Tag Archives: protein

Domain-based mRNA vaccines encoding spike protein N-terminal and receptor binding domains confer protection against SARS-CoV-2 – Science

  1. Domain-based mRNA vaccines encoding spike protein N-terminal and receptor binding domains confer protection against SARS-CoV-2 Science
  2. Trial: Alternative COVID vaccine 75% cross-protective against symptomatic cases in previously infected University of Minnesota Twin Cities
  3. Broadly neutralizing antibodies derived from the earliest COVID-19 convalescents protect mice from SARS-CoV-2 variants challenge | Signal Transduction and Targeted Therapy Nature.com
  4. New Omicron subvariant BA.2.86: A master of immune escape but not taking over yet News-Medical.Net
  5. Efficacy of a bivalent (D614 + B.1.351) SARS-CoV-2 recombinant protein vaccine with AS03 adjuvant in adults: a phase 3, parallel, randomised, modified double-blind, placebo-controlled trial The Lancet
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Midnolin protein plays key role in breaking down short-lived nuclear proteins – News-Medical.Net

  1. Midnolin protein plays key role in breaking down short-lived nuclear proteins News-Medical.Net
  2. Unraveling the Secrets to Brain Diseases – When Proteins Get Stuck at Solid SciTechDaily
  3. The midnolin-proteasome pathway catches proteins for ubiquitination-independent degradation Science
  4. Fundamental understanding of a molecule’s normal function could inform treatments for a variety of brain disorders Medical Xpress
  5. Newly Identified Proteasomal Protein Disposal Mechanism Bypasses Ubiquitin Tagging Genetic Engineering & Biotechnology News
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Targeted protein degradation improves cognition and reduces Alzheimer’s brain pathology in mouse models – FierceBiotech

  1. Targeted protein degradation improves cognition and reduces Alzheimer’s brain pathology in mouse models FierceBiotech
  2. Alzheimer’s and Other “Undruggable” Diseases Could Be Treated With Degraded Modified Proteins SciTechDaily
  3. New drug target shows promise in mice as potential Alzheimer’s treatment New Atlas
  4. Degrading Modified Proteins Could Treat Alzheimer’s and Other “Undruggable” Diseases Neuroscience News
  5. Breaking apart certain proteins may offer a pathway to treat Alzheimer’s diease News-Medical.Net
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Study unveils mechanism regulating the transmission of a protein associated with the progression of Parkinson’s disease – Medical Xpress

  1. Study unveils mechanism regulating the transmission of a protein associated with the progression of Parkinson’s disease Medical Xpress
  2. Brain’s recycling system is blocked by mutation tied to Parkinson’s | Mutation found to aid in buildup of cellular debris in brain cells Parkinson’s News Today
  3. How the Brain’s Recycling System Breaks Down in Parkinson’s Disease Neuroscience News
  4. TNFRSF10B shows promise as therapeutic target in Parkinson’s: Mouse study | High TNFRSF10B protein levels tied to neurodegeneration, motor dysfunction Parkinson’s News Today
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Study unveils mechanism regulating the transmission of a protein associated with the progression of Parkinson’s disease – Medical Xpress

  1. Study unveils mechanism regulating the transmission of a protein associated with the progression of Parkinson’s disease Medical Xpress
  2. AI Semantic Similarity Study Leads to Novel Drug Candidates for Parkinson’s Disease Neuroscience News
  3. Powerful Antibiotics That Kill Superbugs Are Being Found By AI IFLScience
  4. TNFRSF10B shows promise as therapeutic target in Parkinson’s: Mouse study | High TNFRSF10B protein levels tied to neurodegeneration, motor dysfunction Parkinson’s News Today
  5. How IBM’s Supercomputer Found a Hidden New Parkinson’s Drug The Daily Beast
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‘Dead zone’ within tumor promotes cancer spread, helped by a protein secreted by cancer cells – Medical Xpress

  1. ‘Dead zone’ within tumor promotes cancer spread, helped by a protein secreted by cancer cells Medical Xpress
  2. Metastasis from the tumor interior and necrotic core formation are regulated by breast cancer-derived angiopoietin-like 7 | Proceedings of the National Academy of Sciences pnas.org
  3. Largest genomic study focuses on the prognosis of metastatic pheochromocytomas News-Medical.Net
  4. The largest genomic study of rare cancer metastathic pheochromocytoma identifies patients at highest risk of metastasis and those who would respond to immunotherapy EurekAlert
  5. Dead to me? Insights into a tumor’s necrotic core Fred Hutch News Service
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Study explores incidence, severity, and long COVID associations of SARS-CoV-2 reinfections

In a recent study posted to the medRxiv* preprint server, a team of researchers from the United States used electronic health records to characterize the incidence, biomarkers, attributes, and severity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) reinfections and evaluated the association between reinfections and long coronavirus disease (COVID).

