TTHealthWatch is a weekly podcast from Texas Tech. In it, Elizabeth Tracey, director of electronic media for Johns Hopkins Medicine in Baltimore, and Rick Lange, MD, president of the Texas Tech University Health Sciences Center in El Paso, look at the top medical stories of the week.
This week’s topics include urinary tract infections (UTIs) and meat consumption; mental health hospitalizations among youth; genes, a bacterium, and gastric cancer; and reducing air pollution and health.
Program notes:
0:40 Air pollution and the effect of reducing it
1:40 Medicare beneficiaries
2:40 Different countries around the world
3:21 Genes, Helicobacter pylori, and gastric cancer
4:27 A variant plus infection equals increased risk
5:27 Confluence of factors giving rise to cancer
6:25 Pediatric mental health hospitalizations domestically
7:25 Two-thirds suicidal attempt or self harm
8:27 Covid has exacerbated
9:00 Mobile genetic elements and E. coli
10:00 From meat consumption
11:02 Genetic analysis modeling
12:00 End
Transcript:
Elizabeth: How many urinary tract infections are due to meat?
Rick: Does reducing air pollution impact everybody the same?
Elizabeth: How does a common bacterial infection and genetics interact in gastric cancers?
Rick: And what do we know about pediatric mental health hospitalizations over the last decade?
Elizabeth: That’s what we’re talking about this week on TTHealthWatch, your weekly look at the medical headlines from Texas Tech University Health Sciences Center in El Paso. I’m Elizabeth Tracey, a Baltimore-based medical journalist.
Rick: And I’m Rick Lange, president of Texas Tech University Health Sciences Center in El Paso, where I’m also dean of the Paul L. Foster School of Medicine.
Elizabeth: Dean, I’m going to leave it up to you. How would you like to start this week?
Rick: Let’s start with the thing I led off with, air pollution. Does reducing it affect everybody the same? It’s pretty clear that we’re doing our best to decrease air pollution and especially exposure to what’s called fine particulate matter — particles that have a diameter of less than 2.5 μm. We call it PM2.5. The EPA has recognized that air pollution levels are related to mortality really across the country. There is a current effort to get the PM2.5 level down to 12 mcg per cubic meter. It’s now about 20.
Let’s say you do that. Who benefits and do some people benefit more than others? What the authors did was they looked at 623 million person-years of Medicare data from 73 million people over the age of 65 from 2000 to 2016. They estimated two things, one is the annual PM2.5 exposure and the mortality.
But they looked at particular subpopulations. They looked at black versus white. They also looked at income, really low-income, people that were on Medicaid. These are people that are about 200% of the poverty level and then everybody above that. What they discovered is, you can get it down to 12. That’s beneficial. But if you go from 12 to 8, you still get an incremental benefit. Overall it reduces the mortality by about 4% or 5%. It impacts African Americans more than whites and higher-income African Americans more than lower-income African Americans, and even lower-income whites.
That implies that first of all there is an income disparity. More importantly, the racial difference doesn’t have anything to do with the race, it has to do more with where they live. African Americans are more likely to be exposed to higher particulate matter and live in areas, for example, where there were freeways and there is more exposure to it. There is a 45% better mortality reduction among African Americans than there is against whites.
Elizabeth: We certainly have circled around this particular observation many times when we’ve taken a look at proximity to highways and the degree of particulate matter, and specifically in different countries around the world where there is a higher density of a population immediately adjacent to these kinds of structures. It’s unclear to me, though, exactly what we do about this outside of, “Let’s move them out of there.”
Rick: This is one way to decrease health disparities, so I think it’s very helpful. Besides moving — and that’s going to be very difficult — it’s just to reduce particulate matter across the board. The change in the fuel we use, so change in our driving habits. In fact, when you look at the particulate matter density just across the United States, it’s clearly been decreasing. But what this study shows is you can still get incremental benefit going even lower to help decrease some of the health disparities between whites and African Americans.
Elizabeth: That’s in the New England Journal of Medicine. Let’s stay there and let’s turn to this relationship between the common bacterium, Helicobacter pylori, and recombination genes that people may have and their susceptibility to developing gastric cancer.
This is a study that includes a couple of different databases from Japan. One of them is the BioBank Japan. What they did was look at germline pathogenic variants in 27 cancer-predisposing genes and the risk of gastric cancer in a sample of 10,000+ patients who already had gastric cancer and 38,000+ controls who did not, from this BioBank Japan. They also took a look at the combined effect of the pathogenic variants and Helicobacter pylori, or H. pylori, infection status on risk of gastric cancer. This was in 1400+ patients with gastric cancer, just shy of 6,000 controls, from the hospital-based epidemiologic research program at Aichi Cancer Center. What they found was that sure enough if you had one of these pathogenic variants and you had Helicobacter pylori infection, you were more likely to develop gastric cancer.
Rick: I found this one really interesting. The first thing they did was they identified 9 different genes, genetic abnormalities that people were born with, that increased risk of gastric cancer. Eight of these hadn’t really been previously described. Then they said what if you have that and an H. pylori infection — by the way half of the world is infected with H. Pylori — that increases the risk of cancer about 16 fold?
We do know, for example, that H. Pylori helps to cause gene abnormalities in the stomach. These genetic variants that people have predispose them to not be able to fix those genetic variants and it predisposes to cancer. For example, at 85 years of age, a person who has H. pylori infection and one of these variants the cumulative risk of gastric cancer was 45%. For those that were non-carriers of H. pylori, it’s only about 14%.
