12 months but equivalent cardiometabolic effects. Long-term data remain sparse; a 2022 trial of time-restricted eating versus standard restriction (both 1,800 kcal/day) in obese adults showed comparable 6-month losses of ~6-8 kg, with no added benefits from meal timing on energy expenditure or hormones like ghrelin.
Study/SourceDiets ComparedDurationKey Weight Loss OutcomeCitation
DIETFITS RCT (2018)Low-fat vs. low-carb12 months-5.3 kg vs. -6.0 kg (no sig. diff.)
Cochrane Review (2022)Low-carb vs. balanced-carbUp to 2 years<1 kg difference
Network Meta-Analysis (2024) vs. vs. low-fat6-12 monthsSimilar 5-10% reductions
IF vs. CR Meta (2024) vs. continuous restriction3-12 months0.9-1.5 kg greater short-term with IF
Across diet types, meta-analyses highlight adherence as the primary differentiator, with dropout rates of 20-40% in most trials due to palatability and lifestyle fit, leading to equivalent real-world efficacy when energy balance is equated. Long-term maintenance challenges persist uniformly, as evidenced by a 2015 meta-analysis of U.S. studies showing near-complete regain within five years post-intervention, irrespective of initial diet type. These patterns suggest that while specialized diets may offer motivational or physiological edges initially, no approach consistently outperforms others without addressing behavioral and metabolic adaptations.

Risks and Limitations

Physiological Adverse Effects

Caloric restriction and rapid weight loss through dieting often induce metabolic adaptation, characterized by a disproportionate reduction in resting energy expenditure (REE) beyond what is predicted by losses in fat and lean mass. This adaptation, observed in longitudinal studies, can persist for years post-weight loss, as evidenced by participants from the television program The Biggest Loser who exhibited REE deficits of approximately 500-800 kcal/day six years after intervention, independent of body composition changes. Such reductions stem from decreased sympathetic nervous system activity, lower thyroid hormone levels (e.g., triiodothyronine), and enhanced skeletal muscle efficiency, collectively hindering further fat loss and predisposing to regain. Dieting frequently results in significant lean body mass (LBM) loss, particularly when energy deficits exceed 20-25% without adequate protein intake or resistance training. In controlled trials, very-low-calorie diets (VLCDs, <800 kcal/day) have led to LBM reductions of 20-30% of total weight lost, impairing muscle function, strength, and basal metabolic rate. This catabolic state elevates cortisol and promotes proteolysis, exacerbating sarcopenia risk in older adults or those with insufficient exercise. Hormonal disruptions compound these effects, including suppressed gonadal steroids (e.g., testosterone in men, estradiol in women) and elevated ghrelin, which not only drive hunger but also correlate with reduced bone mineral density and reproductive function. Nutrient deficiencies and electrolyte imbalances arise from macronutrient manipulation or elimination diets, leading to physiological strain such as hypokalemia, hyponatremia, or micronutrient shortfalls (e.g., thiamine, magnesium). Rapid weight loss (>1.5 kg/week) increases formation risk by 10-25% due to bile supersaturation and stasis, as documented in meta-analyses of bariatric and VLCD cohorts. health suffers from chronic energy deficits, with studies showing 1-2% annual declines in bone mineral density, attributable to reduced , increased , and impaired calcium absorption. Additional effects include cold intolerance from lowered , impaired via synthesis deficits, and transient immune suppression reflected in reduced counts. While some adaptations (e.g., mild REE shifts) may stabilize with weight maintenance, severe restriction amplifies these risks, particularly in unsupervised contexts.

Psychological and Behavioral Consequences

Dieting, particularly through caloric restriction, frequently induces psychological distress including preoccupation with , , and depressive symptoms, as observed in controlled studies of semi-starvation where participants exhibited obsessive thoughts about eating and emotional volatility. Longitudinal research indicates that dieting behaviors predict heightened , with individuals engaging in any dieting over 12 months showing elevated symptoms of restraint, eating concern, and shape/weight concern. Moderate dieting in correlates with a fivefold increase in risk among females, escalating to 18-fold for extreme restriction, underscoring dieting as a causal precursor rather than mere . Behaviorally, restriction often triggers compensatory mechanisms such as upon re-exposure to food, a replicated in both experimental paradigms and self-imposed diets, leading to cycles of loss of control over intake. , or yo-yo dieting, exacerbates these issues by fostering , life dissatisfaction, and interpersonal strain, with qualitative analyses revealing self-perceived and social withdrawal tied to repeated regain. While some interventions report short-term gains like reduced anxiety, these are inconsistent across studies and often overshadowed by long-term behavioral , including persistent disordered s that intensify from to adulthood. Overall, prioritizes the maladaptive of dieting, where initial restraint erodes self-regulatory capacity, promoting disinhibited eating and sustained psychological burden.

Evidence of Regain and Yo-Yo Cycling

Studies consistently demonstrate that the majority of individuals who achieve through dieting experience significant regain over time, often returning to or exceeding baseline weights within 1 to 5 years. A of interventions found that only about 20% of and obese participants maintained their long-term after dieting, with the rest exhibiting partial or full regain. Similarly, another reported that just 25% of patients sustained results following low-calorie diets, highlighting the challenge of preventing regain despite initial success. Yo-yo dieting, characterized by repeated cycles of intentional followed by regain, is a common pattern among dieters and is linked to higher subsequent risks. In a study of U.S. women, over 70% reported at least one episode of , with prevalence increasing alongside cardiovascular health declines. Surveys indicate that 50-60% of adults in the U.S. and attempt annually, contributing to widespread cycling behaviors, particularly in fitness-oriented populations where dieting history correlates with multiple regain episodes. Even among normal-weight individuals, dieting has been associated with elevated long-term gain in meta-analyses, suggesting that cycling may predispose to metabolic adaptations favoring fat storage. Longitudinal data from behavioral weight management programs further underscore regain dynamics, with average maintenance masking individual trajectories where approximately half of participants fail to sustain losses beyond program completion, often due to behavioral lapses and physiological counter-regulation. Peer-reviewed analyses confirm that occurs in nearly all dieting cohorts tracked over years, with regain rates approaching 80-95% in non-surgical interventions, independent of diet type. These patterns persist across demographics, though success rates are marginally higher in supervised settings, yet real-world adherence amplifies cycling prevalence.

Implementation Methods

Tracking and Behavioral Strategies

Self-monitoring of dietary intake, , and body weight constitutes a foundational behavioral technique in programs, with systematic reviews indicating that higher frequency of monitoring correlates with greater short-term . In one analysis of 24 studies, participants engaging in consistent self-recording of consumption achieved an average additional 1.5-2.0 kg loss compared to those with lower adherence over 3-6 months. Digital tools, such as mobile applications for logging calories or macronutrients, facilitate this process by providing real-time feedback and reducing estimation errors, though accuracy depends on user diligence in portion assessment. Daily self-weighing emerges as a particularly potent tracking method, with from randomized trials showing it promotes sustained attention to balance and yields 0.5-1.0 kg greater reduction over 12 months versus weekly weighing. This practice enhances awareness of fluctuations driven by caloric surplus or deficit, enabling timely adjustments, though it requires to avoid discouragement from daily variances due to factors like water retention. Comparative data suggest structured tracking outperforms approaches for quantifiable deficits, as the latter often underestimates intake by 20-50% in uncontrolled settings, leading to diminished outcomes. Behavioral strategies complement tracking by addressing adherence barriers through techniques like , , and relapse prevention, drawn from cognitive-behavioral frameworks validated in long-term interventions. Specific aims, such as reducing daily caloric intake by 500 kcal via portion control or substituting high-density foods, improve success rates by 20-30% in group-based programs, as they leverage cue-response modification to minimize impulsive consumption. formation via consistent routines—e.g., pre-planning meals or removing environmental triggers like visible snacks—sustains losses by automating compliance, with reviews confirming these yield 5-10% body weight reduction when integrated with monitoring over 6-12 months. Problem-solving skills training, involving identification of lapses (e.g., stress-induced ) and alternative coping mechanisms, further bolsters efficacy, as evidenced by maintenance trials where such strategies halved regain rates at 18 months follow-up. elements, like accountability partners or apps with progress sharing, amplify these effects by reinforcing , though individual variability in executive function influences uptake. Overall, combining tracking with these targeted behaviors outperforms isolated efforts, yet long-term retention hinges on to counter and external disruptions.

