#Obesity

Obesity and Cancer

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What is obesity?

Obesity is a disease in which a person has an unhealthy amount and/or distribution of body fat (1). Compared with people of healthy weight, those with overweight or obesity are at greater risk for many diseases, including diabetes, high blood pressure, cardiovascular disease, stroke, and at least 13 types of cancer, as well as having an elevated risk of death from all causes (2–5). 

Diagram of the human body highlighting cancers associated with overweight & Obesity. The cancer types are: meningioma, adenocarcinoma of the esophagus, multiple myeloma, kidney, endometrium, ovary, thyroid, breast, liver, gallbladder, upper stomach, pancreas, and colon & rectum.
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To determine if someone has obesity, researchers commonly use a measure known as the body mass index (BMI). BMI is calculated by dividing a person’s weight (in kilograms) by their height (in meters) squared (commonly expressed as kg/m2). BMI provides a more accurate measure of obesity than weight alone, and for most people it is a good (although imperfect) indicator of body fatness. 

The National Heart Lung and Blood Institute has a BMI calculator for adults. The standard weight categories based on BMI for adults ages 20 years or older are:

BMI in kg/m2Weight Category
Below 18.5Underweight
18.5 to 24.9Healthy
25.0 to 29.9Overweight
30.0 to 39.9Obese
40.0 or higherSeverely obese

The Centers for Disease Control and Prevention (CDC) has a BMI percentile calculator for children and teens. Overweight and obesity for people younger than 20 years old, whose BMI can change significantly as they grow, are based on CDC’s BMI-for-age growth charts. 

BMIWeight Category
BMI-for-age below the sex-specific 5th percentileUnderweight
BMI-for-age at or above the sex-specific 5th percentile, but less than the 85th percentileHealthy  
BMI-for-age at or above the sex-specific 85th percentile, but less than the 95th percentileOverweight
BMI-for-age at or above the sex-specific 95th percentileObese
BMI-for-age at or above 120% of the sex-specific 95th percentile*Severe obesity
*Based on recommendations from experts (6)

Measurements that reflect the distribution of body fat are sometimes used along with BMI as indicators of obesity and disease risks. These measurements include waist circumference, waist-to-hip ratio (the waist circumference divided by the hip circumference), waist-to-height ratio, and fat distribution as measured by dual-energy X-ray absorptiometry (DXA or DEXA) or imaging with CT or PET.

These measures are used because the distribution of fat is increasingly understood to be relevant to disease risks. In particular, visceral fat—fat that surrounds internal organs—seems to be more dangerous, in terms of disease risks, than overall fat or subcutaneous fat (the layer just under the skin). 
 

How common are obesity and severe obesity?

Obesity and severe obesity have become more common in the United States in recent years (7). 

  • In 2011, 27.4% of adults ages 18 or older had obesity or severe obesity.
  • By contrast, in 2020, 31.9% of adults ages 18 or older had obesity or severe obesity. 

The percentage of children and adolescents ages 2–19 years with obesity or severe obesity has also increased (6). 

  • In 2011–2012, 16.9% of 2–19-year-olds had obesity and 5.6% had severe obesity.
  • By contrast, in 2017–2018, 19.3% of 2–19-year-olds had obesity and 6.1% had severe obesity. 

According to the CDC, the prevalence of obesity in the United States differs among racial and ethnic groups (7). In 2020, the proportions of adults ages 18 years or older with obesity or severe obesity were:

  • Non-Hispanic Black, 41.6% 
  • American Indian/Alaska Native, 38.8%
  • Hawaiian/Pacific Islander, 38.5%
  • Hispanic, 36.6% 
  • Non-Hispanic White, 30.7%
  • Asian, 11.8% 

In 2017–2018, the proportions of obesity among children and adolescents ages 2–19 years were (6):

  • Mexican American, 26.9%
  • Hispanic, 25.6%
  • Non-Hispanic Black, 24.2%
  • Non-Hispanic White, 16.1%
  • Non-Hispanic Asian, 8.7%

The prevalence of obesity has increased more quickly recently, possibly due to the COVID-19 pandemic (8). CDC has state-level estimates of adult obesity prevalence in the United States. 

What is known about the relationship between obesity and cancer?

Nearly all of the evidence linking obesity to cancer risk comes from large cohort studies, a type of observational study. However, data from observational studies cannot definitively establish that obesity causes cancer. That is because people with obesity or overweight may differ from people without these conditions in ways other than their body fat, and it is possible that these other differences—rather than their body fat—explain their increased cancer risk.

An International Agency for Research on Cancer (IARC) Working GroupExit Disclaimer concluded that there is consistent evidence that higher amounts of body fat are associated with an increased risk of a number of cancers. The table below shows the risks reported in representative studies. 

Cancer type (reference)Compared with people without obesity or overweight, this cancer is 
Endometrial (9, 10)7 times as likely in people with severe obesity*
2–4 times as likely in people with obesity or overweight
Esophageal adenocarcinoma (11)4.8 times as likely in people with severe obesity
2.4–2.7 times as likely in people with obesity
1.5 times as likely in people with overweight
Gastric cardia (12)2 times as likely in people with obesity
Liver (13, 14)2 times as likely in people with obesity or overweight
Kidney (15, 16)2 times as likely in people with obesity or overweight
Multiple myeloma (17)1.1–1.2 times as likely in people with obesity or overweight
Meningioma (18)1.5 times as likely in people with obesity
1.2 times as likely in people with overweight
Pancreatic (19)1.5 times as likely in people with obesity or overweight
Colorectal (20)1.3 times as likely in people with obesity
Gallbladder (21, 22)1.6 times as likely in people with obesity
1.2 times as likely in people with overweight
Breast
    Postmenopausal (23, 24)       Premenopausal** (24, 25)
1.2–1.4 times as likely in people with obesity or overweight
1.2 times as likely for every 5-unit increase in BMI 0.8 times as likely in people with obesity or overweight
Ovarian*** (26, 27)1.1 times as likely for every 5-unit increase in BMI
Thyroid (28)1.3 times as likely in people with obesity
1.26 times as likely in people with overweight
BMI = body mass index.
*Risk for type I endometrial cancer
**Hormone receptor–positive premenopausal breast cancer
***Higher BMI is associated with a slight increase in the risk of ovarian cancer overall, particularly in women who have never used menopausal hormone therapy (26). The association differs by ovarian cancer subtypes, with strongest risk increases observed for rare, non-serous subtypes (27).

