Hong Kong’s No 2 official has sought to calm public panic over a possible outbreak of chikungunya fever, expressing confidence that infections can be contained with government workers stepping up mosquito control efforts.
Chief Secretary Eric Chan Kwok-ki made the appeal as Hong Kong reported five imported cases in a week, while Tuen Mun recorded high mosquito index levels that prompted authorities to speed up implementing pest control measures.
“The public does not need to panic as all the cases are from the mainland or imported from overseas. The most important thing is to take good care of yourself and be careful,” Chan told a radio programme on Saturday.
“We absolutely must prevent mosquitoes that might be carrying the virus from biting anyone. So, we have intensified mosquito eradication efforts at all our border crossings.”
His assurance came as the latest mosquito data released by the government suggested a boom in the pest’s numbers over the past month in So Kwun Wat in Tuen Mun.
The area recorded a Gravidtrap index reading of 16.4 per cent, the highest among the results made available for the 13 districts surveyed.
In this randomized controlled trial, we aimed to evaluate the effect of low-dose esketamine on POD in 108 older patients with fragile brain function undergoing thoracoscopic lung cancer surgery. Patients were randomly assigned to receive either esketamine (0.25 mg/kg during induction, 0.1 mg/kg/h for 30 min during maintenance) or normal saline. We found that the esketamine group had a significantly lower incidence of POD at 24 h post-surgery (3.8% vs. 15.1%, P = 0.046) but not at 72 h. Serum levels of interleukin-6 and S100β, markers of inflammation, were significantly lower in the esketamine group on the first postoperative day. Additionally, esketamine use was associated with reduced sufentanil consumption, shorter extubation time, recovery room stay, and total hospital stay, as well as higher post-extubation SpO2 and lower rescue analgesia rates, without increasing adverse events like dizziness or nausea. These findings highlight esketamine’s potential to mitigate early POD, inhibit inflammation, and accelerate postoperative recovery in this vulnerable patient population.
Patients with fragile brain function are often complicated by a history of stroke, imaging-confirmed cerebral infarction, cerebral vascular stenosis, alzheimer’s disease, parkinson’s disease, and other conditions. These patients have weaker neural plasticity and recovery capabilities, making them more susceptible to the effects of surgical anesthesia, which leads to a higher incidence of POD. Therefore, this study focuses particularly on this special older population.
Research has shown that sub-anesthetic doses of esketamine may effectively reduce the incidence of delayed neurocognitive recovery and may improve early postoperative cognitive function in older patients undergoing gastrointestinal surgery [10]. Other studies have found that continuous intraoperative infusion of esketamine may help prevent sleep disorders after gynecological laparoscopic surgery, potentially reducing the risk of POD and cognitive dysfunction [15]. This study references the aforementioned literature and, based on preliminary trials, adopted an intravenous bolus dose of 0.25 mg/kg for esketamine and a continuous infusion at 0.1 mg/kg/h for 30 min during surgery.
POD is one of the common and serious complications in older patients, especially for those with fragile brain function, where the incidence and harm are more significant. In this study, compared with the control group, the incidence of POD in the esketamine group was significantly decreased 24 h after surgery, while there was no significant difference in the incidence of POD 72 h after surgery between the two groups. This suggests that a small dose of esketamine may have advantages in preventing early POD, though further research is needed to confirm this effect in broader patient populations. Esketamine may act on multiple receptors such as NMDA, γ-aminobutyric acid (GABA), cholinergic, opioid, and dopamine receptors [16], suggesting potential mechanisms for its effects. Its protective effect on the central nervous system may be a key factor. On the one hand, esketamine may regulate the neurotransmitter system, such as inhibiting the excessive release of excitatory amino acids and stabilizing the membrane potential of nerve cells, thereby reducing the damage and inflammatory response of nerve cells. Research has shown that esketamine may reduce neuroinflammation by regulating the activity of microglia and inhibiting their overactivation, thereby reducing damage to neurons and the release of inflammatory mediators [17], which helps to maintain the stability of brain function to a certain extent and reduce the risk of POD. On the other hand, the analgesic effect of esketamine may indirectly reduce the stress response caused by postoperative pain, and stress response is often an important factor in inducing POD.
