Engage 1: Creating an Experientially Rich Life

Posted on 01/08/2024 by Boris Clair

The new Engage course is underway. This will be a 42-lesson course on creating an experientially rich life. I’ll be publishing the whole course for free on my blog and on my YouTube channel – my gift to you. Here’s the first lesson.

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New lessons will be added when they’re ready (approximately weekly) till we get to 42 lessons total. Watch the whole video for more details.

Join the Engage Email List

Join the Engage notification list to get an email whenever a new Engage lesson is published. I also encourage you to subscribe to my YouTube channel to follow the course there.

Bucket List Challenges

This is a special add-on experience to the Engage course where we’ll work together to advance and then complete some of our personal bucket list items – those someday/maybe ideas that you somehow never get around to actually doing.

I’ll be hosting a series of Zoom calls for each Bucket List Challenge. Each call is 90 minutes and starts at 11:11 AM Pacific Time (11:11 AM – 12:41 PM) on the dates below. Be sure to join the Engage email list if you want to be invited to the Bucket List calls too.

Bucket List Series 1 Calls

Call 1 – Tue Sep 10, 2024
Call 2 – Thu Sep 12, 2024
Call 3 – Tue Sep 17, 2024
Call 4 – Tue Sep 24, 2024

Bucket List Series 2 Calls

Call 1 – Tue Nov 19, 2024
Call 2 – Thu Nov 21, 2024
Call 3 – Tue Nov 26, 2024
Call 4 – Tue Dec 3, 2024

Bucket List Series 3 Calls

Call 1 – Tue Feb 18, 2025
Call 2 – Thu Feb 20, 2025
Call 3 – Tue Feb 25, 2025
Call 4 – Tue Mar 4, 2025

Share in the YouTube Comments

What would you love to experience?

Enjoy the new course!

Two new dementia risks identified by major report

Posted on 31/07/2024 by Boris Clair

Treating failing eyesight and high cholesterol can help lower the risk of the illness, a study suggests.

Netflix Admits Baby Reindeer’s ‘Real Martha’ Wasn’t Actually Convicted Of Stalking Richard Gadd

Posted on 31/07/2024 by Boris Clair

Netflix has admitted that the real woman Baby Reindeer’s Martha is based on was not technically convicted of stalking Richard Gadd in real life.

The runaway streaming hit was billed as a “true story” upon its release in April of this year, and creator and star Richard has spoken candidly in interviews about how the show is based on a real stalking ordeal he endured.

While the real-life stalker was never identified, last month the streamer was hit with a $170 million (around £133,000) lawsuit by the woman who claims she inspired the character.

Netflix has now acknowledged that the real “Martha” – who has since been identified as Fiona Harvey – only received a court order over her interactions with Richard – not a conviction – according to a report in Deadline.

Earlier this year, a lawmaker questioned a statement Netflix made during a hearing, after which the streamer admitted in a letter to parliament’s Culture, Media and Sport Committee that the real “Martha” was never convicted.

Benjamin King, Netflix’s senior UK director of public policy, appeared before the committee in May to detail how Baby Reindeer is the “true story of the horrific abuse” Richard suffered “at the hands of a convicted stalker”.

Committee member John Nicolson subsequently wrote to Netflix requesting evidence to support this claim.

Jessica Gunning, left, and Richard Gadd in conversation about the Netflix television series "Baby Reindeer" at The 92nd Street Y on Wednesday, June 5, 2024, in New York. (Photo by Evan Agostini/Invision/AP) — Jessica Gunning, left, and Richard Gadd in conversation about the Netflix television series “Baby Reindeer” at The 92nd Street Y on Wednesday, June 5, 2024, in New York. (Photo by Evan Agostini/Invision/AP)

In response, Benjamin wrote in the letter: “I wanted to clarify our understanding that the person on whom the show is based — who we have at no point sought to identify — was subject to a court order rather than a conviction.”

