How is obesity diagnosed?
Obesity is defined as having a body mass index (BMI) of greater than or equal to 30 kilograms per meters squared (kg/m2; “meters” meaning a person’s height). The categories are designated as follows:[2]
| BMI | Category |
|---|---|
| 25–29.9 | overweight |
| 30–34.9 | class I obesity |
| 35–39.9 | class II obesity |
| ≥40 | class III obesity |
While BMI is a generally useful measurement at the population level, because it only accounts for total body mass, individuals who are tall and/or muscular may have a BMI that qualifies as “obese”. As such, it’s useful to factor other measures like body fat percentage into an evaluation of whether someone has obesity.[3]
What are some of the main medical treatments for obesity?
The primary treatment for obesity in patients without other health conditions is lifestyle modifications (i.e., changes to diet and exercise); sometimes, weight loss medications are also used. If lifestyle modifications do not work after trying for a long time, or if the person has class II or III obesity with additional chronic conditions like heart disease or diabetes, then bariatric surgery may be considered.[2]
Have any supplements been studied for obesity?
Many dietary supplements and dietary ingredients have been studied for weight loss. In a recent meta-analysis of 67 randomized trials, the dietary ingredients chitosan, glucomannan, and conjugated linoleic acid were shown to help reduce weight by 1–1.9 kilograms. Other ingredients commonly studied for weight loss include green-tea-extract, green-coffee-extract, bitter orange, and Garcinia cambogia. Evidence about their effects is limited.[4]
How could diet affect obesity?
Diet is central to both the development and the management of obesity and the mainstay of dietary interventions for treating obesity involves calorie restriction. A commonly used approach includes limiting daily calorie intake to 1200–1500 kilocalories (calories adjusted to a person’s weight) for women and 1500–1800 kilocalories for men. Another approach is eating a diet with a 500–750 kilocalorie deficit. Many different types of diets have been used for weight loss; the diet that will be most beneficial over time will vary from person to person, and adherence to the diet is crucial.[2]
Are there any other treatments for obesity?
Physical activity and behavioral therapies are important in the treatment of obesity. Increasing physical activity increases calories burned and works in tandem with calorie-restricting diets for obesity. Engaging in 200–300 minutes of physical activity per week is recommended for those with obesity. Behavioral therapy usually involves regular self-monitoring of food intake, physical activity, and changes to weight.[2]
What causes obesity?
Obesity happens after a prolonged time of eating more calories than what is needed and used by the body. Extra calories are stored as fat. The factors that determine caloric need differ for each person. Factors that affect weight include genetic makeup, overeating, eating high-fat foods, and not being physically active.[1]
Examine Database: Obesity
Research FeedRead all studies
Frequently asked questions
Obesity means having more body fat than what's calculated to be healthy. Obesity increases the risk of diabetes, heart disease, stroke, arthritis, and some cancers. In people with obesity, losing even 5–10% of the total weight can delay or prevent some of these other conditions.[1]
Metabolically healthy obesity (MHO) refers to a subset of people with a BMI ≥30 who display a relatively normal metabolic profile and a reduced risk of disease when compared to people with a BMI ≥30 who have the more typical profile of increased cardiometabolic risk, which is referred to as metabolically unhealthy obesity (MUO).[26][27] Basically, people with MHO don’t seem to have increased cardiometabolic risk despite their elevated BMI.
While the general concept of MHO is clear, standardized criteria have yet to be defined. In fact, more than 30 different definitions of MHO have been used in the scientific literature.[28] Most definitions are based on the criteria for metabolic syndrome outlined by the National Cholesterol Education Program Adult Treatment Panel III,[29] with the presence of 2 or less of the 5 metabolic syndrome components commonly qualifying as MHO.