People who have a higher BMI at the time their cancer is diagnosed (29) or who have survived cancer (30, 31) have higher risks of developing a second, unrelated cancer (a second primary cancer).

How might obesity increase the risk of cancer?

Several possible mechanisms have been suggested to explain how obesity might increase the risks of some cancers (32, 33).

  • Fat tissue (also called adipose tissue) produces excess amounts of estrogen, high levels of which have been associated with increased risks of breast, endometrial, ovarian, and some other cancers.
  • People with obesity often have increased blood levels of insulin and insulin-like growth factor-1 (IGF-1). High levels of insulin, a condition known as hyperinsulinemia, is due to insulin resistance and precedes the development of type 2 diabetes, another known cancer risk factor. High levels of insulin and IGF-1 may promote the development of colon, kidney, prostate, and endometrial cancers (34).
  • People with obesity often have chronic inflammatory conditions such as gallstones or non-alcoholic fatty liver disease. These conditions can cause oxidative stress, which leads to DNA damage (35) and increases the risk of biliary tract and other cancers (36).
  • Fat cells produce hormones called adipokines that can stimulate or inhibit cell growth. For example, the level of an adipokine called leptin in the blood increases with increasing body fat, and high levels of leptin can promote aberrant cell proliferation. Another adipokine, adiponectin, is less abundant in people with obesity than in people with a healthy weight and may have antiproliferative effects that protect against tumor growth.
  • Fat cells may also have direct and indirect effects on other cell growth and metabolic regulators, including mammalian target of rapamycin (mTOR) and AMP-activated protein kinase.

Other possible mechanisms by which obesity could affect cancer risk include impaired tumor immunity and changes in the mechanical properties of the scaffolding tissue that surrounds developing tumors (37).

In addition to biological effects, obesity can lead to difficulties in screening and management. For example, women with overweight or obesity have an increased risk of cervical cancer compared with women of healthy weight, likely due to less effective cervical cancer screening in these individuals (38).

How many cancer cases may be due to obesity?

A nationwide cross-sectional study using BMI and cancer incidence data from the US Cancer Statistics database estimated that each year in 2011 to 2015 among people ages 30 and older, about 37,670 new cancer cases in men (4.7%) and 74,690 new cancer cases in women (9.6%) were due to excess body weight (overweight, obesity, or severe obesity) (39). The percentage of cases attributed to excess body weight varied widely across cancer types and was as high as 51% for liver or gallbladder cancer and 49.2% for endometrial cancer in women and 48.8% for liver or gallbladder cancer and 30.6% for esophageal adenocarcinoma in men.

Globally, a 2019 study found that in 2012, excess body weight accounted for approximately 3.9% of all cancers (544,300 cases), with the burden of these cancer cases higher for women (368,500 cases) than for men (175,800 cases) (40). The proportion of cancers due to excess body weight varied from less than 1% in low-income countries to 7% or 8% in some high-income Western countries and in Middle Eastern and Northern African countries.

Does losing weight lower the risk of cancer?

Most of the data about whether losing weight reduces cancer risk comes from cohort and case–control studies. Observational studies of obesity and cancer risk should be interpreted with caution because they cannot definitively establish that obesity causes cancer and people who lose weight may differ in other ways from people who do not.

Some of these studies have found decreased risks of breast, endometrial, colon, and prostate cancers among people with obesity who had lost weight. For example, in one large prospective study of postmenopausal women, intentional loss of more than 5% of body weight was associated with lower risk of obesity-related cancers, especially endometrial cancer (41). However, unintentional weight loss was not associated with cancer risk in this study. 

A follow-up study of weight and breast cancer in the Women’s Health Initiative (42) found that, for women who were already overweight or obese at the beginning of the study, weight change (either gain or loss) was not associated with breast cancer risk during follow-up. However, in a study that pooled data from 10 cohorts, sustained weight loss was associated with lower breast cancer risk among women 50 years and older (43).

To better understand the relationship between weight loss among people with obesity and cancer risk, some researchers are examining cancer risk in people with obesity who have undergone bariatric surgery (surgery performed on the stomach or intestines to provide maximum and sustained weight loss). Studies have found that bariatric surgery among people with obesity, particularly women, is associated with reduced risks of cancer overall (44); of hormone-related cancers, such as breast, endometrial, and prostate cancers (45); and of obesity-related cancers, such as postmenopausal breast cancer, endometrial cancer, and colon cancer (46).

How does obesity affect cancer survivors?

Most of the evidence about obesity in cancer survivors comes from people who were diagnosed with breast, prostate, or colorectal cancer. Research indicates that obesity may worsen several aspects of cancer survivorship, including quality of life, cancer recurrence, cancer progression, prognosis (survival), and risk of certain second primary cancers (29, 30, 47, 48).

For example, obesity is associated with increased risks of treatment-related lymphedema in breast cancer survivors (49) and of incontinence in prostate cancer survivors treated with radical prostatectomy (50). In a large clinical trial of patients with stage II and stage III rectal cancer, those with a higher baseline BMI (particularly men) had an increased risk of local recurrence (51). Death from multiple myeloma is 50% more likely for people with the highest levels of obesity compared with people at healthy weight (52).

Is weight loss after a cancer diagnosis beneficial for people with overweight or obesity?

Most studies of this question have focused on breast cancer. Several randomized clinical trials in breast cancer survivors have reported weight loss interventions that resulted in both weight loss and beneficial changes in biomarkers that have been linked to the association between obesity and prognosis (53, 54). 

However, there is little evidence about whether weight loss reduces the risk of breast cancer recurrence or death (55). The NCI-sponsored Breast Cancer WEight Loss (BWEL) Study, an ongoing randomized phase III trial, is examining whether participating in a weight loss program after breast cancer diagnosis affects invasive disease-free survival and recurrence in overweight and obese women (56).

What research is being done on obesity and cancer?

Many studies are exploring mechanisms that link obesity and cancer (34, 57). One research area involves understanding the role of the microbes that live in the human gastrointestinal tract (collectively called the gut microbiota, or microbiome) in both type 2 diabetes and obesity. Both diseases are associated with dysbiosis, an imbalance in the community of these microbes. For example, the gut microbiomes of people with obesity differ from and are less diverse than those of people of healthy weight. Imbalances in the gut microbiota are associated with inflammation, altered metabolism, and genotoxicity, which may in turn be related to cancer. 

