Arxiu d'etiquetes: aging

White, brown or red?

For many people summer is synonymous of beach and tan. But there are people who are not tan during winter. Some people prefer to use UVA tanning booths a few months before, and others take the sun without protection to catch some colour. What consequences can this have? Then I will talk about the skin and the effect of radiation on it.


The skin is the largest organ of our body, has an area between 1.5 and 2m2 of surface and a weight around 3.5-5kg. Their functions are:

  • Protection: protects the internal organs from trauma and prevents the loss of water and electrolytes from the inside.
  • Thermoregulation: the blood vessels increase or decrease the temperature of the skin. When it is very hot the sweat refreshes the skin surface.
  • Sensitivity: the perception of touch, pressure, temperature, pain and itching is done through the skin.
  • Secretion: the skin protects the body from dehydration.
  • Excretion: through the skin we eliminate about 350ml per day of water, which we have to recover by moisturizing. In certain diseases you can get rid of a lot of protein and sulfur.

The skin has two basic cells: keratinocytes (80%) and melanocytes (10%). The melanin, which gives the tan, is found inside the melanocytes and accumulates in some bags (melanosomes). When it does not touch the light it remains in deep strata, whereas when it touches the sun goes up by the keratinocytes (Figure 1).

Figure 1. Melanin (arrows) rising towards the keratinocytes (Source: Salud del Siglo XXI)

Tan is the synthesis of new melanin. Not all people produce the same amount of melanin. We all have the same number of melanocytes, but the difference is in the number of melanosomes.

Our skin is formed by 3 layers that are, ordered from superior to inferior, epidermis, dermis and hypodermis (Figure 2).

capes pell
Figure 2. Skin layers: A) epidermis, B) dermis and C) hypodermis (Source: MedlinePlus)

The tanning process passes into epidermis, which is the top layer of the skin. Epidermis is 0.2mm thick and subdivided into 4 or 5 layers, depending on the body part. For example, the palms of the hands and soles of the feet are formed by 5 layers, where the extra layer gives more resistance. The thickness of the skin in these areas is 1-2mm, in contrast, in other areas, as in the eyelids, is lower (0.004mm). In the inner or deep layers, the cells are younger and more active, and along the cycle, they ascend to the outer or superficial area, becoming dead cells, without nucli and formed basically by keratin (dead skin).

Below, there is dermis that gives elasticity to the skin, where you find the nerves and blood vessels and is where the hairs and nails grow. Finally, hypodermis is below everything and is where the glands are.


The sun emits radiation with wavelengths ranging from 0.1 to 17,000nm. But only the radiations between 280 and 3,000nm arrive to the Earth (the others remain in the ozone layer).

Radiation that affects living organisms involves spectrum of 280-800nm (UVB, UVA, visible light and a part of infrared) (Figure 3).

Figure 3. Electromagnetic spectrum (Source: J. E. Martin Cordero. Agentes Físicos Terapéuticos (2009))

Not all radiation penetrates in the same way on our skin. Table 1 shows the level of penetration:

Table 1. Penetration according to the different radiation.



Level of penetration










Visible light




Infrared IR >700nm


It is important to know that prolonged exposure, without taking precautions, can not only produce skin cancer, but can also have other effects. UVB radiation is the most common cause of sunburn, erythema or redness. It is also the most common cause of skin cancer. In contrast, UVA radiation rarely causes burns, but is responsible for most photosensitization (abnormal increase in skin sensitivity to UV radiation) and may be carcinogenic in the presence of certain substances that enhance its effect. In addition, it causes aging of the skin (Figure 4).

In tanning booths 30% of the radiation is UV. Mostly it is UVA radiation, but there is also UVB radiation (albeit to a lesser extent). The remaining percentage is infrared radiation and visible light.

Figure 4. UVA (aging) and UVB radiation (burns) effects (Source:

The amount of irradiation is greater when the more near is the Earth of the Sun (zone of the Equator, between the Tropics of Cancer and Capricorn, or between 12 and 16 hours). This irradiation can damage our DNA, causing breaks in the DNA strand that can cause mutations.

