Officials want to investigate whether the vaccine is related to blood clots and other rare but dangerous problems.Denmark will extend its suspension of the AstraZeneca vaccine until April 15, the Danish Health Authority announced on Thursday, as other European countries are restarting use of the vaccine.Officials in Denmark want to further investigate whether AstraZeneca vaccine is the cause of an unusual disease picture involving low blood platelets, bleeding and blood clots in unexpected places in the body, the head of the Danish Health Authority, Soren Brostrom, said.The European Medical Agency, the continent’s top drug regulator, said last week that it had found no sign of the vaccine causing such rare but dangerous problems, and strong evidence that its lifesaving benefits “outweigh the risk of the side effects.”The agency announced on Thursday that it was convening a group of external medical experts to help assess the safety of the vaccine.Denmark was the first country to suspend use of the AstraZeneca vaccine, on March 11. It has reported two deaths from brain hemorrhages among people who had received the shot.Officials acknowledged that continuing the suspension would lead to delays in the vaccination process.“We are very conscious that a continued hold on vaccination with the Covid-19 vaccine from AstraZeneca delays the Danish vaccination program,” Mr. Brostrom said. “However, the vaccines are already in the refrigerator. If we decide to recommence vaccination with the Covid-19 vaccine from AstraZeneca, we can quickly distribute and use the vaccines.”The health authorities in Sweden, which last week suspended the use of the AstraZeneca vaccine, said on Thursday that the country would resume its use for people over 65.In other developments around the world:Schools in Romania will close for four weeks starting next month as the Eastern European country fights to curb its latest wave of Covid-19 cases. Most schools will close from April 2 to May 4, Sorin Cimpeanu, Romania’s education minister, said on Thursday, extending the usual break for Orthodox and Catholic Easter.Travelers flying to Germany will need to show proof they tested negative for Covid-19 before boarding flights starting on Sunday, the country’s health ministry said on Thursday. Germans rushed to book flights and hotels in Portugal and Spain for Easter and Holy Week holidays after the government took those nations off its “at risk” list that require people to quarantine upon return to Germany.

Alzheimer’s disease seems to progress faster in women than in men. The protein tau accumulates at a higher rate in women, according to research from Lund University in Sweden. The study was recently published in Brain.
Over 30 million people suffer from Alzheimer’s disease worldwide, making it the most common form of dementia. Tau and beta-amyloid are two proteins known to aggregate and accumulate in the brain in patients with Alzheimer’s.
The first protein to aggregate in Alzheimer’s is beta-amyloid. Men and women are equally affected by the first disease stages, and the analysis did not show any differences in the accumulation of beta-amyloid. Memory dysfunction arises later, when tau starts to accumulate. More women than men are affected by memory problems due to Alzheimer’s, and it was for tau that the researchers found a higher rate of accumulation in women.
“Tau accumulation rates vary greatly between individuals of the same sex, but in the temporal lobe, which is affected in Alzheimer’s disease, we found a 75% higher accumulation rate in women as a group compared to men,” explains Ruben Smith, first author of the study.
The accumulation of tau is faster in patients who already have a pathological accumulation of beta-amyloid, and are in the early phase of the disease. The discovery that the accumulation rate of tau is higher in women remained even after adjusting for age and the levels of tau they had at the beginning. Together with data from three similar cohorts in the USA, the project contains 209 women and 210 men.
“The next step would be to examine why this accumulation is faster in women,” says Sebastian Palmqvist, the researcher responsible for the cognitive assessment of the patients.
The study did not investigate the reasons for the higher rate of tau accumulation in women.
“Our study strongly indicates that the faster spread of tau makes women more prone to develop dementia because of Alzheimer’s pathology compared to men. Future experimental studies will be important to understand the reasons behind this,” concludes Professor Oskar Hansson.
Story Source:
Materials provided by Lund University. Note: Content may be edited for style and length.

