Aging progressively decreases testosterone levels by about 1% per year after the age of 30 or 40. How does it interact with an individual’s diet?

A new study published in the Journal of the American Urological Association concludes that men who follow a more proinflammatory diet appear to have a higher risk of testosterone deficiency, indicating the important role of a healthy diet in male reproductive health.

Alejandro Monzó – Neolife Nutrition and Nursing Unit

Industrial food consumption and sedentary lifestyles in the spotlight

.

Testosterone is an androgen or steroid hormone. It is produced mainly in the testes and ovaries (1). In men, it is the main male sex hormone and also an anabolic steroid. Testosterone fulfills different functions, which help to maintain:

• • Bone density
  • The distribution of fat
  • Muscle mass and strength
  • Facial and body hair
  • The production of red blood cells
  • Sex drive and sperm production

Hypogonadism impairs the ability to produce normal amounts of testosterone due to a problem with the testes or with the pituitary gland that controls the testes (1). Hormone replacement therapy with testosterone, administered as injections, tablets, patches or gels, may improve the symptoms of low testosterone in men, a very common treatment at Neolife

Nowadays, the average testosterone level in men has reduced significantly in recent decades. Although loss of testosterone is common as men age, scientific evidence shows that it is often associated with diabetes, abdominal obesity, sexual dysfunction, depression, and other adverse conditions (2).

According to new research published in the Journal of the American Urological Associationa diet rich in proinflammatory foods, including foods that contain refined carbohydrates and sugar, as well as polyunsaturated fats, may lead to testosterone deficiency in men (3). This study investigated the link between dietary inflammatory index and sex hormones in a representative sample of nearly 4,200 adult men. They provided a 24-hour dietary intake history and underwent sex hormone tests. For men on the more proinflammatory diet, the odds of testosterone deficiency were approximately 30% higher compared to men on the more anti-inflammatory diet.

The authors state that the study’s findings do not prove causality; however, they support previous research suggesting that this type of diet may contribute to testosterone deficits, in addition to other potential health problems. Men with low testosterone levels have higher levels of proinflammatory cytokines, small proteins released by cells during injury or infection or in response to inflammatory factors in the environment.

A proinflammatory diet is generally characterized by the consumption of refined carbohydrates, processed meats, trans fats, poor quality oils, and sugary drinks. In short, foods belonging to the fast food group, industrial and ultra-processed foods, all of them rich in fat, sugar, and salt. In an antioxidant diet, there is more consumption of vegetables, fruits, legumes, and nuts. New research published in the Journal of the American College of Cardiology shows that certain dietary patterns have the potential to significantly increase cardiovascular risk, so that appropriate intervention at this point may result in an effective disease prevention strategy (4, 5) (Figure 1).

Figure 1. Proinflammatory diet vs. anti-inflammatory diet: potential effects (5).

No isolated food ‘per se’ induces an increase in testosterone. However, an unhealthy proinflammatory diet, especially due to its effect on obesity and increased cardiovascular risk, may produce a decrease in testosterone(6). There is increasing evidence that poor eating habits are associated with a variety of chronic diseases, such as cardiovascular disease, type 2 diabetes or obesity, which is key to understanding their interaction with declining testosterone levels.

Therefore, a healthy, balanced, antioxidant diet may have a beneficial effect on testosterone levels. Intakes of complex carbohydrates, fiber, healthy fats, vitamins, and minerals, such as those mentioned below, have demonstrated the important role of a healthy diet in men’s health (6, 7, 8):

• A high consumption of vegetables, especially cruciferous vegetables, such as broccoli, Brussels sprouts, cauliflower, in addition to helping prevent cancer, favor the increase of testosterone levels.
• Restrictive diets, especially when it comes to fat, may also reduce serum testosterone levels in men. Cholesterol is necessary for the production of testosterone, so consuming natural fats, from quality meats, fish and eggs, nuts, extra virgin olive oil, coconut and avocado, may be a suitable option.
• In particular, minerals such as zinc, selenium, and magnesium play a relevant role in optimizing testosterone levels and fertility. Adequate consumption of nuts, liver, eggs, dark chocolate, seafood, and crustaceans may also be of interest.

Finally, there are several factors associated with a decrease in testosterone, such as advanced age, environmental pollution, lifestyle, the presence of structural alterations in the reproductive system, diseases such as obesity, and an unhealthy diet. At Neolife, our medical-nutritional team works with each individual and particular case; this is where dietary-nutritional advice is of special interest due to its great ability to prevent disease and potentially improve testosterone levels.

BIBLIOGRAFÍA

(1) Mayo Clinic. (2021). “Sexual health: testosterone”. URL: https://www.mayoclinic.org/healthy-lifestyle/sexual-health/in-depth/testosterone-therapy/art-20045728

(2) Kalvaitis, K. (2007). “Generational decline in testosterone levels observed”. Endocrinetoday. Healio. URL: https://www.healio.com/news/endocrinology/20120325/generational-decline-in-testosterone-levels-observed

(3) Zhang, C. y otros. (2021). “The Association between dietary inflammatory indcex and sex hormones among men in the United States”. Vol. 206, 1-7. American Urological Association. URL: https://www.auajournals.org/doi/10.1097/JU.0000000000001703

(4) De Luis Román, D.A. Bellido Guerrero, D. García Luna, P.P. Olivera Fuster, G. (2017). “Dietoterapia, nutrición clínica y metabolismo”. Tercera edición. Sociedad Española de Endocrinología y Nutrición. Grupo Aula Médica, S.L. Madrid, España.

(5) Li, J. y otros. (2020). “Dietary Inflammatory potential and Risk of cardiovascular disease among men and women in the U.S.”. Journal of the American College of Cardiology. Vol. 76 (19). URL:https://www.sciencedirect.com/science/article/abs/pii/S0735109720371904?via%3Dihub

(6) Camarero, A. (2019). “La alimentación insana puede producir un descenso de testosterona”. El Confidencial: Alimente. URL: https://www.alimente.elconfidencial.com/bienestar/2019-12-17/dieta-insana-descenso-testosterona_2379316/

(7) Guadalupe G-R, L. y otros. (2018). “Nutrición y fertilidad”. Nutrición hospitalaria. Vol. 35(6): 7-10. URL: https://scielo.isciii.es/pdf/nh/v35nspe6/1699-5198-nh-35-nspe6-00007.pdf

(8) Vázquez, M. (2013). “Aumenta tus niveles de testosterona, de manera natural”. Fitness Revolucionario. URL: https://www.fitnessrevolucionario.com/2013/05/19/aumenta-tus-niveles-de-testosterona-de-manera-natural-parte-ii/

La entrada Proinflammatory Diet and Testosterone se publicó primero en Neolife.

We live in mutualistic symbiosis with these microorganisms that inhabit our gut; we need each other.

Having a healthy microbiota is vital for our mental health, weight and appetite control, rest, lowering our cardiovascular risk, lowering our risk of developing diabetes, lowering our risk of developing cancer, having a proper immunity, preventing the development of autoimmune diseases, intolerances, allergies, migraine, diarrhea, constipation and abdominal pain, infertility, etc…

Dr. Alfonso Galán González – Neolife Medical Team

The microbiota is of utmost importance to our immune system.

You may know it as gut microbiota, microbiome, or gut flora in more colloquial terms. By now, we all know that we have healthy bacteria in our intestine that live with us and provide beneficial effects to our bodies. But do you really know how important they are? Did you know that changes in our microbiota are linked to pathologies? Did you know that we can study it…and repair it?

We also have microbiota in our skin and mucous membranes in physiological terms (except for the conjunctiva of the eye, which is sterile by definition). Approximately 80% of our immune system cells are in the gut and communicate via blood and lymph with the rest of the body.