Adjuncts Like Exercise and Hydration

Exercise, when combined with caloric restriction, augments short-term weight loss by increasing energy expenditure and preserving , though its independent contribution to fat reduction is modest compared to dietary changes alone. A meta-analysis of randomized controlled trials indicated that structured interventions incorporating exercise alongside diet yield greater than diet or exercise in isolation, with combined approaches achieving approximately 2-3 kg more loss over 6-12 months. , such as brisk walking or for at least 150 minutes weekly, reduces and waist circumference by 1-2 cm on average, primarily through elevated post-exercise oxygen consumption and fat oxidation. In contrast, resistance training mitigates the loss of during dieting—up to 20-30% of weight loss can be lean mass without it—while enhancing metabolic rate via increased muscle protein synthesis, as evidenced in trials among older adults where resistance groups retained 1-2 kg more fat-free mass than aerobic-only groups. Combining both modalities proves superior for overall , reducing intermuscular by 15-20% more than either alone in dieting obese individuals. Long-term adherence remains challenging, with dropout rates exceeding 50% in unsupervised programs, limiting sustained benefits. Hydration supports dieting by promoting and modest metabolic enhancements, particularly when replaces caloric beverages or is consumed preemptively. Randomized trials demonstrate that drinking 500 ml of 30 minutes before meals reduces subsequent energy by 13-20% in non-obese adults, correlating with 1-2 kg greater over 12 weeks via gastric distension and delayed gastric emptying. A of clinical studies found increased daily (1.5-3 liters) associated with average weight reductions of 0.4-8.8 kg over follow-up periods, attributed to enhanced and suppressed appetite hormones like . In maintenance phases, habitual high consumers exhibit twofold higher rates of sustained loss compared to those substituting diet drinks, with mechanisms including from water-induced energy expenditure (up to 50 kcal/day) and substitution effects. However, effects diminish in habitually hydrated individuals, and overemphasis on hydration without caloric control yields negligible independent impact.

Role of Supplements and Pharmaceuticals

Dietary supplements marketed for weight loss, such as extract, cambogia, , and fiber products like , generally demonstrate limited efficacy in s. A of over 100 trials found that while some supplements produced statistically greater weight loss than (typically 0.5-2 kg over 1-3 months), the effects were clinically insignificant and often confounded by poor study quality, small sample sizes, and industry funding biases. Similarly, a 2023 meta-analysis of nutraceuticals identified modest benefits for (up to 3-5 kg loss) and certain herbal extracts like , but emphasized high heterogeneity and lack of long-term data, with no supplement achieving sustained reductions beyond 5% body weight. The U.S. concludes that evidence for most weight-loss supplements is insufficient to recommend their use, citing risks of contamination, interactions, and claims unsupported by randomized controlled trials. Pharmaceutical interventions, particularly (GLP-1) receptor agonists, offer more robust evidence for weight reduction when combined with lifestyle changes. (Wegovy), approved by the FDA in 2021 for chronic in adults with BMI ≥30 or ≥27 with comorbidities, led to mean weight losses of 14.9% at 68 weeks and approximately 15% at 104 weeks in phase 3 trials like STEP 1-5, compared to 2-3% with . (Zepbound), a dual GLP-1/GIP agonist approved in 2023, showed superior outcomes with 15-21% at 72 weeks in the SURMOUNT-1 trial. Older agents like (Xenical), which inhibits fat absorption, yield 2-3 kg greater loss than over a year but with gastrointestinal side effects in up to 20% of users. Network meta-analyses rank GLP-1 agonists highest for efficacy, though real-world adherence yields smaller losses (e.g., 12.9% at 12 months for ) due to discontinuation rates exceeding 50%. Long-term maintenance requires indefinite use, as weight regain averages 2/3 of lost weight within a year of discontinuation, per STEP 1 extension data showing only 48% retaining ≥5% loss at 120 weeks off-drug. Common adverse effects include nausea (20-44%), vomiting, and diarrhea, with rare risks of pancreatitis, gallbladder disease, and thyroid tumors in rodents (human data inconclusive). Cardiovascular benefits, such as reduced major adverse events, emerge in trials like SELECT (semaglutide reduced events by 20% in overweight patients without diabetes). These agents address hormonal dysregulation in obesity but do not alter underlying caloric imbalance without dietary adherence, positioning them as adjuncts rather than standalone solutions. Meta-analyses caution against over-reliance, noting higher dropout due to side effects compared to lifestyle interventions alone.

Societal and Cultural Dimensions

Obesity Epidemic and Attribution Debates

The prevalence of has risen sharply in many countries since the late , marking what authorities describe as an . In the United States, adult rates increased from approximately 13% in the early to 30.5% by 1999–2000 and reached 41.9% by 2017–March 2020, with severe tripling over the same period from 1999 to 2020. Globally, the reports that adult has more than doubled since 1990, affecting 1 in 8 people worldwide by 2022, with adolescent quadrupling over the same timeframe. These trends coincide with increased availability of calorie-dense foods and declining levels, though some recent data suggest possible stabilization or slight declines in certain demographics, such as U.S. , potentially linked to interventions like GLP-1 receptor agonists. Attribution of the epidemic centers on sustained positive energy balance—where caloric intake exceeds expenditure—as the proximate cause, but debates persist over the primary drivers. Proponents of the caloric model emphasize aggregate increases in energy consumption (e.g., from 1,800–2,000 kcal/day in the mid-20th century to over 2,500 kcal/day in recent decades in high-income nations) alongside reduced daily energy expenditure due to mechanized labor and sedentary lifestyles. This view, supported by epidemiological data, posits that obesity results from voluntary overconsumption and underactivity, with twin studies indicating heritability explains only 40–70% of variance, leaving substantial room for behavioral factors. Critics, however, argue this overlooks how modern environments facilitate overeating; for instance, randomized trials show ultra-processed foods (UPFs) promote excess intake of 500+ kcal/day compared to unprocessed equivalents, independent of conscious portion control, due to hyper-palatability and rapid digestion. Hormonal mechanisms, particularly insulin dynamics, feature prominently in alternative causal models challenging pure caloric reductionism. High-glycemic carbohydrates and added sugars, ubiquitous in processed diets, trigger insulin spikes that promote fat storage and suppress fat oxidation, fostering insulin resistance—a precursor to obesity observed in longitudinal studies where rising body fat correlates with diminished insulin sensitivity. Evidence links UPF consumption, often exceeding 50% of calories in Western diets, to obesity via disrupted satiety signals and metabolic dysregulation, rather than mere caloric surplus; meta-analyses associate higher UPF intake with 20–50% elevated obesity risk, even after adjusting for total energy. These findings suggest food composition alters hunger hormones like leptin and ghrelin, making energy balance harder to maintain than in ancestral environments with whole foods. Debates also encompass environmental versus individual agency, with some sources attributing the epidemic to systemic factors like agricultural subsidies favoring corn-derived sugars (e.g., consumption peaking at 60 lbs/person/year in the U.S. by 2000) and discouraging activity. Peer-reviewed analyses highlight gene-environment interactions, where thrifty genotypes evolved for scarcity now maladapt to abundance, but emphasize that rates vary widely within similar environments, underscoring personal choices in diet adherence. While institutions like the WHO frame as multifactorial with policy levers (e.g., taxing sugars), empirical trials of such interventions yield modest effects (1–2 kg ), suggesting overreliance on external fixes undervalues behavioral self-regulation, as evidenced by successful low-carb interventions reducing insulin demand and yielding sustained loss. Mainstream attributions often downplay metabolic causation in favor of socioeconomic narratives, potentially reflecting institutional biases toward collectivist explanations over individual .