Influenza vaccines need to be evaluated every year to ensure they remain effective against new influenza viruses. Will the same apply to COVID-19 vaccines? In order to gauge whether and to what extent this may be necessary, a team of researchers from Charité — Universitätsmedizin Berlin compared the evolution of endemic ‘common cold’ coronaviruses with that of influenza viruses. The researchers predict that, while the pandemic is ongoing, vaccines will need to undergo regular updates. A few years into the post-pandemic period, however, vaccines are likely to remain effective for longer. This study has been published in Virus Evolution.
Influenza viruses are masters at evading the human immune system. They undergo such rapid changes that antibodies produced by the immune system in response to a previous infection or vaccination become unable to neutralize them. This is why the complex task of evaluating and updating the seasonal influenza vaccine has to be repeated every year. Mutations within SARS-CoV-2 have already produced a number of variants, some of which (such as the South African variant) partially evade the body’s immune response. As a result, some vaccine manufacturers have already started to develop new versions of their vaccines. What does this mean for the future? Will COVID-19 vaccines mirror influenza vaccines in requiring regular updates?
In order to gauge whether, over the long term, SARS-CoV-2 is likely to demonstrate an immune evasion capability on par with that of influenza viruses, Charité virologists have studied the genetic evolution of the four currently known ‘common cold’ coronaviruses. These relatively harmless coronaviruses are known to be responsible for approximately 10 percent of common colds in the world and have been in circulation in humans significantly longer than SARS-CoV-2. Just like SARS-CoV-2, they enter human cells using the ‘spike protein’, a surface protein which gives the virus its characteristic crown-like appearance (and name). The spike protein also forms the target of all current COVID-19 vaccines.
For their study, the researchers focused on the two longest-known coronaviruses (termed 229E and OC43), tracing changes in the spike gene approximately 40 years into the past. The researchers started by comparing sequences from a range of old samples which had been deposited in a genetic sequence data bank. Based on the mutations which had emerged over time, they then produced phylogenetic trees for both coronaviruses. The researchers compared their findings with the phylogenetic tree of H3N2, an influenza subtype which is particularly effective at evading the human immune response.
The researchers’ calculations revealed one feature which was common to the phylogenetic reconstructions of both the coronaviruses and the influenza virus: all three had a pronounced ladder-like shape. “An asymmetrical tree of this kind likely results from the repeated replacement of one circulating virus variant by another which carried a fitness advantage,” explains the study’s first author, Dr. Wendy K. Jó from Charité’s Institute of Virology. “This is evidence of ‘antigenic drift’, a continuous process involving changes to surface structures which enable viruses to evade the human immune response. It means that these endemic coronaviruses also evade the immune system, just like the influenza virus. However, one also has to look at the speed with which this evolutionary adaptation happens.”
For this step, the researchers determined the three viruses’ evolutionary rates. While the influenza virus accumulated 25 mutations per 10,000 nucleotides (genetic building blocks) per year, the coronaviruses accumulated approximately 6 such mutations in the same timeframe. The rate of change of the endemic coronaviruses was therefore four times slower than that of the influenza virus. “As far as SARS-CoV-2 is concerned, this is good news,” summarizes Prof. Dr. Christian Drosten, Director of the Institute of Virology and a researcher at the German Center for Infection Research (DZIF).
SARS-CoV-2 is currently estimated to change at a rate of approximately 10 mutations per 10,000 nucleotides per year, meaning the speed at which it evolves is substantially higher than that of the endemic coronaviruses. “This rapid genetic change in SARS-CoV-2 is reflected in the emergence of numerous virus variants across the globe,” explains study lead Prof. Dr. Jan Felix Drexler, a researcher at both the Institute of Virology and the DZIF. “This, however, is likely due to the high rates of infection seen during the pandemic. When infection numbers are so high, a virus is able to evolve more rapidly. Based on the rates of evolution seen in the endemic common cold coronaviruses, we expect that SARS-CoV-2 will start to change more slowly once infections start to die down — meaning once a large proportion of the global population has developed immunity either as a result of infection or through vaccination. We expect therefore that COVID-19 vaccines will need to be monitored regularly throughout the pandemic and updated where necessary. Once the situation has stabilized, vaccines are likely to remain effective for longer.”