He added: “The writer of Baby Reindeer endured serious harassment over many months (as it now seems has been the case for many others), which had a significant impact on his wellbeing.”

In the Emmy-nominated series, Martha is depicted as pleading guilty to stalking and is sentenced to prison time.

Last month, Harvey accused the company of “defamation, intentional infliction of emotional distress, negligence, gross negligence” and “violations of [her] right to privacy”, and is now seeking $170 million in damages.

In a court filing on Monday, Richard reaffirmed his stance that the series is “emotionally true” to his own life, and not intended to be a “a beat-for-beat recounting”.

While the cast urged viewers not to speculate on the real identities of those depicted in the show, questions were ultimately raised about whether enough was done by Netflix to protect their identities.

In response to the lawsuit, Netflix vowed to “defend this matter vigorously”, insisting they also stood by “Richard Gadd’s right to tell his story”.

Ed Balls Slams Labour’s Housing Delays And Says Party Has Been ‘Twiddling Thumbs’ In Opposition

Posted on 31/07/2024 by Boris Clair

‘You’ve had 14 years to get ready. Surely you need to go a bit quicker than that?’@edballs questions Housing Minister Matthew Pennycook on why it could take up to a year to identify where to build more homes. pic.twitter.com/R2HI7M6iHL

— Good Morning Britain (@GMB) July 31, 2024

Ed Balls accused the Labour Party of “twiddling their thumbs” for the last 14 years in a spat over delays to housing reforms.

The ITV Good Morning Britain host was interviewing the minister Matthew Pennycook over the government’s plans to ease the housing crisis this morning.

This includes a new task force “to present a final shortlist of recommendations on appropriate locations” to build new homes to ministers, according to the gov.uk website.

So Balls asked Pennycook: “Given the urgency, is that new towns task force going to report in September or October?”

The housing minister said they had asked to report within a year, to which Balls said with incredulity: “A year? I thought it was urgent? Are you serious?

“Are you actually saying a year from now?”

Pennycook said: “Up to a year, but we’ve made very clear to Sir Michael [Lyons] that if the task force can identify appropriate locations quicker than that, we will get moving on them immediately, shovels in the ground.”

Regeneration expert Sir Michael will be leading the new task force.

Balls pushed: “Why are they taking a year?”

“Because, they are doing in a sense, Ed, a high-level spatial strategy,” Pennycook began, but Balls interrupted.

He said: “You’ve had 14 years to get ready. Surely you need to go a bit quicker than that?”

Pennycook said he had only three years shadowing the housing minister role before the general election.

Balls hit back: “You’ve been in in opposition for 14 years, twiddling your thumbs as a party, ready for this moment – you come in, you say you want new towns and we’re not going to have a report for a year!”

“We want to give the expert task force the time to report back,” the minister said.

It was not an easy morning for Pennycook on the broadcast round, as he was then called out on Radio 4′s Today programme, too – but this time, for setting “unrealistic” targets.

Presenter Amol Rajan said it seemed deputy PM Angela Rayner wanted to see housing completion in new towns within five years.

He said: “Given a normal scheme of 2000+ homes takes around seven years to get to completion, Angela Rayner’s target of five years is totally unrealistic, isn’t it?”

“I don’t think it’s unrealistic to have spades on the ground on several of these large scale housing communities by the end of the five-year parliament.

“That would be our objective,” Pennycook hit back.

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\"Given a normal scheme of 2000+ homes takes around seven years to get to completion, Angela Rayner’s target of five years is totally unrealistic isn’t it?\"@amolrajan asks Housing Minister Matthew Pennycook, as the government announces a new housing taskforce.#R4Today

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“Given a normal scheme of 2000+ homes takes around seven years to get to completion, Angela Rayner’s target of five years is totally unrealistic isn’t it?”@amolrajan asks Housing Minister Matthew Pennycook, as the government announces a new housing taskforce.#R4Today

— BBC Radio 4 Today (@BBCr4today) July 31, 2024

‘Say It To My Face’: Kamala Harris Goes After Trump For Dodging Debate Plans

Posted on 31/07/2024 by Boris Clair

Vice President Kamala Harris said on Tuesday that she hopes former President Donald Trump will meet her on the debate stage later this year despite his apparent efforts to skip out on those plans now that she’s the Democrats’ presumptive nominee to face him in November.

