Definition and diagnostic criteria of clinical obesity

In the paper

“Typically, scoring and staging systems and treatment algorithms for obesity are based on the presence of other diseases (often referred to as comorbidities), rather than clinical manifestations of obesity itself.”

What the sources say

• ?Not checked — no full text of the sourcecites [16] Sharma, 2009, A proposed clinical staging system for obesity, Int J Obes source
• ?Not checked — no full text of the sourcecites [17] Aasheim, 2011, Assessment of obesity beyond body mass index to determine benefit of treatment, Clin Obes source
• Disputed

  The guideline’s discussion of the Edmonton Obesity Staging System says it considers metabolic, physical and psychological parameters to guide treatment, rather than relying on the presence of other diseases instead of clinical manifestations. Its Level 3 recommendation likewise proposes the system to assess obesity severity and guide decisions. The cited paper therefore does not support the claimed contrast. (LLM, conf=0.79)

  Checked by a reasoning model — may be wrong.

  cites [18] Wharton, 2020, Obesity in adults: a clinical practice guideline, CMAJ sourceExperimental — accuracy not yet measured

In the paper

“Other anthropometric measures, such as waist circumference, waist-to-hip ratio, and weight-to-height ratio have been suggested as alternative methods to BMI for diagnosis of obesity. However, these anthropometric measures also have notable limitations.45”

What the sources say

• ?Could not verify

  The Results section on high BMI reports its attributable disease burden, while the Methods section discusses outcomes associated with high BMI. Neither addresses limitations of waist circumference, waist-to-hip ratio, or weight-to-height ratio as obesity measures. Searches for those measures and for limitations of anthropometric alternatives found no passage supporting the cited claim. (LLM, conf=0.76)

  cites [45] Stanaway, 2018, Lancet sourceExperimental — accuracy not yet measured

In the paper

“Furthermore, overall diet quality and physical activity or fitness level are potent modulators of the risk associated with any BMI value, regardless of body composition.44”

What the sources say

• Partly supported

  The section 'Lifestyle and prevention/remission of T2D in visceral obesity' (page unavailable) links healthier diets and physical activity to lower cardiovascular risk and identifies fitness as a powerful risk predictor. 'From obesity to obesities' (page unavailable) also describes risk variation within BMI categories. The paper does not establish that these factors modulate risk at any BMI regardless of body composition; it emphasizes visceral adiposity as an important source of risk variation. (LLM, conf=0.84)

  cites [44] Després, 2021, Management of obesity in cardiovascular practice: JACC Focus seminar, J Am Coll Cardiol sourceExperimental — accuracy not yet measured

In the paper

“For example, many population studies have shown that within every BMI category considered, the larger the waist circumference, the greater the morbidity or mortality risk.36”

What the sources say

• Supported

  In “Identifying the high-risk obesity phenotype” (page not provided), the paper states that adults with higher waist circumference have greater adverse health risk within any given BMI category. It also reports pooled cohort findings of higher mortality with greater waist circumference in every BMI category examined. (LLM, conf=0.94)

  cites [36] Ross, 2020, Waist circumference as a vital sign in clinical practice: a consensus statement from the IAS and ICCR Working Group on Visceral Obesity, Nat Rev Endocrinol source

In the paper

“The current definition of obesity on the basis of BMI has several limitations.38,39”

What the sources say

• ?Not checked — no full text of the sourcecites [38] Blüher, 2019, Obesity: global epidemiology and pathogenesis, Nat Rev Endocrinol source
• Supported

  Section 3, “Limitations of the BMI,” explicitly says BMI has serious limitations for evaluating individuals with excess adiposity and understanding the heterogeneity of obesity. The Abstract identifies several specific deficiencies, including its failure to measure fat distribution and its limited usefulness for diagnosing obesity in an individual. (LLM, conf=0.94)

  cites [39] Bray, 2023, Beyond BMI, Nutrients source

In the paper

“Other ectopic fat depots, including liver fat, also contribute to variations in health risk.50”

What the sources say

• Supported

  The Introduction states that variation in fat accumulation at ectopic sites such as the liver is associated with differing cardiometabolic disease risk. The Conclusions report distinct risk profiles for visceral and liver fat, supporting the claim that fat distribution contributes to variations in health risk. (LLM, conf=0.91)

  cites [50] Tejani, 2022, Cardiometabolic health outcomes associated with discordant visceral and liver fat phenotypes: insights from the Dallas Heart Study and UK Biobank, Mayo Clin Proc source

In the paper

“This definition has been widely adopted and used in epidemiological studies, clinical practice, and public health policy.35”

What the sources say

• Partly supported

  The Introduction says BMI has long been the primary way to diagnose obesity, has been used in many epidemiological studies, and has been recommended for clinical practice. The Methods identify standardized BMI cutoffs, but the paper does not establish that this definition has been adopted or used in public health policy. (LLM, conf=0.84)

  cites [35] Romero-Corral, 2008, Accuracy of body mass index in diagnosing obesity in the adult general population, Int J Obes (Lond) sourceExperimental — accuracy not yet measured

In the paper

“However, eliminating individuals from the analysis on the basis of such factors can plausibly create biases.45,46”

What the sources say

• ?Could not verify

  The Methods section describes incorporating current, former, and occasional smokers into exposure estimates, while Discussion > Limitations discusses how smoking histories were reconstructed (page numbers unavailable). Neither passage addresses whether excluding individuals because of smoking history or occult disease creates bias; searches for exclusion, selection bias, and occult disease found no passage that does. (LLM, conf=0.73)

  cites [45] Stanaway, 2018, Lancet sourceExperimental — accuracy not yet measured
• ?Could not verify

  The paper’s “To the Editor” section discusses recalibrating BMI thresholds by race, ethnicity, and sex, but does not address excluding people from an analysis because of smoking history or occult disease. Searches for those factors and for exclusion or selection bias found no relevant passage in our copy. (LLM, conf=0.76)

  cites [46] Stanford, 2019, Race, ethnicity, sex, and obesity: is it time to personalize the scale?, Mayo Clin Proc sourceExperimental — accuracy not yet measured

