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Note for the web: If you find the text overly professional, let me point out that the chapter on longevity is the penultimate chapter about the effects. When you read the book from the beginning, you will already be familiar with most technical terms and concepts. Therefore, understanding will be more comfortable.

Reading time: approx 19 min 

13. Sauna effects on Longevity and Ageing

If you could choose at this point, how long would you like to live? Would you prefer 85 years, maybe 120, 150 or even 1000 and more years?

 

If you could choose at this point, how long would you like to live? Would you prefer 85 years, maybe 120, 150 or even 1000 and more years? Be careful before answering this question. Don't make the same mistake as Eos, the goddess of dawn from Greek mythology, who asked the god Zeus to grant her lover Tithonus immortality while forgetting to ask for eternal youth as well. As a result, Tithonus grew old but did not die, causing his power to wither to such an extent that he could no longer move. All he could do was blabber on; in the end, it is supposed that he turned into a cricket, hoping that death would come for him, too. At least, that's what the legend says. Long life, therefore, does not make much sense if it is associated with illness and suffering. But, it is entirely different if age is accompanied by health and vitality. And that's what we're going to focus on in this chapter. Simultaneously, we'll learn about the impact of sauna bathing on ageing and longevity.

History is full of myths and exaggerations about human's longevity and the longest-living people, (1) from biblical mythologies to famous local anecdotes. For example, Methuselah was supposed to live for 969 years! Hard to accept even for the most ardent believers, explains Israeli researcher Dr Nir Barzilai. One famous, more local story describes a Chinese man named Li Ching-Yuen, who is said to have died in 1933 after living 256 years. Another is about an Indonesian named Mbah Gotho, who claimed to be 145 years old and even had an official government-issued identity card supporting his claim. (2) The oldest officially-recognised person is Jeanne Calment, who died in 1997 at 122 years and 164 days. (3) Her longevity is the most thoroughly confirmed age claim, which some researchers nevertheless oppose, as they associate it with manipulation and the avoidance of financial difficulties. (4)

Another myth about longevity is that the present human lives longer than he once did a thousand years ago because of a supposed extended lifespan. This misunderstanding is often associated with semantic slippage when the longest lifespan is confused with life expectancy. Sometimes, however, such an opinion may be due to a misinterpretation of the data or other, even opportunistic reasons, such as avoiding military service or pension fraud. (1) The maximum life span, which is supposed to be determined by the longest living people, has not changed significantly in the last 100,000 years and remains around 125 years. (5) This high number is also more theoretical, still mostly unattainable in modern times. Previously, when the conditions for survival were much more complicated, the probability was even lower, despite the human body's theoretical ability to live that long. During the entire development period, man's main concern was survival until the offspring could reproduce. Therefore, old age was, in fact, more or less an unknown phenomenon. It is essential to understand that increasing individual longevity has no particular value in terms of species survival. Anything more than ensuring reproductive success would be unproductive from an evolutionary perspective, a waste of resources. The price for it is incredibly high in biological terms. (5) The best strategy for the survival of the species was to invest energy in development from birth to adulthood, but not in maintaining the body indefinitely. (6) Thus, fifty thousand and more years ago, most people died relatively young. After we learned to use available resources and tackled important issues such as more accessible access to food and avoiding predators, the survival curve began to change (Figure 1). Over time, an individual's life expectancy – which refers to a person's average life expectancy over time – has increased. However, it increased mainly during the twentieth century. Especially in developed countries, where it rose from about 49 years, in 1900, to about 76 years, in 1997. (7)Thus, a 27-year increase in life expectancy over less than a hundred years is equivalent to the increased life expectancy that occurred from ancient Rome to 1900, so, in about 2500 years. This remarkable change in such a short time is primarily the result of successfully dealing with the causes of death in the period from birth to young adulthood. The leading causes of death at a young age were infectious diseases, which were eliminated mainly by implementing relatively simple measures in improving hygiene and discovering antibiotics and vaccines.

Figure 1

Much harder than influencing survival in youth, experts say, is to extend life span on the other side of the life curve in old age. There are several reasons for this. Undoubtedly the most important is the complexity of the organism and its molecular mechanisms.