Our gut microbiota accompanies us from the moment we are born (some studies now suggest that the amniotic fluid in which we swim before birth already carries bacteria that begin to populate our gut). As we pass through the birth canal, lay on our mother’s breast, receive kisses from family members, and suckle for the first time, we receive bacteria that colonize our gut. Our flora matures during the first 4-5 years of life, as we are exposed to different environments and foods.

Symbiosis and health

We live in mutualistic symbiosis with these microorganisms; we need each other. And we say microorganisms because they are not only bacteria, but also fungi and yeasts, viruses, protozoa, and archaea.

Some interesting facts:

• We have 100 trillion bacteria in our gut. This is 10 times more than the number of cells in the entire body!
• We have more than 1000 different species of bacteria.
• About 2 kg of our body weight is comprised of microbiota.
• They make up 48% of the weight of our stool.
• Our body is comprised of 21% protein, and we are not able to synthesize many amino acids (the components of proteins), but our microbiota can.
• More than 30% of the substances circulating in our blood are produced by the microbiota.

Our microbiota need multi-species communities to live and complete their metabolic capacity to degrade nutrients, obtain energy, and synthesize essential compounds for the community.

Having a healthy microbiota is vital for our mental health, weight and appetite control, rest, lowering our cardiovascular risk, lowering our risk of developing diabetes, lowering our risk of developing cancer, having a proper immunity, preventing the development of autoimmune diseases, intolerances, allergies, migraine, diarrhea, constipation and abdominal pain, infertility, etc…

I hope I got your attention with this last paragraph. Everything it says has been rigorously and scientifically proven, and, as always, we will get into it in greater detail.

The microbiota is of utmost importance to our immune system; 80% of our immune system cells are in the gut and communicate via blood and lymph with the rest of the body. It influences the maturation and correct functioning of our immune system by “training” it continuously and teaching it what to attack and what not to attack.

It constitutes a physical and biochemical barrier to prevent the entry of pathogens. If our microbiota is not in balance, we enter into what we call dysbiosis which leads to inflammation and disease.

It behaves like a real “second brain”. The enteric nervous system contains as many neurons as our medulla. Sixty percent of the information that reaches our brain comes from our gut, and it produces neurotransmitters in even greater quantities than the central nervous system (CNS). With our CNS, it is permanently in communication through these neurotransmitters, the hypothalamic-pituitary-adrenal axis (which we covered here), the bacterial metabolites, and cytokines secreted, etc… Who hasn’t felt nervousness, fear, hope, all kinds of emotions in “the gut”? They are closely related.

Functional groups

The most important and most studied group of gut microbiota are bacteria. As already mentioned, there are over 1000 species that are grouped into a number of functional groups, with similar functions. This facilitates their study and analysis.

We should make a distinction between the group of medium stabilizing bacteria and the group of facultative pathogens. Within the group of those that control the stability and homeostasis of the intestinal environment, we find bacteria that are protective, immunomodulatory, muconutritive, primary saccharolytic, and neuroactive. We’ll discuss their functions and the consequences of their alteration below.

Among the facultative pathogenic microorganisms, we find proteolytic bacteria, and fungi and yeasts.

The following depend on the functional stability of our microbiota:

• Food digestion
• The absorption of nutrients
• Normal immune, metabolic, and neuroactive performance

Immunoregulatory Microbiota

The most important bacteria in this group are apathogenic Escherichia coli and Enterococcus faecalis.

They locally regulate all the components involved in immune response, ensure a continuous training of the immune system, are able to induce non-specific immune responses, and collaborate with the immune system in the phenomena of immune identification or immunotolerance (identifying pathogens as pathogens and harmless molecules as non-pathogenic and therefore not susceptible in order initiate the correct immune reaction).

If we have a test result that shows a level that is below the normal range for these bacteria, the subject has an increased susceptibility to immune disorders such as autoimmune diseases, allergies, or immunodeficiencies.

Protective Microbiota

These are mainly bacteria like as Lactobacillus, Bifidobacterium and Bacteroides.

They stabilize the intestinal environment by maintaining the necessary acid pH in the intestine, and synthesize bacteriocins and hydrogen peroxide, protecting us from the growth and colonization of pathogenic microorganisms. Additionally, they strengthen and repair tight junctions, the junctions between the cells of the intestinal epithelium; when these fail, they lead to the very common symptoms of intestinal permeability.

If their number is low, we lose this barrier function against pathogens; the environment is destabilized, favoring dysbiosis, and nutrient absorption is compromised.

Muconutritive Microbiota

The most important bacteria in this group are Faecalibacteroium prausnitzii and Akkermansia muciniphila.

They stabilize the mucus layer that lines the intestinal epithelium, where our microbiota lives. They renew this mucus layer by degrading it and the intestinal fiber, producing oligosaccharides and SCFA (short-chain fatty acids) that serve as food for the intestinal cells and the rest of the microbiota. They modulate inflammation, and in a very important and characteristic way, they regulate neoglycogenesis, that is, the synthesis of glucose in the liver.

When these bacteria are low, we have an increased susceptibility to suffer from inflammatory pathologies such as Crohn’s disease and ulcerative colitis, and metabolic diseases such as type 2 diabetes, metabolic syndrome, obesity, or non-alcoholic fatty liver disease.

Primary saccharolytic Microbiota

The most important bacteria in this group are Bifidobacterium adolescentis and Ruminococcus Bromii

They support muconutritive microbiota in the digestion of long and complex carbohydrate chains. They stimulate other species to degrade dietary fiber normally. They are essential for the primary degradation of resistant starch and oligofructose, producing butyric and lactic acid that nourish intestinal cells and acidify the medium respectively.

A low count in this functional group, therefore, means that we cannot digest complex carbohydrates well and do not effectively produce the aforementioned SCFA.

Neuroactive Microbiota

Once again, Bifidobacterium adolescentis and lactobacillus plantarum are the most important bacteria in this group.

Neuroactive microbiota are able to synthesize GABA (Gamma amino butyric acid), which is an essential neurotransmitter especially in cases of anxiety. They also modulate neurotransmitter receptors and stabilize the gut-brain axis, the immune system, and visceral pain. Their ability to synthesize neurotransmitters like those in our brain means that our bacteria and our brain have a common language that functionally consolidates this gut-brain axis. We know that by administering Lactobacillus plantarum to stressed individuals, their stress and anxiety is reduced, with a correlation in the levels of neurotransmitters like GABA, serotonin, dopamine, and norepinephrine. Depressed patients show intestinal dysbiosis and alterations in neurotransmitter levels, affecting the gut-brain axis.

Proteolytic Microbiota

Proteolytic microbiota is composed of various bacteria that are facultative pathogens. That is, in the right balance and quantity, they do favorable work for the host, but if they get out of control, they can harm us.

They contribute to the digestion of proteins by generating good degradation products such as amino acids, and potentially harmful ones such as biogenic amines (some known as histamine and others with disturbing names like putrescine or cadaverine), ammonia, etc….

If we have an overgrowth of proteolytic bacteria, the pH of the intestine – which, remember, should be physiologically acidic – becomes more alkaline, favoring the development of pathogens. Our system tries to acidify the intestine again at the cost of overloading the liver and consuming our blood bicarbonate, leading to further acidification of the environment. These proteolytic bacteria injure the intestinal mucosa producing chronic inflammation and altering intestinal permeability.

Fungal Microbiota

Composed of fungi and yeasts, the most important of these is Candida.. If it grows above normal levels, it becomes pathogenic and releases toxic metabolites; it may also behave as a reservoir of fungi so that we may present infections in other areas such as the mouth (thrush), vagina (yeast infection), etc.