Researchers are also studying how obesity alters the tumor microenvironment, which may play a role in cancer progression. For example, studies in mouse models show that obesity (induced by feeding mice a high-fat diet) creates a competition for lipids between tumor cells and T cells that makes the T cells less effective at fighting the cancer (58). 

Another area of investigation is the role of insulin receptor signaling in cancer. Many cancer cells express elevated levels of IR-A, a form of the insulin receptor that has a high affinity for insulin and related growth factors. Researchers are investigating how these factors contribute to metabolic disease and cancer and whether they may be useful targets for therapeutic interventions to prevent obesity-related cancers.

Investigators are also exploring whether the associations of obesity with cancer risk and outcomes vary by race or ethnicity (59). Also, researchers are investigating whether different cutoffs for overweight and obesity should be used for different racial/ethnic groups. For example, the World Health Organization (WHO) has suggested the alternate thresholds of 23.0 and 27.5 kg/m2 for overweight and obesity for people of Asian ancestry (60).

The NCI Cohort Consortium is an extramural–intramural partnership that combines more than 50 prospective cohort studies from around the world with more than seven million participants. The studies are gathering information on body mass index, waist circumference, and other measures of adiposity from each cohort. The large size of the consortium will allow researchers to get a better sense of how obesity-related factors relate to less common cancers, such as cancers of the thyroid, gallbladder, head and neck, and kidney.

Another area of study is focused on developing more precise and effective interventions to prevent weight gain and weight regain after weight loss. This area of research includes two NIH-based initiatives—the Accumulating Data to Optimally Predict Obesity Treatment (ADOPT) Core Measures (61) and the Trans-NIH Consortium of Randomized Controlled Trials of Lifestyle Weight Loss Interventions (62)—both of which aim to identify predictors of successful weight loss and maintenance and to incorporate information on genetic, psychosocial, behavioral, biological, and environmental factors into predictive profiles to enable more precise and, ultimately, more effective weight loss interventions.

NCI supports research on obesity and cancer risk through a variety of activities, including large cooperative initiatives, web and data resources, epidemiologic and basic science studies, and dissemination and implementation resources. For example, the Transdisciplinary Research on Energetics and Cancer (TREC) initiative supports ongoing training workshops for postdocs and early career investigators to enhance the ability to produce innovative and impactful transdisciplinary research in energetics and cancer and clinical care. The Trans-NCI Obesity and Cancer Working Group promotes the exchange of information and cross-cutting interests in obesity and cancer research within NCI by identifying and sharing state-of-the-science knowledge about obesity and cancer to document what is known and what is needed to move the science forward. 

Continued Treatment With Tirzepatide for Maintenance of Weight Reduction in Adults With Obesity

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Key Points

Question  Does once-weekly subcutaneous tirzepatide with diet and physical activity affect maintenance of body weight reduction in individuals with obesity or overweight?

Findings  After 36 weeks of open-label maximum tolerated dose of tirzepatide (10 or 15 mg), adults (n = 670) with obesity or overweight (without diabetes) experienced a mean weight reduction of 20.9%. From randomization (at week 36), those switched to placebo experienced a 14% weight regain and those continuing tirzepatide experienced an additional 5.5% weight reduction during the 52-week double-blind period.

Meaning  In participants with obesity/overweight, withdrawing tirzepatide led to substantial regain of lost weight, whereas continued treatment maintained and augmented initial weight reduction.

Abstract

Importance  The effect of continued treatment with tirzepatide on maintaining initial weight reduction is unknown.

Objective  To assess the effect of tirzepatide, with diet and physical activity, on the maintenance of weight reduction.

Design, Setting, and Participants  This phase 3, randomized withdrawal clinical trial conducted at 70 sites in 4 countries with a 36-week, open-label tirzepatide lead-in period followed by a 52-week, double-blind, placebo-controlled period included adults with a body mass index greater than or equal to 30 or greater than or equal to 27 and a weight-related complication, excluding diabetes.

Interventions  Participants (n = 783) enrolled in an open-label lead-in period received once-weekly subcutaneous maximum tolerated dose (10 or 15 mg) of tirzepatide for 36 weeks. At week 36, a total of 670 participants were randomized (1:1) to continue receiving tirzepatide (n = 335) or switch to placebo (n = 335) for 52 weeks.

Main Outcomes and Measures  The primary end point was the mean percent change in weight from week 36 (randomization) to week 88. Key secondary end points included the proportion of participants at week 88 who maintained at least 80% of the weight loss during the lead-in period.

Results  Participants (n = 670; mean age, 48 years; 473 [71%] women; mean weight, 107.3 kg) who completed the 36-week lead-in period experienced a mean weight reduction of 20.9%. The mean percent weight change from week 36 to week 88 was −5.5% with tirzepatide vs 14.0% with placebo (difference, −19.4% [95% CI, −21.2% to −17.7%]; P < .001). Overall, 300 participants (89.5%) receiving tirzepatide at 88 weeks maintained at least 80% of the weight loss during the lead-in period compared with 16.6% receiving placebo (P < .001). The overall mean weight reduction from week 0 to 88 was 25.3% for tirzepatide and 9.9% for placebo. The most common adverse events were mostly mild to moderate gastrointestinal events, which occurred more commonly with tirzepatide vs placebo.

Conclusions and Relevance  In participants with obesity or overweight, withdrawing tirzepatide led to substantial regain of lost weight, whereas continued treatment maintained and augmented initial weight reduction.

Introduction

Obesity is a serious chronic, progressive, and relapsing disease.1 Lifestyle interventions are a cornerstone of obesity management; however, sustaining weight reduction achieved through lifestyle-based caloric restriction is challenging.

Therefore, current guidelines recommend adjunctive antiobesity medications to promote weight reduction, facilitate weight maintenance, and improve health outcomes in people with obesity.2–4 Randomized withdrawal studies of antiobesity medications to date have consistently demonstrated clinically significant body weight regain with cessation of therapy.5,6 There is also evidence that antiobesity medications, including long-acting glucagon-like peptide-1 (GLP-1) receptor agonists, naltrexone/bupropion, phentermine/topiramate, and orlistat, may help maintenance of achieved weight reduction.5,7–12

Tirzepatide is a single molecule that combines glucose-dependent insulinotropic polypeptide (GIP) and GLP-1 receptor agonism13 resulting in synergistic effects on appetite, food intake, and metabolic function.14–16 Tirzepatide is approved in many countries, including the US, EU, and Japan, as a once-weekly subcutaneous injectable for type 2 diabetes and for the treatment of obesity in the US and UK.16–18 In a placebo-controlled trial of participants with obesity or overweight without diabetes, tirzepatide led to mean reductions in body weight up to 20.9% after 72 weeks of treatment.17,18

The aim of the SURMOUNT-4 trial was to investigate the effect of continued treatment with the maximum tolerated dose (ie, 10 or 15 mg) of once-weekly tirzepatide, compared with placebo, on the maintenance of weight reduction following an initial open-label lead-in treatment period in participants with obesity or overweight.

