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Friday, May 2, 2025

Gastric Cancer Prevention: New AGA Update

Clinicians can help reduce gastric cancer incidence and mortality in high-risk groups through endoscopic screening and surveillance of precancerous conditions, such as gastric intestinal metaplasia (GIM), according to a new clinical practice update from the American Gastroenterological Association (AGA).

The AGA update supports additional gastric guidance published so far in 2025, including a clinical guideline on the diagnosis and management of gastric premalignant conditions (GPMC) from the American College of Gastroenterologists (ACG) and upper GI endoscopy quality indicators from ACG and the American Society for Gastrointestinal Endoscopy (ASGE).

“The synergy of these three publications coming out at the same time helps us to finally establish surveillance of high-risk gastric conditions in practice, as we do in the colon and esophagus,” said Doug Morgan, MD, professor of medicine in gastroenterology and hepatology and director of Global Health programs in gastroenterology at the University of Alabama at Birmingham, Alabama.

Morgan, who wasn’t involved with the AGA update, served as lead author for the ACG guideline and co-author of the ACG-ASGE quality indicators. He also co-authored the 2024 ACG clinical guideline on treating Heliobacter pylori infection, which has implications for gastric cancer.

“The AGA and ACG updates provide detail, while the QI document is an enforcer with medical, legal, and reimbursement implications,” he said. “We have an alignment of the stars with this overdue move toward concrete surveillance for high-risk lesions in the stomach.”

The clinical practice update was published in the February 2025 issue of Gastroenterology.

Gastric Cancer Screening

Gastric cancer remains a leading cause of preventable cancer and mortality in certain US populations, the authors wrote. The top ways to reduce mortality include primary prevention, particularly by eradicating H pylori, and secondary prevention through screening and surveillance.

High-risk groups in the United States should be considered for gastric cancer screening, including first-generation immigrants from high-incidence regions and potentially other non-White racial and ethnic groups, those with a family history of gastric cancer in a first-degree relative, and those with certain hereditary GI polyposis or hereditary cancer syndromes.

Endoscopy remains the best test for screening or surveillance of high-risk groups, the authors wrote, since it allows for direct visualization to endoscopically stage the mucosa, identify any concerning areas of neoplasia, and enable biopsies. Both endoscopic and histologic staging are key for risk stratification and surveillance decisions.

In particular, clinicians should use a high-definition white light endoscopy system with image enhancement, gastric mucosal cleansing, and insufflation to see the mucosa. As part of this, clinicians should allow for adequate visual inspection time, photodocumentation, and systematic biopsy protocol for mucosal staging, where appropriate.

As part of this, clinicians should consider H pylori eradication as an essential adjunct to endoscopic screening, the authors wrote. Opportunistic screening for H pylori should be considered in high-risk groups, and familial-based testing should be considered among adult household members of patients who test positive for H pylori.

Endoscopic Biopsy, Diagnosis

In patients with suspected gastric atrophy — with or without GIM — gastric biopsies should be obtained with a systematic approach, the authors wrote. Clinicians should take a minimum of five biopsies, sampling from the antrum/incisura and corpus.

Endoscopists should work with their pathologists on consistent documentation of histologic risk-stratification parameters when atrophic gastritis is diagnosed, the authors wrote. To inform clinical decision-making, this should include documentation of the presence or absence of H pylori infection, severity of atrophy or metaplasia, and histologic subtyping of GIM.

Although GIM and dysplasia are endoscopically detectable, these findings often go undiagnosed when endoscopists aren’t familiar with the characteristic visual features, the authors wrote. More training is needed, especially in the US, and although artificial intelligence tools appear promising for detecting early gastric neoplasia, data remain too preliminary to recommend routine use, the authors added.

Since indefinite and low-grade dysplasia can be difficult to identify by endoscopy and accurately diagnosis on histopathology, all dysplasia should be confirmed by an experienced gastrointestinal pathologist, the authors wrote. Clinicians should refer patients with visible or nonvisible dysplasia to an endoscopist or center with expertise in gastric neoplasia.

Endoscopic Management, Surveillance

If an index screening endoscopy doesn’t identify atrophy, GIM, or neoplasia, ongoing screening should be based on a patient’s risk factors and preferences. If the patient has a family history or multiple risk factors, ongoing screening should be considered. However, the optimal screening intervals in these scenarios aren’t well-defined.

