Does Owning a Dog Increase Quality of Life?

Owning a dog has been linked to increased physical activity and improved mental health. Dog owners typically engage in more exercise than non-owners, as they are responsible for walking, playing, and caring for their pets. This increased physical activity helps reduce the risk of cardiovascular diseases, hypertension, and obesity (American Heart Association, 2021). In addition to physical benefits, dog ownership has a positive impact on mental health. Interactions with dogs stimulate the release of oxytocin, dopamine, and serotonin—neurotransmitters associated with happiness and stress relief. These chemicals help reduce symptoms of depression and anxiety. Moreover, dog owners tend to have lower levels of cortisol, the body’s primary stress hormone, compared to non-dog owners (Beetz et al., 2012).

Dogs also encourage outdoor activity and social interaction. Visits to parks or dog-friendly spaces increase opportunities for positive human interactions, which can alleviate social isolation and anxiety. The act of caring for a dog promotes emotional well-being by fostering a sense of responsibility and connection. In short, dog ownership offers a range of physical and mental health benefits, for improving overall well-being.

References:

American Heart Association. (2021). Healthy Bond for Life: Do Dog Owners Live Longer? Retrieved from https://www.heart.org/en/healthy-living/healthy-bond-for-life-pets/do-dog-owners-live-longer

Beetz, A., Uvnäs-Moberg, K., Julius, H., & Kotrschal, K. (2012). Psychosocial and psychophysiological effects of human-animal interactions: The possible role of oxytocin. Frontiers in Psychology, 3, 234. doi: 10.3389/fpsyg.2012.00234

It Doesn't Count in College...Right?

Even if you yourself have not said this in your time in college, you probably know someone who has said “it doesn’t count when you’re in college” about things like drinking alcohol or smoking nicotine. Many college students are social drinkers or smokers that participate in these activities more than once a week. Of course, there is nothing wrong with enjoying your time, but it is important to notice signs from your body that it may be time to take things a bit more seriously.

Think about how many times you or your friends get heartburn, does it happen regularly? It can’t be that significant, everyone has it at some point in their lives right? Acid reflux due to the malfunction of the cardiac sphincter in the stomach and at the base of the esophagus could be a slippery slope to much more serious issues. If acid reflux occurs daily over the span of months or years, you may be at risk of developing Barrett’s esophagus. This happens when the body tries to heal itself and replaces the esophagus lining with tissue resembling that of the small intestine. 

You’re probably thinking, “okay, how does that relate to drinking and smoking?” Here’s how: smoking and heavy alcohol use can increase the risk of esophageal cancer, and if you have acid reflux, it can quickly become an issue without warning. Even though it is rare, making up about 1% of all cancers in the U.S. and occurring in people over the age of 55, these activities college students are participating in could increase their chances of experiencing issues with the esophagus. 

I have seen it in a 46 year old who was an alcoholic in his twenties and an avid smoker, the only symptom he had was acid reflux that suddenly worsened over the span of a month. In my time with him, 16 years, he had only picked up alcohol at holiday events, but nicotine or vaping was an everyday occurrence. This type of cancer can also happen in young adults that have never smoked and have healthy lifestyles.

So surely doing these things in college doesn’t count. Surely these habits will stop once you graduate. Do yourself and your loved ones a favor and take that acid reflux seriously! Barrett's esophagus is just as important to look out for!

The steroid era in the MLB had to have been AWESOME

 Do you ever just find yourself thinking about how baseball, Americas greatest passing time has just been on the decline this past decade. Well let me take you back to 2001 when Barry Bonds notched 73 home runs in 1 season, not to mention this guy hit 762 home runs in his career (https://www.youtube.com/watch?v=cL3vNXIsEPM) !!! Mark McGwire, Sammy Sosa, A-ROD, all these legends have something in common and I am not talking about talent, I'm talking about performance enhancing drugs (PED) or what I like to call it "That Juice." 

