Genesis Perez-Melara, M.D.

​Infant feeding is still discussed as if it were a simple matter of personal choice. The familiar slogans, “breast is best” and “fed is best” dominate the conversation, yet neither fully reflects the realities facing families and clinicians. The better questions are: What do the data really show about the benefits of breastfeeding for infants, and what barriers determine whether breastfeeding is even realistic?

The evidence suggests that breastfeeding does provide real infant benefits, but the research is more nuanced than public messaging often suggests. A recent AAP-published systematic review in Pediatrics, accompanied by a full AHRQ evidence report, found associations between breastfeeding and lower risk of ear infections, severe respiratory and gastrointestinal infections, asthma, childhood obesity, childhood leukemia, and infant mortality. At the same time, the review emphasizes that much of this literature comes from observational studies, meaning that the strength and certainty of the findings vary. In other words, the benefits should not be dismissed, but they also should not be oversold.

That is where the current divide can become less helpful than it appears. The phrase “Fed is best,” popularized in part by the Fed Is Best Foundation, emerged from a legitimate concern: some newborns need supplementation quickly, and families should not be shamed when breastfeeding is not going well. This concern is grounded in real clinical risks. Insufficient milk intake in the early days of life can contribute to jaundice, dehydration, excessive weight loss, and poor weight gain, all of which may require prompt evaluation and, at times, supplementation.

At the same time, some breastfeeding advocates worry that an overly casual approach to formula feeding can obscure important differences between human milk and formula. That concern is also valid. Formula has become increasingly sophisticated, with additives such as human milk oligosaccharides, milk fat globule membrane components, and lactoferrin designed to mimic some of the biologically active components of breast milk. Early studies suggest these additives may offer benefits, including softer stools, fewer night awakenings, possible reductions in some respiratory infections, and potential immune or cognitive support. However, recent reviews note that the direct health impact of many of these additives remains less clear than the marketing surrounding them.

The challenge is that families are often navigating these decisions without enough support. In some clinics and hospitals, lactation consultants are not readily available, and clinicians may have limited time or training to address breastfeeding problems before they become urgent. As a result, many parents face high-stakes feeding decisions without the guidance they need to make informed choices. Understanding those decisions requires looking beyond individual families and the healthcare system to the broader social and economic conditions in which infant feeding occurs.

The United States guarantees only unpaid federal leave for eligible workers through the FMLA, while paid leave depends on states and employers. Although formula is expensive, breastfeeding is not “free.” A recent Journal of Perinatology perspective argued that once pumps, added food needs, supplements, and the value of a parent’s time are counted, breastfeeding can carry substantial hidden costs. For a parent working an hourly job with little flexibility, protected pumping time that is unpaid may still be a major barrier. That makes infant feeding not just a maternal-child health issue, but also a labor, benefits, and health policy issue.
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My broader takeaway is that nutrition is rarely determined by knowledge or willpower alone. What people eat is shaped by the policies that govern them, the jobs they have, the benefits available to them, their income, and the environments in which they live. That reality applies even to infants. Clinicians should therefore talk about breastfeeding the way good scientists talk about evidence: with honesty, humility, and appropriate context. The infant benefits are meaningful enough to deserve recognition. The evidence is nuanced enough to require careful interpretation. And the barriers many families face are significant enough that counseling should be practical, supportive, and noncoercive, reflecting the realities of everyday life rather than idealized assumptions.

​Diet and health: truth in an old English idiom.
There’s an old English idiom that goes, “One man’s meat is another man’s poison.” It reminds us that what is healthy or enjoyable for one person might be unpleasant for another. This idea becomes relevant when it comes to changing our diets to mitigate the risk of chronic metabolic diseases. Nutrition isn’t one‑size‑fits‑all, and there are many other factors that shape how diet affects health. This is important when we look at a condition strongly shaped by diet, such as metabolic dysfunction-associated steatotic liver disease (MASLD).

