Test makers target monkeypox market as cases surge

 

Diagnostic companies are racing to develop tests for monkeypox, hoping to tap into a new market as governments ramp up efforts to trace the world's first major outbreak of the viral infection outside of Africa.

The scramble started last month, much like early 2020 when companies rushed to make kits to help diagnose COVID-19, creating a multibillion-dollar boon for test makers.

But demand for monkeypox tests will be a fraction of what it was for COVID, given monkeypox is not as transmissible nor as dangerous as COVID - it typically spreads through close contact and can cause flu-like symptoms and pus-filled skin lesions that usually resolve on their own within weeks.

And unlike the sudden emergence of COVID, there are vaccines, treatments and tests that can already help curb the spread of monkeypox.

A niche new market could soften - but won't make up for - the anticipated slowing of COVID diagnostic sales as the need to test for the SARS-CoV-2 virus ebbs and concern about monkeypox grows, analysts say.

Roche, for instance, made 1.9 billion Swiss francs ($2.0 billion) in COVID test sales in the first quarter, and Barclays analyst Emily Field estimates the tests will generate 3 billion Swiss francs in total for the company in 2022.

"It would be very difficult for monkeypox revenues to offset this in any meaningful way," she said.

More than 550 confirmed cases of monkeypox have been reported by about 30 countries since early May. The majority were in Europe and not linked to travel to Africa, where the virus is endemic. Public health authorities suspect some degree of community transmission. No deaths have been reported.

Still, the World Health Organization (WHO) has said it expects infections to rise as surveillance expands and its Europe head warned the spread could accelerate as people gather for parties and festivals over the summer.

This outbreak is significant on the monkeypox scale, but there is not yet a need for hundreds of thousands of tests, which was the case when COVID emerged, said Daniel Bausch, senior director, emerging threats and global health security at FIND, the global alliance for diagnostics.

"This isn't going to be the next COVID ... so I don't think the needs are massive. I don't anticipate [test] supply to be an issue."

TESTING, TESTING

Some countries, including Switzerland and the Netherlands which have reported only a handful of cases, say that for now they have sufficient testing capacity for monkeypox. Britain, where nearly 200 cases have been confirmed, is working on expanding capacity.

Although researchers previously had fragmented access to the chemicals and other materials needed to conduct PCR tests for monkeypox, kits being developed by companies such as Roche theoretically allow them to have everything they need in one place to process a sample in a lab.

Kits like Roche's have not been cleared by regulators for use as a medical diagnostic - however, they are available for research purposes only.

Meanwhile, more than a dozen listed Chinese firms, including Jiangsu Bioperfectus Technologies, say they have added the European Union's CE mark of quality to their kits.

The regime allows test-makers to self-certify that they are complying with EU regulations, and can accordingly be sold in the region.

Broadly there are two types of test: PCR and antigen tests are designed to detect whether a person is currently or very recently infected, while antibody tests show whether a person has previously been infected.

The monkeypox virus is part of the orthopoxvirus family that also includes smallpox and cowpox

PCR tests are the gold standard test for the detection of monkeypox, according to the WHO, while the way antigen and antibody tests are designed makes it less likely that a positive result is definitively indicative of monkeypox.

It is unclear whether infected but symptomatic individuals can spread the virus, says the WHO, so it's not known if precautionary testing of suspected cases is needed.

However, since suspected cases are expected to isolate for up to 21 days, rapid antigen tests could be useful, given there are currently no pox virus diseases that have broadly spread across populations, said Carlos Maluquer de Motes, who runs a research group studying poxvirus biology at Surrey University.

Most diagnostic makers are focused on PCR tests for monkeypox. A few others, including Tetracore Inc, are working on rapid antigen tests.

However, caution is warranted.

