Hot days put our bodies to the test

“It sounds fine and well, doesn’t it, to warn the public of high temperatures. But when should this warning be given, what should it contain, and how do we check if it has the desired effect? At the moment, there is a lot of assumptions being made regarding

these issues,” says Petter Ljungman, cardiologist and researcher at the Institute of Environmental Medicine at Karolinska Institutet. Today, SMHI sends out a message to the public

when the next 72 hours are expected to have heat peaks of at least 26 degrees. If the heat peaks are expected to be higher than 30 degrees, SMHI will instead issue a class 1 warning, and if it is expected to last for at least five consecutive days, or if the temperature peaks are expected to be at least 33 degrees for three days straight, they will issue a class 2 warning. However, the summer’s weather warnings are received differently than those issued in winter, where we have procedures for ploughing and roof clearing as well as a public awareness of black ice.

“Swedes are more prepared for cold, and we are not used to considering the risks of hot weather. But we are moving towards a climate with more extreme weather, where heatwaves are expected to become more common. Our infrastructure and our buildings are not adapted for this,” says Petter Ljungman.

Increased risk of cardiac arrest

When the temperature rises, it takes the heaviest toll on the heart. Studies carried out based on data from Paris in the heatwave of 2003 show a clear increase in cardiac arrests, but not in heart attacks or other heart diseases. One possible explanation is that the heat is stressful for the body, raising both the heart rate and the blood pressure. The stress can stimulate palpitations, which can disrupt the heart rhythm and result in cardiac arrest. Whether this is primarily triggered by high temperature spikes, rapid temperature increases or high temperatures over a long time is unknown.

What is known, however, is that certain groups run a higher risk than others of dying from heart failure in high temperatures. It is generally more difficult for the elderly to regulate body temperature, and they do not feel thirst to the same extent. People with diabetes are also more vulnerable to heat, for similar reasons.

More unexpected is that people suffering from mental illness of a wide variety, such as depression or dementia, are at increased risk of dying from heart failure during a heatwave. One possible explanation could be that certain drugs have a diuretic effect or an impact on temperature regulation. Another explanation could be that mental illness may impair the ability to deal with the heat in practical terms, for example by acquiring a fan or seeking out cool places.

People with pulmonary diseases, such as COPD, are more vulnerable to heart disease and this risk appears to increase when the heat is combined with air pollution, which makes certain urban environments more risky.

But suicide rates also appear to increase in high temperatures. The scientific literature includes several studies indicating that the number of suicides rises in high temperatures, but there is no answer as to why that is.

“I can only guess. Generally speaking, heat can be excruciating and stressful. If you don’t have access to a cooler space or the possibility of lowering the temperature indoors, it is imaginable that this would give a sense of not being able to escape. That can cause anxiety, which in combination with dehydration may impact your judgement. We need to be better at considering environmental exposure in mental illness. It seems there are mechanisms we have not thought about,” says Petter Ljungman.

Brown fat generates heat

The body is constantly generating its own heat through metabolism. Every single process in the body, such as creating a protein, breaking down a sugar or reading DNA, entails a certain loss of energy, which causes heat. When the muscles and the brain are working, several metabolic processes occur, which generate a greater loss of energy and consequently a higher body temperature.

The body’s thermostat is located in the brain, in the hypothalamus, where signals are sent indicating how warm different body parts are. The thermostat then decides what to do in order to regulate the body temperature, such as dilating or constricting blood vessels, sweating or shivering. In the cold, the brain and internal organs are prioritised, which means constricting the peripheral blood vessels.

But the body has another way of raising body temperature. That is to use the brown fat, which is stored in adults between the lungs and in the neck.

Researchers previously believed that only babies had brown fat. But around ten years ago, it was discovered that brown fat, which has a number of good and health-preserving properties, is also found in adults – to be exact, we appear to have approximately 60 grammes each of this tissue.

If needed, the brown fat can be activated in order to generate heat. In order to regenerate, this fatty tissue uses blood sugar and blood lipids from the circulatory system. This is undeniably an appealing concept for the modern human with our lifestyle issues – the brown fat can literally burn our excess fat.

But if we do not need to raise our body temperature, perhaps because we are dressed in winter clothes, or choose to go inside when we get cold, then this function is never activated. Nor is it entirely clear what makes the brown fat cells start generating heat, but it is likely caused primarily by nerve signals from the brain.

