Tuesday, July 31, 2018

Natural Product Polyphenols Against Cancer

Natural product polyphenols that can be obtained through diet can have anti-cancer properties, particularly with respect to cancer driven by chronic inflammation.  Modulation of signaling pathways and transcription factors may be involved in this anti-cancer effect. Abstract:

Inflammation is one of the major causative factor of cancer and chronic inflammation is involved in all the major steps of cancer initiation, progression metastasis and drug resistance. The molecular mechanism of inflammation driven cancer is the complex interplay between oncogenic and tumor suppressive transcription factors which include FOXM1, NF-kB, STAT3,Wnt/β- Catenin, HIF-1α,NRF2, androgen and estrogen receptors. Several products derived from natural sources modulate the expression and activity of multiple transcription factors in various tumor models as evident from studies conducted in cell lines, pre-clinical models and clinical samples. Further combination of these natural products along with currently approved cancer therapies added an additional advantage and they considered as promising targets for prevention and treatment of inflammation and cancer. In this review we discuss the application of multi-targeting natural products by analyzing the literature and future directions for their plausible applications in drug discovery.

Tea tree oil

I am abroad, in a country where each pharmacy carries a wide variety of essential oils. They are displayed right next to the pharmacists. There is no way a client would miss the rows or small pretty containers. 

The oils come with amazing practical advice on how to safely use them. Below is a part of a leaflet that came with a small bottle of tea tree oil. I bought it because I have been using this oil and already know its benefits for my acne-prone skin. However, I was not aware of all other applications of the oil.
Melaleuca alternifolia is the Latin name of the botanical species.

What is the tea tree oil used for?

  • It restores and balances oily skin, decreases skin pore size, prevents acne.
  • It counteracts the unpleasant smell of sweaty feet; neutralizes bad breath.
  • It regenerates and strengthens the hair, removes dandruff.
  • It cleanses the air and neutralizes unpleasant room odors.

How to use the tea tree oil?
  • For massage, to each 100 ml of almond oil (or any other plant-based oil) add 20 drops of tea tree oil.
  • To strengthen your hair and remove the dandruff, enrich your hair shampoo or conditioner by adding 10 -15 drops of tea tree oil for each 100 ml of shampoo or conditioner.
  • To neutralize bad breath, rinse the mouth with a solution prepared with three drops of tea tree oil per 100 ml of water.
  • Against sweating, soak yourself in a bathtub with 6 - 8 drops of tea tree oil.
  • To stop the unpleasant smell of your feet, soak them in a container with water and 5 - 6 drops of tea tree oil.
  • To freshen up your room, prepare a spray bottle of 250 ml water and 15 - 20 drops of tea tree oil.
  • For acne remedy and clean skin, I have previously published my concoction of apple cider vinegar, tea tree oil and witch hazel. I use this solution to clean my face in the evening and in the morning, or after any strenuous/dirty job to unplug the skin pores. I have always been pimple-prone; however, since I started using this cleanser, my face has been quite clean and almost pimple-free. The added benefit is that the vinegar brightens some of the age spots.

Keep in mind that all essential oils are not recommended for pregnant women, mothers who breastfeed, children, and individuals with intolerance to any of the essences. The best approach to use is first to test whether you are sensitive to the oil.  
Store all essential oils tightly closed, away from sunlight.

Here is a useful video for acne-spot treatment with tea tree oil:


Monday, July 30, 2018

A life of leisure

Feeling burnt out? Need to watch something that you will never have and yet, is entertaining?  

Watch Jeeves and Wooster - a show about a British gentleman, whose entire life is filled with leisure, leisure and more leisure.  

I am sure that I would adore my life if filled with these activities and dynamism. It is the life of no real worries and perpetual childhood that we all wish for.

It gets even better, Jeeves is the man that makes your life a song. Jeeves takes care of you and your possessions. Jeeves advises you in any situation; therefore, you do not strain yourself to resolve any issues. 

Yes, it may get boring after time, but I would like to try the life of Wooster, or maybe this of Jeeves.





Wednesday, July 25, 2018

Cannabinoids For Metastatic Colon Cancer?