"Virtually none of the kits, whether listed for research or otherwise, have gone through extensive validation," said Bausch. "It would be interesting to order all the tests that have suddenly come on the market and see what you get."

https://www.marketscreener.com/quote/stock/JIANGSU-BIOPERFECTUS-TECH-130784079/news/Test-makers-target-monkeypox-market-as-cases-surge-40628714/

Supplements for slowing age-related macular degeneration

 The Age-Related Eye Disease Studies (AREDS and AREDS2) established that dietary supplements can slow progression of age-related macular degeneration (AMD), the most common cause of blindness in older Americans. In a new report, scientists analyzed 10 years of AREDS2 data. They show that the AREDS2 formula, which substituted antioxidants lutein and zeaxanthin for beta-carotene, not only reduces risk of lung cancer due to beta-carotene, but is also more effective at reducing risk of AMD progression, compared to the original formula. A report on the study, funded by the National Institutes of Health, published in JAMA Ophthalmology.

"Because beta-carotene increased the risk of lung cancer for current smokers in two NIH-supported studies, our goal with AREDS2 was to create an equally effective supplement formula that could be used by anyone, whether or not they smoke," said Emily Chew, M.D., director of the Division of Epidemiology and Clinical Application at the National Eye Institute (NEI), and lead author of the study report. "This 10-year data confirms that not only is the new formula safer, it's actually better at slowing AMD progression."

AMD is a degenerative disease of the retina, the light-sensitive tissue at the back of the eye. Progressive death of retinal cells in the macula, the part of the retina that provides clear central vision, eventually leads to blindness. Treatment can slow or reverse vision loss; however, no cure for AMD exists.

The original AREDS study, launched in 1996, showed that a dietary supplement formulation (500 mg vitamin C, 400 international units vitamin E, 2 mg copper, 80 mg zinc, and 15 mg beta-carotene) could significantly slow the progression of AMD from moderate to late disease. However, two concurrent studies also revealed that people who smoked and took beta-carotene had a significantly higher risk of lung cancer than expected.

In AREDS2, begun in 2006, Chew and colleagues compared the beta-carotene formulation to one with 10 mg lutein and 2 mg zeaxanthin instead. Like beta-carotene, lutein and zeaxanthin are antioxidants with activity in the retina. The beta-carotene-containing formation was only given to participants who had never smoked or who had quit smoking.

At the end of the five-year AREDS2 study period, the researchers concluded that lutein and zeaxanthin did not increase risk for lung cancer, and that the new formation could reduce the risk of AMD progression by about 26%. After the completion of the five-year study period, the study participants were all offered the final AREDS2 formation that included lutein and zeaxanthin instead of beta-carotene.

In this new report, the researchers followed up with 3,883 of the original 4,203 AREDS2 participants an additional five years from the end of the AREDS2 study in 2011, collecting information on whether their AMD had progressed to late disease, and whether they had been diagnosed with lung cancer. Even though all the participants had switched to the formula containing lutein and zeaxanthin after the end of the study period, the follow up study continued to show that beta-carotene increased risk of lung cancer for people who had ever smoked by nearly double. There was no increased risk for lung cancer in those receiving lutein/zeaxanthin. In addition, after 10 years, the group originally assigned to receive lutein/zeaxanthin had an additional 20% reduced risk of progression to late AMD compared to those originally assigned to receive beta-carotene.

"These results confirmed that switching our formula from beta-carotene to lutein and zeaxanthin was the right choice," said Chew.

The study was funded by the NEI Intramural program (EY000546) and through contracts (AREDS2 contract HHS-N-260-2005-00007-C; ADB contract NO1-EY-5-0007; AREDS Contract NOI-EY-0-2127, and contract HHS-N-263-2013-00005-C). The AREDS2 contracts were supported by the NIH Office of Dietary Office of Dietary Supplements, the National Center for Complementary and Alternative Medicine, the National Institute on Aging, the National Heart, Lung, and Blood Institute, and the National Institute of Neurological Disorders and Stroke. The study took place at the NIH Clinical Center.

Story Source:

Materials provided by NIH/National Eye Institute. Note: Content may be edited for style and length.