MASLD, once known as non-alcoholic fatty liver disease (NAFLD), occurs when fat builds up in the liver. It is the most common chronic liver disease worldwide, affecting 2 in 5 adults. With the rise of the childhood obesity epidemic, MASLD prevalence has risen among children and adolescents, affecting approximately 10% of the pediatric population and up to 35% of youth with obesity. The primary strategy for preventing MASLD is lifestyle modifications, such as making healthful diet changes – e.g., reducing added sugar intake in foods and beverages, focusing on whole foods as opposed to process foods, and consuming healthy fats instead of trans and saturated fats. Yet lifestyle alone is not the only piece of the puzzle; genetic factors play a role as well.
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Our DNA helps explain why diet affects people differently.
When it comes to metabolic diseases like MASLD, one gene of particular interest is the PNPLA3 gene, which provides instructions for making an enzyme that regulates fat storage and the breakdown in liver and fat cells. For this reason, the PNPLA3 gene is strongly associated with the risk of obesity, type 2 diabetes, and MASLD. According to some studies, individuals who have the high-risk genotype of PNPLA3 are 88% more likely to develop MASLD than their lower-risk counterparts, highlighting the importance of identifying protective factors in this vulnerable subgroup.

To investigate potentially protective dietary habits and their interactions with PNPLA3 genotype, in a study with my colleagues, we used data from 381 adolescents in the Denver-based EPOCH cohort. Specifically, we characterized a dietary pattern that is inversely associated with liver fat and investigated whether this association varies by an individual’s level of genetic risk. We found that a dietary pattern composed of vegetables, fruit, nuts and seeds, oatmeal, sports bars, crackers and sandwiches, and beef was associated with lower liver fat, especially among youth with the high-risk allele for PNPLA3. While foods like veggies, fruits, nuts, and whole grains, align with protection against metabolic disease, other foods, such as sports bars, crackers, and sandwiches, were unexpected, as these are ultra-processed, refined, and typically linked to unfavorable health outcomes. We hypothesized that this dietary pattern captures an active, on-the-go lifestyle that may be especially beneficial for adolescents with elevated genetic risk for metabolic disease.

Is the “active, on-the-go” dietary the golden ticket to preventing MASLD?
Not exactly. Because our dietary habits and daily routines do not exist in isolation, the on-the-go dietary pattern may reflect a broader active lifestyle, which could be the real protective factor. Although our analysis accounted for physical activity levels, there may still be differences in activity that our data could not fully capture. We also note that these findings should not overshadow the importance of maintaining a balanced diet. Regularly consuming foods such as fruits and vegetables, whole grains, and nutritious snacks remains an important strategy for supporting overall health, including liver health. Ultimately, further research is needed to better understand how specific foods and nutrients within this dietary pattern contribute to MASLD risk, as well as the underlying biological mechanisms that may explain these associations and, accordingly, lend credence to our findings.
At the same time, this research delivers a hopeful message: even for individuals with a high genetic risk of MASLD, lifestyle changes may still make a meaningful difference. Encouraging dietary patterns that are both nutritious and realistic for adolescents could help pave the way for more personalized and effective strategies to prevent and manage MASLD and other leading metabolic diseases.

Author 
Wei Perng is an Associate Professor in the Department of Epidemiology at the Colorado School of Public Health. Her research revolves around perinatal origins of childhood obesity and related metabolic consequences. She has two boys and one dog, and enjoys napping (see former) in her free time. 
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Kyle Salmon is a Senior Data Analyst and Database Coordinator at the Colorado School of Public Health at the University of Colorado Anschutz Medical Campus. She completed her MSPH in Human Nutrition at the Johns Hopkins Bloomberg School of Public Health. Her research interest includes chronic disease prevention from a nutrition lens, food security, and food as medicine. Kyle enjoys traveling, hiking, camping, skiing, and seeing live music. 

Sanika Chakkamadathil 

​A plate of oysters or mussels might look like a healthy seafood choice but hidden inside could be dangerous levels of per- and polyfluoroalkyl substances (PFAS). Known as “forever chemicals,” these toxic substances are commonly used in nonstick cookware and fast-food wrapping papers, and are even present in waterways, food items, and the air. While the U.S. Environmental Protection Agency (EPA) only classifies a select few PFAS, such as PFOS and PFOA, as official hazardous substances, the entire chemical class poses a serious threat to public health and the environment.
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​In 2024, the U.S. EPA passed legislation in the National Primary Drinking Water Regulation, regulating PFAS for the first time and creating a Maximum Contaminant Level (MCL) for six different types of PFAS in drinking water: PFOA, PFOS, PFHxS, PFNA, HFPO-DA (GenX chemicals), and PFBS mixtures. The EPA set enforceable drinking water limits of 4 parts per trillion (ppt) for PFOA and PFOS and required public water systems to comply by 2029. The EPA also required companies to disclose the amount of PFAS they were using and releasing, under the Toxic Substances Control Act. 
 