Discussion

The SURMOUNT-4 trial results emphasize the need to continue pharmacotherapy to prevent weight regain and ensure the maintenance of weight reduction and its associated cardiometabolic benefits.22 At least 5 trials (including the present study) across various classes of medications, including potent antiobesity medications such as semaglutide, have demonstrated that weight is substantially regained after cessation of pharmacotherapy.5,6,23,24

The consistency of these data across therapeutic classes spanning more than 2 decades suggests that obesity is a chronic metabolic condition similar to type 2 diabetes and hypertension requiring long-term therapy in most patients.

A notable finding in the SURMOUNT-4 trial is that after switching to placebo for 1 year, participants ended the study with substantial body weight reduction (9.9%). However, much of their initial improvement in cardiometabolic risk factors had been reversed. Further studies are needed to understand the potential long-term benefits and risks (ie, legacy effects) of such short-term therapy.

The health benefits seen with continued treatment with the maximum tolerated dose of tirzepatide during this study were achieved with a safety profile consistent with that previously reported in SURMOUNT and SURPASS trials and in studies of incretin-based therapies approved for the treatment of obesity and overweight.18,25–32

The strengths of this study include its large sample size and the randomized withdrawal design. The duration of the open-label lead-in period allowed the study to assess the maintenance of body weight reduction. Dose escalation protocols during the open-label lead-in period helped to maximize tolerability and reflect dose adjustment strategies that may be helpful to future prescribers.

Limitations

This study has limitations. First, the design of this study did not allow dose adjustments after randomization and did not evaluate the effects of intensive behavioral therapy on the maintenance of body weight reduction. Second, those who tolerated initial treatment with 10-mg or 15-mg tirzepatide may represent a subgroup of the general population.

Conclusions

After achieving clinically meaningful weight reduction during a 36-week tirzepatide lead-in treatment period, adults with obesity or overweight who continued treatment with maximum tolerated dose tirzepatide for an additional 52 weeks demonstrated superior weight maintenance and continued weight reduction compared to those who switched to placebo.

Could a vibrating, ingestible capsule help treat obesity?

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Researchers have developed a vibrating ingestible capsule that may help treat obesity. DKart/Getty Images

  • Obesity is a known risk factor for a number of health concerns and diseases.
  • Current noninvasive and invasive treatments for obesity have risks and barriers people may need to overcome.
  • The newest treatment for obesity comes from researchers at MIT, who developed an ingestible capsule that vibrates within the stomach.
  • The way this capsule works is by tricking the brain into thinking it is full.

As of 2020, about 38% of the world’s population is considered to have obesity or overweight, with that percentage expected to jump to 42% by 2025.

Obesity is a known risk factor for a variety of health concerns, including high blood pressureTrusted Source, high cholesterolTrusted Source, sleep apneaTrusted Source, and depression.

Additionally, obesity may increase a person’s chance of developing diseases such as cardiovascular diseaseTrusted Source, type 2 diabetesTrusted Source, osteoarthritisTrusted Source, dementiaTrusted Source, and even certain cancersTrusted Source.

Although there are treatments available for obesity, some interventions, such as making dietary changesTrusted Source can be difficult for a person to stick with for a long time, and others, such as weight loss surgeryTrusted Source also have barriers that may keep a person from that treatment.

To help provide a new option for noninvasive obesity treatment, researchers from the Massachusetts Institute of Technology (MIT) have developed an ingestible capsule that vibrates within the stomach, tricking the brain into thinking it is full.

Information on this new research was recently published in the journal Science Advances.

Finding new noninvasive treatments for obesity

Dr. Shriya Srinivasan, a former MIT graduate student and postdoc who is now an assistant professor of bioengineering at Harvard University, and the lead author of this study, told Medical News Today that the development of new noninvasive methods for treating obesity is of importance in confronting the multifaceted challenges posed by this global health crisis.

“Traditional interventions, such as invasive surgeries, can be associated with significant risks, costs, and lifestyle modifications, limiting their applicability and effectiveness,” Dr. Srinivasan continued. “Noninvasive methods for treating obesity offer alternatives to invasive procedures, reducing associated risks and costs while improving accessibility for a broader population.”

In developing the ingestible capsule, she explained they wanted to develop a method that relied on the body’s natural signaling mechanisms in a closed-loop fashion.

“We believe that relying on these mechanisms will minimize side effects. Relying on mechanostimulationTrusted Source has not yet been explored in this application and may offer a new modality that could lead to increased efficacy, overcoming the limitations of current methods. (And) a capsule-based solution offers scalability and minimization of costs, making this accessible to global populations,” she added.

40% less food intake with the capsule

According to researchers, the ingestible pill is about the size of a multivitamin and is powered by a small silver oxide battery.

Dr. Srinivasan said the ingestible capsule is swallowed about 20 minutes prior to a meal.

“It turns on when it makes contact with gastric fluid in the stomach. It then vibrates and activates the stretch receptorsTrusted Source to signal that the stomach is distended or full. This will then make the subject less hungry, limiting intake,” she explained.

“We feel satiated, or full, primarily when stretch receptors in the stomach indicate that the stomach is ‘full’ of food. We can activate these stretch receptors with just vibration — even in an empty stomach — thereby ‘tricking’ the stomach into feeling full.”
— Dr. Shriya Srinivasan

Dr. Srinivasan and her team conducted research on how well the ingestible capsule might work via an animal model. They found animals given the pill 20 minutes before eating reduced their food intake by about 40%.

“Given the neurophysiology and metabolic results in the study, we expected the [vibrations] to indeed decrease intake, consistent with the mechanism and physiological principles governing hunger and feeding,” Dr. Srinivasan said.

“However, we were impressed by the level to which it was effective, especially in the swine model as these animals normally have a large appetite. It was a very consistent effect, which supports our hypotheses about the working mechanism,” she said.

