Months after retiring from professional sports Olympic medalist Clara Hughes is publicly fragile in her frank openness about her brush with depression prompting her involvement to reduce the stigma of denying depression within Bell Canada’s, Let’s Talk campaign.
“Sport that consumed me for over two decades . . . is now gone. Now it’s just me. No pressure, no expectations, no need to be fast, good, strong or to even improve. Yet I can’t let go of this idea that I always need to be more than I am. And it is eating me alive”— Clara Hughes, in a January 2013 blog post http://www.thestar.com/authors.scallan_niamh.html Niamh Scallan News reporter
“Life in permanent off-season,” ‘Hughes called it in her poignant January blog post, which chronicled some of the mental and emotional difficulties she’s faced since completing her final race at the 2012 London Games.’ ‘Clara Hughes knew the transition wouldn’t be easy, but little prepared her for life after professional sport.’
‘The majority of her time once consumed by gruelling training regimens, the six-time Olympic medallist in cycling and speed skating found herself struggling late last year — at a time she would usually begin winter training — when she began to realize that her life was no longer geared toward the next big race.’ ‘Having slipped into a depression once before, she decided two years ago to come forward with her own story and speak nationally as part of the Bell Canada Let’s Talk campaign about the need to break down barriers and support mental health programs.’
“I want to eradicate stigma around mental illness in Canada … I hope my story can help,” ‘Launched in 2010, the Let’s Talk campaign is a five-year, multimillion-dollar charitable initiative focused on reducing stigma and supporting both research and mental health-related programs. Last Tuesday, as part of its annual Let’s Talk Day, Bell donated five cents for every text and long-distance call made by Bell customers, as well as any Facebook share of the Let’s Talk image or tweet using the #BellLetsTalk hashtag.’
‘According to Health Canada, one in five Canadians will experience a mental health issue in their lifetime. The Canadian Medical Association, meanwhile, reports that only about half of Canadians would tell a friend or co-worker if they had a family member who struggled with mental health issues.’
‘As someone who once tried to cope alone, Hughes now shares the story of when she began to lose control shortly after the 1996 Olympics. Fixated on her training, she said, she felt isolated and began to gain weight and cry every day. To cope, she threw herself even further into a rigorous training plan that only worsened her mental state.’
“The hole was dug and I was piling the dirt on top of myself,” she said.
‘It wasn’t until a training camp in British Columbia, when Hughes’ doctor mentioned depression, that she reached out for help and began to turn herself around. With the support of professionals, friends and family, she focused on improving her health and went on to win several more Olympic medals before her retirement last summer.’
‘Her professional sports career now over, Hughes said she continues to work daily on keeping herself mentally healthy and wants to encourage others, especially youth, to do the same.’
“The only reason I (shared my story) is to try to help other people,” she said. “I really hope that enough people connect to this so, collectively, we can make this happen … I want to erase stigma.”
Clara Hughes’ star on the Walk of Fame in Toronto represents someone who rewrote the history books of Olympic sport – and not only in Canada. First she captured two bronze medals in cycling at the Atlanta 1996 Olympic Games. Six years later she had switched to speed skating and collected a bronze in 5,000 metres at the 2002 Olympic Winter Games. There, in Salt Lake City, she became just the fourth Olympian to win a medal in the summer and winter Games. Then she entered uncharted waters. At the Torino 2006 Olympic Winter Games, Hughes won gold in 5,000 metres and silver in team pursuit. She was then the world’s only athlete to win multiple medals at a single summer and a single winter Games. But she slipped into a deep depression despite all the Olympic glory. What happens inside Clara Hughes to tear a part the very fabric of her spunkiness, where is depression inside of us ? Where does depression lurk like a sink hole capable of swallowing whole one of the world’s best athletes ?
This essay is dedicated to Clara Hughes to bring out into the open the frailness that we all share. This slippery slope that can bring anyone, I mean anyone into the darkness of depression that can last for years. Where do you start with depression ? You start with the physiology of panic, the stark triggering fear of heights, of loneliness, of rejection, of snakes and the list goes on. Only psychopaths do not have this primal fear, the shattered inner balance of respect for life, of tenderness twisted into distortions of expressed evil. If Clara Hughes were an astronaut reporting from the International Space Station with a wobble in her voice, speaking softly only to her mission controller over a private line, whispering, “I can’t go on.” What do you think would be the reaction back on the ground in Houston? Would it be, “We have to get her out of there,” or maybe “The radiation is getting to her,” but the reaction would not be, “What’s happening to her balance?” What does balance have to do with depression? The previous essay was all about the primary signalling system within the vestibular system capable of engaging the entire brain’s resources with ‘ambient vision.’ Basically Clara Hughes cry for help was from a brain lit up with calculations. Calculations employing everything in her peripheral flow vision where she was out-of-place. Her balance was exquisitely off, yet that sense is never queried. But the very choice of words leads us in that vector, “My life is out of balance.” These are not shallow words, let’s examine what some scientists are saying about depression, analysing the changes that are starting to be reported.