Inflammatory response plays an important role in the occurrence and development of POD. Surgical trauma induces a systemic inflammatory response, and inflammatory cytokines can cross the blood-brain barrier and activate microglia, triggering neuroinflammation, which may induce POCD and POD [7] This study found that there was no statistically significant difference in the serum concentration of IL-6 and S100β between the two groups before surgery, but on the first postoperative day, both IL-6 and S100β in the esketamine group were significantly lower than those in the control group.This suggests that esketamine may effectively inhibit the excessive activation of postoperative inflammatory response, though further research is needed to confirm this potential effect. Research has shown [18] that esketamine significantly reduces inflammation levels by regulating the expression of multiple cytokines. As an important inflammatory mediator, IL-6 is released in large quantities after surgical trauma, triggering a systemic inflammatory response, which in turn affects brain function and increases the incidence of delirium. S100β is a sensitive indicator reflecting brain damage and blood-brain barrier disruption. The decrease in its level indicates that esketamine may play a protective role in the microscopic structure of the brain, reducing brain damage caused by surgery and brain function disorders mediated by inflammation, which is consistent with the reduction in the incidence of POD, further revealing that the potential mechanism of esketamine in preventing POD may be closely related to inhibiting inflammatory response and reducing brain damage.
Research has found that esketamine can reduce the consumption of opioid medications during surgery [19]. The results of this study are consistent with previous reports. In this study, the use of sufentanil in the esketamine group and the rate of rescue analgesia in the recovery room were lower than those in the control group, and the esketamine group had a higher SpO2 after extubation compared with the control group. The discrepancy in sufentanil usage between the two groups in this study may be attributed to two key mechanisms. First, during skin incision at the commencement of surgery, supplemental sufentanil (5–10 µg) was administered based on individual stress responses. Esketamine may antagonizes the N-methyl-D-aspartate (NMDA) receptor, possibly inhibits the activation and maintenance of the pain center, and also has a certain µ-receptor antagonistic effect, producing a strong analgesic effect mitigated stress reactions during incision in the esketamine group, thereby potentially reducing the need for sufentanil. Second, esketamine may alleviate postoperative hyperalgesia caused by remifentanil [20, 21], potentially reducing the need for rescue analgesia with sufentanil in the recovery room. Collectively, these factors contributed to lower overall perioperative sufentanil consumption in the esketamine group. In addition, esketamine may directly stimulate the respiratory center, thereby potentially counteracting the respiratory depression induced by opioids [22]. Research has also found that multi-component interventions can effectively reduce the incidence of POD [23], and multimodal analgesia is an important part of this approach. In this study, the esketamine group adopted a multimodal analgesia regimen with esketamine combined with non-steroidal anti-inflammatory drugs and paravertebral nerve block, which reduced the rate of rescue analgesia, decreased the consumption of opioids, and did not increase the incidence of adverse reactions. In terms of postoperative recovery indicators, the postoperative extubation time, recovery room stay time, and total hospital stay in the esketamine group were also shorter than those in the control group. These results suggest that esketamine may be beneficial to the early postoperative respiratory function recovery and rapid rehabilitation of patients and could potentially shorten the hospital stay by reducing postoperative pain and complications, reducing the economic burden on patients and the occupation of medical resources. Its rapid rehabilitation advantage may stem from its regulation of the overall stress response of the body and its effective control of postoperative pain and inflammation, thus creating a more favorable physiological and psychological state for patients’ recovery.