An alternative to GLP-1 medications like Ozempic

In addition to the reduced food intake, researchers also found the animals in the study gained weight more slowly during periods when they were treated with the vibrating pill.

“We know that consistent limited intake leads to decreased weight gain,” Dr. Srinivasan said. “Since the [vibrations from the capsule] leads to decreased intake, this tool may be useful to people seeking to minimize their weight gain.”

While GLP-1 receptor agonists have recently become very popular as a way to potentially lose weight, the scientists noted there are some potential barriers to these medications, including cost, availability, and the need for them to be self-injected.

“For a lot of populations, some of the more effective therapies for obesity are very costly,” Dr. Srinivasan said.

“At scale, our device could be manufactured at a pretty cost-effective price point. I’d love to see how this would transform care and therapy for people in global health settings who may not have access to some of the more sophisticated or expensive options that are available today,” she added.

Natural ways to feel “full” 

MNT also spoke with Dr. Mir Ali, a bariatric surgeon and medical director of MemorialCare Surgical Weight Loss Center at Orange Coast Medical Center in Fountain Valley, CA, about this new research.

While Dr. Ali said this is an interesting noninvasive concept, he mentioned some potential hurdles.

“First, the stomach empties within an hour, so the longest this thing would give you that effect would be like an hour,” he detailed. “You can’t keep swallowing one of these every hour, so they have to figure out a way for it to last longer in the stomach. If that’s possible, then that can be an alternative.”

“The other issue is it has batteries and batteries are notorious for causing lots of problems in the GI tract. In fact, when a child swallows a battery, like one of those little button batteries, it’s a surgical emergency. So a patient purposely swallowing batteries is not usually a good idea,” Dr. Ali continued.

He said it is important for researchers to develop new noninvasive obesity treatments because although weight loss surgery has been around for many years and is still the most effective treatment, a lot of patients are apprehensive about it.

“In fact, of the patients that qualify for weight loss surgery, only about 2% or so actually end up having surgery because there’s a lot of fear and misconceptions about surgery, insurance issues, psychosocial issues, and other hurdles to achieving surgery,” he explained.

Dr. Ali also said there are ways people can naturally “trick” their stomach and brain into feeling full to help them lose weight.

“Things that are more dense in calories like proteins will typically make the patient feel full for longer. So we emphasize to the patient to eat more protein and vegetables. Things like carbohydrates and sugars are digested more rapidly, so they typically feel full for a shorter period of time,” he said.

What’s the link between obesity and diabetes?

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The link between obesity and type 2 diabetes is well established, with both conditions listed as comorbidities of the other.

Insulin explained

Insulin is a naturally occurring hormone that regulates blood glucose in the body. Obesity – especially abdominal fat distribution – can lead to insulin resistance, where the body cannot produce enough insulin, or is unable to properly use the insulin it does produce. Insulin resistance can lead to high blood sugar levels, which greatly increases the risk of developing type 2 diabetes.

Insulin is necessary for carbohydrates, fat, and protein to be metabolised. Therefore, with the compromised insulin function that comes with type 2 diabetes, the risk of obesity also increases.

Because of the significant overlap between these two diseases, they share many of the same lifestyle changes – namely nutrition and physical activity – needed to help keep them in check. While lifestyle factors play an important role in treating obesity and diabetes, in some circumstances, other interventions such as pharmacotherapy may be required.

Individual risk of obesity

Obesity is increasingly common, with close to 2 billion people predicted to be living with obesity by 2035. Obesity develops due to excess body fat, taking the form of a chronic disease or long-lasting condition.

Obesity often suffers from the stigma of being considered a lifestyle disease. However, lifestyle is just one part of that equation. Everyone’s own body, metabolism, and genetics form a unique equation. Science has given us a better understanding of how different genetics are naturally predisposed to an increased risk of obesity.

Not only is obesity a major risk factor for type 2 diabetes, but it is also likely to increase the rate at which type 2 diabetes progresses. Therefore, maintaining a healthy body weight and avoiding weight gain is crucial for diabetes management and prevention. Every day that a person lives with excess weight also increases their risk of adverse cardiovascular outcomes such as heart attack and stroke.

Is obesity genetic?

When does overweight become obesity?

Obesity is a complex chronic disease in which abnormal or excess body fat impairs health, increases the risk of long-term medical complications and reduces lifespan. Obesity is defined using the body mass index (BMI; weight/height2). Obesity is defined as a BMI exceeding 30 kg/m2 and is subclassified into class 1 (30–34.9), class 2 (35–39.9) and class 3 (≥ 40). At the population level, health complications from excess body fat increase as BMI increases.

BMI is a tool to estimate body fat and screen for obesity and health risks. It can be calculated with a BMI calculator and classifies people as being underweight, overweight, and obese based on their height and weight. BMI is calculated by dividing weight in kilograms by height in meters and then comparing your result to the BMI classes. Body mass index (BMI) can also be correlated to type 2 diabetes risk.

There are six weight status categories:

What is a healthy BMI?

Overweight25 – 29.9
 Class I 30.0 – 34.9
 Class II 35.0 – 39.9
 Class III Above 40

Find your BMI and health risks

Metric /ImperialHeight

cmWeight

kg

Start your change now

People who fall into the overweight category should talk to their doctor about how to slow the progression or potentially prevent obesity. If you are in obesity class I, II or III you should talk to a doctor about managing your obesity and your type 2 diabetes risk.

How to reduce your risk of obesity & type 2 diabetes

Nutrition and physical activity are key recommendations for reducing the risk or slowing the progression of obesity and type 2 diabetes. While weight management and nutrition can often seem straightforward on paper, it’s rarely as simple in practice. What works for one person might not work as effectively for another.

Our genetic variations mean we all store and spend energy differently. Even as we go about improving our health, our bodies and our metabolism react differently to our changing fitness levels, which means our approach – and often our nutrition – may also need to evolve.

Our ability to make healthy choices – such as being able to access and afford healthy food, or having the time and energy to engage in physical activity – is directly linked to our economies, our living situations, and the environments in which we live.

There is no one-size-fits-all solution to health. What is right at the beginning of a journey might not be right down the line. That means you need to find the right solution, or the right level of change for you. Nobody can achieve everything overnight, so start with what’s manageable and work towards realistic improvement goals.