Rimonabant, which interacts with cannabinoid receptors, inhibits canonical Wnt signaling in colorectal cancer cells; this form of Wnt signaling is often deregulated in cancer.  An opposing signaling pathway, non-canonical Wnt signaling, is upregulated in some, but not all, colorectal cancer cells.  This reagent also reduced tumor growth in a mouse model of colon cancer.  Thus, the authors conclude that: “Obtained data heavily supported the rationale for the use of cannabinoids in combined therapies for metastatic CRC harbouring activating mutations of β-Catenin” – although of course more research is needed.  Abstract:

In a high percentage (≥85%) of both sporadic and familial adenomatous polyposis forms of colorectal cancer (CRC), the inactivation of the APC tumor suppressor gene initiates tumor formation and modulates the Wnt/β-Catenin transduction pathways involved in the control of cell proliferation, adhesion and metastasis. Increasing evidence showed that the endocannabinoids control tumor growth and progression, both in vitro and in vivo. We evaluated the effect of Rimonabant, a Cannabinoid Receptor 1 (CB1) inverse agonist, on the Wnt/β-Catenin pathway in HCT116 and SW48 cell lines carrying the genetic profile of metastatic CRC poorly responsive to chemotherapies. In these models, Rimonabant inhibited the Wnt/β-Catenin canonical pathway and increased β-Catenin phosphorylation; in HCT116 cells, but not in SW48, the compound also triggered the Wnt/β-Catenin non canonical pathway activation through induction of Wnt5A and activation of CaMKII. The Rimonabant-induced downregulation of Wnt/β-Catenin target genes was partially ascribable to a direct inhibition of p300/KAT3B histone acetyltransferase, a coactivator of β-Catenin dependent gene regulation. Finally, in HCT116 xenografts, Rimonabant significantly reduced tumor growth and destabilized the nuclear localization of β-Catenin. Obtained data heavily supported the rationale for the use of cannabinoids in combined therapies for metastatic CRC harbouring activating mutations of β-Catenin.

Epigenetic Cancer Therapy

Possible epigenetic-based cancer therapy for tumors with certain mutations; abstract:

The lysine methyltransferase KMT2C (also known as MLL3), a subunit of the COMPASS complex, implements monomethylation of Lys4 on histone H3 (H3K4) at gene enhancers. KMT2C (hereafter referred to as MLL3) frequently incurs point mutations across a range of human tumor types, but precisely how these lesions alter MLL3 function and contribute to oncogenesis is unclear. Here we report a cancer mutational hotspot in MLL3 within the region encoding its plant homeodomain (PHD) repeats and demonstrate that this domain mediates association of MLL3 with the histone H2A deubiquitinase and tumor suppressor BAP1. Cancer-associated mutations in the sequence encoding the MLL3 PHD repeats disrupt the interaction between MLL3 and BAP1 and correlate with poor patient survival. Cancer cells that had PHD-associated MLL3 mutations or lacked BAP1 showed reduced recruitment of MLL3 and the H3K27 demethylase KDM6A (also known as UTX) to gene enhancers. As a result, inhibition of the H3K27 methyltransferase activity of the Polycomb repressive complex 2 (PRC2) in tumor cells harboring BAP1 or MLL3 mutations restored normal gene expression patterns and impaired cell proliferation in vivo. This study provides mechanistic insight into the oncogenic effects of PHD-associated mutations in MLL3 and suggests that restoration of a balanced state of Polycomb-COMPASS activity may have therapeutic efficacy in tumors that bear mutations in the genes encoding these epigenetic factors.

Tuesday, July 24, 2018

Porcupine, Wnt, And Fertility

The factor porcupine is involved in the Wnt signaling pathway.  Modulation of porcupine shows that Wnt signaling is important in regulating fertility and “successful embryo implantation.”  Also see this.  Modulating porcupine and/or Wnt signaling more directly may possible become part of treatments for fertility problems.







