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The human gut is home to more than 100 trillion microorganisms, collectively known as the microbiome. This incredibly diverse and highly complex community performs numerous tasks for us. Our gut flora plays an important role in digestion and metabolism, but also in immune defence, and it even influences the hormonal system.
The microbiome can be imagined as a microcosm of its own. The gut flora is even involved in the development of inflammatory processes. In addition, it is closely connected with other organs such as the liver and the brain.
The composition of microorganisms is unique in every person. What matters is that the composition of the bacteria, or diversity, remains balanced. This multitude of tasks can only be handled by a healthy and stable microbiome. When disease-causing and harmful microorganisms predominate, this is referred to as dysbiosis.
However, dysbiosis rarely develops without cause. If we do not provide beneficial bacteria with an optimal environment, their numbers decline and harmful microorganisms eventually become dominant. Our lifestyle can have an enormous influence on this balance: diet, physical activity, medication use and environmental factors all affect our personal microbiome. Numerous studies have now shown that an imbalanced gut microbiome plays an important role in chronic diseases, including chronic inflammatory bowel diseases, obesity, type 2 diabetes, cardiovascular disease and cancer.
In 2017, a study conducted at Lund University found that dysbiotic gut flora accelerates the progression of Alzheimer’s disease. A gut-friendly diet rich in whole grains, fruit and vegetables may therefore help prevent Alzheimer’s disease.
Good to know: A change in diet – for example, from a diet rich in animal products to a predominantly plant-based diet – can cause a remarkable microbial shift within just 24 hours.
There is no doubt that diet shapes the composition and diversity of the microbiome, and does so remarkably quickly. The links between the gut microbiome, diet and systemic inflammation suggest that a high-fibre diet beneficially shapes the composition of the microbiome. Fibre increases the number of beneficial bacteria, inhibits the growth of disease-causing microorganisms and reduces harmful serum cholesterol in the microbiome. It also promotes the production of important short-chain fatty acids.
In countries where a high-fibre, low-fat diet is preferred, the population also achieves the highest life expectancy.
The microbiome undergoes major changes as we age. It develops during the first three years of life and then remains relatively stable until middle adulthood. However, the ageing process generally appears to be favourably influenced by a balanced interaction between different immunological processes. The gut microbiome can support or even enhance anti-inflammatory activity and thereby counterbalance the increased pro-inflammatory activity that occurs in all older adults. The balance of the microbiome is crucial for healthy ageing. Healthy older people maintain stable and diverse gut flora well into old age.
Short-chain fatty acids, or SCFAs, appear to be central compounds in this process. They are produced through the bacterial fermentation of fibre in the large intestine and influence many processes in the body. For example, they can trigger processes that stop the growth of tumour cells and promote apoptosis, meaning the programmed death of harmful cells. SCFAs also have a positive effect on insulin sensitivity and are important for healthy fat metabolism.
It has been found that younger test subjects have higher levels of SCFAs than older individuals. Reduced health in old age is therefore believed to be associated with lower SCFA levels.
Cream cake, pork schnitzel, burgers and similar foods – some people would prefer to eat almost nothing else. They can hardly expect to remain healthy into old age. By contrast, the right diet gives us a good chance of maintaining our health and extending our lifespan. There is strong scientific evidence that healthy eating habits significantly increase the likelihood of longevity.
For a long time, it was assumed that our life expectancy was determined mainly by our genes. Researchers have disproved this. Using model calculations, they found that the importance of genes in determining our lifespan has been greatly overestimated: genes are likely to account for only around 10 percent of our life expectancy. Approximately 90 percent of the factors that determine how long we live therefore appear to be linked to our lifestyle. Sufficient physical activity and a healthy diet that promotes longevity are particularly important.
Key finding: Genes account for only around 10 percent of our life expectancy – the remaining 90 percent is determined by our lifestyle, above all by our diet.
What this means in practical terms can be learned from populations living in regions of the world with an unusually high number of very old people. These include Abkhazia on the Black Sea, the mountain village of Vilcabamba in Ecuador, certain areas of the Mediterranean island of Sardinia and, in particular, Okinawa in Japan, where longevity is almost the norm and the number of very old people is highest.
These longevity societies share certain characteristics, such as regular moderate physical activity, a predominantly plant-based diet low in meat and a strong attachment to traditions.
