Monday, April 22, 2013

Stress, Sweets, & Syndromes

How stress can drive insulin resistance, metabolic syndrome, & diabetes

We know psychosocial stress can set one at risk for all sorts of disease. To add one more to the list - risk for developing type 2 diabetes has its correlations with the body’s stress response as well, specifically, a chronic stress response.

Individuals living with type-2 diabetes are often warned that stress can acerbate their conditions, putting their health at risk. In humans’ hunting and foraging days, our stress response helped us get out of trouble quick. And by trouble I mean, that hog we just tried to spear and missed is looking pretty angry, charging at our gut with six-inch tusks. Our stress response would be triggered, seconds later releasing more glucose into our bloodstream, to provide our bodies an energy boost to scramble up a tree to safety. We rarely suffer these same problems anymore, but our bodies wouldn’t know the difference.

Photo courtesy of Sidereal
In a diabetic individual (type-2) with insulin resistance, glucose cannot adequately be taken up into storage and accumulates in the bloodstream. You may have already seen the connections; the glucose that gets unpacked and moved into the blood under stressful circumstance can unnecessarily add dangerous amounts to the diabetic’s blood supply. These elevated levels can lead to all sorts of another serious problems then.

But how can stress lead to diabetic, pre-diabetic or dysglycemic conditions?

There is a complex path on the way to
diabetes that stress can lead a primary role in, holding your hand the whole way. It starts with a sugar craving. If you’re anything like me, you – well, first, have quite the sweet tooth to start out with – but also, grab for anything sugary when feeling stressed out.

Many people cope with their stress by overeating or pursuing incentives. So, if your vice has always been sugar, you’re going to crave it when you’re stressed. Our brains release dopamine - that works on the pleasure-pathways (mentioned in my depression post) - at the beginning of a stressful event if there is a high probability of reward at the end of it (Sapolsky, 2004). Additionally, corticotropin-releasing factor (CRF) – experienced by us when we’re under stress – exaggerates cravings for a reward (Serwach, 2006). Humans have had a long and loving relationship with sugar; unsurprisingly, it is definitely reward enough for most of us.

Additionally, our bodies utilize increased levels of cortisol to mobilize glucose into the bloodstream when stressed. This is quickly followed by a rise in insulin levels, re-storing the glucose, to rebalance those circulating glucose levels. This quick rise and subsequent drop in blood sugar can leave us craving another quick form of relief from a quickly-metabolized sugar source.

As I’m sure you are exceedingly aware by now, psychosocial stress throws our bodies into a biological stress response a great many times in our modern era - most often without a physical means of energy expenditure to match. When work has us mentally running rampant and time is not on our side, we may find that a quick snack loaded with sugar holds us over just enough to make it through the day. Our brains employ a large amount of glucose to operate, but do not directly store it itself, so it must have a consistent supply from the blood. Heavy mental work can prompt a craving for sugar; that spike of energy may get the job done. However, continuing this pattern can lead to serious dysglycemic conditions, defined as a imbalance in sugar metabolism and energy production, characterized my abnormal blood glucose levels and associated with related diseases.

If this glucose yo-yoing keeps up a number of conditions can ensue. The first of which is hypoglycemia, literally referring to decreased amounts of glucose in the bloodstream. This is commonly associated with individual with diabetes but can be caused by a number of other reasons, including drug-related side effects and fasting. What we are concerned with here though is hypoglycemia in reaction to eating, specifically refined sugars. After a spike in glucose from a refined sugar, insulin takes effect, moving the glucose out of the bloodstream. In many cases, this results in an abnormally low level in blood sugar. If this effect is frequently occurring, we’ve got a hypoglycemic condition.

Hypoglycemia is often associated with insulin resistance in which beta-cells overproduce insulin and cause hypoglycemic conditions. Though insulin resistance syndrome is thought to involve a variety of genetic, lifestyle and dietary factors, psychosocial stress seems to play an important role in its emergence. Human clinical studies have linked chronic stress to enhanced sympathoadrenal reactivity, which increases fasting levels of glucose, insulin and lipids. Chronic stress has also been connected with a reduction in insulin-like growth factor-1 (IGF-1), the reduction of which is linked to glucose intolerance. Additionally, chronic stress has shown numerously to have a relationship with insulin resistance. The underlying mechanism between psychosocial stress and insulin resistance may include stress-related elevations in proinflammatory cytokines, which have been related to symptoms of depression, anxiety, cognitive impairment and traits such as anger, hostility and aggression which have been touched upon in previous posts. (Innes, Vincent & Taylor, 2007)

Insulin resistance syndrome is sometimes used synonymously with metabolic syndrome, previously known as syndrome x, but this condition actually describes multiple factors beyond just insulin resistance. Both, however, are used as indicators for risk of diabetes mellitus (type-2). Metabolic syndrome involves a group of risk factors for cardiovascular disease and stroke as well, including abdominal/visceral fat deposition, high triglyceride levels, low HDL cholesterol levels, high blood pressure and high blood sugar levels.

And guess what? The body’s stress response, characterized by the activation of the sympathetic nervous system and hormonal release of glucocorticoids, further stress these factors because they are causally linked. Psychosocial stress is significantly correlated with high blood pressure, atherosclerosis, increased levels of circulating cholesterol and triglycerides, increased blood sugar and fat deposition in the abdominal area. 