Story Source:
Materials provided by Charité – Universitätsmedizin Berlin. Note: Content may be edited for style and length.

Cholinesterase inhibitors are a group of drugs recommended for the treatment of Alzheimer’s disease, but their effects on cognition have been debated and few studies have investigated their long-term effects. A new study involving researchers from Karolinska Institutet in Sweden and published in the journal Neurology shows persisting cognitive benefits and reduced mortality for up to five years after diagnosis.
Alzheimer’s disease is a cognitive brain disease that affects millions of patients around the world. Some 100,000 people in Sweden live with the diagnosis, which has a profound impact on the lives of both them and their families. Most of those who receive a diagnosis are over 65, but there are some patients who are diagnosed in their 50s.
The current cost of care and treatment for people with dementia is approximately SEK 60 billion a year in Sweden. This is on a par with the cost of care and treatment of cardiovascular diseases and is twice as high as cancer care.
In Alzheimer’s disease changes to several chemical neurotransmitters in the brain are found, and thus to the ability of the neurons to communicate with each other. Acetylcholine is one such substance and plays a key role in cognitive functions such as memory, attention and concentration.
There are three drugs that work as cholinesterase inhibitors and that are used in the treatment of Alzheimer’s disease: galantamine, donepezil and rivastigmine.
The effects of cholinesterase inhibitors have, however, been debated, partly because there are relatively few longitudinal clinical studies. Researchers at Karolinska Institutet and Umeå University have now conducted a registry study of patients with Alzheimer’s disease over a period of five years from point of diagnosis.
The study is based on data from SveDem (the Swedish Dementia Registry) on 11,652 patients treated with cholinesterase inhibitors and a matched control group of 5,826 untreated patients.
The results showed that treatment with cholinesterase inhibitors was associated with slower cognitive decline over five years, and 27 per cent lower mortality in patients with Alzheimer’s disease compared with the controls.
“Of all three drugs, galantamine had the strongest effect on cognition, which may bedue to its effect on nicotine receptors and its inhibiting effect on the enzyme acetylcholinesterase, which breaks down the neurotransmitter acetylcholine,” says the study’s first author Hong Xu, postdoctoral researcher at the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet.
“Our results provide strong support for current recommendations to treat people with Alzheimer’s disease with cholinesterase inhibitors, but also shows that the therapeutic effect lasts for a long time,” says the study’s last author and initiator Maria Eriksdotter, professor at the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet.
Story Source:
Materials provided by Karolinska Institutet. Note: Content may be edited for style and length.

Orthopaedic researchers are one step closer to preventing life-long arm and leg deformities from childhood fractures that do not heal properly.
A new study led by the University of South Australia and published in the journal Bone, sheds light on the role that a protein plays in this process.
Lead author Dr Michelle Su says that because children’s bones are still growing, an injury to the growth plate can lead to a limb in a shortened position, compared to the unaffected side.
“Cartilage tissue near the ends of long bones is known as the growth plate that is responsible for bone growth in children and, unfortunately, 30 per cent of childhood and teen fractures involve this growth plate which is highly susceptible to injuries,” Dr Su says.
Instead of the rubbery cartilage tissue regenerating, bone tissue lodges in and around the injury site, causing different limb lengths and angulations.
Researchers from Adelaide, Perth and Shanghai used a rat model to investigate the role of this protein called bone morphogenetic protein (BMP). Dr Su says scientists are aware of the importance of BMP in bone development and normal bone fracture healing, but little is known about its role in growth plate repair.
The researchers found that levels of BMP were greater at the injured growth plate, and that inhibiting BMP suppressed growth plate bony repair and prevented degeneration of the surrounding uninjured region.
“This finding could be the first step in creating a biological treatment in place of correcting deformities by surgery, which can be complicated, extremely invasive and often ineffective,” Dr Su says.
Surgery involves inserting pins, plates, wires or screws to correct the damaged limbs, with a long period of recovery, which is not 100 per cent guaranteed.