However, this study also has certain limitations. Firstly, the sample size of this study is relatively limited. Although the results are statistically significant, larger-scale multicenter clinical trials are still needed to further verify its reliability and universality. Secondly, this study only observed the changes in short-term postoperative indicators, and the effects of esketamine on patients’ long-term cognitive function and quality of life are still unclear. Future studies need to further extend the follow-up time to comprehensively evaluate its long-term efficacy and safety. In addition, “fragile brain function” is a conceptual framework rather than a reference to a specific metric, we did not develop a new score, this is a research gap. Future investigation could attempt to construct a integrated scoring systems that combine cognitive, imaging, and biological data to better characterize brain vulnerability. Such scores could enhance risk stratification and guide personalized perioperative care.
You might not know every platinum-group metal by name, but they’re in use all around you. This group of metals — which includes platinum and five other related elements — is used in everything from catalytic converters to cellphones, jewelry, electrochemical manufacturing, cancer research, and more. PGMs are also particularly important for renewable energy, as these metals power technology such as hydrogen fuel cells and some lithium-ion batteries.
Despite the multifaceted utility of these metals, however, there are a number of environmental and health concerns related to their widespread use.
The power consumed during PGM mining is one of the key issues, as are the health impacts of accumulated platinum-group elements in living creatures. A study in the journal Reviews of Environmental Contamination and Toxicology found that PGE exposure has been linked to “asthma, miscarriage, nausea, hair loss, skin diseases, and, in humans, other serious health problems.” Additionally, the smelting of PGMs has been linked to persistent levels of toxic sulphur dioxide, which has been linked to other serious health risks.
Fortunately, researchers have found a way to recycle PGMs more effectively, reducing the need for mining while simultaneously preventing the accumulation of more PGEs in the environment.
The research, which was published in the journal Sustainable Resource Management, looked at a dual recycling process involving both pyrometallurgical and hydrometallurgical processes. The former uses high temperatures to extract and refine metal components, while the latter uses water-based solutions.
In this case, scientists used sodium carbonate to recover leached metals. In this process, it reacts with the collected metals to cause the formation of solid metal precipitates, allowing the researchers to filter them out of the solution. Their method was highly successful, achieving what the study described as “an exceptionally high rate of recovery (≥99%) from the selective collector-metal leachate.”
The study’s innovative method also reduced toxic environmental pollution and waste typically generated by PGM recycling processes.
“These quantifiable improvements in recovery efficiency and environmental performance underscore the potential of this process as a sustainable and economically competitive strategy for industrial-scale PGM recycling,” the researchers explained.
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Share on PinterestThe human body experiences rapid changes around age 50, according to a new study. Maskot/Getty Images
Past studies show that human aging doesn’t necessarily happen at the same pace throughout our life.
There is still much to discover about the aging process, especially when it comes to how it impacts the body’s organs.
A new study found that by focusing on aging-related protein changes in the body, there is an acceleration in aging of organs and tissues around the age of 50.
And of these proteins, scientists found that expressions of 48 of them linked to diseases increased with age, such as cardiovascular and liver disease.
While we can try to slow it down, human aging is something we currently can’t stop from happening. However, past studies show that aging doesn’t necessarily happen at the same pace throughout our life.
Instead, there are certain ages when a person’s body may experience a burst of aging. Previous studies show that the body may undergo rapid aging around the ages of 44 and 60.
And there is still much to discover about the aging process, especially when it comes to how it impacts the body’s organs.
“Aging, as a systemic, degenerative process that spans multiple organs and biological strata, remains one of the most profound unresolved questions in the life sciences,” Guang-Hui Liu, PhD, regenerative medicine researcher at the Chinese Academy of Sciences, explained to Medical News Today.
“Throughout the extended human lifespan, two fundamental issues persist: Do all organ systems adhere to a unified aging rhythm? Does a molecular spatiotemporal hub exist that orchestrates organism-wide senescence? Despite their centrality to understanding the essence of aging, these questions have long lacked systematic, empirical resolution.”
Liu is the corresponding author of a new study recently published in the journal Cell that has found that by focusing on aging-related protein changes in the body, they can get a clearer picture of how the body’s organs and tissues age over time, including an aging acceleration around the age of 50.