Innes, K. E., Vincent, H.K., & Taylor, A. G. (2007). Chronic Stress and Insulin            
            Resistance-Related Indices of Cardiovascular Disease Risk, Part 1:
            Neurophysiological Responses and Pathological Sequelae. Alternative
            Therapeutic Health Medicine. 13(4) pp 46-52. Retrieved from
Sapolsky, Robert M. (2004). Why Zebras Don’t Get Ulcers: The Acclaimed Guide to
            Stress, Stress-Related Diseases, and Coping. New York: St. Martin’s Griffin
Serwach, Joe (2006). Bitter Truth: Stress Drives Sweet Craving. The University
            Record Online: The Regents of the University of Michigan. Retrieved

Friday, April 5, 2013

Chronic Stress on Cognitive Functioning

Image by Slowgogostock;

I’m going to take a step back from focusing on the traits of my family to discuss what effects stress can have on our mental capacity. If you’re like me, you have surely had many nights, studying and stressing for hours on end, preparing for a class, a presentation or an exam. But, when the time comes to showcase what you’ve learned, mentally you feel worse off than before you started.

Our lives are inevitably riddled with stressful events that require our optimum alertness and insight to handle. Once again, our biology in that face of chronic stress seems to be more harmful than helpful. Long-term stress can have evitable effects on our cognition and memory in negative ways.

It is helpful to understand a little background information about how our brains allot effort in storing different kinds of memory. There are two important regions in the brain that work in memory storage and retrieval: the cortex and the hippocampus. Without any elaboration, the cortex specializes in storing memories, while the hippocampus places and accesses memories in the cortex.

Memories are stored in patterned displays of excited neurons, called neural networks. This is why all sorts of approximate contextual information, such as a certain smell, can trigger memory recollection. Multiple routes of exciting a certain neural network can extract memory and information.

The cortex and hippocampus make use of a neurotransmitter called glutamate that is critical in creating memory. Glutamate is a uniquely acting neurotransmitter. In glutamatergic synapses, a small amount of glutamate released activates no response. A bit more is released and still nothing happens. It is not until a threshold of glutamate is passed along to the second neuron that an extensive wave of excitation is triggered. This is when we ‘learn’ something. This is when something ‘clicks.’

Once a synapse has experienced a certain number of glutamate-driven excitations, the synapse is strengthened. It becomes persistently more excitable and takes less of a signal the next time to reach that excited state. The strengthened synapse has just been ‘potentiated.’

Time to fit chronic stress back into the picture.

As we move along the stress scale, from no stress, to mild stress, to temporary moderate stress – memory improves. As we continue along to severe and chronic stress, we see a decline in memory. High stress and glucocorticoid levels are certainly the culprits. It could be that these things make for a generally compromised brain altogether, affecting other areas as well, but memory recollection is the most notable.

Interestingly, these conditions seem to more greatly disrupt eliciting prior explicit memory rather than the formation of new memory. Correspondingly however, stress does disrupt what’s called the ‘executive function’ in forming and storing and retrieving new and old memory (Sapolsky, 2004). This concerns what is done with the information, whether it’s organized strategically and how it guides judgments and decisions.

There are several ways that stress evidentially damages the neural networks of the hippocampus. First, the hippocampus neurons do not perform as well. Even in the absence of glucocorticoids, an overactive sympathetic nervous system can disrupt long-term potentiation of the hippocampus; the neurons are not firing as effectively. High and chronic levels of glucocorticoids only elevate the problem.

The hippocampus has two types of receptors for glucocorticoids, one of which is ten times better at accepting the hormone than the other. The low-affinity receptors are only activated by major or long-standing stress, while the high-affinity receptors are activated all the time. These high-affinity receptors enhance potentiation of neural networks; the low-affinity receptors do the opposite. (Sapolsky, 2004)

Second, long-term stress disconnects neural networks. Under prolonged stress and excessive exposure to glucocorticoids, the neural branches – axons and dendrites – begin to atrophy and retract. The good news: it appears that once the stressor is over with these neurons can re-grow or re-strengthen their connections. The memory is still there, you just have to draw from more associative cues to extract it because the neural network is less efficient than before. (Sapolsky, 2004)

Another happy fact: contrary to what you have probably been told, as I was, certain areas in the brain do make new neurons. There are two main areas of the brain that do this - one of them being the hippocampus! And now for the bad news: the third way in which stress detrimentally affects cognition is in inhibiting the creation of new neurons in the hippocampus. Once again the underpinning bullies are glucocorticoids and an overactive sympathetic nervous system. (Sapolsky, 2004)

Fourthly, the neurons in the hippocampus become more susceptible to damage under chronic stress conditions. During a continuous stressor, glucose levels eventually even out to their normal resting levels. As the stressor continues, glucose to the brain is inhibited, specifically to the hippocampus, by about 25 percent less than normal levels due to high glucocorticoids. This would be tolerable for healthy neurons. However, in weak neurons, like those experiencing a severe neurological stressor, the neuron is far liker to just die off. (Sapolsky, 2004)

Moreover, stress can burden cognition simply by allocating more energy to stress-related intrusive thoughts and avoidance behavior, which can furthermore be exacerbated by the perception of stress. In fact, high levels of perceived stress and diagnosed PTSD both equally elicit high occurrences of cognitive failure – meaning forgetfulness and/or lack of attentiveness.  There is much growing research surrounding PTSD and the notion of whether it is the traumatic event or the subjective response to the event that more heavily tips the scale to induce chronic stress and complications with cognition. (Boals & Banks, 2012)

Conclusively, stress isn’t just a pain in your side (sometimes, literally), it’s a pain in your head. We often think of stress as an abstract concept or state of being that comes and goes. In reality, stress is rooted deeply in our biology and can leave its trace (in chronic conditions) even when the stressor has passed.