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Journal Reference:

1. Emily Y. Chew, Traci E. Clemons, Elvira Agrón, Amitha Domalpally, Tiarnán D. L. Keenan, Susan Vitale, Claire Weber, Douglas C. Smith, William Christen, John Paul SanGiovanni, Federick L Ferris, Ronald P Danis, Barbara A Blodi, Alan J Ruby, Andrew Antoszyk, Michael Klein, Ivana Kim, Gary Edd Fish, Wai T Wong, David H Orth, Kourous Rezaei, Susan B Bressler, G Baker Hubbard, Michael J Elman, Suresh Chandra, Thomas Friberg, Michael Tolentino, Darmakusuma Le, Mary B Lansing, Jay B Stallman, Paul A Edwards, Carl W Baker, Michael A Novak, Ricky D Isernhagen, Todd E Schneiderman, Lawrence Halperin, Michael Lee, David Boyer, Philip Rosenfeld, Pamela Rath, Marc Levy, Robert H Rosa, John Hoskins, Clement K Chan, David M Brown, Craig Greven, J Michael Jumper, Linda Margulies, William Rosenthal, Richard Rosen, Glenn Stoller, Fadi El Baba, W Copley McLean, Ronald Kingsley, Alice Lyon, Jeffrey Heier, Anne Fung, Ingrid Scott, John Wells, Michael Banach, Paul Beer, James Folk, Joseph Maguire, SriniVas Sadda, Richard Garfinkel, Judy E Kim, Paul Berstein, Michael Rauser, Richard Alan Lewis, Barron C Fishburne, Suber Huang, Nelson R Sabates, Nicola Kim, Robert N Frank, Brian Joondeph, Odette Houghton, Dean Hainsworth, Edward Chaum, Robert Millay, Raymond Iezzi, Rajendra Apte, Ron Adelman, Anita Agrawal, Neelakshi Bhagat, Lawrence Ulanski, Steven Schwartz, Cynthia Owsley, Alan J Letson, Yu-Guang HE, Cynthia Toth, Lawrence Morse, Michael Cooney, Sandeep Grover, Henry Ferreyra, Alexander J Brucker, David DiLoreto, Aaron Weinberg. Long-term Outcomes of Adding Lutein/Zeaxanthin and ω-3 Fatty Acids to the AREDS Supplements on Age-Related Macular Degeneration Progression. JAMA Ophthalmology, 2022; DOI: 10.1001/jamaophthalmol.2022.1640

https://www.sciencedaily.com/releases/2022/06/220602121430.htm

High fat diet, unregulated athletic exercise endurance enhancers linked to risk of pancreatic cancer

 Researchers at the University of Michigan Rogel Cancer Center have found a cell nuclear receptor activated by high fat diets and synthetic substances in unregulated athletic performance enhancers fuels the progression of precancerous pancreas lesions into pancreatic cancer.

Pancreatic ductal adenocarcinoma is a highly lethal form of cancer with rising occurrence, and strategies to prevent and treat the disease are urgently needed. Most cases of pancreatic cancer arise from pre-cancerous lesions called pancreatic intraepithelial neoplasia; about 55-80% of adults over 40 are estimated to have these low grade pre-cancerous silent pancreatic lesions. A study published in Nature Communications, led by Imad Shureiqi, M.D., shows that, pre-cancerous pancreatic lesions in mice, similar to those found in humans, contain higher levels of the transcriptional receptor peroxisome proliferator activated receptor-delta (PPARδ).

PPARδ regulates the expression of a wide spectrum of key genes that influences biological processes like lipid metabolism and cancer formation. Activation of PPARδ dramatically accelerates the progression of pre-cancerous lesions into pancreatic cancer. Shureiqi previously worked at MD Anderson Cancer Center at the University of Texas where he conducted much of this study, specifically in partnership with Xiangsheng Zuo, M.D., Ph.D., before moving his research to the cancer center in 2020.

"We became interested in studying the effects of PPARδ on pancreatic carcinogenesis because our prior observations showed that PPARδ strongly promoted other gastrointestinal cancers. But there's very limited information about PPARδ's role in pancreatic cancer's development," said Shureiqi.

Activation of PPARδ correlates with excessive exposure to certain ligands, both natural and synthetic. Some ligands naturally occur in high fat diets, which have been associated with increased risk for pancreatic cancer in humans and animal models. High fat diets are enriched with fatty acids that are natural ligands of PPARδ.