In the paper

“Specific examples include gaps in referral to bariatric or metabolic surgery,66 with only <1% of qualified surgical candidates being referred for such operations,67”

What the sources say

• ?Not checked — no full text of the sourcecites [66] Holmes, 2022, Gaps in referral to bariatric surgery for patients with type 2 diabetes seen in endocrinology clinics, Can J Diabetes source
• Partly supported

  The Introduction (page not provided) says that fewer than 1% of severely obese U.S. adults undergo bariatric surgery annually; it does not say that fewer than 1% are referred. The Discussion (page not provided) identifies referral as a step toward surgery and calls for better understanding of referring-provider practices, but gives no referral rate. (LLM, conf=0.87)

  cites [67] Funk, 2015, Patient and referring practitioner characteristics associated with the likelihood of undergoing bariatric surgery: a systematic review, JAMA Surg sourceExperimental — accuracy not yet measured

In the paper

“This state of positive energy balance maintained over a prolonged period—or energy burden—drives adipocyte hypertrophy and, to a lesser extent, hyperplasia, as well as weight gain.85,86”

What the sources say

• ?Not checked — no full text of the sourcecites [85] Leibel, 1995, Changes in energy expenditure resulting from altered body weight, N Engl J Med source
• Partly supported

  The Introduction reports weight gain during overfeeding and explains that a small energy surplus can produce substantial weight gain over time. It does not say that prolonged positive energy balance causes adipocyte hypertrophy or hyperplasia, or that hypertrophy occurs to a greater extent. (LLM, conf=0.86)

  cites [86] Rosenbaum, 2010, Energy intake in weight-reduced humans, Brain Res sourceExperimental — accuracy not yet measured

In the paper

“Consistently, scoring and staging systems of obesity, and policies for coverage of treatments, estimate the clinical effect of obesity on the basis of the presence of other diseases, often referred to as comorbidities.16–18”

What the sources say

• ?Not checked — no full text of the sourcecites [16] Sharma, 2009, A proposed clinical staging system for obesity, Int J Obes source
• ?Not checked — no full text of the sourcecites [17] Aasheim, 2011, Assessment of obesity beyond body mass index to determine benefit of treatment, Clin Obes source
• Partly supported

  The guideline’s discussion of the Edmonton Obesity Staging System says it uses metabolic, physical and psychological parameters to assess severity and guide treatment, supporting the point that staging considers health effects beyond BMI. The Step 5: Follow-up and advocacy and Implementation sections discuss treatment coverage and access, but do not say coverage policies estimate obesity’s clinical effect from the presence of comorbidities. The staging description also does not reduce its assessment to the presence of other diseases. (LLM, conf=0.86)

  cites [18] Wharton, 2020, Obesity in adults: a clinical practice guideline, CMAJ sourceExperimental — accuracy not yet measured

In the paper

“Although Foster and colleagues’ study was conducted many years ago, similar biases among health-care professionals still persist.11”

What the sources say

• Supported

  The Summary of evidence section says that weight bias has been reported among numerous types of health-care professionals in the United States and worldwide. It also states that weight stigma has persisted despite the increased prevalence of obesity, supporting the claim that such biases still persist. (LLM, conf=0.91)

  cites [11] Rubino, 2020, Joint international consensus statement for ending stigma of obesity, Nat Med source

In the paper

“This view could contribute to delays in seeking medical care for obesity.57,58”

What the sources say

• ?Not checked — no full text of the sourcecites [57] Kaplan, 2018, Perceptions of barriers to effective obesity care: results from the national ACTION study, Obesity source
• Supported

  The Discussion states that believing weight loss is one's own responsibility, or that one already knows how to lose weight, may substantially delay seeking help from healthcare providers. The Results also link these beliefs to not discussing weight management with providers. (LLM, conf=0.94)

  cites [58] Sharma, 2019, Perceptions of barriers to effective obesity management in Canada: results from the ACTION study, Clin Obes source

In the paper

“However, studies over the past decade or more have questioned the role of sedentary lifestyle as an explanation for increased obesity rates in extant societies.84”

What the sources say

• Supported

  The Abstract reports that Hadza foragers had higher physical activity than Westerners but similar daily energy expenditure after accounting for body size, challenging models that link Western lifestyles to reduced expenditure and obesity. The Introduction also describes debate over whether reduced activity or changes in diet better explain rising obesity. (LLM, conf=0.90)

  cites [84] Pontzer, 2012, Hunter-gatherer energetics and human obesity, PLoS One source

In the paper

“These attitudes and behaviours towards obesity and its care appear to be widely shared by people with obesity across different regions globally.60–62”

What the sources say

• Supported

  The Methods describe a survey of people with obesity in 11 countries across different world regions. The Discussion reports shared patterns in their attitudes and weight-management behaviours and concludes that the findings reveal a global need for improved obesity-care education. This supports the claim’s hedged description of attitudes and behaviours appearing widely shared. (LLM, conf=0.88)

  cites [60] Caterson, 2019, Gaps to bridge: misalignment between perception, reality and actions in obesity, Diabetes Obes Metab source
• ?Not checked — no full text of the sourcecites [61] Lee, 2019, Attitudes and perceptions of the general public on obesity and its treatment options in Singapore, Obes Res Clin Pract source
• ?Not checked — no full text of the sourcecites [62] Tham, 2024, Action APAC: understanding perceptions, attitudes and behaviours in obesity and its management across south and Southeast Asia, Clin Obes source

In the paper

“In one study of 2545 participants in Canada, only 28% of people with obesity reported that a follow-up appointment was scheduled.58”

What the sources say

• Partly supported

  The Results (People with obesity–healthcare provider relationship; page not provided) report that 28% of people with obesity who had discussed weight with a healthcare provider said a weight-related follow-up appointment or call was scheduled—not 28% of all people with obesity surveyed. The Participants table (page not provided) gives 2,545 total participants, including 2,000 people with obesity. (LLM, conf=0.88)

  cites [58] Sharma, 2019, Perceptions of barriers to effective obesity management in Canada: results from the ACTION study, Clin Obes sourceExperimental — accuracy not yet measured

In the paper

“Obesity probably accelerates heart failure via effects on haemodynamic, metabolic, cellular, inflammatory, and mechanical pathways,112 but the relative contributions of each pathway are not well established.”

