The core experiences of depression – changes in energy, activity, thinking and mood – have been described for more than 10,000 years. The word “depression” has been used for about 350 years.

Given this long history, it may surprise you that experts don’t agree about what depression is, how to define it or what causes it.

But many experts do agree that depression is not one thing. It’s a large family of illnesses with different causes and mechanisms. This makes choosing the best treatment for each person challenging.

Reactive vs endogenous depression

One strategy is to search for sub-types of depression and see whether they might do better with different kinds of treatments. One example is contrasting “reactive” depression with “endogenous” depression.

Reactive depression (also thought of as social or psychological depression) is presented as being triggered by exposure to stressful life events. These might be being assaulted or losing a loved one – an understandable reaction to an outside trigger.

Endogenous depression (also thought of as biological or genetic depression) is proposed to be caused by something inside, such as genes or brain chemistry.

Many people working clinically in mental health accept this sub-typing. You might have read about this online.

But we think this approach is way too simple.

While stressful life events and genes may, individually, contribute to causing depression, they also interact to increase the risk of someone developing depression. And evidence shows that there is a genetic component to being exposed to stressors. Some genes affect things such as personality. Some affect how we interact with our environments.

What we did and what we found

Our team set out to look at the role of genes and stressors to see if classifying depression as reactive or endogenous was valid.

In the Australian Genetics of Depression Study, people with depression answered surveys about exposure to stressful life events. We analysed DNA from their saliva samples to calculate their genetic risk for mental disorders.

Our question was simple. Does genetic risk for depression, bipolar disorder, schizophrenia, ADHD, anxiety and neuroticism (a personality trait) influence people’s reported exposure to stressful life events?

You may be wondering why we bothered calculating the genetic risk for mental disorders in people who already have depression. Every person has genetic variants linked to mental disorders. Some people have more, some less. Even people who already have depression might have a low genetic risk for it. These people may have developed their particular depression from some other constellation of causes.

We looked at the genetic risk of conditions other than depression for a couple of reasons. First, genetic variants linked to depression overlap with those linked to other mental disorders. Second, two people with depression may have completely different genetic variants. So we wanted to cast a wide net to look at a wider spectrum of genetic variants linked to mental disorders.

If reactive and endogenous depression sub-types are valid, we’d expect people with a lower genetic component to their depression (the reactive group) would report more stressful life events. And we’d expect those with a higher genetic component (the endogenous group) would report fewer stressful life events.

But after studying more than 14,000 people with depression we found the opposite.

We found people at higher genetic risk for depression, anxiety, ADHD or schizophrenia say they’ve been exposed to more stressors.

Assault with a weapon, sexual assault, accidents, legal and financial troubles, and childhood abuse and neglect, were all more common in people with a higher genetic risk of depression, anxiety, ADHD or schizophrenia.

These associations were not strongly influenced by people’s age, sex or relationships with family. We didn’t look at other factors that may influence these associations, such as socioeconomic status. We also relied on people’s memory of past events, which may not be accurate.

How do genes play a role?

Genetic risk for mental disorders changes people’s sensitivity to the environment.

Imagine two people, one with a high genetic risk for depression, one with a low risk. They both lose their jobs. The genetically vulnerable person experiences the job loss as a threat to their self-worth and social status. There is a sense of shame and despair. They can’t bring themselves to look for another job for fear of losing it too. For the other, the job loss feels less about them and more about the company. These two people internalise the event differently and remember it differently.

Genetic risk for mental disorders also might make it more likely people find themselves in environments where bad things happen. For example, a higher genetic risk for depression might affect self-worth, making people more likely to get into dysfunctional relationships which then go badly.

What does our study mean for depression?

First, it confirms genes and environments are not independent. Genes influence the environments we end up in, and what then happens. Genes also influence how we react to those events.

Second, our study doesn’t support a distinction between reactive and endogenous depression. Genes and environments have a complex interplay. Most cases of depression are a mix of genetics, biology and stressors.

Third, people with depression who appear to have a stronger genetic component to their depression report their lives are punctuated by more serious stressors.

So clinically, people with higher genetic vulnerability might benefit from learning specific techniques to manage their stress. This might help some people reduce their chance of developing depression in the first place. It might also help some people with depression reduce their ongoing exposure to stressors.

If this article has raised issues for you, or if you’re concerned about someone you know, call Lifeline on 13 11 14.

Jacob Crouse, Research Fellow in Youth Mental Health, Brain and Mind Centre, University of Sydney and Ian Hickie, Co-Director, Health and Policy, Brain and Mind Centre, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

One of the earliest descriptions of someone with cancer comes from the fourth century BC. Satyrus, tyrant of the city of Heracleia on the Black Sea, developed a cancer between his groin and scrotum. As the cancer spread, Satyrus had ever greater pains. He was unable to sleep and had convulsions.

