Day: 01/16/2024

Measles, trends, and collective amnesia.

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Yesterday I got a Google News alert: “Measles.” Yes, measles. In the 21st century. At the height of winter. (Measles typically spreads in spring.) What’s going on?

This sure seems like a lot. Is measles increasing?

A measles case here or there is not abnormal. We see them every year. Cases typically come from international travelers, but sometimes locally acquired outbreaks emerge among unvaccinated pockets.

Cases today are still far, far, far below rates in the 1950s and ’60s thanks to vaccines. However, when we zoom into the past 10 years, we see a slow but steady rise. This shouldn’t be a surprise, given the reduction in routine vaccination coverage and the increase in vaccine exemptions.

As you may also notice above, measles has epidemic cycles. It flares up every four to five years—2008, 2011, and 2019. We can also see this pattern during the pre-vaccine era (see below).

It is exactly 5 years since the last flare-up, which suggests this may be a bad year. Of course, the pandemic could throw off patterns, but we aren’t off to a great start.

What is (and is not) a way forward?

Measles is preventable. And, in the PA outbreak, one unvaccinated child went to daycare while infected, defying isolation.

People are disappointed and shocked that fellow parents wouldn’t vaccinate their children. People are angry that their loved ones may get exposed as a result, especially since babies under 12 months old cannot be vaccinated.

I share a lot of the frustration. But I remember what Dr. Sandro Galea said during the pandemic, “We cannot finger-wag our way to a healthier world.”

Is there collective amnesia? Let’s fix it.As generations age, the memory of mid-20th-century diseases like measles fade. This is a blessing and a curse. Some don’t know why this disease is bad or if this vaccine is safe. This is understandable. The onus is on public health—we need to equip trusted messengers to start communicating, as measles is:

  • The most contagious disease, with an infected person infecting an average of 12-18 others (assuming no immunity in the population). In some cases, a single person has infected hundreds of people.
  • It’s not “just a fever or a rash.” While most people who get measles will recover, it can harm the body in every way possible. Measles can wipe out a huge fraction of immune memory to other diseases, causing an increase in all-cause deaths. 
  • The risks of infection far outweigh the risks of the vaccine, as shown beautifully by the New York Times below.
(Source: New York Times)

Is this a consequence of individualism? Let’s engage. One of the biggest challenges is the rise of individualism, as it goes against public health’s DNA: a collective response for the good of the population. We desperately need to engage with people who find individualism increasingly important. Develop interventions with them.

Is this due to a recent and dramatic decline in trust? Let’s do something about it. Mistakes were made during the pandemic. Misinformation is supercharged by social media. Bad actors, like the disinformation dozen, drive the majority of anti-vax content. Politics are further dividing individual health. Many people talk about these challenges (it’s even the theme of Davos this week!), but I’m getting increasingly frustrated with inaction.

Bottom line

Unfortunately, measles is off to a great start in 2024. We expect trends to increase.

We need to heed the underlying warning. A laissez-faire approach to public health, on both sides, will not work. Harrowing stories like Roald Dahl’s below will creep into the 21st century. We can do better.

What is the link between intermittent fasting and headaches?

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Some people undertaking intermittent fasting may experience headaches. This can be due to several factors, such as hypoglycemia, dehydration, and caffeine withdrawal.

Intermittent fasting is an eating method that a person may adopt for religious, dietary, or health reasons. It involves cycling between periods of eating and fasting.

Intermittent fasting may provide some health benefits, such as weight loss and decreased risk of certain diseases. However, fasting may not be suitable for all people, and some individuals may experience side effects, such as headaches.

Can intermittent fasting result in headaches?

Design by MNT; Photography by Blasius Erlinger/Getty Images & MirageC/Getty Images

People doing intermittent fasting may experience headaches. The results of a small 2023 study suggest that roughly 61%Trusted Source of individuals experience headaches while on an intermittent fast.

Secondary headaches refer to headaches that people can trace back to a specific cause. Common triggers of secondary headaches are changes to homeostasis. This term describes the internal system that helps regulate bodily functions.

As such, intermittent fasting can disturb homeostasis and result in headaches.

However, not everyone will experience headaches. Factors such as individual differences, fasting methods, and a person’s overall health may play a part in whether someone will have a headache during an intermittent fast.

Fasting headache symptoms

Older research suggests that fasting headaches either occur in the frontal region, meaning a person feels the pain at the front of their head, or are diffuse, meaning the pain spreads. Usually, a fasting headache may also be non-pulsating and of mild or moderate intensity.

In addition to a headache, a person undertaking intermittent fasting may also experience feelings of dizziness and weakness.