The progress in our knowledge of age-related diseases is significant. In many ways, it goes far beyond the progress in understanding the fundamental processes of ageing. It sometimes seems that somewhere in the distance, there is a light at the end of the tunnel and that the day will come when we will be able to control even the most severe diseases. However, successfully tackling or eliminating the most common fatal diseases such as cancer, Alzheimer's disease, and atherosclerosis would extend life expectancy by only about fifteen years. (5) This way, we could study how death would occur without the disease, but this is still far from the longevity dream that humans always have. Besides, the experience of decades of "battles" against this or that form of cancer, unfortunately, proves that efforts to eradicate the disease definitively are more than not a pious desire. The Geriatric model of coping with pathology, therefore, does not bring the desired effects. And come to think of it, it can't work. The number of the most various pathological changes that can potentially manifest, most often several simultaneously, is too large. By not addressing the causes, the endless struggle with them is reminiscent of Don Quixote's fights with windmills or the caricature showing someone struggling to mop the floor in a flooding bathroom instead of turning off faucets. It may well turn out that the light is not an exit from the tunnel but a warning light of the costs becoming an increasing burden for society due to tackling ageing diseases. The growth of the ageing population in the coming years also poses significant health and socio-economic challenges. Addressing these challenges requires multidisciplinary approaches and more excellent knowledge of the basic biochemical mechanisms of ageing. Therefore, for some time, experts have been proposing more attention to fundamental research on ageing on which vulnerability to pathologies is actually based. (8) Unfortunately, health policymakers are not paying attention to this, although ageing is, in fact, a major risk factor for most chronic diseases. (5) 

Perhaps this attitude is also due to many disappointments over the so-called elixirs of youth. They have been a regular accompaniment of the urge for a longer life throughout human history and have all proved ineffective so far. As a result, even scientifically, dealing with longevity has long been stigmatised and often even ridiculed. However, things have changed dramatically in the last thirty years, at least in academic circles. The realisation that ageing is not something mysterious or enigmatic that we absolutely do not and will never understand is slowly but steadily coming to the forefront. Loud individuals, as well as new scientific findings, have a lot of credit for this. One such discovery is that ageing is not the result of a dedicated program that is supposed to be driven by genes. (9) And if the ageing gene does not exist, then what is it that makes you age?

What is ageing, and why do we age?

Recently, one morning my car didn't start. The battery had gone flat. I didn't replace it right away. That morning, I asked a friendly neighbour to help me start the engine with jumper cables. For the next few weeks, everything was normal until the battery finally gave up. There was nothing left but to replace it. After I did it, I found that it was not only the battery that was not working: all electronic controls connected to the steering wheel broke down.

Consequently, turn signals and all other devices operated via the steering wheel did not work, including the horn, cruise control and car computer display. I was informed at the garage that they would need some time before they got the spare part, so I had left the car parked in the parking lot for most of the time. I only used it to drive to the closest grocery store, to which there was no need to use turn signals. I waited for more than two months; therefore, I went to pick groceries more times than I planned. One day, as I drove back to the store, I noticed an unpleasant odour spreading from under the hood. I opened the hood and was horrified to see the oil frying and smoking from the engine. Since I was right in front of the store, I bought a one-litre bottle of oil, poured it in and checked to see if it was enough. There was still too little oil. I purchased the next bottle and checked again. Then the next bottle and the next bottle, and there was still not enough oil. I was horrified to find that it was missing as much as five litres. However, this was not the worst at all. By driving a short way without enough oil, I had caused additional damage to the car engine, which cost me dearly. I realised how stupid of me to damage the engine due to an untimely battery replacement. Instead of a few bucks, it would cost me thousands.

At first glance, this seems illogical. However, with a bad battery, I first caused damage to the electronics that connect the steering wheel controls to the main computer and screen. Because the computer screen did not work, I could not see the oil warning on time, resulting in engine damage. Suddenly, the car, though not new but fit, was full of problems and ultimately useless. 

That's how I see ageing. First, something stings here or hurts there, which is usually solved acutely, many times with a painkiller, for example. Then one (masked) problem leads to another that causes a third, and we are suddenly facing the systemic problem. Unfortunately, we do not usually solve this systemically and entirely but partially. Instead of understanding, for example, diabetes as a systemic problem that can be solved by lifestyle change, we settle for a few pills that we reckon will do the impossible. In other words, instead of understanding the body as a systemic "device" that needs a systemic approach, we solve or, most of the time, mask the problem until there is too late and the body fails. It is, therefore, helpful to understand the body and ageing better. Although we cannot prevent it, it will be easier to manage the process of ageing and thus remain a valuable part of society for as long as possible while still having fun and rejoicing every day.