Individual Responsibility vs Systemic Factors

The debate over individual responsibility versus systemic factors in dieting outcomes centers on whether personal choices and agency primarily determine weight management success or if broader environmental, economic, and societal influences predominate. Empirical evidence from behavioral interventions indicates that sustained weight loss is achievable through self-regulated strategies such as goal-setting and habit formation, with studies showing that adults who maintain medium- to long-term adherence to dietary and activity changes experience significant reductions in body mass index (BMI). For instance, a large community-based trial found that participants setting specific weight-loss targets achieved greater long-term losses compared to those without, underscoring the role of personal motivation and planning. Twin studies further support genetic predispositions to obesity, with heritability estimates for BMI ranging from 40% to 70%, yet post-adolescent environmental influences appear minimal, suggesting that adult behavioral agency can override shared systemic exposures. Proponents of individual responsibility argue that personal accountability aligns with causal mechanisms of energy balance, where caloric intake and expenditure are directly modifiable through volitional actions, independent of external pressures. Peer-reviewed analyses of programs demonstrate that intrinsic motivation and predict adherence and outcomes, with participants exhibiting autonomous regulation sustaining losses over years. Surveys of public attitudes reinforce this view, with nearly 90% attributing healthy dieting to personal effort rather than external forces. Critiques of overemphasizing systemic factors highlight that such narratives can undermine agency, as evidenced by successful interventions in diverse socioeconomic groups where behavioral yields consistent results, challenging claims of insurmountable barriers. Systemic factors, including the proliferation of ultra-processed foods and obesogenic environments, are cited as contributors to the obesity epidemic, with critiques noting increased portion sizes and marketing since the 1970s correlating with rising prevalence. Socioeconomic disparities show higher rates in lower-income populations, potentially linked to food deserts and economic constraints on healthy options, though these explain variance rather than inevitability. Environmental exposures like endocrine-disrupting chemicals in processed foods have been proposed as drivers, yet their causal role remains contested, with genetic and behavioral factors showing stronger predictive power in longitudinal data. While systemic interventions like policy reforms are advocated, evidence indicates they have limited impact without individual compliance, as populations exposed to similar environments exhibit wide BMI distributions attributable to differential choices. Reconciling the two, first-principles analysis of reveals that fundamentally arises from sustained positive energy balance, which individuals can counteract through deliberate restriction and activity, even amid systemic temptations. tempers but does not eliminate responsibility, as modifiable behaviors account for non-shared environmental variance in twin models. Overreliance on systemic explanations risks excusing inaction, whereas empirical success in self-directed programs—such as digital tools yielding 5-10% losses in over half of users—affirms the primacy of personal agency in dieting efficacy.

Cultural Norms and Stigmatization

In Western societies, cultural norms have increasingly emphasized thinness as a marker of , , and since the mid-19th century, coinciding with the rise of industrialization and the of body weight. This shift marked a departure from earlier eras where fuller figures symbolized wealth and status, as seen in and pre-20th-century European depictions; by the , aesthetics and subsequent trends solidified the "," linking slenderness to discipline and success. Dieting emerged as a normative response, with practices like calorie counting promoted as accessible paths to , though empirical data indicate sustained weight loss rates below 20% long-term for most adherents. Media and social platforms amplify these norms, portraying idealized thin bodies in and influencer content, which correlates with heightened body dissatisfaction among adolescents and adults; a review of 50 studies across 17 countries found exposure linked to and negative self-perception in over 70% of cases examined. This cultural pressure extends to professional spheres, where individuals face hiring biases—studies report 26% lower callback rates for job applications with heavier-set photos—and workplace discrimination, often rationalized by assumptions of lower productivity despite evidence of equivalent performance when controlled for health factors. Such norms reflect causal links between excess adiposity and comorbidities like and , with prevalence exceeding 40% in the U.S. by 2020, prompting societal emphasis on as a imperative. Stigmatization of , however, manifests as , with individuals experiencing in healthcare settings; surveys indicate 60-70% of obese patients report provider disrespect, leading to avoidance of medical care and delayed screenings, such as a 2-3 times higher rate of skipping cancer checks among stigmatized women. Peer-reviewed analyses link this stigma to elevated levels and stress-induced eating, potentially exacerbating in a feedback loop, though longitudinal data suggest bidirectional where underlying obesity risks precede stigma exposure. Critically, while stigma correlates with 32% higher depression odds independent of BMI, some evidence questions its net motivational effect, as repeated internalizes helplessness rather than spurring sustained behavioral change. Academic sources, often influenced by advocacy for reduced stigma, may underemphasize how norms counter rising obesity rates driven by caloric surplus, with global data showing inverse correlations between thin-ideal cultures and average BMI in comparative studies. Cross-culturally, norms vary: Pacific Island societies historically valorized larger bodies as signs of prosperity, correlating with higher tolerance and BMI averages above 30 kg/m², whereas East Asian contexts enforce stricter thinness standards, with dieting prevalence over 50% among urban youth and lower stigma thresholds tied to collectivist emphases. In contrast, Western frames dieting as personal agency, yet this fosters when norms overlook metabolic realities; ethnographic data reveal that in low-stigma environments like certain Mauritanian groups, deliberate fattening rituals persist, underscoring how cultural priors shape weight perceptions beyond universal optima. These differences highlight that stigmatization, while harmful in excess, may serve adaptive functions in signaling deviations from population-level fitness norms, though overgeneralization risks perpetuating without addressing root causes like sedentary lifestyles.

Controversies and Debates

Caloric Reductionism vs Hormonal Models

Caloric reductionism, also known as the energy balance model (EBM), posits that body weight is primarily determined by the difference between energy intake and expenditure, with resulting from chronic positive energy balance due to overconsumption relative to activity levels. This view emphasizes creating a through reduced intake or increased output, treating the body as a closed where excess calories are stored as fat. Proponents argue it aligns with fundamental laws of physics, as demonstrated in controlled feeding studies where precise energy surpluses lead to predictable . In contrast, hormonal models, such as the carbohydrate-insulin model (CIM), contend that obesity arises from dysregulated hormones—particularly insulin, driven by high diets—that promote fat storage and suppress fat mobilization, independent of total calories. Advocates like argue that refined carbohydrates elevate insulin chronically, partitioning calories toward while increasing hunger and reducing energy expenditure, rendering simple caloric restriction unsustainable. This framework prioritizes macronutrient composition over total energy, suggesting low-carbohydrate diets lower insulin, enhance fat oxidation, and improve satiety signals via hormones like and . Empirical evidence highlights limitations of pure caloric reductionism. A study of participants who lost 10-15% body weight via caloric restriction found persistent hormonal adaptations, including a 24% drop in resting energy expenditure beyond predicted levels, suppressed , and elevated , fostering regain despite ongoing deficits. Such adaptations explain high rates, with over 80% of dieters regaining weight within 5 years under calorie-focused regimens. Meta-analyses of randomized trials comparing low-carbohydrate (typically <130g/day carbs) and low-fat diets (<30% fat) support hormonal influences. A 2015 analysis of 17 trials (n=1,144) showed low-carb diets yielded greater short-term weight loss (-1.15 kg at 6-12 months) and improved triglycerides and HDL cholesterol, attributed to reduced insulin and better metabolic partitioning. A 2020 meta-analysis confirmed low-carb superiority for weight reduction (mean difference -1.3 kg) and lipid profiles over 6-12 months, with effects persisting longer in adherent participants. However, some trials, like the 2018 DIETFITS study (n=609), found equivalent 12-month weight loss (~5-6 kg) between healthy low-fat and low-carb arms, suggesting individual metabolic responses—potentially hormone-driven—mediate outcomes more than model alone. Critics of caloric reductionism note its failure to predict real-world dieting outcomes, as it overlooks endocrine feedback loops that amplify intake post-restriction. Hormonal proponents counter that EBM conflates correlation (energy imbalance) with causation, ignoring how insulin resistance and carbohydrate-induced hyperphagia precede surplus. While both paradigms acknowledge thermodynamics, hormonal models better integrate causal mechanisms like peripheral energy sensing and appetite regulation, informing interventions like ketogenic diets that sustain losses by targeting insulin dynamics. Mainstream adoption lags, potentially due to entrenched low-fat paradigms in nutrition guidelines, though mounting trial data challenges reductionist primacy.