Study: SARS-CoV-2 Reinfection is Preceded by Unique Biomarkers and Related to Initial Infection Timing and Severity: an N3C RECOVER EHR-Based Cohort Study. Image Credit: Ralf Liebhold/Shutterstock

Background

The emergent SARS-CoV-2 variants are increasing the incidence of breakthrough infections. Mutations in spike protein regions of these variants that increase immune escape, combined with the waning of the immunity induced by coronavirus disease 2019 (COVID-19) vaccines and previous SARS-CoV-2 infections are resulting in a rise in reinfections. Studies based on whole genome sequences of the SARS-CoV-2 variants isolated from reinfected patients have revealed that the variants responsible for reinfections are distinct from those that caused the earlier infections. However, there is a dearth of information on whether reinfections differ from the initial infection in their incidence, severity, and attributes, as well as on the long COVID complications after SARS-CoV-2 reinfections.

About the study

In the present study, the team used electronic health record data of a cohort exceeding 1.5 million individuals involved in the National COVID Cohort Collaborative (N3C), which is a part of the National Institute of Health’s Researching COVID to Enhance Recovery (RECOVER) initiative. This data was used to evaluate the incidence, biomarkers, and attributes of SARS-CoV-2 reinfections and understand the association between post-acute sequelae of SARS-CoV-2 infection (PASC) and reinfections.

Reinfection was defined based on a positive SARS-CoV-2 antigen or polymerase chain reaction (PCR) test more than 60 days after the index date for the initial SARS-CoV-2 infection. Long COVID was defined based on the International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM) codes.

Reinfections were also examined according to the epochs of SARS-CoV-2 variants, with the epoch of the wild-type strain spanning the March to November 2020 period, the Alpha, Beta, and Gamma variants dominating the December 2020–May 2021 period, and the Delta variant epoch spanning the June 2021–October 2022 period. The Omicron epoch was divided into two parts for the Omicron variant and the Omicron BA variants, corresponding to November 2021–March 2022 and March–August 2022, respectively.

Biomarkers such as inflammation, coagulopathies, and organ dysfunction can be used to characterize SARS-CoV-2 infections. A wide range of biomarkers, including laboratory measurements of white blood cell counts, erythrocyte sedimentation rates, C-reactive protein, serum creatinine, albumin, and many more, were used to characterize reinfections.

COVID-associated hospitalization data was used to determine the severity of reinfections. Mild infections included those that did not require a visit to the emergency department or hospitalization, while those requiring hospitalization were categorized as moderately severe, and cases requiring hospitalization, invasive mechanical ventilators, vasopressors, or extracorporeal membrane oxygenation were considered severe infections.

The period between reinfection and long COVID diagnoses was compared with that between the initial infection and diagnosis of long COVID to understand the relationship between reinfections and PASC.

Results

The results indicated that most individuals in the cohort had one reinfection, with a small group comprising largely of non-Hispanic White males and older individuals having had three or more reinfections. The largest number of reinfections during the Omicron epoch were among individuals who had initial SARS-CoV-2 infections during the epochs of the wild-type, Alpha, Beta, and Gamma strains, followed by reinfections among those with initial Delta infections.

Analyses of biomarkers revealed that compared to the initial SARS-CoV-2 infection, reinfections showed lower elevation of hepatic inflammation markers such as alanine transaminase (ALT) and aspartate transaminase (AST). However, albumin levels were consistently low in reinfection patients.

Furthermore, the severity of reinfections was found to be associated with the severity of the initial SARS-CoV-2 infections. A majority of the cohort experienced mild symptoms during the initial infections and reinfections and did not require hospitalization or a visit to the emergency department. Compared to the initial infection, the percentage of individuals who required hospitalization or succumbed to the infection after reinfection was marginally lower (14.4% vs. 12.6%). Close to half the patients who experienced a severe initial SARS-CoV-2 infection had moderate symptoms requiring hospitalization or emergency department visits during reinfection. Additionally, 7.4% of the individuals who had a severe initial infection had severe infections, and 5.7% succumbed to the reinfection.