“Depression has significant adverse effects on the course and outcome of coronary heart disease (CHD). Depressed patients are twice as likely as non-depressed patients to have a major cardiac event within 12 months of the diagnosis of coronary artery disease, and they are significantly more likely to die in the years following the diagnosis. Depression also increases the risk of dying after an acute myocardial infarction, an episode of unstable angina, or coronary artery bypass graft surgery. Although some studies have failed to find a relationship between depression and mortality in patients after myocardial infarction (MI), most have found depression to be a significant risk factor for mortality and/or cardiac morbidity. Although the relationship between depression and cardiac events is well established, the mechanisms underlying this relationship remain unclear.
“Dysregulation of the autonomic nervous system (ANS) is one of the most plausible candidates, which is a pivot point of balance between the basic biological response of flight or fight. Such a dynamic shift will reveal a reduced parasympathetic nervous system (PNS) interlinked with an increased sympathetic nervous system (SNS) activity. [ In the human body, the most abundant catecholamines are epinephrine (adrenaline), norepinephrine (noradrenaline) and dopamine, all of which are produced from phenylalanine and tyrosine. Release of these hormones epinephrine and norepinephrine from the adrenal medulla of the adrenal glands is part of the fight-or-flight response.] Such a dynamic parasympathetic versus sympathetic output can lower the threshold for myocardial ischemia, ventricular tachycardia, ventricular fibrillation, and sudden cardiac death in patients with coronary heart disease. Furthermore, coronary artery disease is a chronic inflammatory process that is triggered by injury to the vascular endothelium, and high levels of circulating catecholamines may contribute to recurrent endothelial injury. Elevated catecholamines may also promote pro-coagulant processes by potentiating platelet activation through direct agonist effects, by increasing hemodynamic stress on vascular walls, or by inhibiting vascular eicosanoid synthesis. Both inflammatory and platelet coagulant processes are also associated with depression.” excerpted from Psychosomatic Medicine 67, Supplement 1:S29–S33 (2005) Depression, the Autonomic Nervous System, and Coronary Heart Disease authored by Robert M. Carney, Kenneth E. Freedland and Richard C. Veith In the research article titled: Panic, agoraphobia and vestibular dysfunction Am J Psychiatry April 01, 1996 the authors describe agoraphobia as an anxiety disorder characterized by anxiety in situations where the sufferer perceives the environment as being difficult to escape or get help.
Here in their words, is part of their abstract, ” Otoneurological abnormalities have been reported in panic disorders to which we wish to discern whether vestibular dysfunction was associated with specific symptoms.” Their results are revealing. ” Vestibular abnormalities were common in all the groups, patients with uncomplicated panic disorder (without agoraphobia or with only mild agoraphobia), patients with panic disorder with moderate to severe agoraphobia, patients with anxiety or panic attacks and normal for comparison patients. Vestibular dysfunction was associated with space and motion discomfort and with frequency of vestibular symptoms between, but not during panic attacks. There were no major differences between the two panic groups in anxiety levels during vestibular testing. Exploratory data analysis indicated that the constellation of vestibular tests most specific for agoraphobia was one indicating compensated peripheral vestibular dysfunction.” The authors concluded with, ” Subclinical vestibular dysfunction, as identified by clinical tests, may contribute to the phenomenology of panic disorder, particularly to the development of agoraphobia in panic disorder patients. ”
How do you assess a clinical test for subclinical vestibular dysfunction ? Is this basically a balance test ? Don’t concussed athletes have balance tests to determine the extent of their concussion towards establishing abnormal body sway ? Don’t concussed athletes suffer from depression after their concussions some times for a long time? What is happening here ? Depression is strongly associated with cardiac problems, should Clara Hughes have her cardiac parameters checked ? Are Clara Hughes fractal pattern from her cardiac pacing signals different in their patterns, what is going on here ? Is depression roped into post concussion syndrome, where is the overlap occurring within the brain networks? At this point our medical capacity to both analyze and rationalize patterns vanishes, for the simple reason we do not know how the vestibular balance system integrates into our brain. The dynamic capacity for the vestibular system to shift dynamically compensating its operational strategy is still a distant concept that has not even been modelled let alone derived into predictable analysis. The whole vestibular thing in the human brain is output from a black box.
