Brief Bulletins from the Healthcare Front

As I looked over the medical and healthcare news in the various publications (and also online, of course) my takeaway was that, in spite of some distinctly bad items like a new flu subtype and the definitely negative news about the effects of obesity on deaths from infection, most of what has turned up is positive. I’ll put the negative items up front, hoping that you can get through them to the good news.

Let’s start off with a look at the flu picture.

This flu season was predicted to be the worst in 25 years

That dire prediction came from the Centers for Disease Control and Prevention (CDC), which, as you know, is a US federal agency under the Department of Health and Human Services. The flu season runs from fall to the following spring, so we’re talking about the 2025 -2026 flu season. The CDC estimated that by the third of January 2026, there were at least 15 million illnesses, 180,000 hospitalizations, and 7,400 deaths, and the flu season still had several months to do more damage. Considering that during the 2024- 2025 season, their estimate was that the flu was the cause of 51 million illnesses, 710,000 hospitalizations, and 45,000 deaths, the CDC’s prediction for the span of time after January 3 this year was dire indeed. The numbers come from an online CDC platform entitled “FluView.”

However, that prediction has so far turned out to be needlessly dire.

As it turns out, seasonal flu activity has significantly decreased across the United States, following that peak back in January. As of late spring, the CDC estimates that the season has caused at least 27 million illnesses, 350,000 hospitalizations, and 22,000 deaths, which is less than half of the deaths predicted earlier.

Flu cases are declining across most of the country, the CDC said, with influenza A viruses waning and influenza B viruses showing varying levels of activity. That trend actually follows the typical seasonal flu virus patterns. As of the most recent tests at the beginning of May , the proportion that were positive for flu fell to 9.8%, down from 11.5% the previous week, and the proportion of outpatient visits for flu remained below the national baseline for the second straight week, falling from 2.8% to 2.6%.

For the season overall, influenza A viruses have been the most frequently reported. Of the influenza A viruses collected so far, 92.7% have belonged subclade K, which contains mutations that developed after this season’s flu vaccine strains were selected.

Weekly hospital admissions for flu also declined, dropping from 5,640 the previous week to 3,050. But an additional four pediatric deaths were reported during the last week in April, bringing the total for the season to 127. Although the CDC has classified the current flu season as moderate for adults, for children it has been a high severity season.

The dire prediction about this flu season came from an interview with Yonatan Grad, a professor of immunology and infectious diseases at Harvard. He suggested that at least part of the problem is a new virus strain labeled subclade K, which has crucial differences from the strains that were used to formulate this year’s vaccine. As you know, each year a flu vaccine is developed based on whatever information exists about the most current flu strains.

The information guiding the formulation of flu vaccines comes mostly from virus samples obtained from regions where the flu emerges earlier. The flu variants causing the disease in South America, are used as the basis for developing a vaccine that (it is hoped!) will be effective in North America. The South American flu season happens about six months earlier than the one in North America, because their winter is our summer (and vice versa). Of course, this assumes that the flu variant manifest earlier, in the South American winters, than in our winters up North. That assumption is not always correct. Some of the new variants pop up in the Northern Hemisphere sooner than in the Southern Hemisphere, in which case the vaccine does not protect us against those variants.

The classification of flu strains is complex, and developing a vaccine that is effective against the specific flu strain that is circulating and making people sick requires extensive investigation. The two main classes of influenza are designated A and B.

Within the influenza A type, H3N2 and H1N1 are the two subtypes that have been circulating for nearly 50 years. Usually, one influenza A subtype dominates in a season, although the B subtype is still around causing disease. This year, H3N2 is the villain. The specific H3N2 strain used in the current vaccine appears to be essentially different from the circulating H3N2 strain. This suggests that the immune response elicited by the vaccine might not offer enough protection against the flu strain that is currently circulating.

A critical factor (of course!) is how much of the population actually gets vaccinated. Here’s a little table showing the numbers of people that contracted the flu each of the past seven seasons.

Flu Cases in the United States

And the current estimates for the 2025 – 2026 season as stated above, (~27 million cases), are much lower than those for the 2024 – 2025 season, although more than twice the rate for the 2021 -2022 season.

Why did the numbers of flu cases decline so markedly in 2021 – 2022? Professor Grad’s guess is that many, many more people got the flu vaccine in that period, because that’s when everybody was super alert to the COVID 19 pandemic. COVID vaccines had become available, and our populace was urged to get vaccinated. Lots of people got the flu vaccine at the same time, and the rate of incidence took a very large dip. And another factor that certainly contributed to the large decrease in flu infections in that period was social isolation and protective masking, again due to heightened awareness of COVID. But once the COVID pandemic receded a bit, people relaxed their concern and fewer people got vaccinated, so in 2022 – 2023 the number of flu cases bounced back to 40 million.