Another Natural Wnt Inhibitor

A plant-derived natural product inhibits Wnt signaling; maybe of potential therapeutic value.  Abstract:

The Wnt/β-catenin pathway is essential for embryonic development and homeostasis, but excessive activation of this pathway is frequently observed in various human diseases, including cancer. Current therapeutic drugs targeting the Wnt pathway often lack sufficient efficacy, and new compounds targeting this pathway are therefore greatly needed. Here, we report that the plant-derived natural product parthenoide (PTL), a sesquiterpene lactone, inhibits Wnt signaling. We found that PTL dose-dependently inhibits Wnt3a- and CHIR-induced transcriptional activity assessed with the T-cell factor/lymphoid enhancer factor(TCF/LEF)-firefly luciferase (TOPFlash) assay in HEK293 cells. Further investigations revealed that PTL decreases levels of the transcription factors TCF4/LEF1 without affecting β-catenin stability or subcellular distribution. Moreover, this effect of PTL on TCF4/LEF1 was related to protein synthesis rather than to proteasome-mediated degradation. Of note, siRNA-mediated knockdown of RPL10, a ribosome protein that PTL binds, substantially decreased TCF4/LEF1 protein levels and also Wnt3a-induced TOPFlash activities, suggesting a potential mechanism by which PTL may repress Wnt/β-catenin signaling. In summary, PTL binds RPL10 and thereby potently inhibits the Wnt/β-catenin pathway.

Monday, July 23, 2018

Chocolate Milk For Exercise Recovery?

There’s an exercise paradigm suggesting that chocolate milk (CM) is an ideal post-exercise recovery drink.  Someone actually evaluated this, and the outcome was not extremely supportive of the paradigm, but did not refute it either: “CM provides either similar or superior results when compared to placebo or other recovery drinks.”  At best, CM seems marginally better than placebo or other recovery drinks, but more studies, with larger sample sizes, are required.  Abstract:

BACKGROUND/OBJECTIVES:Chocolate milk (CM) contains carbohydrates, proteins, and fat, as well as water and electrolytes, which may be ideal for post-exercise recovery. We systematically reviewed the evidence regarding the efficacy of CM compared to either water or other "sport drinks" on post-exercise recovery markers.SUBJECTS/METHODS:PubMed, Scopus, and Google scholar were explored up to April 2017 for controlled trials investigating the effect of CM on markers of recovery in trained athletes.RESULTS:Twelve studies were included in the systematic review (2, 9, and 1 with high, fair and low quality, respectively) and 11 had extractable data on at least one performance/recovery marker [7 on ratings of perceived exertion (RPE), 6 on time to exhaustion (TTE) and heart rate (HR), 4 on serum lactate, and serum creatine kinase (CK)]. The meta-analyses revealed that CM consumption had no effect on TTE, RPE, HR, serum lactate, and CK (P > 0.05) compared to placebo or other sport drinks. Subgroup analysis revealed that TTE significantly increases after consumption of CM compared to placebo [mean difference (MD) = 0.78 min, 95% confidence interval (CI): 0.27, 1.29, P = 0.003] and carbohydrate, protein, and fat-containing beverages (MD = 6.13 min, 95% CI: 0.11, 12.15, P = 0.046). Furthermore, a significant attenuation on serum lactate was observed when CM was compared with placebo (MD = -1.2 mmol/L, 95% CI: -2.06,-0.34, P = 0.006).CONCLUSION:CM provides either similar or superior results when compared to placebo or other recovery drinks. Overall, the evidence is limited and high-quality clinical trials with more well-controlled methodology and larger sample sizes are warranted.

Sunday, July 22, 2018

Preventing Neuronal Disease Through The Microbiota

Once again, modifying the microbiota through diet can prevent neuroimmune and neuroinflammatory disease.

The gut-brain-axis refers to the bidirectional communication between the enteric nervous system and the central nervous system. Mounting evidence supports the premise that the intestinal microbiota plays a pivotal role in its function and has led to the more common and perhaps more accurate term gut-microbiota-brain axis. Numerous studies have identified associations between an altered microbiome and neuroimmune and neuroinflammatory diseases. In most cases, it is unknown if these associations are cause or effect; notwithstanding, maintaining or restoring homeostasis of the microbiota may represent future opportunities when treating or preventing these diseases. In recent years, several studies have identified the diet as a primary contributing factor in shaping the composition of the gut microbiota, and in turn, the mucosal and systemic immune systems. In this review, we will discuss the potential opportunities and challenges with respect to modifying and shaping the microbiota through diet and nutrition in order to treat or prevent neuroimmune and neuroinflammatory disease.

