Workplace Bullying Interventions

At left, possible workplace bullying?

Public Domain, https://commons.wikimedia.org/w/index.php?curid=393839

A paper on workplace bullying is found here, two sections from the abstract are reproduced below:

BACKGROUND: Bullying has been identified as one of the leading workplace stressors, with adverse consequences for the individual employee, groups of employees, and whole organisations. Employees who have been bullied have lower levels of job satisfaction, higher levels of anxiety and depression, and are more likely to leave their place of work. Organisations face increased risk of skill depletion and absenteeism, leading to loss of profit, potential legal fees, and tribunal cases. It is unclear to what extent these risks can be addressed through interventions to prevent bullying.

AUTHORS' CONCLUSIONS: There is very low quality evidence that organisational and individual interventions may prevent bullying behaviours in the workplace. We need large well-designed controlled trials of bullying prevention interventions operating on the levels of society/policy, organisation/employer, job/task and individual/job interface. Future studies should employ validated and reliable outcome measures of bullying and a minimum of 6 months follow-up.

So, there is only “low quality evidence” that the interventions actually do any good to prevent workplace bullying. One possibility is that the organizational interventions are pushed by administrators who want to “cover themselves from potential liability (“see – we did something!”) or to burnish their resumes with their “impressive intervention sessions.” Or, we may have “experts” without actual data to back up their assertions, as well as (possibly well-meaning) individuals who do not know how to best approach the problem. As the authors state: “Future studies should employ validated and reliable outcome measures of bullying and a minimum of 6 months follow-up.”

Banana Bread Pudding

I have not baked bread pudding until now. Recently, got inspired by Kirsten Wick and her video.

So, I decided to make my own recipe. First, went through one of the cookbooks I had and then, the substitutions of ingredients started. No sugar, but bananas. No milk, but some unsweetened apple sauce and peaches in light syrup. I did not substitute the butter, however.

I also made a double batch, so that I could freeze a few delicious breakfasts.

Here is the recipe:

Banana bread pudding

Ingredients:
5 frozen ripe bananas
10 slices Oatnut bread (or any other bread you prefer), sliced in cubes
1 stick butter (melted in the microwave for the oiling of the pan and for the pudding mixture)
8 oz unsweetened apple sauce (I use two 4-oz cups)
14.5-oz sliced peaches in water (the peaches were cut into small pieces)
1 cup raisins
3 Tbsp vanilla extract
1 Tbsp cinnamon powder
7 eggs

Directions:
Preheat the oven to 400 F and butter a pan (mine is 10' x 13'). Combine the peaches with their syrup, the apple sauce, the raisins, vanilla, cinnamon and the bread cubes. In a separate bowl, beat the eggs and mix with the mashed bananas and melted butter. Add to the bread cubes and mix well. Bake for 30-35 minutes or until set and slightly golden on top. Cut when the pudding cools down.

Cruciferous Vegetables, Sulforaphane, And The Nervous System

At left, Brussel sprouts, By Eric Hunt - Own work, CC BY 2.5, https://commons.wikimedia.org/w/index.php?curid=1318818

Can agents found in the diet help with neural stem cell proliferation and differentiation, therefore possibly being of benefit for nervous system diseases and disorders?

It seems that sulforaphane, found in cruciferous vegetables, can enhance neural stem cell proliferation (growth) and differentiation (maturation into mature neural cells) as described in this paper here.

I myself always like to eat Brussel sprouts, and these findings increase my desire for that food.

Exercise For Hip Osteoarthritis

Can a specific exercise program enhance hip muscle strength and therefore be of benefit to patients suffering from hip osteoarthritis?  Here is a paper that says yes, abstract:

PURPOSE: To evaluate the effect of an exercise therapy concept (the Tübingen exercise therapy approach THüKo) for increasing hip muscle strength (HMS) in patients with hip osteoarthritis (OA), and to investigate whether patients do adhere to the intervention and if there are any adverse events related to the intervention.
METHODS: A total of 210 hip OA patients (89 females, 121 males) were randomized into a 12-week exercise intervention (THüKo) including group sessions (1/week) and home exercising (2/week), a placebo ultrasound group (1/week) or a control group (no treatment). HMS was measured as isometric peak torque of hip abduction, adduction, flexion, and extension. Adherence to exercise and safety aspects were monitored as additional outcomes.
RESULTS: Baseline adjusted post intervention HMS of the THüKo group were higher compared to the control group (differences of 0.11-0.27 Nm/kg, p < 0.01) and to the placebo ultrasound group (differences of 0.09-0.19 Nm/kg, p < 0.01). Adherence to exercise was high (about 90%). No subject had to refuse from training because of an exercise related adverse event and exercise related pain was only of intermittent nature without sustainable adverse effects.
CONCLUSIONS: The Tübingen exercise therapy approach has shown to have a significant positive effect on HMS. Its implementation has shown to be feasible and safe according to the percentage of exercise participation and the absence of sustainable adverse events.

More details about the exercise program can be found in this paper here.  If you have hip osteoarthritis, this may be something you can discuss with your physician.

The evil in your medicine

About a week ago, I listened to the podcast of Peter Attia, MD, with Kathrine Eban, the author of the book Bottle of Lies. It was one of the longest podcasts Attia has produced, and yet, I could not stop listening. It was a captivating and anxiety-inducing narrative about generics, the cheaper version of the brand-name medications.

As the minutes turned into hours, the discussion revealed the depths of a global crime with the main motivation being the GREED. 

After the podcast, I obtained the book and read it in three days. Several times through the book, I started crying (yes, I am a cry-baby). Several times, I had to stop reading because the words felt like punches to my chest and left me breathless. I was facing one of the most detailed and harrowing accounts of EVIL.

And here is some of the story.

First was the GREED of global pharma. The drugs were developed based upon huge intellectual and research effort, and yes, based upon lots of funds. But the profits exceeded the expenses beyond any imagination. The drug prices that pharmaceutical companies extracted from the patients and the US health system supported the companies’ manicured headquarters and campuses, the lavish caviar-and-champagne office parties, the helicopters and the multi-million-dollar salaries and bonuses of the executives.

The second layer of GREED story was revealed when the pharmaceutical companies in China and India were allowed to deliver the cheaper versions of the brand-name medicines – the generics. The lower price, however, compromised the quality of the medications. As noted in Kathrine Eban’s book, each drug is a poison, and its therapeutic range is rather narrow. Anything outside this range could damage or kill. If to the not-so-precise dosing of the generics, one adds impurities, carcinogens, fast degradation/decomposition or deregulated bioavailability of the active ingredients, then the result is a generic drug that acts as a placebo (the best case scenario), or functions as a lethal weapon. 

The death of the pharmaceutical manufacturing in the USA, the rise of pharma in India and China, the resulting genocide in the form of substandard or murderous generics, and the inability (unwillingness?) of the federal government to address this genocide are all documented in Bottle of Lies.

If you, your family and friends rely on any medication, you should listen to the podcast of Attia and read the book Bottle of Lies.

What can you do when prescribed and dispensed a generic medication that might make you sicker, kill you or is just ineffective?

I hate to say that there is no hope or solution to this tragedy. But for most people who are not aware of what is happening, there is no solution. Many patients would end up poisoned or even killed by the medications. 

And yet, you may try to fight the established system by insisting that your doctor and pharmacy give you the brand version of the medicine. It will certainly cost you.

There is also the very first online pharmacy Valisure, that analyzes for reliability all drugs they dispense. They also keep a list of Indian and Chinese companies that they would never order drugs from. Learn more about this company from another podcast of Dr. Attia, this of his conversation with David Light.  

Finally, eat healthy, move, destress so that your dependence on drugs is decreased. Above all, read the book, be aware. Let your friends and family know the truth.

If you live in Europe, you will find this video revealing and troubling:  How Safe Are Our Medicines.

Immune Defect As A Cause Of Alzheimer's Disease

An interesting hypothesis, abstract:

Inflammation is an immune activity designed to protect the host from pathogens and noxious agents. In its low-intensity form, presence of an inflammatory process must be inferred from appropriate biomarkers. Occult neuroinflammation is not just secondary to Alzheimer's disease (AD) but may contribute to its pathogenesis and promote its progression. A leaky blood-brain barrier (BBB) has been observed in early AD and may play a role in its initiation and development. Studies of the temporal evolution of AD's biomarkers have shown that, in AD, the brain's amyloid burden correlates poorly with cognitive decline. In contrast, cognitive deficits in AD correlate well with synapse loss. Oligomeric forms of amyloid-beta (oAβs) can be synaptotoxic and evidence of their deposition inside synaptic terminals of cognition-associated neurons explains early memory loss in AD better than formation of extracellular Aβ plaques. Among innate immune cells that reside in the brain, microglia sense danger signals represented by proteins like oAβ and become activated by neuronal damage such as that caused by bacterial endotoxins. The resulting reactive microgliosis has been implicated in generating the chronic form of microglial activation believed to promote AD's development. Genome-wide association studies (GWASs) have yielded data from patients with sporadic AD indicating that its causes include genetic variation in the innate immune system. Recent preclinical studies have reported that β-hydroxybutyrate (βOHB) may protect the brain from the adverse effects of both the nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome and the deacetylation of histone. Consequently, there is an urgent need for clinical investigations designed to test whether an orally administered βOHB preparation, such as a ketone ester, can have a similar beneficial effect in human subjects.

Immune problems and inflammation may be at the heart of many chronic disorders.  Hopefully, β-hydroxybutyrate  will be helpful.  Doing everything possible to improve immune function and reduce (unnecessary) inflammation may be helpful as well.

Flex your financial muscle

I have previously written about financial independence because it is my goal.  

I have always been thrifty; yet, in my early years no one told me that I could be more financially disciplined and more purposeful with my money. These days, however, I look around my house and instead of stuff, I see money I could have invested. I see days of freedom I would never recover.

How am I going to get rid of all the material junk? This is another question that frightens me. One day, I would like all my belongings to fit in two suitcases. And then a reasonable bank account would propel me into my adventure.

Luckily, some young people today are well aware of what they can achieve financially and how they can achieve it. Some of them even preach it online (see below)! Therefore, my child does not have to follow the road of extreme slavery that describes my everyday life.

For the past three or four years, I have listened to various podcasts on early retirement and financial independence; however, with time, these became a bit repetitive and boring.

Eventually, I switched to videos on investing. At this point, I do not need the impetus that is constantly drummed up in podcasts. All I need is to know more about the tools and the detailed implementation of a successful personal financial plan.

Here are some of the useful (and entertaining) video resources I have found in the past months:

Personal finances, taxes, investing: Money and Life TV with Mike the CPA

Investing, dividends, passive income: Joseph Carlson 

Investing, real estate, practical advice: Graham Stephan

Investing, passive income: Andrei Jikh

If you have kids, let them watch Graham Stephan and Adrei Jikh. After all, peer-to-peer advice is ranked higher than parent-to-child! 

I wish you profitable watching!

Epigenomics And Cancer Heterogeneity

There can be considerable heterogeneity in cancers, and this can contribute to progression and resistance to therapy.  This heterogeneity can arise not only from DNA sequence changes (i.e., mutation) but also from epigenetic changes - changes in the modifications of chromosomes - on a single cell level, making one cell different than another with respect to gene expression, even if the gene sequences remain the same.  A paper of interest, abstract:

Cell-to-cell heterogeneity is a major driver of cancer evolution, progression, and emergence of drug resistance. Epigenomic variation at the single-cell level can rapidly create cancer heterogeneity but is difficult to detect and assess functionally.

RESULTS: We develop a strategy to bridge the gap between measurement and function in single-cell epigenomics. Using single-cell chromatin accessibility and RNA-seq data in K562 leukemic cells, we identify the cell surface marker CD24 as co-varying with chromatin accessibility changes linked to GATA transcription factors in single cells. Fluorescence-activated cell sorting of CD24 high versus low cells prospectively isolated GATA1 and GATA2 high versus low cells. GATA high versus low cells express differential gene regulatory networks, differential sensitivity to the drug imatinib mesylate, and differential self-renewal capacity. Lineage tracing experiments show that GATA/CD24hi cells have the capability to rapidly reconstitute the heterogeneity within the entire starting population, suggesting that GATA expression levels drive a phenotypically relevant source of epigenomic plasticity.
CONCLUSION: Single-cell chromatin accessibility can guide prospective characterization of cancer heterogeneity. Epigenomic subpopulations in cancer impact drug sensitivity and the clonal dynamics of cancer evolution.

Identifying these epigenetic changes can be the first step in developing novel approaches to reverse the changes and/or target those cells containing such changes, for therapeutic benefit.