Long COVID diagnoses also occurred in a shorter time frame for infections or reinfections during the Omicron epoch, as compared to infections during the Delta epoch or those with other variants.

Conclusions

Overall, the results indicated that the severity of SARS-CoV-2 reinfections was similar to those of the initial infection, with individuals who experienced mild to moderate symptoms during the first infection having similar symptoms during reinfection, while individuals who experienced a severe initial infection having similar reinfection symptoms or succumbing to the disease after reinfection.

Additionally, the study reported that long COVID diagnoses during the Omicron epoch occurred much closer to the index date of the infection or reinfection, and the number of long COVID diagnoses also showed an increase after reinfections with recent variants.

*Important notice

medRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.

Journal reference:

  • Emily Hadley, Yun Jae Yoo, Saaya Patel, Andrea Zhou, Bryan Laraway, Rachel Wong, Alexander Preiss, Rob Chew, Hannah Davis, Christopher G Chute, Emily R Pfaff, Johanna Loomba, Melissa Haendel, Elaine Hill, Richard Moffitt. (2023). SARS-CoV-2 Reinfection is Preceded by Unique Biomarkers and Related to Initial Infection Timing and Severity: an N3C RECOVER EHR-Based Cohort Study:  and the N3C and RECOVER consortia. medRxiv. doi: https://doi.org/10.1101/2023.01.03.22284042 https://www.medrxiv.org/content/10.1101/2023.01.03.22284042v1

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Free spike proteins in the blood appear to play a role in myocarditis post-COVID mRNA vaccine

Following the large-scale rollout of the messenger ribonucleic acid (mRNA) vaccines developed to prevent infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and symptomatic coronavirus disease 2019 (COVID-19), several cases of myocarditis were reported, mostly among healthy young people.

A recent study published in the journal Circulation examines the immunological picture in this scenario, looking for clues to the etiology of this rare and potentially serious complication.

Study: Circulating Spike Protein Detected in Post–COVID-19 mRNA Vaccine Myocarditis. Image Credit: Design_Cells / Shutterstock

Introduction

The development of myocarditis following mRNA vaccination is rare, occurring in <2 per 100,000 individuals. It remains an unpredictable mysterious occurrence. Some have suggested that it is linked to the overproduction of antibodies or abnormal immune responses.

Autoantibody production due to polyclonal B cell activation and proliferation has also been suggested, as has immune complex formation and inflammation. Finally, some think that cardiac antigens closely resembling the spike protein are targeted by autoantibodies formed as a result of molecular mimicry.

The immune response to these vaccines in these patients needs to be better understood in order to determine why and how it happens. It is imperative to study the role of male hormones since young male patients are most often affected.

The researchers in this study looked at blood samples from 16 myocarditis patients, confirmed to have high levels of serum cardiac troponin T. All developed myocarditis after receiving the COVID-19 vaccine, typically within a week of the second dose. However, a few became sick after the first dose or booster dose. Over 80% were male.

They were studied by antibody profiling, including antibodies to the virus, autoantibodies or antibodies to the virome, and the analysis of T cells specifically directed against the virus. In addition, cytokine and antigen profiles were determined. These measurements were compared with those of 45 vaccinated controls, who were of similar age and health.

What did the study show?

All subjects and controls showed a rise in anti-spike antibodies and antibodies to the receptor binding domain (RBD), of all immunoglobulin (Ig) subclasses, IgA, IgM, and IgG. Functional differences were not perceived either, with Fc effector functions being similar in both categories. In short, all vaccinated individuals showed evidence of a protective immune response against the virus.

We found no indication that a specific antibody response is associated with myocarditis.”

Additionally, these patients did not show evidence of increased autoantibody production or antibody production against other respiratory pathogens that differed in magnitude or range from the controls.

T cells of all relevant subtypes, including naïve, memory, and effector memory T cells, showed similar distributions in both groups. T cells also showed similar proportions of spike-specific memory CD4 T cells and activated CD4 and CD8 T cells. The only exceptions were the observation of small elevations in effector memory cells and PD-1-expressing bulk CD4 T cells in the myocarditis group.

The findings indicated that antibody and T-cell responses could not distinguish between post-vaccine myocarditis subjects and vaccinated controls. The only significant difference was a slight elevation in cytokine production in the former.

The exciting difference was the high level of circulating full-length spike protein in the plasma of myocarditis patients, at a mean of ~34 pg/mL. Furthermore, the protein was not bound to antibodies and remained detectable for up to three weeks from the vaccination date. In contrast, controls did not have free spike protein in their blood.