“Further studies are needed to pinpoint the exact BMP members and other signalling components that are involved in causing the growth plate dysrepair,” she adds.
Falls account for close to half (46 per cent) or around 30,000 hospitalised injury cases involving children every year in Australia, according to the Australian Institute of Health and Welfare.
Overall, boys are 1.5 times more likely to sustain fractures than girls, but this varies with age — from 1.3 times for those aged between 0-4 and 1.8 times for those aged 10-14 years.
Story Source:
Materials provided by University of South Australia. Note: Content may be edited for style and length.

Supersized alcopops are ready-to-drink flavored alcoholic beverages with high alcohol content that are disproportionately consumed by underage drinkers. There can be up to 5.5 standard alcoholic drinks in a single 24 ounce can, so consuming only one can of supersized alcopop is considered binge drinking, and consuming two cans can cause alcohol poisoning. Still, these products remain under-regulated and are available inexpensively at gas stations and convenience stores, where they are more readily accessible by underage youth.
New research led by George Mason University’s College of Health and Human Services found that nearly one-half (46.3 %) of all calls to U.S. poison control centers involving supersized alcopop consumption were made for consumers below the legal drinking age. Additionally, in every year studied, the proportion of calls for supersized alcopops among underage drinkers greatly exceeded the proportion of calls that were for underage drinkers for other types of alcohol.
Dr. Matthew Rossheim, an expert on supersized alcopop consumption and related health outcomes, led the study published in Drug and Alcohol Dependence. This study is the first report of clinical data within the last decade to examine negative effects from supersized alcopop consumption.
“A number of studies we’ve conducted have shown that supersized alcopops are commonly consumed by underage drinkers, which often results in serious negative consequences,” explains Rossheim. “Our latest data show a clear trend of supersized alcopop consumption among underage young people requiring poison center services. In this way, supersized alcopops appear to pose a distinct threat to youth.”
Rossheim and colleagues from the National Capital Poison Center and Emory University analyzed data from the National Poison Data System repository of calls to U.S. poison control centers from 2010 through 2019. This included 1,719 calls for consumption of supersized alcopops, many of whom consumed these products in combination with other substances. Acute care facilities such as emergency departments served as the management site for most calls (67.4 %), with another 14.3% referred to acute care.
While the large majority of consumption (more than 80%) was intentional for most age groups, 91% of the calls for children 0-11 years old who consumed supersized alcopops were for unintentional consumption. This suggests that the packaging and flavoring of these products can be attractive to children who do not understand how much alcohol these products contain or that they contain any alcohol at all.
“Better regulation and policies are urgently needed. Limiting their alcohol content and retail availability are immediate steps regulators must take in order to protect our youth.”
Story Source:
Materials provided by George Mason University. Original written by Danielle Hawkins. Note: Content may be edited for style and length.

Testing and vaccination — these are the pillars on which humanity is trying to get a grip on the Coronavirus pandemic. Although it is taking longer than many had expected, it is believed that it is only a matter of time before we are all vaccinated and thus protected. However, time is also working for the virus, which has now mutated several times, with variants B.1.1.7 from the United Kingdom, B.1.351 from South Africa and P.1 from Brazil spreading rapidly. These viruses have mutations in the so-called spike protein, the structure on the surface of the virus that is responsible for attachment to host cells. At the same time, the spike protein is also the major target of the immune response. Antibodies generated in response to SARS-CoV-2 infection or vaccination bind to the spike protein, thereby blocking the virus.
A team led by Markus Hoffmann and Stefan Pöhlmann of the German Primate Center — Leibniz Institute for Primate Research and Jan Münch of the Ulm University Medical Centre has found that the SARS-CoV-2 variants B.1.351 and P.1 are no longer inhibited by an antibody used for COVID-19 therapy. In addition, these variants are less efficiently inhibited by antibodies from recovered patients and vaccinated individuals. Thus, convalescence from COVID-19 as well as vaccination may offer only incomplete protection against these mutant viruses (Cell).