Advanced cancers in that part of the body were regarded as inoperable, and there were no drugs strong enough to alleviate the agony. So doctors could do nothing. Eventually, the cancer took Satyrus’ life at the age of 65.

Cancer was already well known in this period. A text written in the late fifth or early fourth century BC, called Diseases of Women, described how breast cancer develops:

hard growths form […] out of them hidden cancers develop […] pains shoot up from the patients’ breasts to their throats, and around their shoulder blades […] such patients become thin through their whole body […] breathing decreases, the sense of smell is lost […]

Other medical works of this period describe different sorts of cancers. A woman from the Greek city of Abdera died from a cancer of the chest; a man with throat cancer survived after his doctor burned away the tumour.

Where does the word ‘cancer’ come from?

The word cancer comes from the same era. In the late fifth and early fourth century BC, doctors were using the word karkinos – the ancient Greek word for crab – to describe malignant tumours. Later, when Latin-speaking doctors described the same disease, they used the Latin word for crab: cancer. So, the name stuck.

Even in ancient times, people wondered why doctors named the disease after an animal. One explanation was the crab is an aggressive animal, just as cancer can be an aggressive disease; another explanation was the crab can grip one part of a person’s body with its claws and be difficult to remove, just as cancer can be difficult to remove once it has developed. Others thought it was because of the appearance of the tumour.

The physician Galen (129-216 AD) described breast cancer in his work A Method of Medicine to Glaucon, and compared the form of the tumour to the form of a crab:

We have often seen in the breasts a tumour exactly like a crab. Just as that animal has feet on either side of its body, so too in this disease the veins of the unnatural swelling are stretched out on either side, creating a form similar to a crab.

Not everyone agreed what caused cancer

In the Greco-Roman period, there were different opinions about the cause of cancer.

According to a widespread ancient medical theory, the body has four humours: blood, yellow bile, phlegm and black bile. These four humours need to be kept in a state of balance, otherwise a person becomes sick. If a person suffered from an excess of black bile, it was thought this would eventually lead to cancer.

The physician Erasistratus, who lived from around 315 to 240 BC, disagreed. However, so far as we know, he did not offer an alternative explanation.

How was cancer treated?

Cancer was treated in a range of different ways. It was thought that cancers in their early stages could be cured using medications.

These included drugs derived from plants (such as cucumber, narcissus bulb, castor bean, bitter vetch, cabbage); animals (such as the ash of a crab); and metals (such as arsenic).

Galen claimed that by using this sort of medication, and repeatedly purging his patients with emetics or enemas, he was sometimes successful at making emerging cancers disappear. He said the same treatment sometimes prevented more advanced cancers from continuing to grow. However, he also said surgery is necessary if these medications do not work.

Surgery was usually avoided as patients tended to die from blood loss. The most successful operations were on cancers of the tip of the breast. Leonidas, a physician who lived in the second and third century AD, described his method, which involved cauterising (burning):

I usually operate in cases where the tumours do not extend into the chest […] When the patient has been placed on her back, I incise the healthy area of the breast above the tumour and then cauterize the incision until scabs form and the bleeding is stanched. Then I incise again, marking out the area as I cut deeply into the breast, and again I cauterize. I do this [incising and cauterizing] quite often […] This way the bleeding is not dangerous. After the excision is complete I again cauterize the entire area until it is dessicated.

Cancer was generally regarded as an incurable disease, and so it was feared. Some people with cancer, such as the poet Silius Italicus (26-102 AD), died by suicide to end the torment.

Patients would also pray to the gods for hope of a cure. An example of this is Innocentia, an aristocratic lady who lived in Carthage (in modern-day Tunisia) in the fifth century AD. She told her doctor divine intervention had cured her breast cancer, though her doctor did not believe her.

From the past into the future

We began with Satyrus, a tyrant in the fourth century BC. In the 2,400 years or so since then, much has changed in our knowledge of what causes cancer, how to prevent it and how to treat it. We also know there are more than 200 different types of cancer. Some people’s cancers are so successfully managed, they go on to live long lives.

But there is still no general “cure for cancer”, a disease that about one in five people develop in their lifetime. In 2022 alone, there were about 20 million new cancer cases and 9.7 million cancer deaths globally. We clearly have a long way to go.

Konstantine Panegyres, McKenzie Postdoctoral Fellow, Historical and Philosophical Studies, The University of Melbourne

This article is republished from The Conversation under a Creative Commons license. Read the original article.