Botox injections may reduce depression, study finds

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People who received Botox (botulinum toxin) injections for certain conditions reported less depression less often compared to patients who did not receive the injections for similar diagnoses, according to a study published Thursday in the journal Scientific Reports.

“For years, clinicians have observed that Botox injected for cosmetic reasons seems to ease depression for their patients,” said Ruben Abagyan, Ph.D., professor of pharmacy and one of the lead researchers of the study, in a statement.

“It’s been thought that easing severe frown lines in the forehead region disrupts a feedback loop that reinforces negative emotions. But we’ve found here that the mechanism may be more complex because it doesn’t really matter where the Botox is injected," the author stated in a news release.

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The research team at Skaggs School of Pharmacy and Pharmaceutical Sciences at University of California San Diego combed through the U.S. Food and Drug Administration (FDA)’s Adverse Effect Reporting System (FAERS) database to see the side effects reported by nearly 40,000 people who received Botox injections for various reasons, according to a news release by the university.

The treatments were not just in the forehead but included several different sites, including the neck, limbs and forehead. The release stated the researchers used an algorithm to find significant statistical differences between patients who used Botox and those who did not for the same issue.

The treatments were not just in the forehead but included several different sites, including the neck, limbs, and forehead. (iStock)

The researchers found depression was reported 40 to 88 percent less often by Botox users for six of the eight conditions and injection sites, according to the release.

“This finding is exciting because it supports a new treatment to affect mood and fight depression, one of the common and dangerous mental illnesses — and it’s based on a very large body of statistical data, rather than limited-scale observations,” Tigran Makunts, PharmD, one of the researchers in the study, stated in the release.

More research is needed to determine how Botox potentially acts as an antidepressant, according to the study. The researchers have a few theories that need further investigation. For instance, Botox being absorbed systemically to the central nervous system, which is involved in mood or emotions, they hypothesized, or possibly Botox indirectly affecting a person’s depression because the Botox helped relieve an underlying chronic condition that may have been a contributing factor to the patient’s depression.

Health experts say Botox is commonly used not only for cosmetic reasons, such as combatting wrinkles but also for muscle spasms, tight muscles, migraines, temporomandibular joint dysfunction, as well as other conditions including excessive sweating and bladder conditions.

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The FAERS data used in this study was not exclusively gathered for the purpose of investigating the link between Botox and depression, according to the news release.  The data represents only a subgroup of Botox users who reported experiencing negative side effects. The authors note they excluded data from patients who were taking antidepressants; however, in some of the cases, the use of medications could have been underreported.

The release stated there is a clinical trial underway that is directly investigating Botox treatment for people with depression, but it is only testing forehead injection sites,. The authors said additional clinical trials are necessary to investigate which site is best to specifically inject to treat depression.

According to the World Health Organization, an estimated more than 264 million people worldwide experience depression.

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Vascular development may be at risk in autism

A Canadian collaboration led by Dr. Baptiste Lacoste has undertaken the first ever in-depth study of vasculature in the autistic brain. The product of four years of work, a paper published today in Nature Neuroscience lays out several lines of novel evidence that strongly implicate defects in endothelial cells—the lining of blood vessels—in autism.

Dr. Lacoste, a scientist at The Ottawa Hospital and an assistant professor in the University of Ottawa’s Faculty of Medicine and Brain and Mind Research institute, heads a lab that specializes in neurovascular interactions in health and disease. In collaboration with researchers at McGill University, Laval University, and the National Research Council of Canada, Dr. Lacoste’s team used a mouse model with one of the most common genetic mutations found in autism spectrum disorder—16p11.2 deletion, or “16p” for short.

The team, in which Dr. Lacoste’s graduate student Julie Ouellette and research associate Dr. Xavier Toussay played prominent roles, also used cells derived from the tissue of human autistic adults who carry the 16p mutation.

Nerves and blood vessels not in synch

“If you imagine you have a luxury car—a Ferrari—and it’s beautiful, sitting in your garage. But if you don’t put gas in the tank, the car won’t drive,” says Dr. Lacoste. “It’s exactly the same with the brain. It’s the most complex organ, but if you don’t have blood supply, the brain just doesn’t work properly.”

Normally, when brain cells light up, blood rushes to the active brain region, a phenomenon called ‘neurovascular coupling’. But when neurons of mice with the 16p deletion are stimulated, this study found that vascular responses in those brain regions were delayed and weaker.