Boals, Adriel & Banks, Jonathan B. (2012): Effects of traumatic stress and perceived
            Stress on everyday cognitive functioning, Cognition & Emotion, 26:7, 1335
            -1343. Doi:
Sapolsky, Robert M. (2004). Why Zebras Don’t Get Ulcers: The Acclaimed Guide to
            Stress, Stress-Related Diseases, and Coping. New York: St. Martin’s Griffin

Wednesday, March 27, 2013

Family Profile C: A Family Trait - Personality, Temperament & Proneness to Stress

Image provided by Jo Singer;
found at {}

Stress is such a variable experience for each of us. The interpersonal interactions we experience each day out in world can be a pleasant interlude for some of us or evoke a cascade of stress-triggered hormones for others. So what makes one person activate a stress-response and the other maintain without a single jump in heart rate? Are some people more prone to stressors?

The obvious answer is yes, but there is a deeper interplay acting out here. Stress is a curious thing, specifically in how we physiologically react to it. It must be one of the only mechanisms that exchange stimuli between our thoughts and our biology in a certain way that can psych our health out of allostatic balance. What I mean to say is our perception of reality has much to do with our proneness to stress.

The stress-response can be altered or even caused by psychological factors, like a loss of outlets for frustration and social support, a perspective of things worsening, lack of control and lack of predictability. To many extents, certain stressors do not vary in the factors just mentioned. However, we differ in how we psychological perceive stressors in our lives. And some of these filters can create a far more stressful looking world than others. For instance, a depressed person will tend to perceive low control around stressors in their lives and their general state of being. This can cause each new stressor to be perceived as more stressful than necessary with a physiological response to match.

Many times there is a harmful affiliation between how stressful a person sees the world and how stressful it actually is. Your temperament, personality, attitude and perspective can greatly vary your perception of opportunities of control when faced with a stressor. It can alter your view of a situation as having mostly outcomes of good news or bad news. It can also modulate your willingness to take advantage of social support.

There are several ways these factors, unique to each of us, can set a person up for more stressors and a higher risk of stress-related diseases. When there is mismatch between the degree of perceived stress/stress-response and the degree of actual stress, a person may respond either in a hostile manner or an anxious withdrawal. The individual may make matters worse for themselves as well when they do not seek coping methods that are available to them, as in some sort of perceived control or help in the form of social support.

Anxiety disorders are a perfect example of this. They seem to biologically involve the initial response in coping with stress, with high levels or epinephrine and norepinephrine but not glucocorticoids (signaling giving up coping) (Sapolsky, 2004). But most things that give us anxiety are learned. This falls back on our perception of the world. This condition is further instilled with time. The amygdala, that controls anxiety and fear, respond readily to stress and glucocorticoids, creating more synapses and making them more excitable.

There is another quality of personality that has gain popular heights among stress-health fields that make one much more susceptible to certain stress-related diseases. This personality type, and a specific expressions of it, are common in my family so much so that it has developed somewhat of a hackneyed term used to describe it: the ‘Stout trait’ or sometimes the ‘Stout temper.’

This is certainly not to say that each member of my family has the same personality or is dominated by the insinuated characteristics of the Stout trait. But to give you a rough idea of what I’m talking about, let me briefly explain. The Stout trait tends to describe a personality of high energy and a constant sense of urgency, governed by the second hand of the clock. This leads to impatience and multitasking. Stouts exhibit a high work involvement in their undertakings but all as a means to get things finished. They may then tend to not enjoy their accomplishments because they are preoccupied with the next goal to finish. They often are very overachieving in there undertakings that they usually carry out solely. Stouts can be quite competitive. They can many times have a tendency to overreact or anger easily.

This may sound familiar to some of you. It describes one part of an over-generalized dualism is personalities: type A and type B. I have just described type A. This personality type just so happens to predispose individuals to heart disease. In fact, Type A carries as much a cardiac risk as does smoking or high levels of cholesterol. Evidently enough, cardiovascular ailments claim the health of many in my family. 

Although, it isn’t just being type A that predispose someone to cardiac risk though. It is specifically having that time-pressured, hostile tendency that does. Intuitively, a full expression of anger triggers a powerful cardiovascular response. Furthermore, repressing the expression of strong emotions generates an even more intense physiological reaction of the cardiovascular system (Sapolsky, 2004).

Some of the cardiac risk is likely exacerbated in some type A, hostile-prone individuals’ by behavioral factors, in which they’re more likely to smoke, eat poorly or drink excessively. Plus, it makes sense that hostile people lack the social support to cope with stress more than most because they drive people away. Certainly, these other factors are not the sole source of the risk though. Its interesting to know that the type A proneness to stress may be moderated with therapy to reduce the hostility aspect and in so reducing health risks (Sapolsky, 2004).

Supplementary studies have shown that personality and coping behaviors correspond greatly. Among the Big Five personality dimensions - extraversion (E), openness to experience (O), conscientiousness (C), agreeableness (A), and neuroticism (N) – the first four are positively related to coping with interpersonal, anger-eliciting stressful situations. Coping methods that correlate with neuroticism often include disengagement, withdrawal, wishful thinking, and focusing of negative emotions. (Geisler, Wiedig-Allison, & Weber, 2009)

Furthermore, highly functional coping methods towards interpersonal stressors predict a positively perceived personality (Geisler, Wiedig-Allison, & Weber, 2009). This complements the notion stated earlier, that hostile personalities would have a more difficult time dealing with stress because of lack of social support. Other people would not perceive these type A’s as having a positive personality. It makes sense that a hostile-type personality would tend to score lower in openness and agreeableness in relation to this study. This personality type views life as full of ominous stressors that require overly attentive coping methods that necessitate a hostile nature.

So having a higher cardiac risk because of personality is not deterministic, as with many things. Dealing with everyday situations in a hostile manner is. This behavior is learned and can be unlearned. It makes me wonder if the ‘Stout temper’ is exaggerated in members of my family because it is learned as a method of coping with stressful situations. Perhaps the ‘Stout temper’ is prominent among my family not only because of type A personalities but because hostile behavior is learned through dealing with some hostile behavior (hint: the ‘Stout temper’).