As for the fortunate 2025 – 2026 data, showing that the numbers of flu cases, hospitalizations, and deaths were about half of what was predicted at the start of the season, I have seen no clear explanations. It is possible that the flu variants this past season were less active.

I must acknowledge that many people are highly skeptical about vaccination. Flu vaccines without doubt are associated with negative effects. The common side effects, essentially of little or no concern, include soreness and swelling right at the injection site, also fatigue and perhaps a headache. Children especially may experience low fevers. These side effects are a normal part of the vaccination process. They indicate that the body is generating antibodies to the disease itself. Some individuals may experience rashes or itching near the injection site, or mild pain in their backs or necks. Very rarely, flu shots cause symptoms that require a consultation with a healthcare provider. These include chest pain, difficulty breathing, hives, and, in the case of a small surface wound, bleeding that does not resolve promptly.

However, if we take into account the robust fact that during the 2024 – 2025 season, flu was the cause of 45,000 deaths in the US, the flu vaccine side effects seem negligible. Speaking for myself, I will accept them and get my flu shot every year.

About one in ten deaths from infection may be attributed to obesity

That scary assertion comes from a recent article in Lancet (March 7, 2026). The data comes from two studies in Finland (in 1998 and 2002), and repeated studies in the UK Biobank (from 2006 to 2010). The study participants were classified in five categories – healthy weight, overweight, and three categories of obesity, and followed up based on national hospitalization and mortality registries which tracked hospital admissions and deaths from infectious diseases. The data about obesity prevalence estimates comes from the Global Burden of Diseases, Injuries, and Risk Factors Study database (Institute for Health Metrics and Evaluation). The study estimated the proportion of fatal infections attributable to obesity regionally and by country for the years 2018 (before), 2021 (during), and 2023 (after) the COVID-19 pandemic.

The study analyzed data from almost 120,000 adults in the Finnish cohort and about 480,000 from the UK Biobank. None of the study subjects had any recent history of infection at baseline severe enough to require hospitalization. During the follow-up period, the subjects in the Finnish study experienced 8,230 infections of enough severity to require hospital admission, and subjects in the UK study had almost 82,000 similarly severe infections. Compared with individuals whose weight was assessed as healthy, the individuals in the highest class of obesity had triple the risk of either hospital admission or mortality.

The weight assessment was based on the Body Mass Index (BMI), a screening tool which calculates a person’s body fat using weight in kilograms divided by height in meters squared. This can be translated into a calculation using weight in pounds divided by height in feet and inches squared. I should insert here my profound distrust of BMI as a tool to determine whether a person’s weight is healthy. The tool has several basic defects. For one, it does not take into consideration the essential difference between fat and muscle mass, or between fat and bone. Also, it does not consider differences between men and women.

The article in Lancet mostly emphasizes the greatly increased risk in persons classified in the highest obesity category according to their BMI. A person with a BMI below 18.5 is considered underweight. So-called “healthy weight” is defined as BMI between 18.5 and 24.9. Individuals with a BMI between 25.0 and 29.9 are in the overweight category, and those with a BMI above 30.0 are ranked as obese. However, the Lancet article focuses on the risk in persons with a BMI above 40.0. For example, for me to get to a BMI of 40.0, I would have to gain approximately 130 pounds, and I am not underweight.

The National Institute of Diabetes and Digestive and Kidney Diseases, which is part of NIH, has a lengthy and detailed web documented titled “Understanding Adult Weight Gain and Obesity,” which lists thirteen significant health problems linked to obesity. I will not list all thirteen, but serious infection is not one of them. Just to give you a notion of the severity of the consequences of significant overweight, the first four listed are type 2 diabetes, high blood pressure, heart disease, and stroke.

The Lancet article focuses only on statistics and does not speculate on the mechanism, i.e., how does obesity actually cause life-threatening infection? To get a bit more insight, I had to do more sleuthing and came upon an article entitled “Obesity: A Chronic Low-Grade Inflammation and Its Markers,” (D. Khana, Cureus. 2/28, 2022:14(2). The article states that there is much unknown regarding the association between obesity and inflammation. The Cureus article is essentially a deep review of the literature and not a clinical study. Here’s a key quote:

“Researchers found the adipose tissue of lean individuals predominantly secretes anti-inflammatory markers, while in obese individuals more pro-inflammatory markers are secreted. Many studies found that adipose tissue in obese individuals showed a shift in immune cells from anti-inflammatory M2 macrophages to pro-inflammatory M1 macrophages, which was also correlated with insulin resistance. Obese individuals generally present with higher levels of hormones such as leptin, visfatin, and resistin.”