But (excuse the pun) let’s not get depressed, there are tools to measure individuals who may have their sensitivity to develop panic disorders with or without agoraphobia. Jacob et al. have developed and validated just such a questionnaire, which is the Situational Characteristics Questionnaire (SitQ). The first inkling that vestibular sensibilities might be identified happened over two decades ago in the Journal of Psychopathology and Behavioral Assessment December 1993, Volume 15, Discomfort with space and motion: A possible marker of vestibular dysfunction assessed by the situational characteristic questionnaire by Rolf G. Jacob, Sheila R. Woody, Duncan B. Clark, Scott O. Lilienfeld, Barry E. Hirsch, Gail D. Kucera, Joseph M. Furman, John D. Durran
“Anxiety is highly prevalent in patients with balance disorders. About 30% of patients with vestibular disorders report persistent panic and agoraphobic symptoms or generalized anxiety. The same logic applies in reverse, vestibular dysfunction is common among patients with anxiety disorders. ” While many anxious patients have symptoms of imbalance or dizziness spells they don’t think these types of sensations are important enough on their own to be medically investigated, so they go largely unreported.
Balance symptoms in agoraphobics only rarely include rotational vertigo. Yet in the everyday world these subtle irregularities pass as if unrelated as subtle threading episodes inside familiar locales that suddenly change character within the architecture of their surroundings.
These architectural volumes are termed situationally specific symptoms which include
‘‘supermarket syndrome’’ or “visual vertigo” These subtle situationally specific symptoms have labeled this patterns of situationally specific symptom elicitation as ‘‘space and motion discomfort” (SND). Jacob has devised a specific questionnaire that reveals these subtle immersive situations on the very edge of our awareness the cues of what we pay attention to.
Malcolm Gladwell author of The Tipping Point:How Little Things Make a Difference (2000) has also reported on this peripheral visual relationship with the threatening aspect of how if a public space is well maintained there is less crime committed as a result. If authorities are lazy about removing graffiti with its attendant general brokeness, such disarray becomes a signal to a potential mugger that it is OK to rob people because the architecture is menacing, and there is no surveillance. On the other hand if there are no broken tiles, with diligent regular maintenance, in other words, in efforts to promote organized cleanliness then crime does not increase in that situation. All of these amazing observations panned out within New York’s subway system. Dirty subway stations have more crime than clean subway stations. Yet if you stop commuters in the clean subway station to ask, ‘What do you notice about this station ? ‘ They most likely cannot pinpoint the express differences that order and cleanliness which is surrounding them. This visual perception is part of a general alerting referencing behaviour for evaluating subconscious threats of the type, ‘Is this a safe place?’
“Space and motion discomfort (SMD) refers to the situational specificity of symptoms occurring in some patients with vestibular dysfunction, such as those with balance disorders and some with panic disorder. SMD occurs in situations characterized by inadequate visual or kinesthetic information for normal spatial orientation. We report the results of two studies of the construct validity of the Situational Characteristics Questionnaire (SitQ), which has two subscales, both of which measure SMD: the SMD-I and SMD-II. In Study 1, the SitQ was administered to members of a self-help group for balance disorders, a psychiatric sample consisting of patients with panic disorder, non-panic anxiety disorders, depression, and a sample of normals. SMD levels were the highest in the self-help balance group, next to the highest in the panic groups, and lowest in the remaining groups. In Study 2, the SitQ was administered to otolaryngological patients with vestibular dysfunction and to patients with hearing loss. SMD levels were higher in the vestibular patients. Data on internal consistency, test-retest reliability, and convergent and discriminant validity are presented. The SitQ, particularly the SMD-II, is recommended for quantifying space and motion discomfort in patients with anxiety and/or balance disorder.” This questionnaire evaluates the presence of symptoms such as dizziness, vertigo, and instability under specific conditions. The SitQ comprises two subscales that measure SMD and one subscale for agoraphobia that measures agoraphobia avoidance behaviours.”
“The instrument has two sections. The first section is composed of the SMD-1 and agoraphobia subscales containing 19 and 7 items respectively. Each item consists of two contrasting descriptors of a specific situation or environment. The respondent is required to indicate to what extent the two described situations or environments cause discomfort. Each item includes a ‘criterion’ descriptor for the situation ( ie a descriptor that is presumed to engender SMD) and an alternative (non-criterion) descriptor. The second section comprises the SMD-II scale; this scale is composed of 9 criterion situations, for which the non-criterion situations are not supplied. The questionnaire takes about 20 minutes to complete.”