This difference could not be attributed to poor neutralizing capacity in the myocarditis group, which showed comparable neutralization relative to the control group.

Concordantly, myocarditis patients had cytokine release patterns resembling those found in multisystem inflammatory syndrome in children (MIS-C). This might indicate that the innate immune response was overactive, leading to elevations in interleukin (IL)-8, IL-10, IL-4, IL-6, tumor necrosis factor (TNF)-α, and interferon (INF)-γ relative to healthy controls. IL-8 was most closely associated with raised cardiac troponin T and antigen levels.

Alongside, leukocytes, especially neutrophils, were at higher mean levels in this group than controls, though still within normal range.

What are the implications?

The study shows that the immunological response elicited by the mRNA vaccine was very similar in those who developed post-vaccination myocarditis and others. In other words, myocarditis could not be associated with abnormal autoantibodies, viral infections other than SARS-CoV-2, or excessive production of antibodies elicited by the mRNA vaccine.

In vaccinated patients, infection with the virus was not likely to be a cause or contributing factor for myocarditis since anti-Nucleoprotein IgG was not found in these patients.

In contrast to controls, the finding of high levels of unbound full-length spike protein in myocarditis patients may point to the mechanism by which this condition arises. Similarly, MIS-C patients had circulating SARS-CoV-2 antigens.

The spike protein appears to evade immune antibodies found at normal levels in these patients, with adequate functional and neutralization capacity. The spike may damage the cardiac pericytes or endothelium, perhaps by reducing the expression of the angiotensin-converting enzyme 2 (ACE2), reducing nitric oxide production in the endothelium, or activating inflammation via integrins, causing the endothelium to become abnormally permeable.

Thus, the spike antigen itself, which evades antibody recognition rather than invoking immune hyperactivation, may contribute to myocarditis in these individuals.”

This finding does not amount to evidence against the benefit of vaccination with these vaccines, which effectively protect against severe COVID-19 outcomes. Therefore, current vaccine recommendations are unlikely to be altered due to these results.

Understanding the immunopathological mechanisms associated with postvaccine myocarditis will help improve safety and guide the development of future coronavirus disease 2019 (COVID-19) vaccines. These findings also suggest that administration of anti-spike antibodies, if spike antigenemia is detected, could potentially prevent or reverse postvaccine myocarditis.”

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Free spike proteins in the blood appear to play a role in myocarditis post-COVID mRNA vaccine

Following the large-scale rollout of the messenger ribonucleic acid (mRNA) vaccines developed to prevent infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and symptomatic coronavirus disease 2019 (COVID-19), several cases of myocarditis were reported, mostly among healthy young people.

A recent study published in the journal Circulation examines the immunological picture in this scenario, looking for clues to the etiology of this rare and potentially serious complication.

Study: Circulating Spike Protein Detected in Post–COVID-19 mRNA Vaccine Myocarditis. Image Credit: Design_Cells / Shutterstock

Introduction

The development of myocarditis following mRNA vaccination is rare, occurring in <2 per 100,000 individuals. It remains an unpredictable mysterious occurrence. Some have suggested that it is linked to the overproduction of antibodies or abnormal immune responses.

Autoantibody production due to polyclonal B cell activation and proliferation has also been suggested, as has immune complex formation and inflammation. Finally, some think that cardiac antigens closely resembling the spike protein are targeted by autoantibodies formed as a result of molecular mimicry.

The immune response to these vaccines in these patients needs to be better understood in order to determine why and how it happens. It is imperative to study the role of male hormones since young male patients are most often affected.

The researchers in this study looked at blood samples from 16 myocarditis patients, confirmed to have high levels of serum cardiac troponin T. All developed myocarditis after receiving the COVID-19 vaccine, typically within a week of the second dose. However, a few became sick after the first dose or booster dose. Over 80% were male.

They were studied by antibody profiling, including antibodies to the virus, autoantibodies or antibodies to the virome, and the analysis of T cells specifically directed against the virus. In addition, cytokine and antigen profiles were determined. These measurements were compared with those of 45 vaccinated controls, who were of similar age and health.

What did the study show?

All subjects and controls showed a rise in anti-spike antibodies and antibodies to the receptor binding domain (RBD), of all immunoglobulin (Ig) subclasses, IgA, IgM, and IgG. Functional differences were not perceived either, with Fc effector functions being similar in both categories. In short, all vaccinated individuals showed evidence of a protective immune response against the virus.