And remember, nobody needs to take that journey alone. Beyond the advice below, your starting point should always be to seek advice from your doctor.Share

DID YOU KNOW…

The chance of inheriting obesity through genetics is estimated between 40-70%

-McPherson R. Genetic contributors to obesityShare ThisShare This

6 scientifically proven obesity treatment options to manage weight

Nutrition

While nutrition is a key driver of health for everybody, regardless of body size, there is no one-sizefits-all healthy eating plan. You should choose an eating plan that supports your best health and that you can maintain long term.

Short-term diets, or severely restricting the amount you eat, can cause metabolic adaptation which may make any weight loss difficult to sustain after the period of dietary restriction.

Talk to your healthcare provider about how a healthy food plan can help you support your health goals. See a registered dietitian for an individualised approach and support.

Read more on managing diabetes and obesity:

How to manage diabetes with diet

Obesity management programme: How to find the best exercises for you

Diabetes & obesity – what you need to know

Physical activity

Physical activity It’s recommended that everyone should exercise moderately for at least 30 minutes per day, five times a week – not only to manage weight and blood sugar, but also to reduce cardiovascular risk. For some people, this could be high-intensity training, for others, it might be light yoga.

Everybody is different, and the level of physical activity you take on needs to be achievable for your existing level of fitness. Taking on too much too soon can lead to injury or exhaustion. Motivation also tends to be more sustainable with incremental progress.

If you haven’t engaged in physical activity in a long time, start with something light, like a daily walk at a nearby park. Increase distance and pace from week to week so that you keep your pulse up and gradually increase your aerobic fitness. The important thing is to maintain progress. As your fitness improves, so too will your metabolism. To keep improving your health, you should gradually increase the intensity of your physical activity.

Regular physical activity supports a wide range of health benefits in adults across all BMI categories, even without weight loss. Aerobic and resistance exercise can favour the maintenance or improvements in cardiorespiratory fitness, mobility, strength, and muscle mass during weight management.

Read more on managing diabetes and obesity:

Obesity management programme: How to find the best exercises for you

How to manage diabetes through exercise

Psychological factors 

Depression and insomnia can both be linked to weight gain. The health of the body and mind are intrinsically linked – when one starts to falter, it may invariably impact the other.

With mental health, it can also be difficult to pinpoint the exact cause of symptoms or make changes on your own, so it’s advisable to seek guidance from your doctor if problems persist.

8 ways to manage stress and overcome mental barriers to weight loss

Always talk to your doctor

Obesity is complex and difficult to manage. Seek the advice of your doctor when considering lifestyle changes and to better understand the support available.

Managing Obesity in Heart Failure: A Chance to Tip the Scales?

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Abstract

Obesity is associated with incident heart failure (HF), independent of other cardiovascular risk factors. Despite rising rates of both obesity and incident HF, the associations remain poorly understood between: 1) obesity and HF outcomes; and 2) weight loss and HF outcomes. Evidence shows that patients with HF and obesity have high symptom burdens, lower exercise capacity, and higher rates of hospitalization for HF when compared with patients with HF without obesity. However, the impact of weight loss on these outcomes for patients with HF and obesity remains unclear. Recent advances in medical therapies for weight loss have offered a new opportunity for significant and sustained weight loss. Ongoing and recently concluded cardiovascular outcomes trials will offer new insights into the role of weight loss through these therapies in preventing HF and mitigating HF outcomes and symptom burdens among patients with established HF, particularly HF with preserved ejection fraction.

Highlights

•Obesity is highly associated with the risk for incident HF, independent of other CV risk factors.
•Among patients with established HF, obesity is associated with a higher risk of hospitalization for HF, higher symptom burden, and lower quality of life.
•Ongoing trials of weight loss will help to identify the role of weight loss in managing HF-related clinical outcomes and symptom burden.

Why some experts think obesity may increase autoimmune risk

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What link is there between obesity and autoimmunity?

  • Immune-mediated and autoimmune diseases are linked with the irregular activity of the immune system. Common examples of these diseases include psoriasis, rheumatoid arthritis, multiple sclerosis, and type 1 diabetes.
  • A​ recent perspective piece in the journal Science suggests that obesity may contribute to autoimmune disease risk due to overactive nutrient and energy-sensing pathways.
  • The author of the essay suggests that reducing caloric intake and using certain medications may help counteract the associated risk for autoimmune diseases from obesity.

The immune system’s role is to defend against what is dangerous to the body. However, it does not always work as it should, which can lead to health problems.

There is a great need for research to understand what triggers autoimmunity — where the body turns against itself or acts abnormally.

A​ recent perspective piece published in Science by Dr. Giuseppe Matarese, a professor of immunology at the University of Naples Federico II in Naples, Italy, discusses how obesity and overnutrition could influence the regulation of the immune system.

Autoimmune, immune-mediated diseases

Note: There is a difference between autoimmune conditions and immune-mediated conditions. The term “immune-mediated” is an umbrella term for disorders with abnormalities in immune system activity. Autoimmune diseases are a subcategory of immune-mediated diseases. Expert commenters and the perspective piece author have chosen to use the term “autoimmune disorders” as an umbrella term instead of “immune-mediated.”

Over 23.5 million peopleTrusted Source in the United States have some type of autoimmune disease. Autoimmune diseases occur when the body’s immune system attacks healthy body tissues.

The specific tissues affected will impact how the disease develops and doctors’ treatment approaches. For example, psoriasis is an autoimmune disease that affects the skin, while hemolytic anemia damages the body’s red blood cells. Inflammation is a common component of many autoimmune diseases.

It is not completely clear what causes autoimmune and immune-mediated diseases. Research is ongoing to understand modifiable and non-modifiable risk factors.

For example, someone’s genetics may play a role in developing an autoimmune disease, but so can certain lifestyle choices. One area of interest is how diet and weight may affect the risk for autoimmune and immune-mediated diseases.

Dr. Jason Balette, a bariatric surgeon with Memorial Hermann in Houston, TX, explained to Medical News Today:

“There appears to be a clear correlation with obesity and autoimmune diseases like MS. This association has been demonstrated through cell signal pathways between adipose cells (fat cells) and the immune system. Just as malnutrition has been shown to decrease immune function, overnutrition (obesity) has been demonstrated to increase immune function leading to autoimmune diseases. Clearly, there is much to learn about these relationships and cell signals to help guide us with treatment plans in the future.”