The Cureus article gives no clue as to any underlying reasons for that basic difference between the adipose tissue of the lean population and their obese counterparts, nor about that shift in their respective immune cells. A bit of further sleuthing came up with this:

“Obese individuals have pro-inflammatory (M1) macrophages because hypertrophied (enlarged) adipose cells become stressed and die, releasing signals that recruit monocytes, which then polarize into M1 macrophages. This creates a chronic low-grade inflammation due to hypoxia, lipid accumulation, and increased production of pro-inflammatory cytokines like TNF-α and IL-6.”

This was from “The Macrophage Switch in Obesity Development,” by Angela Castoldi. (Front Immunol 2016 Jan 5;6:637). Other adverse consequences of enlarged fat cells include insulin resistance, accumulation of amyloid-beta and tau in the brain, reduced cerebral blood flow, and several other strongly negative factors. Amyloid-beta and tau in the brain are, as you know, key markers of Alzheimer’s disease.

However (this is pure speculation) I suspect that those highly obese individuals that the Lancet article focuses on – those with a BMI of 40 or higher – are reluctant to come under the scrutiny of a doctor, lest they be stigmatized for being fat, and firmly instructed to lose weight. It’s possible that the new generation of weight loss drugs such as Wegovy (semaglutide) and Zepbound (tirzepatide), which we have discussed in these missives, may make a significant difference in the prevalence of infectious diseases in the individuals who have successfully slimmed down. I’ll look out for further data.

Positive developments in the management of Alzheimer’s disease

One of these developments points to earlier detection of Alzheimer’s and the other to an entirely new (potential!) treatment option.

We have discussed the large benefit of initiating the treatment of progressive diseases in the early phases, as well as the harm in letting the disease progress to later stages before initiating treatment. For example, the U. S. Preventive Services Task Force (USPTF) has put forward recommendations that severely limit testing for prostate cancer. Their statement recommends “weighing small potential benefits against risks of overdiagnosis and overtreatment” for men aged from 55 to 69. For men aged 70 or older, the USPSTF recommends against routine testing because the harms outweigh potential benefits, in their estimation. The harms noted by the USPSTF are false positives, unnecessary biopsies, and treatment complications like incontinence/erectile dysfunction. These recommendations – or perhaps condemnations – have of course led to reduced screening rates, which according to PubMed strongly correlated with an increase in the incidence of metastatic prostate cancer. Hopefully, the USPSTF will not meddle with recommendations regarding tests for Alzheimer’s disease (AD).

The ability to diagnose AD earlier took a huge step forward in May of 2025 when the FDA gave its blessing to the first blood test for early detection of the condition. The test, called Luminpulse, was developed by a Japan-based company, Fujirebio Diagnostics. The test is for persons aged 55 or older with signs or symptoms of the disease.

Before this encouraging development, other blood tests for AD have been available for clinical use. These previous tests do not have FDA approval, FDA safety regulation, or any insurance coverage. Thus, the tests have not been part of the standard of care for diagnosis. If an individual wants to be tested for AD using one of these novel tests, he/she must pay for it out of his/her own pocket. These tests cost between $300 and $1,750, and are not widely used.

Up to now, our healthcare system has relied on two other tests, both approved by the FDA. As it happens, these tests are more complicated, more invasive, and more expensive than the new blood tests. However, they are currently covered by insurance to confirm the presence of Alzheimer’s. One of these tests is a positron emission tomography (PET) scan of the brain. The other is a lumbar puncture, or “spinal tap,” which can detect AD biomarkers in a sample of fluid surrounding the brain and spinal cord.

This new Luminpulse test analyzes a blood sample to look for several proteins that are characteristic of Alzheimer’s. As we have discussed in the past, one of these proteins is amyloid-beta 42 (αβ-42). The test calculates the ratio of αβ-40, which is naturally present in the brain and considered normal, to αβ-42, which is involved in forming Alzheimer’s brain plaques. The test also looks for a type of tau protein (phosphorylated τ-217) that causes tangles in brain cells.

Usually the blood test is either strongly positive or strongly negative, a result that’s accurate more than 90% of the time. If the blood test is clearly negative, the patient is given the reassuring news that his/her memory issues are not due to Alzheimer’s. Such patients are normally informed that their memory problems will be addressed by other means. If after a period of about six months, his/her memory issues are still unresolved, he/she is referred to a memory specialist to look for other causes of dementia. If the test is neither clearly positive nor negative, the patient is referred to a specialist for either an amyloid PET scan or a lumbar puncture to zero in on the correct diagnosis.