At this time usually the drug of choice was called Androstenedione (andro). This is a steroidal hormone produced by the male and female gonads. Utilized to increase testosterone levels, and thought and "proven" to be an athletic performance enhancer by building muscle, reduce fats, increase energy, maintain healthy RBC's and also increase sexual performance. Nevertheless this drug is banned by almost all athletic committees, including the MLB :(. 

Andro works negatively by converting into more potent hormones like estradiol and testosterone, which really can disrupt your hormone balance (Badway). Estradiol also was known to stimulate cell growth, potentially promoting cancer development. On this study The big take home they were concerned about was how bad it affects the male sperm count. 

In another study done with mice, Andro was seen to cause liver cancer in mice and likely contribute to higher risk of liver cancer in men compared to women (Rooney). Male mice were found to be more susceptible to liver cancer because they have higher androgen receptor activation, This mechanism showed that andro's metabolism is linked to liver tumor development based on sex within mice (Rooney). Also according to the Mayo clinic Andro was seen to cause damage in the heart and blood vessels, to anyone who takes it (Mayo clinic). 

So would taking Androstenedione be worth it, at the expense of liver cancer. I say "Commence the moonshot bombs." 

Badawy, M. T., Sobeh, M., Xiao, J., & Farag, M. A. (2021). Androstenedione (a Natural Steroid and a Drug Supplement): A Comprehensive Review of Its Consumption, Metabolism, Health Effects, and Toxicity with Sex Differences. Molecules (Basel, Switzerland), 26(20), 6210. https://doi.org/10.3390/molecules26206210 

ESPN. (2012, December 5). The Steroids Era. ESPN.com. https://www.espn.com/mlb/topics/_/page/the-steroids-era

Rooney, J. P., Ryan, N., Chorley, B. N., Hester, S. D., Kenyon, E. M., Schmid, J. E., George, B. J., Hughes, M. F., Sey, Y. M., Tennant, A., MacMillan, D. K., Simmons, J. E., McQueen, C. A., Pandiri, A., Wood, C. E., & Corton, J. C. (2017). From the Cover: Genomic Effects of Androstenedione and Sex-Specific Liver Cancer Susceptibility in Mice. Toxicological sciences : an official journal of the Society of Toxicology, 160(1), 15–29. https://doi.org/10.1093/toxsci/kfx153

Mayo Clinic . (2023, June 27). Performance-enhancing drugs: Know the risks. Mayo Clinic; Mayo Foundation for Medical Education and Research. https://www.mayoclinic.org/healthy-lifestyle/fitness/in-depth/performance-enhancing-drugs/art-20046134

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Would you wish this on your worst enemy?

In the myth of Ondine, a water nymph falls in love with a mortal, giving up her immortality for him. When he betrays her, she curses him: he will continue breathing only as long as he stays awake. The moment he falls asleep, his body will stop breathing, leading to his death. This curse mirrors the rare medical condition called Congenital Central Hypoventilation Syndrome (CCHS), where affected individuals must consciously breathe or rely on ventilators, especially during sleep, as their bodies “forget” to breathe automatically. 

CCHS is primarily caused by mutations in the PHOX2B gene, which plays a crucial role in the development of the autonomic nervous system (ANS). The ANS regulates involuntary bodily functions like heart rate, digestion, and breathing. In healthy individuals, the ANS monitors carbon dioxide (CO₂) levels in the blood and adjusts breathing rates accordingly to maintain homeostasis.

Although CCHS is usually present at birth, individuals can acquire Central Hypoventilation Syndrome (CHS) from trauma to the brainstem. In a case study I found, a patient acquired CHS after undergoing a posterior fossa craniectomy to remove a hemangioblastoma in the cerebellomedullary cistern. The surgery affected the brainstem, which controls breathing, leading to problems after the operation. Although the patient breathes normally while awake, they had difficulty breathing during sleep, resulting in apneic episodes. Continuous monitoring confirmed the diagnosis of acquired CHS as a result from the surgery. The patient underwent a tracheostomy on the fifth day and was started on respiratory stimulants, but there was no improvement. After 14 days in the hospital, they were discharged against medical advice due to financial reasons. This case study poses several ethical dilemmas. What do you think is the most important ethical consideration in this situation?