Efficacy of Willpower Narratives

The prevailing narrative in popular dieting discourse posits that successful weight loss and maintenance primarily depend on individual willpower, framing obesity as a consequence of personal failing in self-discipline against caloric excess. This view, often promoted in self-help literature and media, suggests that adherence to restrictive diets through sheer resolve can overcome appetitive drives. However, empirical data from long-term studies indicate that such narratives overestimate the sustainability of willpower-driven efforts, with meta-analyses revealing that over 80% of lost weight is regained within five years across diverse interventions. Physiological adaptations undermine the efficacy of willpower alone, as caloric restriction triggers metabolic slowdown and hormonal shifts that intensify hunger and reduce energy expenditure. For instance, participants in intensive weight loss programs like exhibited persistent reductions in resting metabolic rate—up to 500-800 calories per day below predicted levels—even years post-intervention, independent of regained weight, illustrating how the body resists deficit through evolved survival mechanisms rather than lapses in resolve. Hormones such as ghrelin (which stimulates appetite) rise while leptin (which signals satiety) falls during energy restriction, creating biological pressures that exceed voluntary control in most cases, as evidenced by neuroimaging studies showing altered brain reward responses to food cues. Psychological models of willpower, including the concept of ego depletion—wherein self-control acts as a depletable resource—have been invoked to explain dieting relapses, yet replication failures and meta-analyses have cast doubt on its robustness, suggesting motivation fluctuates more with incentives and habits than finite reserves. Long-term maintenance rates remain low, with only about 20% of individuals achieving substantial, sustained loss through behavioral means alone, often requiring comprehensive lifestyle overhauls beyond intermittent restraint. These findings imply that willpower narratives foster cycles of guilt and attrition by attributing failure to moral weakness rather than addressing causal factors like environmental hyperpalatability or genetic predispositions, which epidemiological data link to obesity trends more strongly than self-control deficits.

Critiques of Fat Acceptance Movements

Critics of fat acceptance movements, including the associated Health at Every Size (HAES) paradigm, contend that these initiatives promote the notion that health can be decoupled from body weight, thereby minimizing the empirically demonstrated risks of obesity and potentially deterring efforts to address modifiable causes such as caloric imbalance. Such movements have been accused of fostering obesity denialism by framing excess adiposity as largely unchangeable or benign, which contradicts evidence that sustained weight reduction via dietary restriction and increased physical activity lowers morbidity and mortality rates. For instance, HAES approaches have drawn scrutiny for implying indefinite postponement of weight management interventions, accepting elevated body mass index (BMI) levels despite data linking BMI over 30 kg/m² to heightened disease incidence. Obesity substantially elevates risks for comorbidities driving premature death, including type 2 diabetes mellitus, dyslipidemia, hypertension, cardiovascular disease, stroke, certain cancers, and obstructive sleep apnea, with global epidemiological data attributing roughly 5 million annual deaths to excess body weight as of recent estimates. In the United States, adult obesity prevalence reached 42.4% during 2017–2018, correlating with increased all-cause mortality, particularly among younger adults where obesity triples cardiovascular death risk compared to normal weight cohorts. Critics argue that fat acceptance rhetoric overlooks these causal links, where adipose tissue dysfunction triggers inflammation and metabolic dysregulation, rather than attributing harms solely to societal stigma, which lacks robust evidence as a primary driver of obesity progression. By emphasizing acceptance over intervention, these movements may undermine personal agency and behavioral change, as surveys indicate many obese individuals already underestimate their weight status, with only 6% self-identifying as obese despite clinical metrics. This complacency could exacerbate healthcare burdens, given obesity's role in elevating costs through preventable conditions; for example, U.S. medical expenditures for obese adults averaged $1,861 higher annually than for normal-weight peers in 2008 data, adjusted for inflation. Empirical reviews of HAES interventions reveal limited long-term efficacy in improving cardiometabolic markers beyond short-term psychological benefits, with small sample sizes and exclusion of high-risk groups highlighting methodological weaknesses that fail to refute weight loss's superior outcomes. Proponents of critiques further assert that fat acceptance contravenes public health imperatives by eroding norms favoring leanness, which historically aligned with reduced chronic disease prevalence prior to the post-1980s obesity surge, potentially reversing gains in cardiovascular mortality decline. While acknowledging weight stigma's existence, detractors prioritize causal realism—wherein energy surplus directly engenders fat accumulation and attendant pathologies—over narratives reallocating responsibility to environmental or genetic factors without proportionate evidence for immutability. Intentional weight loss of 5–10% body mass has been shown to ameliorate insulin resistance, hypertension, and dyslipidemia, underscoring that acceptance sans action sustains rather than resolves these risks.

Recent Advances and Alternatives

Pharmacological Interventions

Pharmacological interventions for weight loss primarily target appetite regulation, gastrointestinal absorption, or central nervous system stimulation to facilitate caloric deficits. Glucagon-like peptide-1 (GLP-1) receptor agonists, such as semaglutide and liraglutide, mimic incretin hormones to slow gastric emptying, enhance satiety, and reduce food intake, leading to average weight reductions of 12-17% of body weight over 68 weeks in randomized trials when combined with lifestyle changes. Tirzepatide, a dual GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) agonist, achieves even greater losses, up to 20-22% at 72 weeks in phase 3 trials. These agents are FDA-approved for chronic weight management in adults with obesity or overweight with comorbidities, with semaglutide demonstrating sustained efficacy over four years in the SELECT trial, where participants lost approximately 10% body weight versus 1.5% with placebo. However, discontinuation often results in substantial weight regain, with studies showing 48% of semaglutide-induced loss maintained at one year off-drug but higher regain thereafter, underscoring that these drugs manage symptoms rather than address underlying causes like hormonal dysregulation or behavioral patterns. Gastrointestinal adverse effects, including nausea (up to 44%), vomiting (24%), and diarrhea (30%), affect over 70% of users initially and contribute to dropout rates of 7-10% in trials. Rare but serious risks include pancreatitis, gastroparesis, bowel obstruction, and gallbladder disease, with meta-analyses reporting 1.4- to 9-fold increased odds for these events compared to non-users. Cardiovascular benefits, such as reduced major adverse events in high-risk patients, have been observed with semaglutide, though benefits may partly stem from weight loss rather than direct effects. Older agents like orlistat, which inhibits pancreatic lipase to block ~30% of dietary fat absorption, yield modest losses of 2.9-5.4 kg over one year versus placebo, with gastrointestinal side effects like steatorrhea limiting adherence. Phentermine, a sympathomimetic approved for short-term use (up to 12 weeks), suppresses appetite via norepinephrine release, achieving 3-7% weight loss, but lacks long-term data and carries risks of hypertension and insomnia. Combination therapies, such as phentermine/topiramate, extend efficacy to 8-10% loss over one year by combining appetite suppression with enhanced GABA signaling, though teratogenicity restricts use in women of childbearing age. Meta-analyses indicate GLP-1 agonists outperform older drugs in magnitude of loss but require ongoing use, with real-world adherence challenged by injection requirements, high costs (often >$1,000 monthly without insurance), and shortages as of 2023-2025. While effective adjuncts to diet and exercise, no pharmacological intervention eliminates the need for sustained behavioral changes, and long-term safety beyond five years remains understudied, with potential for and dependency.