Patients with confirmed gastric atrophy should undergo risk stratification, the authors wrote. Those with severe atrophic gastritis or multifocal/incomplete GIM would likely benefit from endoscopic surveillance, particularly if they have other risk factors such as family history. Surveillance should be considered every 3 years, though shorter intervals may be advisable for those with multiple risk factors such as severe GIM.

Patients with high-grade dysplasia or early gastric cancer should undergo endoscopic submucosal dissection (ESD), with the goal of en bloc, R0 resection to enable accurate pathologic staging and the intent to cure. Eradicating active H pylori infection is essential — but shouldn’t delay endoscopic intervention, the authors wrote.

In addition, patients with a history of successfully resected gastric dysplasia or cancer should undergo endoscopic surveillance. Although post-ESD surveillance intervals have been suggested in other recent AGA clinical practice updates, additional data are needed, particularly for US recommendations, the authors wrote.

Although type 1 gastric carcinoids in patients with atrophic gastritis are typically indolent, especially if less than 1 cm, endoscopists may consider resecting them and should resect lesions between 1and 2 cm. Patients with lesions over 2 cm should undergo cross-sectional imaging and be referred for surgical resection, given the risk for metastasis.

Patient-Centered Approach

The guideline authors suggested thinking about screening and surveillance on a patient-level basis. For instance, only those who are fit for endoscopic or potentially surgical treatment should be screened for gastric cancer and continued surveillance of GPMC, they wrote. If a person is no longer fit for endoscopic or surgical treatment, whether due to life expectancy or other comorbidities, then screening should be stopped.

In addition, to achieve health equity, clinicians should take a personalized approach to assess a patient’s risk for gastric cancer and determine whether to pursue screening and surveillance, the authors wrote. Modifiable risk factors — such as tobacco use, high-salt and processed food diets, and lack of health care — should also be addressed, since most of these risk factors disproportionately affect high-risk patients and represent healthcare disparities, they added.

“This update provides clinicians with a framework for understanding the natural history and epidemiology of gastric polyps, as well as guidance on best practices for the endoscopic detection and classification of gastric polyps, best practices for the endoscopic resection of gastric polyps, and best practices for endoscopic surveillance following resection,” said Hashem El-Serag, MD, professor and chair of medicine at the Baylor College of Medicine and director of the Texas Medical Center Digestive Diseases Center in Houston.

El-Serag, who wasn’t involved with the clinical practice update, has researched and published on consensus around the diagnosis and management of GIM.

“Stomach polyps are commonly found during routine endoscopic procedures. They are mostly asymptomatic and incidental, and therefore, clinicians may not be prepared ahead of time on how to deal with them,” he said. “The appropriate management requires proper identification and sampling of the polyp features and the uninvolved gastric mucosa, as well as a clear understanding of the risk factors and prognosis. Recent changes in the epidemiology and endoscopic management of gastric polyps makes this update timely and important.”

The update received no particular funding. The authors disclosed receiving grant support, having consultant relationships with, and serving in advisory roles for numerous pharmaceutical, biomedical, and biotechnology firms. Morgan and El-Serag reported having no relevant disclosures.

https://www.medscape.com/viewarticle/gastric-cancer-prevention-new-aga-update-reflects-latest-2025a1000aqq

Inflammation and Obesity: Which Starts the Cycle?

The understanding of fat has evolved in recent decades. Once regarded as nothing more than passive storage reservoirs for fat, adipocytes are now recognized as critical players in metabolic and endocrine processes. Fat may even be regarded as an endocrine organ, with the metabolic contribution of adipocytes changing as they enlarge in tandem with increasing obesity. Expanding adipose tissue undergoes alterations that not only promote insulin resistance but also produce pro-inflammatory factors.

“It’s become clear from the literature that people with obesity often have a pro-inflammatory state, based on various biomarkers measured in the blood,” Karen Corbin, PhD, RD, associate investigator of Translational Research Institute, AdventHealth, Orlando, Florida, told Medscape Medical News.

Mechanisms linking obesity and inflammation are intricate and far-reaching, according to Alan Saltiel, PhD, professor of medicine and director of the Diabetes Research Center, University of California San Diego. “In recent decades, the quest to find a mechanism connecting the pathogenesis of obesity to insulin resistance and diabetes has shed light on a close relationship between caloric excess and activation of the innate immune system in most organs that play a role in energy homeostasis,” he told Medscape Medical News.

Inflammation may represent a “bridge” linking obesity to its comorbid conditions, such as type 2 diabetes. Understanding inflammation may also illuminate what drives obesity, beyond excess caloric intake.