Other synthetic forms of PPARδ ligands, like Cardarine (GW501516), are found in exercise supplements, aimed to boost physical performance and endurance. GW501516 was originally designed by pharmaceutical companies to encourage the body to use more fat and treat noncancerous conditions like obesity and hyperlipemia. Pharmaceutical development of GW501516 and other similar potent PPARδ agonists for medical use has long been discontinued given their potential procancerous side effects. Though studies on how PPARδ affects colorectal cancer date back to 1999, and pharmaceutical companies have halted synthetic PPARδ ligand development, unregulated internet outlets still sell substances like Cardarine. Ads are largely marketed to young people, claiming it will help them build muscle endurance and burn fat.

Shureiqi explains that, initially, researchers found that these synthetic ligands reduced fatigue in mice. This news made its way to major media outlets, who nicknamed it "exercise in a pill." "Unfortunately, what the media didn't address was the dark side of PPARδ. Like muscle cells, synthetic PPARδ ligands also help cancer cells get more energy from fats as a fuel source," he said.

"It's shocking to me," Shureiqi continued. "Animal models repeatedly show the strong relationship between PPARδ and cancer promotion in the case of colorectal cancer and stomach cancer. Now we're gaining more information about how it affects pancreatic cancer."

Critical factors that promote the progression of silent pancreatic precancerous lesions to pancreatic cancer remain poorly defined, especially those that are easy to target. While most of these pre-cancerous lesions don't develop into cancer, understanding how they progress is still crucial to finding interventions to address the rising rate of pancreatic cancer. Findings from this study indicate that people who have silent precancerous lesions, even those that are low grade, could increase their risk of developing pancreatic cancer by consuming PPARδ natural activators, like in high fat diets, or synthetic ones, like Cardarine. Future development of effective agents to block PPARδ activation could be a new approach to prevent the progression of precancerous lesions into pancreatic cancer. Limiting exposure to high fat diets could also be considered for those with a high prevalence of pre-cancerous pancreatic lesions. But for now, the prevalent sales and use of those athletic boosting synthetic PPARδ activating substances causes the most pressing concern.

"This new information should alert individuals to the potential serious health risks from using synthetic PPARδ agonists," Shureiqi said. "We're trying to spread the message that's using those substances is not a good idea. It might enhance muscle endurance, but it also enhances cancer's ability to use energy and grow."

Funding: National Cancer Institute grants R01CA266223, R01CA142969, R01CA195686, R01-CA206539, R01CA236905 R03CA235106, K08CA234222; the Cancer Prevention and Research Institute of Texas grants RP150195 RP140224;, DDC seed fund. This study made use of the MD Anderson Cancer Center Genetically Engineered Mouse Facility, Functional Genomics Core, Flow Cytometry and Cellular Imaging Facility, the Next Generation Sequencing Core and Research Animal Support Facility -- Smithville Laboratory Animal Genetic Services, supported by Cancer Center Support Grant P30CA016672. The Next Generation Sequencing Core was also supported by CPRIT Core Facility Support Grant RP120348.

Story Source:

Materials provided by Michigan Medicine - University of Michigan. Original written by Anna Megdell. Note: Content may be edited for style and length.

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Journal Reference:

1. Yi Liu, Yasunori Deguchi, Daoyan Wei, Fuyao Liu, Micheline J. Moussalli, Eriko Deguchi, Donghui Li, Huamin Wang, Lovie Ann Valentin, Jennifer K. Colby, Jing Wang, Xiaofeng Zheng, Haoqiang Ying, Mihai Gagea, Baoan Ji, Jiaqi Shi, James C. Yao, Xiangsheng Zuo, Imad Shureiqi. Rapid acceleration of KRAS-mutant pancreatic carcinogenesis via remodeling of tumor immune microenvironment by PPARδ. Nature Communications, 2022; 13 (1) DOI: 10.1038/s41467-022-30392-7

https://www.sciencedaily.com/releases/2022/06/220601170205.htm

Alternate origins of Alzheimer's disease plaques

 A breakdown in how brain cells rid themselves of waste precedes the buildup of debris-filled plaques known to occur in Alzheimer's disease, a new study in mice shows.

The field argued for decades that such plaques, containing the protein amyloid beta, built up outside of cells as a crucial first step toward the brain damage observed in Alzheimer's disease. Led by researchers at NYU Grossman School of Medicine and the Nathan Kline Institute, the new study challenges this idea, known as the amyloid cascade hypothesis.

