It seems like an odd thing to want to know. Why don’t zebras get ulcers? Is there something magical about zebras like unicorns that protect them from ulcers? As it turns out, it’s more than just zebras that don’t get ulcers: most of the animal kingdom doesn’t get them. The reason why they don’t is a combination of factors; the most critical, to the book’s point of view, is stress.
I started seeing pointers to Sapolsky’s work across multiple books. Why Zebras Don’t Get Ulcers and his name kept showing up. How Children Succeed mentioned the book directly and others like Grit mentioned Sapolsky’s work on stress and its impacts. Ultimately, it was The End of Memory and my quest to understand more about Alzheimer’s that pushed me to reading about zebras now.
This review will be broken into three pieces. This component, which covers the importance of the impacts of stress and why we’re different than zebras, is subtitled The Physical Impact of Stress. The next portion of the review will cover The Psychological and Neurological Impacts of Stress. The final part of the review will cover The Causes and Cures for Stress.
Let’s get started with the physical impacts.
Mind Over Matter
The starting point when looking at the relationship between stress and the body is to realize that, though there are physiological processes in operation, they are mediated by three factors. The first factor is our genetics – our equivalent of hardware. That is, genes drive our susceptibility and reactivity to stress. The second factor is our experiences. That is, what stressors we were exposed to in utero and after our birth. Surprisingly, stresses during our gestation can influence our outcomes much later in life. The final factor is how our brain manages stress. In essence, this is our software; how we cope with our situation. These three factors each influence our susceptibility to ulcers and other long-term effects of stress. There’s no one factor that can rule out the others. They work together to determine our risk.
With definitive thinking, we assume that if we have one factor, like genetics, then we must accept the outcome. However, as The Halo Effect points out, we live in a probabilistic, not a deterministic, world. We all roll the dice and hope that we get the outcome we want. We don’t directly influence the outcome. We only influence the factors.
However, in this case, one of the major factors is the software, how we process stress. Many years ago, the Intel Pentium processors had a defect in its floating point division. The Pentium FDIV bug was a hardware problem, but one for which software workarounds were devised and used. Software was being used to work around what was a known hardware problem. In much the same way, our brains have the capacity to mediate the impacts of the biology that drives our stress responses and potentially mediate some of the negative effects.
If you’re a zebra on the plains and you see a lion, you’ve got a short time to get away before becoming lunch. The stress response leads you to “flight or fight”; given your odds against a lion it’s pretty much always flight as a zebra. The body mobilizes all of the energy it can to allow you to run faster. This means shutting down anything that is long-term and consumes resources, and it also means taking the biological equivalent of high-interest payday loans to get glucose (cash) into the system – NOW.
It’s a nice piece of evolution. Keep long-term processes running except for the few times that you need immediate results, and in that case shut everything down that you don’t need and borrow against future needs to make sure you have a future.
Humans Can Simulate
This elegant set of evolutionary programming gets disrupted when you add the primate – and particularly human – ability to simulate events and to plan. Instead of the stress response being activated for the eminent attack from a lion, the response is activated when we aren’t sure how we’ll pay the mortgage next month. On the surface, the extra energy seems like a good thing – and it can be – but as you look deeper you realize that all the enhanced performance while in the stressful state must be paid for at some point in the future.
By activating the stress response when we’re thinking about how we’re going to pay the mortgage, we can focus attention on it and plan a course of action. However, at the same time, we’re potentially over-activating our stress response – particularly if we’re constantly worried about how we’re going to pay the mortgage.
Thus, we as humans subsumed a process designed for short-term improvements in performance and have started to engage it for longer-term stressors. The problem is that at some point the debts accrued while being physiologically stressed must be paid for. These “debts” sometimes cannot be repaid, as they’ve already done permanent damage in some cases and created challenges that will recover only if tended to over the long term.