What the sources say

• Supported

  Section 5 describes obesity-related changes in cardiac structure, metabolism, circulation, and systemic inflammation that can lead to heart failure with preserved ejection fraction (HFpEF). Section 5.3 also describes mechanical restraint from epicardial fat and potential inflammatory effects on the heart. Together, these support the hedged account of multiple pathways, although the review focuses on HFpEF. (LLM, conf=0.88)

  cites [112] Borlaug, 2023, Obesity and heart failure with preserved ejection fraction: new insights and pathophysiological targets, Cardiovasc Res source

In the paper

“Hyperinsulinaemia, however, can contribute to certain obesity complications or related diseases, including hormonal disorders related to sex hormones and cancer (ie, mitogenic effect of insulin).98,99”

What the sources say

• Partly supported

  Section 2, “The Pathogenetic Role of Insulin Resistance in PCOS” (page unavailable), says that compensatory hyperinsulinaemia stimulates ovarian androgen production and increases androgen levels, supporting the sex-hormone-disorder portion of the claim. The passages found do not address cancer or a mitogenic effect of insulin, and the paper’s discussion is specific to PCOS rather than obesity complications generally. (LLM, conf=0.87)

  cites [98] Armanini, 2022, Controversies in the pathogenesis, diagnosis and treatment of PCOS: focus on insulin resistance, inflammation, and hyperandrogenism, Int J Mol Sci sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [99] Gallagher, 2020, Hyperinsulinaemia in cancer, Nat Rev Cancer source

In the paper

“Individuals predisposed to glucotoxicity and lipotoxicity of β cells have a gradual decline in insulin secretion, which becomes insufficient for normal metabolism of glucose, proteins, and lipids.97”

What the sources say

• Partly supported

  Section IV (page unavailable) says that continued overnutrition in insulin resistance can culminate in β-cell failure, likely due in part to glucose and lipid toxicity. It does not establish a gradual decline in secretion among predisposed individuals or specifically link that decline to insufficient metabolism of proteins as well as glucose and lipids. (LLM, conf=0.84)

  cites [97] Petersen, 2018, Mechanisms of insulin action and insulin resistance, Physiol Rev sourceExperimental — accuracy not yet measured

In the paper

“Importantly, the genetic factors that help determine fat distribution are largely distinct from those that affect overall adiposity as estimated by BMI.78,94”

What the sources say

• Partly supported

  The Introduction (page not specified) describes genetic variants associated with waist–hip ratio adjusted for BMI, supporting the idea that fat distribution can be studied separately from overall adiposity. The paper does not establish that the genetic factors determining fat distribution are largely distinct from those affecting BMI. The low overlap reported in Methods concerns BMI and body-fat-percentage variants, not fat-distribution variants. (LLM, conf=0.78)

  cites [78] Martin, 2022, Disease consequences of higher adiposity uncoupled from its adverse metabolic effects using Mendelian randomisation, eLife sourceExperimental — accuracy not yet measured
• Partly supported

  The Results (‘Overlap with findings from previous GWAS’; page unavailable) identify 29 body-fat-distribution signals not previously associated with an anthropometric trait, supporting some genetic distinction. But the same section reports that the strongest arm-fat-ratio associations occur at known BMI and adiposity loci, while ‘Correlation between fat ratios and anthropometric traits’ reports a strong genetic correlation between arm fat ratio and BMI in females. The blanket description ‘largely distinct’ omits this substantial overlap and variation by fat compartment and sex. (LLM, conf=0.87)

  cites [94] Rask-Andersen, 2019, Genome-wide association study of body fat distribution identifies adiposity loci and sex-specific genetic effects, Nat Commun sourceExperimental — accuracy not yet measured

In the paper

“Genome-wide association studies have identified several hundred common variants that influence food intake, basal metabolic rate, and the energy used during a fixed amount of exercise.92–94”

What the sources say

• Partly supported

  In “Gene discovery for polygenic obesity” (page unavailable), the review reports that a BMI GWAS identified more than 750 loci. In “Insights from genetic loci linked to common obesity” (page unavailable), it links the FTO locus to food intake, but says there is no evidence to date linking that locus to energy expenditure. The copy does not establish that the identified variants influence basal metabolic rate or energy used during a fixed amount of exercise. (LLM, conf=0.88)

  cites [92] Loos, 2022, The genetics of obesity: from discovery to biology, Nat Rev Genet sourceExperimental — accuracy not yet measured
• Not checked yet

  Checked before — its earlier verdict is held back until a new check runs.

  cites [93] Farooqi, 2015, Genetic, molecular and physiological mechanisms involved in human obesity: Society for Endocrinology medal lecture 2012, Clin Endocrinol source
• ?Could not verify

  The Introduction (page unavailable) says GWAS have identified hundreds of loci associated with body mass and body fat distribution, not variants influencing food intake, basal metabolic rate, or energy used during a fixed amount of exercise. Searches for those three outcomes found no passage in our copy addressing the attributed claim. (LLM, conf=0.76)

  cites [94] Rask-Andersen, 2019, Genome-wide association study of body fat distribution identifies adiposity loci and sex-specific genetic effects, Nat Commun sourceExperimental — accuracy not yet measured

In the paper

“Evidence from studies of families, twins, and adopted children shows that at least 40–70% of the variation in body weight is explainable by genetic factors (heritability).90–92”

What the sources say

• ?Not checked — no full text of the sourcecites [90] Stunkard, 1990, The body-mass index of twins who have been reared apart, N Engl J Med source
• ?Not checked — no full text of the sourcecites [91] Stunkard, 1986, A twin study of human obesity, JAMA source
• Supported

  The Obesogenic environment passage (labeled Abstract; page not provided) links genetic factors to variation in body weight and states that twin, family, and adoption studies estimate obesity heritability at 40–70%. This supports the citing sentence’s paraphrase. (LLM, conf=0.94)

  cites [92] Loos, 2022, The genetics of obesity: from discovery to biology, Nat Rev Genet source