Karn M, Mahato BK, Sah R, Kandel D, Sapkota S. "You Sleep, You Die": A Rare Clinical Case of Ondine's Curse after Posterior Fossa Surgery. Case Rep Surg. 2023 Sep 11;2023:3113428. doi: 10.1155/2023/3113428. PMID: 37727799; PMCID: PMC10506874.

Don't trip...or Maybe Do! The Efficacy of Shrooms for TRD

    Psilocybin, a naturally occurring psychedelic compound found in certain mushrooms, is gaining attention in the field of mental health, especially for its potential effects on treatment-resistant depression (TRD). Traditional antidepressants primarily target monoamine neurotransmitters like serotonin, norepinephrine, and dopamine. However, they often fall short for individuals with TRD, where typical therapies don’t produce meaningful improvement. Although non-FDA approved, psilocybin shows promising results for people who haven’t found relief with standard treatments. Understanding the physiological mechanisms behind psilocybin’s effects offers insights into its unique therapeutic potential. 

    At a cellular level, psilocybin acts as a partial agonist for serotonin (5-HT) receptors, particularly the 5-HT2A receptor, which is densely expressed in the prefrontal cortex, striatum, and areas of the limbic system. Activation of this receptor is thought to underlie the hallucinogenic and consciousness-altering effects of psilocybin, as well as its impact on mood and perception (Carhart-Harris et al., 2016). This receptor activation promotes the release of the serotonin neurotransmitter, strengthens communication between neurons, and triggers a cascade of cellular responses that contribute to "synaptic plasticity," or the brain's ability to rewire itself. Enhanced synaptic plasticity is crucial for individuals with TRD, as it helps in forming new pathways that may counteract the negative, rigid thought patterns often seen in depression.

    Research has also shown that psilocybin can reduce the activity of the brain's default mode network (DMN), a network active during self-referential thinking and rumination. Hyperactivity in the DMN is common in depression, leading to repetitive negative thinking. By reducing DMN activity, psilocybin allows the brain to "reset" and potentially disengage from these persistent negative thought loops. Studies using functional MRI show that psilocybin creates a highly interconnected brain state, fostering communication between regions that typically don’t interact. This effect appears to be associated with sustained relief from depressive symptoms, even after just one or two sessions. In fact, research shows that it relieves depressive symptoms in adolescents with MDD after a single therapeutic session (Goodwin et al., 2023). Psilocybin's impact on serotonin pathways, synaptic plasticity, and brain network dynamics provides a promising avenue for the treatment of TRD and a unique outlook on how altering neurochemistry with psilocybin can support recovery and remission in TRD.

Reference articles: 

Goodwin, G. M., Croal, M., Feifel, D., Kelly, J. R., Marwood, L., Mistry, S., O'Keane, V., Peck, S. K., Simmons, H., Sisa, C., Stansfield, S. C., Tsai, J., Williams, S., & Malievskaia, E. (2023). Psilocybin for treatment resistant depression in patients taking a concomitant SSRI medication. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 48(10), 1492–1499. https://doi.org/10.1038/s41386-023-01648-7. 

Carhart-Harris, R. L., Bolstridge, M., Rucker, J., Day, C. M., Erritzoe, D., Kaelen, M., Bloomfield, M., Rickard, J. A., Forbes, B., Feilding, A., Taylor, D., Pilling, S., Curran, V. H., & Nutt, D. J. (2016). Psilocybin with psychological support for treatment-resistant depression: an open-label feasibility study. The lancet. Psychiatry, 3(7), 619–627. https://doi.org/10.1016/S2215-0366(16)30065-7. 