Causes

There are several potential reasons why a person may experience a headache while fasting intermittently. These may include:

  • Hypoglycemia: Some people may experience hypoglycemia, or low blood sugar levels, duringTrusted Source periods of fasting. When blood sugar levels fall too low, a person may experience symptoms such as a headache.
  • Caffeine withdrawal: Many people rely on caffeine to stay alert or focused. During fasting, a person may reduce or eliminate their caffeine consumption. This can cause withdrawal symptomsTrusted Source, such as headaches.
  • Dehydration: Dehydration occurs when a person does not consume enough fluids. Headaches are a commonTrusted Source symptom of dehydration. When a person is undergoing an intermittent fast, the lack of regular meals may mean a person is not consuming enough fluids.
  • Stress and anxiety: Fasting can causeTrusted Source a person’s cortisol levels to increase. Cortisol is a hormone that can rise in response to feelings of stress and anxiety. Other research suggests a relationship between stress and the occurrence of headaches.

Prevention tips

For people undertaking intermittent fasting, there are a few precautionary steps they can take to avoid having a headache. These may include:

  • Gradually transitioning: If a person is new to intermittent fasting, they may want to startTrusted Source with short periods and gradually increase their fasting duration. This may help the body adapt without triggering headaches.
  • Staying hydrated: It is important to be mindful of water consumption during the fasting period. A person can consume a variety of beverages, such as herbal teas and water with electrolyte supplements.
  • Monitoring blood sugar levels: Experts advise watching for symptoms of hypoglycemia. These can includeTrusted Source shakiness, dizziness, and sweating. Having a small snack or sugary beverage may help return glucose levels to a healthy range. However, it is best to consult a doctor about managing blood sugar levels.
  • Managing stress: Incorporating stress-reduction techniques, such as meditation, deep breathing exercises, and yoga, can help manage stress during fasting.
  • Moderating caffeine intake: If planning to eliminate caffeine during fasting, a person can try to gradually reduce their caffeine intake to minimize withdrawal symptoms, such as headaches.

If a person experiences severe or persistent headaches when fasting, it is best to consult a healthcare professional. They will be able to provide personalized guidance and ensure there are no underlying health issues causing the headaches.

Other possible side effects of intermittent fasting

As well as headaches, there are several other side effects that a person may experience while intermittent fasting. These may include:

  • Cravings: Research suggestsTrusted Source that short-term food deprivation, such as fasting, can increase food cravings.
  • Digestive changes: If a person’s body is not familiar with fasting, they may experience digestive discomfort, such as a stomachache or constipation. Additionally, individuals with preexisting digestive conditions may experience an exacerbationTrusted Source of symptoms.
  • Irritability and fatigue: Short-term fasting may causeTrusted Source a person to experience low mood, fatigue, and irritability.
  • Bad breath: During periods of fasting, a person may experience bad breath, which is also known as halitosis. Maintaining good oral hygiene and drinking plenty of water can help address this issue.
  • Sleep issues: Research is inconclusiveTrusted Source on whether intermittent fasting affects sleep. Anecdotal evidence suggests some people may experience disturbed sleep while fasting.
  • Malnutrition: Extended and unbalanced fasting can lead to malnutrition. It is important to ensure that during periods of eating, a person is consuming essential nutrients.

Additionally, it is important to consider that intermittent fasting may not suit all individuals. For example, experts advise not fasting if a person is ill or living with certain health conditions, such as diabetes.

Summary

Intermittent fasting is a dietary approach with various potential health benefits, but it can sometimes lead to headaches and other side effects.

To help prevent fasting headaches, it is essential to maintain proper hydration, manage blood sugar levels, and manage stress effectively. Gradually transitioning into fasting and consulting healthcare professionals as necessary can also make fasting more comfortable, particularly for individuals with preexisting health conditions.

While fasting headaches are common, many people may be able to fast intermittently with minimal side effects. However, a person should listen to their body and make adjustments as necessary to find the fasting routine that works best for them.

Everything you need to know about DHT

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The male sex hormone dihydrotestosterone (DHT) may play a key role in hair loss. Pattern hair loss, or androgenetic alopecia, is the most common type of hair loss among males.

Hair loss affects around half of all males over the age of 50 years, and around 50 million males in the United States (U.S.). Hair loss also impacts roughly 30 million females in the U.S. and is more likely to occur after menopause.

DHT is a hormone that plays a role in hair production. While DHT stimulates hair growth in the hair follicles, too much DHT is partly responsible for hair loss, in addition to other factors, such as genetics.

What is DHT?

domoyega/Getty Images

DHT is a sex hormone with androgenic properties. This means that it stimulatesTrusted Source characteristics that people typically associate with males. However, while people relate androgens with masculine features, females also produce androgen hormones such as DHT.

The body produces DHT through converting another hormone, known as testosterone. The amount of DHT in the body relates to the amount of testosterone present for the body to convert. As such, when testosterone levels increase, so does DHT levels. The gonads, which refers to either the testes or the ovaries, are typically responsible for producing testosterone.

The hypothalamus and pituitary gland carefully regulate the amount of testosterone in the body. The hypothalamus releases gonadotropin-releasing hormone (GnRH), which travels to the pituitary gland. This stimulates the gland to release luteinizing hormone into the bloodstream.

This hormone then travels to special cells in the testes and stimulates them to produce more testosterone. In people assigned female at birth, the ovaries and and adrenal glands also play a role in testosterone production.