Surgical and Technological Options

Surgical interventions for , collectively known as bariatric or metabolic , primarily target severe by altering gastrointestinal anatomy to restrict intake, reduce absorption, or both. Common procedures include Roux-en-Y gastric bypass (RYGB), which reroutes the to bypass part of the and , leading to and reduced caloric intake; laparoscopic (SG), which removes about 80% of the to create a smaller, sleeve-shaped reservoir that limits volume and decreases production; and adjustable gastric banding (AGB), which places an inflatable band around the upper to create a small pouch, adjustable via port. RYGB typically yields the greatest excess (EWL), averaging 56.7% at 10+ years, followed by SG at around 50-60% EWL and AGB at 45.9%. Long-term outcomes favor RYGB over SG for sustained weight reduction and (T2DM) remission, with RYGB achieving 23% total at 10-20 years and superior glycemic control (e.g., 1.4% greater HbA1c reduction at 7 years versus medical management). SG offers comparable short-term results to RYGB (e.g., similar EWL up to 3 years) but with lower risks of nutritional deficiencies and reoperations, though meta-analyses indicate RYGB's edge in 5-year T2DM remission and resolution. Complications across procedures include leaks, infections, and nutrient , with perioperative mortality under 0.3%; however, RYGB and SG outperform AGB in durability, as banding often requires revisions due to slippage or inadequate loss. Technological advancements complement with less invasive endoscopic bariatric therapies (EBTs), such as intragastric balloons (IGBs) that occupy space for temporary (6-12 months) restriction, yielding 10-15% total but with higher removal rates due to intolerance. Endoscopic gastroplasty (ESG) uses sutures to reduce volume without resection, achieving 15-20% at 2 years with fewer complications than traditional SG, positioning it as a bridge for surgery-ineligible patients. Emerging devices include aspiration systems like AspireAssist, which enable post-meal drainage of 30% of ingested calories via a tube, resulting in 20-25% over 1 year but requiring patient compliance. Investigational implants, such as the BariaTek BariTon, mimic bypass effects reversibly by partitioning stomach and intestine, aiming for without permanent alteration, though remain preliminary as of 2024. Bioelectronic implants delivering targeted neural stimulation or hormone-regulating cells represent frontier technologies, with prototypes showing promise in preclinical models but lacking large-scale human efficacy trials by 2025. Robotic assistance in bariatric procedures enhances precision, reducing operative times and errors, particularly in RYGB and SG. Overall, while surgical options demonstrate superior durability to non-invasive alternatives, technological innovations prioritize reversibility and lower risk, though long-term data lag behind established surgeries.

Emerging Personalized Approaches

Personalized approaches to dieting integrate individual biological and behavioral data to customize dietary interventions, aiming to enhance efficacy beyond standardized recommendations. Nutrigenomics, the study of gene-nutrient interactions, identifies genetic variants that influence metabolic responses, such as polymorphisms in the associated with altered oxidation or APOE variants affecting handling, enabling tailored macronutrient ratios. Recent reviews highlight how such can guide or intake to mitigate risk, though clinical translation requires validation beyond association studies. Gut microbiome profiling emerges as a predictive tool for dietary success, with baseline compositions forecasting responses to interventions like caloric restriction or supplementation. For example, higher abundance of taxa correlates with greater on high-fiber diets, while taxa like or Dorea predict poorer outcomes, reflecting interindividual efficiency and energy harvest variations. A 2022 review of intervention trials underscores resilience to short-term changes but variability in predicting sustained loss, suggesting pre-diet sequencing could stratify responders. Biomarker-driven personalization, incorporating continuous glucose monitoring, lipid profiles, and , further refines plans by matching diets to metabolic phenotypes—e.g., low favoring low-carbohydrate approaches for fat-burners. The 2024 PREVENTOMICS randomized trial (n=347, 18 weeks) tested a multi-input program using glucose, triglycerides, , and history, yielding 2.17 kg mean versus 0.30 kg in controls, with adherent participants achieving 4.7% body weight reduction alongside reduced triglycerides (0.21 mmol/L) and waist circumference (2.94 cm). Such digital integrations predict short-term adherence via behavior tracking and long-term success via baseline markers like signatures. Despite promise, these methods face evidentiary limits: most data derive from small or observational cohorts with reproducibility challenges, modest effect sizes dependent on adherence, and underrepresentation of diverse populations. Implementation barriers include high costs for testing and algorithmic opacity, necessitating larger trials to confirm superiority over generic advice.