The chief criminal in the case of human ulcers isn’t stress. The chief criminal is Helicobacter pylori. Despite decades of scientific belief that stress – and stress alone – caused ulcers, it was discovered that a stomach-surviving bacteria called H. pylori was the root cause. This discovery didn’t come easy when the Australian pathologist named Robert Warren wasn’t believed when he made the discovery. It took him literally ingesting H. pylori and showing that he developed ulcers shortly after this to get the scientific community’s attention and eventually acceptance.
To understand the relationship between ulcers and H. pylori, we first should understand that it can survive in the stomach. Despite the acidic environment, it protects itself with a layer of bicarbonate. With its protective armor on it can live relatively peacefully in the stomach. Where things get troublesome for you and I is when our stomach breaks down just a bit and H. pylori decides that the stomach itself is for lunch.
Our stomachs expend massive amounts of energy protecting themselves from the acidic environment that they create. Our stress response does a relatively rapid shutdown of the energy that’s routed for digestion. Sometimes that rapid shutdown can leave the stomach less protected than it should be. When the stress abates for a bit and power is restored to the digestive system, it starts pumping out acid – sometimes before the protective linings have been fully restored. Some of the stomach is killed by the acid and H. pylori starts its attack.
In most cases, H. pylori and the stomach are in a state of homeostasis. There’s enough going on in the stomach to keep the amount of H. pylori in check. In fact, in our bodies, there are numerous bacteria that are kept in check. Our immune system doesn’t attempt to totally eradicate them, nor does it allow them to overwhelm the system. They’re kept in a sense of balance. Our digestive tract needs some of these bacteria to function properly. If our immune system were to kill off everything foreign, it finds it would kill off some of the bacteria that we need to survive. If you don’t believe me check out fecal microbiota transplant.
The problem with H. pylori and the ulcers that it causes aren’t the presence of the bacteria – it’s the fact that the systems are out of homeostasis. The problem is that the stress response caused disruption in the balance and started turning the knobs of the immune system response.
Immune System Response
It’s no secret that when you’re stressed your immune response is lowered – except that isn’t the case. In fact, the immune system sculpts its response differently, both in terms of time and in terms of how it’s going to address invaders. Consistent with the idea that it will take payday loans that will ultimately have a high payback cost, it changes in a way that has the highest probability of short-term success at the expense of long-term success.
To understand the impact on the immune system, it’s important to understand there are three kinds of immune response cells. There are the T-cells, which are killer cells that seek out and kill. These are the ninja assassin of the group for short-term quick response. There are B-cells, which are created in the long-term to address specific kinds of invaders. They are the antibodies. The last type, the NK-cells, address tumors and viral invaders. These cells are called Lymphocytes collectively. (-cyte means cell, so these are lymphatic cells.) Shortly after an immediate threat, the T-cells are activated and are engaged to address the problem. This is the short-term spike in the immune response.
However, after a sustained release of the glucocorticoids (which are the main actor in stress, described in detail in a moment), they will start to kill the lymphocytes. It appears that this first affects the older lymphocytes, which presumably are able to destroy the invader. If the condition causes a stress response then it’s probably important enough to let the newer, younger cells handle the job. So, there are less lymphocytes circulating, but the ones that are left should be those most capable of subduing the threat.
Glucocorticoids also encourage the return of the lymphocytes into the lymph nodes, which are the store houses of the immune system. In other words, there are fewer guards out on patrol in the circulatory system to identify and confront invaders quickly.
It turns out that it’s the glucocorticoids that are the main actor in the endocrine system. They’re what happens when we get stressed.
Most of the time when we’re talking about the fight or flight response, we’re talking about adrenaline. (Adrenaline is the British name; in American terms, we’re speaking of epinephrine.) This is the initial “hit” that we get from our adrenal gland. The adrenal gland is triggered to produce epinephrine (and cortisol) through Adrenocorticotropic hormone (ACTH). ACTH is released from the anterior pituitary gland – which was triggered by the hypothalamus. For something that happens very, very quickly, there is a long chain of things that must happen. However, epinephrine is a fast-acting chemical. It gives a short burst of energy that is backed up by the glucocorticoids.