Another hormone known as 5-alpha reductase then converts testosterone into DHT. DHT is much more potent than testosterone. Increasing levels of DHT production is thought to be responsible for the start of puberty in male teenagers. Namely, DHT causes the development of the genitals and growth of pubic and body hair. While less is known about DHT in females, it also likely plays a role in the development of body and pubic hair growth.

Hair growth and hair loss

DHT plays a role in the stimulation of body hair. However, it also plays a role in the thinning and eventual loss of hair.

Three phases of hair growth

Hair growth is split into three main phasesTrusted Source:

  • Anagen (growth): This is the active phase when the hair follicle produces a hair fiber. This phase can last for several years. The longer it lasts, the longer the hair grows.
  • Catagen (transition): This phase typically lasts a few weeks. The follicle starts to become inactive and the hair thins. It allows the hair follicle to renew itself.
  • Telogen (rest): This is the resting phase. The follicle lies dormant for a few months to roughly a year and hair growth does not occur.

Some people may also refer to the exogen phase. This is essentially a part of the telogen stage and is when hair is shed from the follicle. After completing the telogen phase, the anagen phase typically starts again.

Hair loss

Hair loss occurs due to the miniaturization of the hair follicle. This change causes hair to grow for shorter periods of time and become smaller, finer, and lighter. Eventually, the terminal, or thick hairs reduce to the vellus stage, which refers to fine, wispy hair that is often present all over the body.

Effects

The growth of scalp hair is not dependent on androgens, such as DHT. However, they play a role in the development of pattern hair loss, or androgenetic alopeciaTrusted Source. This can occur in males and females.

Higher levels of DHT in hair follicles can lead to a shorter cycle of hair growth. It can also result in the growth of shorter and thinner hair and extend how long hair stays in the resting phase.

The shorter cycle occurs due to the repeated activation of the androgen receptor on the hair follicle, which leads to miniaturization. Testosterone can bind and active the androgen receptor on hair follicles. However, DHT can bind and activate the receptor with five times greater affinity, which is why high DHT levels can lead to hair loss.

Read on to learn more about male pattern hair loss and female pattern hair loss.

Medication

If a person has excessively high levels of DHT resulting in hair loss, medications are available to manage DHT-related hair loss. Typically, these medications work by blocking DHT from binding to androgen receptors or inhibiting the body’s production of DHT.

Some examples include:

Finasteride

Finasteride is a 5-alpha-reductase inhibitor. Doctors may prescribe this medicine to treat male pattern hair loss or benign prostatic hyperplasia (BPH). Finasteride acts as a DHT blocker. It works by blocking 5-alpha-reductase, decreasing the amount of circulating DHT, which can help prevent hair loss.

Minoxidil

Topical minoxidil is a treatment for hair loss. It is typically available as a solution or foam that a person can massage directly into areas of hair loss on their scalp. It is suitable for both male and female use.

It is a vasodilator, meaning it helps to widen blood vessels to allow blood to pass through more easily. This additional blood flow may help to shorten the resting phase of hair follicles and stimulate hair growth.

Evidence on the use of vitamins and minerals for preventing hair loss is inconclusive. If a person should tell their healthcare provider if they are taking supplements, as they can interfere with medication. While there is currently not enough supportive evidence, some people may anecdotally recommend the following supplements:

  • biotin
  • pygeum bark
  • pumpkin seed oil
  • caffeine
  • vitamin B12 and B6

Other causes of hair loss

In addition to DHT, evidence also highlights the role of genetics in hair loss. Pattern hair loss may be hereditary for both male and female pattern hair loss.

Experts consider the genetic component of pattern hair loss to be polygenic. This means that is involves many genes. Evidence suggests that the genes relating to pattern hair loss may include:

  • the androgen receptor gene
  • the estrogen recepetor-beta gene
  • the aromatase gene

Frequently asked questions

Some FAQs on DHT may include:

What does DHT do to you?

DHT is a sex hormone that most adults produce. It contributes to the development of sexual structures and characteristics in people assigned male at birth. However, people assigned female at birth may also produce the hormone. It plays a role in body, facial, and pubic hair growth.

Is blocking DHT good or bad?

If people have excessive levels of DHT, they may experience pattern hair loss. As such, these people may consider DHT blockers. Generally, DHT blockers are safe, but some medications and products may cause side effects. For example, some evidence suggests that finasteride may cause male factor infertility.

What causes high DHT?

High levels of DHT often results from excessive testosterone production. Different health conditions can cause DHT levels to rise. These can include prostate problems, issues with the adrenal glands, polycystic ovary syndrome (PCOS), and certain medications, such as anabolic steroids.

How do you reduce DHT levels?

Methods to reduce DHT levels typically include the use of DHT blockers. While more research is necessary, some anecdotal evidence suggests that dietary changes, such as including onions and pumpkin seeds, and lifestyle changes, such as regular exercise, quitting smoking, and reducing stress, may help reduce DHT levels.

Summary

Dihydrotestosterone (DHT) is a sex hormone that most adults produce. One of the functions of DHT includes stimulating the growth of body and pubic hair. However, it also plays a role in hair loss on the scalp.