For this study, researchers analyzed 516 samples of 13 types of human tissues collected from 76 organ donors between the ages of 14 and 68 who had passed away from traumatic brain injury.
The tissue samples included cardiovascular, digestive, respiratory, endocrine, and musculoskeletal samples, as well as immune system, skin, and blood samples.
Next, researchers documented the types of proteins found in the organ and tissue samples, allowing them to create what Liu called “a proteomic aging atlas” that spans 50 years of human life.
“Covering seven physiological systems and thirteen pivotal tissues, the atlas presents a panoramic, dynamic portrait of organismal aging from a protein-centric perspective,” Liu explained. “The more than 20,000 proteins encoded by the genome serve as the structural bedrock of cells; their dynamic networks exquisitely orchestrate physiological homeostasis and act as the principal executors of virtually every biological process.”
“Consequently, systematically charting a panoramic, lifespan-wide atlas of proteomic dynamics and dissecting the reprogramming rules of protein networks at organ- and system-level scales are pivotal for accurately identifying the core drivers of aging and for establishing precise intervention targets,” he added.
At the study’s conclusion, researchers found that the biggest aging changes in the body’s organs and tissues seems to occur around age 50.
The critical aging window
“Ages 45–55 are identified as a landmark inflection point: most organ proteomes undergo a ‘molecular cascade storm,’ with differentially expressed proteins surging explosively, marking this interval as the critical biological transition window for systemic, multi-organ aging.” — Guang-Hui Liu, PhD
“Notably, the aortic proteome is reshaped most dramatically; its secretome and the circulating plasma proteome evolve in tight concordance, indicating that senescence-associated secreted factors (senokines) may serve as the hub mechanism broadcasting aging signals throughout the body,” Liu explained.
Additionally, Liu and his team found that expressions of 48 of the proteins linked to diseases, including cardiovascular disease, fatty liver disease, tissue fibrosis, and liver-related tumors, increased with age.
“Organ aging is the essence of human chronic disease; each geriatric illness is merely a specific manifestation of this underlying organ aging,” Liu added.
MNT had the opportunity to speak with Cheng-Han Chen, MD, a board certified interventional cardiologist and medical director of the Structural Heart Program at MemorialCare Saddleback Medical Center in Laguna Hills, CA, about this study.
“This study found that protein changes in the body associated with aging seem to accelerate roughly around age 50, depending on the type of body tissue. This is an interesting finding that helps us better understand the types of biochemical changes that underlie aging and potentially provide targets for therapy at different stages of someone’s life.” — Cheng-Han Chen, MD
“Science is only beginning to understand the biological mechanisms involved in aging,” Chen said. “Studies like this help us to identify the basis of normal aging, and in turn provides insight into how deviations in normal biology lead to diseases such as cardiovascular disease and fatty liver disease. Ultimately, this will help us understand how to keep our patients healthy and aging well. It may also help us to develop new therapies for diseases that result from accelerated aging.”
“Future research should attempt to expand on these findings in more diverse demographic groups and as well as in other important organs such as the brain and kidneys,” he added.
MNT also talked to Manisha Parulekar, MD, chief of the Division of Geriatrics at Hackensack University Medical Center in New Jersey, about this research.
How aging affects the whole body
“The idea that our cells lose the ability to maintain a healthy and functional proteome (the collection of proteins) is a cornerstone of modern aging theory. The accumulation of misfolded proteins, like amyloids, is the classic example, best known in neurodegenerative diseases like Alzheimer’s disease. This study’s finding of widespread amyloid accumulation across many tissues confirms that this isn’t just a brain-specific problem but a systemic feature of aging.” — Manisha Parulekar, MD
“This research is about transforming medicine from a reactive, disease-focused model to a proactive, health-focused one,” she continued. “By understanding the what and the when of aging, we can develop the tools to compress morbidity — allowing people to live not just longer, but healthier and more vibrant lives.”
“A longitudinal study, following the same individuals over decades will be helpful,” Parulekar added when asked what she would like to see as next steps for this research. “This would track their personal proteomic changes over time, allowing us to study genetic and lifestyle differences between people and providing additional confirmation for the ‘age 50 inflection point’.”