These are steroids that are important in the regulation of glucose – the sugar that powers our biology. The glucocorticoids are what allows us to sustain a heightened rate over minutes or hours. It’s also the glucocorticoids that leave us with the most lingering effects of stress. Because they linger in the body and they have so many effects across our physiology, they have the greatest potential for long-term damage. The most prominent damage isn’t from ulcers – the most prominent damage is a vascular system problem called atherosclerosis.
Our body’s circulatory system runs through the thousands upon thousands of blood vessels traversing our bodies. These are the streets of our circulatory system, and they’re designed to accommodate the normal blood flow that we need. However, there are numerous things that can impact the flow of blood. Inflammation temporarily reduces the carrying capacity of the blood vessels, while plaque buildup more permanently restricts the flow of blood. As it turns out, glucocorticoids play a role in encouraging the naturally-occurring crud floating in the blood stream to accumulate on the walls of the blood vessels. The result is the plaque that causes circulatory problems.
Circulatory problems can be their own issue by reducing the flow of blood to the body, or triggering the body to respond with higher blood pressures – to get the same volume of blood needed through the blood vessels that are smaller than they’d normally be without the plaque. This increased blood pressure causes additional stress on the blood vessels and on the pump at the heart of the system – the heart.
Heart disease can be caused directly because of atherosclerosis, or indirectly through the development of diabetes.
Diabetes is a disease with two basic types which indicate problems with processing glucose in the blood. The first type is when the cells in the pancreas, which produce insulin, are destroyed by the immune system. The second type of diabetes, which is far more common, is where the body develops a resistance to the insulin that is being produced.
Insulin is critical to the absorption of glucose. If there’s not enough insulin in the body – or if the cells resist its effect – then the cells get less energy, causing the body’s response to increase the glucose level in the blood. By increasing the concentration of glucose in the blood, even a smaller fractional percentage of the absorption feeds the cells adequately. This seems like a very useful adaptation – and it is – except that it creates a secondary set of problems.
Excess glucose in the blood makes it sticky, like honey or maple syrup. Thus, the blood is harder to pump through the blood vessels, and it has more “crud” floating in it. This drives atherosclerosis and directly increases the strain on the heart.
Glucocorticoids’ name comes from the combination of glucose + cortex + steroid. The effect of glucocorticoids over the long term seems to be the development of insulin resistance, which drives the body into increasing the glucose in the blood. However, there’s more to the glucose problem than just the direct effect of the glucocorticoids in the blood: there’s also how it changes our habits.
Dieting is big business. Our natural glucose imperative drives a great deal of our behavior. As an evolutionary mechanism, we are rewarded whenever the brain detects something with high calories. A little shot of dopamine rewards finding the sweet, and therefore sustaining, food. This system works great when food supplies are low and you’re creating a system biased towards finding the least expensive fuel possible. However, in today’s world, most of us are not starving, and don’t need to hunt out sweets – but we still do.
Fighting this urge towards sweetness might be the greatest test of willpower that we’ve ever faced. (See Willpower for more about this fight.) Even folks who have a great deal of willpower in most situations will find that dieting and avoiding sweets will be difficult. One of the times that people struggle with making healthy food choices – as opposed to caloric ones – is when their blood sugar is low. In effect, our prefrontal cortex receives less energy and is partially suppressed – giving the amygdala and hypothalamus nearly uninhibited access to scarf down large quantities of glucose.
The other challenge is something called stress eating – or emotional eating. That is, when we’re emotional – or stressed – we tend to eat more caloric items and in higher quantities than normal – even if we’re not hungry. In short, when we’re stressed, the urge to self-soothe and get little squirts of dopamine is powerful.
Of course, eating more calories than we consume means the body stores those extra calories as fat, and fat further increases insulin resistance.
Heading to the Brain
There are many more impacts of stress on the body, but the next part of the review is about its impact on the brain.