“Vestibular dysfunction can give rise to situational discomfort, i.e., SMD because three sensory channels (vision, proprioception and vestibular) are involved in balance control. When sensory conflict arises, the postural control system adjusts the sensory integration process toward an appropriate sensory channel or away from the channel providing any misleading information. Normal healthy adults, when exposed to misleading balance information, downgrade the importance in terms of attentional balance weighing of this to upgrade weighing from information from the misleading sensory channels which provide correct information. Patients with vestibular disorders are prone to develop SMD because they become unusually dependent on information from the non-vestibular channels. They become sensitized to misleading information in these channels. For example, a person who is visually dependent due to a shift away from vestibular dysfunction would be expected to experience particularly high levels of ‘height vertigo.’ Visual information is degraded due to the absence of motion parallax and reduction of retinal slip resulting from the long visual distances characteristic of height combined with a lack of a reliable vestibular channel. SMD is observed not only in patients with balance disorders, but also in individuals unable to flexibly adjust the inter-sensory integration e.g. those who are either visually dependent or surface dependent. Some patients with anxiety disorders, particularly those with panic disorder and agoraphobia seem especially prone toward developing SMD.” These authors conclude that a generalized balance abnormality in patients with excessive SMD is dominant rather than a problem limited to sensory integration in situations involving sensory conﬂict.
“Recent basic science studies have suggested a possible neuroanatomical based neurophysiological basis for their study results. They point to anatomical relationships between the vestibular system the (network) circuitry involved in anxiety and panic disorders. This brainstem network includes (1) connections between the locus coeruleus and the lateral vestibular nucleus (2) vestibular inputs to the raphe nuclei (3) serotonergic effects on vestibular processes (4) vestibular–respiratory connections. Also, the nucleus parabrachialis receives vestibular and visceral input and is connected with the limbic system, including the central nucleus of the amygdala The amygdala and other parts of the limbic system are essential for the conditioning of fear responses. Of particular interest is the potential for these various connections to interact specifically with the lateral vestibular nuclei, which are known to have strong projections to the vestibulospinal system.”
The control zone for these structures lies in the oldest part of our brain. Incredibly, the same named vestibular anatomical structures are implicated within the astronauts micro gravity and hyper gravity experiences during their space flights. So what appears to have happened within Clara Hughes during her worst depressive panic attacks was as if her brain was being accelerated then decelerated. So to quote the oft sneering response of reacting to someone with depression, ‘ It’s only in your head,’ as if nothing were really happening. Now think of a female astronaut riding a rocket into space or flying between zones within the International Space Station. In both situations her brain responds to each massive gravity shift along its continuum. Now make the same comment as if the astronaut were only feeling things in her head. Clara Hughes depression was like a gravity hit to her brain, provoking at the strongest apex force at the pinnacle point, tipping over the entire hierarchy of the mammalian brain. Don’t forget, in a previous cerebrovortex essay the observation was expressed that the vestibular system determines the autonomic system output. The oldest mammalian sense, the sense of balance responds to the omnipresent gravity vector to pace the cardiac output. Depression is like a gravity storm affecting the entire brain which can literally knock you off your feet.
In the diagram below of the fiber tracts within the brain we are taught to pay attention to the tract directions in terms of their relevance. These tracts both originate somewhere and travel to somewhere, somewhat like Bell Canada’s telephone early wire network. These tracts are the line connections linking the whole network of circuits. This is a false perception. This image is not revealing within the design of a floating tension network that is assembled using Nature’s rules of balancing tension to compression throughout the continuum of the entire brain volume. The phrase, ‘hard wired’ is also no longer an appropriate phrase to describe the brain. Our brain is a dynamic network within networks capable of rewiring itself within seconds depending on the exigencies of demand. Our brain is a hierarchy of intranets all linked within systems of dynamic interactions that are based on a floating tension sensitive to the direction of a gravity vector orienting each cell to a position in 3-dimensional flexible space. The sensing of gravity is the heritage behind each element of the brain’s structure. Our brains are not ‘hard-wired’ they are a floating tension net interacting in a time volume of communication capacity and delivery. We are only beginning to sense this new universe of communication within each of us involving billions of connections.
In the beginning of this essay I had referenced autonomic dysregulation of the autonomic nervous system as a plausible point of reference within depressive cardiac pacing anomalies. There is such a general bias with the stigma that depression is ‘just in your head,’ the typical response attitude being, ‘It’s not that bad, you’ll get over it, just tough it out.’ The problem with that very superficial response is that there is no basis in the physiology being expressed in the moment by the person experiencing it. The experience is as live as if the event were happening. One of the training methods used by elite athletes is called ‘visualizing.’ Take an Olympic ski-racer or an Olympic luge competitor, standing at the starting gate with eyes closed running the upcoming course in their mind’s eye. The observer watches, fascinated, as their bodies dip to gyrate on the jarring surface chatter flowing at great downhill velocity as if they are on their course run. They are imaging being in the gravity flow pulling their bodies down the course.