So what is ageing, and why do we age? What regulates longevity? Researchers have been asking these questions for a long time, and some hard-to-expect answers are finally popping up. Slowly but steadily, the mechanisms and processes of ageing are beginning to be recognised. With the growing interest in this field and a serious scientific approach to molecular processes, reports and various theories on ageing's causes began to accumulate. Scientists call them free radical theory (10) or mitochondrial theory (11), inflammation theory (12), immunological theory (13), and so on. There are still many unknowns in this area, but one is for sure: despite possible different views, we know that there is no single cause for ageing, but several of them. Therefore, experts agree that the various ageing theories that have begun to emerge should not be seen as mutually exclusive but complementary. (14) Thus, they formed a consensus that, at the biological level, ageing is an accumulation of a wide variety of molecular and cellular damage over time. This leads to a gradual loss of physiological integrity or a reduction in physical and mental capacity, increasing the risk of disease and, eventually, death. (10) This gradual loss of physiological integrity is a major risk factor for the most critical human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Ageing could also be defined as a general loss of molecular ability to repair damage resulting from metabolism or an organism's functioning. (9) Or, as Aubrey de Gray, the Chief Science Officer of the SENS Research Foundation, explains: "Ageing is not something specific to biology. It is just a fact of physics. Ageing is a phenomenon that is fundamentally the same in a living organism as it is in any human-made machine with moving parts, like the car or an aeroplane. It is simply a fact of physics that any machine with moving parts will do itself damage throughout its existence as an inevitable consequence of its normal operation. And that damage is going to accumulate. And that is fine for a while. Because any machine, living or not, is set up to tolerate a certain amount of damage. That is why, for example, cars work perfectly fine for a few years, and you don't have to take them into the garage. It is also why humans work pretty well for a few decades. You don't have to take them into the hospital, either. But eventually, the tolerable threshold of damage is reached and exceeded, and that's when things start to go downhill. And that is all that Ageing is." And he adds that the ageing of a living organism can be described in just three words: METABOLISM - DAMAGE - PATHOLOGY. (Figure 2)

Figure 2

METABOLISM (by this word, we mean everything the body does at any given moment to sustain us) creates damage. DAMAGE is constantly accumulating throughout our lives, and eventually, an age-specific PATHOLOGY occurs. Therefore, we can say that ageing is simply a side effect of life.

Let's take a closer look at the 'equation' above. On the one hand, we have METABOLISM. There is no life without it, so we cannot just abolish it. However, it can be influenced. One of the somewhat effective methods is calorie restriction, confirmed by many animal model experiments. To date, this is the only intervention that consistently shows to slow down ageing and increase the average and maximum life expectancy of short-lived animals. (16) However, it is still unclear whether long-term calorie restriction had a similar effect in long-lived animal and human species. A few signs suggest that this could be the case. Mainly due to the positive impact on cardiovascular disease and some other age-related diseases, including cancer. However, it has not been explored yet how such an intervention would affect the quality of life or cause other health problems.

On the other side of the 'equation' is PATHOLOGY. We have a lot of experience in dealing with various types of pathologies. It is associated with a lot of suffering and unpredictable outcome. Despite the tremendous advances in medicine, the results are not encouraging. 

There is a third option left, elimination, reduction or management of DAMAGE resulting from metabolism or external factors before the accumulated cause pathological changes in the organism. In this regard, Aubrey suggests focusing on developing systems that would periodically repair the damage. Like, say, some regular car service. He goes a little further and offers the so-called "seven deadly things" that cause pathology, and he also suggests ways to eliminate them. Although a pioneer in many ideas, Aubrey is not the only one who sees matters and solutions in this direction. More and more researchers agree that eliminating damage before they cause pathological changes is the key to healthier ageing.

In 2013, the scientific journal Cell published an article entitled 'Hallmarks of Aging' (17), which in many ways, confirms Aubrey's ideas. The report has a significant impact on the entire research field of ageing. A group of scientists from Spain, France, and the United Kingdom summarised nine probably essential ageing hallmarks (Figure 3). These are the common denominators of ageing in different organisms. As they wrote in the article, the main challenge facing them is to break down and recognise the interrelationships between recognised hallmarks and their relative contribution to ageing, with the ultimate goal of setting pharmaceutical goals to improve human health with minimal side effects. It may help form the basis for future studies on the molecular mechanisms of ageing and design interventions to improve human health.

Figure 3

The proposed nine hallmarks of ageing are classified into three categories. At the top are those that are the main causes of cell damage. The common characteristic of the primary hallmarks is the fact that they are all unequivocally negative. In the middle are those that are considered part of compensatory or antagonistic responses to damage. These responses initially mitigate the damage, but eventually, if chronic or exacerbated, they become harmful. At the bottom are integrative hallmarks, which are the end-result of the previous two groups and are ultimately responsible for the functional decline associated with ageing. The main criteria by which these ageing hallmarks were selected are three. The first is that they always show up during normal ageing. The second is that if the experiment caused deterioration of a particular hallmark, this would accelerate ageing. And the third criterion is that its "experimental" improvement should inhibit the normal ageing process and increase life expectancy. The mentioned article's importance is in presenting and describing ageing hallmarks and presenting potential interventions or solutions. The solutions are not yet fully developed, but they have a strong theoretical basis.