DHT is very potent in stimulating hair follicles. When DHT levels are too high, they can overstimulate hair follicles. This can result in the miniaturization of the hair follicle, causing hair to become smaller, finer, and lighter. Eventually, this can result in hair loss known as pattern hair loss.

As such, some treatments for hair loss may aim to block or inhibit the effect of DHT on hair follicles to preserve hair growth.

Newborns Exposed to Endocrine Disruption

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Even newborns can’t escape plastic contaminants

Measurement of Bisphenol A Diglycidyl Ether (BADGE), BADGE derivatives, and Bisphenol F Diglycidyl Ether (BFDGE) in Japanese infants with NICU hospitalization history; BMC Pediatrics, Jan. 8, 2024.

Bisphenol A diglycidyl ether (BADGE) and Bisphenol F diglycidyl ether (BFDGE) are plastics used to construct intravenous sets, syringes, catheters and other single-use equipment used in hospitals.

To quantify neonatal exposure to BADGE and BFDGE investigators enrolled 10 infants admitted to the neonatal intensive care unit (NICU) and analyzed their blood at 1-2 months and 7 months after their discharge. The researchers also surveyed the infants’ parents about their diet and home environment.

One form of BADGE, BADGE-2H2O was found at various concentrations in all infants at both time points. However, blood values were lower at 7 months. Researchers could not detect BADGE-H2O, BADGE and BFDGE at either time point.

One of two children who received mechanical ventilation showed “substantially increased” levels of the plastic BADGE-2H2O. There was no significant difference between children who ate commercial baby food at least once per week and those who did not.

Studies have shown that BADGE and BFDGE disrupt the endocrine system and are toxic to both genes and cells. Endocrine disruption was of particular concern to researchers for its potential to affect newborn growth and development.

More microbiome science, please

Boosting microbiome science worldwide could save millions of children’s lives; Nature, Jan. 8, 2024.

Promoting microbiome science beyond its current European and North American leanings could save millions of children’s lives per year, according to a study in Nature.

The human microbiome is the collection of bacteria, viruses, yeast, fungi and other microorganisms that inhabit our bodies.

Although Europe and the U.S. make up just 15% of the world’s population they are the subjects of 70% of published human microbiomes and about 85% of the high-quality microbiomes of children under age 4.

Just one component of the human microbiome, the gut microbiome, has been implicated in both beneficial and harmful events — for example, heart disease and inflammation.

Scientists are working on drugs that target the microbiome, but because microbiomes vary regionally the drugs must be designed for specific populations. If world health authorities pursue this tack, 17 million children’s lives could be saved each year.

Low vitamin A levels linked to increased risk of respiratory infections

Recurrent respiratory tract infections in children might be associated with vitamin A status: a case-control study; Frontiers in Pediatrics, Jan. 5, 2024.

A Chinese study found that the less vitamin A in a child’s bloodstream the greater their risk for having recurrent respiratory tract infections (RRTIs).

Investigators recruited 2,592 children ages 6 months to 14 years from China’s Heilongjiang province. Parents completed a diet questionnaire on behalf of 1,039 children experiencing RRTIs and 1,553 who did not.

Blood concentrations of vitamin A in the RRTI group were significantly lower than for healthy control subjects. Children with moderately low vitamin levels had a 32% higher chance of being in the RRTI group, and those who were seriously deficient were 50% more likely.

Among children with respiratory tract infections on the day they entered the study, those with moderately low vitamin A were 48% more likely to have started in the RRTI group, and those with severely low levels were 5.5 times more likely.

Children with low intake of vitamin A-rich foods (carrots, spinach, broccoli and meat, especially organ meats) also had a lower incidence of RRTIs.

Autism associated with inflammation

Evaluation of serum interleukin-17 A and interleukin-22 levels in pediatric patients with autism spectrum disorder: a pilot study; BMC Pediatrics, Jan. 5, 2024.

Egyptian investigators found a connection between elevated levels of interleukin-17 A (IL-17A) and interleukin-22 (IL-22), cytokines involved in systemic inflammation, in children with autism spectrum disorder (ASD).

The group enrolled 24 children with ASD (median age 5.25) and 24 non-autistic controls (age 6).

Combined elevated cytokine levels strongly associated with an ASD diagnosis and IL-22 levels predicted ASD severity. But when the cytokines were analyzed together no link emerged between IL-17A plus IL-22 levels and ASD symptom severity.

Children with pre-existing inflammatory or allergic diseases were excluded from the study as they likely already had high cytokine levels.

The authors were attempting to establish the cytokine-ASD link to lay the groundwork for the discovery of future ASD treatments targeting inflammatory processes.

However, they note that factors like breastfeeding and gut microbiome composition, which were not controlled in their study, could also contribute to the development of ASD.

Why some kids are more vulnerable to mercury exposure

Factors associated with blood mercury concentrations and their interactions with three glutathione S-transferase genes (GSTT1, GSTM1, and GSTP1): an exposure assessment study of typically developing Jamaican children; BMC Pediatrics, Jan. 4, 2024.