The lastest study findings argue instead that neuronal damage characteristic of Alzheimer's disease takes root inside cells and well before these thread-like amyloid plaques fully form and clump together in the brain.

Publishing as the cover article in the journal Nature Neuroscience online June 2, the study traced the root dysfunction observed in mice bred to develop Alzheimer's disease to the brain cells' lysosomes. These are small sacs inside every cell, filled with acidic enzymes involved in the routine breakdown, removal, and recycling of metabolic waste from everyday cell reactions, as well as from disease. Lysosomes are also key, researchers note, to breaking down and disposing of a cell's own parts when the cell naturally dies.

As part of the study, researchers tracked decreasing acid activity inside intact mouse cell lysosomes as the cells became injured in the disease. Imaging tests developed at NYU Langone Health and Nathan Kline (to track cellular waste removal) showed that certain brain cell lysosomes became enlarged as they fused with so-called autophagic vacuoles filled with waste that had failed to be broken down. These autophagic vacuoles also contained earlier forms of amyloid beta.

In neurons most heavily damaged and destined for early death as a result, the vacuoles pooled together in "flower-like" patterns, bulging out from the cells' outer membranes and massing around each cell's center, or nucleus. Accumulations of amyloid beta formed filaments inside the cell, another hallmark of Alzheimer's disease. Indeed, researchers observed almost-fully formed plaques inside some damaged neurons.

"Our results for the first time sources neuronal damage observed in Alzheimer's disease to problems inside brain cells' lysosomes where amyloid beta first appears," says study lead investigator Ju-Hyun Lee, PhD.

"Previously, the working hypothesis mostly attributed the damage observed in Alzheimer's disease to what came after amyloid buildup outside of brain cells, not before and from within neurons," says Lee, a research assistant professor in the Department of Psychiatry and NYU Langone Health and research scientist at Nathan Kline.

"This new evidence changes our fundamental understanding of how Alzheimer's disease progresses; it also explains why so many experimental therapies designed to remove amyloid plaques have failed to stop disease progression, because the brain cells are already crippled before the plaques fully form outside the cell," says study senior investigator Ralph Nixon, MD, PhD.

"Our research suggests that future treatments should focus on reversing the lysosomal dysfunction and rebalancing acid levels inside the brain's neurons," says Nixon, a professor in the Department of Psychiatry and the Department of Cell Biology at NYU Langone, as well as director of the Center for Dementia Research at Nathan Kline.

Researchers say they are already working on experimental therapies to treat the lysosomal problems observed in their studies.

A recent study (published in April in Science Advances) by the NYU Langone team sourced one cause of the cell's waste disposal problems to a gene called PSEN1. The gene has long been known to cause Alzheimer's disease, but its additional role in causing the illness (through lysosomal dysfunction) is only now becoming clear.

Their recent work also showed that the neuronal damage in a PSEN1 mouse model of Alzheimer's disease could be reversed by restoring proper acid levels in lysosomes.

This work is covered by United States Patent 9,265,735 that is directed to methods of treating Alzheimer's disease based on reversing lysosomal de-acidification, the underlying cause of waste buildup. The terms and conditions of the patent are being managed in accordance with the policies of the health system.

According to the National Institute on Aging, more than 6 million Americans, most of them age 65 or older, have dementia, a progressive loss of thinking, remembering, and reasoning, due to Alzheimer's disease.

Funding for these studies was provided by National Institute of Health grants P01AG017617, P50AG025688, and R01AG062376.

Besides Lee and Nixon, other NYU Langone and Nathan Kline study investigators involved in this research are Dun-Sheng Yang, Chris Goulbourne, Eunju Im, Philip Stavrides, Ann Pensalfini, Cynthia Bleiwas, Martin Berg, Chunfeng Huo, James Peddy, Monika Pawlik, Efrat Levy, and Mala Rao. Additional co-investigators are Han Chan and Cedric Bouchet-Marquis, at Thermo-Fisher Scientific in Hillsboro, Ore.; and Mathias Staufenbiel, at the University of Tubingen in Germany.