Diet appears to be the central factor. The residents of Okinawa in Japan demonstrate what a diet designed to support healthy ageing can look like: they eat mainly root vegetables, especially sweet potatoes, green and yellow vegetables and soy-based foods. They consume seafood, lean meat, fruit, herbs, tea and alcohol in moderate amounts. Following the dietary principles of the people of Okinawa reduces oxidative stress, may modulate age-related biological pathways, lower the risk of developing chronic age-related diseases and thereby promote healthy ageing and longevity overall.
The fundamental principles of this type of diet can also be found in the Mediterranean diet, which is considered particularly healthy in this part of the world. It appears to help prevent cardiovascular disease and age-related diseases in general. The Mediterranean diet is based on a high proportion of unrefined carbohydrates, moderate protein intake with an emphasis on plant proteins, fish and lean meat. A relatively low fat content is also important, with unsaturated fatty acids predominating. At the same time, the diet should be rich in omega-3 fatty acids. This type of diet is associated with anti-inflammatory effects, is believed to optimise cholesterol balance and may also have a beneficial effect on other risk factors for age-related diseases.
A strongly plant-based diet also results in a comparatively low calorie density, meaning that fewer calories are generally consumed. This type of diet also has a low glycaemic index (GI) and a low glycaemic load (GL), both of which are generally considered particularly healthy. The GI, and therefore also the GL of a food, indicates how a carbohydrate-containing food affects blood sugar levels. The lower the GI, the smaller and slower the rise in blood sugar.
Glycaemic load, by contrast, is considered an indicator of the insulin requirement triggered by a meal. Foods with a high GI, such as products made from white flour, sweets or sugary drinks, cause blood sugar levels to rise rapidly. This is accompanied by an increase in insulin levels in the blood. Insulin promotes the uptake of sugar into body cells as well as the formation and storage of fat, while making fat breakdown more difficult – effects that are not beneficial to our health.
Our diet and our genes also appear to influence one another in relation to ageing. The gene known as “Forkhead box protein O3”, abbreviated as FOXO3, seems to play a central role in ageing processes. Its effects are probably dependent on diet, with fasting appearing to be more favourable for the ageing process and overeating less favourable, according to scientists from the Cluster of Excellence “Inflammation at Interfaces” at Kiel University.
According to the researchers, the first evidence that the FOXO3 gene affects lifespan emerged as early as 1993. At that time, scientists observed that the lifespan of nematode worms doubled when FOXO3 was activated. The gene was subsequently studied more closely in humans, and it became clear that FOXO3 may promote longevity. Studies of very old people suggest that increased expression of the FOXO3 gene favours a long lifespan, an effect that had already been observed in a similar way in worms, flies and mice.
However, the life-extending effect of the gene apparently only comes into play when the diet is not high in calories, meaning when the person concerned tends to eat less rather than consume too much food. This appears to be linked to evolution. Studies of human skeletons from the Neolithic period show that the longevity-related variant of the FOXO3 gene was more common in the population at that time than it is today. For people living in that period, who were frequently forced to endure hunger, this may have provided a survival advantage.
When our ancestors later became sedentary and began consuming more carbohydrates, animal protein and fats, longevity variants may have become less common, according to the Kiel researchers.
Experiments on flatworms also suggest that hunger may have a positive effect on healthy ageing. These animals have an unusually high regenerative capacity and can even regrow individual body parts. They also have special survival strategies during periods of food scarcity. In such situations, the animals shrink and only begin to grow again once sufficient food is available. This process is regulated through the length of the so-called telomeres. These are protective caps located at the ends of chromosomes. They become shorter with each cell division, which is interpreted as part of the ageing process. During starvation, the stem cell pool from which the organism regenerates is modulated in such a way that cells with long telomeres predominate. From the researchers’ perspective, this points to a rejuvenating effect of fasting periods on cells.
The effects of a healthy diet are likely to be greatest when these principles are followed throughout life and from childhood onwards. However, studies show that changing one’s diet in middle age can still be effective. The principle is simple: more whole grains, fruit, vegetables, fish and nuts. This can clearly reduce the risk of death. In particular, deaths caused by cardiovascular disease are less common with this type of diet, and cancer-related mortality is also lower.
In brief: A radical diet is not necessary. Simply adding one serving of nuts or legumes each day and replacing one serving of processed meat or red meat can already make a difference. What matters is an overall improvement in the dietary pattern, not the elimination of one individual food.
We explore how nutrition interacts with other lifestyle factors in greater depth in the article Silent inflammation and an anti-inflammatory diet. Those who would also like to learn how their lifestyle affects cellular ageing can find further information in the article What biological age reveals. We also discuss the interaction between metabolic pathways such as mTOR, fasting and nutrition in detail in the article Longevity and mTOR.