The way you walk affects mood and memory

     It is well known that there is a significant connection between physical activity and depression. However, other studies now show that there is a close relationship between walking patterns and depression such that patients suffering from major depression not only walked slower, but also had smaller arm-swing amplitudes, smaller amplitude of vertical movements of the upper body, larger amplitudes of lateral body sway, and a more slumped posture than healthy controls. Yet, changes in motor and activity levels can have profound effects on emotional information processing. As such, manipulations of the muscular-skeletal system can affect memory and cognitive processes. 

    In a study, researchers manipulated participants’ gait to adopt happy or depressed walking behaviors using the biofeedback method, measuring how many negative and positive words the participants recalled from a previously presented list of items. Participants were randomly assigned to the depressed or happy gait feedback and were asked to walk on the treadmill according to their assigned walking patterns. After walking for four minutes under biofeedback conditions, an experimenter read 40 terms randomly to the participants. While the participants were still walking, they had to recall as many words as possible. The participants were not aware of the main objective of the study and were instead told that the purpose was to determine the ability of people to change their gait patterns in response to real-time feedback.

    As a result, there was a significant difference in the affective memory bias between the happy and depressed groups, such that the happier the person walked, the higher the proportion of positive self-relevant material recalled. By manipulating walking styles and patterns, biased memory towards self-referent negative material changed, thus, changing the central pathological mechanism of Major Depressive Disorder (MDD). As such, in addition to increasing general activity levels, changes in gait patterns can affect the way people process negative and positive material, which can help those suffering from MDD. For this reason, being mindful of the way you walk can improve mood and memory bias recall. Furthermore, other studies have shown that fewer arm swings when walking is associated with a decline in memory and thinking while an unsteady walk can be an early sign of memory problems. Therefore, gait is important to be aware of as it is indicative of health issues relating to memory and cognition.

Daylight Saving Time and Cardiovascular Health: Don't Spring Into a Heart Attack!

 Daylight Saving Time (DST) is often a contentious subject. While we're luckily "falling back" an hour (and hopefully soaking up the extra hour of sleep!), the adverse effects of the bi-annual time change are often commonly shared. In particular, the "spring forward" shift may actually increases the chance of experiencing a myocardium infarction, or heart attack.

In 2018, responding to Finland's EU representation's call for the abolition of DST, researchers at the University of Ferrara in Ferrara, Italy conducted a review on the relationships between DST, circadian rhythms, and cardiovascular health. In this, they found that the available evidence suggests an association between DST and a decent increase in the occurrence of acute myocardial infarction, particularly in the first week after the time change. 

We're all fairly familiar with our individual circadian rhythms (especially after the sleep challenge). However, the physiology of this concept is a little more complex than it just being a 24-hour cycle. Circadian rhythms are driven by the central and peripheral clocks.  Circadian clocks consist of proteins that generate positive and negative transcriptional feedback loops with a free-running period of ~24 hours. The central circadian clock, or master clock, is located within superchiasmatic nucleus (SCN) of the hypothalamus. Peripheral circadian clocks also exist and are often found within most mammalian cells and tissues. Central and peripheral circadian clocks can influence numerous functions, including sleep/rest, either directly or indirectly. The cardiovascular system has biological clocks as well, often found in the cardiomyocytes of the heart, in blood vessels, and in the vascular endothelial cells. The circadian clock within cardiomyocytes directly regulates myocardial metabolic gene expression, most likely in anticipation of the sleep/wake and feeding/fasting cycle. As such, results obtained on murine models show that the circadian clock within the cardiomyocytes allows for the rapid adaptation of the heart to the prolongation of fasting. Thus, a desynchronization of an organism with its environment, through circadian clock derangements, may also contribute to the development of CV diseases.