Though some of us can experience stress where others do not, our perception and attitude have the largest influence on that. Psychiatric disorders and certain personalities do indeed involve dealing poorly with stress. However, our personality and experiences can prompt us to behavior or view the world in a certain way that alleviate the strenuousness of stress. Those behaviors, perspectives, and coping methods that help one deal successfully or unsuccessfully with stress are learned. So poor coping methods, regardless of personality, can be upgraded to better handle the stress-provoking lifestyles we’re accustom to and create.

Geisler, Fay C. M., Wiedig-Allison, Monika, & Weber, Hannelore (2009). What Coping
            Tells about Personality. European Journal of Personality. 23: 289-306.
            doi: 10.1002/per.709.
Sapolsky, Robert M. (2004). Why Zebras Don’t Get Ulcers: The Acclaimed Guide to
            Stress, Stress-Related Diseases, and Coping. New York: St. Martin’s Griffin

Family Profile B: Stress & Depression

Image provided by Ruth and Dave's photo stream;
found at {}

Depression may be one of the most misperceived of disease; it certainly is approached in many different ways. Take into concentration the variation in neurotransmitters, hormone ratios and genetics in depressive individuals and you might be in accord with the biologist. Deem the cognitive attributes of the depressive, a pessimistic and hopeless attitude about their own skill and life, and you might side with the psychologists. Or, as many undoubtedly wonder if depressed people simply experience the same hum-drumness as the rest of us but simply overindulge in it, you might fall into another perspective category altogether.  

Depression is quite a commonly used word and its clinical meaning can sink into the over-usage of it. Life can deliver upsetting or disappointing events that make us depressed feeling, however this is different than a major depressive state, as it would be diagnosed.  There are in fact parameters that have distinct biological signifiers of depression.

The concentration of this blog is on stress and its effects on health and disease. Depression is a peculiar disease in this case, though powerfully correlated to the stress response, whether causally or consequentially, it is less often viewed in this way. Before, however, I get into that correlation, I’ll reference a bit of the diagnostic factors that distinguish a major depressive state from the absence of one.

What do the symptoms of depression look like?

The foremost distinguishing factor of depression is an inability to feel pleasure. Whether from food, humor, sex, achievement, hobbies or friendships, the feeling towards these things are typically as inert as any unmemorable moment would deliver. The depressed person will often feel nothing. In some cases something, but a negative something - that it doesn’t count, or that the thing or event is undeserved.

In fact, these repercussions compare to what is called vegetative symptoms, in which eating and appetite decline, as well as sleep and sleeping patterns. A depressed individual will typically have no trouble falling asleep, but for short spurts of time and with disturbed sleeping cycles between deep, shallow, and dream sleep states. Similarly, depressed people commonly feature what is called psychomotor retardation, in which the person has to exert immense effort and concentration in the littlest things. The person may speak slower because simply adding to a conversation is arduous. Or they may take twice the amount of time putting on their socks in the morning, because lifting their leg to their hands requires exhaustive amounts of energy.

There are defining parallels between cognitive patterns and depressive states quite naturally. For the majority of non-depressed people, there is a complex array of emotion. Strongly positive emotion and strongly negative emotion are not inversely related; they can be felt simultaneously to different degrees. As in a depressed state, this emotional relationship collapses inversely, often characterized by few positive emotions and many negative emotions, though not felt simultaneously. Depression is also characterized by a distorted view of facts, over- or under- analyzed to the extent that conclusions are drawn that things are awful, getting worse and with a loss of agency to do anything about it.

Family Profile B: Stress and Depression

Before I begin to annotate the stress-depression relationship, let me present Family Profile B, a young adult female family member of mine who has experience depression for much of her life adolescent and adult years. She does not believe in taking medication for her depression. Her symptoms seem to come and go regularly in waves. ‘B’ would describe herself as being prone to depression because she stresses easily. To cushion this proneness she finds, eating well, exercising, thinking positively and working incessantly on stress-management benefits her the most.

She also considers this proneness due to hereditary, because she handles stress similarly to the rest of the family. She has always been a very emotionally responsive person, which ‘B’ believes has to do with initiating depressive moods. Similarly, she finds herself sometimes wallowing in despairing thoughts – about her abilities, about her emotions, about her relationships, about her prospects. She explains that she is an overly analytical person as well, basically picking herself apart and arriving at negative conclusions.

‘B’ describes that she experiences physical symptoms often times. She fits well into the depressed-person’s sleeping patterns: falling asleep quick, waking up often and tired. Many times she feels general muscle achiness all over. This may be related to psychomotor retardation, which she agrees that she experiences exhaustiveness in small, easy tasks. She explains how she is always hungry but never for anything in particular. And food does not taste that good when she is eating. This corresponds with a lack of feeling pleasure in any and everything that is characteristic of depressive people.

In describing the stress-depression correlation, she agrees that this is accurately fits her general idea of her depression. ‘B’ even says, quite understandably, that her depressive symptoms seem to spiral out of control when she is stressed. She even explains that high-strung, jittery yet exhausted feeling inside, as she says, it’s like “too much energy and no outlet.”

What causes depression?

You likely have heard that depression is related to imbalances in neurotransmitters – the most probable focus being on dopamine, norepinephrine, and serotonin. These imbalances are not easily understood. Basically, these neurotransmitters have been held responsible because drugs that increase the level of signaling by these neurotransmitters seem to assist in treating depression. Though surely, other neurotransmitters and factors are at work here.