This disconnect—or ‘neurovascular uncoupling’—was shown to originate in the blood vessels themselves: Arteries isolated from these mice and kept alive in a medium also showed a weak and sluggish response to chemicals that induce dilation of blood vessels. The team further isolated the source of the deficit in the endothelium, as opposed to the other cell types, such as muscle cells, that surround blood vessels.

Difficulties in development

Dr. Lacoste’s work further shows that problems with blood vessels begin very early in life for those who carry the 16p deletion. In a petri dish, both human-derived and mouse endothelial cells with the mutation were unable to sprout the extensions that normally connect blood vessels to each other, allowing the vascular network to expand and grow. Endothelial cells in the brains of newborn autistic mice had the same problem.

By adolescence, the mice still showed reduced vascular density in their brains. Interestingly, in contrast to the problems in the circulatory system, the researchers found that the neurons in the brains of these young mice appeared to be surprisingly well organized.

As the mice grew, other cells in the brain compensated for their dysfunctional endothelial cells, so that by adulthood they had developed a full network of blood vessels. However, as the researchers’ previous experiments showed, these blood vessels remained dysfunctional in adult mice.

“It’s a bit like if a plumber comes to your house and does a bad job installing the pipes,” says Dr. Lacoste. “You will have trouble getting the right water pressure in your sink from then on.”

Blood vessels and autistic behavior

When a person or mouse carries a 16p mutation, that genetic difference is replicated in every cell in their body. This makes it harder to pin down the cause of systemic developmental differences.

To address this difficulty, Dr. Lacoste’s team generated mice that only expressed the mutation in their endothelial cells—so-called “conditional mutants”. These mice showed similar deficits in their vascular development as whole-body mutants.

Remarkably, although every other cell in their brain and body was genetically normal, these conditional mutants displayed some behavioral signs of autism: hyperactivity, stereotypic movements, and motor learning impairment.

This indicated that the problems in the blood vessels contributed to neuronal dysfunction, which in turn led to the outward signs and symptoms of autism.

Further avenues of inquiry

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Types of flu people encounter in childhood may affect susceptibility to different flu strains later in life

A team of researchers from the University of Pennsylvania, the University of Pittsburgh, Centro Nacional de Diagnóstico y Referencia, Nicaragua, and the University of Michigan has found that the strains of influenza virus that infect people when they are young may influence their susceptibility to other influenza strains later in life. In their paper published in Proceedings of the National Academy of Sciences, the group describes their study of influenza strains in ferrets and human blood samples and what they found.

As the researchers note, most people are first infected with an influenza virus at age five, when they first go to school. Thereafter, most people are exposed to and are infected by several influenza viruses throughout their lifetimes. Prior research has shown that the antibody response by an individual person to a specific influenza virus can be boosted by infections by other strains. In this new effort, the researchers sought to find out if the strain of influenza that infects a person early in their life might affect their ability to fight off other strains later in life. To find out, they conducted tests with two well-known strains of influenza, lab ferrets and human blood.

The experiments involved infecting ferrets or blood samples with one strain of an influenza virus and then attempting to infect them again with another strain—and also attempting to infect blood samples from people who had already had one or the other types of infection earlier in their life.

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Stopping the clones may help win skin cancer battle

Targeting large clones of skin cells caused by ultraviolet irradiation (UV) may help reduce skin cancers, according to University of Queensland research.

Professor Kiarash Khosrotehrani said the study found proliferation of these large clones was concentrated around hair pores and not evenly distributed.

“Using genetic engineering of skin epidermal stem cells, we were able to track the growth, regression and cancerisation of individual clones that resulted from UV exposure.

“We found large clones regressed in size as soon as skin irradiation stopped, highlighting the importance of sun protection,” Professor Khosrotehrani said.

Keratinocyte cancers, or basal and squamous cell carcinomas, are one of the main cancers in Australia, affecting one in three people, and are strongly linked to sun exposure.

Dr. Edwige Roy said skin cancers were more likely to be found in large clones.

“While surgery is extremely effective in treating individual keratinocyte cancers, it doesn’t prevent a high proportion of patients from developing subsequent tumours in the same sun damaged area,” Dr. Roy said.

“In Queensland, about four per cent of people experience 10 or more skin cancers every three years.

“For these patients, skin cancer is a chronic disease with multiple surgeries and regular skin checks required during their lifetime.