Consequently, MHO is a misnomer of sorts — people with MHO are typically not truly healthy; they just have fewer cardiometabolic abnormalities than their MUO peers. People with MHO may lack certain cardiometabolic risk factors,[30] but still generally have a higher risk of cardiovascular disease,[31][32] type 2 diabetes,[33] nonalcoholic fatty liver disease,[34][35] and all-cause mortality[30][36][37] than people who are metabolically healthy and have a normal BMI.
To cast further doubt on the seemingly benign nature of MHO, evidence suggests that MHO is not a stable condition and 30%–50% of people with MHO transition to MUO after 4 to 20 years of follow-up.[28] In a large prospective cohort study published in 2018, only about 15% of women with MHO at baseline remained metabolically healthy over 20 years of follow-up.[38]
Lastly, several observational studies have found that increased liver fat is a crucial risk factor for cardiometabolic disease and is associated with an increased risk of transitioning from MHO to MUO;[39][40][41][42] however, very few studies have considered liver fat as part of the criteria for MHO.
In sum, MHO is a misleading term on the basis of the common criteria used to classify it. People with MHO may be at a lower risk of cardiometabolic disease than people with MUO, but their risk is still higher than that of people who are metabolically healthy and have a normal BMI. Additionally, people with MHO commonly transition to MUO over time. As such, just like people with MUO, obesity treatment is indicated for people with MHO to improve long-term health outcomes.[26]
Metabolically healthy obesity (MHO) is most common in women, younger adults, people with a BMI <35, and people of European ancestry.[28] Compared to people with metabolically unhealthy obesity (MUO), people with MHO have greater insulin sensitivity and insulin secretion, as well as less inflammation.[26][43] People with MHO also seem to have greater levels of physical activity and cardiorespiratory fitness.[44]
Evidence suggests that differences in body fat distribution — which is controlled by genetics, age, sex, and total body fat content — explain a large part of the difference in cardiometabolic risk between people with MHO and MUO.[45] Specifically, people with MHO have more subcutaneous fat and less visceral and skeletal muscle fat.[46][47]
People with MHO that consume excess calories display a much greater capacity for subcutaneous fat expansion via the formation of new fat cells than people with MUO who primarily accommodate excess calories by increasing the size of existing fat cells.[45][48] Subcutaneous fat expansion via new fat cell formation prevents fat deposition into visceral fat and results in smaller fat cells, attenuating the negative metabolic effects of obesity.
The term “gut-brain axis” refers to the bidirectional communication system between the gastrointestinal system and the brain. For example, the gastrointestinal tract secretes various hormones to signal the brain to regulate food (energy) intake. The most-studied gut hormones include ghrelin, glucagon-like peptide-1 (GLP-1), cholecystokinin (CCK), pancreatic polypeptide (PP), peptide YY (PYY), and oxyntomodulin.
Ghrelin, secreted by the intestines, increases food intake and gastric motility; in obesity, its secretion is abnormal, and bariatric surgery seems to reduce its secretion after eating. GLP-1, secreted by the intestines, reduces appetite, slows gastric emptying, and suppresses glucagon secretion. Postmeal GLP-1 levels are reduced in people with obesity, and bariatric surgery seems to correct the reduction. In fact, GLP-1 agonists are a medication class that mimics this hormone, and they are used therapeutically for obesity. CKK, secreted by the duodenum, reduces appetite and slows gastric motility. In obesity CKK’s effects on the appetite are blunted, and these effects seem to normalize after bariatric surgery.