UV rays easily pass through clouds and water vapor, but are partially absorbed by atmospheric pollution. It has been seen that in areas where there are holes in the ozone layer the incidence of skin cancer is higher. This is because the damage caused in the ozone layer allows the passage of more amount of UVB rays. Here the importance of not damaging the ozone layer, as it protects us from these rays.


Since the light can be reflected by several substances, it is necessary to take into account that, to direct rays of the sun, can be added those that arrive tangentially on a bright day and that are reflected by sand, water, soil, gel, snow…

Radiation doses are cumulative and may add to the effects of ionizing radiation (X-rays). The presence of skin cancer can be observed many years after an acute burn. This has been observed in American sailors who were in the Pacific during World War II, and who were exposed for months or years to high intensity solar radiation. These sailors have developed over the years different types of skin cancer.

For this reason it is very important to take the correct sun protection measures: use photoprotectors, avoid long periods in the sun, especially in hours of maximum solar intensity; and moisturize often.



Nutritional genomics: À la carte menu

When Hipprocrates said “let food be your medicine and medicine be your food” he knew that food influences our health. And it tells us that nutritional genomics, which I will discuss in this article; a new science appeared in the post genomic era as a result of the sequencing of human genome (all DNA sequences that characterize an individual) and the technological advances that allow the analysis of large amounts of complex information.   


The aim of nutritional genomics is to study the interactions of genes with elements of the human diet, altering cellular metabolism and generating changes in the metabolic profiles that may be associated with susceptibility and risk of developing diseases.

This study wants to improve the health and to prevent diseases based on changes in nutrition. It is very important not understand nutritional genomics how that specific food or nutrients cause a particular answer to certain genes.

When we talk about diet we have to distinguish between what are nutrients and what are food. Nutrients are compounds that form part of our body, while foods are what we eat. Food can take many nutrients or only one (such as salt).


Within nutritional genomics we find nutrigenomics and nutrigenetics, but although their names we may seem to mean the same is not the case (Figure 1).

Nutrigenomics is the study of how foods affect our genes, and nutrigenetics is the study of how individual genetic differences can affect the way we respond to nutrients in the foods we eat.

Figure 1. Schematic representation of the difference between nutrigenomics and nutrigenetics (Source: Mireia Ramos, All You Need is Biology)


Nutrients can affect metabolic pathways and homeostasis (balance) of our body. If this balance is disturbed chronic diseases or cancer may appear, but it can also happen that a disease, which we have it, be more or less severe. It means that impaired balance can give the appearance, progression or severity of diseases.

The aim of nutrigenomics is that homeostasis is not broken and to discover the optimal diet within a range of nutritional alternatives.

Thus, it avoids alterations in genome, in epigenome and/or in expression of genes.


Free radicals are subproducts that oxidise lipids, proteins or DNA. These can be generated in mitochondria, organelles that we have inside cells and produce energy; but we can also incorporate from external agents (tobacco, alcohol, food, chemicals, radiation).

In adequate amounts they provide us benefits, but too much free radicals are toxic (they can cause death of our cells).

Antioxidants neutralize free radicals. But where can we get these antioxidants? There are foods that contain them, as Table 1 shows.

Table 1. Example of antioxidants and some foods where we can find them (Source: ZonaDiet)

The way we cook food or cooking is important for avoid to generate free radicals. In barbecues, when we put the meat on high heat, fats and meat juices fall causing fire flames. This produces more flame and it generates PAHs (a type of free radicals). These adhere to the surface of the meat and when we eat it can damage our DNA.


Epigenome is the global epigenetic information of an organism, ie, changes in gene expression that are inheritable, but they are not due to a change in DNA sequence.

Epigenetic changes may depend on diet, aging or drugs. These changes would not have to exist lead to diseases as cancer, autoimmune diseases, diabetes…

For example, with hypomethylation, in general, cytosines would have to be methylated are not. What does it mean? Hypomethylation silenced genes and then, they cannot be expressed. Therefore, we need methylated DNA. A way of methylate DNA is eating food rich in folic acid.


There are agents (UV rays) that activate pathways that affect gene expression. Occurring a cascade that activates genes related to cell proliferation, no differentiation of cells and that cells survive when they should die. All this will lead us cancer.

It has been found that there are foods which, by its components, can counteract activation of these pathways, preventing signal transduction is given. For example curcumin (curry), EGCG (green tea) or resveratrol (red wine).