They anticipate their body curling in for the approach of a particularly challenging curve that must be taken flat-out in a seamless drift that arcs across the icy terrain. They loosen their entire body as if in temporary flight then BAM they’re back onto the ground in a spray of braking. The entire sequence of their descent is in perfect harmony with the actual experience. If you were to have sensors in their various muscle groups while they sight run their event, the time-line triggering of contracting muscles over the entire course could literally be a traced onto paper. Comparing the real thing with the simulated imaginary run reveals both tracings are exactly identical.
But wait! What is happening here, how is a practice run in the tempo of the mind the same as the real thing you might query? What is it about a mental experience being the same physiological response as if the athlete were actually participating? Our life flow as we experience it, is the same if the intensity is generated imagining it or actually doing it. The experience within the brain’s networks is visually comparable. The simulation can duplicate the real event, our brain is that good. Apple Computer would kill for knowing the inner computer code that accomplishes that task. Imagine playing a hockey game on a simulator that mimics a real hockey game. You come away from your shift out of breath leg muscles aching the blocked puck you received on your ankle making you limp, yet there you are in your pyjamas on a Sunday morning, playing Apple’s latest Immersive Gaming Platform with 3-dimensional goggles perched over your forehead feeling the still residual vibration on the balance platform on your feet. US Navy pilots practicing only on flight simulators can land their jets onto a pitching aircraft carrier landing their aircraft the very first time, because their accumulated simulator flight time is the same as real world experiences. They can also crash their flight simulator without the consequences of plunging into the ocean as they learn to acquire their landing skills without the risk of their death. Mimicking simulation using the vestibular system imprints the brain learning as if the practised experience is real.
Clara Hughes can visualize with that same level of intensity toward perfection, she has Olympic medals to show for her very superior preparation. The loss-the drift-the absolute agony of no longer competing ring true in her revealing blog feelings, “….it was eating me alive.” But what of Clara Hughes heart -what of the pacing within the muscle of the pumping during the anguish of feeling of being eaten alive, what of the beating of Clara Hughes heart, was the depression affecting the pacing behaviour? Let’s investigate further.
If a doctor were to sample a patient in deep depression, what concerns might the doctor think drawing blood from the forearm of such an anxious patient?
“The interpretation of plasma norepinephrine (NE) concentration is complex. When plasma NE is sampled from antecubital venous blood, it reflects local sympathetic activity in the forearm, but it may or may not reflect cardiac or total body sympathetic activity levels. Moreover, high levels of circulating NE could result from increased NE release because of sympathetic hyperactivity, diminished NE clearance, or both. These complexities make it difficult to interpret elevations in plasma or urinary NE in human studies. It is possible to obtain better estimates of systemic sympathetic activity by employing arterialized venous sampling and plasma NE kinetic techniques that rely on dilution of radiolabeled NE and mathematical modeling to provide estimates of postganglionic NE release and NE clearance. Using this approach, Veith et al. demonstrated that the elevated levels of circulating plasma NE in medically healthy patients with major depression are a result of increased total body sympathetic activity. ” Which means in terms of a hierarchical segmentation that is not only a local control event within the forearm but a stronger central command sequence is now being regulated at the very core of the cardiac control networks actively, by dynamically regulating the balance of the sympathetic versus the parasympathetic systems toward running the pacing demands to optimize the profile of performance to the hearts pumping profile. “The resting heart rate has been studied in depressed patients along with measures of catecholamines levels or other markers of autonomic function. Most of these studies have found higher heart rates in depressed patients than in non-depressed controls, consistent with altered cardiac autonomic nervous system (ANS) function. Elevated resting heart rate is a risk factor for sudden cardiac death, even in the general population.” Severely depressed people can literally die from a breaking heart, its called Takotsubo cardiomyopathy, which I have written about in an earlier cerebrovortex essay.