In the paper

“Inflammation and hormonal dysfunction of adipose tissue exacerbates insulin resistance in most, but not all, people with obesity.95”

What the sources say

• Supported

  The “Obesity and Insulin Resistance” section says adipose tissue inflammation and disrupted endocrine function contribute to insulin resistance. The “Metabolically Healthy Obesity (MHO)” section identifies a subgroup of people with obesity who remain insulin-sensitive, supporting the “but not all” qualification. (LLM, conf=0.88)

  cites [95] Chait, 2020, Adipose tissue distribution, inflammation and its metabolic consequences, including diabetes and cardiovascular disease, Front Cardiovasc Med source

In the paper

“Such patients are at high risk of developing overt type 2 diabetes.97”

What the sources say

• Supported

  The Introduction states that insulin resistance is the best predictor of a future type 2 diabetes diagnosis and describes how increased pancreatic workload can lead to overt disease. This supports the risk claim for insulin-resistant patients, although the supplied citing sentence does not identify who “such patients” are. (LLM, conf=0.85)

  cites [97] Petersen, 2018, Mechanisms of insulin action and insulin resistance, Physiol Rev source

In the paper

“Evidence in the past several years shows relatively rapid and sizeable improvements in major heart failure symptoms with drug-induced and lifestyle-induced weight loss among people with heart failure with preserved ejection fraction.110,111”

What the sources say

• Partly supported

  The Results report sizeable symptom improvement with semaglutide over 52 weeks, and the Discussion reports that a caloric-restriction trial found symptom reductions. Both findings concern patients with HFpEF and obesity. The cited paper does not establish that the lifestyle-related improvement was relatively rapid or sizeable, and it says the extent to which semaglutide’s benefits are attributable to weight loss rather than other effects is unknown. (LLM, conf=0.85)

  cites [110] Kosiborod, 2023, Semaglutide in patients with heart failure with preserved ejection fraction and obesity, N Engl J Med sourceExperimental — accuracy not yet measured
• Supported

  This source supports the lifestyle-induced weight-loss part of the sentence. In older obese patients with stable HFpEF, the Discussion reports improved exercise capacity after caloric restriction; the Results report a clinically meaningful improvement in heart-failure-specific quality of life over the 20-week intervention. The paper does not study drug-induced weight loss, which the sentence also cites another source for. (LLM, conf=0.88)

  cites [111] Kitzman, 2016, Effect of caloric restriction or aerobic exercise training on peak oxygen consumption and quality of life in obese older patients with heart failure with preserved ejection fraction: a randomized clinical trial, JAMA source

In the paper

“Emerging evidence supports the concept that deposition of ectopic fat within pancreatic islets, possibly inside β cells themselves, contributes to progressive impairment of β-cell function (which is reversible with weight loss)115 in individuals who are genetically susceptible.116–118”

What the sources say

• ?Not checked — no full text of the sourcecites [115] Taylor, 2018, Remission of human type 2 diabetes requires decrease in liver and pancreas fat content but is dependent upon capacity for β cell recovery, Cell Metab source
• Partly supported

  The Pathogenesis section (page unavailable) links lipid accumulation in and around the pancreas with β-cell pathology and reports restored β-cell function alongside reduced pancreatic fat after dietary energy restriction. It does not locate the fat specifically within islets or β cells, or establish that this mechanism applies to genetically susceptible individuals. The citing sentence attaches a separate citation to reversibility with weight loss. (LLM, conf=0.86)

  cites [116] Reed, 2021, A review of current trends with type 2 diabetes epidemiology, aetiology, pathogenesis, treatments and future perspectives, Diabetes Metab Syndr Obes sourceExperimental — accuracy not yet measured
• Supported

  The citation is attached to the parenthetical claim that β-cell impairment is reversible with weight loss. In “Time-course of reversal of pathogenic factors” (page unavailable), the paper reports restored β-cell sensitivity after substantial weight loss and notes that this reversal is not necessarily seen beyond the first few years after diagnosis. (LLM, conf=0.90)

  cites [117] Taylor, 2008, Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause, Diabetologia source
• Partly supported

  The paper’s introductory discussion says that many type 2 diabetes-associated genetic variants relate to islet function, and its Outlook says acquired and inherited factors can impair insulin secretion. But the passages found do not link genetic susceptibility to fat deposition within islets or β cells; the weight-loss findings discussed concern liver fat and insulin resistance, not reversal of β-cell impairment. (LLM, conf=0.78)

  cites [118] Roden, 2019, The integrative biology of type 2 diabetes, Nature sourceExperimental — accuracy not yet measured

In the paper

“Compounding the adverse effects of weight stigma is internalised weight bias, which can negatively affect health-care interactions and access to health care.146”

What the sources say

• Supported

  The Discussion (page not provided) reports that higher internalized weight bias was associated across six countries with poorer doctor interactions, more healthcare avoidance, and fewer regular checkups among adults engaged in weight management. This supports the claim's cautious wording about interactions and access to care. (LLM, conf=0.92)

  cites [146] Puhl, 2021, The roles of experienced and internalized weight stigma in healthcare experiences: perspectives of adults engaged in weight management across six countries, PLoS One source

In the paper

“Also, it is well established that developmental trauma and childhood adversity are associated with a higher likelihood of developing obesity in adulthood.135,136”

What the sources say

• Supported

  The Introduction says systematic reviews consistently report a higher risk of adult obesity after childhood adversity and defines adversity to include traumatic events. The Conclusion reports a higher risk of obesity in young adulthood among men exposed to childhood adversity. (LLM, conf=0.94)

  cites [135] Wimmelmann, 2024, Childhood adversity trajectories and weight status in young adult men: a register-based study including 359,783 Danish men, Int J Obes source
• Supported

  The Results report a higher pooled odds ratio for overweight or obesity among people with multiple adverse childhood experiences (ACEs). The Discussion specifies that the comparison is between individuals with at least four ACEs and those with none; the paper describes the association as weak or modest, not causal. (LLM, conf=0.90)

  cites [136] Hughes, 2017, The effect of multiple adverse childhood experiences on health: a systematic review and meta-analysis, Lancet Public Health source