However, this policy was recently rewritten to only regulate two major PFAS chemicals, PFOA and PFOS, and extend the deadline for these companies from 2029 to 2031. Meanwhile, the European Union has already taken some legislative measures to begin reducing PFAS in its packaging. A single non-polymeric PFAS compound is limited to 25 ppb (parts per billion) and total PFAS (including polymeric) must be less than 50 ppm (parts per million). Currently, no legislation in the U.S has been passed to regulate the amount of PFAS in any other source of contact other than water. If no action is taken, more communities will become polluted and the attempt to reduce its presence will only become more laborious.
 
An important next step in reducing PFAS exposure is regulating PFAS contamination in food. A recent study found PFOA concentrations as high as 62500 ng/kg in shellfish – including clams, mussels, scallops, whelks, and oysters – from China’s Bohai Sea. Compared to the other studies which had measured the levels of PFAS in seafood in regions in Africa, Europe, and the U.S, this was an extremely high concentration of one individual chemical. Research shows that the Bohai Sea is well known for oil refineries on the coast, resulting in high levels of pollution. Seafood, particularly shellfish, is often identified as a significant source of PFAS exposure because these organisms can accumulate contaminants from polluted aquatic environments. As filter feeders, shellfish absorb PFAS and other pollutants from their surroundings, potentially increasing human exposure through consumption. Reducing PFAS contamination of shellfish will require stronger measures to prevent industrial pollution, especially in waters used for seafood harvesting.
 
Policymakers must prioritize monitoring and regulating PFAS contamination in seafood, particularly in shellfish harvested from contaminated waters. While federal drinking water regulations represent an important step toward reducing exposure, seafood remains an underregulated pathway for PFAS intake. Expanding PFAS regulations beyond drinking water and addressing contamination in the food supply are essential to protecting public health and reducing long-term exposure to these persistent chemicals.  

Author 
Sanika Chakkamadathil is a junior at River Hill High School, working under the guidance of Dr. Pi-I Debby Lin. Her research is focused on how the government can reduce the presence of PFAS chemicals in the environment. More specifically, she is looking into the levels of PFAS in diet, the dangers of PFAS, and the communities who are at risk for PFAS exposure. In her free time, she likes to dance, bake, and spend time with her friends and would like to pursue a career in healthcare in the future. 

Wei Perng, PhD, MPH

For years, type 2 diabetes (T2D) has been treated as a single disease. If someone has high blood sugar but does not meet criteria for type 1 diabetes or another form of diabetes, they are diagnosed with T2D. But researchers are starting to rethink what we call “type 2 diabetes” as multiple distinct conditions that all lead to elevated blood sugar.

Why one size does not fit all.
As discussed in a recently published commentary, not everyone develops T2D in the same way. For some individuals, the problem starts with insulin resistance (when the body stops responding to insulin properly). This is often associated with obesity. For others, their bodies don’t produce enough insulin, sometimes due to genetics and/or environmental factors that damage the pancreas. These differences matter and provide hints on the sequence of biological events that culminate in disease. A study in European populations suggest that these differences may help explain why some T2D patients manage their diabetes with lifestyle changes, others require medications, and some develop serious complications – like kidney or heart disease, or even early mortality. Identifying distinct root causes, as well as the progression of biological events responsible for high blood sugar is key to the effective prevention, treatment, and management of T2D – and can look very different from person to person.

The DEFINE-T2D Consortium.
To better understand this complexity, the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) launched the Definition, Etiology, Function: INtegration to Enhance T2D treatment (DEFINE-T2D) Consortium in 2024. This large research effort brings together data from 13 observational cohort studies, 4 randomized controlled trials, and 6 electronic health record systems and biobanks. Together, these resources include information from more than 4.8 million individuals, many with prediabetes or established T2D. The scale of the project gives researchers an unprecedented opportunity to better understand different forms of T2D. DEFINE-T2D researchers are examining multiple layers of information, including traditional clinical measures (such as blood sugar levels, blood pressure, weight, and medications), genetics (inherited risk factors), omics data (a catch-all term for advanced lab measures using proteins (via proteomics) and metabolites (via metabolomics) to uncover disease pathways at the molecular level).