References

  1. https://pmc.ncbi.nlm.nih.gov/articles/PMC8017325/
  2. https://www.tandfonline.com/doi/full/10.1080/08870446.2017.1316849
  3. https://www.rcseng.ac.uk/library-and-publications/library/blog/do-you-bant/
  4. https://pmc.ncbi.nlm.nih.gov/articles/PMC10937533/
  5. https://pmc.ncbi.nlm.nih.gov/articles/PMC9798029/
  6. https://pmc.ncbi.nlm.nih.gov/articles/PMC7416131/
  7. https://pmc.ncbi.nlm.nih.gov/articles/PMC4903943/
  8. https://pmc.ncbi.nlm.nih.gov/articles/PMC3352786/
  9. https://www.mayoclinic.org/healthy-lifestyle/weight-loss/basics/weightloss-basics/hlv-20049483
  10. https://pmc.ncbi.nlm.nih.gov/articles/PMC3302369/
  11. https://www.ncbi.nlm.nih.gov/books/NBK221839/
  12. https://www.health.harvard.edu/healthbeat/5-principles-of-a-healthy-diet
  13. https://www.sciencedirect.com/science/article/pii/S0753332221005710
  14. https://www.betterhealth.vic.gov.au/health/healthyliving/weight-loss-a-healthy-approach
  15. https://pmc.ncbi.nlm.nih.gov/articles/PMC9052419/
  16. https://www.gastrojournal.org/article/s0016-5085%2817%2930158-0/fulltext
  17. https://www.logansportmemorial.org/blog/dieting-vs-lifestyle-changes
  18. https://www.canr.msu.edu/news/weight_loss_diet_change_vs_dietary_lifestyle
  19. https://pmc.ncbi.nlm.nih.gov/articles/PMC3313649/
  20. https://pmc.ncbi.nlm.nih.gov/articles/PMC5764193/
  21. https://www.nature.com/articles/s43016-023-00868-w
  22. https://journals.sagepub.com/doi/10.1177/00469580221090397
  23. https://pmc.ncbi.nlm.nih.gov/articles/PMC6917653/
  24. https://www.health.harvard.edu/blog/what-is-a-successful-mindset-for-weight-loss-maintenance-202205112742
  25. https://www.nejm.org/doi/full/10.1056/NEJMoa1014296
  26. https://pmc.ncbi.nlm.nih.gov/articles/PMC7833027/
  27. https://pmc.ncbi.nlm.nih.gov/articles/PMC3764867/
  28. https://www.mdpi.com/2673-4168/2/2/11
  29. https://www.nationalgeographic.com/history/article/diet-advice-food-health-ancient-greeks-romans
  30. https://pubmed.ncbi.nlm.nih.gov/15107945/
  31. https://www.thelancet.com/journals/lancet/article/PIIS0140673610610653/fulltext
  32. https://www.ncbi.nlm.nih.gov/books/NBK581942/
  33. https://onlinelibrary.wiley.com/doi/10.1007/s00268-004-7373-9
  34. https://www.smithsonianmag.com/science-nature/doctor-pioneered-counting-calories-century-ago-were-still-dealing-with-consequences-180984282/
  35. https://www.smithsonianmag.com/arts-culture/how-americans-got-hoooked-counting-calories-more-than-century-ago-180984428/
  36. https://www.cambridge.org/core/journals/journal-of-american-studies/article/eat-your-way-to-health-a-history-of-ability-in-the-progressive-era/8C65543385E3E082BEF0019A8AEA1F3F
  37. https://www.forhers.com/news/history-weight-loss-drugs
  38. https://pmc.ncbi.nlm.nih.gov/articles/PMC3482033/
  39. https://www.bbc.com/news/magazine-20695743
  40. https://www.weightwatchers.com/au/ww-evolution
  41. https://www.company-histories.com/Weight-Watchers-International-Inc-Company-History.html
  42. https://www.thoughtful-nutrition.com/the-history-of-diet-culture-a-timeline-of-societys-obsession-with-thinness/
  43. https://www.dietaryguidelines.gov/sites/default/files/2019-05/1980%2520DGA.pdf
  44. https://www.bmj.com/content/361/bmj.k2392
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC5916427/
  46. https://www.pbs.org/wgbh/pages/frontline/shows/diet/themes/lowfat.html
  47. https://www.dietaryguidelines.gov/about-dietary-guidelines/history-dietary-guidelines
  48. https://www.northwell.edu/news/the-latest/us-dietary-recommendations-changes-last-50-years
  49. https://scholarsbank.uoregon.edu/items/911e72ae-8585-49a0-acd6-cf50607ba6b2
  50. https://www.levels.com/blog/how-and-why-the-food-pyramid-diet-recommendations-changed
  51. https://med.stanford.edu/news/insights/2019/03/a-skeptical-look-at-popular-diets-the-lowdown-on-low-carb-3.html
  52. https://usafacts.org/articles/obesity-rate-nearly-triples-united-states-over-last-50-years/
  53. https://www.cdc.gov/nchs/fastats/obesity-overweight.htm
  54. https://www.who.int/activities/controlling-the-global-obesity-epidemic
  55. https://www.cdc.gov/mmwr/preview/mmwrhtml/rr5807a1.htm
  56. https://pmc.ncbi.nlm.nih.gov/articles/PMC3056747/
  57. https://bmcpublichealth.biomedcentral.com/articles/10.1186/1471-2458-11-136
  58. https://www.health.harvard.edu/blog/crumbling-confusing-food-pyramid-replaced-by-a-plate-201106032767
  59. https://www.niddk.nih.gov/health-information/health-statistics/overweight-obesity
  60. https://pmc.ncbi.nlm.nih.gov/articles/PMC3024813/
  61. https://pmc.ncbi.nlm.nih.gov/articles/PMC3401553/
  62. https://pmc.ncbi.nlm.nih.gov/articles/PMC4035446/
  63. https://pmc.ncbi.nlm.nih.gov/articles/PMC506782/
  64. https://nutritionandmetabolism.biomedcentral.com/articles/10.1186/1743-7075-1-15
  65. https://pmc.ncbi.nlm.nih.gov/articles/PMC5568065/
  66. https://pmc.ncbi.nlm.nih.gov/articles/PMC9036397/
  67. https://nutritionandmetabolism.biomedcentral.com/articles/10.1186/s12986-021-00587-8
  68. https://pmc.ncbi.nlm.nih.gov/articles/PMC8852805/
  69. https://pmc.ncbi.nlm.nih.gov/articles/PMC6513301/
  70. https://www.nejm.org/doi/full/10.1056/NEJMoa1105816
  71. https://academic.oup.com/jcem/article/95/11/5037/2835281
  72. https://pmc.ncbi.nlm.nih.gov/articles/PMC5357888/
  73. https://pmc.ncbi.nlm.nih.gov/articles/PMC3856718/
  74. https://diabetesjournals.org/care/article/38/7/1253/30929/Calorie-Restriction-and-Matched-Weight-Loss-From
  75. https://pubmed.ncbi.nlm.nih.gov/12055988/
  76. https://www.mdpi.com/1422-0067/25/24/13438
  77. https://www.ncbi.nlm.nih.gov/books/NBK592402/
  78. https://pmc.ncbi.nlm.nih.gov/articles/PMC2990627/
  79. https://www.sciencedirect.com/science/article/pii/S1530891X2101380X
  80. https://pmc.ncbi.nlm.nih.gov/articles/PMC3673773/
  81. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4989512/
  82. https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/does-adaptive-thermogenesis-occur-after-weight-loss-in-adults-a-systematic-review/726FC60518DA67349B9C3EC1D75A7156
  83. https://pmc.ncbi.nlm.nih.gov/articles/PMC7484122/
  84. https://journals.lww.com/nsca-jscr/fulltext/2022/10000/metabolic_adaptations_to_weight_loss__a_brief.39.aspx
  85. https://www.uab.edu/news/research-innovation/weight-loss-may-take-longer-than-expected-due-to-metabolic-adaptation
  86. https://nutrition.org/high-protein-diets-may-counteract-adaptive-thermogenesis-during-weight-maintenance-after-weight-loss/
  87. https://pmc.ncbi.nlm.nih.gov/articles/PMC7657334/
  88. https://www.uab.edu/reporter/research-innovation/does-your-body-really-fight-against-weight-loss-this-scientist-explains-why-the-research-says-no
  89. https://ajcn.nutrition.org/article/S0002-9165%2822%2900943-1/fulltext
  90. https://www.uab.edu/ccts/news-events/center-news/ccts-bionutrition-set-point-theory
  91. https://www.tandfonline.com/doi/full/10.1186/1550-2783-11-7
  92. https://pubmed.ncbi.nlm.nih.gov/20416018/
  93. https://pubmed.ncbi.nlm.nih.gov/15588283/
  94. https://pmc.ncbi.nlm.nih.gov/articles/PMC7539343/
  95. https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2022.935234/full
  96. https://journals.lww.com/jnsm/fulltext/2025/01000/low_fat_versus_low_carbohydrate_diet.1.aspx
  97. https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-023-02874-y