Mercury exposure through consumption of canned fish and plant foods high in mercury leads to higher-than-normal blood mercury levels — but this effect is most pronounced in children carrying one specific gene.

U.S. and Jamaican researchers enrolled 375 typically developing 2- to 8-year-olds to explore the association between the consumption of canned fish (a staple of Jamaican diets), starches, grains and beans — sources of mercury exposure — and blood-mercury concentrations.

The only significant difference among subjects was which version of the GST (glutathione S-transferase) gene they carried.

GST is an enzyme that helps the body eliminate mercury, lead and other dangerous heavy metals. Some variants of this gene are more effective than others.

The researchers found that the consumption of canned sardines and mackerel significantly raised blood mercury concentrations, but only among children with two specific GST variants. Humans express eight different families of GST and dozens of subvariants.

By identifying subgroups of children most likely to experience the ill effects of mercury exposure, the study points toward future mercury exposure studies that concentrate on this particularly vulnerable population.

Thousands of U.S. Cities Could Become Virtual Ghost Towns by 2100

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These projected findings about depopulation in U.S. cities are shaped by a multitude of factors, including the decline of industry, lower birth rates and the impacts of climate change

an city empty street in downtown Jackson, Mississippi
Jackson, Mississippi, United States.

The Urban U.S. could look very different in the year 2100, in part because thousands of cities might be rendered virtual ghost towns. According to findings published in Nature Cities, the populations of some 15,000 cities around the country could dwindle to mere fractions of what they are now. The losses are projected to affect cities everywhere in the U.S. except Hawaii and Washington, D.C.

“The way we’re planning now is all based on growth, but close to half the cities in the U.S. are depopulating,” says senior author Sybil Derrible, an urban engineer at the University of Illinois Chicago. “The takeaway is that we need to shift away from growth-based planning, which is going to require an enormous cultural shift in the planning and engineering of cities.”

Derrible and his colleagues were originally commissioned by the Illinois Department of Transportation to conduct an analysis of how Illinois’s cities are projected to change over time and what the transportation challenges will be for places that are depopulating. As they got deeper into the research, though, they realized that such predictions would be useful to know for cities across the entire U.S.—and not just for major ones, such as New York City, Chicago and Los Angeles. “Most studies have focused on big cities, but that doesn’t give us an estimation of the scale of the problem,” says lead study author Uttara Sutradhar, a doctoral candidate in civil engineering at the University of Illinois Chicago.

The authors analyzed data collected from 2000 to 2020 by the U.S. Census and the American Community Survey, an annual demographics survey conducted by the U.S. Census Bureau. This allowed them to identify current population trends in more than 24,000 cities and to model projections of future trends for nearly 32,000.  They applied the projected trends to a commonly used set of five possible future climate scenarios called the Shared Socioeconomic Pathways. These scenarios model how demographics, society and economics could change by 2100, depending on how much global warming the world experiences.

The authors’ resulting projections indicated that around half of cities in the U.S., including Cleveland, Ohio, Buffalo, N.Y., and Pittsburgh, Pa., are likely to experience depopulation of 12 to 23 percent by 2100. Some of those cities, including Louisville, Ky., New Haven, Conn., and Syracuse, N.Y., are not currently showing declines but are likely to in the future, according to the findings. “You might see a lot of growth in Texas right now, but if you had looked at Michigan 100 years ago, you probably would have thought that Detroit would be the largest city in the U.S. now,” Derrible says.

Regionally, the Northeast and Midwest will most likely be the most heavily affected by depopulation, the authors found. And on a state level, Vermont and West Virginia will be the hardest hit, with more than 80 percent of cities in each of these two states shrinking. Illinois, Mississippi, Kansas, New Hampshire and Michigan could also see about three quarters of their cities decline in population.

While the authors’ analysis of current trends found that 43 percent of the more than 24,000 cities are losing residents, around 40 percent are now growing, including major cities such as New York City, Chicago, Phoenix and Houston. In general, though, the places that are projected to most likely gain population by 2100 tend to be located in the South or West.

The new analysis does not explore the factors that are driving the projected trends. But Sutradhar says there is probably a complex mix of variables at play that differ by location, including the rising cost of homes in some places, the decline of industry, lower birth rates, different levels of state taxes and the impacts of climate change.

Justin Hollander, an urban planning scholar at Tufts University, who was not involved in the research, says that the new study’s methods were sound and that the findings are original. “I have never seen a national study that looked so far into the future,” he says. He warns, however, that making specific projections this far in advance is “pretty reckless,” given the amount of uncertainty the future holds.

He appreciates, though, that the paper calls attention to future depopulation in general, which he agrees the data do support. “These are not isolated problems to the Detroits of the world,” he says. “Depopulation is everywhere, and the paper is right to demand that cities face this fact and begin to honestly prepare for this possible future.”

The authors hope that their paper serves as a wake-up call to policy makers to begin moving away from growth-based planning and to start finding place-specific solutions for cities that are likely to depopulate in the years ahead. “We should see this not as a problem but as an opportunity to rethink the way we do things,” Derrible says. “It’s an opportunity to be more creative.”