Chicken vs Egg

The relationship between obesity and inflammation might be seen as a “tough chicken-and-egg question,” said Saltiel. “Obesity definitely causes inflammation; and inflammation, in turn, makes people more susceptible to weight gain through reducing energy expenditure and possibly through mechanisms in the brain that we don’t fully understand, which reduce the brain’s sensitivity to satiety hormones.”

Research supports the role of both the “chicken” and the “egg.” For example, a population-based study found that an array of baseline inflammatory markers (eg, high-sensitivity C-reactive protein [hs-CRP], interleukin-1 receptor antagonist, IL-1Ra, IL-6, tumor necrosis factor–a, and high-molecular-weight adiponectin) were strongly associated with indicators of obesity (elevated weight, body mass index [BMI], waist circumference, and body fat percentage). After adjustment for obesity predictors, hs-CRP and IL-1Ra were inversely associated with changes in obesity indicators during 7-year follow-up. Almost all associations were attenuated after further adjustment for baseline BMI. “These findings suggest that the inflammatory markers, although highly associated with obesity, do not predict weight gain,” the authors concluded. “This could translate into inflammation being a result of obesity, rather than a contributing factor to it.”

On the other hand, inflammation may contribute to fat storage, according to a paper by Jianping Ye and Jeffrey N. Keller. The inflammatory response may induce energy expenditure “in a feedback manner to fight against energy surplus in obesity.” A deficient feedback system (sometimes called inflammation resistance) reduces energy expenditure, leading to energy accumulation, and in turn, contributing to obesity. Caloric restriction may inadvertently contribute to energy saving, which may be one reason it’s so difficult for people with obesity to lose weight and sustain their weight loss.

The Power of Fat Cells

Saltiel’s research focuses on “trying to understand the signaling pathways in cells.” He described fat cells as playing an important part in controlling metabolism, “If you look at pictures of fat cells, at first glance, they look like marshmallows. But they’re much more than simply ‘blobs.’ They’re actually on the cutting edge of sensing the energy in our bodies.” These cells go through a “decision-making process of whether it’s a good time to store or to burn energy.” The cells must be able to sense “how much energy they have on board and send a signal to the other cells in the brain, liver, and tissues, instructing them what to do.”

Fat cells have hormonal receptors that are sensitive to adrenaline, insulin, and other hormones, Saltiel explained. “They’re very plastic, so they enlarge when we feed them and shrink when we fast.” He noted that pictures of fat cells in mice deprived of food for 24 hours, showed cells that are half the size of fat cells in recently fed mice.

However, he continued, there are types of fat cells, some more adaptable than others. “In a normal setting, fat cells shrink when we fast and expand when we feed. When they expand and shrink, they sense that they have more or less energy and release hormones accordingly. Pathways in fat cells sense the breakdown or storage of energy, and then change the expression of genes that encode for these hormones.”

Leptin, discovered in the 1990s, is the most well-known hormone released in response to feeding, he said. “After we eat and the fat cell is full, it releases leptin, which travels to the brain, tells the brain we’re satiated and we should stop eating, and tells the brain to release hormones that increase the breakdown of fat and increase energy expenditure.” Saltiel described this as a “rheostat” or “feedback loop.”

“When we fast, we release fatty acids from fat cells,” Saltiel stated. “They travel to the liver, muscle, brain, and pancreas to instruct those cells to perform a variety of functions, including the release of other hormones.”

In the setting of inflammation, this process can be disrupted. Inflammation dampens the responsiveness of the fat cell to these signals, so they become less plastic and less adaptable. “Adipose tissue responds to overnutrition by mounting an immune response.” The resulting inflammation induces insulin resistance. Additionally, the adipose cells “become more efficient at storing rather than releasing energy, and inflammation may be implicated in suppressing the release of energy and promoting its storage.”

Several questions about this process are subjects of current investigation, Saltiel said. “The first is what triggers the inflammatory response in adipose tissue that occurs in the setting of positive energy balance and drives storage rather than release.” Trying to understand this entails looking at immune cells residing in adipose tissue; what leads to changes in those cells and how those changes take place.

“One hypothesis, which I think is an oversimplification, is that it’s mechanical stress on the fat cell that triggers inflammation,” Saltiel commented. “It’s been suggested that the fat cell expands to accommodate the fat, but it ‘hits a wall’ because there isn’t enough room to expand. That process could trigger inflammation.”