SARS-CoV-2 viruses invade lung cells in order to multiply. For the virus to enter a cell, it must first attach to the cell surface. For this, the virus uses its so-called spike protein, which is located on the viral envelope. The spike protein is also the target for therapies and vaccines aimed at preventing the virus from replicating in the body.
At the beginning of the pandemic, SARS-CoV-2 was relatively stable, but recently several viral variants have been detected and are spreading rapidly. Variants B.1.1.7, B.1.351, and P.1, which first appeared in the United Kingdom, South Africa, and Brazil, respectively, have mutations in the spike protein and some are located in areas targeted by currently used antiviral agents and vaccines. “This is worrisome because the rapid spread of variants that might not be efficiently inhibited by antibodies could undermine our current vaccination strategy,” says Stefan Pöhlmann, an infection biologist at the German Primate Center in Göttingen. Therefore, the team led by Pöhlmann and Münch investigated how effectively the mutant viruses are inhibited by drugs and antibodies.
“We found that certain antiviral agents that block host cell entry and are in (pre)clinical development inhibit the mutant viruses just as well as the original virus. Variant B1.1.7, which is currently spreading rapidly in Germany, was also efficiently inhibited by antibodies, including antibodies induced by vaccination. In contrast, an antibody used for COVID-19 therapy did not inhibit variants B.1.351 and P.1. Moreover, these variants were less well inhibited by antibodies from convalescent or vaccinated individuals, they partially bypassed the neutralizing effect of the antibodies,” says Jan Münch.
The use of the currently available vaccines makes sense and a rapid expansion of the vaccination efforts in Germany is desirable. However, it is possible that vaccination or recovery from COVID-19 may offer reduced protection from SARS-CoV-2 variants B.1.351 and P.1.” Clinical studies must now show the extent to which this fear is true.
“Our findings show that it is important to limit the spread of the virus as much as possible until widespread vaccination is feasible. Otherwise, we risk the emergence of new variants that cannot be effectively controlled by the currently available vaccines,” says Markus Hoffmann, first author of the study.
Story Source:
Materials provided by Deutsches Primatenzentrum (DPZ)/German Primate Center. Note: Content may be edited for style and length.

Humans are born with tens of thousands of hematopoietic stem cells (HSCs) that collectively ensure lifelong production of blood and immune cells that protect us from infections. HSCs can either duplicate to produce more stem cell progeny or differentiate to produce distinct immune cell lineages, an extremely critical decision that ensures that the body achieves the fine balance between having enough immune cells to fight invaders while still retaining enough HSCs to maintain future blood production. As we age, HSCs accumulate mutations that lead to the emergence of genetically distinct subpopulations. This common phenomenon known as clonal hematopoiesis (CH) is known to start in early fifties and is frequently associated with loss of function mutations in the DNMT3A gene. CH is associated with a significantly higher risk of blood cancers, cardiovascular disease, stroke and all-cause mortality.
A study led by Dr. Katherine King, associate professor at Baylor College of Medicine and Texas Children’s Hospital, shows for the first time that long-term infection and chronic inflammation drive CH mediated by the loss of Dnmt3a function. In addition, the study offers key insights into the mechanism by which chronic inflammation leads to CH and demonstrates the critical role of DNMT3a in regulating normal HSC responses to infections. The study was published in the journal Cell Stem Cell.
“Previously, we showed that chronic infection significantly impairs the ability of wild-type HSCs to remain in a quiescent stem cell state. Prolonged (lasting several months) exposure to a systemic bacterial infection promoted extensive differentiation of HSCs. While this produced sufficient immune cells to fight the infection, it also reduced the number of bone marrow HSCs by 90%,” King said. “In contrast, HSCs in mice lacking Dnmt3a gene did not differentiate much. In fact, they underwent self-renewal to produce more HSCs. We undertook the current study to test our prediction that defective differentiation and increased duplication of Dnmt3a HSCs allows them to overtake and outcompete normal HSCs when fighting chronic infections or facing long-term inflammatory conditions.”