PP, secreted by the pancreas, seems to be able to both decrease and increase appetite, depending on where it exerts its effect. PP is structurally related to PYY, which is secreted by the intestines and decreases appetite and gut motility. PYY secretion was found to be reduced in people with obesity, and it increased after bariatric surgery. Oxyntomodulin, secreted by the intestines, reduces food intake and gastric motility. It acts on similar receptors as GLP-1 but produces a smaller incretin effect (the release of insulin in response to increased glucose in the blood). Since the incretin effect regulates blood glucose, there is interest in using oxyntomodulin to treat obesity in people without diabetes, who do not need help regulating blood glucose.[51][52]
Obesity is defined as having a body mass index (BMI) of greater than or equal to 30 kilograms per meters squared (kg/m2; “meters” meaning a person’s height). The categories are designated as follows:[2]
| BMI | Category |
|---|---|
| 25–29.9 | overweight |
| 30–34.9 | class I obesity |
| 35–39.9 | class II obesity |
| ≥40 | class III obesity |
While BMI is a generally useful measurement at the population level, because it only accounts for total body mass, individuals who are tall and/or muscular may have a BMI that qualifies as “obese”. As such, it’s useful to factor other measures like body fat percentage into an evaluation of whether someone has obesity.[3]
BMI is not a highly accurate measure of obesity. That being said, it can be useful as a complementary datum. BMI has a high rate of false negatives, particularly among females, with nearly half of obese people being classified as normal or overweight in some studies. The amount of false positives, on the other hand, is surprisingly small: less than 5% in men and 1% in women, according to one study.
What is BMI
BMI, or Body Mass Index, is a simple formula using a person's height and weight to calculate a number which is supposedly representative of their level of body fat.
The formula itself is:
- Weight (kg) / Height (m)2
or
- (Weight (lbs) * 703) / Height (in)2
And the numerical value fits into the following categories:
-
18.5 is seen as underweight
- 18.5-24.9 is seen as average weight and is usually a target range
- 25-29.9 is seen as overweight
- 30 and above is seen as obese
In the obese category, it is further divided into 30-34.9 (Class I Obesity), 35-39.9 (Class II Obesity) and 40+ (Morbid Obesity). The first two classes are seen as at-risk populations whereas health complications associated with obesity are assumed in a state of Morbid Obesity.
Obesity as defined by alternate means
BMI is not the only measurement of obesity, although it is the most commonly used.
Many studies report obesity rates as a function of body fat percentage (BF%), which is more accurate but requires special tools to assess; even then, the tools may not be highly accurate.
The standard for obesity as defined by body fat percentage is greater than 25% body fat for men and greater than 35% for females; this is the World Health Organization's (WHO) reference standard made in 1995.[17] A more recent (2009) proposal from the American Society of Bariatric Physicians suggest lowering the values to 25% and 30% for men and women, respectively, and these values are used in some studies.[18][19]
Uses of BMI
BMI tends to be used in large-scale population research and surveys as it can be calculated from height and weight, either self-reported or taken quickly and non-invasively by a researcher.
It has the benefits of being quick, easy to calculate, and a measure of body fat in which most of the population will consent to (unlike calipers which are invasive due to touching skin with cold metal objects, and hydrostatic weighing which dunks people in water without oxygen in their lungs).
An exception to this is the NHANES series of studies, a large scale series of studies conducted in the US that assesses persons by calipers.
Accuracy of BMI as it pertains to individuals
Youth
In a study of 1,676 young girls (aged 5-16) it was found that although ethnicity differences existed in body fat that 89.9-92.4% of girls were accurately diagnosed with BMI.[20] Results from NHANES 1999-2004 (three different NHANES surveys) found that 86.9%-89.1% of youth between the ages of 5-18 (both genders) were accurately diagnosed with BMI when compared against skin-fold calipers.[21]
Adults
A cross-sectional study of 13,601 subjects in the US[22] compared BMI against BIA (Bioelectrical Impedence Analysis). BMI defined 21% of men and 31% of women as obese, and BIA indicated 50% of men and 61% of women. Results from this study should be taken with a bit of scrutiny, as BIA is a measure of body fat with high variability based on hydration status.