Another hypothesis he cited is that “bacterial products are released into circulation because of the ‘leaky gut’ that occurs during obesity, resulting in inflammation.” Other mechanisms include adipocyte death and hypoxia, which develops due to the expansion of adipose tissue and reduction in oxygen tension. “However,” Saltiel noted, “it’s unclear whether this hypoxia is a consequence of adipose tissue expansion or whether it directly causes obesity-associated metabolic disease.”

Saltiel thinks the answer probably incorporates several hypotheses, together with “other changes in circulating nutrients that make inflammation more likely to happen and prime the fat cell to mount an inflammatory response.”

He noted that inflammation in obesity is “ low-grade and chronic, rather than acute. The long-term effects of inflammation have downstream impact, which is the second major question we’re trying to understand.”

The third question is which particular pathways, triggered by inflammation, change energy balance, promote energy storage, and repress energy use. “A lot of us are working on that question, and there’s controversy surrounding the mechanisms.” Some studies have utilized an anti-inflammatory antibody or small molecule, with “results that are mixed or modest, or show no effect at all.” The problem, Saltiel explained, is that “there’s probably a redundancy of pathways, so we don’t know which specific pathway to target or whether to target a combination of pathways.”

But if the main action of inflammation in obesity is to reduce energy expenditure, then blocking that process by increasing energy expenditure alone is “likely to have a modest effect, at best. This may be why it doesn’t always help to tell people to ‘simply exercise more.’ People get hungrier and compensate by eating more to balance out the energy expenditure.”

Anti-inflammatory therapy could potentially work if combined with therapy that blocks energy intake, such as a glucagon-like peptide 1 receptor agonists (GLP-1 RAs), Saltiel speculated. “But no one has conducted that study yet; and commonly used anti-inflammatory agents like nonsteroidal anti-inflammatory drugs, for example, won’t target inflammation in adipose tissue. It would be interesting to see if other anti-inflammatory drugs coupled with GLP-1 drugs could work together to improve weight loss and metabolic effects.”

Gut Microbiome: Key Player

The gut microbiome is garnering increasing attention as a potential connector between inflammation and adipose tissue function. A growing body of research demonstrates that disruption of gut microbiota activates the adaptive and innate immunity in the intestine and raises the inflammatory level.

Corbin has studied the role of gut microbiota in obesity. Her research focuses on the role of gut microbiota in directly contributing to energy balance by “harvesting energy” from undigested components of the diet.

“Of the calories a person eats, most are absorbed in the small intestine,” she explained. “Calories from fiber and resistant starch aren’t digestible, so they end up in the colon. The role of high-fiber diets in preventing illnesses such as colon cancer, or promoting cardiovascular health, is well-known. But what we didn’t know 50 years ago is that, with the right kinds of microbes, nondigestible carbohydrates will be fermented. This is beneficial because fermentation produces primarily short-chain fatty acids, an energy source, and these get reabsorbed by the human being.”

Corbin and her collaborators discovered that the energy produced by the microbes in a healthy colon affects energy balance. They measured energy intake, energy expenditure, and energy output (fecal and urinary) in participants in a metabolic ward, under strictly controlled environmental conditions. Compared with the standard Western diet, the Microbiome Enhancer Diet (MBD) led to an additional 116 ± 56 kcals (P < .0001) lost in feces daily, with no changes in energy expenditure, hunger/satiety or food intake (P > .05).

“When we fed people the MBD, high in fiber and resistant starch and low in processed foods, people lost more calories in excretion and had massive growth and remodeling of the microbes,” summarized Corbin, a spokesperson for The Obesity Society.

These findings may lay the groundwork for potential “precision nutrition,” although several questions still need to be elucidated, said Corbin. Does the gut microbiota play a causal, not merely an associational, role in linking diet and human obesity? What’s the magnitude of its effect size? What’s the impact of caloric restriction or overfeeding on the microbiome? Does inflammation contribute to the dynamics of microbiota involvement? And do individuals with obesity benefit from some version of the MBD, not only in terms of weight loss but also in reducing inflammation?

Diets that include foods associated with lower inflammation might be linked to improvements in microbiome diversity and function. Typically, these include consumption of unrefined and minimally processed foods, nutrients including fiber, mono- and poly-unsaturated fatty acids and lean protein sources, and avoidance of red meat, high-fat dairy foods, saturated and trans fats, and processed foods. The Mediterranean diet, for example, has been shown to reduce inflammatory markers and overweight/obesity, and has improved the population of the gut microbiota. “Given that our MBD had many of the same components as the Mediterranean diet, one could hypothesize that inflammation is a means whereby the microbiome is related to energy balance and adipose function,” Corbin suggested.