And we again come to our regular question: what does this have to do with the sauna? 

Can the sauna influence the mentioned hallmarks of ageing or the physiological changes that contribute to ageing? Let's look at each of them and try to determine if sauna bathing might have any effect on them.

 

A. Primary hallmarks of ageing - the main causes of cell damage and consequent ageing:

 

1 - Genomic instability

Genomic instability (also called genetic instability) means a high incidence or frequency of mutations within the genome of a cell line* and has long been recognised as a primary causative agent of ageing. (18)

Cell lines * are cells that are grown under controlled conditions, usually outside their natural environment. First, the cells of interest are isolated from living tissue, then maintained under carefully controlled conditions. They are often used in the laboratory instead of primary cells to study biological processes.

As we know, our cells are constantly exposed to various external and internal sources of DNA damage. From UV radiation and various toxic, so-called mutagenic substances from the environment or reactive oxygen species from bodily functioning, which causes so-called oxidative stress. Damaged DNA means the faulty construction of proteins, which then do not do the necessary work and can cause disease. To deal with tens of thousands of such attacks per day, cells have evolved a complex network of genome maintenance systems that remove damage and repair DNA. Despite extremely sophisticated mechanisms, it can sometimes happen that systems do not perform their function accurately enough, and cell misrepresentation and mutation occur. Especially with ageing, these systems are becoming less responsive and efficient. Genomic instability is increasing, and as a result, a wide variety of forms of genetic damage begin to accumulate, resulting in ageing and increasing the chances of disease. Recognising the importance of genomic stability, scientists have begun to explore ways to repair the damage. In doing so, different researchers take different approaches. Some suggest strengthening the signalling and repair mechanisms, while others suggest eliminating damaged cells. No matter which approaches proves more effective in the future, the fact is that we already have a tool at our disposal. The evidence shows that this tool stimulates DNA repair mechanisms (19) and reduces oxidative stress, an important generator of DNA damage (20). Of course, I am talking about sauna and the associated acute hyperthermia, a short-term rise in body temperature. The tests show that sauna bathing reduces oxidative stress (21,22) and stimulates the repaired mechanisms of DNA. (19,23) So, the first box checked.

2. Telomere attrition

Telomeres protect the ends of chromosomes, much like the aglets, a plastic caps at the end of shoelaces, thus preventing DNA breakdown. With each cell division, the telomeres shorten. Telomere wear is a usual accompaniment to normal ageing. However, research results have shown that accelerated telomere shortening is directly related to accelerated ageing and increased mortality. Researchers have even found that telomere length could indicate a body's ability to absorb damage that accumulates in cells (24). Critically short telomeres are recognised by cellular repair mechanisms as defective DNA and stop cell division. Cells enter an ageing period and die. Experts, therefore, see a potential solution in telomere reactivation. Recent studies have confirmed it as a potential therapeutic target for age-related diseases. But it has also been found that abnormal telomerase expression and telomerase mutations are associated with many different types of human tumours (25). However, there is another option using more natural methods. One of these is the activation of the 'Heat shock factor 1' gene, which researchers report protects telomeres (26). Acute heat stress activates this vital gene, and sauna bathing is a perfect way to generate heat stress, as we already know very well. So, another box checked.

3. Epigenetic alterations

There is evidence to suggest that epigenetic * changes accompany ageing (27,28). These findings may be bad or good news.

Epigenetics * is a study of inherited gene expression changes (active versus inactive genes) that do not involve DNA changes, affecting how cells read the gene. Therefore, epigenetic modifications are changes that result from changes in gene expression and not in their transformation. (More in the chapter on epigenetics)

The bad news is that even if we inherited good genes for a healthy and long life, we could unwisely waste this rich dowry with wrong decisions. On the other hand, the good news is the realisation that with a proper, healthy lifestyle, even slightly inferior genes can be neutralised through epigenetic changes, at least to some extent. DNA methylation, a process in which specific molecules (scientists call them methyl groups) bind to DNA molecules, is the main control program that alters, most often silences or reduces, gene expression (27). Unfortunately, this process can also reduce the activity of good genes, such as the genes responsible for beneficial repair mechanisms to take care of metabolism and fight against oxidative stress. Consequently, it reduces the ability to neutralise stress in the cell leading to ageing and age-related disease (28.5). Epigenetic changes are fortunately reversible. The fact that the epigenome can be manipulated gives scientists the prospect of improving age-related pathologies and prolonging healthy lifestyles. At least that is what it seems, judging by the increasingly intensive research in this area. Therefore, it is not surprising that there are high expectations in treating the disease associated with the use of so-called "epigenetic drugs" that can modulate the activity of enzymes that causes epigenetic changes (29). However, there is growing evidence that heat acclimation also affects epigenetic changes (30). It involves the availability of DNA and transcription factors, thereby regulating gene expression and controlling the phenotype * (31).