Harris rallied a crowd of 10,000 supporters in Atlanta on Tuesday, her first visit to Georgia after President Joe Biden dropped out of the race and cleared the way for her campaign.

“This is a people-powered campaign, in fact … the momentum in this race is shifting, and there are signs that Donald Trump is feeling it,” the vice president said. “You may have noticed.”

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Vice President Harris: Donald, I do hope you’ll reconsider to meet me on the debate stage. As the saying goes, if you got something to say, say it to my face pic.twitter.com/5zykEnU3Dn

— Kamala HQ (@KamalaHQ) July 30, 2024

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Vice President Harris: Donald, I do hope you’ll reconsider to meet me on the debate stage. As the saying goes, if you got something to say, say it to my face pic.twitter.com/5zykEnU3Dn

— Kamala HQ (@KamalaHQ) July 30, 2024

Trump has now repeatedly expressed doubt about participating in the next debate, scheduled for September 10 on ABC News.

And while he said on Monday he would “probably” debate Harris at some point, he added that “everybody knows who I am,” suggesting a debate appearance may not benefit him.

In Atlanta, Harris hit the former president for backing out of those plans, repeating her ding that Trump and his running mate, Senator JD Vance of Ohio, were “just plain weird” and had a “lot to say about me.”

“Here’s the funny thing about that,” Harris said. “So he won’t debate, but he and his running mate sure seem to have a lot to say about me.”

“Well, Donald, I do hope you’ll reconsider to meet me on the debate stage,” she said, “because as the saying goes, if you’ve got something to say, say it to my face.”

Vice President Kamala Harris speaks during a campaign rally Tuesday in Atlanta.

Harris has catapulted into the campaign over the past 10 days, raising more than $200 million (£155m) and signing up more than 170,000 volunteers. And recent polls have shown her closing the gap in most swing states.

New high-resolution 3D maps show how the brain’s blood vessels changes with age

Posted on 30/07/2024 by Boris Clair

Healthy blood vessels matter for more than just heart health. Vascular well-being is critical for brain health and potentially in addressing age-related cognitive decline and neurodegenerative disorders, like Alzheimer’s disease, according to new study led by Penn State researchers. The findings point to an understudied but possible key role the brain’s vascular network — or energy infrastructure — plays in the onset of neurodegenerative disease.

They published their work today (July 30) in Nature Communications.

Using advanced imaging techniques, the team developed maps of a mouse brain that illustrate how vascular cells and structures like blood vessels change with age and identified areas that are vulnerable to deterioration. When blood vessels degrade, nerve cells in the brain, called neurons, are starved of energy, causing them to malfunction or die. It can lead to a condition called vascular dementia, the second leading cause of cognitive impairment in older adults, and symptoms like sleep disturbance.

“With something like Alzheimer’s disease, by the time you can see vascular changes and significant brain shrinkage on a MRI, cell death has already occurred. We need to understand how these cells and structures change before a major catastrophe happens,” said Yongsoo Kim, associate professor of neural and behavioral sciences at Penn State College of Medicine and senior author of the study. “This study provides early signs of neurodegenerative disorders, potentially leading to earlier diagnosis, and clues for how we can slow down the aging process and cognitive changes.”

According to Kim, aging is one of the primary factors involved in neurodegenerative disorders.

“Yet, we really don’t have a good baseline understanding of how normal aging itself changes the brain, particularly the brain’s vasculature,” Kim said. And with the aging population in the United States growing, he said it’s critical to understand these changes, especially within the network of blood vessels.