Friday, July 20, 2018

The Opiod Epidemic As A Model For The Tobacco Problem

Using the opioid epidemic as a model to deal with the broader tobacco problem may be a useful approach.  Read this:

On October 26, 2017, President Trump declared the opioid epidemic a public health emergency. Although some commentators have debated its merits, the declaration has already been successful in 1 regard: it has focused national attention on the problem of opioid misuse and abuse. Indeed, the opioid epidemic is a pressing problem. In 2015, opioids were implicated in 33 000 deaths, representing a 4-fold increase since the early 2000s.1 Mortality attributable to opioids is particularly concentrated among younger adults, with an estimated 1 million years of potential life lost annually.2
As devastating as the opioid epidemic is, however, its toll is modest compared to that of another substance: tobacco. Even though tobacco use has rarely made headlines in recent years, cigarette smoking is associated with an estimated 480 000 deaths in the United States annually, totaling approximately 5 million years of potential life lost each year.3,4 Of these deaths, approximately 41 000 are attributed to secondhand smoke exposure, a number that alone exceeds the number of US residents who die of an opioid overdose.3 Public outcry over the opioid crisis is by no means misplaced, but the contrast between the relative attention garnered by the opioid epidemic compared with tobacco use highlights the extent to which concern over tobacco has receded, despite the enormous adverse effects of tobacco on the health of society.
Why has the opioid crisis generated intense public concern and interest while tobacco has not? One reason might be that the trajectories of the 2 epidemics are quite different. The opioid epidemic is a relatively recent phenomenon that appears to be accelerating at a concerning pace. Tobacco use, by contrast, has been steadily decreasing in the United States, with smoking rates declining by more than half during the past 60 years.
The decline in smoking rates, while encouraging, can obscure the ways in which tobacco is still a real and pressing problem. First, the burden of disease attributable to tobacco remains substantial. For every person who dies from using tobacco, 30 live with serious tobacco-related illness.3 Second, and perhaps more insidiously, tobacco use has become more concentrated in vulnerable populations: among the poor, those with mental illness, and those with low educational attainment. Smoking prevalence has declined to less than 10% among those with a college education or more, whereas among those without a high school diploma, approximately 24% of the population smokes.5 Tobacco is becoming a key driver of health disparities in the United States.
The perceived importance of tobacco use has critical consequences for tobacco control and prevention efforts. Over the past decade, public funding for tobacco control has remained stagnant. State spending on tobacco control has been well below revenue generated by tobacco sales and represents a fraction of what tobacco companies spend on marketing. In some cases, states have elected to defund tobacco control programs entirely. For example, the state of New Jersey devoted zero state dollars to tobacco control and prevention between 2013 and 2017, suggesting that tobacco use was declining and that funding for tobacco control measures was not needed.
Despite declining or stagnant efforts on the state and local levels, tobacco control has received renewed attention from a key agency: the US Food and Drug Administration (FDA).6 In August 2017, the FDA announced a proposal to regulate and reduce the amount of nicotine in combustible cigarettes. High-quality (albeit short-term) data suggest that lowering nicotine levels in tobacco reduces nicotine dependence without promoting compensatory smoking.7 While the actual effects of such a policy remain to be seen, the policy represents a novel and aggressive approach to reducing cigarette consumption. The FDA has also proposed regulating noncombustible nicotine products, including electronic nicotine-delivery systems, and has suggested that these products may have a role in a broader harm-reduction strategy.
Implementing these policies will not be straightforward. The FDA’s authority to regulate nicotine in cigarettes was established by statute in 2009. Eight years have elapsed since this authority was granted, highlighting the difficulties of regulating nicotine. Vested interests, including tobacco companies, will surely oppose the policy. Policy makers concerned about local economic effects may also oppose and challenge the FDA’s authority. Even public health advocates and public health agencies wary of unintended consequences may challenge this approach.8
In many ways, the challenges faced by tobacco control are similar to those of the opioid epidemic: a profoundly addictive substance, use concentrated among marginalized and vulnerable populations, powerful interests that profit from consumption, and harm-reduction strategies that require a shift in approach. Perhaps a key difference is that the opioid epidemic has generated intense public concern as well as broad bipartisan political support. While the opioid epidemic has not yet abated, this public and political support has been critical at key policy junctures, including in shaping debate around the future of the Affordable Care Act and the structure of the Medicaid program, which are important in funding treatment for substance use disorders. Such support could likewise be critical in carrying the FDA proposal forward.
Perhaps public concern over the opioid epidemic can provide an opportunity to renew a sense of urgency around tobacco control. Indeed, the epidemics are not completely distinct. The communities most deeply affected by the opioid crisis also have some of the highest smoking rates, and individuals who use tobacco are also more likely to develop prescription opioid misuse. These overlapping epidemics suggest that common conditions may contribute to both and that common solutions may be useful. This moment, with attention focused intently on the opioid epidemic, may also provide the chance to address addiction to nicotine and thereby substantially reduce the harms caused by these 2 threats to health.