Several celebrities have publicly discussed their experiences with pre-diabetes. From Hollywood actor Viola Davis, who was diagnosed with pre-diabetes and has become an advocate for diabetes education and awareness, to veteran actor Tom Hanks. The Oscar-winning actor was diagnosed with type 2 diabetes, and had revealed that his blood sugar levels were elevated in his 30s, indicating pre-diabetes. Also read | Prediabetes can damage your health; know all the complications, prevention tips from experts
Study shows that the ability to chew properly helps improve blood sugar levels in Type 2 diabetes patients. (Pexels)
Pre-diabetes in younger individuals
These celebrities’ stories highlight the importance of awareness, education, and lifestyle changes in managing pre-diabetes. In an interview with HT Lifestyle, Dr Suchismitha Rajamanya, lead consultant and HOD, internal medicine, Aster Whitefield Hospital, Bengaluru, highlighted how pre-diabetes in younger Indians is an increasingly concerning issue.
She said, “Pre-diabetes, a state where blood sugar levels are higher than normal without yet being classified as type 2 diabetes, is an increasingly common diagnosis in younger people in their 20s and 30s in India. As we are seeing, pre-diabetes is on the rise due to sedentary lifestyles, irregular eating habits, stress levels and poor sleep patterns — all behaviours young people subscribe to in urban areas today.”
She added, “Prediabetes isn’t a diagnosis it’s a warning signal. If you make the right changes keep a healthy diet, exercise regularly, manage stress, and get the HbA1c test every year you may be able to completely reverse the risk factor. The trick is early detection. With increasing rates of type 2 diabetes in India, particularly in younger adults, pre-diabetes screening is not an option anymore; it is a necessity.”
What is pre-diabetes and why is it dangerous?
According to Dr Rajamanya, pre-diabetes is difficult to detect due to the absence of recognised symptoms. “You may feel perfectly well and full of energy, but your body’s management of blood levels may already be affecting your health. If no action is taken, a typical person will develop diabetes within 5-10 years and in some circumstances, less. The recent Indian Council of Medical Research (ICMR)-INDIAB study found that 15.3 percent of Indians have pre-diabetes many of which are unaware. Most concerning is that this is increasingly affecting the younger generation.”
Why you should care about the HbA1c test
Dr Rajamanya said an HbA1c (glycated hemoglobin) test is a very simple blood test. “It provides you with an alternative way of computing your average blood sugars from the last 2 to 3 months. Although a fasting sugar test would have only assessed your blood sugar at that moment, an HbA1c gives you a better snapshot of your blood sugars over a lengthier period of time. It is a great way to investigate your blood sugar levels before you enter the pre-diabetic stage when you might have the option to make lifestyle changes that could potentially reverse your diagnosis completely,” she explained.
Per the American Diabetes Association, Dr Rajamanya shared HbA1c results are used to determine:
⦿ Under 5.7 percent – normal
⦿ 5.7 percent to 6.4 percent – pre-diabetes
⦿ 6.5 percent and over – diabetes
“If you are a younger person having a family history of diabetes, or high BMI, or PCOS for women, or any metabolic disease history or problems, it is good practice to have an annual HbA1c test as a preventative measure,” she added.
Why are young Indians at risk?
According to Dr Rajamanya, these factors play a role:
1. Carbohydrate-heavy diet + long sitting breaks: Most of the Indian diet of refined carbohydrates and sugars can result in some younger adults who have long desk hours with hardly any movement.
2. Stress metabolic effects + sleep deprivation: Chronic stress and irregular sleep have metabolic effects, causing hormonal imbalance in the body, which can negatively impact insulin sensitivity.
3. Failure to have health appointments: Many individuals under the age of 35 are not routinely screened unless symptoms appear- and by that time the damage potentially has commenced.