Single-Dose Psilocybin Treatment for Major Depressive Disorder

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Abstract

Importance  Psilocybin shows promise as a treatment for major depressive disorder (MDD).

Objective  To evaluate the magnitude, timing, and durability of antidepressant effects and safety of a single dose of psilocybin in patients with MDD.

Design, Setting, and Participants  In this phase 2 trial conducted between December 2019 and June 2022 at 11 research sites in the US, participants were randomized in a 1:1 ratio to receive a single dose of psilocybin vs niacin placebo administered with psychological support. Participants were adults aged 21 to 65 years with a Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition diagnosis of MDD of at least 60 days’ duration and moderate or greater symptom severity. Exclusion criteria included history of psychosis or mania, active substance use disorder, and active suicidal ideation with intent. Participants taking psychotropic agents who otherwise met inclusion/exclusion criteria were eligible following medication taper. Primary and secondary outcomes and adverse events (AEs) were assessed at baseline (conducted within 7 days before dosing) and at 2, 8, 15, 29, and 43 days after dosing.

Interventions  Interventions were a 25-mg dose of synthetic psilocybin or a 100-mg dose of niacin in identical-appearing capsules, each administered with psychological support.

Main Outcomes and Measures  The primary outcome was change in central rater–assessed Montgomery-Asberg Depression Rating Scale (MADRS) score (range, 0-60; higher scores indicate more severe depression) from baseline to day 43. The key secondary outcome measure was change in MADRS score from baseline to day 8. Other secondary outcomes were change in Sheehan Disability Scale score from baseline to day 43 and MADRS-defined sustained response and remission. Participants, study site personnel, study sponsor, outcome assessors (raters), and statisticians were blinded to treatment assignment.

Results  A total of 104 participants (mean [SD] age, 41.1 [11.3] years; 52 [50%] women) were randomized (51 to the psilocybin group and 53 to the niacin group). Psilocybin treatment was associated with significantly reduced MADRS scores compared with niacin from baseline to day 43 (mean difference,−12.3 [95% CI, −17.5 to −7.2]; P <.001) and from baseline to day 8 (mean difference, −12.0 [95% CI, −16.6 to −7.4]; P < .001). Psilocybin treatment was also associated with significantly reduced Sheehan Disability Scale scores compared with niacin (mean difference, −2.31 [95% CI, 3.50-1.11]; P < .001) from baseline to day 43. More participants receiving psilocybin had sustained response (but not remission) than those receiving niacin. There were no serious treatment-emergent AEs; however, psilocybin treatment was associated with a higher rate of overall AEs and a higher rate of severe AEs.

Conclusions and Relevance  Psilocybin treatment was associated with a clinically significant sustained reduction in depressive symptoms and functional disability, without serious adverse events. These findings add to increasing evidence that psilocybin—when administered with psychological support—may hold promise as a novel intervention for MDD.

Discussion

In this phase 2 study, treatment with a 25-mg dose of psilocybin administered with psychological support was associated with a statistically and clinically significant reduction in depressive symptoms compared with a niacin placebo, assessed as change in total MADRS score and as rates of sustained response. The 15.9% difference in sustained remission rates between the groups was not significantly different. Improvements in depression were apparent within 8 days of psilocybin dosing, consistent with a rapid onset of action, and were maintained across the 6-week follow-up period, without attenuation of the effect, and with higher point prevalence rates of MADRS-defined response and remission than has been observed in recent psilocybin studies of TRD.10,14 Although an MCID was not specified a priori for this study, the 12.3-point difference in change in score between the psilocybin and niacin groups is larger than the upper limit active placebo difference in the literature of 9 points and the 19.1-point reduction in MADRS score from baseline to day 43 in the psilocybin group is larger than the 12-point difference shown to reflect substantial clinical improvement in patients with TRD.25 In contrast to prior psilocybin trials for depression,8,14,15 there was not a significant reduction in depressive symptoms or a psilocybin/placebo difference in depressive symptom status at the day 2 assessment (ie, 1 day after dosing) (Figure 2 and Table 2). This may reflect the fact that to maintain central rater blinding, the 7-day recall period used for all other MADRS assessments was maintained at day 2, with the result that the majority of recall period for the day 2 assessment covered the predosing period during which depressive symptoms remained elevated, based on results from the Symptoms of Major Depressive Disorder Scale (eTable 7 in Supplement 3).