A smaller scale study (1,691 persons) using DEXA scans (seen as a valid body fat measuring device) found that there was a 34.7% discrepancy between BMI and DEXA for women and 35.2% for men.[23] However, BMI appeared to misclassify women as less fat as they were by DEXA; notable misclassifications include 20.3% of women being obese via BMI while DEXA showed 37.1%, 24.8% of men being obese via BMI compared with 38.4% of men being obese via DEXA. These results have been replicated in which persons in the normal BMI range were actually obese according to body fat percentage (20% of men, 9.2% of females) and more persons in the overweight BMI range were actually obese by body fat percentage (67.2% of men, 84.2% of females).[24] High obesity rates in this study may be partially explained by socioeconomic issues, as it comprised Mexican persons (n=538) living in the southern USA. Finally, another study utilizing DEXA on a sample size of 1,393 persons found that 26% of persons were classified obese by BMI while 64% of persons were obese by DEXA; a misclassification rate (false negatives) of 25% for men and 48% for women was noted.[18]
This trend of BMI underreporting obesity has been replicated in a small (82) sample of active police officers,[21] and for child-bearing aged women where BMI suggests 36.9% of these persons are obese and the WHO standard of 35% body fat indicates an obesity rate of 63.1%.[25]
One meta-analysis on the subject suggests that BMI fails to classify half of persons with excess body fat, reporting them as normal or overweight despite having a body fat percentage classifying them as obese.[19]
Summation
If you are normal weight or overweight according to BMI (18.5-29.9) there is still a chance you are actually obese, and thus is primarily due to low levels of lean mass (muscle, water, and glycogen).
If you are obese according to BMI, you are most likely obese according to body fat percentage as well. When sampling from the general population, over 95% of men and 99% of women identified as obese by BMI were obese via body fat levels.[22]
Outliers to this dataset, those who have enough lean mass to be classified as obese by BMI but not by body fat percentage, are far and few in society. These persons would normally be highly active athletes or dedicated 'weekend warriors', and it is unlikely sedentary persons or those with infrequent exercise habits would be these outliers.
The primary treatment for obesity in patients without other health conditions is lifestyle modifications (i.e., changes to diet and exercise); sometimes, weight loss medications are also used. If lifestyle modifications do not work after trying for a long time, or if the person has class II or III obesity with additional chronic conditions like heart disease or diabetes, then bariatric surgery may be considered.[2]
Glucagon-like peptide 1 (GLP-1) is a hormone that is released from cells in our intestines and colon when we eat food. When GLP-1 binds to its receptor, it stimulates the release of insulin and inhibits the release of glucagon by the pancreas. GLP-1 receptors are located throughout the body, and therefore, the binding of GLP-1 can have effects unrelated to blood glucose lowering, including increased feelings of fullness and satiety, reduced hunger, and decreased food intake.[49]
Synthetic GLP-1 agonists such as liraglutide, semaglutide, and terzepatide mimic the effects of GLP-1 in the body. Furthermore, synthetic GLP-1 agonists have a longer half-life in the body than the native hormone, making for longer-lasting therapeutic effects. Specifically, while the half-life of native GLP-1 is 1–2 minutes, the half-life of GLP-1 analogs can range from 11–15 hours (liraglutide) to 155–184 hours (semaglutide), allowing semaglutide to be administered just once per week by subcutaneous injection.[50]
Many dietary supplements and dietary ingredients have been studied for weight loss. In a recent meta-analysis of 67 randomized trials, the dietary ingredients chitosan, glucomannan, and conjugated linoleic acid were shown to help reduce weight by 1–1.9 kilograms. Other ingredients commonly studied for weight loss include green-tea-extract, green-coffee-extract, bitter orange, and Garcinia cambogia. Evidence about their effects is limited.[4]
Diet is central to both the development and the management of obesity and the mainstay of dietary interventions for treating obesity involves calorie restriction. A commonly used approach includes limiting daily calorie intake to 1200–1500 kilocalories (calories adjusted to a person’s weight) for women and 1500–1800 kilocalories for men. Another approach is eating a diet with a 500–750 kilocalorie deficit. Many different types of diets have been used for weight loss; the diet that will be most beneficial over time will vary from person to person, and adherence to the diet is crucial.[2]
In most cases, someone undertaking a diet with the goal of losing weight — regardless of what diet it is — will experience initial weight loss, followed by a significant amount of weight regain.[5][6] But do “95% of diets fail”, as is sometimes claimed?
