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Health & Fitness

How Does Stress Make Us ill?

Before we get stuck in, though, let’s just remind ourselves of the evidence that stress, particularly chronic stress, does make us ill.  Many people, particularly people with no interest in reading about this kind of thing, often write off stress as “all in the mind” but it’s not as simple as that.

The evidence that stress makes us ill

There is plenty of evidence to suggest that people who suffer from chronic stress have been shown to be more likely to:

Develop an episode of clinical depression, Monroe and Hadjiyannakis, The Social Environment and Depression: Focusing on Severe Life Stress, in Gotlib and Hammen, Handbook of Depression, 2002

Experience symptoms of upper respiratory infections following viral exposure, Miller and Cohen, Infectious Disease and Psychoneuroimmunology, in Vedhara and Irwin, Human Psychoneuroimmunology, 2005

Suffer from allergic reactions or autoimmune conditions, Wright, Rodriquez and Cohen, Review of psychosocial stress and asthma: an integrated biopsychosocial approach, Thorax, 1998

Show accelerated progress of chronic diseases, including AIDS, Pereira and Penedo, Psychoneuroimmunology and chronic viral infection: HIV infection, in Vedhara and Irwin, Human Psychoneuroimmunology, 2005

Suffer increased risk of cardiovascular disease, Rozanski, Blumenthal and Kaplan, Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy, Circulation, 1999

And this effect is very substantial, it is not a slightly worse effect.  In some cases, exposure to chronic stress triples or quadruples the chances of adverse medical conditions.

Is that really true?

Come one, surely these are just a few studies that you’ve picked out carefully to present your case?

No actually, in Psychological Stress and the Human Immune System: A Meta-Analytic Study of 30 Years of Inquiry, by Suzanne Segerstrom and Gregory Miller, Psychological Bulletin, 2004, the authors note that by 2004 there had been over 300 studies done over a 30 year period that demonstrated that stress causes an immune response in humans (i.e. not counting animal studies).

That’s a lot more evidence to suggest stress makes you ill than there is for idea that saturated fat causes heart disease…

Stress makes you sick.  Sicker than eating hamburgers all the time, in fact.  Case closed, my lord.

So how does stress make us ill?

Well, there are a number of different ways in which stress makes us ill, some of which have been more well-studied than others.  In my reading, I have uncovered the following different pathways but there may be more:

Cardiovascular disease – in the case of cardiovascular disease, stress causes hypertension, which is a key cause of heart disease.  Malcolm Kendrick discusses this at the end of his book, The Great Cholesterol Con.

Metabolic syndrome – if you read most stress researchers, they will talk about the curious effect of how stress seems to raise appetite.  However, if you consider the basic effects of the fight-or-flight response, you’ll see that this mechanism causes a massive release of glucose into the bloodstream, which to my simple mind provides an obvious pathway to diabetes.  I’ll talk more about this mechanism next week.

Impaired immunity – this is the interesting one, which gets all the die-hard Pasteur fans hopping mad.  Stress, even psychological stress, causes the immune system to take a dive.  Now why would that be?  Let’s take a look.

Stress and the immune system

OK, buckle up my friends.  This is going to get technical in a hurry.  Let’s start with the basic guide to how the immune system functions. The immune system has two basic classifications of immune responses: natural and specific.

Natural responses are those that pretty much all organisms have, including basic organisms like sponges.  They respond fairly quickly to pathogens entering the body.

Specific responses are more dependent on the type of creature involved and take longer to respond to enemy agents.

OK so far?  Let’s look at the natural and specific responses individually.

Natural responses

We can break down the cells involved in natural immune responses as follows:

Granulocytes – these are white blood cells that are characterised by having granules in their cytoplasm (cell contents).  Most of the granulocytes are phagocytes (eating cells) that can be further subdivided into things like neutrophils and macrophages.  Phagocytes attack foreign bodies and eat them.  They congregate at the site of the infection and either release toxic chemicals to damage the invaders or envelop and consume them whole.

While all this is going on, the granulocytes also release cytokines, which are communicating molecules that have broader effects on the body, including fever and inflammation, and which promote wound healing.

Natural killer cell – these cells work by recognising that the invaders are not made of the same cellular material as the body.  They release toxic substances onto the invader to damage them.

The complement system – the complement system or family of proteins assists or “complements” the other aspects of the immune system and increases their effectiveness.