Signs you should not ignore
While there are no definitive symptoms of pre-diabetes, as per Dr Rajamanya, common signs include the following, and it is advisable to visit your physician and get tested for these signs:
⦿ Unexplained fatigue
⦿ Excessively thirsty or urinating excessively
⦿ Unexplained changes in weight
⦿ Dark patches of skin on the neck or armpits- acanthosis nigricans
⦿ Recurrent infections or wounds that take longer to heal
Note to readers: This article is for informational purposes only and not a substitute for professional medical advice. Always seek the advice of your doctor with any questions about a medical condition.
On one of the most memorable days of my life, I walked into a doctor’s office with an incipient migraine and walked out half an hour later pain-free. It was the early ’90s, and I’d been suffering from the headaches—often accompanied by nausea and vomiting, occasionally somewhat eased by ibuprofen—since the age of 14. I can’t recall why on that day I decided to request an appointment, but I can still see the doctor fumbling with the wrapping of a cartridge encasing a hypodermic needle filled with a new drug. She got migraines, too, she’d told me, so when she placed the cartridge on my arm and pressed the button delivering the shot, we both exhibited the curious anticipation of experimenters, wondering if something miraculous was in the offing.
It was. Within five minutes, the nagging throb that had bloomed on my right temple a few hours earlier had vanished. That made us both giddy. Whether the new drug, sumatriptan (marketed as Imitrex), also worked for that doctor, I’ll never know. But I was lucky. Over the decades that followed, sumatriptan has reliably tamed the migraines that have intermittently plagued me, rescuing me from countless hours of misery. Whenever anyone complains about Big Pharma or fantasizes about having been born in an earlier era, my ironclad response is that I can’t imagine my life without sumatriptan—or, rather, I can, and the thought is chilling.
I’m lucky. As the journalist Tom Zeller Jr. recounts in his illuminating new book, The Headache, people with migraines or cluster headaches (Zeller’s own affliction) often find that recommended treatments either don’t work or decline in effectiveness over the course of months. Cluster headaches, like migraines, are called “primary headaches,” Zeller explains, “meaning the head pain and accompanying battery of other neurological effects constitute disorders unto themselves, rather than symptoms of some other underlying disease.” Even the fairly common migraine is poorly understood by those who don’t get them. I once worked with a colleague who was convinced I was being careless with my health because I didn’t regard my headaches as symptoms of some grave condition that could, and ought, to be cured.
By Tom Zeller Jr. Mariner Books.
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The Headache is an account of what we have learned about migraine and cluster headaches (less than you’d think) and the state of research developing treatments. The newest of those treatments are blockers that inhibit the uptake of calcitonin gene-related peptide, CGRP, a “key chemical messenger in the nervous system’s pain communication pathway,” according to Zeller. Researchers knew that CGRP could induce migraines in experimental subjects (all praise the sacrifices of those heroes!), and this new class of drugs binds to the chemical to prevent it from binding to neural receptors.
Cluster headaches are relatively rare, but migraines are not, and one study calculated the cost to the U.S. economy of migraines alone is as much as $1 trillion. Yet research into the causes and cures for primary headaches has been sluggish, for reasons that are highly contested. While the medical explanations in The Headache occasionally made my eyes glaze over, Zeller’s accounts of feuds among headache researchers and their combined wrath at what they insist is inadequate National Institutes of Health funding for their work offers a delectable blend of dish and substance. When one scientist likened migraine research to a massive Airbus plane requiring four fully fueled engines to get it off the ground, Zeller asked him what, exactly, was keeping the plane on the tarmac. “Too many female passengers,” was the reply.
Female migraineurs outnumber their male counterparts by 3 to 1, while the gender breakdown is reversed for cluster headaches. Many headache experts believe that this explains why migraine isn’t taken seriously by the medical establishment, whose tendency to dismiss pain in female patients has been well documented. Zeller observes that cluster headache sufferers, by contrast, tend to hide their condition, something he himself did during an early stint at the New York Times.The Headache includes the story of an air traffic controller who concealed his cluster headaches for three decades, knowing that the condition would trigger an automatic medical disqualification from a job he loved. He resorted to keeping his medications (which did not impair his performance) secret and ducking out of work during an episode to inhale oxygen from a tank he kept in his car.