We found no indication that a specific antibody response is associated with myocarditis.”

Additionally, these patients did not show evidence of increased autoantibody production or antibody production against other respiratory pathogens that differed in magnitude or range from the controls.

T cells of all relevant subtypes, including naïve, memory, and effector memory T cells, showed similar distributions in both groups. T cells also showed similar proportions of spike-specific memory CD4 T cells and activated CD4 and CD8 T cells. The only exceptions were the observation of small elevations in effector memory cells and PD-1-expressing bulk CD4 T cells in the myocarditis group.

The findings indicated that antibody and T-cell responses could not distinguish between post-vaccine myocarditis subjects and vaccinated controls. The only significant difference was a slight elevation in cytokine production in the former.

The exciting difference was the high level of circulating full-length spike protein in the plasma of myocarditis patients, at a mean of ~34 pg/mL. Furthermore, the protein was not bound to antibodies and remained detectable for up to three weeks from the vaccination date. In contrast, controls did not have free spike protein in their blood.

This difference could not be attributed to poor neutralizing capacity in the myocarditis group, which showed comparable neutralization relative to the control group.

Concordantly, myocarditis patients had cytokine release patterns resembling those found in multisystem inflammatory syndrome in children (MIS-C). This might indicate that the innate immune response was overactive, leading to elevations in interleukin (IL)-8, IL-10, IL-4, IL-6, tumor necrosis factor (TNF)-α, and interferon (INF)-γ relative to healthy controls. IL-8 was most closely associated with raised cardiac troponin T and antigen levels.

Alongside, leukocytes, especially neutrophils, were at higher mean levels in this group than controls, though still within normal range.

What are the implications?

The study shows that the immunological response elicited by the mRNA vaccine was very similar in those who developed post-vaccination myocarditis and others. In other words, myocarditis could not be associated with abnormal autoantibodies, viral infections other than SARS-CoV-2, or excessive production of antibodies elicited by the mRNA vaccine.

In vaccinated patients, infection with the virus was not likely to be a cause or contributing factor for myocarditis since anti-Nucleoprotein IgG was not found in these patients.

In contrast to controls, the finding of high levels of unbound full-length spike protein in myocarditis patients may point to the mechanism by which this condition arises. Similarly, MIS-C patients had circulating SARS-CoV-2 antigens.

The spike protein appears to evade immune antibodies found at normal levels in these patients, with adequate functional and neutralization capacity. The spike may damage the cardiac pericytes or endothelium, perhaps by reducing the expression of the angiotensin-converting enzyme 2 (ACE2), reducing nitric oxide production in the endothelium, or activating inflammation via integrins, causing the endothelium to become abnormally permeable.

Thus, the spike antigen itself, which evades antibody recognition rather than invoking immune hyperactivation, may contribute to myocarditis in these individuals.”

This finding does not amount to evidence against the benefit of vaccination with these vaccines, which effectively protect against severe COVID-19 outcomes. Therefore, current vaccine recommendations are unlikely to be altered due to these results.

Understanding the immunopathological mechanisms associated with postvaccine myocarditis will help improve safety and guide the development of future coronavirus disease 2019 (COVID-19) vaccines. These findings also suggest that administration of anti-spike antibodies, if spike antigenemia is detected, could potentially prevent or reverse postvaccine myocarditis.”

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How Much Protein Should I Eat Every Day?

A stroll through a grocery store used to include lots of packages touting the sought-after term “low fat.” Years later, it was replaced with exciting-looking “low carb” claims. These days, “high in protein” is a benefit you’ll see touted on lots of products, whether they’re protein powder, bone broth, salty snacks or just about anything else. But people are more confused than ever about how much protein they should eat.

How much protein do you really need? We spoke with experts who explained its importance, why it’s not a one-size-fits-all nutrient and how to figure out what your body needs.

Why You Need Protein

It’s a pretty simple situation: Protein is good for us, and we ought to eat some every day. What’s most important to remember is that our body really does need what protein provides.

“Most people think of eating protein simply to maintain or help improve muscle size, but it does far more in our bodies,” said Michael J. Ormsbee, a Florida State University professor in the department of nutrition and integrative physiology and director at the Institute of Sports Sciences and Medicine. “Proteins serve as enzymes, hormones, receptors, signaling molecules and much more.”

Because protein is not something our bodies keep in reserve, like body fat, it’s a daily essential, explained Floris Wardenaar, an assistant professor at the College of Health Solutions at Arizona State University. “Protein provides essential amino acids, which we need to consume as part of our daily diets,” he said. “That’s because the body constantly breaks down protein to create the building blocks for new protein, resulting in a loss that needs to be replaced with food.”