There are two theories involved here in how drugs treat depression. The first states that its too high levels of neurotransmitters, which generate depressive symptoms. So when these drugs, that increase these levels of neurotransmitters, are given, one would think the depressive symptoms would increase. And they do, at first. After a certain amount of time, the receptor cells to these neurotransmitters decrease, or down-regulate, decreasing excessive signaling and balance the recognized levels. And the person feels better. (Sapolsky, 2004)

The second theory states that its really too little neurotransmitters communicating between neuron A and neuron B. Not only does neuron B have receptor sites for neurotransmitters, but neuron A has them as well as a means of regulating the amount of neurotransmitters it releases. If it recognizes too much, it will produce less. If it recognizes too many, it will produce more. But what happens when neuron A decrease or down-regulates its receptor sites or autoreceptors? It would recognize too low amounts of neurotransmitters released and accordingly, release more. (Sapolsky, 2004)

Though the problem gets increasingly more complicated. If neuron A starts synthesizing more amounts of neurotransmitters, then neuron B may down-regulate its receptor sites. We’re now back close to the first theory.

Why do these neurotransmitters cause depression?

It helps to know what function these neurotransmitters help to regulate. Serotonin is thought to relate to incessant ideation in depression, the looped thought patterns of failure, doom and despair. Norepinephrine plays a role in alerting other areas of the brain – activating them or lowering their threshold for response. This is thought to perhaps explain how psychomotor retardation in depressed people makes small daily tasks exhaustive. Dopamine is related to the ‘pleasure pathway.’ Robert Sapolsky sums up this stimulate pathway quite well:

“Something along the lines of “Aaaaah, boy, that feels good. It’s kind of like getting your back rubbed but also sort of like sex or playing in the backyard in the leaves when you’re a kid and Mom calling you in for hot chocolate and then you get into your pajamas with the feet…”” (Sapolsky, 2004)

Of course the complication with treating depression arises since there are many other factors that can contribute to it. Things like the body inducing a stress response over a sad abstract thought (Sapolsky, 2004). Genetics are also heavily at play in the manifestation of depression. However, genetics rarely destine the health of an individual, it depends on the environment in how they are expressed. Certain hormones often go hand in hand with depression.

Perhaps most interestingly, depression and stress are closely linked. In some instances, people who are prone to depression experience stressors at a higher rate. On the other hand, people who are enduring many stressors are more likely to give way to depressive states.

It is common to find elevated levels of glucocorticoid (one of those stress hormones) in depressed individuals (Sapolsky, 2004). Often, people with depression are viewed as lethargic, mopey and perhaps even lazy. In fact, it is more accurate to see them as high-strung, strenuous, alert and on edge, but all internally. This creates a dynamic and overwhelming battle within a person where they feel exhausted and drained with every little task but at the same time, overflowing with panicky apprehension.

So what does the stress-depression relationship look like?

Typically, clinically depressed people have abnormal levels of glucocorticoids, whether abnormally low or high. It is more often the case that these levels are too high, coupling an overactive stress-response and an overactive sympathetic nervous system. That ‘jittery yet exhausted’ feeling fits like a glove over the chronic stress-response profile. These elevated levels of glucocorticoid found in depressives appear to arise from too much of a stress signaling in the brain.

The brain is less effective at shutting off the glucocorticoid-secreting stress response, activated by the sympathetic nervous system. Glucocorticoids have a strong influence of those neurotransmitters described earlier – serotonin, norepinephrine, and dopamine – namely in the amount of each synthesized, how fast they are broken down, how many receptors there are for the neurotransmitters and how well the receptors work. It is easy to see, in this case, how chronically high levels of glucocorticoid in a depressed person’s system would throw this delicate chemical balance off.

A sustained stress response depletes dopamine from that ‘pleasure pathway’ and norepinephrine from alerting other areas of the brain. Furthermore, stress modifies all sorts of areas of synthesis, release, efficacy and recycling of serotonin. Sustained high levels of glucocorticoids can alter manifold of other mechanisms in the body, but specifically in relation to depression, it has been found to damage the hippocampus, which deals with, among other things, memory – specifically, declarative memory. The frontal cortex of the brain seems to be markedly sensitive to glucocorticoids as well. Decreased volume of the frontal cortex and the hippocampus is commonly found in depressed individuals and may have a detrimental correlation with glucocorticoids. (Sapolsky, 2004)

All of these aspects and more make depression so sufferable and tricky to climb out of. This is why it is all to commonly heard of that depression reaches a vicious cyclical nature in which individuals will continually fall back into depression soon after relief of it. Similarly, being in a depression is enormously stressful in and of itself, stimulating more glucocorticoid secretion and deepening that chaotic cycle.

On a lighter note though, it may be hopeful to consider that depression can often be triggered by stress and not just a mysterious imbalance in brain chemicals. Although this imbalance ensues with the stress response, it may be easier and less detrimental to practice better methods of stress-management rather than find the right antidepressant that best represents your body’s optimal levels of neurotransmitters.

Sapolsky, Robert M. (2004). Why Zebras Don’t Get Ulcers: The Acclaimed Guide to
            Stress, Stress-Related Diseases, and Coping. New York: St. Martin’s Griffin

Monday, March 18, 2013

Family Profile A: Stress & Cardiovascular Health

Also see my Family Profile project mission statement to get some background info.

Image by Daniel Newcombe; found
at {}

In my last year of high school, I got a call late one night. It was concerning family member ‘A’ – she had just had a heart attack. Before I go any further, she made it through fine. It was a mild heart attack as far as heart attacks go. I was and am still very close to this woman, so I know her habits and lifestyle well. She has the ‘Stout temper’ personality that seemingly no Stout can escape without.