“We need a happy, healthy, well-fed microbiome,” she added. “In addition to upgrading one’s diet to include prebiotics and reducing foods associated with inflammation and damage to the microbiota, incorporating some extra physical exercise will also help promote negative energy balance.”

Today’s discoveries may revolutionize our understanding of the mechanisms that drive obesity, including inflammation. Both experts hope that these new insights into inflammatory mechanisms will lead to improved management of obesity and its sequelae.

Saltiel is a founder of Elgia Therapeutics. Corbin disclosed no relevant financial relationships.

https://www.medscape.com/viewarticle/inflammation-and-obesity-which-starts-cycle-2025a1000aqk

Low- and No-Calorie Sweeteners Aren’t the ‘Dietary Boogeyman’

I wish it astonished me that people are still publishing studies about non-nutritive sweeteners’ purported links to weight gain despite the lack of any such finding in formal trials or in the post-market surveillance of these additives’ longstanding and widespread use.

I say “I wish” because I wholly understand that in part, study topics and designs are influenced by public interest, and no doubt there has always been interest in the demonization of non-nutritive sweeteners, as well as in the interest of finding a simple solution to the complex issue of societal weight gain. This interest probably stems from the common naturalistic fallacy that posits that “artificial” equals bad and “natural” equals good, a fallacy spurred on by the likes of America’s new Department of Health and Human Services Secretary Robert F. Kennedy, Jr, and the MAHA (Make America Healthy Again) movement.

How badly do people want to believe non-nutritive sweeteners are a danger? Consider this recent crossover study where researchers examined the impact of consuming a beverage consisting of sucralose and water vs one consisting of sucrose and water on functional MRI (fMRI)-measured hypothalamic blood flow, as well as plasma glucose, insulin and glucagon-like peptide 1 (GLP-1). The researchers were measuring these things as surrogates for hunger. I will come back to the results in a moment, but skipping straight to the first line of their conclusion, “Our findings indicate that the non-caloric sweetener sucralose can affect key mechanisms in the hypothalamus responsible for appetite regulation,” would certainly lead one to think that the sucralose arm was uniquely, for lack of a better word, hungrifying. And indeed, the researchers found those surrogate hunger markers did seem to differ between the sucralose and sucrose crossovers whereby with sucralose the surrogate markers were skewed toward levels supportive, based on their belief of the markers’ predictive utility, of heightening hunger.

As to this very small crossover study’s extensive coverage, it near uniformly spoke to sucralose increasing hunger. From social media posts on X (many from healthcare professionals who in turn serve as nutrition, obesity, or science influencers), to science publications mainstream media outlets, nearly all wrote with at times emphatic concern regarding sucralose consumption and the broad genesis of hunger and, of course, weight.

When it comes to non-nutritive sweeteners and weight, I’m not aware of any randomized controlled trial (RCT) that has shown meaningful weight gain consequent to their consumption (something you might expect if they increase hunger). And meta-analyses of RCTs and other sustained interventions also conclude that the use of low- and no-calorie sweeteners in weight management, despite the fMRI findings reported above, is in fact beneficial to weight loss.

But back to that fMRI study that has influencers, doctors, professors, and the media warning about sucralose, hunger, and weight gain, there are two rather important shortcomings. Firstly, weight and dietary intake were not measured. But, happily, researchers, rather than simply collecting fMRI measurements and blood biomarker values, also collected something else perhaps important: subjective reports of hunger.

Certainly, based off the coverage and assuming you want to ignore the wealth of evidence showing if anything the use of low- and no-calorie sweeteners are helpful to weight loss efforts, you’d think those subjective reports would be dramatic. That consuming sucralose and water would see subjects reporting heightened hunger. You’d be wrong though, which brings me to the second important shortcoming: The study found that subjective hunger did not differ between sucralose-sweetened water consumption and consumption of just plain old water. Unless you believe consuming water heightens hunger significantly, this study is not a cause for concern.

I, too, would love there to be a dietary boogeyman to blame for our various diet related ills and concerns, especially obesity, but low- and no-calorie sweeteners almost certainly aren’t it.