If you notice that you feel fuller after a protein-rich meal, you’ve discovered another of protein’s benefits. “It keeps us satisfied and fuller for longer,” said Jane Burrell, an associate teaching professor at Syracuse University.

What’s The Magic Number?

How much protein is enough to realize all of these benefits? As a basic guideline, the Food and Drug Administration recommends that adults consume 50 grams of protein a day as part of a 2,000-calorie diet. But other experts take a more nuanced approach.

“Adequate protein intake isn’t one number or target to hit, but more of a range that depends on your age, sex, overall health and lean body mass,” said registered dietitian Jaclyn London.

“A generally healthy person who’s not very active should consume 0.8 to 1 gram of protein for each kilogram of body weight a day as a minimum,” she advised. (That would be about 68 grams of protein for someone who weighs 150 pounds.)

“Someone who’s super active with things like running, cycling or training for an endurance event will require more, about 1.2-1.7g/kg per day,” which would be from 82 to 116 grams of protein for a 150-pound person, she continued. “When I’m working with individuals who are active and generally healthy, I typically recommend something closer to 1.2g/kg per day to 1.5g/kg per day.”

Not all proteins are created equal. Consider the amount of cholesterol in bacon and eggs, compared to vegetarian-based proteins or even chicken or fish.

The Best Protein Sources

“Proteins can not only be found in animal-based foods, but also in plants,” said board-certified naturopathic physician Dr. Kellyann Petrucci. “In fact, some studies have indicated that getting protein from non-meat sources could actually be better for your health. Think low-fat dairy products, fish, beans and soy. These foods are delicious, and they may even help lower blood pressure and cholesterol levels.”

Pay attention to fat content, which can go hand-in-hand with high-protein foods. “Not all protein is created equal,” Petrucci said. “Bacon, sausage or processed meats might be high in protein, but they’re also high in saturated fat, which could be harmful for your heart.”

Finally, food is always better than a supplement or a powder, London said. “Protein powders are everywhere these days, and since they’re considered dietary supplements, they’re not overseen by the FDA,” she said. “When it comes to meeting your nutritional needs, dietary supplements are meant to be used only to fill in the gaps from what might be missing in your diet, not to take the place of attempting to meet nutrient needs through food sources.”

High-Protein Foods

Protein content in foods (one-ounce portions unless noted), according to Johns Hopkins Medicine:

  • Beef or turkey jerky: 10 to 15 grams of protein
  • 5 ounces Greek yogurt: 12 to 18 grams of protein
  • Roasted edamame: 13 grams of protein
  • 3/4 to 1 1/3 cup of high-protein cereal: 7 to 15 grams of protein
  • Meat or fish: 7 grams of protein
  • 1/3 cup of hummus: 7 grams of protein
  • 2 tablespoons of peanut butter: 7 grams of protein
  • 1 Egg: 6 grams of protein

Spreading Out Your Protein Intake

How much protein you eat is important, but so is when you eat it. “I encourage people to aim for 15 to 25 grams of protein each time they eat,” Burrell said. “If you eat that amount of protein only at lunch and dinner, but not at other times of day, you might be left feeling unsatisfied or hungry.”

You need to get enough calories overall to give that protein what it needs to be most effective, she added. “I work with college students, and many will be on high-protein diets, but they don’t eat enough calories overall,” Burrell said. “For protein to be used to build new proteins, first you need enough calories. Otherwise, your body will just use this extra protein for energy. And if carbohydrate intake is low, your body will break down functioning proteins and use some of those amino acids to make glucose in order to maintain blood glucose.”

Popular Myths About Protein

There’s a lot of misinformation out there about protein, experts said. Here’s one example: “We still hear that protein causes kidney damage,” Ormsbee said. “The data simply do not support this.”

On its own, protein can’t make you bulk up, either, they agreed. “One misconception about protein is that eating it means you’ll get big muscles,” Petrucci said. “In fact, muscle growth is a complicated process that takes into account protein consumption, exercise and hormones. Athletes may have higher protein needs compared to their peers, but eating this way doesn’t mean they’ll get bigger muscles.”

In fact, smart protein choices are an important part of a nutritious diet. “It’s an absolute essential component of meals and snacks, especially for people looking to adopt small-but-impactful strategies or habits that can result in weight loss or weight management over time,” London said.

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