In the paper

“Weight discrimination is reported by 19–42% of adults with higher BMI, particularly women.11”

What the sources say

• Supported

  The Summary of evidence section, under “Prevalence of weight bias, stigma, and discrimination,” reports weight discrimination in 19–42% of adults with obesity. It also says rates are higher at higher BMI and among women than men; no page number is provided in our copy. (LLM, conf=0.94)

  cites [11] Rubino, 2020, Joint international consensus statement for ending stigma of obesity, Nat Med source

In the paper

“Obesity can also contribute to the development of peripheral neuropathy, independent of glycaemic status.129,130”

What the sources say

• Supported

  The Discussion explicitly describes obesity as an emerging risk factor for neuropathy independent of hyperglycemia and says the study supports obesity as a potential cause. It also reports neuropathy among obese participants with normal glycaemic status. (LLM, conf=0.94)

  cites [129] Callaghan, 2020, Central obesity is associated with neuropathy in the severely obese, Mayo Clin Proc source
• Supported

  The Key Summary Points report peripheral neuropathy in people with obesity despite normoglycaemia and suggest that obesity-related risk factors contribute to its development. The Introduction also states that obesity has been associated with peripheral neuropathy independent of hyperglycaemia. (LLM, conf=0.92)

  cites [130] Lim, 2022, The peripheral neuropathy prevalence and characteristics are comparable in people with obesity and long-duration type 1 diabetes, Adv Ther source

In the paper

“Obesity can be a cause of impaired fertility.98,121,122”

What the sources say

• ?Could not verify

  Section 6 (page unavailable) lists both infertility and obesity as features associated with PCOS, but does not say obesity causes impaired fertility. Searches for obesity, fertility, anovulation, and weight loss found no passage in our copy establishing that causal link. (LLM, conf=0.72)

  cites [98] Armanini, 2022, Controversies in the pathogenesis, diagnosis and treatment of PCOS: focus on insulin resistance, inflammation, and hyperandrogenism, Int J Mol Sci sourceExperimental — accuracy not yet measured
• Partly supported

  The Pathophysiology section says obesity can cause testosterone deficiency in men, and the Management options section discusses erectile dysfunction in obese men. These passages support a link to impaired male reproductive function, but the paper does not directly state that obesity impairs fertility or extend the finding beyond men. (LLM, conf=0.78)

  cites [121] Fernandez, 2019, Male obesity-related secondary hypogonadism—pathophysiology, clinical implications and management, Eur Endocrinol sourceExperimental — accuracy not yet measured
• Supported

  The Introduction states that obesity impacts reproductive function, and the Sperm and Semen Parameters section describes a negative effect on male reproductive function. These passages support the qualified claim that obesity can impair fertility, specifically in men. (LLM, conf=0.90)

  cites [122] Sultan, 2020, Male obesity associated gonadal dysfunction and the role of bariatric surgery, Front Endocrinol source

In the paper

“In women, hormonal dysfunction of adipose tissue and hyperinsulinaemia (which can act as a gonadotrophin) from insulin resistance constitute the main links to development of functional hyperandrogenism or polycystic ovary syndrome.98”

What the sources say

• Partly supported

  Section 2 describes hyperinsulinaemia resulting from insulin resistance and says insulin acts as a co-gonadotropin, increasing androgen production. Section 3 implicates adipose-tissue dysfunction in a possible cycle involving PCOS, but does not identify hormonal dysfunction of adipose tissue as a main link to its development; it says these observations need confirmation. Page numbers are unavailable in our copy. (LLM, conf=0.85)

  cites [98] Armanini, 2022, Controversies in the pathogenesis, diagnosis and treatment of PCOS: focus on insulin resistance, inflammation, and hyperandrogenism, Int J Mol Sci sourceExperimental — accuracy not yet measured

In the paper

“Obesity is associated with increased risk of mortality in patients with cancer due to altered drug metabolism, chemotherapy resistance, accelerated carcinogenesis, or a combination of these.134”

What the sources say

• Partly supported

  The Discussion reports increased mortality with obesity in some cancers, while the Conclusions note reduced mortality in lung cancer and melanoma. The Introduction and Discussion propose possible mechanisms, but they do not establish altered drug metabolism, chemotherapy resistance, or accelerated carcinogenesis as causes of the mortality association. The Discussion mentions possible chemotherapy undertreatment, which is not the same as chemotherapy resistance. (LLM, conf=0.88)

  cites [134] Petrelli, 2021, Association of obesity with survival outcomes in patients with cancer: a systematic review and meta-analysis, JAMA Netw Open sourceExperimental — accuracy not yet measured

In the paper

“Weight stigma is shamefully prevalent among health-care professionals, including obesity specialists.11”

What the sources say

• Supported

  The Summary of evidence, under “Prevalence of weight bias, stigma, and discrimination,” reports weight bias among healthcare professionals, including those engaged in the clinical management of obesity. The consensus statements say many healthcare professionals hold negative attitudes and call stigma especially unacceptable among specialists in obesity care. Page numbers are not provided in our copy. (LLM, conf=0.92)

  cites [11] Rubino, 2020, Joint international consensus statement for ending stigma of obesity, Nat Med source

In the paper

“A belief held by most people with obesity is that weight loss is their responsibility.57”

What the sources say

• ?Not checked — no full text of the sourcecites [57] Kaplan, 2018, Perceptions of barriers to effective obesity care: results from the national ACTION study, Obesity source

In the paper

“Research surveys also suggest that only about half of people with obesity believe that an individual’s weight could negatively affect future health, considerably fewer than reported by health-care professionals.57”

What the sources say

• ?Not checked — no full text of the sourcecites [57] Kaplan, 2018, Perceptions of barriers to effective obesity care: results from the national ACTION study, Obesity source

In the paper

“Once conversations regarding obesity treatment do occur during patient consultations, follow-up care is not routine.”