  98. https://www.sciencedirect.com/science/article/pii/S0002916523274274
  99. https://www.nature.com/articles/ijo2014216
  100. https://jissn.biomedcentral.com/articles/10.1186/s12970-015-0100-0
  101. https://www.ahajournals.org/doi/10.1161/01.CIR.98.9.935
  102. https://jamanetwork.com/journals/jama/fullarticle/200094
  103. https://www.nejm.org/doi/full/10.1056/NEJMoa0804748
  104. https://examine.com/articles/low-fat-vs-low-carb-for-weight-loss/
  105. https://pubmed.ncbi.nlm.nih.gov/39408357/
  106. https://www.nature.com/articles/s41430-023-01311-w
  107. https://www.bmj.com/content/389/bmj-2024-082007
  108. https://pmc.ncbi.nlm.nih.gov/articles/PMC12309044/
  109. https://www.nejm.org/doi/full/10.1056/NEJMoa2114833
  110. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2811116
  111. https://hsph.harvard.edu/news/intermittent-fasting-may-be-effective-for-weight-loss-cardiometabolic-health/
  112. https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-024-03716-1
  113. https://www.mdpi.com/2072-6643/16/20/3533
  114. https://pmc.ncbi.nlm.nih.gov/articles/PMC9108547/
  115. https://www.ncbi.nlm.nih.gov/books/NBK599543/
  116. https://pmc.ncbi.nlm.nih.gov/articles/PMC7238914/
  117. https://www.researchgate.net/publication/289914441_The_Effect_of_Elimination_Diet_on_Weight_and_Metabolic_Parameters_of_Overweight_or_Obese_Patients_Who_Have_Food_Intolerance
  118. https://www.michiganmedicine.org/health-lab/can-elimination-diet-help-you-lose-weight
  119. https://www.jandonline.org/article/s2212-2672%2812%2900743-5/fulltext
  120. https://www.hopkinsmedicine.org/health/wellness-and-prevention/fodmap-diet-what-you-need-to-know
  121. https://my.clevelandclinic.org/health/treatments/22466-low-fodmap-diet
  122. https://pmc.ncbi.nlm.nih.gov/articles/PMC6647066/
  123. https://pmc.ncbi.nlm.nih.gov/articles/PMC8004139/
  124. https://pmc.ncbi.nlm.nih.gov/articles/PMC8684475/
  125. https://www.ncbi.nlm.nih.gov/books/NBK612514/
  126. https://www.cdrnet.org/vault/2459/web/files/Franz.pdf
  127. https://www.nature.com/articles/s41598-024-60547-z
  128. https://ijbnpa.biomedcentral.com/articles/10.1186/s12966-024-01657-9
  129. https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2771095
  130. https://pmc.ncbi.nlm.nih.gov/articles/PMC10996390/
  131. https://www.nature.com/articles/s41598-022-15770-x
  132. https://pmc.ncbi.nlm.nih.gov/articles/PMC4198155/
  133. https://pubmed.ncbi.nlm.nih.gov/11684524/
  134. https://pmc.ncbi.nlm.nih.gov/articles/PMC8953094/
  135. https://pmc.ncbi.nlm.nih.gov/articles/PMC3904491/
  136. https://onlinelibrary.wiley.com/doi/full/10.1002/oby.22769
  137. https://link.springer.com/article/10.1007/s13679-025-00619-x
  138. https://www.nature.com/articles/s41598-020-74302-7
  139. https://pmc.ncbi.nlm.nih.gov/articles/PMC4578963/
  140. https://www.ahajournals.org/doi/10.1161/CIRCOUTCOMES.122.009348
  141. https://jamanetwork.com/journals/jama/fullarticle/2673150
  142. https://www.bmj.com/content/369/bmj.m696
  143. https://pubmed.ncbi.nlm.nih.gov/35088407/
  144. https://www.mdpi.com/2072-6643/12/12/3774
  145. https://pmc.ncbi.nlm.nih.gov/articles/PMC11945412/
  146. https://journals.lww.com/md-journal/fulltext/2024/10180/the_impact_of_3_different_dietary_interventions_on.65.aspx
  147. https://www.sciencedirect.com/science/article/pii/S0939475324004393
  148. https://www.sciencedirect.com/science/article/pii/S0002916523063748
  149. https://pmc.ncbi.nlm.nih.gov/articles/PMC4989512/
  150. https://www.ncbi.nlm.nih.gov/books/NBK572145/
  151. https://www.sciencedirect.com/science/article/pii/S0002916523661842
  152. https://pubmed.ncbi.nlm.nih.gov/40247012/
  153. https://www.embopress.org/doi/10.15252/emmm.202114418
  154. https://www.ncbi.nlm.nih.gov/books/NBK603752/
  155. https://www.sciencedirect.com/science/article/pii/S0002916522008280
  156. https://pubmed.ncbi.nlm.nih.gov/8655907/
  157. https://www.sciencedirect.com/science/article/pii/S147101532400045X
  158. https://www.nationaleatingdisorders.org/statistics/
  159. https://pubmed.ncbi.nlm.nih.gov/8002684/
  160. https://www.news-medical.net/news/20240129/Study-highlights-the-negative-consequences-linked-to-yo-yo-dieting.aspx
  161. https://pubmed.ncbi.nlm.nih.gov/35997170/
  162. https://pubmed.ncbi.nlm.nih.gov/23983018/
  163. https://psycnet.apa.org/record/1994-38711-001
  164. https://ajcn.nutrition.org/article/S0002-9165%2823%2906374-8/fulltext
  165. https://www.mdpi.com/2072-6643/14/6/1259
  166. https://www.cuimc.columbia.edu/news/yo-yo-dieting-linked-heart-disease-risk-women
  167. https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2022.851887/full
  168. https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/is-dieting-a-risk-for-higher-weight-gain-in-normalweight-individual-a-systematic-review-and-metaanalysis/8405D783824B0F5A55365630ABCBBA03
  169. https://pmc.ncbi.nlm.nih.gov/articles/PMC11205792/
  170. https://pmc.ncbi.nlm.nih.gov/articles/PMC3268700/
  171. https://pubmed.ncbi.nlm.nih.gov/21185970/
  172. https://www.cambridge.org/core/journals/public-health-nutrition/article/systematic-review-of-the-use-of-dietary-selfmonitoring-in-behavioural-weight-loss-interventions-delivery-intensity-and-effectiveness/476B83589088637C6740BA801B92185D
  173. https://link.springer.com/article/10.1007/s12170-024-00746-5
  174. https://ijbnpa.biomedcentral.com/articles/10.1186/s12966-023-01555-6
  175. https://www.sciencedirect.com/science/article/pii/S0195666324001624
  176. https://www.sciencedirect.com/science/article/pii/S2212267223001661
  177. https://cdnsciencepub.com/doi/10.1139/apnm-2013-0026
  178. https://www.mdpi.com/2072-6643/17/4/617
  179. https://pmc.ncbi.nlm.nih.gov/articles/PMC9662257/
  180. https://bmcpublichealth.biomedcentral.com/articles/10.1186/s12889-024-17848-9
  181. https://jamanetwork.com/journals/jama/fullarticle/2702878
  182. https://bmjpublichealth.bmj.com/content/2/2/e000246
  183. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2828487
  184. https://www.nejm.org/doi/full/10.1056/NEJMoa1616338
  185. https://pubmed.ncbi.nlm.nih.gov/33839788/
  186. https://www.ncbi.nlm.nih.gov/books/NBK572051/
  187. https://pmc.ncbi.nlm.nih.gov/articles/PMC6209729/
  188. https://pubmed.ncbi.nlm.nih.gov/31657610/
  189. https://diabetes.org/newsroom/press-releases/water-instead-diet-drinks-associated-two-fold-rate-diabetes-remission-women
  190. https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2016.00018/full
  191. https://pmc.ncbi.nlm.nih.gov/articles/PMC8231729/
  192. https://www.sciencedirect.com/science/article/pii/S1043661823003006
  193. https://ods.od.nih.gov/factsheets/WeightLoss-HealthProfessional/
  194. https://www.nejm.org/doi/full/10.1056/NEJMoa2032183
  195. https://www.nature.com/articles/s41591-022-02026-4
  196. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2823644
  197. https://jamanetwork.com/journals/jama/fullarticle/2528211
  198. https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370%2824%2900599-6/fulltext
  199. https://newsroom.clevelandclinic.org/2024/09/13/cleveland-clinic-study-identifies-key-factors-that-can-impact-long-term-weight-loss-in-patients-with-obesity-who-were-prescribed-glp-1-ra-medications
  200. https://dom-pubs.onlinelibrary.wiley.com/doi/10.1111/dom.14725
  201. https://www.sciencedirect.com/science/article/pii/S2665913124000396