Well, I hope this has conveyed just how important it is to have a balanced microbiota, where we have the right amount of all the bacteria and microorganisms necessary, without an overgrowth of facultative pathogens or a weak protective microbiota.

Environmental and toxic factors

Unfortunately, the life we live may lead us to a real extinction of our intestinal bacteria, favoring cases of dysbiosis.

These are just a few of the external factors that may affect you:

• Diet; an excess of meat, sugar, or low fiber intake alter our flora.
• A sedentary lifestyle favors dysbiosis.
• Rest; circadian rhythm disorders and deregulation also favor dysbiosis.
• Chemicals; from additives to endocrine disruptors, these alter our gut bacteria.
• Drugs; especially antibiotics and proton pump inhibitors (the famous Omeprazole and drugs of that family).
• The very same aging process is related to a decrease in the population of protective bacteria and an increase in proteolytic bacteria.

It is more than likely that you have identified with one or more of these symptoms, which may be an indication of an imbalance in your microbiota.

At Neolife, we may now assess your intestinal microenvironment in the most scientific and advanced way with a simple stool sample. Our medical team will correlate your symptoms to the test findings and propose the best way to restore balance in your microbiota and correct the problem.

BIBLIOGRAFÍA

(1) Role of the normal gut microbiota. World J Gastroenterol 2015 August 7; 21(29): 8787-8803

(2) Enterococcus faecalis Inhibits Hyphal Morphogenesis and Virulence of Candida albicans Melissa R. Cruz, Carrie E. Graham, Bryce C. Gagliano, Michael C. Lorenz, Danielle A. Garsin Infection and Immunity January 2013 Volume 81 Number 1. 189-200

(3) Review Article: Association between Faecalibacterium prausnitzii Reduction and Inflammatory Bowel Disease: A Meta-Analysis and Systematic Review of the Literature Hindawi Publishing Corporation Gastroenterology Research and Practice Volume 2014, Article ID 872725, 7 pages

(4) Exploring the influence of the gut microbiota and probiotics on health: a symposium report Linda V. Thomas, Theo Ockhuizen and Kaori Suzuki. British Journal of Nutrition (2014), 112(S1), S1–S18

(5) Role of the Microbiota in Immunity and Inflammation Yasmine Belkaid and Timothy W. Hand Cell 157, March 27, 2014 ª2014 Elsevier Inc. 121-141

(6) Contribución de la microbiota intestinal y del género «Bifidobacterium» a los mecanismos de defensa del huésped frente a patógenos gastrointestinales Y. Sanz, M.C. Collado, J. Dalmau Acta Pediatr Esp. 2006; 64: 74-78

(7) Probiotics and prebiotics and health in ageing populations Sylvia H. Duncan∗, Harry J. Flint Maturitas 75 (2013) 44– 50

La entrada Gut Microbiota se publicó primero en Neolife.

Obesity is a growing epidemic and one of the leading causes of preventable death worldwide. Unhealthy eating habits and a sedentary lifestyle are most responsible for weight gain and fat accumulation.

Obesity is a disease that affects over 650 million people worldwide. It’s a global public health problem, and it costs over 150 billion annually to treat acute and chronic obesity conditions. Recently, a promising study has been published, which has demonstrated the action mechanism and preclinical efficacy of a protein called BAM15, effective in the treatment of obesity and related metabolic disorders.

Alejandro Monzó – Neolife Nutrition and Nursing Unit

BAM15 is a protein that prevents weight gain and fat accumulation, while reducing blood sugar levels

Advances in small molecule screening and biochemical engineering have led to a renewed interest in mitochondrial agents directed towards the treatment of metabolic disease, such as obesity. Currently, only four medicines (orlistat, phentermine-topiramate, naltrexone-bupropion, and liraglutide) are approved for the treatment of obesity (2, 3). However, they are limited when it comes to effectively providing long-term weight loss.

Their limitations are due, in part, to the difficulty in identifying bioactive compounds with a wide therapeutic range that address the multifactorial causes and effects of obesity. Recently, the scientific journal EMBO Molecular Medicine published research that reveals a very promising step in addressing obesity. The protein BAM15, a mitochondrial proton translocator, may be used to treat this chronic, non-communicable disease (3).

In general, existing medications work by reducing appetite or calories absorbed after food intake (2). The protein BAM15 differs greatly from these drugs, as its potential lies in decreasing the efficiency of cellular mitochondria, resulting in their “burning” more energy (3). Mitochondria are the cellular organelles responsible for supplying most of the energy needed for cellular activity, acting as power plants and releasing ATP, which is the fuel for most cellular processes (4).

Researchers have shown in trials with mice that those who received BAM15 burned more calories and therefore had a lower weight gain than the mice in the control group (3). After obtaining these results, the authors noted that this protein may be used to treat obesity, in addition to other diseases related to it, such as diabetes, liver disease, and some forms of cancer. Additionally, the study shows numerous other benefits of this protein (Figure 1):

• It lowers blood sugar and insulin levels, regardless of weight loss.
• It improves sensitivity of skeletal muscles to the effects of insulin.
• It reduces total fat accumulation by restricting fat deposit in the liver, kidneys, and blood.

Generally speaking, BAM15 prevents weight gain, fat accumulation, and lowers blood sugar levels. Mitochondria burn more energy, and this way, the body composition and blood sugar levels of overweight and obese patients may be modulated. This compound is proposed as a treatment option for these patients, where scientists point out very good results in animal models.

Obesity is currently the result of a positive energy balance. The underlying causes of this positive balance are usually modifiable: a high calorie intake, a reduction in the body’s energy consumption due to decreased physical activity or, more commonly, a combination of both situations. Also, the socio-economic changes we’ve experienced in recent decades have led to a wider availability of food and the production of energy-dense and very nutritionally poor processed foods. At the same time, physical activity has been drastically reduced in the population, due to more sedentary work and the generalization of means of transport. Additionally, we need to add the neuro-hormonal regulation of energy metabolism, which plays a permissive role in the development of obesity (5,6,7).

Despite the search for new drugs and treatments to prevent obesity, there is solid scientific evidence pointing to the change in habits that a person must make to achieve a healthy lifestyle and prevent obesity. A healthy diet has proven to be the fundamental component in the treatment of obesity and should be part of a comprehensive program that includes behavioral therapy and physical exercise, with the aim of, beyond reducing body weight, changing lifestyle habits (5, 6, 7). Therefore, the FESNAD-SEEDO consensus states that the dietary management of obesity should (6):

• Decrease body fat while preserving lean mass to the maximum
• Takes place in the long term
• Be effective in the long run, maintaining weight
• Prevent future weight gains
• Include nutrition education that eliminates bad eating habits and mistakes
• Decrease cardiovascular risk factors associated with obesity (high blood pressure, dyslipidemia, prediabetes or diabetes mellitus)
• Improve comorbidities linked to excess weight (sleep apnea, osteoarthritis, neoplastic risk, etc.)
• Induce psychosomatic improvement with the recovery of self-esteem
• Improve functional capacity and quality of life

Finally, at Neolife, we’ve developed a comprehensive program for the health promotion and disease prevention of our patients. Our approach to obesity through medical and nutritional treatment is one of Neolife’s specialties, with the highest positive results. Looking ahead, the use of new facilitative treatments, such as the use of the protein BAM15, may prove promising to improve body composition and metabolic balance outcomes. We will, therefore, be on the lookout for the latest results of the clinical trials conducted with this protein.