“Higher average heart rate, measured as beats per minute, also increases the risk for progression of atherosclerosis, ventricular arrhythmias, myocardial ischemia, and plaque disruption in acute coronary syndromes in individuals with coronary heart disease (CHD). Mean 24-hour heart rate has been found to be higher in depressed than non-depressed patients with CHD, with differences ranging from 5 to 11 bpm (beats per minute). Depression is associated with exaggerated heart rate responses to physical and psychological stressors in medically well subjects, and it increases cardiovascular reactivity to physical stressors in patients with CHD. In one study, heart rate was measured at rest and during orthostatic challenge in 50 depressed and 39 medically comparable non- depressed patients with CHD. NE did not differ between the depressed patients and the controls, but this may have been a result of a measurement artifact. Resting heart rate did differ between the groups, with a mean of 69.9 bpm +/-10.4 bpm in the depressed and 63.6 bpm +/-10.2 bpm in the nondepressed groups with a significance of (p = 0.005). The changes from supine (lying flat horizontally) heart rate at 2, 5, and 10 minutes after standing were significantly greater in the depressed patients than the nondepressed controls (p = 0.02, 0.004, and 0.02, respectively), with depressed patients having a mean maximum change in heart rate of 11.9 bpm +/-6.8 bpm, compared with 7.9 bpm +/-6.8 bpm among the nondepressed controls. These differences remained significant even after adjusting for covariance. Thus, depressed patients with CHD have higher 24-hour heart rates and higher heart rate responses to physical stressors than non-depressed patients. To our knowledge, heart rate responses to psychological stressors have not yet been studied in depressed patients with CHD. ” There’s that real-versus-simulated anomaly, that stimga reflex response of , “It’s only in your head approach.” How many times has medicine in its insistence that, “No, that can’t be the real answer,” doesn’t match the real physiology of the flow of the physiology. Medicine has revealed this essential flaw since doctors first started their interactions of intervention by practicing, trial and error fashion to seek what works, at the same, trying to understand the bewildering expressions of a patients symptoms before them. Many Nobel prize winners were initially treated as quacks, sometimes for decades, by their colleagues dumfounded by the new real truth, in contrast to their supposed knowledge that the new insight was now challenging. Sadly human nature is unwilling to readily accept the new insight of truths compared to the accepted dogma of understanding, treating the presenting observer as if they were deranged, by ridiculing their exacting observations as totally unfitting, to the way things must work.
“Heart rate variability (HRV) is one of the most widely used methods for measuring cardiac autonomic activity in humans. Beat-to-beat variability in the heart’s rhythm is determined primarily by autonomic system (ANS) modulation of the intrinsic cardiac pacemakers. HRV, then, reflects the balance between the sympathetic and parasympathetic regulatory control of the heartbeat; low HRV suggests excessive cardiac sympathetic modulation, inadequate cardiac parasympathetic modulation, or both. Low HRV also predicts mortality in patients with a recent myocardial infarct (MI) or with stable coronary disease.”
The consensus keeps returning to the hierarchical importance of the central cardiac control zones at the design of the failing heart. We are burdened with the concept that the heart pump within the actual muscle of the heart is failing not being able to squeeze precious life blood around the with the body pulse. Yet, we are not comfortable from a neurocardiology point of reference which is diminished balancing control determining within the failing brain control system that is provoking the dying heart, tracing its decline on the beeping cardiac monitor as the flickering descent of the pacing signal. The heart pump fails because the brain control system fails first. What Clara Hughes is telling us is that an electrocardiogram can help open her diagnosis with depression when she cries out, ” …it’s eating me alive.” is as strong as the flickering electrocardiogram tracing from an injured heart. This is the paradigm shift that a very courageous yet frail Olympic athlete, Clara Hughes has taken upon herself. She is giving us an Olympian’s singular perspective on her broken heart, and her broken heart is real, it’s within the physiology. For Clara Hughes, she has not finished her final race. She has started the greatest race of her life. Her determined efforts will save millions of people. Clara Hughes deserves our very best support, she is a pathfinder to a new understanding toward depression. Depression is all about balance control, depression is about visual peripheral sensation of the flow of vision, depression is about cardiac pacing, depression is about a destabilised internal balance where everything can go off within the autonomic system, the balancing of parasympathetic with sympathetic flow control.
“Many studies have found HRV to be lower in depressed psychiatric patients compared with controls, although some have not. There is more consistent evidence that HRV is lower in depressed than nondepressed patients with stable coronary disease or with a recent history of acute MI. ”
“In the Multicenter Post Infarction Project study, log(n) of very low frequency power 5.2 was associated with a relative risk of 4.7 for cardiac mortality over the 2.5 years after the acute MI. In our study of post-MI patients, 7% of the nondepressed patients and 16% of the depressed patients had very low-frequency power below this value, a difference that was significant even after adjusting for covariates (p =0 .006). Thus, mean 24-hour HRV is low enough in depressed patients with medically stable CHD and after an acute MI to have prognostic significance. ” “Low HRV has consistently been found in studies of de- pressed CHD patients, but in only approximately half of the studies of medically well depressed patients. Furthermore, although several HRV indices are highly predictive of cardiac mortality, the relative contributions of the sympathetic and parasympathetic nervous systems and other physiological processes remain unclear. HRV clearly has the potential to explain much of the effect of depression on cardiac mortality, but more work is needed to delineate the underlying physiological processes.”
Kevin Van Paassen /The Globe and Mail) Heart rate variability (HRV) is the physiological phenomenon of variation in the time interval between heartbeats. It is measured by the variation in the beat-to-beat interval.