“While it’s still unclear what processes drive the formation of skin cancer, our study helps clarify the influence of UV irradiation in its development by evaluating clone size dynamics in skin exposed to chronic ultraviolet irradiation,” she said.

“It also considers whether specific clones have more propensity to form skin cancer.

“Our findings have major implications for reducing skin cancer through sun protection and reducing the size of skin clones.

“Chemoprevention treatment could play a significant role in addition to sun protection by reducing the size of skin cancer clones, lowering keratinocyte cancers rates in Australia.”

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We may be able to eliminate coronavirus, but we’ll probably never eradicate it. Here’s the difference

Compared to many other countries around the world, Australia and New Zealand have done an exceptional job controlling COVID-19.

As of May 7, there were 794 active cases of COVID-19 in Australia. Only 62 were in hospital.

The situation in New Zealand is similar, with 136 active cases, only two of whom are in hospital.

If we continue on this path, could we eliminate COVID-19 from Australia and New Zealand?

Control –> elimination –> eradication

In order to answer this question, we first to need to understand what elimination means in the context of disease, and how it differs from control and eradication.

Disease control is when we see a reduction in disease incidence and prevalence (new cases and current cases) as a result of public health measures. The reduction does not mean to zero cases, but rather to an acceptable level.

Unfortunately, there’s no consensus on what is acceptable. It can differ from disease to disease and from jurisdiction to jurisdiction.

As an example, there were only 81 cases of measles reported in Australia in 2017. Measles is considered under control in Australia.

Conversely, measles is not regarded as controlled in New Zealand, where there was an outbreak in 2019. From January 1, 2019, to February 21, 2020, New Zealand recorded 2,194 measles cases.

For disease elimination, there must be zero new cases of the disease in a defined geographic area. There is no defined time period this needs to be sustained for—it usually depends on the incubation period of the disease (the time between being exposed to the virus and the onset of symptoms).

For example, the South Australian government is looking for 28 days of no new coronavirus cases (twice the incubation period of COVID-19) before they will consider it eliminated.

Even when a disease has been eliminated, we continue intervention measures such as border controls and surveillance testing to ensure it doesn’t come back.

For example, in Australia, we have successfully eliminated rubella (German measles). But we maintain an immunization schedule and disease surveillance program.

Finally, disease eradication is when there is zero incidence worldwide of a disease following deliberate efforts to get rid of it. In this scenario, we no longer need intervention measures.

Only two infectious diseases have been declared eradicated by the World Health Organisation – smallpox in 1980 and rinderpest (a disease in cattle caused by the paramyxovirus) in 2011.

Polio is close to eradication with only 539 cases reported worldwide in 2019.

Guinea worm disease is also close with a total of just 19 human cases from January to June 2019 across two African countries.

What stage are we at with COVID-19?

In Australia and New Zealand we currently have COVID-19 under control.

Importantly, in Australia, the effective reproduction number (Reff) is close to zero. Estimates of Reff come from mathematical modelling, which has not been published for New Zealand, but the Reff is likely to be close to zero in New Zealand too.

The Reff is the average number of people each infected person infects. So a Reff of 2 means on average, each person with COVID-19 infects two others.

If the Reff is greater than 1 the epidemic continues; if the Reff is equal to 1 it becomes endemic (that is, it grumbles along on a permanent basis); and if the Reff is lower than 1, the epidemic dies out.

So we could be on the way to elimination.

In both Australia and New Zealand we have found almost all of the imported cases, quarantined them, and undertaken contact tracing. Based on extensive community testing, there also appear to be very few community-acquired cases.

The next step in both countries will be sentinel surveillance, where random testing is carried out in selected groups. Hopefully in time these results will be able to show us COVID-19 has been eliminated.

It’s unlikely COVID-19 will ever be eradicated

To be eradicated, a disease needs to be both preventable and treatable. At the moment, we neither have anything to prevent COVID-19 (such as a vaccine) nor any proven treatments (such as antivirals).

Even if a vaccine does become available, SARS-CoV-2 (the virus that causes COVID-19) easily mutates. So we would be in a situation like we are with influenza, where we need annual vaccinations targeting the circulating strains.

The other factor making COVID-19 very difficult if not impossible to eradicate is the fact many infected people have few or no symptoms, and people could still be infectious even with no symptoms. This makes case detection very difficult.

At least with smallpox, it was easy to see whether someone was infected, as their body was covered in pustules (fluid-containing swellings).

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