To test their hypothesis, researchers used a combination of experimental and mathematical modeling experiments to test how HSCs from Dnmt3a mutant mice respond to long-term infection and chronic inflammation. For experimental validation, they generated mosaic mice that were generated by transplanting a mixture of whole bone marrow from Dnmt3a-mutant mice and normal mice into irradiated mice, which allowed them to track how each subpopulation of HSC contracts or grows relative to one another over time when infected for several months with Mycobacterium avium bacteria.
Using this model that mimics chronic infection in humans, they found long-term infection caused specific expansion of Dnmt3a-loss of function HSCs along with a concomitant reduction in their ability to differentiate into immune cells, which is contrary to the behavior exhibited by normal HSCs to chronic infection. Moreover, compared to the normal HSCs, Dnmt3a HSCs were more resistant to exhaustion and were less sensitive to stress-induced apoptosis (‘cell death’) upon chronic infection. Collectively, this indicates how a minor population of Dnmt3a HSCs could eventually overtake a major population of normal HSCs in the presence of chronic infection.
A number of viral or bacterial infections and chronic inflammatory stress conditions including tuberculosis, hepatitis, herpetic infections, and inflammatory bowel disease trigger the release of interferon gamma (IFN?) by the immune system, which in turn, initiates a cascade of protective immune responses. The team found that compared to wild-type HSCs, Dnmt3a-loss of function HSCs exhibited an entirely opposite set of cellular responses and global changes in gene expression patterns in response to IFN?, which tended towards preserving or even increasing the numbers of stem cells at the expense of mounting an effective response against imminent invaders or stress.
“We are excited by the findings of this study which opens several areas of future investigations. We have shown for the first time how chronic inflammation due to long-term infections or autoimmune conditions such as rheumatoid arthritis, ulcerative colitis or Crohn’s disease dampen the body’s immune response as we age. Moreover, it sheds light on the critically important role of DNMT3a in modulating immune responses during chronic infection or stress and also explains how aging and inflammation are linked to blood cancers,” King concluded.
Other authors involved in the study are Daniel Hormaechea-Agulla, Katie Matatall, Duy Le, Grant Challen, and Marek Kimmel. They are affiliated with one or more institutions: Baylor College of Medicine, Rice University, Silesian University of Technology, and Washington University School of Medicine. Grants from the National Institutes of Health, Dan L. Duncan Cancer Center, and Polish National Science Center supported this work.
Story Source:
Materials provided by Texas Children’s Hospital. Note: Content may be edited for style and length.

Fish oil supplements are a billion-dollar industry built on a foundation of purported, but not proven, health benefits. Now, new research from a team led by a University of Georgia scientist indicates that taking fish oil only provides health benefits if you have the right genetic makeup.
The study, led by Kaixiong Ye and published in PLOS Genetics, focused on fish oil (and the omega-3 fatty acids it contains) and its effect on triglycerides, a type of fat in the blood and a biomarker for cardiovascular disease.
“We’ve known for a few decades that a higher level of omega-3 fatty acids in the blood is associated with a lower risk of heart disease,” said Ye, assistant professor of genetics in the Franklin College of Arts and Sciences. “What we found is that fish oil supplementation is not good for everyone; it depends on your genotype. If you have a specific genetic background, then fish oil supplementation will help lower your triglycerides. But if you do not have that right genotype, taking a fish oil supplement actually increases your triglycerides.”
Ye’s team, including first author and graduate student Michael Francis, examined four blood lipids (fats) — high-density lipoprotein, low-density lipoprotein, total cholesterol and triglycerides — that are biomarkers for cardiovascular disease. The data for their sample of 70,000 individuals was taken from UK Biobank, a large-scale cohort study collecting genetic and health information from half a million participants.