Phenotype * (from the Greek pheno "display" and type as in the variety) is a term used in genetics for an organism's observable characteristics or traits. An organism's phenotype derives from two primary factors: the expression of the organism's genetic code, its genotype, and environmental factors. Both aspects can interact, which further affects the phenotype.

Increased availability of DNA means easier access and transcription, thus more straightforward (necessary) protein synthesis.
It is unknown whether thermal adaptation can "remove or cleanse" accumulated unwanted epigenetic changes in the ageing process. However, research to date has confirmed that heat acclimation causes positive epigenetic changes. This notion is also indicated by the study of the Israeli scientist Michal Horowitz. She showed that heat acclimation enables cross-tolerance * to new stressors and thus more efficient cellular function and cytoprotection* throughout epigenetic changes (32,33,33.5).

Cross-tolerance * means that exposing the body to one stress can lead to resistance to others.
Cytoprotection * is the process by which chemical compounds protect cells against harmful substances.

Thus, we can say that regular sauna bathing expresses more robust defence mechanisms in the cells against external and internal damaging factors that affect ageing also through epigenetic changes. Box checked.

4 - Loss of proteostasis (protein homeostasis)

Ageing and some age-related diseases are associated with impaired protein homeostasis, also named proteostasis. Cellular protein homeostasis is critical to cell health. It requires close control of protein synthesis, folding, conformational maintenance, and degradation. If the system does not work, many problems can occur. We discussed this extensively in the Protein Chapter. Among others, it can cause what is known as protein aggregation. The protein aggregation into clusters is the basis for various age-related neurodegenerative disorders, including Alzheimer's and Parkinson's disease (34,35). The correct relationship between synthesis and degradation is necessary for the normal functioning of cells and the whole organism. Heat shock proteins (HSPs) help fold proteins or repair them if necessary. If this is not possible, HSPs cooperate with other cellular systems to break down irreparably damaged proteins in a process called autophagy *. Therefore, the body must maintain optimum HSPs.

Autophagy * is a natural, regulated mechanism of the cell that removes unnecessary or non-functional components. It enables orderly decomposition and recycling of cellular components. Its malfunction accelerates cell collapse.

For the normal functioning of cells and the whole organism, the correct relationship between protein synthesis and degradation is necessary. With age, the ability to produce HSPs in cells decreases.

It is well-known that regular use of a sauna stimulates heat shock proteins production and contributes to protein homeostasis, positively affecting ageing (36,37). So, another box checked.

 

B. Antagonistic hallmarks - cellular response to damage

After reviewing the primary hallmarks, we can see that regular sauna use and, consequently, thermal acclimatisation seem to impact all four major causes of damage positively. Whether this impact is significant enough to be reflected in healthy ageing and possibly even more extended life, we will discover a bit later. Before that, let's look at whether sauna bathing affects the next group of ageing hallmarks, so-called antagonistic ones. They represent the cellular response to damage caused by primary hallmarks and are, to some extent, helpful, the cell's protective response until they grow into a harmful factor of ageing.

 

5 - Deregulated nutrient sensing

Have you ever wondered why some people have a large belly even though they are not very obese? The answer lies in the deregulated nutrient sensing.
As long as the organism is young and the cellular mechanisms for repairing metabolic damage are sufficiently active, we are relatively safe from ageing pathology. The exceptions are rare types of genetic diseases. However, as repair mechanisms become less effective over the years, cellular damage becomes increasingly problematic. One of the longest-preserved defence responses to cellular damage caused by metabolic processes is nutrient-sensing deregulation. In other words, as we age, when cells are no longer able to repair the damage caused by metabolism, they begin to respond defensively by reducing nutrient intake, thus achieving a longer lifespan. The response has similar characteristics and results, such as lowering energy intake with a low-calorie diet. This has been demonstrated in many studies of a wide variety of organisms (38-40).

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Note: In continuation, the chapter explains the effects of sauna bathing on ageing's other remaining hallmarks. It concludes with summaries of the findings of studies on the effects of ageing and answers whether the claim that sauna positively impacts ageing and longevity is a myth or a fact. The chapter contains five sketches and 89 reference notes to research to support the text.

Reading time: approx 19 min 

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