Psilocybin also improved psychosocial functioning compared with niacin as shown by mean difference in SDS score change. Similar results were observed in the per-protocol population and in sensitivity analyses. Psilocybin treatment was associated with improvement in various exploratory end points, including reduced overall disease severity, anxiety and self-reported depressive symptoms, and improved quality of life (eTables 4-7 in Supplement 3). Psilocybin treatment did not evince the type of emotional blunting reported with standard antidepressant medicines (eTable 8 in Supplement 3).31

Psilocybin was generally well-tolerated, with most AEs being of mild or moderate severity and generally limited to the acute dosing period. The 8% rate of severe adverse events in participants receiving psilocybin was similar to the 10% rate reported in the study by Goodwin et al in participants with TRD treated with a single 25-mg dose of psilocybin.14 However, in contradistinction to the study by Goodwin et al, no clinically confirmed active suicidal ideation or suicidal behavior occurred in either randomized group. No serious TEAEs were reported in the current study; however, psilocybin treatment was associated with a higher rate of overall AEs and a higher rate of severe AEs compared with niacin, with these severe AEs being known effects of psilocybin.17 Moreover, psychedelics may produce AEs not captured by standard rating scales or may induce unrecognized new psychiatric conditions even as they improve target syndromes.3

Conclusions

In this randomized trial, a single 25-mg dose of psilocybin administered with psychosocial support was associated with clinically and statistically significant reductions in depressive symptoms and improvement in measures of functional disability compared with a 100-mg dose of niacin placebo administered under an identical protocol. No serious TEAEs occurred during the study, but psilocybin treatment was associated with an increase rate of overall, solicited, and severe TEAEs, most of which occurred during or immediately after the dosing period. These findings add to evidence that psilocybin—when administered with psychological support—may hold promise as a novel intervention for MDD.

Astronomers Puzzled by Galaxy With No Stars

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It could be a never before seen part of the cosmos.

The Big Empty

Astronomers have accidentally found an entire galaxy that appears to have plenty of gas — but no visible stars to speak of.

Their findings, which were presented this week at the annual meeting of the American Astronomy Society, may seem paradoxical on their face, but the discovery could provide a rare, possibly never-before-seen insight that challenges our understanding of how stars and galaxies are formed.

The eerily empty object, called J0613+52, is located 270 million light years away, according to a Big Think writeup on the discovery, and at the very least appears to be a low-surface brightness galaxy (LSB).

As the name suggests, an LSB is significantly less bright than other glimmering objects that populate the night sky because the gasses it contains are so spread out that few stars are formed.

Still, this classification holds that such a galaxy would at least have some stars, and J0613+52, with seemingly none at all, could be something even more rare and elusive: a dark, primordial galaxy.

“This could be our first discovery of a nearby galaxy made up of primordial gas,” Karen O’Neil, a senior scientist of the Green Bank Observatory, said in a statement about the research.

Gassy Galaxy

O’Neil and her team stumbled on the object thanks to a fortuitous error made while studying LSBs. Basically, they realized there was a discrepancy in the data between two telescopes they were using, which led to them double-checking where they were looking at.

“The [Green Bank Telescope] was accidentally pointed to the wrong coordinates and found this object,” O’Neil said.

Not only did they find that the galaxy was lacking stars despite being rich in gas — they believe it contains between one and two billion solar masses of hydrogen — it was also extremely isolated.

“It’s too far from other galaxies for them to help trigger star formation through any encounters,” O’Neil said. “J0613+52 appears to be both undisturbed and underdeveloped.”

That last part — “undisturbed and underdeveloped” — is key. It would suggest that over the billions of years of its existence, the “dark” galaxy has remained stable to an unparalleled degree, with no significant gravitational interactions occurring that would lead to gas clumping together to form stars, and no nearby galaxies to intrude on its near-perfect equilibrium.

In other words, it’s an uncannily preserved relic of the early years of the cosmos, so perfect that it almost defies understanding.

Future observations will have to bear out these findings. As Big Think notes, astronomers will likely follow up by searching for heavy metals that indicate the presence of stars. If none are found, it’ll be strong evidence in favor of J0613+52 indeed being the fabled dark galaxy that has for so long eluded detection.

The WHO Is About to Declare Aspartame a Possible Carcinogen

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That’s a huge decision.

Getty

Aspartame, one of the most widely used artificial sweeteners in the world, will be declared as a possible carcinogen by the cancer research arm of the World Health Organization (WHO), Reuters reports.

The upcoming July ruling from the WHO group, the International Agency on Cancer Research (IARC), will list aspartame as “possibly carcinogenic to humans.” According to the report, the assessment considers all published evidence, but does not account for the amount a person can safely consume.

It’s ample cause for alarm. The sugar substitute has long been a staple of low or zero calorie drinks like Diet Coke, and is also used in thousands of other products including ice cream, chewing gum, and cereal.

But it’s worth noting that the classification of “possibly carcinogenic” only denotes that there is some evidence that a substance can cause cancer, and that the findings are overall considered inconclusive. There are still two categories above this: “probably carcinogenic,” indicating strong evidence, and simply “carcinogenic,” meaning there is consensus on a proven link.

Those are important distinctions. But no matter the technicalities involved, putting a “possibly” next to cancer is always ominous.

As such, the IARC has repeatedly faced criticism for causing alarm from its rulings. Over the years, it’s faced backlash for categorizing eating red meat or working night shifts as “probably carcinogenic,” as well as using cell phones as “possibly carcinogenic.”

Given the stakes involved, the food industry has already began to speak against the IARC’s impending ruling.

“IARC is not a food safety body and their review of aspartame is not scientifically comprehensive and is based heavily on widely discredited research,” said Frances Hunt-Wood, the secretary general of the International Sweeteners Association, as quoted by Reuters.