Elizabeth: What it does for me is it nails down some of the hypotheses that have been circulating for quite a long time about the confluence of factors that ultimately end up giving rise to cancer. One of the questions I have is, is it possible that these pathogenic variants in the genes actually predispose to persistent H. pylori infection?
Rick: Elizabeth, that’s an interesting question. This particular study doesn’t answer it. It does say that one of the ways we can reduce the risk of gastric cancer, then, is to eradicate H. pylori infection, especially with those that have one of these genetic variants.
Elizabeth: At 85 years of age, this higher cumulative risk, it’s kind of like, “Wow, you’re 85 when you develop this?” That’s not that I’m not sympathetic, but we do develop things the older we get.
Rick: We do. But if you knew that giving someone an antibiotic could reduce your risk by 67%, that’s a pretty effective cancer prevention method.
Elizabeth: Yep, I agree with that.
Rick: Elizabeth, let’s move from the older population to the pediatric population. This is in JAMA, and it’s looking at pediatric mental health hospitalizations from 2009 to 2019. Why this is relevant is, if you just go back about 4 or 5 years, it was shown that approximately 1 in 6 youths in the U.S. have a mental health condition. Unfortunately, less than half received any mental health services.
When you take a look just around the country, if you look at rural counties, more than half of them don’t have any outpatient mental health facility that provides treatment for children. Even in the urban setting, more than a third don’t have it. Over the last several decades, we’ve decreased the capacity to treat kids as an outpatient. Ask yourself, what’s that done to inpatient hospitalizations?
They looked at that database and they looked at over 4.7 million pediatric hospitalizations. What happened is if you looked at those that were just due to mental health, during that period they increased from about 160,000 to almost 202,000. Unfortunately, when you look at the major causes for that, about two-thirds to three-fourths of it is due to depression. About two-thirds of those there is actually a suicidal attempt or self-injury. That’s increased to 160% over that decade and it’s primarily affecting kids in the adolescent range 10 to 14 or 11 to 14. This is an epidemic of huge proportion, and it affects our most vulnerable population.
Elizabeth: I think this is just such an incredibly difficult problem. I’m glad that this study is pointing to it and providing us with some data. We’ve talked a lot about the incidence of mental health issues during the pandemic.
On the converse, I have also been hearing a lot of discussion about why are we telling adolescents that they’re abnormal? This is normal for them to experience some mood swings and all kinds of things. Then what’s the role of social media in this? That’s why I say, gosh, it’s just really a thorny problem.
Rick: It is Elizabeth. Because this particular study covers a period from 2009 to 2019, it predates COVID. These were the mental health issues before COVID. You and I have talked before, based upon data, of how it’s exacerbated it even more. It clearly needs to be addressed.
Elizabeth: How would you approach it?
Rick: As you mentioned, some of this is what I don’t want to call normal behavior, but it’s a normal part of the life cycle. It’s even worse when there is social instability or there is peer or family conflict, and as you’ve mentioned social media as well.
But what’s made things even worse is the fact there has been a decrease in outpatient facilities where you’d like to treat the kids and also a decrease in inpatient facilities. Increasing access to outpatient care is going to be imperative.
Elizabeth: Finally, let’s turn to the journal One Health, mobile genetic elements to identify E. coli infections in people that are not in the intestine.
They basically did a comparative genomic analysis of a large collection of contemporaneous, geographically-matched, clinical and meat-source E. coli isolates. Then they identified among that population 17 source-associated mobile genetic elements. Those are plasmids and bacteriophages. What we know about those is, those are like the jumping genes. They help E. coli acquire different characteristics during its lifespan, if you will, and they ultimately ended up, by the incorporation of their model, and the study of both transposons and plasmids, that 8% of human, mostly urinary tract, infections in their study population were caused by these things that ultimately arose from zoonoses and they say from meat. That’s a large number of UTIs that we can finger and say, “This came from a meat source — a dietary meat source.”
Rick: Elizabeth, there is a huge emphasis on what’s called One Health now. It’s not just to focus on human health, but it’s how health across all the animal spectrum affects human health. We know, by the way, that most E. coli infections that are transmitted from animals or meat to humans are actually GI infections. People close down meatpacking plants and they take meat off the shelves. But this thought that meat can actually cause urinary tract infections, that’s kind of novel. The fact that it’s an animal-to-human transmission is pretty remarkable.
Now you say 8% is not very high, but you have to remember that E. coli causes approximately 6 to 8 million urinary tract infections each year in the U.S. That means about 8%, somewhere between a half of a million and two-thirds of a million arise from the meat that we eat.
The main value of this study, though, is it uses certain techniques and genetic analysis to identify the source of these infections. These are genetic analysis modeling that hasn’t been done before. This can transmit to other zoonotic infections.
Elizabeth: I think we’re going to see, if I were a betting gal, a whole lot more of this kind of analysis coming down the pike.
Rick: It is. One of the things that our listeners need to be aware of is the fact that many of these animals are fed antibiotics to help them to grow and to be healthy before they’re sent to the packing plant. These particular infections were resistant to some of the usual antibiotics we typically use. This issue of transmission from animals to humans and back and forth really is clinically irrelevant.
Elizabeth: On that note then, that’s a look at this week’s medical headlines from Texas Tech. I’m Elizabeth Tracey.
Rick: And I’m Rick Lange. Y’all listen up and make healthy choices.
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