Extracellular Vesicles And Neurodegeneration

Extracellular vesicles have effects on Alzheimer’s disease and other neurodegenerative diseases, mostly negative but possibly also some positive.  Thus can be a target for therapeutic intervention.  Abstract:

Extracellular vesicles (EVs), based on their origin or size, can be classified as apoptotic bodies, microvesicles (MVs)/microparticles (MPs), and exosomes. EVs are one of the new emerging modes of communication between cells that are providing new insights into the pathophysiology of several diseases. EVs released from activated or apoptotic cells contain specific proteins (signaling molecules, receptors, integrins, cytokines), bioactive lipids, nucleic acids (mRNA, miRNA, small non coding RNAs, DNA) from their progenitor cells. In the brain, EVs contribute to intercellular communication through their basal release and uptake by surrounding cells, or release into the cerebrospinal fluid (CSF) and blood. In the central nervous system (CNS), EVs have been suggested as potential carriers in the intercellular delivery of misfolded proteins associated to neurodegenerative disorders, such as tau and amyloid β in Alzheimer's Diseases (AD), α-synuclein in Parkinson's disease (PD), superoxide dismutase (SOD)1 in amyotrophic lateral sclerosis and huntingtin in Huntington's disease. Multiple studies indicate that EVs are involved in the pathogenesis of AD, although their role has not been completely elucidated. The focus of this review is to analyze the new emerging role of EVs in AD progression, paying particular attention to microglia EVs. Recent data shows that microglia are the first myeloid cells to be activated during neuroinflammation. Microglial EVs in fact, could have both a beneficial and a detrimental action in AD. The study of EVs may provide specific, precise information regarding the AD transition stage that may offer possibilities to intervene in order to retain cognition. In chronic neurodegenerative diseases EVs could be a novel biomarker to monitor the progression of the pathology and also represent a new therapeutical approach to CNS diseases.

Thursday, July 19, 2018

Diaphragm Fatigue And Lower Pack Pain


The diaphragm plays an important role in spinal control. Increased respiratory demand compromises spinal control, especially in individuals with low back pain (LBP). The objective was to determine whether individuals with LBP exhibit greater diaphragm fatigability compared to healthy controls. Transdiaphragmatic twitch pressures (TwPdi) were recorded in 10 LBP patients and 10 controls, before and 20 and 45 min after inspiratory muscle loading (IML). Individuals with LBP showed a significantly decreased potentiated TwPdi, 20 min (-20%) (p=0.002) and 45 min (-17%) (p=0.006) after IML. No significant decline was observed in healthy individuals, 20 min (-9%) (p=0.662) and 45 min (-5%) (p=0.972) after IML. Diaphragm fatigue (TwPdi fall ≥ 10%) was present in 80% (20 min after IML) and 70% (45 min after IML) of the LBP patients compared to 40% (p=0.010) and 30% (p=0.005) of the controls, respectively. Individuals with LBP exhibit propensity for diaphragm fatigue, which was not observed in controls. An association with reduced spinal control warrants further study.

Further study can, among other things, look at cause and effect.  Does diaphragm fatigue lead to spinal problems and lower back pain?  Or is it the reverse?  Or is spinal problems and back pain not directly related, but that one leads to the other through the intermediate step of diaphragm  fatigue?  Is there some way to make the diaphragm less "fatigable" - perhaps by increasing ease of breathing through weight loss of conditioning through exercise?