Time Domain Analysis are based on the beat-to-beat or NN intervals, which are analysed to give variables such as:
- SDNN, the standard deviation of NN intervals. Often calculated over a 24-hour period. SDANN, the standard deviation of the average NN intervals calculated over short periods, usually 5 minutes. SDANN is therefore a measure of changes in heart rate due to cycles longer than 5 minutes. SDNN reflects all the cyclic components responsible for variability in the period of recording, therefore it represents total variability.
- RMSSD, the square root of the mean squared difference of successive NNs.
- NN50, the number of pairs of successive NNs that differ by more than 50 ms.
- pNN50, the proportion of NN50 divided by total number of NNs.
- NN20, the number of pairs of successive NNs that differ by more than 20 ms.
- pNN20, the proportion of NN20 divided by total number of NNs.
Frequency Domain Analysis Several methods are available. Power spectral density (PSD), using mathematical parametric or nonparametric methods, provides basic information on the power series distribution across frequencies. One of the most commonly used PSD methods is the discrete Fourier transform. Methods for the calculation of PSD may be generally classified as nonparametric and parametric. In most instances, both methods provide comparable results. The advantages of the nonparametric methods are (1) the simplicity of the algorithm used (fast Fourier transform [FFT] in most of the cases) and (2) the high processing speed, while the advantages of parametric methods are (1) smoother spectral components that can be distinguished independent of pre-selected frequency bands, (2) easy postprocessing of the spectrum with an automatic calculation of low- and high-frequency power components with an easy identification of the central frequency of each component, and (3) an accurate estimation of PSD even on a small number of samples on which the signal is supposed to maintain stationarity. (Thank you Wikipedia for some brief explanations of the mathematics of the heart’s tracing interpretations.)
At first glance some of these mathematical treatments can appear daunting to the novice. The heart beat has a complexity aspect to its rhythms that are misleading in a fast taking of a few minutes worth of a electrocardiogram’s tracings. There are all kinds of interesting details that appear as you learn more and more about what is a signal measurement in Nature. The daily rhythms also are influenced depending on the time of day so false interpretations can be of referenced too easily arrived at can be misleading if the underlying mechanisms are not fully brought into the resolution of the pacing of the heart. I do not want to get into more detail for fear of losing the reader, but there are layers of detail that are needed to be taken into account which is the basis from a fractal point of reference how Nature controls things.
“Ventricular tachycardia can be precipitated by cardiac autonomic imbalance, as reflected by lower HRV, and this is the arrhythmia that usually precedes ventricular fibrillation and sudden cardiac death. One study found that depressed patients with stable coronary artery disease and preserved ventricular function had more frequent and longer runs of ventricular tachycardia than medically comparable nondepressed patients. Twenty-three percent of the depressed patients in this study and 3.5% of the nondepressed patients with stable CHD had episodes of ventricular tachycardia (p =0.008). Depression remained a significant predictor of ventricular tachycardia even after controlling for potential confounds (p =0.01). The relative risk for ventricular tachycardia among the depressed patients was 8.2 (95% confidence limits). Research is needed to determine whether the increased prevalence of ventricular tachycardia in depressed patients, especially those with poor left ventricular function, explains the increased risk for sudden cardiac death in these patients. ”
“The QT interval is the electrocardiographic representation of ventricular repolarization time. Variability in the QT interval reflects beat-to-beat fluctuations in myocardial recovery time, and increased variability is a significant predictor of arrhythmic events and sudden cardiac death. Postural challenge and isoproterenol infusion have been shown to increase QT interval variability, which suggests that ventricular repolarization is modulated, at least in part, by the SNS.”
“In the only study to date of depressed cardiac patients, QT variability was found to be significantly higher in the depressed patients than in a group of age-matched and gender- matched nondepressed CHD patients during two of eight sampling periods over 24 hours of ambulatory monitoring. Sudden cardiac death has been shown to have a circadian pattern, with the peak incidence occurring in the early morning hours. The difference in QT variability between depressed and non-depressed patients was greatest during the early morning, just after 6:00 AM. This may reflect a greater increased risk for arrhythmias and sudden death for depressed patients during this normally high-risk time. Thus, depression may increase the risk of mortality after an acute MI by contributing to dysregulation of ventricular repolarization. ”
“A number of studies have examined the effects of various treatments for depression on heart rate and HRV. Tricyclic antidepressants tend to increase heart rate and decrease HRV, presumably because of their anticholinergic side effects, and they are generally not recommended for treatment of depression in patients with heart disease. The selective serotonin reuptake inhibitors appear to have no significant cardio-toxic side effects and are recommended for treating depression in these patients. In a preliminary study among healthy volunteers, short-term sertraline administration suppressed circulating plasma NE appearance, which is compatible with a reduction in total body SNE activity. [Sertraline hydrochloride (trade names Zoloft, Lustral) is an antidepressant of the selective serotonin reuptake inhibitor class (SSRI) class. It was introduced to the market by Pfizer in 1991. Sertraline is primarily used to treat major depressive disorder in adult outpatients as well as obsessive-compulsive, panic ans social anxiety disorders in both adults and children. In 2011, it was the second-most prescribed antidepressant on the U.S. retail market, with 37,208,000 prescriptions.] However, some studies have shown that treatment of depression with selective serotonin reuptake inhibitors improves HRV, while others have found only temporary or no improvements.”