If the blood test comes back positive for Alzheimer’s, he/she will be referred to a neurologist or another specialist to discuss possible treatment, such as an amyloid-targeting therapy.

The Lumipulse test is not the only test that looks for Alzheimer’s blood markers. However, it is the only test that has attained FDA approval, a highly challenging process. This is a milestone that’s considered a game changer.

FDA approval means that the blood test has been evaluated by scientists and has been demonstrated to do what it claims. Thus, it has the potential to improve treatment for individuals with memory issues. The next step is for the test to be covered by insurance, particularly Medicare and Medicaid. When that happens, which is expected soon, the test will likely become the standard of care. There will be a pathway for early detection of Alzheimer’s, before the deposition of those brain-clogging substances leads to extensive permanent harm. A blood test that produces relatively prompt and accurate results will allow healthcare providers to start treatment immediately. And, as we’ve repeatedly observed, the sooner a treatment program gets going, the better the odds are that it will result in genuine benefit.

“Alzheimer’s disease impacts too many people, more than breast cancer and prostate cancer combined,” said FDA Commissioner Martin A. Makary, M.D., M.P.H. “Knowing that 10% of people aged 65 and older have Alzheimer’s, and that by 2050 that number is expected to double, I am hopeful that new medical products such as this one will help patients.”

… and another promising Alzheimer’s bit of news

That being the role of lithium in Alzheimer’s disease. A team led by Dr Bruce Yankner, a professor of genetics and neurology at Harvard Medical School, published groundbreaking research showing that lithium is a natural, biologically important element in the brain, which has the potential to prevent or even reverse Alzheimer’s disease. This is a substantial forward marker in understanding a disease that affects more than 50 million people worldwide, and that so far has proved frustratingly difficult to treat.

The team’s research demonstrated that lithium is naturally present in the brain and assists the normal function of major brain cell types. Their research also showed that lithium depletion is one of the earliest changes in Alzheimer’s disease. Additionally, their work demonstrated that reduced lithium levels occurred when amyloid beta 42 (αβ-42) plaques bind lithium, essentially inactivating it and further reducing the amount available to support normal brain function. When the team reproduced this level of lithium depletion in the mouse brain, it dramatically accelerated the formation of αβ-42 plaque and led to memory loss.

In the early stages of research into the mechanisms of Alzheimer’s disease, amyloid was thought to be an inert byproduct of the disease. But the researchers found that far from being a harmless byproduct, αβ-42 was in fact toxic to neurons, suggesting that it might play a causal role in Alzheimer’s. That finding is foundational to recently FDA approved drugs such as lecanemab and donanemab.

However, a troublesome contradiction emerged. Some people can have brains riddled with these αβ-42 plaques and have relatively intact cognition, while others who have similar amounts of these plaques are severely impaired.

The recent findings about the effect of lithium on our brains provide a potential explanation. By showing that amyloid binds to and neutralizes lithium, and that aging individuals can vary in their baseline lithium levels, the team may be starting to understand the imperfect correlation between αβ-42 plaques and disease symptoms.

Further investigation by the team suggested that a novel lithium compound, lithium orotate, resulted in a reduction of toxic lithium binding by αβ-42 plaques. The early finding that this compound could prevent and reverse Alzheimer’s pathology and memory loss in mouse models suggests that lithium orotate might have a similar effect in human models.

I should emphasize that at this point it’s only a possibility that lithium could be a useful and effective agent in dealing with Alzheimer’s disease. Prospective drugs that have desirable effects in mice frequently disappoint when tested in humans. Besides, like most drugs, lithium comes with side effects.

The most common side effects are increased urination, shakiness of the hands, and increased thirst. More serious side effects include hypothyroidism, diabetes, and potential toxicity. If lithium levels become too high, patients might experience diarrhea, vomiting, poor coordination, sleepiness, and ringing in the ears. Blood level monitoring is recommended to decrease the risk of toxicity.

A study in Lancet found that elevated blood lithium concentrations were also significantly linked with chronic kidney disease. Odds of developing stage 3 or higher kidney disease increase as lithium concentrations increase, ranging from nearly triple the risk to more than quadruple the risk. And analyses showed that age, initial estimated glomerular filtration ratio (eGFR), diabetes, and history of acute kidney injury were also significant risk factors for developing stage 3 or higher chronic kidney disease. The eGFR ratio indicates how well (or poorly) the kidneys are functioning in removing waste from the blood. (Lancet 11:12 1002-1011 Dec 2024)

Lithium can also cause significant birth defects, especially if used in the first semester of pregnancy. This is not a major factor in evaluating lithium as a treatment to prevent or delay the onset of Alzheimer’s, since the risk of Alzheimer’s becomes significant well after the age at which women are apt to become pregnant.