Tuesday, July 17, 2018

Pigeon Crop Milk

This is not relevant to human health, but may be of interest to pigeon enthusiasts.  Abstract: 

The pigeon (Columba livia) is one of the few birds capable of secreting nutrients to nourish squabs. During the incubation period, the crop of the parent pigeon will be thickened. When squabs are hatched, the crop milk will be secreted from the crop and fed to squabs. The nutritional benefits are similar between the pigeon crop milk and mammalian milk, and both of them are regulated by prolactin. Prolactin stimulates the proliferation of crop epithelial cells, which eventually slough to form the crop milk. Evidence suggests that the complex process may be associated with the transcription of the AnxIcp35 gene and the activation of JAK/STAT and Wnt signal pathways. In this review, we summarize the main components and the biological function of the crop milk, the histological changes of the crop and the regulatory mechanism of crop milk secretion.

Sunday, July 15, 2018

The Appendix and IBD

Take home points: The appendix most likely is not just a “vestigial remnant” but may play a role as a “microbiota reservoir.”  Also, the appendix may play a role in inflammatory bowel disease, particularly ulcerative colitis, and for some of these patients, an appendectomy may be helpful.  Abstract:

The human appendix has long been considered as a vestigial organ, an organ that has lost its function during evolution. In recent years, however, reports have emerged that link the appendix to numerous immunological functions in humans. Evidence has been presented for an important role of the appendix in maintaining intestinal health. This theory suggests that the appendix may be a reservoir or 'safe house' from which the commensal gut flora can rapidly be reestablished if it is eradicated from the colon. However, the appendix may also have a role in the development of inflammatory bowel disease (IBD). Several large epidemiological cohort studies have demonstrated the preventive effect of appendectomy on the development of ulcerative colitis, a finding that has been confirmed in murine colitis models. In addition, current studies are examining the possible therapeutic effect of an appendectomy to modulate disease course in patients with ulcerative colitis. This literature review assesses the current knowledge about the clinical and immunological aspects of the vermiform appendix in IBD and suggests that the idea of the appendix as a vestigial remnant should be discarded.

Friday, July 13, 2018

Genetics of X Inactivation

By Michael Bodega - I (Michael Bodega) created this work entirely by myself., Public Domain, https://commons.wikimedia.org/w/index.php?curid=16831523

X inactivation shuts off many (but not all!) genes of one of the X chromosomes in the cells of female mammals, to balance gene expression with cells of males that have only one X chromosome.  The inactivation tends to be random (as to which of the pair of X chromosomes experiences inactivation in each cell), and has phenotypic consequences for health and disease  and also affects fur color in female cats.  The set of inactivated X chromosome genes in female human cells has been analyzed, which may help in understanding X-linked disorders in females.  Abstract:

X chromosome inactivation (XCI) silences transcription from one of the two X chromosomes in female mammalian cells to balance expression dosage between XX females and XY males. XCI is, however, incomplete in humans: up to one-third of X-chromosomal genes are expressed from both the active and inactive X chromosomes (Xa and Xi, respectively) in female cells, with the degree of 'escape' from inactivation varying between genes and individuals. The extent to which XCI is shared between cells and tissues remains poorly characterized, as does the degree to which incomplete XCI manifests as detectable sex differences in gene expression and phenotypic traits. Here we describe a systematic survey of XCI, integrating over 5,500 transcriptomes from 449 individuals spanning 29 tissues from GTEx (v6p release) and 940 single-cell transcriptomes, combined with genomic sequence data. We show that XCI at 683 X-chromosomal genes is generally uniform across human tissues, but identify examples of heterogeneity between tissues, individuals and cells. We show that incomplete XCI affects at least 23% of X-chromosomal genes, identify seven genes that escape XCI with support from multiple lines of evidence and demonstrate that escape from XCI results in sex biases in gene expression, establishing incomplete XCI as a mechanism that is likely to introduce phenotypic diversity. Overall, this updated catalogue of XCI across human tissues helps to increase our understanding of the extent and impact of the incompleteness in the maintenance of XCI.