BIBLIOGRAPHY

(1) (2020). “Obesity and overweight”. World Health Organization. URL: https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight

(2) Mayo Clinic. (2020). “Obesity: prescription weight-loss medication”. URL: https://www.mayoclinic.org/diseases-conditions/obesity/diagnosis-treatment/drc-20375749

(3) Axelrod, C.L. et al. (2020). “BAM15-mediated mitocondrial uncoupling protects against obesity and improves glycemic control”. EMBO Molecular Medicine e12088. URL: https://www.embopress.org/doi/10.15252/emmm.202012088

(4) (2020). “Mitochondria”. National Human Genome Research Institute. URL: https://www.genome.gov/genetics-glossary/Mitochondria

(5) Liliana P. Rodota y María Eugenia Castro. “Nutrición clínica y dietoterapia” [Clinical nutrition and diet therapy]. Editorial Médica Panamericana, 1ª Edición, 2012.

(6) De Luis Román, D.A. Bellido Guerrero, D. García Luna, P.P. Olivera Fuster, G. (2017). “Dietoterapia, nutrición clínica y metabolismo” [Diet therapy, clinical nutrition and metabolism]. Third Edition. Sociedad Española de Endocrinología y Nutrición. Grupo Aula Médica, S.L. Madrid, Spain.

(7) Redondo S., M.R. & González R., L.G. (2015). “Nutriguía: manual de nutrición clínica” [Nutrition Guide: Clinical Nutrition Manual]. 2^nd Edition. Editorial Médica Panamericana.

La entrada A Protein that Fights Obesity se publicó primero en Neolife.

The way our genetic material works is that some genes are transcribed, that is, that their information is read and used to create a protein with a particular function, and that other genes, however, are not read, are not transcribed despite being encoded in our DNA.

Whether a cell becomes a neuron, a skin cell, or a muscle cell is determined by which genes are being read in each case. DNA methylation, in fact, regulates which genes are expressed and which are not. Simply put, methylated regions silence genes, and nonmethylated regions express genes. As previously mentioned, as we age, our DNA methylation levels decrease, and we have less control over our DNA.^.

Dr. Alfonso Galán González – Neolife Medical Team

Unlike the permanent mutations in our genes, which we cannot change, we do have the ability to change this epigenome.

In this blog post, we’ll present one of the famous 9 “Hallmarks of Aging”, or factors that determine aging, which are, in fact, reversible. We’re talking about epigenetic alterations.

Epigenetics is not the easiest thing to explain, but we’ll give it a try. If we consider the word “epigenetics”, we may see it means something that is “epi” or “over” or “on top of” our genes. Something that is not written in our genes, in our DNA, but that impacts how our genes are going to work. The way our genetic material works is that some genes are transcribed, that is, that their information is read and used to create a protein with a particular function, and that other genes, however, are not read, are not transcribed despite being encoded in our DNA. Whether a cell becomes a neuron, a skin cell, or a muscle cell is determined by which genes are being read in each case, even though all these cells have the same genetic material. So, our genome is the complete list of all the genes that we can potentially read or not read, activate or not, turn ON or OFF, and what determines this? Our epigenome.

Our epigenome are a series of markers added to our DNA without modifying its sequence, but which determine exactly that, what should be expressed and what should not.

All our cells have 23 chromosomes. Chromosomes are a tangle of chromatin, formed by nucleosomes, which look like the beads of a necklace, which are in turn made up of DNA coiled around proteins called histones. This is how structural support is given to the chromosomes and they fit in the nucleus of the cell.

Epigenetic alterations consist of changes in this chromatin and may be changes in both the histones and chromatin structure, as well as the addition of methyl groups to the DNA. These alterations may be inherited by daughter cells and therefore perpetuated.

Let’s delve deeper into the issue of DNA methylation (1).

DNA methylation, in fact, regulates which genes are expressed and which are not. Methylation patterns change over time. Simply put, though it’s actually a bit more complicated, methylated regions silence genes, and nonmethylated regions express genes. As previously mentioned, as we age, our DNA methylation levels decrease, and we have less control over our DNA (3).

This influences the function of the cells, harming them and predisposing them to the appearance of a pathology. Yes, indeed, we’re talking about the often mentioned diseases associated with aging. We now know that these epigenetic alterations, namely this change in DNA methylation patterns predispose to cancer, neurodegenerative diseases, obesity, diabetes, insulin resistance, inflammation, cardiovascular disease, immune disorders, etc. (2). These epigenetic alterations accumulate as we age, and we can measure them. Multiple “epigenetic clocks” such as Horvath’s and more complete current ones have been designed, which are used to measure just how methylated a series of genes are, giving us an idea of our biological age as opposed to our chronological age. Tests are now available that measure the methylation of millions of sites in the genome when initially only a few hundred (4) were available.

Unlike the permanent mutations in our genes, which we cannot change, we can modify this epigenome, and there are multiple studies that show how we can make these clocks start working backwards and rejuvenate our biological age, based on what they measure.

How can we do this?

Well, you’ve probably heard all this before: exercise, a balanced diet, and supplementation.

A systematic review of the scientific literature published in January this year shows us that strength training in humans induces epigenetic alterations in pathways associated with energy metabolism and insulin sensitivity, contributing to skeletal muscle health. Aerobic exercise also causes modifications in biomarkers associated with metabolic alterations through changes in specific DNA methylation and mRNA expression. It seems that the best strategy is a combination of both types of exercise (6).

Calorie restriction, which we’ve already discussed in previous blog posts, prevents a decrease in DNA methylation levels, even in different organs (5).

Calorie restriction mimetics, like metformin or resveratrol have also demonstrated these benefits.

Smoking and psychological trauma lead to changes in methylation patterns.

The availability of methyl group donor molecules influences our methylation levels. Betaine (trimethyl glycine –TMG-) is a safe supplement that helps us with this task (7). Additionally, it lowers homocysteine levels; you may see why this is important here.

In short, a decrease in DNA methylation leads to pathology and aging. This process may be reversed through exercise, a proper diet, and supplements like TMG.

We cannot emphasize enough how important it is to exercise and maintain a good diet. This is just more scientific proof of their incredible benefits.

BIBLIOGRAPHY

(1) Moore LD, Le T, Fan G. DNA methylation and its basic function. Neuropsychopharmacology. 2013 Jan;38(1):23-38. doi: 10.1038/npp.2012.112. Epub 2012 Jul 11. PMID: 22781841; PMCID: PMC3521964.

(2) Sallustio F, Gesualdo L, Gallone A. New findings showing how DNA methylation influences diseases. World J Biol Chem. 2019 Jan 7;10(1):1-6. doi: 10.4331/wjbc.v10.i1.1. PMID: 30622680; PMCID: PMC6314879.

(3) Heyn H, Li N, Ferreira HJ, Moran S, Pisano DG, Gomez A, Diez J, Sanchez-Mut JV, Setien F, Carmona FJ, Puca AA, Sayols S, Pujana MA, Serra-Musach J, Iglesias-Platas I, Formiga F, Fernandez AF, Fraga MF, Heath SC, Valencia A, Gut IG, Wang J, Esteller M. Distinct DNA methylomes of newborns and centenarians. Proc Natl Acad Sci U S A. 2012 Jun 26;109(26):10522-7. doi: 10.1073/pnas.1120658109. Epub 2012 Jun 11. PMID: 22689993; PMCID: PMC3387108.

(4) Bell CG, Lowe R, Adams PD, Baccarelli AA, Beck S, Bell JT, Christensen BC, Gladyshev VN, Heijmans BT, Horvath S, Ideker T, Issa JJ, Kelsey KT, Marioni RE, Reik W, Relton CL, Schalkwyk LC, Teschendorff AE, Wagner W, Zhang K, Rakyan VK. DNA methylation aging clocks: challenges and recommendations. Genome Biol. 2019 Nov 25;20(1):249. doi: 10.1186/s13059-019-1824-y. PMID: 31767039; PMCID: PMC6876109.