The team divided the sample into two groups, those taking fish oil supplements (about 11,000) and those not taking fish oil supplements. Then they performed a genome-wide scan for each group, testing for 8 million genetic variants to compare. After running over 64 million tests, their results revealed a significant genetic variant at gene GJB2. Individuals with the AG genotype who took fish oil decreased their triglycerides. Individuals with the AA genotype who took fish oil slightly increased their triglycerides. (A third possible genotype, GG, was not evident in enough study volunteers to draw conclusions.)
Determining your genotype is not as far-fetched as it sounds, thanks to direct-to-consumer genetic testing companies. Companies may not report that specific genetic variant yet, but a tech-savvy consumer should be able to download the raw data and look at the specific position to discover the genotype, according to Ye. The ID for the variant is rs112803755 (A >G).
The study’s findings may also shed light on previous trials, most of which found that fish oil provides no benefit in preventing cardiovascular disease.
“One possible explanation is that those clinical trials didn’t consider the genotypes of the participants,” Ye said. “Some participants may benefit, and some may not, so if you mix them together and do the analysis, you do not see the impact.”
Now that Ye has identified a specific gene that can modify an individual’s response to fish oil supplementation, his next step will be directly testing the effects of fish oil on cardiovascular disease.
“Personalizing and optimizing fish oil supplementation recommendations based on a person’s unique genetic composition can improve our understanding of nutrition,” he said, “and lead to significant improvements in human health and well-being.”
Story Source:
Materials provided by University of Georgia. Original written by Allyson Mann. Note: Content may be edited for style and length.

In “Hooked,” Michael Moss explores how no addictive drug can fire up the reward circuitry in our brains as rapidly as our favorite foods.In a legal proceeding two decades ago, Michael Szymanczyk, the chief executive of the tobacco giant Philip Morris, was asked to define addiction. “My definition of addiction is a repetitive behavior that some people find difficult to quit,” he responded.Mr. Szymanczyk was speaking in the context of smoking. But a fascinating new book by Michael Moss, an investigative journalist and best-selling author, argues that the tobacco executive’s definition of addiction could apply to our relationship with another group of products that Philip Morris sold and manufactured for decades: highly processed foods.In his new book, “Hooked,” Mr. Moss explores the science behind addiction and builds a case that food companies have painstakingly engineered processed foods to hijack the reward circuitry in our brains, causing us to overeat and helping to fuel a global epidemic of obesity and chronic disease. Mr. Moss suggests that processed foods like cheeseburgers, potato chips and ice cream are not only addictive, but that they can be even more addictive than alcohol, tobacco and drugs. The book draws on internal industry documents and interviews with industry insiders to argue that some food companies in the past couple of decades became aware of the addictive nature of their products and took drastic steps to avoid accountability, such as shutting down important research into sugary foods and spearheading laws preventing people from suing food companies for damages.PenguinRandomHouseIn another cynical move, Mr. Moss writes, food companies beginning in the late 1970s started buying a slew of popular diet companies, allowing them to profit off our attempts to lose the weight we gained from eating their products. Heinz, the processed food giant, bought Weight Watchers in 1978 for $72 million. Unilever, which sells Klondike bars and Ben & Jerry’s ice cream, paid $2.3 billion for SlimFast in 2000. Nestle, which makes chocolate bars and Hot Pockets, purchased Jenny Craig in 2006 for $600 million. And in 2010 the private equity firm that owns Cinnabon and Carvel ice cream purchased Atkins Nutritionals, the company that sells low-carb bars, shakes and snacks. Most of these diet brands were later sold to other parent companies.“The food industry blocked us in the courts from filing lawsuits claiming addiction; they started controlling the science in problematic ways, and they took control of the diet industry,” Mr. Moss said in an interview. “I’ve been crawling through the underbelly of the processed food industry for 10 years and I continue to be stunned by the depths of the deviousness of their strategy to not just tap into our basic instincts, but to exploit our attempts to gain control of our habits.”A former reporter for The New York Times and recipient of the Pulitzer Prize, Mr. Moss first delved into the world of the processed food industry in 2013 with the publication of “Salt Sugar Fat.” The book explained how companies formulate junk foods to achieve a “bliss point” that makes them irresistible and market those products using tactics borrowed from the tobacco industry. Yet after writing the book, Mr. Moss was not convinced that processed foods could be addictive.