Researchers are also looking beyond biology. The analyses will also integrate these “below-the-skin” factors with “above-the-skin” influences (known as environmental and social factors) including things like access to education, health care, and grocery stores or indirect exposures including diet, exercise, sleep, and stress. By combining all of this, DEFINE-T2D investigators hope to identify distinct T2D subtypes and determine whether they each carry their own risks for complications and comorbidities.

What does this mean for clinical care?
If researchers can identify distinct forms of T2D, it could change how we approach care for those who are at high risk of or have the disease. Clinicians may eventually be able to predict how their patient’s disease will progress more accurately and choose treatments that work best for that specific individual. A better understanding of T2D subtypes will also help identify high-risk patients earlier and offer tailored prevention strategies. This approach, called precision medicine, moves away from a one-size-fits-all model and towards more personalized care.
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Why this matters.
T2D affects hundreds of millions of people worldwide, yet the effects of this disease vary from person to person. Understanding why is one of the most important next steps in precision diabetes research. The DEFINE-T2D Consortium represents one of the largest efforts ever undertaken to better understand the biology of T2D. While the work is still in its early stages, it has the potential to reshape the prevention, diagnosis, treatment, and management for T2D patients, and lead to better outcomes for people living with this chronic disease.

Food insecurity or inconsistent or inadequate access to enough food for a healthy life is a well-documented social determinant of health. But it is not experienced equally across the population. Our new preliminary research using the Massachusetts Statewide Food Access Survey reveals a striking picture: in 2024, more than half of LGBTQ+ adults in the Commonwealth were food insecure, and many are not using the systems designed to help.

​A Persistent Disparity
Using data from 9,169 Massachusetts residents surveyed between 2022 and 2024, we measured food insecurity with the 10-item USDA Household Food Security Survey Module. Among LGBTQ+ adults, food insecurity rose from 45% in 2022 to 56% in 2024, significantly higher than non-LGBTQ+ adults each year. These numbers are staggering, though not entirely surprising. A 2017 Williams Institute analysis found that 26.7% of American LGBTQ+ adults experienced food insecurity in the prior year, roughly double the national average. Furthermore, LGBTQ+ adults are about twice as likely to experience poverty compared to non-LGBTQ+ adults, a direct consequence of the historical and ongoing discrimination and stigma that likely drives high rates of food insecurity.

Many Aren't Getting Help
Beyond measuring food insecurity, this study examines whether LGBTQ+ adults are using available assistance. In 2024, only one-third used food pantries, and fewer than half used SNAP (the Supplemental Nutrition Assistance Program). LGBTQ+ adults reported multiple barriers to pantry access more frequently than non-LGBTQ+ adults. For example, many pantries are housed in religious settings that haven't always been welcoming to LGBTQ+ people. Transgender and gender nonconforming individuals may face additional, concrete obstacles when applying for benefits if they are unable to receive accurate identification documents. More broadly, discrimination and stigma in housing, employment, and healthcare can make it harder to trust the systems meant to help. Even SNAP, which offers more privacy than visiting a pantry in person, poses barriers and proposed federal policy changes that would make access harder.

Why This Matters and What Can Be Done
Food insecurity isn't just about hunger; it has cascading effects across physical and mental health. The association of food insecurity with poor health outcomes, including mental illness and chronic diseases, has been well-documented, but research has increasingly called for closer examination of how food insecurity affects LGBTQ+ individuals specifically. Given that LGBTQ+ adults already face elevated rates of depression, anxiety, and other chronic conditions, the added burden of food insecurity is particularly dangerous for their health outcomes.
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Our forthcoming research findings show that addressing food insecurity among LGBTQ+ adults requires more than just making programs available. We need multi-level interventions that are designed with input from LGBTQ+ communities themselves to address the unique barriers they face and begin to minimize the burden of food insecurity in this population.

Author
Austin R. Waters is a postdoctoral fellow through the Dana-Farber Cancer Institute and the Harvard LGBTQ Health Center of Excellence. He received his PhD in Health Policy and Management from the University of North Carolina at Chapel Hill. His research focuses on prevention, access, and outcomes among LGBTQ+ and adolescent and young adult (AYA) patient populations. The common threads of his research revolve around health equity, health-related social needs, economic instability, cost-related barriers to care, the influence of policy, and technology use.