However, what is peculiar about her case is that she lives a very health-conscious lifestyle. Let me elaborate. ‘A’ has always had a more balanced diet on her off days than I average at my best. Her meals typically consist of ample vegetables and some sort of animal protein. Her diet is not unusually high in lipid or carbohydrate content. And, because of her naturally healthy appetite, she does not diet, so it stays very consistent. She takes vitamins every morning and even does regular cleanses that include a nearly all-vegetable diet and extra amounts of water. She is in tune enough with her body to know when it is stressed whether by nutritional, physical or psychological means. She exercises regularly (nearly daily), usually with balanced cardio and weight lifting. She has used exercise as a method of stress-management for most of her life.

‘A’ was fifty-two when she had the heart attack. Her diet and exercise routines had not changed. She was at a very healthy weight, most likely around 125 - 135 pounds at five feet four inches. She had a well-providing, stable job. There was only one thing that was different at this point in ‘A’s’ life; she was right in the middle of a divorce that was ending an 18 year marriage, with three children.  

As you might assume, the doctors could not find a clear cause of the heart attack. She was perfectly healthy. The best explanation they could give was an irregular heartbeat. They kept her an extra day just to run tests because they could not come up with a positive causal problem that had triggered the attack. ‘A’ had a pretty good idea though. She was psychologically overwhelmed with the burden of the divorce and her concern with her kids. She even suggested it to the doctors herself – “it was stress.”

So how does stress physiologically strain the cardiovascular system so much that it can give a perfectly healthy individual a heart attack?

The obvious answer? – Stress. Though, it is far more complicated than that. From an evolutionary perspective, the stress response of our cardiovascular system is ideal. Say you are living 100,000 years ago. You and couple of your tribal peers go out hunting for a boar. You find one, have it in sight. You begin strategizing your method to catch it. But something unplanned happens – the boar starts charging you! Stress response activated: your digestive tract shuts down and your breathing rate surges. Your body inhibits the release of sex hormones, while others like epinephrine (adrenaline), norepinephrine and glucocorticoids spill into your bloodstream, activating the sympathetic nervous system. Heart rate increase to pump oxygen quicker throughout the body, glucose energy reserves are released, attention and response centers in the brain are heightened, and blood flow to skeletal muscles are top priority. With all this in place, you have a pretty good chance of escaping that charging boar intact.

This heightened blood flow is well and great when we have the metabolic demand to match. However, like family member ‘A’, if these physiologic responses are chronic, you are continually diverting as much blood flow to your limbs, straining the heart and overlooking other areas of the body. This is when we see damaging effects.

The cardiovascular system was just not made to take the continual beating that the stress-induced rise in blood pressure generates. So the first condition in developing stress-related heart disease is hypertension. The problem becomes more tricky and engrained when high blood pressure occurs more often. This causes the capillaries (the small ends of the arteries before they branch back together to form veins), which regulate blood pressure as a means to optimize the amount of oxygen and nutrients to local sites, to build up thick layers of muscle to control this blood flow. Consequently, this thicker muscle makes the vessels more rigid and actually increases hypertension. At a certain point, it will increase so much that chronic hypertension has developed.

This is not great for the heart either as blood is returning to the heart with greater force. And as a means for the heart to resist and control this thrashing, it builds up its muscle mass as well. However, it is just the left ventricle bearing the brunt of this force and so is the quadrant to develop the most muscle. This condition is called “left ventricular hypertrophy” and causes the mass of the heart to become lopsided. This in turn increases the risk of an irregular heartbeat, increasing cardiovascular risk. 

A blood vessel with atherosclerotic plaque.
Image by The Other Side of Life; found at
Hypertension has its damaging effect on the blood vessels as well. As the blood whips faster through the vessels, the branching points suffer much of the force, creating weak spots in the smooth muscular lining. Eventually, that lining tears and craters begin to form. This injury initiates an inflammatory response to heal the tears. Cells from the immune system and foam cells full of fatty nutrients collect there to restore the vessel lining. However, the hormones involved in the stress response make the blood more viscous by increasing blood platelets (which help the blood clot with injury) likelihood of sticking together. What’s more hazardous is that those stress hormones increase the levels of fat, glucose and cholesterol circulating in the bloodstream. All sorts of things can then amass at this weak place in the vessel wall. At this point, we’ve got atherosclerotic plaque formation.

And if this plaque is dislodged and starts freely moving through the bloodstream (as a thrombus), it has a chance of getting caught in some narrower blood vessel causing all sorts of serious problems. As with ‘A’, something to this effect may have happened with the thrombus blocking a coronary artery and causing a myocardial infarct, a heart attack. If the same thing happens to the arteries leading to the heart, one can develop coronary heart disease, myocardial ischemia and more awful health risks. Block up a blood vessel leading to the brain, and a brain infarct ensues, a stroke. Comparatively, this actually happened twice to ‘A’s’ father, eventually getting the best of him.

These conditions simply accumulate upon each other, making any additional stressor that much more detrimental. Under stressful conditions, the sympathetic system is activated. The sympathetic system and parasympathetic system have an inverse relationship. So if you’re chronically stressed, then the sympathetic nervous system is chronically active and the parasympathetic nervous system is chronically inactive. Under these circumstances, it becomes harder and harder to switch on the parasympathetic nervous system to diminish the stress response. So in some cases, the stress response itself ensures that it continues.

What is interesting is that strong emotions increase cardiac vulnerability, which is worsened under stressful conditions. A strong, adverse emotion, like anger, doubles the risk of a heart attack during the succeeding time period (Sapolsky, 2004). Actual causes are tough to study since you can’t predict when a traumatizing event is going to happen to someone and interview them to find out how they were feeling before and afterwards.