(5) Gensous N, Franceschi C, Santoro A, Milazzo M, Garagnani P, Bacalini MG. The Impact of Caloric Restriction on the Epigenetic Signatures of Aging. Int J Mol Sci. 2019 Apr 24;20(8):2022. doi: 10.3390/ijms20082022. PMID: 31022953; PMCID: PMC6515465.

(6) Barrón-Cabrera E, Ramos-Lopez O, González-Becerra K, Riezu-Boj JI, Milagro FI, Martínez-López E, Martínez JA. Epigenetic Modifications as Outcomes of Exercise Interventions Related to Specific Metabolic Alterations: A Systematic Review.

Lifestyle Genom. 2019;12(1-6):25-44. doi: 10.1159/000503289. Epub 2019 Sep 23. PMID: 31546245; PMCID: PMC6921698.

(7) Zhao G, He F, Wu C, Li P, Li N, Deng J, Zhu G, Ren W, Peng Y. Betaine in Inflammation: Mechanistic Aspects and Applications. Front Immunol. 2018 May 24;9:1070. doi: 10.3389/fimmu.2018.01070. PMID: 29881379; PMCID: PMC5976740.

La entrada Epigenetics and DNA Methylation: Why Should you care? se publicó primero en Neolife.

Preventive medicine seeks to detect diseases or dysfunctions before irreversible problems occur. The use of specific biomarkers in the monitoring of our patients is absolutely essential. Ferritin is one of these. Higher levels of ferritin may be due to multiple causes, but it deserves special attention.

Iron deposits are evaluated by determining the levels of ferritin. In some inflammatory diseases, it rises as a reactant. However, high levels of ferritin may be concealing a disease with serious repercussions: hemochromatosis.

Dr. Celia Gonzalo Gleyzes – Neolife Medical Team

Hemochromatosis is characterized by an increase in iron absorption from the food we consume

.

Before we begin, a brief history to put us in the proper context. In 1865, Armand Trousseau observed a link between liver cirrhosis, diabetes mellitus, and skin hyperpigmentation, in a 28-year-old Parisian newspaper salesman. He calls this disease bronze diabetes. In England, in 1899, Von Recklinghausen began using a new term: “hemochromatosis“.

What is hemochromatosis?

Hemochromatosis is an autosomal recessive genetic disorder (the mutation of the two copies of the gene will result in the disorder at its greatest extent). It is characterized by an increase in the absorption of iron from our diet. This metal is accumulated due to a problem in the excretion mechanisms, causing toxic effects.

In this type of hemochromatosis, iron is deposited in parenchyma cells, but additionally (due to excess transfusions, hemolysis, etc.), it accumulates in the cells of the reticuloendothelial system.

The different types of hereditary hemochromatosis (HH) are:

1. Type 1 (related to the HFE-hemochromatosis gene protein- with C282Y and H63D being the most common mutations of this gene): classic form of autosomal recessive inheritance of hereditary hemochromatosis.
2. Type 2 (mutations in the hemojuvelin gene) and type 2b (mutations in the hepcidin gene): autosomal recessive. Onset of the disease at about 15-20 years of age.
3. Type 3 (mutations in the transferrin receptor 2 gene): autosomal recessive, onset at 30-40 years of age.
4. Type 4 (mutations in the ferroportin gene): autosomal dominant, variable onset between 10-80 years of age.

Epidemiology

Hereditary hemochromatosis is the most common autosomal recessive disease amongst white people (the risk is 6 times higher than in the black population), with a prevalence of 1 in 300-500 individuals. Type 1 is more common in individuals of northern European descent.

Men are affected 2-3 times more than women. Symptoms appear in men (in non-juvenile forms) over the age of 50 and in women later (60 years of age). This is because the later “release iron” throughout their lives through menstruation.

Excess iron and oxidative stress

Iron fulfills an essential role in multiple cellular functions, but can be harmful because of its ability to release free radicals that will in turn cause:

1. Fibrosis: your cells will be replaced by fibrotic tissue.
2. Enzyme inactivation.
3. Carcinogenic effects: mutations, possible activation of oncogenes (especially in the liver).

Manifestations of the disease

We can say that this pathology has a multi-systemic involvement, including organs such as the liver, pancreas, heart, thyroid gland, joints, gonads, and pituitary gland.

Alcohol consumption speeds up liver and pancreatic damage.

The following are the system alterations:

• Liver damage: cirrhosis is present in 70% of patients with hemochromatosis. Increased risk of liver cancer.
• Pancreas: iron accumulates affecting organ functions, such as insulin secretion, resulting in secondary diabetes. It is worth noting that heterozygous patients may present this alteration.
• Joints: pain without destruction. Calcium pyrophosphate crystals are detected in synovial liquid.
• Heart: risk of congestive heart failure secondary to dilated cardiomyopathy and arrhythmias. Left ventricle dysfunction may sometimes be reversible.
• Pituitary gland and hypothalamus: effects on sex hormones, risk of androgen deficiency, impotence, etc.
• Skin: “bronze” skin tone, hyperpigmentation that is produced by the accumulation of iron and melanin.
• Immunity: worsening of phagocytosis, risk of infection with Listeria, Yersinia enterocolitica, and Vibrio vulnificus (raw mollusks should be avoided).
• Thyroid gland: increased risk of hypothyroidism.
• Adrenal and parathyroid glands: some cases of adrenal insufficiency and hypoparathyroidism have been described (1).

Curiosities: mutations with certain benefits.

The different variants of a gene are called polymorphisms. It is no coincidence that HFE gene mutations have continued to be transmitted over the centuries in Caucasian populations. Apparently, they offer advantages in the health of their carriers (immune system and fertility). Additionally, they reduce the risk of pathologies such as Parkinson’s disease, Alzheimer’s disease, amyotrophic lateral sclerosis, and atherosclerosis. Heterozygous patients (individuals with an altered copy of the gene) may benefit from the slight increase in levels of iron caused by these mutations. Benefits in homozygous individuals (two altered copies) may occur during childhood and in young adults, before iron overload (2).

Treatment

In patients diagnosed with hemochromatosis, it is important to provide dietary advice to limit the intake of iron and vitamin C. Therapeutic phlebotomy (extraction of 500 ml of blood) should be prescribed when ferritin levels are too high.

The doctor will need to rule out complications associated with hemochromatosis and treat them, if there are any. The patient may need the intervention of different specialists (digestive system, endocrinology, transplant center, cardiology, rheumatology and dermatology).

BIBLIOGRAFÍA

(1) Porter JL, Rawla P. Hemochromatosis. 2020 Jun 18. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan–. PMID: 28613612.

https://pubmed.ncbi.nlm.nih.gov/28613612/

(2) Katsarou MS, Papasavva M, Latsi R, Drakoulis N. Hemochromatosis: Hereditary hemochromatosis and HFE gene. Vitam Horm. 2019;110:201-222. doi: 10.1016/bs.vh.2019.01.010. Epub 2019 Feb 8. PMID: 30798813.

https://pubmed.ncbi.nlm.nih.gov/30798813/

La entrada Weakened by Iron se publicó primero en Neolife.

It is very important to know how efficient our cells are when producing ATP (adenosine triphosphate), a process which depends on how efficient each mitochondria is, how many normo-functional mitochondria there are, and how effective the cell is at eliminating the useless mitochondria. We could define mitochondrial dysfunction as a state in which ATP production by our mitochondria decreases. Mitochondrial dysfunction directly or indirectly affects all chronic diseases associated with aging.

Mitochondria are very special organelles within our cells, so much so that they even have their own genetic material (mitochondrial DNA), and they are, among other important functions, responsible for producing ATP through a process called cellular respiration in which the nutrients we ingest and absorb are combined with the O2 we breathe to convert them into CO2 and H2O, producing ATP along the way.