Tom Zeller Kristine Paulsen
For Zeller’s part, he found it difficult to admit how debilitated he was by a disorder that many people conflate with the discomfort caused by a hangover. Cluster headaches, however, are often ranked among the worst pain a human can experience. While migraineurs tend to retreat to dark quiet rooms to wait out their affliction, people with cluster headaches are restless, often pacing, rocking, and pounding their heads. While cluster headaches don’t last all day like a migraine, they can recur every day or multiple times per day within the window of a period that can last weeks or months, followed by a period of remission. In The Headache, Zeller relates the story of a young man whose cluster headaches proved so relentless and tormenting that he took his own life, grimly confirming the disorder’s nickname: suicide headaches. Zeller himself recounts a period when, while working on a demanding story, he experienced a cluster attack and resorted to “medicating myself with absurd tides of chemical experimentation and excess,” ranging from caffeine, steroids, and magnesium to a CGRP blocker called verapamil—a drug on which he overdosed, passing out.
Though we have different kinds of headaches, there’s much that’s familiar to me in Zeller’s account. I, too, have found it difficult to convey just how disabling a mere headache can be. And I certainly recognized Zeller’s almost superstitious hoarding of medication doses, splitting them to stretch the supply, and the way Zeller would “jealously count those blue injections like a Scrooge, worrying over their limited number, wondering whether they’d last.” These drugs are the treasure we require to placate an angry god. Insurance companies can be stingy with the number of doses they allow per month, so it’s imperative to keep renewing the prescription regularly, even in the absence of headaches, so that you hit any future bad period with an ample supply. The fear of running out is petrifying—although, thankfully, well in the past for me now that sumatriptan has gone generic and can be bought online. The more recently developed CGRP blockers, however, can be brutally expensive. And most primary headache medications only work for half the people who try them, and then often only half the time.
Maddeningly, scientists still can’t say what causes primary headaches. Fierce debate rages among them over whether these are disorders of the vascular system—dilated blood vessels pressing against nerves—or of the central nervous system, arising from some dysfunction in the brain. The hypothalamus, which regulates the autonomic nervous system, seems implicated in cluster headaches, with their mysterious link to the body’s circadian rhythms. Migraines vary widely from person to person, but also in the same person during the course of a lifetime. My migraines once were synced to hormonal cycles. Now they only come at night, and especially when it rains or the humidity tops 75 percent. Or when my blood sugar gets too low. Or when I drink wine. I never experienced migraine aura—a disturbance in vision—until about 15 years ago. Now, my eyesight will occasionally be marred by a crescent of shimmering silver triangles (a classic migraine aura), but with no subsequent headache attached.
No wonder headache scientists are stumped, although several of the sources Zeller spoke with also complained that the stigma attached to primary headaches as an “unserious” medical condition has kept gifted researchers away from the field. Former NIH director Story Landis told Zeller that the agency—which has demonstrably underfunded headache research relative to the impact primary headaches have on society—simply didn’t get enough high-quality grant proposals in the area. Landis suggested, Zeller writes, “that headache researchers had been poorly conditioned by industry to focus on pills and shots, rather than foundational science,” such as identifying the cause or causes of the disorders. But if Big Pharma is the only source of funding for headache research, who can blame them?
When an advocate for headache sufferers asked Zeller what he’d learned in all his admirably extensive research for The Headache, the author found himself stammering and backtracking, qualifying his own suffering as not “the worst of what cluster headaches can inflict on a person,” adding that “there are bigger problems.” Then he pulled up. For millions of people of all races and genders—including Zeller himself!—primary headaches are a literal torment. Though I seldom endure that myself now, I remember all too well what a full-blown migraine was like. “It’s not just a headache” is the answer Zeller finally comes up with, and on that we should all agree.
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