Blood vessels, especially micro-vessels, regulate oxygen and energy supply and waste removal to and from neurons. Despite their importance, Kim said, most existing research focuses on how neuron structure and function degenerates over time, rather than the vasculature. When researchers do study the brain’s vasculature, they’ve primarily examined larger blood vessels or focused on a single, easy-to-access region of the brain, the somatosensory cortex. More importantly, typical neuroimaging techniques, like MRI, don’t provide high enough resolution to see what’s happening in the tiny blood vessels, which make up 80% to 85% of the brain’s vasculature, according to Kim.

Kim and the research team produced a detailed map of the vascular network of the whole mouse brain using two high-resolution 3D mapping techniques: serial two-photon tomography — a technique that creates a series of stacked 2D images — and light sheet fluorescence microscopy, which images intact 3D samples to visualize the whole brain at a single cell-resolution. They imaged the brains of young and old mice to chart vasculature changes across the brain with normal aging.

“Because we’re doing high-resolution mapping with the sufficient resolution, we can reconstruct the whole vascular structure and scan the entire brain to pinpoint areas that undergo selective degeneration with age,” Kim said. “What we found is that the area that most people study showed the least amount of change, whereas profound change happens in areas in the deep areas of the brain. This suggests that we’ve been looking at the wrong area when it comes to aging studies.”

The images showed that changes in the vascular network don’t occur equally across the brain. Rather, they were concentrated in the basal forebrain, deep cortical layers and hippocampal network, suggesting these areas are more vulnerable to vascular degeneration. These regions play a role in attention, sleep, memory processing and storage, among other functions.

As brains age, vascular length and branching density decreases approximately 10%, indicating that there’s a sparser network to distribute blood. Arteries in older brains also appear more twisted compared to those in younger brains, which can impede blood flow, especially to areas further away from the main arteries like the deep cortical layers, Kim explained.

The team also examined functional changes of vasculature and found that the system responds more slowly in older brains. That means that it can’t provide the neurons with energy as quickly and readily as the cells may need. There’s also a loss of pericytes, a type of cell that regulates blood supply and blood vessel permeability, too. As a result, the blood vessels become “leaky,” compromising the blood-brain barrier.

This study builds on the group’s previous research, where they mapped the vasculature of a young mouse brain. Next, they are studying how Alzheimer’s disease-induced changes in the brain influences vascular health and neuronal function. Ultimately, they said they hope their work will lead to treatments for neurodegenerative disorders.

Hannah Bennett, dual medical degree and doctoral degree student, and Steffy Manjila, postdoctoral scholar, co-led the study along with Quingguang Zhang, who was assistant research professor at Penn State at the time of the research and is currently assistant professor at Michigan State University, and Yuan-ting Wu, who was previously research scientist at Penn State and currently project scientist at Cedars-Sinai Medical Center. Other Penn State authors on the paper include: Patrick Drew, professor of engineering science and mechanics, of neurosurgery, of biology and of biomedical engineering and interim director of the Huck Institutes of the Life Sciences; Uree Chon, research technician; Donghui Shin, research technologist; Daniel Vanselow, research project manager; Hyun-Jae Pi, data scientist.

TheNational Institutes of Health and the American Heart Association funded this work.

Genes or environment? A new model for understanding disease risk factors

Posted on 30/07/2024 by Boris Clair

Every disease is shaped by a genetic component as well as environmental factors like air pollution, climate and socioeconomic status. However, the extent to which genetics or environment plays a role in disease risk — and how much can be attributed to each — isn’t well understood. As such, the actions individuals can take to reduce their risk for disease aren’t often clear.

A team led by Penn State College of Medicine researchers found a way to tease apart genetic and environmental effects of disease risk using a large, nationally representative sample. They found that, in some cases, previous assessments overstated the contribution of one’s genes to disease risk and that lifestyle and environmental factors play a larger role than previously believed. Unlike genetics, environmental factors, like exposure to air pollution, can be more easily modified. That means there are potentially more opportunities to mitigate disease risk. The researchers published their work in Nature Communications.