Dr. Alfonso Galán González – Neolife Medical Team

Mitochondrial dysfunction is at the bottom of metabolic syndrome, cancer, cardiovascular disease, autoimmune diseases, sarcopenia, fatigue, etc. It also has a close relationship with inflammation and immunity.

We have talked in detail in these articles about the 9 “Hallmarks of Aging” that can be seen in the figure below.

These are the 9 mechanisms that science recognizes as causing aging at the molecular and cellular level, as well asdiseases associated with aging such as osteoarthritis, osteoporosis, cardiovascular disease, cancer, diabetes, Alzheimer’s, Parkinson’s, etc.

As I am writing these lines, science is advancing to seek ways to “combat” each of these mechanisms. For many of them we already have effective ways to intervene that have been proven in experiments of different scopes (at the laboratory level, experiments in animals, and experiments in humans). The challenge is to find solutions that are safe and viable in humans.

But we also wonder: Are any of these mechanisms more important than the others? Would it be interesting to focus our efforts more on one rather than another? If I have to treat just one, which one should I choose?

Here, we are going to present the candidacy of mitochondrial dysfunction.

What is mitochondrial dysfunction? What relationship do they have with ageing?

Mitochondria are very special organelles within our cells, so special that they even have their own genetic material (mitochondrial DNA), and they are, among other important functions, responsible for producing ATP (adenosine triphosphate) through a process called cellular respiration in which the nutrients we ingest and absorb are combined with the O2 we breathe to convert them into CO2 and H2O, producing ATP along the way.

ATP is responsible for providing energy for 90% of the processes that take place in our body.

Therefore, it is very important to know how efficient our cells are when producing ATP, a process which depends on how efficient each mitochondria is, how many normo-functional mitochondria there are, and how effective the cell is at eliminating the useless mitochondria.

We could define mitochondrial dysfunction as a state in which ATP production by our mitochondria decreases.

When the production of ATP decreases, we have less energy to undertake our internal processes and the entire system slows down.

Mitochondrial dysfunction directly or indirectly affects all chronic diseases associated with aging.

It is estimated that the signs and symptoms of mitochondrial dysfunction come approximately 10 years before the problem actually sets in, some of those symptoms are:

• Fatigue
• Muscle weakness
• Loss of muscle coordination.
• Alterations in sight and hearing.
• Mental fog or cognitive problems, etc.

What are the causes of mitochondrial dysfunction?

Among the causes associated with lifestyle, nutrition plays a very important role. The worse we eat, the worse the state of our mitochondria will be and the worse they will be able to do their job. Physical activity also is a fundamental factor: as we get older, we tend to be more sedentary. The less demand we have to produce energy in the mitochondria, the less ATP it will produce and this will make our processes slower and we’ll be able to do less exercise, putting us into a very negative vicious circle.

Among the most precise causes of mitochondrial dysfunction, we can list:

• Changes in morphology.
• Alteration of balance between fusion and fission. Fusion is the process by which the smaller and somewhat damaged mitochondria join together with larger mitochondria to form a matrix where they share genetic material and which compensates for the loss of function that they may have. Fission, on the other hand, is the process activated by something called mitophagy, which is a special form of autophagy, mentioned in other entries on this blog, in which mitochondria are fragmented, something essential for removing damaged mitochondria. As we age, accumulated and a decrease in ATP production harm mitophagy and the balance between fusion and fission is broken, with a predominance of fusion over fission, and damaged mitochondria are not recycled as a result.
• Reactive oxygen species (ROS) increase. These occur as a consequence of these energy production processes when some of the electrons produced combine with oxygen, yielding these ROS that can damage mitochondrial DNA. Mitochondrial DNA has a much lower repair capacity than nuclear DNA and, therefore, has a much higher mutation rate.
• Levels of NAD+ (which is a fundamental electron acceptor for cellular respiration) decline as we age, affecting ATP production.

So, what importance does mitochondrial dysfunction have in the aging process and the development of illnesses?

Mitochondrial dysfunction is at the bottom of metabolic syndrome, cancer, cardiovascular disease, autoimmune diseases, sarcopenia, fatigue, etc.

It also has a close relationship with inflammation through something called mtDAMPs (mitochondria-derived damage-associated molecular patters), as it activates the release of proinflammatory cytokines. Likewise, it has a relationship with immunity, affecting innate immunity and T cells, with this being one of the reasons why older people are more susceptible to infections.

Why mitochondrial dysfunction?

Mitochondrial dysfunction is the target of our efforts because in one way or the other it is related with practically all the other 8 “Hallmarks of Aging” (González-Freire et al). For example, telomeric shortening is related to lower mitochondrial biogenesis (Sahin et al). The sirtuins, a group of enzymes that we have talked about on other occasions which are very related to altered nutrient sensitivity, influence autophagy/mitophagy and the recycling of damaged mitochondria, as well as the expression of many respiratory chain enzymes (Giralt et al). They also affect the production of ROS. D’Aquila et al. have additionally researched their relationship with epigenetic modifications.

What can we do?

Having seen all the negative aspects of mitochondrial dysfunction, one can get the idea that when it happens, all is lost. Fortunately, that is not the case. Mitochondrial dysfunction can be reversible if it is caught early enough. Interventions on the nutritional, supplementation, exercise, and hormonal levels have proven to improve mitochondrial functioning.

1. Nutrition

What we eat and how we eat it influences the functioning of our mitochondria a lot. We should eat non-processed, organic, and natural foods like meat, fish, dried fruits, seeds, eggs, and leafy green vegetables with vivid colors that are rich in antioxidants. Health fats like fish oil, avocado, coconut oil, olive, etc.

How we eat is also important. Intermittent fasting, as is known and as we have explained here , has great properties and here is yet another: it improves the fission/fusion balance, improves the burning of fatty acids, and activates the AMPk pathway (explained here), which is involved in obtaining energy in the form of ATP.

2. Supplementation

Various compounds have been shown to improve mitochondrial function, including:

• Group B vitamins.
• Vitamin C.
• Vitamin E
• Iron.
• Selenium.
• Zinc.
• Magnesium.
• Alpha lipoic acid.
• Coenzyme Q10.
• NAD in the form of its precursors, nicotinamide mononucleotide and nicotinamide riboside (NMN and NR).
• Ellagitannins present in red berries.
• Detoxifiers. Periodically undertaking a detox schedule to get rid of medicines, pollutants, etc. that have accumulated is beneficial for mitochondrial function.

3. Exercise

Exercising, staying active, and, more specifically, high intensity interval training (HIIT) has been shown to increase the efficiency of mitochondria in ATP production, as well as the number of mitochondria (Robinson et al), and it helps with mitophagy (Schiavi et al).

If we subject the system to stress and ask for energy from it to undertake muscle exercise this will lead to improved ATP synthesis, the creation of new mitochondria (biogenesis), the activation of autophagy (which allows for the recycling of damaged mitochondria, mitophagy), and it will increase ROS. Yes, I know that earlier in this article we spoke about the negative effect of ROS; however, here we have to introduce, just for a moment, the concept of mitohormesis: a small amount of damage because of the production of ROS, leading to improved mitochondrial function, signaling, and biogenesis (Son et al, Sena et al, Hekimi et al). When this production is excessive, damage to proteins and DNA occurs.

4. Hormones

The presence of estrogen and androgen receptors and hormone response elements in mitochondria led to research into the effects of 17β-estradiol and testosterone on mitochondrial functions and their relationship with aging. Both steroids trigger a complex molecular mechanism involving a cross-dialogue between the mitochondria, nucleus, plasma membrane, and cytoskeleton — leading to mitochondrial protection (Vasconsuelo et al).

BIBLIOGRAPHY

(1) Schiavi A, Ventura N. The interplay between mitochondria and autophagy and its role in the aging process. Exp Gerontol. 2014;56:147-153.