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Story Source:

Materials provided by NYU Langone Health / NYU Grossman School of Medicine. Note: Content may be edited for style and length.

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Journal Reference:

1. Lee, JH., Yang, DS., Goulbourne, C.N. et al. Faulty autolysosome acidification in Alzheimer’s disease mouse models induces autophagic build-up of Aβ in neurons, yielding senile plaques. Nat Neurosci, 2022 DOI: 10.1038/s41593-022-01084-8

https://www.sciencedaily.com/releases/2022/06/220602114220.htm

Transcript: Edwards Lifesciences at Bernstein strategic Decisions Conference

 https://www.marketscreener.com/quote/stock/EDWARDS-LIFESCIENCES-CORP-12521/news/Transcript-Edwards-Lifesciences-Corporation-Presents-at-Bernstein-38th-Annual-Strategic-Decisions-40625189/

Chicago, Philadelphia, LA County record first monkeypox cases

 Chicago, Philadelphia and Los Angeles County all announced their first monkeypox cases Thursday amid growing concerns about the outbreak in the United States.

All three locations’ public health departments are currently awaiting final confirmation from the Centers for Disease Control and Prevention (CDC) for the presumed cases.

“The patient is an adult resident who recently traveled and had a known close contact to a case. Although the patient is symptomatic, they are doing well and not hospitalized. They are isolated from others,” the Los Angeles County announcement said, assuring that the general public’s risk of monkeypox remains low.

“The Chicago Department of Public Health and Illinois Department of Public Health, announced today a single presumptive monkeypox case in an adult male Chicago resident with recent travel history to Europe,” wrote the Chicago agency in its announcement.

“The threat to Philadelphians from monkeypox is extremely low,” said Health Department Acute Communicable Disease Program Manager Dana Perella, with the health department adding that any details about the patient’s case will remain anonymous to protect the privacy of the patient.

“Monkeypox is much less contagious than COVID-19 and is containable particularly when prompt care is sought for symptoms,” Perella added. “Vaccine to prevent or lessen the severity of illness is available through the CDC for high-risk contacts of persons infected with monkeypox, as is antiviral treatment for patients with monkeypox. I believe that residents and visitors should feel safe to do all the fun things Philadelphia has to offer, with the proper precautions.”

The CDC has confirmed monkeypox cases in 10 states so far, not including states that have pending confirmation. The state of Georgia announced its first CDC-confirmed case on Thursday.

A man in Massachusetts had the first confirmed U.S. monkeypox case after traveling to Canada in the middle of last month. That came following several confirmed cases throughout Europe.

The CDC urges anyone who has a rash that looks like monkeypox to speak with their health care provider and warns that men who have sex with men may be at higher risk, though notes that any person who comes in close contact with someone with monkeypox can become infected.

https://thehill.com/healthcare/3509950-chicago-philadelphia-la-county-record-first-monkeypox-cases/

 The White House has compounded its problems — again — this time in addressing a baby formula shortage that President Biden admitted he was not personally aware of until months after the shutdown of a plant that manufactured a significant chunk of the nation’s products.

Biden’s admission that he wasn’t aware of the gravity of the situation until April, when store shelves were already empty, confounded some observers who saw it as a political mistake that made the optics of the administration’s response worse. 

“I almost couldn’t believe what I was hearing,” said one Democratic strategist. “He has to show that he’s on top of these situations. The last thing they want is to be the subject of another Republican talking point.” 

The administration had already been struggling to handle questions on the baby formula shortage, and Biden’s statement left it scrambling to lay out a clear timeline of who was working on the issue in February and March and why the president was not informed sooner.

It’s far from the first time the White House has had to deal with such a problem.

The strategist pointed to the White House being caught flat-footed on a number of issues dated back almost one year ago. 

“Almost everything since the Afghanistan withdrawal foul-up has been Biden and the White House playing catch up,” the strategist said.

A second strategist added, “This looks so bad. It raises questions about competency and the more that comes out, the worse it looks.” 

Administration officials for weeks have said they’ve been working to address the shortage since February, when a recall of Abbott Nutrition products, the maker of Similac baby formula, left the administration seeking to bring in products from other countries. Biden in May invoked the Defense Production Act in a bid to increase supply. 