Yoni Freedhoff, MD

Associate Professor, Department of Family Medicine, University of Ottawa; Medical Director, Bariatric Medical Institute, Ottawa, Ontario, Canada

Disclosure: Yoni Freedhoff, MD, has disclosed the following relevant financial relationships:
Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: Bariatric Medical Institute; Constant Health
Received research grant from: Novo Nordisk
Publicly share opinions via Weighty Matters and social media

https://www.medscape.com/viewarticle/low-and-no-calorie-sweeteners-arent-dietary-boogeyman-2025a10009xf

US adds 10 more mining projects to fast-track permitting list

The Trump administration on Friday added 10 more US mining projects to a fast-track permitting list aimed at expanding critical minerals production across the country.

The projects – which would supply copper, palladium and other minerals – have been granted FAST-41 status, a federal initiative launched in 2015 to streamline approvals of critical infrastructure.

The Trump administration last month had named an initial 10 projects to the list and said that more would be added in the future.

All of the projects are listed on a US federal website where their permitting progress can be publicly tracked, part of what the administration calls a push for greater transparency and faster permitting.

The latest 10 include a proposed copper and nickel mine in Minnesota from a joint venture of Glencore and Teck Resources; a New Mexico uranium project from Energy Fuels; expansion of a Montana palladium project from Sibanye Stillwater; an Alaskan silver project from Hecla; and a Georgia titanium dioxide project from Chemours.

South32’s Hermosa zinc-manganese project in Arizona was fast-tracked by former President Joe Biden, the first mine to receive the FAST-41 treatment.

President Donald Trump also last month ordered a probe into potential new tariffs on all US critical minerals imports, a major escalation in his dispute with global trade partners and an attempt to pressure industry leader China.

https://www.mining.com/web/us-adds-10-more-mining-projects-to-fast-track-permitting-list/

Government cash mailings to random Americans draw Senate DOGE leader’s ire: ‘Complete waste’

Federal agencies and contractors have been mailing small amounts of cash to hundreds of thousands of Americans in recent years, according to an investigation by the Republican leader of the Senate’s DOGE caucus.

Now, Sen. Joni Ernst (R-Iowa) wants the Elon Musk-inspired Department of Government Efficiency to put an end to the giveaways — which are meant to entice Americans to open government mailings.

“While it is said that a penny saved is a dollar earned, a dollar bill mailed is a complete waste,” Ernst told The Post this week. “I look forward to DOGE and the Trump administration ending the madness, because money does not grow on trees.”

In one egregious example, Ernst said, a Food and Drug Administration contractor mailed out 145,000 $1 bills in order to boost participation in a so-called “Health and Media Study.”

“We knew taxpayers were getting nickel and dimed but blindly mailing $145,000 in cash is shocking even for Washington,” said Ernst.

Recipients of the mailing were “welcome to keep the enclosed $1 in appreciation for their time,” but were not actually required to fill out the online survey.

Individuals who did answer the questions were “offered $25 to complete the online survey before April 30, 2025, and a bonus $5 ($30 total) if they do so on or before April 1, 2025,” according to a copy of the letter seen by The Post.

RTI International, a research institution out of California, organized the survey for the FDA.

Several other agencies engaged in similar initiatives.

In 2019, the Census Bureau sent out $5 bills to randomly selected individuals who were sent the National Survey of Children’s Health, with a $40 bonus for actually completing the questionnaire. The survey was sent by the Maternal and Child Health Bureau, is part of the Department of Health and Human Services’ Health Resources & Services Administration.

The Federal Reserve Board has similarly used cash prizes for its Survey of Consumer Finances and examined the effectiveness of that perk.

“Our evidence indicates that a single $15 pre-paid incentive increases response rates and maintains similar levels of interviewer burden and data quality, relative to a single $5 pre-paid incentive,” an April 2024 Fed study on that survey found.

In a Friday letter to Musk, Ernst reminded her billionaire recipient that the US Postal Service frequently admonishes Americans to “never send cash in the mail.”

“In no world is this the most efficient or professional way to do things,” she wrote. “There’s a reason most private sector surveys rely on digital incentives, avoiding the risk associated with the mail system, and delivering them upon completion.”

“Paying Americans for their time to participate in government surveys is one thing. But randomly

sending loose cash in the mail in hopes that recipients will participate in surveys is exactly the type of thing the American people want you to stop.”

The Post reached out to the FDA.

https://nypost.com/2025/05/02/us-news/government-cash-mailings-to-random-americans-draws-senate-doge-leaders-ire-complete-waste/

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