In the paper

“People with obesity report not initiating conversations about their weight primarily because of the belief that weight management is their own responsibility and that they already know what is needed to be successful.57”

What the sources say

• ?Not checked — no full text of the sourcecites [57] Kaplan, 2018, Perceptions of barriers to effective obesity care: results from the national ACTION study, Obesity source

In the paper

“A 2022 meta-analysis of studies about weight bias among health-care professionals found that physicians, nurses, dietitians, psychologists, physiotherapists, occupational therapists, speech therapists, podiatrists, and exercise physiologists all held implicit or explicit (or both), weight-biased attitudes toward people with obesity.65”

What the sources say

• ?Not checked — no full text of the sourcecites [65] Lawrence, 2021, Weight bias among health care professionals: a systematic review and meta-analysis, Obesity (Silver Spring) source

In the paper

“Obesity-related conditions (including sleep disturbance, eating behaviours and disorders, disability, weight stigma, low self-esteem, and psychosocial impairment) act to impair quality of life with both conditions.”

In the paper

“Since 2021, research in a large US paediatric health-care system reported that children and adolescents with obesity were 22–104% more likely to be diagnosed with two or more obesity-related diseases as primary diagnoses, depending upon the severity of obesity, compared with people classified as without obesity.151”

What the sources say

• ?Not checked — no full text of the sourcecites [151] Nussbaum, 2021, Distribution of comorbidities as primary diagnoses by obesity class among patients in a large US paediatric healthcare system, Clin Obes source

In the paper

“Associations between obesity and anxiety are unclear, as positive, negative, and null relationships are reported.137–139”

What the sources say

• ?Not checked — no full text of the sourcecites [137] Milaneschi, 2019, Depression and obesity: evidence of shared biological mechanisms, Mol Psychiatry source
• ?Not checked — no full text of the sourcecites [138] Jokela, 2023, Obesity as a causal risk factor for depression: systematic review and meta-analysis of Mendelian randomization studies and implications for population mental health, J Psychiatr Res source
• ?Not checked — no full text of the sourcecites [139] Amiri, 2019, Obesity and anxiety symptoms: a systematic review and meta-analysis, Neuropsychiatr source

In the paper

“Weight stigma adversely affects mental and physical health beyond that of obesity itself through internalised stigma, stress, social isolation, low self-esteem, anxiety, depression, and substance abuse.”

In the paper

“The higher the childhood BMI,148 the higher the risk of developing obesity-related non-communicable diseases in adulthood.149,150”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [148]
• ?Not checked — no full text of the sourcecites [149] Meyer, 2021, Associations between body mass index and height during childhood and adolescence and the risk of coronary heart disease in adulthood: a systematic review and meta-analysis, Obes Rev source
• ?Not checked — no full text of the sourcecites [150] Horesh, 2021, Adolescent and childhood obesity and excess morbidity and mortality in young adulthood—a systematic review, Curr Obes Rep source

In the paper

“Skin integrity is compromised by obesity.”

In the paper

“As BMI can overestimate and underestimate the presence of excess adiposity, especially at levels around the traditional thresholds used for the definition of obesity, we recommend that obesity status should be verified by at least one additional anthropometric measure (eg, waist circumference, waist-to-hip ratio, or waist-to-height ratio), or, where available, direct fat mass measurement (eg, by D”

In the paper

“A 2018 study has shown that remitting from overweight by late adolescence can reduce the risk of type 2 diabetes.152”

What the sources say

• Not checked yet

  Checked before — its earlier verdict is held back until a new check runs.

  cites [152] Bjerregaard, 2018, Change in overweight from childhood to early adulthood and risk of type 2 diabetes, N Engl J Med source

In the paper

“Such practices can effectively, and unfairly, deny access to care among many people who already have objectively ill health due to obesity alone.”

In the paper

“It is common practice to require the presence of another disease (so-called obesity plus criteria) for indication to and coverage of obesity treatment.”

What the sources say

• ?Not checked — no full text of the sourcecites [24] Gebran, 2020, Insurance coverage criteria for bariatric surgery: a survey of policies, Obes Surg source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [25]

In the paper

“Thus, the current definition of obesity inherently lacks enough sensitivity and specificity for clinical use, justifying concerns about a blanket definition of obesity as a standalone disease state.”

In the paper

“However, alterations of adipose tissue function are not always necessary for the effect of obesity on health, as this can also occur through other mechanisms.”

In the paper

“By contrast, dysfunctional adipose tissue can induce insulin resistance and metabolic alterations in the absence of excess adiposity (eg, lipodystrophy).”

In the paper

“In fact, physical effects of excess fat mass on organs (eg, restrictive lung capacity and musculoskeletal complications) or the whole individual can affect health in the absence of functional alterations.”

In the paper

“Second, the risk associated with obesity does not refer to a specific illness, but to a broad number of other ailments, including type 2 diabetes, cancer, and mental disorders.”

In the paper

“For example, in people with more bone or skeletal muscle mass, such as athletes, BMI can overdiagnose obesity; famous examples of such misclassifications are legendary boxers and US National Football League quarterbacks.42”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [42] Armstrong, 2019

In the paper

“Also, persons matched for visceral adiposity can show differences in their risk-factor profile.”

In the paper

“Many conditions can predispose one to future disease, yet are not considered diseases themselves. For example, although monoclonal gammopathy of uncertain significance can be a precursor of multiple myeloma, it is not deemed a disease itself.37”

What the sources say

• Not checked yet

  Checked before — its earlier verdict is held back until a new check runs.

  cites [37] Landgren, 2019, Association of immune marker changes with progression of monoclonal gammopathy of undetermined significance to multiple myeloma, JAMA Oncol source

In the paper

“However, there is ample evidence that excess adiposity itself can directly induce structural and functional alterations in multiple tissues and organs (eg, liver, heart, lungs, kidneys, and musculoskeletal system), causing objectively ill health, independent of the onset of other diseases.”

In the paper

“This possibility is objectively true for some people with obesity, who appear to be able to live a relatively healthy life for many years, or even a lifetime.”