The fear of getting older

When we are children we look forward to the day of our birthday. That day is own, friends and family give us presents and we blow the candles hoping that all our wishes will fulfil. Over the years gifts decrease and we value that they remember us. But that special day is linked to the fear of getting older. In this article I will talk about what is aging and its genetics.


Rembrandt Harmensz van Rijn (1606 – 1669) was a Dutch painter and etcher. He is considered one of the greatest painters and printmakers in European art. He liked painting self-portraits (Figure 1). There are a lot of his self-portraits and we can look the course of time in his face and his aging.

Figure 1. Self-portraits by Rembrandt (Source: El Mundo)

We relate the word aging with the verb gain (gain experience, gain weight, gain wrinkles) and the verb lose (lose hair, lose loved ones, lose abilities). But what is aging?

Aging is a process that there is a deterioration of homeostatic mechanisms. Homeostasis is a system in which variables are regulated so that internal conditions remain stable and relatively constant (pH, oxygen pressure…). All organs and systems of our body are part of homeostatic mechanisms.

Then, as we age, in our organism the following occurs: decrease the organic functions, as with the stomach, which works worse and it is more difficult to digest; and it is more difficult to adapt, most old people are more easily dehydrated. All this is linked to a tissue atrophy and decrease cell turnover, since the balance between cells that form and cells that are destroyed is lost with age.

Aging is a physiological process, not a disease, although in this physiological situation there is more pathological events.


Sometimes when we talk about aging is easily confused with the term senescence. Aging refers to the whole body, while senescence is the aging process at the cellular and organic part.

When a cell suffer a senescent stimulus occurs an arrest cell cycle and DNA damage. It means that cell stops growing because its DNA is damaged. The diminution of cellular proliferation, for example in bone marrow it can cause anaemia.

Tissue cells can enter senescence due to UV radiation and a series of proteins are generated, activating macrophage recruitment of immune cells. These macrophage cells, as part of the immune system, are responsible for removing other harmful cell to the body. Then they kill senescent cells and leave holes, which are covered by new cells. This is what happens in normal skin.

If this process occurs in an old skin, some senescent cells can not die because there are not enough macrophages. Then the tissue will be thinned by their inability to form new cells.


There are a number of factors, including genetic and epigenetic factors that contribute to aging (Figure 2):

  1. Genomic instability: there has to be balance between DNA damage and repair pathways. It has to repair DNA to not have a senescent phenotype in the cell.
  2. Telomere attrition: they are the ends of chromosomes and will shorten after each cell division. When they are very short the cell dies.
  3. Epigenetic alterations: how environment influences in gene expression.
  4. Loss of proteostasis: changes in degradation capacity of proteasome, a complex which eliminates unneeded or damaged proteins.
  5. Deregulated nutrients sensing: the elderly do not control well their desire to eat, or they eat too much or they eat very little. They have not a good sensitivity to signals of satiety and appetite. The same applies to the sensation of thirst. The elders never thirst and this can cause dehydration.
  6. Mitochondrial dysfunction: mitochondria provide energy for cellular activity.
  7. Cellular senescence: cell damage processes occur.
  8. Stem cell exhaustion: stem cell formation decreases. In muscle cells there are not new cells to repair muscle fibres and muscle is becoming smaller, causing the person is getting weaker.
  9. Altered intercellular communication: different cellular pathways do not work well.
hallmarks aging
Figure 2. The 9 hallmarks of aging (Source: The Hallmarks of Aging)

You can propose a number of alternatives or interventions in each of the above factors that could lengthen the average life of the organism, but still not have the tools necessary to assess all factors that may be involved in aging, although much has been achieved in recent years.

However, the interpretation of what is pathological and what is not supposed one of the main challenges to solve.


  • F. Rodier, J. J. Campisi. Four faces of cellular senescence. Cell Biol. 2011; 192(4), 547-56
  • Daniel Muñoz-Espín, Manuel Serrano. Cellular senescence: from physiology to pathology. Nat. Rev. Molecular Cell Biology 2014; 15, 482-496
  • C. López-Otin, M. A. Blasco, L. Partridge, M. Serrano, G. Kroemer. The Hallmarks of Aging. Cell 2013