This, of course, requires defining what is a “diet success”, and there is no universally accepted definition for what this means (and it likely varies according to each person’s needs and preferences). Nevertheless, some researchers have proposed a weight loss of ≥10% of one’s initial body weight after ≥1 year as successful weight loss.[7]
Using that definition, the percentage of people achieving successful long-term weight loss is variable in studies, with rates of 10%,[8] 20%,[7] 26%,[9] and 33%[10] reported over periods of 1–8 years.
These findings suggest that the failure rate of dieting is high, but not as high as 95%. Of course, it's important to note that the previous studies usually included people who were exercising (or were recommended to do so), and physical activity seems to enhance the effect of dietary interventions on weight loss.[6] Furthermore, these studies typically provided participants with counseling, education, and/or support sessions, which likely improves dietary adherence.
Physical activity and behavioral therapies are important in the treatment of obesity. Increasing physical activity increases calories burned and works in tandem with calorie-restricting diets for obesity. Engaging in 200–300 minutes of physical activity per week is recommended for those with obesity. Behavioral therapy usually involves regular self-monitoring of food intake, physical activity, and changes to weight.[2]
Obesity happens after a prolonged time of eating more calories than what is needed and used by the body. Extra calories are stored as fat. The factors that determine caloric need differ for each person. Factors that affect weight include genetic makeup, overeating, eating high-fat foods, and not being physically active.[1]
It’s been suggested that the microbiome may impact body fat gain and obesity risk through various potential mechanisms, including calorie extraction from food, inflammatory signaling, and lipid oxidation pathways.[11] However, available evidence indicates the microbiome may not actually be an important (or, at the very least, modifiable) determinant of body weight in humans.
Several clinical trials have examined whether a process called a fecal microbiota transplant (FMT) can impact body weight. With FMT, the microbiota of a healthy (or, in this case, lower body weight) individual is transferred into the gut of another individual with the intention of colonizing their microbiome with the donor’s microbes. In most cases, these trials have found FMT does not result in weight loss.[12][13][14][15] Oral probiotics, meanwhile, have been shown to result in weight loss, but the effect seems too small to matter — in one meta-analysis of 15 randomized controlled trials, probiotics led to an average weight loss of only 0.6 kg (1.3 pounds).[16]
You can't be optimally healthy when morbidly obese, but health parameters could be improved (to a degree) independent of weight loss with further benefits inducing weight loss
Health and Obesity Correlates
The state of obesity is definitely correlated with exacerbation of several disease states. Several systemic reviews and/or meta-analysis' noted that the state of obesity is associated with worsened symptoms and signs of Polycystic Ovarian Syndrome (PCOS),[53] Pulmonary Function and Cardiovascular Risk,[54][55] Asthma,[56][57] Obstructive Sleep Apnea,[58] Kidney function,[59] Schizophrenia,[60] Bipolar Disorder,[60] Alzheimer's,[61] worsened Breast Feeding potential[62] and heightened risk of Pregnancy complications[63] as well as preeclampsia,[64] and increased risk of Colorectal Adenocarcinoma.[65]
Several Meta-analysis' indicate that obesity is correlated with disease states and appears to be further correlated with worsened disease progression over time (when compared to leaner subjects with the same disease state)
Conversely, BMI appears to be inversely related to success of suicide attempts (although attempts in women only are positively correlated)[66] and the evidence of BMI influencing cancer survival during chemotherapy is mixed.[67][68]
The above studies establish a relationship between obesity and several disease states, but do not per se establish a causative link. However, unless the (obese/overweight) person being assessed is not the statistical norm it is possible these results would apply to them