  202. https://www.sciencedirect.com/science/article/pii/S2667368124000299
  203. https://www.acc.org/About-ACC/Press-Releases/2025/06/20/14/11/American-College-of-Cardiology-Issues-Guidance-on-Weight-Management-Drugs
  204. https://www.nature.com/articles/s41591-025-03978-z
  205. https://pmc.ncbi.nlm.nih.gov/articles/PMC12456317/
  206. https://www.cdc.gov/obesity/adult-obesity-facts/index.html
  207. https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight
  208. https://www.freethink.com/biotech/obesity-rate-falling
  209. https://pmc.ncbi.nlm.nih.gov/articles/PMC10748771/
  210. https://academic.oup.com/edrv/article-abstract/27/7/750/2355230
  211. https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2021.706978/full
  212. https://www.cell.com/cell-metabolism/fulltext/S1550-4131%2819%2930248-7
  213. https://pmc.ncbi.nlm.nih.gov/articles/PMC380258/
  214. https://www.bmj.com/content/384/bmj-2023-077310
  215. https://www.sciencedirect.com/science/article/pii/S2949688825000103
  216. https://www.mdpi.com/2304-8158/13/16/2627
  217. https://pmc.ncbi.nlm.nih.gov/articles/PMC6959843/
  218. https://www.ncbi.nlm.nih.gov/books/NBK278977/
  219. https://www.sciencedirect.com/science/article/pii/S2589936825000313
  220. https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-015-0323-6
  221. https://pmc.ncbi.nlm.nih.gov/articles/PMC5111772/
  222. https://www.nejm.org/doi/full/10.1056/NEJM199005243222102
  223. https://pmc.ncbi.nlm.nih.gov/articles/PMC4346225/
  224. https://ijbnpa.biomedcentral.com/articles/10.1186/1479-5868-9-22
  225. https://pmc.ncbi.nlm.nih.gov/articles/PMC7350775/
  226. https://pubmed.ncbi.nlm.nih.gov/33977636/
  227. https://pmc.ncbi.nlm.nih.gov/articles/PMC9611578/
  228. https://www.sciencedirect.com/science/article/pii/S0939475325000559
  229. https://www.nature.com/articles/s41366-024-01460-3
  230. https://onlinelibrary.wiley.com/doi/10.1111/nbu.12574
  231. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0030153
  232. https://www.jmir.org/2023/1/e44955/
  233. https://sahrc.org/2022/04/diet-culture-a-brief-history/
  234. https://journalofethics.ama-assn.org/article/what-historical-ideals-womens-shapes-teach-us-about-womens-self-perception-and-body-decisions-today/2019-10
  235. https://www.teenvogue.com/story/diet-culture-history-from-ancient-greece-to-ozempic
  236. https://pmc.ncbi.nlm.nih.gov/articles/PMC10032524/
  237. https://pmc.ncbi.nlm.nih.gov/articles/PMC9985585/
  238. https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370%2822%2900138-9/fulltext
  239. https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-018-1116-5
  240. https://www.nature.com/articles/s41366-021-00814-5
  241. https://www.journals.uchicago.edu/doi/10.1086/659309
  242. https://pmc.ncbi.nlm.nih.gov/articles/PMC7824151/
  243. https://www.sciencedirect.com/science/article/pii/S2530018022001767
  244. https://www.nature.com/articles/s41430-022-01179-2
  245. https://ajcn.nutrition.org/article/S0002-9165%2822%2900242-8/fulltext
  246. https://www.nature.com/articles/492155a
  247. https://www.theguardian.com/society/2021/jan/17/gary-taubes-interview-obesity-calories-hormones-case-for-keto
  248. https://meatscience.org/docs/default-source/publications-resources/rmc/2012/01_taubes.pdf?sfvrsn=0
  249. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0139817
  250. https://pubmed.ncbi.nlm.nih.gov/33317019/
  251. https://rachelwilliamsfitness.wordpress.com/2017/06/11/debunking-dr-jason-fungs-criticism-of-cico/
  252. https://www.bmj.com/content/346/bmj.f1050/rr/642656
  253. https://www.health.harvard.edu/blog/exercise-metabolism-and-weight-new-research-from-the-biggest-loser-202201272676
  254. https://www.nature.com/articles/ijo2012114
  255. https://www.psychologytoday.com/us/blog/the-motivated-brain/202012/the-last-thing-you-need-know-about-ego-depletion
  256. https://bmjopen.bmj.com/content/11/7/e047743
  257. https://practicetransformation.umn.edu/continuing-education/the-myth-of-willpower/
  258. https://jeatdisord.biomedcentral.com/articles/10.1186/2050-2974-2-8
  259. https://www.intechopen.com/chapters/73236
  260. https://pmc.ncbi.nlm.nih.gov/articles/PMC5401682/
  261. https://www.ahajournals.org/doi/10.1161/circulationaha.109.192574
  262. https://www.news-medical.net/news/20120103/Many-obese-people-in-denial-mode-Survey.aspx
  263. https://publichealth.uga.edu/fat-shaming-strategy-pushed-by-bioethicist-daniel-callahan-to-help-curb-obesity/
  264. https://flcancer.com/articles/can-we-be-healthy-at-any-size/
  265. https://www.fda.gov/news-events/press-announcements/fda-approves-new-medication-chronic-weight-management
  266. https://www.nature.com/articles/s41591-024-02996-7
  267. https://jamanetwork.com/journals/jama/fullarticle/2810542
  268. https://www.gastrojournal.org/article/S0016-5085%2825%2900845-5/abstract
  269. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2825%2901375-3/fulltext
  270. https://www.ncbi.nlm.nih.gov/books/NBK279038/
  271. https://onlinelibrary.wiley.com/doi/10.1002/oby.23152
  272. https://pmc.ncbi.nlm.nih.gov/articles/PMC11840199/
  273. https://pmc.ncbi.nlm.nih.gov/articles/PMC12476180/
  274. https://medicine.washu.edu/news/study-identifies-benefits-risks-linked-to-popular-weight-loss-drugs/
  275. https://pmc.ncbi.nlm.nih.gov/articles/PMC6320354/
  276. https://pubmed.ncbi.nlm.nih.gov/30293134/
  277. https://asmbs.org/news_releases/new-study-shows-long-term-effectiveness-of-gastric-bypass-in-treating-type-2-diabetes-and-obesity/
  278. https://jamanetwork.com/journals/jama/fullarticle/2815401
  279. https://journals.lww.com/annalsofsurgery/fulltext/2017/03000/laparoscopic_sleeve_gastrectomy_versus.8.aspx
  280. https://bmcsurg.biomedcentral.com/articles/10.1186/s12893-024-02512-1
  281. https://www.cureus.com/articles/284070-long-term-effectiveness-and-outcomes-of-bariatric-surgery-a-comprehensive-review-of-current-evidence-and-emerging-trends
  282. https://jamanetwork.com/journals/jamasurgery/fullarticle/1790378
  283. https://pmc.ncbi.nlm.nih.gov/articles/PMC12250154/
  284. https://www.brainzmagazine.com/post/weight-loss-in-2025-innovations-in-medical-solutions-and-lifestyle-changes
  285. https://www.clinicaltrialsarena.com/news/bariatek-implants-first-device-that-aims-to-mimic-weight-loss-surgery/
  286. https://news.rice.edu/news/2024/rices-biotech-launch-pad-lead-commercialization-bioelectrical-implant-treatment-obesity
  287. https://news.northwestern.edu/stories/2024/10/obesity-diabetes-implant-receives-up-to-34-million-to-fast-track-development
  288. https://peakbariatric.com/technological-advancements-bariatric-surgery/
  289. https://www.nature.com/articles/s41598-024-57724-5
  290. https://pmc.ncbi.nlm.nih.gov/articles/PMC7939775/
  291. https://www.ifm.org/articles/nutrigenomics-personalized-diets-to-meet-patient-needs
  292. https://pmc.ncbi.nlm.nih.gov/articles/PMC7371677/
  293. https://pmc.ncbi.nlm.nih.gov/articles/PMC9537590/
  294. https://med.stanford.edu/news/insights/2023/01/biomarkers-predict-weight-loss-suggest-personalized-diets.html
  295. https://www.nature.com/articles/s41591-024-02951-6
  296. https://www.bmj.com/content/361/bmj.k2173
  297. https://www.ncbi.nlm.nih.gov/books/NBK575794/
Add your contribution
Related Hubs
Contribute something
User Avatar
No comments yet.