(2) D’Aquila P, Bellizzi D, Passarino G. Mitochondria in health, aging and diseases: the epigenetic perspective. Biogerontology. 2015;16(5):569-585.

(3) Robinson MM, Dasari S, Konopka AR, et al. Enhanced Protein Translation Underlies Improved Metabolic and Physical Adaptations to Different Exercise Training Modes in Young and Old Humans. Cell Metab. 2017;25(3):581-592.

(4) Son JM, Lee C. Mitochondria: multifaceted regulators of aging. BMB Rep. 2019;52(1):13-23. doi:10.5483/BMBRep.2019.52.1.300

(5) Sena LA, Chandel NS. Physiological roles of mitochondrial reactive oxygen species. Mol Cell. 2012; 48:158–167.

(6) Hekimi S, Lapointe J, Wen Y. Taking a “good” look at free radicals in the aging process. Trends Cell Biol. 2011; 21:569–576

(7) Giralt A, Villarroya F. SIRT3, a pivotal actor in mitochondrial functions: metabolism, cell death and aging. Biochem J. 2012; 444:1–10

(8) Sahin E, Depinho RA. Axis of ageing: telomeres, p53 and mitochondria. Nat Rev Mol Cell Biol. 2012; 13:397–404.

(9) Gonzalez-Freire M, de Cabo R, Bernier M, et al. Reconsidering the Role of Mitochondria in Aging. J Gerontol A Biol Sci Med Sci. 2015;70(11):1334-1342.

(10) Vasconsuelo, A., Milanesi, L., & Boland, R. (2013). Actions of 17β-estradiol and testosterone in the mitochondria and their implications in aging. Ageing Research Reviews, 12(4), 907–917.

La entrada Is the Mitochondria the Axis of Aging? se publicó primero en Neolife.

The COVID-19 pandemic caused by SARS-CoV-2 continues to be an important problem for health, the economy, and the global society. Since its appearance in December of 2019, a great amount of data, evidence, diagnostics, and treatment options have arisen.

Christmas time will be atypical this year because of the coronavirus crisis. Recently, scientists have noted that measures even more restrictive will be adopted in December, events will be cancelled, home lockdowns will take place, and limits will be placed on family meetings and on social contact in general. These are measures that, without a doubt, will once again modify our nutritional and lifestyle habits.

Alejandro Monzó – Neolife Nutrition and Nursing Unit

Mortality rates are higher amongst those over 60 years old with prior conditions.

Currently, there are no registered medicines to prevent COVID-19 and there is also not a safe vaccine at the moment. Treatment is based mainly on support therapies and treating symptoms, as well as aiming to prevent respiratory insufficiency. As preventative measures, the use of face masks, hand washing, and respecting social distancing rules have all yielded results. Currently, a feasible, tried-and-true way to lower the rate of contagion seems to be the strict measure of a lockdown for the general population (1,2).

In Spain, the autonomous communities will have to try to be restrictive to control the pandemic’s curve at Christmas. This can be done by cancelling social events, limiting the number of people in family meetings, and avoiding closed spaces without ventilation. Home lockdowns have proven to be a good tool to combat the virus’s propagation (3). Nevertheless, this solution is a double edge sword that, unfortunately, can seriously compromise people’s health because of the habit and lifestyle changes that it implies.

It must be remembered that good health is the result of a set of different factors. Eating habits, physical activity and exercise, rest, the environment, the control of stress, our social relationships, our management of emotions, even our gut microbiota (amongst many other factors) play a key role for reaching optimal health.

Firstly, governments are applying lockdown, isolation, and social distancing measures that lead to a prolonged period of time at home. This has yielded reductions in physical activity and changes in dietary intake and is even more noticeable now in this Christmas season as foods rich in calories, sugars, and fat have a greater presence at home (4). In this context, the risk of sarcopenia increases, a deterioration of muscle mass and muscle functions (more prevalent in older populations), as well as increases in body fat. A new study published in the scientific journal GeroScience shows the health effects and consequences of home confinement restrictions due to COVID-19 (Figure 1), where these changes in body composition are associated with a number of chronic lifestyle diseases like cardiovascular diseases, diabetes, osteoporosis, frailty, cognitive impairment, and depression (5).

The generalized loss of skeletal muscle mass and strength is aggravated as a consequence of inactivity and a lack of exercise. The authors note, in addition, that the elderly population suffers from additional problems such as an increase in falls, fractures, reduction of mobility, greater deterioration, and a higher rate of mortality in general. Nevertheless, one of the most noteworthy points of the study is the risk of sarcopenic obesity (people who are losing muscle and gaining fatty tissue at the same time), an added risk factor for chronic diseases that does not only shorten life expectancy but also compromises quality of life (5).

Regarding diet, home confinement and the Christmas period can bring about changes in food choices and diet quality. These changes in eating habits, along with chances in appetite regulation, can increase the risk of weight gain (an average of 3 kilos of fat has been estimated) or, on the contrary, of weight loss (mainly because of the loss of muscle mass) (4,5). The authors even discuss the risk of the immune system working less effectively. In addition, a new Spanish study published in the journal Annals of Medicine has demonstrated that the level of blood sugar helps to predict the prognosis of patients in the hospital with COVID-19, even in those who are not diabetic (6). Therefore, specialists note that hyperglycemia is a risk factor and recommend controlling blood sugar levels. Also worthy of mention are other recent discoveries, like the connection between a deficiency in vitamin D and greater risk in the event coronavirus is contracted A recent study published in the journal Aging Clinical and Experimental Research shows that those countries with greater levels of vitamin D on average have a lesser number of deaths from the virus; therefore, healthy levels of vitamin D could contribute to reducing the risk of respiratory infections (7).

Likewise, the Christmas season along with social isolation could cause emotional and sleep problems. It has been shown that psychological factors, drowsiness, social isolation, and anxiety may play a considerable role in the loss of muscle during the pandemic (5). This could be due to the pandemic’s effects on healthy behaviors like irregular eating habits and physical exercise regimes coupled with stress, which, in turn, are associated with sleep alterations, less time sleeping, and insomnia, which are all affecting general health (4,5)

Another of the key health factors is the advancement and knowledge of gut microbiota. Scientists define microbiota as the set of microorganisms present in a set environment like the intestinal tract (8). It is important because it undertakes multiple defense tasks, as well as nutritional functions, and it influences mood and behavior. Researcher today consider it as if it were an “organ.” Recently, Spanish scientists have undertaken a research project to find the immunological mechanisms through which gut microbiota may protect the body from the coronavirus and reduce the seriousness of symptoms. It has been verified that SARS-CoV-2 can be detected in stool and its receptor is also expressed in the cells of the intestine and colon (9). Therefore, it is important to always consider ahealthy diet a priority, even more so during this Christmas season. What we eat nourishes us and the billions of microorganisms that live in our intestine.

Lastly, during Christmas, following the recommendations of the Spanish Academy of Nutrition and Dietetics against COVID-19 (10), it is important to increase the consumption of fruits and vegetables due to their richness in vitamins, minerals, fiber, and antioxidants and because of their role to combat oxidative stress brought on by a possible loss of muscle. Likewise, their consumption is important to keep the immune system working at its best. Include quality sources of protein, like legumes, meats, fish, and eggs to avoid sarcopenia. Also avoid the consumption of non-healthy fats contained in industrially processed and ultra-processed foods and go for a greater amount of healthy fats like olive oil, dried fruits, fish oils, and avocado (amongst others) due to their energizing and antioxidant properties. Other recommendations include keeping metabolically active; that is, avoiding a sedentary lifestyle and doing activities like walking, physical training at home, cleaning, etc. to guarantee body weight maintenance at Christmas time. Something no less important is to keep up social contact with our loved ones and family members despite the restrictions. This can be done thanks to the use of new technologies (Figure 2).