Commonly, regular disruption of the circadian rhythm cycle can lead to chronic heart disease. Activities such as shift work, a circadian misalignment resulting from a 12-h inversion of the behavioral cycle (including sleep/wake and fasting/feeding cycles), is a typical example of rhythm disruption. Often, shift workers are exposed to a misalignment of their behavioral and environmental cycles, which is a risk factor for hypertension, inflammation, and CV disease. It's been observed that when compared with circadian alignment, circadian misalignment can (a) increase both systolic and diastolic blood pressure (BP); (b) decrease heart rate (HR) during wake periods and increase HR during sleep time; (c) reduce the sleep opportunity-associated dip in BP and HR; (d) affect the 24-h urinary epinephrine and norepinephrine excretion rates; (e) decrease markers of cardiac vagal modulation; (f) increase inflammatory markers, particularly 24-h interleukin-6 (IL-6), 24-h C-reactive protein (CRP), resistin, and tumor necrosis factor (TNF); and (g) decrease plasminogen activator inhibitor-1 (PAI-1) levels. Taken together, all these effects can explain the increased prevalence of CV disease in night workers versus day workers.

By extension, circadian differences in the physiological status of the CV system give rise to rhythmic—and predictable-in-time—variations either in the susceptibility of human beings to morbid and mortal events, or in the ability to precipitate the overt expression of disease. It is known that the occurrence of CV events exhibits varies across the 24 hours of the day. These patterns coincide with the timing variation in the (a) pathophysiological mechanisms that trigger CV events and (b) physiological changes in the body rhythms. A series of factors, though not harmful if considered alone, are capable of triggering unfavorable events when they all occur within the same general temporal window. 

Over the last two to three decades, an evident circadian (morning) rhythm for acute myocardial infarction (AMI) has been understood. It's been estimated that the incidence rate of AMI onset is 40% higher in the morning than throughout the rest of the day, and nearly 28% of morning AMIs (accounting for approximately 9% of all AMIs) are attributable to the morning excess. Moreover, rupture or dissection of aortic aneurysms shows a circadian variation, with an evident morning preference as well. The similarity of these timing patterns of such different acute CV and cerebrovascular events suggests that they share common underlying mechanisms. Several pathophysiologic phenomena, such as increased BP, HR, sympathetic activity, basal vascular tone, vasoconstrictive hormones, increased viscosity, fibrinogen, platelet aggregability, and reduced fibrinolytic activity, exhibit prominent circadian rhythms with phases positively correlated with the timing of excess in CV events. Moreover, the effect of stress on human cardiac, vascular, and hemostatic status appears to be circadian rhythmic, with the effects being greater in the morning. An exaggerated CV response to behavioral challenges has been suggested as a potential factor that enhances the risk of hypertension and CV disease. As such, individuals who exhibit large increases in BP during acute psychological stress are at risk of atherosclerosis, probably secondary to endothelial damage by a BP surge, via increased flow turbulence, and a subsequent release of inflammatory and pro-atherogenic cytokines.

The fact of sleep depravation may also be a factor, as the central master clock is primarily entrained by light, and reduced exposure to light during the day and over exposure to light at night due to artificial lighting may impair the circadian organization of sleep. Changes in sleep architecture during sleep disruption may lead to increased energy intake, reduced energy expenditure, and insulin resistance. Short (< 6 h) sleep has been associated with negative health outcomes including hypertension, diabetes mellitus, obesity, and even mortality. Short sleep, compared with normal sleep, is associated with a significant increase in the relative risk of mortality due to all causes. Moreover, short sleepers have increased rates of obesity (38%), diabetes mellitus (37%), coronary heart disease (26%), and hypertension (17%).

TL;DR - While we're easily soaking up the extra hour of sleep now, come springtime, make sure you're healthily managing your stress levels and taking care of yourself! While the risk increase is slight, it still exists! Keep prioritizing your sleep and maintaining good sleep hygiene, too!

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Source: Manfredini, R., Fabbian, F., Cappadona, R., & Modesti, P. A. (2018). Daylight saving time, circadian rhythms, and cardiovascular health. Internal and emergency medicine, 13(5), 641–646. https://doi.org/10.1007/s11739-018-1900-4