Obesity as a factor in autoimmune disease

The perspective paper in Science looked at how excessive caloric intake and obesity may influence the risk for abnormal immune responses by the body.

Dr. Matarese wrote about the possible underlying mechanisms of obesity and excessive caloric intake that may affect the body’s immune response.

H​e proposed that people who consume an obesogenic Western diet, that is, a diet that can lead to obesity, have changes in their metabolic workload. Put simply, they experience metabolic overload, which has many implications at the cellular level.

First, he proposed that adipose tissues promote increased leptin and cytokine levels. Leptin is a hormone that influences hunger and appetite. CytokinesTrusted Source influence the activity and production of immune cells.

H​e further notes that the circulation of certain nutrients from high-calorie intake in obese individuals is also at work.

H​e proposed that these three factors combined lead to increased inflammatory response and abnormalities in the actions and cells of the immune system. These results then lead to an increased risk for autoimmune disorders.

D​r. Matarese explained some of the critical points of his paper to MNT:

“This perspective summarizes why today we observe a raising in frequency of autoimmune diseases in more affluent countries where there is a strong excess of calorie intake. Calories in excess induce activation of immune cells, thus leading to an increased chance to loose immunological self-tolerance. Generally, the amount of calories and the quality of foods, typically of western diets rich in lipids and carbs, induce inflammation by activating innate and adaptive immune cells and their production of inflammatory mediators, increasing the chance of developing autoinflammation.”

Continuing research and interventions

Based on the ideas he presents in the piece, Dr. Matarese suggests that behavioral interventions may help control the body’s autoimmune response. This could involve intermittent fasting and calorie restriction. It could also include using medications that mimic fasting and reduce the body’s inflammatory response.

Dr. Matarese also discussed that researchers need to go further in investigating different areas. “[We need to] understand specifically if specific diet regimens, not only the amount of calories, predispose to specific diseases more than others,” he told MNT.

Researchers should “also assess whether calorie restriction (CR) can be an effective additional treatment to improve autoimmunity together with specific drug treatments — i.e. there are ongoing trials associating calorie restriction to treat multiple sclerosis together with drugs such as dimethyl fumarate,” he added.

Commenting on the paper, Dr. Balette noted that it points to the importance of maintaining a healthy body weight and what further research could include. He elaborated to MNT:

“The connection between obesity and autoimmune diseases as well as other medical comorbidities related to obesity demonstrates the importance of the need for both surgical and non-surgical weight loss. The further research areas I would like to see would be the continued investigation of the cell signals like leptin, ghrelin and how they change in the post-operative bariatric surgical patient. In addition, further investigation with immunosuppressive and anti-inflammatory drugs and how they function in the obese patient.”

Obesity’s Impact on Uterine Cancer Risk Greater in Younger Age Groups

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Overall risk and risk of endometrioid subtype 20- to 30-fold greater in women younger than 35

TAMPA, Fla. — Obesity poses a significantly greater risk of uterine cancer in younger women as compared with their older counterparts, an analysis of a database from Taiwan showed.

The relative risk of uterine cancer in women with obesity versus normal-weight women increased from 2.6 in the 65+ age group to as much as 39 times greater in women 20 to 24. The risk of endometrioid uterine cancer, the histology most closely associated with obesity, increased from 3.0 in the 65+ age group to 19 and 32 in the 25-34 and 20-24 age groups, respectively.

Among women who met body mass index (BMI) criteria for overweight, the risk of uterine cancer ranged from 1.3 to 7.7 times greater across age groups as compared with normal-weight women, reported Chelsea Stewart, MD, of the University of California Los Angeles, at the Society of Gynecologic Oncologyopens in a new tab or window annual meeting.

“This is the first study to investigate the risk of endometrial cancer based on BMI and age,” said Stewart. “Previous studies lacked information on age and cell type and/or did not evaluate risk of endometrial cancer at a specific age.”

“Overall, compared to normal-weight patients, those who are obese or overweight have a higher risk of uterine cancer,” she added. “Specifically, obesity in younger patients poses a significantly higher risk compared to older patients, up to almost 40-fold higher. Future research should evaluate risk of uterine cancer adjusted for duration of obesity, fat distribution, and lean versus fat mass.”

During a discussion that followed the talk, Megan Clarke, PhD, a research scientist at the National Cancer Institute, asked Stewart for more specifics about the data: the number of cases of uterine cancer in the youngest age group (20-24) with obesity and the confidence intervals associated with the statistically significant risk conferred by obesity in that age group.

Stewart said 11 cases of uterine cancer occurred in women with obesity versus three normal-weight women in the 20-24 age group, and the confidence intervals associated with the risk in that age group ranged from 11 to 139. The researchers performed additional analyses for patients and controls younger than 30 and obtained results associated with a P value <0.001, she added.

In response to another question from Clarke, Stewart said the researchers did not have information about women who had hysterectomies and did not know whether those women had been excluded.

Multiple studiesopens in a new tab or window have documented increasing rates of obesity and a corresponding increaseopens in a new tab or window in rates of uterine cancer. However, studies to date have lacked data directly linking BMI to cancer. U.S. databases do not have the necessary information, leading Stewart and colleagues to analyze records from Taiwan’s Health and Welfare Data Science Center linked to the Statistical Yearbook of Health Promotion. Investigators normalized BMI categories according to Taiwanese standards: normal weight, 18.5-23.0; overweight, 24-27; and obese, ≥27.

From 2008 to 2018, uterine cancer incidence increased from 10 cases per 100,000 to 15.4 per 100,000, representing a 5.9% annual increase. During the same time period, the proportion of overweight and obese individuals increased from 28.4% to 32.4%.

The risk of uterine cancer in overweight versus normal-weight women was 1.3-fold higher in women older than 65 (P<0.001), increasing with age to 7.7-fold higher for women 20-24 (P=0.003). For the comparison of obese versus normal-weight women, the risk of uterine cancer in the 65-or-older age group was 2.6-fold greater, increasing with declining age:

  • 55-64: 3.8
  • 45-54: 4.2
  • 35-44: 10.0
  • 25-34: 16.2
  • 20-24: 38.9

From 2014 to 2018, the risk of endometrioid uterine cancer for obese versus normal-weight women increased from 3.0 per 100,000 in women 65 or older to 31.8 per 100,000 among women 20-24. The risk of serous, carcinosarcoma, and malignant mesenchymal uterine cancer also increased across the age groups.