Obesity and Activity
Sumo wrestlers tend to be a hot topic in regards to 'Health at Every Size®' due to their body mass exceeding the standards of obesity yet the strength and activity level of an average Rikishi exceeding most of the population.[69][70]
In sumo wrestlers, the large amount of daily physical activity conducted in accordance with a high calorie diet and state of obesity does not appear to be enough to normalize some health parameters; Type II diabetes, triglycerides, and hypertension are still higher in highly active sumo wrestlers when compared to age-matched controls of normal BMI status.[71] This study noted no significant differences in blood glucose or total cholesterol but worsened parameters otherwise, and it should be noted that the difference in average weight was a mere 12.2kg (88kg in control, 100.2kg in Rikishi) which is not the size many associate with a 'sumo wrestler'.[71]
The risk of premature death is higher in sumo wrestlers when comparing the heaviest weight class against lower weight cohorts;[72] an increase in risk of death was very significant when compared against age-matched controls, although it is hard to delineate if this is due to obesity or due to professional contact sports, some evidence towards it being weight related is an association between weight and premature cardiovascular death in NFL players of heavier weight but to a lesser extent in lighter weight NFL players.[73][74] Retired NFL players also appear to be at greater risk for metabolic syndrome if their BMI is greater,[75] and the state of obesity in athletes of this caliber is associated with hepatic damage, assessed by ALT levels.[76]
Sumo wrestlers do tend to have a more favorable body fat composition (more subcutaneous and less visceral, which is in accordance with biomarkers for reduced risk of cardiovascular disease[77]) but this same study also noted that it has yet to be shown that exercise interventions less than the heavily intense Sumo training confer this same theoretical protective benefit.[77]
Using sumo wrestlers and National League American Football players as models for 'High adiposity paired with High activity', there still appear to be risks associated with the state of obesity or the high calorie diet that activity cannot compensate for completely (some compensation does seem apparent, however)
Exercise does not appear to be potent enough to normalize all health biomarkers of an obese (BMI greater than 30) person if weight loss does not also occur; this may not hold for overweight persons where the state of health is inherently more favorable (than obese age-matched persons)
Health at Every Size® (HAES®)
According to a few studies, Health At Every Size® (HAES®) is a movement away from weight-centric thinking towards health-centric thinking, and "(addresses) the biological, psychological and sociocultural aspects of weight problem, to emphasize the importance of health and well-balanced life independently of body weight, and to improve lifestyle habits".[78]
Interventions
In overweight women who participate in HAES® intervention (support groups), it appears that a reduction in appetite precedes a reduction in calories.[78] This (appetite reduction) is a phenomena that has been noted previously with HAES® interventions in free-living conditions.[79][80] The success rate of size acceptance appears to be notable in persons who self-identify as 'chronic dieters',[81] especially when delivered via educational platforms such as a 13-week class[82] or Focus groups.[83]
These apparent benefits to appetite and weight control appear to be associated with normalization of eating behaviours and less stress/anxiety surrounding eating.[84][85]
Health At Every Size® interventions appear to be quite effective for normalizing eating habits and reducing subjective reports of appetite, which may be mediated through a reduction in anxiety and stress associated with eating; this effect is slightly more prominent in chronic dieters