In the paper

“Alternative measures, such as waist circumference or body fat percentage, might be more accurate for the detection of excess adiposity and, therefore, as measures of obesity-related health risks.47”

What the sources say

• ?Not checked — no full text of the sourcecites [47] Wildman, 2008, The obese without cardiometabolic risk factor clustering and the normal weight with cardiometabolic risk factor clustering: prevalence and correlates of 2 phenotypes among the US population (NHANES 1999–2004), Arch Intern Med source

In the paper

“These measurements might not accurately reflect subcutaneous and visceral fat accumulation, which is closely associated with an increased risk of metabolic diseases.2”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [2] 2000

In the paper

“Measurements of waist circumference and waist-to-hip ratio can vary across populations and between sexes.”

In the paper

“The risk of underdiagnosis can delay or even prevent access to care; however, the risk of overdiagnosing obesity is particularly concerning for its potential negative ramifications on health-care systems and society.”

In the paper

“As the illness specifically caused by obesity has not been clinically characterised before this Commission, there are currently no available anthropometric measures or biomarkers that have sufficiently robust diagnostic accuracy to conceive a single-criterion, diagnostic model of clinical obesity (as there is for diabetes).”

In the paper

“Such practices effectively lead to a paradox whereby people with objective ill health due to obesity alone (ie, severe symptoms or limitations of daily activities due to effects of obesity on pulmonary, cardiovascular, or musculoskeletal systems) can be denied access to care due to lack of supposed comorbidities.”

In the paper

“Thus, as for BMI, diagnostic methods exclusively based on anthropometric measures can underdiagnose or overdiagnose illness.”

In the paper

“This paradox is evident in current regulatory and insurance policies for antiobesity drugs and bariatric or metabolic surgery that require the presence of one or more comorbidities for indication to, and coverage of, treatment.”

In the paper

“The global rise in the prevalence of obesity is driven by social and environmental factors, in particular easy access to energy-dense, heavily marketed, processed foods that are palatable and inexpensive.81”

What the sources say

• ?Not checked — no full text of the sourcecites [81] Swinburn, 2011, The global obesity pandemic: shaped by global drivers and local environments, Lancet source

In the paper

“The clinical assessment of patients living with obesity and related complications is also fraught with bias and difficulty.”

In the paper

“However, epidemiological, genetic, and trial evidence support stronger links of obesity with incident heart failure than with atherosclerotic cardiovascular disease.”

In the paper

“Recurrent hypoxia and associated activation of the sympathetic nervous system and other stress responses can contribute to higher rates of hypertension, metabolic syndrome, and type 2 diabetes in people with obesity and sleep disordered breathing.102”

What the sources say

• ?Not checked — no full text of the sourcecites [102] Seetho, 2014, Sleep-disordered breathing, type 2 diabetes and the metabolic syndrome, Chron Respir Dis source

In the paper

“This region is crucial for cognitive-based inhibitory control of food intake.93”

What the sources say

• Not checked yet

  Checked before — its earlier verdict is held back until a new check runs.

  cites [93] Farooqi, 2015, Genetic, molecular and physiological mechanisms involved in human obesity: Society for Endocrinology medal lecture 2012, Clin Endocrinol source

In the paper

“Osteoarthritis, particularly affecting large, weight-bearing joints such as the hips and knees, develops as a direct effect of increased body size on these joints.”

In the paper

“Dysregulation in these neural circuits can lead to an imbalance between energy intake and expenditure, promoting uncontrolled fat accumulation, weight gain, and the development of obesity.93”

What the sources say

• Not checked yet

  Checked before — its earlier verdict is held back until a new check runs.

  cites [93] Farooqi, 2015, Genetic, molecular and physiological mechanisms involved in human obesity: Society for Endocrinology medal lecture 2012, Clin Endocrinol source

In the paper

“This mechanism seems to be mediated in part by gut hormonal responses and reductions in the fat-derived hormone leptin, which interact with regulatory regions within the brain to establish a set-point of equilibrium body adiposity.87,88”

What the sources say

• ?Not checked — no full text of the sourcecites [87] Sumithran, 2011, Long-term persistence of hormonal adaptations to weight loss, N Engl J Med source
• ?Not checked — no full text of the sourcecites [88] Rosenbaum, 1999, The role of leptin in human physiology, N Engl J Med source

In the paper

“The hypothalamus is a crucial subcortical brain region that serves as a key control centre for regulating adipocyte mass.93”

What the sources say

• Not checked yet

  Checked before — its earlier verdict is held back until a new check runs.

  cites [93] Farooqi, 2015, Genetic, molecular and physiological mechanisms involved in human obesity: Society for Endocrinology medal lecture 2012, Clin Endocrinol source

In the paper

“Hyperglycaemia results from complex mechanisms that include the development of insulin resistance, combined with relative β-cell dysfunction.”

In the paper

“Upper airway obstruction caused directly by obesity results in development of sleep disordered breathing, which exists on a spectrum, from snoring with increased upper airways resistance, to obstructive sleep apnoea and obesity hypoventilation syndrome.102”

What the sources say

• ?Not checked — no full text of the sourcecites [102] Seetho, 2014, Sleep-disordered breathing, type 2 diabetes and the metabolic syndrome, Chron Respir Dis source

In the paper

“Increased intestinal permeability to bacterial products such as lipopolysaccharide (a potent inflammatory stimulus) also occurs more frequently in people with obesity.100”

What the sources say

• Not checked yet

  Checked before — its earlier verdict is held back until a new check runs.

  cites [100] Massier, 2020, Adipose tissue derived bacteria are associated with inflammation in obesity and type 2 diabetes, Gut source

In the paper

“The development of organ dysfunction and obesity complications, whether cardiometabolic or biomechanical, can arise at different levels of adiposity in different individuals.”