Read also: Natural Remedies For Stress and Anxiety

Specific responses

Specific responses, also called adaptive responses, evolved in the early vertebrates and are not shared with lower organisms.  They take longer to mobilise than natural responses and involve lymphocytes.

Lymphocytes have receptor sites on their cell surfaces, which are the right shape for one particular type of invader.  When activated, these cells divide in a process called the proliferative response and provides a very efficient way of tackling foreign bodies.

However, the proliferative response takes time and in the meantime, the body has to rely on the natural immune responses.

There are three types of lymphocyte involved in specific immune responses, as follows:

T-helper cells – these produce cytokines that communicate with the rest of the immune system and amplify the immune system response

T-cytotoxic cells – these are the cells that identify the bad guys and spray toxic material over the invaders

B cells – these cells produce antibodies, which neutralise bacterial toxins, bind to viruses and increase the effects of the natural immune response.  There are five kinds of antibody but I won’t get into those here.

Is that it?  Not quite, we need to understand one more point about the specific immune response.

Cellular and humoral responses

Human specific immunity comprises cellular and humoral responses.

Cellular responses are those made against invaders that try to get inside our cells (like viruses).  Cellular responses are co-ordinated by a subset of T-helper cells called Th1 cells, which produce cytokines including IL-2 and IFNγ.

Humoral responses are made against larger invaders like parasites and bacteria.  Humoral responses are co-ordinated by a subset of T-helper cells called Th2 cells, which produce different cytokines, including IL-4 and IL-10, which activate B cells and other natural response cells, including mast cells.

So why does stress interfere with that?

Good question.

Basically, the working hypothesis is that stress causes us to stop investing in long-term activities, like building muscle and building up our immune system, in favour of short-term activities, like dumping glucose into the bloodstream and increasing cardiac output, in light of a sprint to the nearest tree to avoid the attacking lion.

So how does it go wrong?  Well, we keep switching on the stress response and eventually realise that no long-term work is going on.

Or in other words, “stress-related disease emerges predominantly out of the fact the we so often activate a physiological system that has evolved for responding to acute physical emergencies but we turn in on for months on end, worrying about mortgages, relationships and promotions,” (Sapolsky).

OK but how does stress affect all of those complicated mechanisms?

The predominantly accepted mechanism for the modulation of the immune response via stress is that lymphocytes have receptors on their cell surfaces and hormones released during the stress response can bind to lymphocytes and influence their responses.

And indeed, human studies have shown that chronic stress is accompanied by:

  • Reduced natural killer cell cytotoxicity
  • Suppressed lymphocyte proliferative response
  • Blunted humoral response to immunisation

Is it that simple?

Well, obviously, the big problem with this for many scientists (at least the sane ones), is that this mechanism doesn’t appear to be evolutionarily adaptive.  Why would the immune system shut down when you might need it?

The standard response is that most stressors in the past would have been physical (i.e. a big cat about to eat you) and that immune function was subsidiary and was suppressed in favour of spending energy on more important things (like running away).

However, as Robert Sapolsky notes, the immune system isn’t just switched off to save energy, it is actively suppressed, which costs energy.  What the hell is going on?

This confusing problem has caused a number of interesting alternative theories to spring up.

Read also: Why Stress is a Natural Part of Life

Alternative theories

The obvious alternative is that acute stress causes an increase in immune system response but chronic stress causes a decrease.  This has some support, as Dhabar and McEwen, Bidirectional effects of stress and glucocorticoid hormones on immune function: possible explanation for paradoxical observations, Psychoneuroimmunology, 2001 have explained.

Another alternative suggests that the balance of cytokines is shifted such that Th1 cytokines, which provide support against cellular invaders, are suppressed and Th2 cytokines, which provide support against external pathogens like parasites, are enhanced.  Interestingly, these cytokines also exacerbate problems with allergies and autoimmune conditions.

Finally, I was interested to note in Hadany, Beker, Eshel and Feldman, Why is stress so deadly? An evolutionary perspective, Proc. Roy. Soc. Bio. Sciences, 2006 that they had done some mathematical modelling to show that it is actually in your genes’ best interests for you to die off during times of scarce resource by helping your offspring make best use of available resources.

But ultimately, we just don’t know at this point.

AboutKara

I’m a writer, new mom and foodie. I love sharing what I know while making others feel beautiful. On this blog, I share my healthy lifestyle, simple meals, fitness tips and experiences.

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