In one instance, however, a physician collected newspaper clippings of sudden cardiac death in individuals. He found a correlation between certain events associated with the deaths, including: the collapse, death or threat of loss of a loved one, acute grief, loss of status or self-esteem, mourning, personal danger, threat of injury, and extreme joy (Sapolsky, 2004). Cardiologists seem to agree that sudden cardiac death is an extreme instance of acute stress causing ventricular arrhythmia or ventricular fibrillation.

With relation to my family member - ‘A’, she was certainly emotionally distressed and chronically stressed. Years of feeling upset, angry, guilty and defeated certainly fueled the fire that stress was raging.  So, as ‘A’s’ case exemplifies, even with a low-fat diet and plenty of exercise, the repercussions of chronic stress can stack up against ones health. All things considered however, it could have been plenty worse. Add in the high-fat diet and sedentism that many post-industrial people call life, and ‘A’s’ heart attack could have been life threatening.

Sapolsky, Robert M. (2004). Why Zebras Don’t Get Ulcers: The Acclaimed Guide to
            Stress, Stress-Related Diseases, and Coping. New York: St. Martin’s Griffin

Family Profile Project: Mission Statement

Image by Delsomething's photostream;
found at {

I’m taking on a project concerning a subject that has long pulled at my curiosity so consistently that, in the end, I have no choice but to explore its implications and causes. The subject is stress, particularly stress as it manifests out of the gene pool of my family.

It has always been clear, not only to me and other family members, but many family acquaintances as well, that the Stout family temperament and personality is quite peculiar. It took my whole childhood growing up, hearing of the ‘Stout temper’ and then experiencing it first hand, to understand how biologically engrained this characteristic is to nearly every Stout. Though I have many individual instances that exemplify the ‘Stout temper’ perfectly, I will not, out of respect for my family, get into that. That is a story unto itself and essentially is not necessary to what I’m trying to accomplish here.

This subject is really quite personal for me, for in embarking on this project it is necessary to divulge not just some personal information concerning myself and Stout members (anonymously of course) but the ways in which the nature of the beast (stress) is essentially tied to these individuals in emotional, cognitive and self-identifying ways.

For these reasons, I will not reveal any actual names or relational ties to myself of the individuals used. My motivation behind this project is to better understand my own biology through studying my family’s, to understand how stress’s effects are genetically, environmentally and temperamentally variable, and to find viable methods of coping with stress effectively when it is unavoidable in our environment.

I hope also that this information is found useful to others. Stress is unavoidable to everyone and intensified in our modern environments. It is a silent killer and its tracks are often brushed off on genetic or behavioral conditions. Though, these have a heavy influence on how stress effects each of us, we are also in full control of managing stress in a healthy way.

I am in school right now, on track to becoming a DO. Though I am just in the midst of my undergraduate, I have a lot of passion in understanding health and disease. I have long been an advocate for healthy lifestyle changes as a way to support a healthy well-being. So, as a way to build my repertoire of understanding how health is a manifestation of many factors - genetic, behavioral, environmental, cognitive and emotional – this will formulate a foundational perspective to build new information on top of. Similarly, in beginning to talk to family members, whom I am close to, about health, stress and lifestyle changes, I am building communicative skills that will be crucial down the road.

I do hope you find this project interesting and hopefully enlightening.

Thank you for reading. 

Friday, March 15, 2013

Just Breathe: The stress-relieving effects of Sudarshan Kriya Yogic Breathing

The feeling is the same for all of us - whether you recognize the symptoms as your hands shake at the start of a speech or when you lay painfully awake thinking about tomorrow’s exam trying to sleep. We all recognize the symptoms of stress, but few understand the bodies underlying mechanisms in dealing with it. Just under the surface of our anxiety is an elaborate and delicate system working itself out.

Stress has its benefits. Its evolutionary roots were selected to keep our ancestors alive. While the stress humans experience today is less severe than what our ancestors put up with, it can still enact equally as taxing a response to our bodies. Perhaps even more so. The same nerve and chemical stimulation that a forager would have escaping for their life, we enable stuck in traffic, late for work.

It seems fairly safe to assume that people today experience less life-threatening, but far more psychosocial stress. So what happens when we’re so continually stressed out our bodies can’t jump our of ‘adrenalate’ mode (commonly expressed as ‘fight or flight’)? Stress easily reaches chronic levels that have harmful, deleterious consequences, ranging anywhere between fatigue and muscle loss to heart disease and diabetes.

But before that sentences alone stresses you out, let me present the good news. Slow breathing techniques, characteristic of yogic breathing, can physiologically reverse the effects of stress by activating the Parasympathetic Nervous System (PNS), also known as the ‘vegetative’ or ‘rest and rebuild’ state. So while stress can have serious consequences to your health, you may be happy to hear you have the final say in managing it.

Before I jump into the findings of Brown and Gerbarg, documenting the effects of Sudarshan Kriya yoga, let me brush up on a bit of biology. The malaffects found caused by chronic stress are hormonal in nature, though it all leads back to what is triggered by our nervous system, through its voluntary and involuntary aspects.

There are two major divisions of the involuntary/autonomic side of that system: the Sympathetic Nervous system (SNS) or ‘fight or flight’ overdrive mode, and the Parasympathetic Nervous system (PNS) or the ‘rest and rebuild’ healing mode. Ideally these two factions have a give and take relationship, trading off the workload when environment is appropriate for one over the other. So as parasympathetic tone goes up, sympathetic tone goes down.

However, its possible for one to try to trump the other for mechanistic control. This can be most damaging when it’s the SNS fighting for attention. And I do mean fighting. The tendency of the SNS is to allocate all possible sources of energy to maximize motor use, leaving less for maintenance and functioning. This means, the SNS is not utilizing energy to repair tissues (i.e. muscle, brain, ect.), metabolize nutrients or fortify the immune system. It is meant to activate quickly and end quickly.