In the paper

“The body responds to weight loss induced by hypocaloric diets through a robust defensive mechanism, which increases hunger and the desire to eat while decreasing energy expenditure.87”

What the sources say

• ?Not checked — no full text of the sourcecites [87] Sumithran, 2011, Long-term persistence of hormonal adaptations to weight loss, N Engl J Med source

In the paper

“The equilibrium body weight is fiercely defended by the brain, regardless of whether this set point represents a so-called healthy weight or an excessive degree of body fat in people with overweight or obesity.89”

What the sources say

• ?Not checked — no full text of the sourcecites [89] Garvey, 2022, Is obesity or adiposity-based chronic disease curable: the set point theory, the environment, and second-generation medications, Endocr Pract source

In the paper

“In obesity, there can be dysregulation in the VTA’s dopaminergic signalling, contributing to the reinforcement of overeating behaviours.93”

What the sources say

• Not checked yet

  Checked before — its earlier verdict is held back until a new check runs.

  cites [93] Farooqi, 2015, Genetic, molecular and physiological mechanisms involved in human obesity: Society for Endocrinology medal lecture 2012, Clin Endocrinol source

In the paper

“Gut microbiota composition and functionality are altered in obesity, skewing towards increased abundance of Proteobacteria and Firmicutes.100”

What the sources say

• Not checked yet

  Checked before — its earlier verdict is held back until a new check runs.

  cites [100] Massier, 2020, Adipose tissue derived bacteria are associated with inflammation in obesity and type 2 diabetes, Gut source

In the paper

“Deposition of ectopic fat in the liver among susceptible individuals can lead to the development of MASLD.124”

What the sources say

• ?Not checked — no full text of the sourcecites [124] Lazarus, 2024, Reply: a multi-society Delphi consensus statement on new fatty liver disease nomenclature, Hepatology source

In the paper

“Idiopathic intracranial hypertension, which typically presents with progressive and severe headaches, visual loss due to papilloedema, or both, is a less common but serious consequence of obesity.128”

What the sources say

• ?Not checked — no full text of the sourcecites [128] Wang, 2022, Idiopathic intracranial hypertension: pathophysiology, diagnosis and management, J Clin Neurosci source

In the paper

“Once MASLD progresses beyond steatosis to steatohepatitis with fibrosis, there is substantial risk of cirrhosis, liver failure, and hepatocellular carcinoma.124,125”

What the sources say

• ?Not checked — no full text of the sourcecites [124] Lazarus, 2024, Reply: a multi-society Delphi consensus statement on new fatty liver disease nomenclature, Hepatology source
• ?Not checked — no full text of the sourcecites [125] Hydes, 2020, Mechanisms, screening modalities and treatment options for individuals with non-alcoholic fatty liver disease and type 2 diabetes, Diabet Med source

In the paper

“Obesity often generates disability that restricts routine activities of daily living, including aspects of its management, such as physical activity, meal preparation, and access to care.131”

What the sources say

• ?Not checked — no full text of the sourcecites [131] Tareque, 2019, Years of life with and without limitation in physical function and in activities of daily living by body mass index among older adults, Int J Obes (Lond) source

In the paper

“Hence, they do not fulfil principles for diagnostic criteria of clinical obesity.”

In the paper

“As with adults, childhood obesity can directly cause organ dysfunction via several pathophysiological mechanisms, ranging from the physical effects of increased adipose tissue mass (eg, obstructive sleep apnoea, genu valgum, or pes planus), the presence of ectopic fat within tissues and organs, metabolic effects, and inflammatory mechanisms, to psychological effects.”

In the paper

“Detrimental effects of excess weight on executive functions determine peoples’ ability to break ingrained actions, such as unhealthy eating and physical exercise habits in obesity.142”

What the sources say

• Not checked yet

  Checked before — its earlier verdict is held back until a new check runs.

  cites [142] Dye, 2017, The relationship between obesity and cognitive health and decline, Proc Nutr Soc source

In the paper

“Excess adiposity intensifies many common inflammatory skin disorders through adipocyte-generated metabolic and inflammatory pathways.143”

What the sources say

• ?Not checked — no full text of the sourcecites [143] Wu, 2018, Impact of weight stigma on physiological and psychological health outcomes for overweight and obese adults: a systematic review, J Adv Nurs source

In the paper

“There is increasing evidence that child and adolescent obesity lays the foundation for other non-communicable diseases, such as type 2 diabetes, coronary heart disease, hypertension, stroke, certain types of cancer, and pulmonary or renal diseases, which are among the leading causes of death and disability.”

In the paper

“Thus, weight stigma can serve as a psychosocial contributor to obesogenic behaviours.145”

What the sources say

• ?Not checked — no full text of the sourcecites [145] Puhl, 2020, Weight stigma as a psychosocial contributor to obesity, Am Psychol source

In the paper

“excess adiposity can also exert direct and negative effects on the functioning of organs, the whole individual, or both, producing the typical clinical manifestations of an illness.”

In the paper

“This approach strongly reduces, although does not eliminate, the risk of misclassification and both overdiagnosis and underdiagnosis of obesity status.”

In the paper

“Individuals with obesity face a pervasive form of social stigma.”

What the sources say

• Not checked yet

  Checked before — its earlier verdict is held back until a new check runs.

  cites [196] O'Keeffe, 2020, Knowledge gaps and weight stigma shape attitudes toward obesity, Lancet Diabetes Endocrinol source

In the paper

“Attempts in the past centuries (eg, polysarcie and corpulence) and more recently (eg, an adiposity-based chronic disease49) have not succeeded in erasing the name obesity from medical, scientific, or common, everyday vernacular use.”

What the sources say

• Not checked yet

  Checked before — its earlier verdict is held back until a new check runs.

  cites [49] Frühbeck, 2019, The ABCD of obesity: an EASO position statement on a diagnostic term with clinical and scientific implications, Obes Facts source

In the paper

“Preclinical obesity therefore confers a variable risk (depending on age, ethnicity, familial predisposition, body fat distribution, etc) to develop obesity-related diseases, clinical obesity itself, or both.”

In the paper

“they implicitly lack specificity as diagnostic methods of obesity as a disease in itself.”

In the paper

“its pathophysiology might therefore include mechanisms of disease additional to those directly associated with obesity.”

In the paper

“Type 2 diabetes, however, is different from hyperglycaemia, which is one of the components of the metabolic cluster we propose as diagnostic of clinical obesity.”

In the paper

“For this reason, anthropometric measures of obesity can only be used as measures of risk for future obesity-related diseases or mortality, not ongoing illness.”