“I had tried to avoid the word addiction when I was writing ‘Salt Sugar Fat,’” he said. “I thought it was totally ludicrous. How anyone could compare Twinkies to crack cocaine was beyond me.”But as he dug into the science that shows how processed foods affect the brain, he was swayed. One crucial element that influences the addictive nature of a substance and whether or not we consume it compulsively is how quickly it excites the brain. The faster it hits our reward circuitry, the stronger its impact. That is why smoking crack cocaine is more powerful than ingesting cocaine through the nose, and smoking cigarettes produces greater feelings of reward than wearing a nicotine patch: Smoking reduces the time it takes for drugs to hit the brain.But no addictive drug can fire up the reward circuitry in our brains as rapidly as our favorite foods, Mr. Moss writes. “The smoke from cigarettes takes 10 seconds to stir the brain, but a touch of sugar on the tongue will do so in a little more than a half second, or six hundred milliseconds, to be precise,” he writes. “That’s nearly 20 times faster than cigarettes.”This puts the term “fast food” in a new light. “Measured in milliseconds, and the power to addict, nothing is faster than processed food in rousing the brain,” he added.Mr. Moss explains that even people in the tobacco industry took note of the powerful lure of processed foods. In the 1980s, Philip Morris acquired Kraft and General Foods, making it the largest manufacturer of processed foods in the country, with products like Kool-Aid, Cocoa Pebbles, Capri Sun and Oreo cookies. But the company’s former general counsel and vice president, Steven C. Parrish, confided that he found it troubling that it was easier for him to quit the company’s cigarettes than its chocolate cookies. “I’m dangerous around a bag of chips or Doritos or Oreos,” he told Mr. Moss. “I’d avoid even opening a bag of Oreos because instead of eating one or two, I would eat half the bag.”As litigation against tobacco companies gained ground in the 1990s, one of the industry’s defenses was that cigarettes were no more addictive than Twinkies. It may have been on to something. Philip Morris routinely surveyed the public to gather legal and marketing intelligence, Mr. Moss writes, and one particular survey in 1988 asked people to name things that they thought were addictive and then rate them on a scale of 1 to 10, with 10 being the most addictive.“Smoking was given an 8.5, nearly on par with heroin,” Mr. Moss writes. “But overeating, at 7.3, was not far behind, scoring higher than beer, tranquilizers and sleeping pills. This statistic was used to buttress the company’s argument that cigarettes might not be exactly innocent, but they were a vice on the order of potato chips and, as such, were manageable.”But processed foods are not tobacco, and many people, including some experts, dismiss the notion that they are addictive. Mr. Moss suggests that this reluctance is in part a result of misconceptions about what addiction entails. For one, a substance does not have to hook everyone for it to be addictive. Studies show that most people who drink or use cocaine do not become dependent. Nor does everyone who smokes or uses painkillers become addicted. It is also the case that the symptoms of addiction can vary from one person to the next and from one drug to another. Painful withdrawals were once considered hallmarks of addiction. But some drugs that we know to be addictive, such as cocaine, would fail to meet that definition because they do not provoke “the body-wrenching havoc” that withdrawal from barbiturates and other addictive drugs can cause.The American Psychiatric Association now lists 11 criteria that are used to diagnose what it calls a substance use disorder, which can range from mild to severe, depending on how many symptoms a person exhibits. Among those symptoms are cravings, an inability to cut back despite wanting to, and continuing to use the substance despite it causing harm. Mr. Moss said that people who struggle with processed food can try simple strategies to conquer routine cravings, like going for a walk, calling a friend or snacking on healthy alternatives like a handful of nuts. But for some people, more extreme measures may be necessary.“It depends where you are on the spectrum,” he said. “I know people who can’t touch a grain of sugar without losing control. They would drive to the supermarket and by the time they got home their car would be littered with empty wrappers. For them, complete abstention is the solution.”