Image by lilycafe3's photostream; found
at {}
However, it is not uncommon in our modern lives to let psychosocial stress take the wheel and control the allocation of energy resources. This can exacerbate pre-conditions and lead to many diseases and illnesses, among them: depression, chronic pain, heart diseases and disorders, immunity disorders, impaired cognition, pre-aging, diabetes and more. Luckily, Brown and Gerbarg have proposed a viable alternative to letting stress run your life (2005).

The best part is, this technique can be used by anyone, anywhere and, aside from learning the technicalities involved in the practice, all you have to do is breathe! For 8,000+ years the yogic masters have claimed that the art of yoga is an exercise in strengthening the connection between the mind and the body. Science is finding more and new ways that our mind affects our brain, which affects our whole body and well-being and visa versa. Many of these pathways are related to the stress-response.

Brown and Gerbarg measured the neurophysiological changes in the body when using mind-body interventions, outlined by Sudarshan Kriya yoga (SKY) techniques, including different rates of breathing, breath-holding, posture, air resistance upon others (2005). If you’re interested, these breathing methods are more detailed and/or efficiently taught by instructors at the Art of Living academy; a link to their site can be found here.

The study focused on stimulation of the autonomic nervous system functions, measured by heart rate variability, cardiac vagal tone, chemoreflex sensitivity (O2 and CO2 levels in blood), baroreflex (blood pressure), and central nervous system excitation (Brown & Gerbarg, 2005). Recent research has even focused on cardiac vagal tone (the PNS is primarily associated with the vagus nerve) as a marker of emotional regulation, psychologic adaptation, emotional reactivity/expression, and empathic response and attachment (Brown & Gerbarg, 2005).

First off, the relationship between breathing and emotion are bidirectional. Breathing is one of the few bodily mechanics under both voluntary and involuntary control through complex feedback mechanisms involving autonomic visceral networks, parts of the brain stem, limbic system, cortical areas and the neuroendocrine system. Breathing that is highly connected to the autonomic nervous system is also highly influential on emotion and mood (Brown & Gerbarg, 2005).

Sudarshan Kriya yoga involves four different components in breathing techniques. Again, if you wish to know more, visit there website to get a more detailed account of the techniques. I’ll refrain from describing them since I’m not a qualified instructor and many nuances are involved that is best explained in person and through practice.

Slow yogic breathing decreases chemoreflex sensitivity (mediated by the vagus nerve), improves cardiovascular and respiratory function and increases arterial baroreflex sensitivity (Brown & Gerbarg, 2005). In other words, this slow breathing decreases the involuntary respiratory responses to small changes in O2 and CO2 levels in the blood, improves circulation and breathing function and increases the vascular system’s sensitivity to changes in blood pressure.

Reducing the chemoreflex sensitivity allows the body to tolerate higher levels of carbon dioxide (which is generated during exercise). In fact, the chemoreflex sensitive affects of yogic breathing practices mimic those found in elite athletes, specifically in that the body is able to sustain higher levels of carbon dioxide, while better utilizing oxygen levels.

Adaptation of pulmonary stretch receptors to deep breathing and chemoreceptors to chronic high levels of carbon dioxide retention increases vagal nerve stimulation to the brain causing physically and emotionally calm effects (Brown & Gerbarg, 2005). And continued yogic breathing practice decreases heart rate, increases vagal tone and increases aerobic capacity, all of which are influenced more so by introducing yogic postures and poses (Brown & Gerbarg, 2005).

Resistant or pressure breathing which is a component of SKY, caused by a slight contraction of the laryngeal muscles, stimulates the somatosensory vagal afferent nerves leading to the brain, increasing vagal tone, in so increasing the PNS (Brown & Gerbarg, 2005). Furthermore, regular slow breathing normalizes baroreflex sensitivity, which is compromised with aging, cardiac disease and hypertension, all of which are exacerbated and even caused by stress (Brown & Gerbarg, 2005). Slow yogic breathing not only lessens the response to stress – it actually reverses it!

The SNS and PNS are constantly dispatching signals to the body with every breath. Normal heart rate increases during inspiration and decreases during expiration. This interplay, however, is influenced by sympathetic and vagal/parasympathetic input and by respiratory rate and volume (Brown & Gerbarg, 2005). Simply enough, exercising the vagal/parasympathetic tone improves (often by decreasing) normal heart rate.

Furthermore, as polyvagal theory purposes, vagal activity is linked to attention, emotion and communication (Brown & Gerbarg, 2005). Slow yoga breathing, stimulating the PNS along with its varied effects mentioned previously, activates the hypothalamic vigilance area and induces a calm but alert state, recharges energy reserves and prepares the body for future stressors. This is the natural state of the nervous system experienced by our evolutionary ancestors – calm, alert and maintained during the majority of experience and heightened by stress to maximum energy output when occasionally needed.

This slow and deep yoga breathing can mechanistically switch off the Sympathetic Nervous system and shift to the Parasympathetic Nervous system via vagal stimulation from vagal somatosensory afferents in the glottis, pharynx, lungs and abdomen (Brown & Gerbarg, 2005). Even without long-term practice, these techniques have shown to improve all the areas mentioned previously and only grow stronger with time.

Often when telling the brain what to do - like “go to sleep” –  enacts the opposite response. So in times of stress, when your mental capacities aren’t doing you anymore good, but you simply find it impossible to escape your thoughts, just breathe…

Brown, R. P. &, Gerbarg, P. L. (2005). Sudarshan Kriya Yogic Breathing in the Treatment
            of Stress, Anxiety, and Depression: Part I—Neurophysiologic Model. The
            Journal of Alternative and Complementary Medicine, 11(2), 189- 201.