Wednesday, July 11, 2018

Baths Vs. Showers

In Japan, people tend to take warm baths rather than showers, and now some Japanese researchers have conducted a study in which they claim baths are better for mental and physical well-being than showers  Take that for what it is worth; I am not going to change my habits based on this one way or the other.  Abstract:

Showering is the most common form of bathing worldwide. Whole-body immersion bathing in warm water (~40°C) is common in Japan and exerts sufficient hyperthermic action to induce vasodilatation and increase blood flow, supplying more oxygen and nutrients to the periphery. Cross-sectional studies report better subjective health status with an immersion bathing habit. This randomized controlled trial compared the effects on health of immersion bathing and shower bathing in 38 participants who received 2-week intervention of immersion bathing in warm water (40°C) for 10 min (bathing intervention) followed by 2-week shower bathing without immersion (showering intervention) or vice versa (n = 19 each group). Visual analog scale scores were significantly better for fatigue, stress, pain, and smile and tended to be better for self-reported heath and skin condition after bathing intervention than after showering intervention. The SF-8 Health Survey showed significantly better general health, mental health, role emotional, and social functioning scores. Profile of Mood State scores were lower for stress, tension-anxiety, anger-hostility, and depression-dejection. Immersion bathing, but not shower bathing, exerts hyperthermic action that induces increased blood flow and metabolic waste elimination, which may afford physical refreshment. Immersion bathing should improve both physical and emotional aspects of quality of life.

Tuesday, July 10, 2018

Can you live beyond external validation



Navy seals learn to live beyond external validation.

This is what someone told me a month ago. Ever since, my mind circled back to this statement many times. It is attractive not to depend on anyone’s opinion, to know for sure what I am worth, to validate my own actions and behaviors.

Interestingly, we do not care about anyone’s opinion when we are born. We are unaware of the approval or disapproval of the surrounding people at our birth and throughout the first years of our lives.

We also die not caring about what everyone else thinks about us and how everyone around assesses us. In the last months or years of our lives, if we are aware of our approaching end, we would likely be disinterested in everyone’s opinion about us.

And yet, between these two events – birth and death – we are entangled in what people think and say about us, in how people perceive us and treat us. This is a most constraining and enduring condition that defines our lives and behaviors. This is also an enormous time trap; we spend countless hours fretting about people’s assessments of us and their behaviors toward us.

The more integrated we are with the society and its structures, the higher is our dependence on external validation. If we work for our living, then we are evaluated on a regular basis. 


I am currently evaluated by many “parties” at my job. The customers, several layers of bosses, and external associates are all assessing my behavior and contributions, my knowledge and even my appearance. This is of course, in addition to colleagues and peers talking about me and doing their “behind-the-scenes” dirty politics. I do not care about the last category anymore, since my salary does not depend on them. For the most part, I can effectively avoid the evil colleagues simply by interacting with them only if it is absolutely necessary. I have witnessed that “friendships” with coworkers are useless and even detrimental. I watched such “associations” burn to ashes. The initial “honeymoon”, when new to each other colleagues overshare personal information is quickly replaced by an open warfare period, when the shared information is turned into a dagger, with which the former “friends” backstab each other.

Whereas the pathetic situations with judgmental, evil and psychotic colleagues might be avoided through limited interactions and more guarded behaviors, the imposed by institutions evaluations such as your annual review with the boss cannot miraculously disappear. We are subjected to these "examinations" since school age, when assessments and grades are given for everything we learn and do. And then, we proceed though our lives by enduring more and more evaluations, as long as we need to work for our living.

The only way out of the vicious trap of assessments and evaluations is to be financially independent. This is obvious when you analyze the behaviors of filthy rich people. Let’s take as an example Elon Musk. Not only the guy does not care about what you and I think about him, he is also creating the same judgment-free environment for his children. 


Musk established a school for his five sons and a few other lucky kids. In this school, “…there are very few formal assessments and no grades are handed out". Emphasis is placed not on the fear of the grades and opinions of teachers and peers, but on creativity: “…Many students go on to create their own websites with what they've learned “, and “…Feedback is given in the form of TED Talk like symposia and presentations to faculty members of nearby universities“. Best of all, “Each year, the curriculum is totally rewritten, with around half of the content decided upon by the students themselves”.

Do you think that kids, who have gone through this school, would grow up to be adults who deeply care about formal assessments and evaluations? I doubt it.

Can you live beyond external validation, rather than seek confirmation and approval by others? Or maybe the right question is, can you afford to not care about external validation?  Is it your life that you are living?