In studies on rats, it has been well documented that exposure to cold activates the brown fat reserves. It has also been clearly established that this has beneficial effects, such as protection against obesity and diabetes, and it has a good effect on blood lipids and blood sugar levels. Studies on humans,

where a smaller number of subjects have spent time in the cold, have produced the same results.  But freezing in order to jumpstart your brown fat is probably a less than appealing prospect for most.

One major question is therefore whether it would be possible to medically induce the brown fat cells to generate heat, regardless of whether the body is cold or not. 

“This is a very intensive research field, which is always being discussed at scientific conferences on obesity and diabetes research. Could we use this fat intentionally to lose weight or to improve our blood lipids and blood sugar levels? How much brown fat do we really need, can we make more, and how could we activate it? These are questions that receive major research grants,” says Jorge Ruas, associate professor at the Department of Physiology and Pharmacology at Karolinska Institutet.

At the same time, a drug like that would likely have the side effect of making you really hot and sweaty. At the same time, a drug like that would likely have the side effect of making you really hot and sweaty.

“We feel uncomfortable and unhappy when we get too hot.

The question is whether it would be an acceptable side effect, if there was an interest in such a drug. But one factor could be that the drug contributes to weight loss down to a level where you no longer risk damage to knees or other joints during physical activity,” says Jorge Ruas.

Fever helps the immune system

Normal body temperature is within the range of 36.0 to 37.8 degrees. When the body temperature goes above 38 degrees, we are considered to have a fever. This is a basic mechanism of our immune system, but it is still unclear whether it is good or bad for the body to have a fever. Perhaps a little of both.

When we are attacked by a virus or a bacterium, an intensive sequence of events is activated in order to bring a large amount of the right type of immune cells to the right place. One of these substances is interpreted by the hypothalamus as the body being too cold, which results in an order to raise the temperature – but this makes the body warmer than what these cells like. At the same time, there is a dilation of blood vessels which makes it possible for the immune cells to go deep into the tissues to combat any intruders that might be hiding there. If you lower your fever with drugs, it becomes more difficult for the cells of the immune system to reach their aim.

“Lowering the fever is a compromise between hindering the immune system and stopping hyperthermia, where the body can no longer regulate its temperature. For a low fever you can skip the medication, but if the fever is slightly higher it is important to lower the body temperature, and in the case of a very high fever, i.e. above 40 degrees, it is vital to do so.”

A bacterium that we have to fight every now and then is Neisseria meningitidis, which normally lives a harmless existence in the nose and throat of around one in ten people. These bacteria, which are sometimes referred to as meningococcus, can spread through sneezing to take up residence in new throats where they can also live out their harmless lives.

Start to multiply dramatically

But they can also suddenly become extremely dangerous. This happens when they start to multiply dramatically, reach the bloodstream and can then cause meningitis. In order to survive, you need to be treated with intravenous antibiotics within hours, but this disease can still have a fatal outcome despite treatment. In 2017, there were 49 reported cases of invasive meningococcal infection in Sweden, which led to ten deaths.

Edmund Loh, research assistant at the Department of Microbiology, Tumour and Cell Biology at Karolinska Institutet, has researched what it is that makes these normally harmless bacteria suddenly become lethal. What appears to happen, according to the researchers’ hypothesis, is that the person carrying the meningococcus develops a fever for some other reason. The bacteria

senses the body’s temperature increase and therefore forms a protective capsule around themselves

which makes them impenetrable to the immune system. This capsule should normally be dismantled when the immune system deescalates, since it consumes a high amount of energy. But a few bacteria may mutate in this reinforced state so that they constantly have a very thick protective capsule that the immune system cannot penetrate. If, for example, the person’s fever was caused by an influenza virus, the constant nose-blowing may have caused small blood vessel ruptures, which allow the bacteria to enter the bloodstream. They can then reach the cerebral membrane in their mutated, lethal state. 

“We have noticed that the incidence increases a couple of days following spikes in the influenza statistics, which supports our hypothesis,” says Edmund Loh.

He and his colleagues have mapped the genome of meningococcus and have discovered the RNA molecules related to temperature gauging, i.e. the RNA that reacts to fever and causes the bacteria to form their capsules. The researchers are now hoping that this knowledge will pave the way for new treatment of meningitis caused by meningococcus. The idea is that a drug could prevent the bacteria from forming their protective shield, which would make them vulnerable to the immune defence again.

“The next step is to try to understand how we can block the thermometer of the bacteria. We also want to look at other bacteria that can cause meningitis, such as pneumococcus and haemophilus. They also form a protective capsule in the event of fever, and we now want to look for the RNA that regulates their thermometers,” says Edmund Loh.