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.

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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. 

References:

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

            http://www.alternative-therapies.com/at/web_pdfs/innes.pdf

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

            Press.

Serwach, Joe (2006). Bitter Truth: Stress Drives Sweet Craving. The University

            Record Online: The Regents of the University of Michigan. Retrieved

            From http://www.ur.umich.edu/0506/Apr17_06/04.shtml

Chronic Stress on Cognitive Functioning

Image by Slowgogostock;
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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.

Reference:

Boals, Adriel & Banks, Jonathan B. (2012): Effects of traumatic stress and perceived

            Stress on everyday cognitive functioning, Cognition & Emotion, 26:7, 1335

            -1343. Doi: http://dx.doi.org/10.1080/02699931.2011.651100.

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

            Press.