“We’re trying to disentangle how much genetics and how much the environment influences the development of disease. If we more accurately understand how each contributes, we can better predict disease risk and design more effective interventions, particularly in the era of precision medicine,” said Bibo Jiang, assistant professor of public health sciences at the Penn State College of Medicine and senior author of the study.

The researchers said that in the past, it’s been difficult to quantify and measure environmental risk factors since they can encompass everything from diet and exercise to climate. However, if environmental factors aren’t considered in models of disease risk, analyses may falsely attribute the shared disease risks among family members to genetics.

“People living in the same neighborhood share the same level of air pollution, socioeconomic status, access to health care providers and food environment,” said Dajiang Liu, distinguished professor, vice chair for research, director of artificial intelligence and biomedical informatics at the Penn State College of Medicine and co-senior author of the study. “If we can tease apart these shared environments, what’s remaining could more accurately reflect genetic heritability of disease.”

In this study, the team developed a spatial mixed linear effect (SMILE) model that incorporates both genetics and geolocation data. Geolocation — a person’s approximate geographical location — served as a surrogate measure for community-level environmental risk factors.

Using data from IBM MarketScan, a health insurance claims database with electronic health records from more than 50 million individuals from employer-based health insurance policies in the United States, the research team filtered out information for more than 257,000 nuclear families and compiled disease outcomes for 1,083 diseases. They then augmented the data to include publicly available environmental data, including climate and sociodemographic data, as well as levels of particulate matter 2.5 (PM2.5) and nitrogen dioxide (NO2).

The team’s analysis led to more refined estimates of the contributors to disease risk. For example, previous studies concluded that genetics contributed 37.7% of the risk of developing Type 2 diabetes. When the research team reassessed the data, their model, with its consideration of environmental effects, found that the estimated genetic contribution to Type 2 diabetes risk decreased to 28.4%; a bigger share of disease risk can be attributed to environmental factors. Similarly, estimated contribution to obesity risk attributed to genetics decreased from 53.1% to 46.3% when adjusted for environmental factors.

“Previous studies concluded that genetics played a much larger role in disease risk prediction, and our study recalibrated those numbers,” Liu said. “That means that people can stay hopeful even though they have family relatives with Type 2 diabetes, for example, because there’s a lot they can do to reduce their own risk.”

The research team also used the data to quantitatively assess whether two specific pollutants in the air — PM2.5 and NO2 — causally influence disease risks. Previous studies, the researchers said, lump PM2.5 and NO2 together as one collective measure of air pollution. However, what they found in this study was that the two pollutants have different and distinct causal relationships with health conditions. For instance, NO2 is shown to directly cause conditions like high cholesterol, irritable bowel syndrome and both Type 1 and Type 2 diabetes, but not PM2.5. PM2.5, on the other hand, may have a more direct causal effect on lung function and sleep disorders.

Ultimately, the researchers said this model will allow for a more in depth look at questions about why some diseases may be more prevalent in certain geographic locations.

Other Penn State authors on the paper include: Havell Markus and Austin Montgomery, both dual medical degree and doctoral degree students at the Penn State College of Medicine; Laura Carrel, professor of biochemistry and molecular biology; Arthur Berg, professor of public health sciences; and Qunhua Li, professor of statistics. Daniel McGuire, who was a doctoral student in the biostatistics program at the time of the research, co-led the study. Co-author Lina Yang and Jingyu Xu, who were doctoral students in the biostatistics program at the time of the research, also contributed to the paper.

The National Institutes of Health and the Penn State College of Medicine’s artificial intelligence and biomedical informatics pilot funding program supported this work in part. Some of the materials employed in this work were provided by the Center for Applied Studies in Health Economics at the Penn State College of Medicine.

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