But Biden, at an event with formula manufacturers on Wednesday, said he “became aware of this problem sometime in early April, about how intense it was. We did everything in our power from that point on.”

“I don’t think anyone anticipated the impact of the shutdown of one facility,” Biden added.

The president’s admission came minutes after executives from some of the leading manufacturers said they knew the shutdown would have a significant impact on formula availability.

Rep. John Joyce (R-Pa.) asked Food and Drug Administration (FDA) Commissioner Robert Califf at a recent hearing when the agency alerted the White House about the closure of the Abbott plant and who was made aware. Califf indicated White House staff knew in early February.

At a press briefing later Wednesday, White House press secretary Karine Jean-Pierre struggled to answer questions about why Biden was not made aware of the severity of the situation until early April. At one point, she claimed to not even know about Biden’s remarks earlier that day. 

“I was in my office. I did not actually hear what the president said,” she told reporters.

Brian Deese, the head of the National Economic Council, went on CNN on Wednesday and acknowledged Americans “are right to be frustrated and concerned.” 

He defended the FDA’s process in investigating how a whistleblower complaint was overlooked and the timeline of looking into the closure of the Abbott plant, calling it “appropriate that they look at that timeline and understand what happened in that context.”

The interview ended abruptly when Deese’s camera on the north lawn of the White House toppled over.

The new revelation about the timeline triggered a fresh wave of questions during Thursday’s White House briefing.

Jean-Pierre said the White House had been working with other agencies for months on the issue. But when pressed on why the president said he did not know about the crisis until April, she suggested he had a lot on his plate and would not specify who eventually notified Biden of the severity of the issue.

“He’s briefed on countless priorities. He is the president of the United States. There are regular channels. He’s briefed by his senior White House staff. And that is just the process that we have,” Jean-Pierre said. “I’m not going to confirm who it was.”

One correspondent noted that the unwillingness to provide specifics seemed “evasive.”

Some Democrats say the White House should be doing more to help parents, who already feel overwhelmed with the recent news centered on last week’s school shooting in Texas and the possible repeal of Roe v. Wade.

“Taking action — even the appearance of action — and showing outrage about this state of affairs, should be a lay-up for President Biden,” said Democratic strategist Christy Setzer. “And yet it feels as though women are getting something between arms-length sympathy and even more outreach to Republicans, who should instead be set up as the contrast and the problem.”

The baby formula shortage has proven to be yet another crisis for the White House to juggle at a time when Biden and his team are struggling to convince much of the public that their agenda is working ahead of the midterm elections.

Inflation has been a persistent issue for months, with gas prices setting record highs in recent days. The war in Ukraine has rattled global supply chains and shows few signs of abating. And a string of mass shootings has pushed the debate over gun laws back to the forefront.

“The baby formula issue, in addition to being a basic survival issue, also reads as an extension of the inflation problem,” Setzer added. “Families can’t access basic household items in the way that they used to.”

To show what tangible steps it has taken, the White House on Thursday launched a dedicated webpage for the public to track progress on increasing formula supply. 

The president has also launched a program dubbed “Operation Fly Formula” which has helped secure millions of additional bottles from Europe and Australia. Biden on Thursday tweeted his administration has gotten another 6.5 million bottles from Nestle, bringing the total coming to U.S. consumers from overseas to nearly 95 million.

But the messaging missteps threaten to overshadow much of that work, with Republicans prepared to portray Biden as out of the loop and late to respond to what formula executives knew would be a problem.

Jean-Pierre would not answer a question on Wednesday about whether Biden was frustrated or disappointed that he was not aware of the crisis until April. Instead, she repeatedly pointed to an FDA review of the handling of the Abbott facility closure and resulting shortages.

“FDA did their part here. But [the FDA commissioner] also admitted that they moved too slowly,” she said. “And once we saw that the supplies were not meeting the demand, we acted. We took urgent action. 

“So, that is the way that it happened,” Jean-Pierre added. “That is the way the timeline was laid out. You may not like my answer, but that is the way we see it.”

https://thehill.com/news/administration/3510242-biden-compounds-his-baby-formula-problems/