Glucagon-like peptide 1 (GLP-1) is a hormone that is released from cells in our intestines and colon when we eat food. When GLP-1 binds to its receptor, it stimulates the release of insulin and inhibits the release of glucagon by the pancreas. GLP-1 receptors are located throughout the body, and therefore, the binding of GLP-1 can have effects unrelated to blood glucose lowering, including increased feelings of fullness and satiety, reduced hunger, and decreased food intake.[49]
Synthetic GLP-1 agonists such as liraglutide, semaglutide, and terzepatide mimic the effects of GLP-1 in the body. Furthermore, synthetic GLP-1 agonists have a longer half-life in the body than the native hormone, making for longer-lasting therapeutic effects. Specifically, while the half-life of native GLP-1 is 1–2 minutes, the half-life of GLP-1 analogs can range from 11–15 hours (liraglutide) to 155–184 hours (semaglutide), allowing semaglutide to be administered just once per week by subcutaneous injection.[50]
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References
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- Weight - Meysam Zarezadeh, Amir Hossein Faghfouri, Nima Radkhah, Elaheh Foroumandi, Masoud Khorshidi, Ahmadreza Rasouli, Mahtab Zarei, Niyaz Mohammadzadeh Honarvar, Nazanin Hazhir Karzar, Mehrangiz Ebrahimi MamaghaniSpirulina supplementation and anthropometric indices: A systematic review and meta-analysis of controlled clinical trialsPhytother Res.(2020 Sep 23)
- Weight - Reihaneh Zeinalian, Mahdieh Abbasalizad Farhangi, Atefeh Shariat, Maryam Saghafi-AslThe effects of Spirulina Platensis on anthropometric indices, appetite, lipid profile and serum vascular endothelial growth factor (VEGF) in obese individuals: a randomized double blinded placebo controlled trialBMC Complement Altern Med.(2017 Apr 21)
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- Low-density lipoprotein (LDL) - Marco Antonio Hernández-Lepe, Abraham Wall-Medrano, José Alberto López-Díaz, Marco Antonio Juárez-Oropeza, Rosa Patricia Hernández-Torres, Arnulfo Ramos-JiménezHypolipidemic Effect of Arthrospira ( Spirulina) maxima Supplementation and a Systematic Physical Exercise Program in Overweight and Obese Men: A Double-Blind, Randomized, and Crossover Controlled TrialMar Drugs.(2019 May 7)
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- Weight - Maria Pfeuffer, Kerstin Fielitz, Christiane Laue, Petra Winkler, Diana Rubin, Ulf Helwig, Katrin Giller, Julia Kammann, Edzard Schwedhelm, Rainer H Böger, Achim Bub, Doris Bell, Jürgen SchrezenmeirCLA does not impair endothelial function and decreases body weight as compared with safflower oil in overweight and obese male subjectsJ Am Coll Nutr.(2011 Feb)
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- Body Fat - Bell ZW, Canale RE, Bloomer RJA dual investigation of the effect of dietary supplementation with licorice flavonoid oil on anthropometric and biochemical markers of health and adiposityLipids Health Dis.(2011 Feb 10)
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- Weight - Kleefstra N, Houweling ST, Jansman FG, Groenier KH, Gans RO, Meyboom-de Jong B, Bakker SJ, Bilo HJChromium treatment has no effect in patients with poorly controlled, insulin-treated type 2 diabetes in an obese Western population: a randomized, double-blind, placebo-controlled trialDiabetes Care.(2006 Mar)
- Body Fat - Douglas S. Kaiman, Carlon M. Colker, Melissa A. Swain, Georgeann C. Torina, Qiuhu ShiA randomized, double-blind, placebo-controlled study of 3-acetyl-7-oxo-dehydroepiandrosterone in healthy overweight adultsCurrent Therapeutic Research.()
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- Body Fat - Lee E, Kolunsarka I, Kostensalo J, Ahtiainen JP, Haapala EA, Willeit P, Kunutsor SK, Laukkanen JAEffects of regular sauna bathing in conjunction with exercise on cardiovascular function: a multi-arm, randomized controlled trial.Am J Physiol Regul Integr Comp Physiol.(2022-Sep-01)
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- Blood glucose - Smedegaard S, Kampmann U, Ovesen PG, Støvring H, Rittig NWhey Protein Premeal Lowers Postprandial Glucose Concentrations in Adults Compared with Water-The Effect of Timing, Dose, and Metabolic Status: a Systematic Review and Meta-analysis.Am J Clin Nutr.(2023-Aug)
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