“To our knowledge, there is only one study that assessed whether heart rate or HRV improves following a psychotherapeutic intervention for depression. Fifty patients with stable CHD and comorbid major depression were given as many as 16 sessions of cognitive behavior therapy, a recognized psychotherapeutic treatment for depression. After completing treatment, 90% of the depressed patients were in full or partial remission. The mean 24-hour heart rate dropped 5 bpm in the depressed patients over the course of treatment, compared with less than 1 bpm in a group of non-depressed controls. There was also a significant increase in an index of HRV (rMSSD) that reflects primarily parasympathetic modulation, and a trend (p = 0.07) toward an increase in an index of HRV (SDNNIDX) that reflects a mixture of sympathetic and parasympathetic influences.”
The clinical significance of these changes is difficult to estimate. However, heart rate reduction is one of the best predictors of improved survival in patients receiving beta blockers, in both short-term and long-term intervention trials. Reduction in heart rate and the percent reduction in mortality and nonfatal reinfarction correlated at approximately 0.60 across the major ß-blockers post-MI intervention trials. On average, heart rate decreased by approximately 11 bpm among patients randomized to ß-blockers in the major trials. The mean heart rate of the severely depressed patients receiving the psychotherapeutic intervention decreased by approximately 5 bpm between the pretreatment and post treatment assessments, or nearly half of the reduction that is typically achieved by giving patients beta-blockers. These results, although intriguing, await replication. However, the implications for treating depression and possibly improving cardiac prognosis are clear. More studies are needed to evaluate the effects of depression treatment on cardiac autonomic function, cardiac morbidity, and mortality. ”
“It is not yet certain that altered ANS activity is responsible for the increased risk of mortality and medical morbidity associated with depression in patients with CHD. Nevertheless, there is considerable evidence of autonomic cardiovascular dysregulation in depressed patients. Furthermore, many indicators of cardiovascular autonomic dysregulation, including elevated resting and 24-hour heart rates, increased heart rate responses to physical stressors, reduced HRV and baroreceptor sensitivity, and high variability in ventricular repolarization, have been associated with increased mortality and cardiac morbidity, especially in vulnerable populations such as post-MI patients. More studies are needed to determine whether these factors mediate the increased risk of mortality in depressed patients with CHD, and to identify clinical interventions that can improve them. ”
The purpose of Clara Hughes to reveal her own weakness is bringing huge focus onto the mental health aspect of our flawed interpretation that a psychological request for probing depression is a sign of weakness is simply not appropriate. Even great Olympic athletes can succumb to depression. This years Let’s talk campaign raised $4, 8 million which according to the Globe & Mail, “The high-profile campaign, which capped off a record third year this week, resulted in $4.8-million in donations as a result of Bell’s offer to donate 5 cents for every message that mentioned the program – which included the company’s name.” Bell says it received more than 96 million calls, texts, Facebook shares and tweets in support of the event. Bell – whose parent company BCE Inc. is one of the country’s largest companies with vast telecom and media holdings – thrust itself into conversations across the country for an entire day, all for slightly more than U.S. advertisers ponied up this year for just 30 seconds in the Super Bowl broadcast.” ”
“We picked a cause that builds awareness and credibility around the brand in a very authentic way,” said Mary Deacon, who runs the Bell Let’s Talk mental health initiative. “As somebody who has been involved in mental health for 15 years and had both brothers die by suicide, I can say this is an absolute godsend for mental health services. But it’s also helped people see Bell in a different, more positive light and made them think about giving Bell a second chance.”
“The company initially promised to inject $50-million into mental health services over five years, but because of the success of its Let’s Talk initiatives, it expects it to be closer to $62-million.”
“Some of that money has already been disbursed – Ottawa’s Royal Ottawa Hospital received $1-million for its telepsychiatry and CAMH Foundation in Toronto received $10-million –while the rest will be disbursed over the next two years.”
Depression appears to be at the tipping point of vulnerability within the brain’s entire networks by influencing the very pacing of the heart within the anguish of despair. Clara Hughes is an angel of hope capable of opening our poor depression physiology knowledge toward combating the stigma of depression.