Another factor that may halt or delay the development of lithium as a treatment for Alzheimer’s is the termination of two critical federal grants to Harvard. These grants support lifesaving research, including the medical uses of lithium. Fortunately, US District Court struck down the cancelation of $2.2 billion in research funding for Harvard. We can hope that the termination of the two other grants will also be struck down.

And, of course, a huge factor will be the terms of the FDA approval, if and when a lithium compound is developed as a treatment for us humans. We can recall the terms of the FDA’s approval of lecanemab, marketed as Leqembi. Here’s the text:

“Leqembi should be initiated in patients with mild cognitive impairment or mild dementia stage of Alzheimer’s disease, the population in which treatment was studied in clinical trials. The labeling states that there are no safety or effectiveness data on initiating treatment at earlier or later stages of the disease than were studied.”

As you see, the FDA’s terms ruled out approval of lecanemab for patients in the earliest stages of Alzheimer’s. The diagnosis of mild cognitive impairment or mild dementia needed to be confirmed empirically, by tests for the detection of those tell-tale αβ-42 plaques by brain scans or analysis of cerebrospinal fluid. That has meant that lecanemab cannot be prescribed early enough to prevent at least some cognitive impairment. Chances are that the FDA’s approval of a lithium compound for Alzheimer’s will be on similar terms, which would likely mean that a lithium compound would have a similarly limited effect on preventing cognitive impairment.

We’re probably a long way from lithium’s seeking approval from the FDA. A factor that will play a major part in the FDA’s approval process is economics. When a prospective drug gets approval from the FDA, that drug will be covered by Medicare. Thus if the approval terms for the drug stated that the lithium compound could be prescribed for individuals with the earliest symptoms of Alzheimer’s, Medicare’s costs would likely skyrocket.

Whether the prospective lithium compound would be highly expensive would depend not on the actual costs of the compound, but on the total development costs. Lithium itself is cheap. As those of us who took high-school physics remember, it’s number three in the periodic table – a soft, flexible metal, not rare and not expensive. But the costs of putting a lithium compound through the clinical trials needed to get FDA approval could be maximally expensive. And who would cover those costs?

There’s no way for a pharmaceutical outfit to get an exclusive patent on a lithium compound. It could get duplicated pretty quickly. Patenting a lithium compound would be like trying to patent aspirin. However, the name under which a lithium compound was marketed could be subject to copyright.

A possibility is that a company attempting to market a lithium compound as a treatment for Alzheimer’s might skip the lengthy and costly process of conducting sufficient clinical trials to convince the FDA and go straight to market, like the thousands of other substances that we see on drugstore shelves.

I have burdened Gumshoe readers with so much speculation about the role of lithium in Alzheimer’s treatment, not because I am hugely optimistic that it will prove transformative, but because Alzheimer’s is a major threat to all of us members of the human tribe. If lithium supplements could significantly decrease that toxic effect of those toxic αβ-42 plaques, it could have a major benefit in the treatment of Alzheimer’s disease.

You are certainly aware of the scope of the Alzheimer’s threat, but here are some recent data. More than 7 million Americans age 65 and older have Alzheimer’s disease at present, and that number is expected to grow to 13.8 million by 2060.

Globally, over 55 million people were estimated to have Alzheimer’s disease in 2020. Looking forward, this scary number will about double every 20 years, reaching 78 million in 2030 and 139 million in 2050. Every three seconds, someone in the world develops Alzheimer’s disease.

Thus, regardless of the many obstacles and serious risks involving the use of lithium as a potential treatment for Alzheimer’s, the recent positive observations are a bright spot. I look forward to further advances on this front, and, of course, to future discoveries of ways to quell this global menace.

* * * * * * * * *

Doc Gumshoe’s previous missive was about nasty viruses and what they do to us. I didn’t get into how the healthcare world attempts to manage viruses. I’m planning to follow that up with a more general look at the management of infections from a broader perspective.

I look forward to your comments.

Best to all, Doc Gumshoe (aka Michael Jorrin)

[ed note: Michael Jorrin, who I dubbed “Doc Gumshoe” many years ago, is a longtime medical writer (not a doctor) and shares his commentary with Gumshoe readers once or twice a month. He does not generally write about the investment prospects of topics he covers, but has agreed to our trading restrictions.  Past Doc Gumshoe columns are available here.]