Stewart acknowledged several limitations to the study: no information on duration of obesity, the lower number of patients in younger cohorts, lack of diversity in the population studied, and the lack of information on genetic risk and use of unopposed estrogen.

The study did not address potential explanations for the association between obesity and uterine cancer. One recent investigationopens in a new tab or window applied Mendelian randomizationopens in a new tab or window to more than a dozen possible molecular risk factors for uterine cancer. The study uncovered “strong evidence” that fasting insulin, bioavailable testosterone, and sex hormone-binding globulin (SHBG) mediate the effect of BMI on uterine cancer risk. The study did not address the variable effect of BMI on cancer risk by age group.

Can Mothers Pass Obesity on to Daughters?

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Approaches to addressing body weight and composition should start early in life, researcher says

A photo of a mom kissing her baby.

Girls were more likely to have obesity if their mother had obesity too, according to a prospective cohort study.

Looking at 240 mother-father-offspring trios from the Southampton Women’s Survey, maternal body mass index (BMI) was positively linked with daughter’s BMI at ages 6 to 7 years (β=0.29, 95% CI 0.11-0.48) and ages 8 to 9 years (β=0.33, 95% CI 0.13-0.54), reported Rebecca Moon, BM, BSc, PhD, of the University of Southampton in England, and colleagues.

While this trend was also seen at age 4, it didn’t reach statistical significance (β=0.14, 95% CI -0.07 to 0.35), the group wrote in the Journal of Clinical Endocrinology & Metabolismopens in a new tab or window.

In addition, fat mass in girls at ages 8 to 9 was also associated with maternal fat mass (β=0.31, 95% CI 0.12-0.49). Moon’s group said this mother-daughter relationship with fat mass appeared to be established by the age of 4.

“The correlations between mother and daughter fat mass and percentage fat mass changed little between offspring ages of 4 years and 8 years, suggesting that these relationships are established early and before the typical period of the adiposity rebound, which usually occurs between 5 and 7 years,” they explained.

Of note, at no age was daughters’ BMI or fat mass significantly linked with paternal BMI or fat mass. Furthermore, at no age was boys’ BMI or fat mass linked with either maternal or paternal BMI or fat mass.

“These findings highlight that girls born to mothers who have obesity or have high amounts of body fat may be at higher risk of gaining excess body fat themselves,” Moon said in a statement. “Further studies are needed to understand why this is happening, but our findings suggest that approaches to addressing body weight and composition should start very early in life, particularly in girls born to mothers with obesity and overweight.”

Lean mass was the only body composition parameter for which there were associations between fathers and daughters, but this was only seen at ages 6 to 7 (β =0.14, 95% CI 0.01-0.26). At no age did boys see this association with either parent.

“There are a number of factors that might determine parent-offspring correlations in body composition, including shared genetics and environmental influences, such as diet and physical activity,” Moon and colleagues noted, adding that “the stronger mother-offspring relative to father-offspring associations with BMI and adiposity also support a possible role for the intrauterine environment in moderating adipose development.”

The authors pointed out they did not take into consideration which parent was the primary caregiver or which parent planned out meals for the children.

For this study, Moon and team included 240 mother-father-offspring trios from the Southampton Women’s Survey, a prospective U.K. population-based pre-birth cohort. Body composition was measured via dual-energy x-ray absorptiometry scans and children were measured at three ages: 4, 6 to 7, and 8 to 9.

At baseline, the mean age of mothers and fathers was 40.8 and 43.6, and median BMI was 25.3 and 27.3, respectively. Over 90% were white, and Moon’s group noted that their findings may not be generalizable to other races/ethnicities.

Estrogen receptor in the heart found to regulate obesity in postmenopausal women

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Estrogen is known to play an important role in the protection of women’s hearts, but once women are postmenopausal and estrogen levels drop, they are at an increased risk of a number of diseases and conditions, including heart disease, obesity and diabetes.

Published in Nature Cardiovascular Research, the study found that reduced ERα in the cells responsible for heart contraction (cardiomyocytes) led to moderate heart dysfunction and increased rates of obesity in female mice, but not in male mice.

Professor Julie McMullen from the Baker Heart and Diabetes Institute said the team identified a sex hormone receptor in the heart that can regulate adiposity (obesity) in females.

“We’ve been interested in trying to understand the role of this estrogen receptor in the heart for some time, to see how it provides protection to the heart,” Professor McMullen said.

“When we blocked this estrogen receptor, we were expecting to see changes and damage largely to the heart. But rather than seeing a dramatic heart phenotype, what we saw was an adiposity phenotype. So, we observed that the female mice were heavier and had more fat mass, which we weren’t expecting at all.”

Genes that are important for contractility of the heart and metabolic function of the heart were also lower in the female heart when ERα was reduced, explaining why the female study hearts did not pump as well.

Associate Professor David Greening, an expert in extracellular vesicle biology at La Trobe University said particles, called extracellular vesicles, that were released from the female hearts with reduced ERα also contained proteins that differed from both the control group and male hearts.

“We found that reducing ERα in heart muscle cells (cardiomyocytes) of female mice leads to transcriptional, lipidomic and metabolic dysregulation in the heart, together with metabolic dysregulation in skeletal muscle and adipose tissue,” Associate Professor Greening said.

“Furthermore, the extracellular vesicles that are released from heart cells with reduced ERα had the capacity to reprogram skeletal muscle cells in cell culture.

“These changes to tissues, the extracellular vesicles proteome and reprogrammed skeletal muscle cells altered the cells’ molecular landscape and function. So rather than energy being expended, energy is instead stored, which explains the increased adiposity in female mice in the absence of Erα,” Associate Professor Greening said.

This important work has implications for preventing and treating heart and metabolic disease in postmenopausal women, but also cardiotoxicity in premenopausal women receiving therapies that may inhibit or reduce ERα in the heart.

“Females who have drugs which can interact with or inhibit this particular receptor, including some chemotherapies, often become obese,” Professor McMullen said.

“Now we have a better understanding of ERα, we’ve got a better chance of identifying therapies to prevent the obesity from occurring.”

Associate Professor Greening said this study demonstrated that “extracellular vesicles—nanovesicles with their packaged molecular cargo—are systemic signaling regulators that can travel to, and impact other organs in the body, including adipose tissue and skeletal muscle.”

“Extracellular vesicles thereby provide a new paradigm in crosstalk between cells, tissues and organs in health and disease,” Associate Professor Greening said.