Though aspartame has been deemed safe by regulators worldwide for decades, including the US Federal Drug Administration (FDA) and the European Food Safety Authority (EFSA), the substitute has never shaken off its stigma.

For its part, the FDA has repeatedly reviewed aspartame’s safety since it was first approved in the 1970s. In 2021, the agency deemed that “no valid conclusion” could be derived from a major Ramazzini Institute study that supposedly found a link between aspartame and cancer in rodents.

That study, along with a large observational study in France involving 100,000 people that also linked aspartame to cancer, have both been criticized for their methodologies. By and large they’re both outliers among an extensive body of research, but in the IARC’s view, it’s enough to warrant concern.

All in all, it’s a bold decision from the WHO group — but according to Reuters, the intent is to encourage more research into aspartame, not to stoke panic.

Scientists Just Discovered Something Horrifying About Artificial Sweeteners

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There’s still a lot we don’t understand about artificial sweeteners.

Futurism

According to a new study, some of the most commonly used artificial sweeteners could potentially cause serious health issues by making the bacteria in our gut invade our intestinal walls.

The study underlines that there’s still a lot we don’t understand about the sweeteners being added to many diet products — and demonstrates that further research is needed.

“There is a lot of concern about the consumption of artificial sweeteners, with some studies showing that sweeteners can affect the layer of bacteria which support the gut, known as the gut microbiota,” said Havovi Chichger, senior lecturer in Biomedical Science at Anglia Ruskin University in the UK, lead author of a paper about the research published in the International Journal of Molecular Sciences, in a press blurb.

The sweeteners — including the ultra-popular saccharin, sucralose, and aspartame — were shown for the first time to cause two types of gut bacteria, E. coli and E. faecalis, to go pathogenic.

These pathogenic bacteria were then able to attach themselves to, take over, and subsequently kill Caco-2 cells, which are the cells that line the walls of the intestines.

All it took was the concentration equivalent of two cans of a diet soft drink. In fact, all three artificial sweeteners increased the adhesion of both kinds of bacteria to the cells of the intestinal walls.

All three sweeteners also increased the formation of biofilms, which made them less sensitive to antimicrobial resistance treatment.

Pathogenic gut bacteria attacking the intestinal walls could be really bad news. Previous research has shown that E. faecalis bacteria that cross the intestinal wall can cause a number of infections, including septicaemia, more commonly known as blood poisoning.

“These changes could lead to our own gut bacteria invading and causing damage to our intestine, which can be linked to infection, sepsis and multiple-organ failure,” Chichger said.

In other words, soft drinks with actual sugars in them may be the healthier option after all.

The WHO Is About to Declare Aspartame a Possible Carcinogen

Posted by

0


That’s a huge decision.

Getty

Aspartame, one of the most widely used artificial sweeteners in the world, will be declared as a possible carcinogen by the cancer research arm of the World Health Organization (WHO), Reuters reports.

The upcoming July ruling from the WHO group, the International Agency on Cancer Research (IARC), will list aspartame as “possibly carcinogenic to humans.” According to the report, the assessment considers all published evidence, but does not account for the amount a person can safely consume.

It’s ample cause for alarm. The sugar substitute has long been a staple of low or zero calorie drinks like Diet Coke, and is also used in thousands of other products including ice cream, chewing gum, and cereal.

But it’s worth noting that the classification of “possibly carcinogenic” only denotes that there is some evidence that a substance can cause cancer, and that the findings are overall considered inconclusive. There are still two categories above this: “probably carcinogenic,” indicating strong evidence, and simply “carcinogenic,” meaning there is consensus on a proven link.

Those are important distinctions. But no matter the technicalities involved, putting a “possibly” next to cancer is always ominous.

As such, the IARC has repeatedly faced criticism for causing alarm from its rulings. Over the years, it’s faced backlash for categorizing eating red meat or working night shifts as “probably carcinogenic,” as well as using cell phones as “possibly carcinogenic.”

Given the stakes involved, the food industry has already began to speak against the IARC’s impending ruling.

“IARC is not a food safety body and their review of aspartame is not scientifically comprehensive and is based heavily on widely discredited research,” said Frances Hunt-Wood, the secretary general of the International Sweeteners Association, as quoted by Reuters.

Though aspartame has been deemed safe by regulators worldwide for decades, including the US Federal Drug Administration (FDA) and the European Food Safety Authority (EFSA), the substitute has never shaken off its stigma.

For its part, the FDA has repeatedly reviewed aspartame’s safety since it was first approved in the 1970s. In 2021, the agency deemed that “no valid conclusion” could be derived from a major Ramazzini Institute study that supposedly found a link between aspartame and cancer in rodents.

That study, along with a large observational study in France involving 100,000 people that also linked aspartame to cancer, have both been criticized for their methodologies. By and large they’re both outliers among an extensive body of research, but in the IARC’s view, it’s enough to warrant concern.

All in all, it’s a bold decision from the WHO group — but according to Reuters, the intent is to encourage more research into aspartame, not to stoke panic.