We are leaving behind 2020, a year marked by the coronavirus pandemic and in which the mechanisms of sarcopenia and its relationship with the effects of lockdowns on physical activity, eating habits, sleep, and stress are associated with a greater risk of coronavirus infection and more serious symptoms. Changes in body composition are frequent in Christmas; therefore, we must be aware and remember the current health context as well. At Neolife, we have become involved in the search for new medical treatments and approaches to prevention. Recently we have added the availability of new COVID-19 tests for the detection of the virus and antibodies in our clinics. There is even a new type of medical checkup know as the “Post-COVID-19 Checkup” which aims to undertake an exhaustive examination to those who have gone through the disease.

We at Neolife wish you happy holidays and a 2021 full of hope, health, and wellbeing!

BIBLIOGRAPHY

(1) Pascarella, G. et. al. (2020). “COVID-19 diagnosis and management: a comprehensive review”. J Intern Med. Vol. Vol. 288(2): 192-206.

URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7267177/

(2) Cevik, M. et. al. (2020). “COVID-19 pandemic-a focused review for clinicians”. Clinical microbiology and infection: the official publication of the European Society of Clinical Microbiology and Infectious Diseases. Vol. 26(7): 842-847. URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7182753/

(3) Dhama, K. et. al. (2020). “Coronavirus Disease 2019 – COVID-19”. Clin Microbiol Rev. Vol. 33(4): e00028-20.

URL: https://cmr.asm.org/content/33/4/e00028-20#sec-25

(4) Ruiz-Roso, MB. et. al. (2020). “COVID-19 Lockdown and changes of the dietary pattern and physical activity habits in a cohort of patients with type 2 diabetes mellitus”. Nutrients. Vol. 12(8): 2327.

URL: https://pubmed.ncbi.nlm.nih.gov/32759636/

(5) Kirwan, R. et. al. (2020). “Sarcopenia during COVID-19 lockdown restrictions: long-term health effects of short-term muscle loss”. GeroScience.

URL: https://link.springer.com/article/10.1007/s11357-020-00272-3#citeas

(6) Carrasco-Sánchez, FJ. et. al. (2020). “Admission hyperglycaemia as a predictor of mortality in patients hospitalized with COVID-19 regardless of diabetes status: data from the Spanish SEMI-COVID-19 Registry”. Annals of Medicine. Vol. 53(1): 103-116.

URL: https://www.tandfonline.com/doi/abs/10.1080/07853890.2020.1836566

(7) Ilie P.C., Stefanescu S. & Smith L. (2020). “The role of vitamin D in the prevention of coronavirus disease 2019 infection and mortality”. Aging Clinical and Experimental Research.

URL: https://link.springer.com/article/10.1007/s40520-020-01570-8

(8) Gut Microbiota for Health. (2020). “Gut microbiota info”.

URL: https://www.gutmicrobiotaforhealth.com/about-gut-microbiota-info/

(9) Hernández Bonilla, JM. (2020). “En busca de la relación entre las bacterias del estómago y el coronavirus”. El País Newspaper. Science.

URL:https://elpais.com/ciencia/2020-11-10/en-busca-de-la-relacion-entre-las-bacterias-del-estomago-y-el-coronavirus.html

(10) (2020). “Recomendaciones de alimentación y nutrición para la población española ante la crisis sanitaria del COVID-19”. Document stating the position of the Spanish Academy of Nutrition and Dietetics and the General Council of Official Associations of Dietitians-Nutritionists.

URL: https://www.academianutricionydietetica.org/noticia.php?id=113

La entrada Christmas in Times of a Pandemic se publicó primero en Neolife.

The 2020 Global Nutrition Report reveals that global and national eating patterns hide significant inequalities within countries and populations.

Last June, the latest 2020 Global Nutrition Report was released, a document that presents the changes that need to be made to our food systems to improve nutrition, health, and food safety. A review is carried out and recommendations are made, such as a more varied production of food and the reformulation of products to make them healthier, in order to improve the state of nutrition on a global scale.

Alejandro Monzó – Neolife Nutrition and Nursing Unit

The number of people who suffer hunger is shrinking, and the number of people who are overweight is increasing at an alarming rate.

Overweight and obesity are defined as an abnormal or excessive accumulation of fat that can be harmful to an individual’s health (1). The Body Mass Index (BMI) is a simple indicator of the ratio of weight to height used to identify overweight and obesity in adults (2). However, it differs from the study of total body composition, which requires a more thorough analysis with anthropometric techniques and tools, such as those available at Neolife. In 2016, the World Health Organization (WHO) estimated that over 1.9 billion adults were overweight, of which over 650 million were obese. Globally, they are linked to a higher number of deaths than underweight (1).

As the world’s leading report on the state of global nutrition (Figure 1.), it examines the critical role of addressing inequality in ending malnutrition in all its forms (3). Inequality is a cause of malnutrition, both malnutrition and overweight, obesity, and other chronic diseases linked to poor diets. The need for more equitable and sustainable food and health systems has never been more urgent. This report highlights the need to integrate nutrition into universal health care as an essential prerequisite for improving diets, saving lives, and reducing health care spending. Reversing the obesity epidemic would also reduce the burden on health systems, as it is one of the most expensive health conditions.

The common consequences of overweight and obesity on health are diverse. Studies show that a high BMI is an important risk factor for chronic noncommunicable diseases, such as the following (1,2):

• Cardiovascular diseases, mainly heart disease and stroke
• Insulin resistance and diabetes
• Disorders of the musculoskeletal system, especially osteoarthritis
• Some types of cancer, like breast, prostate, colon, endometrial, liver, gallbladder, ovarian, and kidney

Today, many low and middle-income countries are facing a so-called “double burden” of morbidity. The Global Nutrition Report presented in 2020 shows that while these countries continue to address the problems of infectious diseases and malnutrition, they are also experiencing a rapid increase in risk factors for noncommunicable diseases, such as obesity and overweight, especially in urban settings (3). Therefore, the authors point out that it is not uncommon to find malnutrition and obesity coexisting in the same country, the same community, and the same home.

Moreover, the authors emphasize that inequality is no longer seen in terms of access to food, but also in terms of access to a varied diet. The same person could be malnourished and, years later, obese. The report presents the case of people who did not receive the necessary nutrients in their early years, or even cases where their mothers did not ingest such nutrients during pregnancy, who later did not have access to healthy eating, but rather to industrial and ultra-processed foods or a rather unbalanced diet (3, 4).

The report states that ultra-processed foods are more readily available, cheaper, and have more intensive marketing. A study published by Foodwatch Netherlands reveals that 70% of the food products we can find in a supermarket are ultra-processed foods. The authors call for a change in legislation, where fresh and perishable foods are more present, as they can significantly improve diets and, consequently, health (3, 5).

Poor diets are not only the result of a personal choice when selecting food items, but also involves composition, something that the food industry is responsible for. The report therefore calls for this industry to adopt appropriate regulations, reformulate its products to make them healthier, use quality raw materials and, finally, provide truthful and transparent information through labelling,and displaying all the ingredients contained in the products they produce (3).

On food composition, the document notes that current agricultural systems focus on the production of commodities such as wheat, rice, or maize. However, others like palm oil, peanuts, sugar beet, sugar cane, soybeans, sunflowers, or tubers account for 72% of crops worldwide. This situation concerns experts, who point to the need for a wide range of healthy and sustainable foods, further diversified into fruits, legumes, and vegetables (3).

It is worth noting the message issued by the expert panel responsible for the report. If appropriate measures are not taken, the problems associated with poor nutrition will be exacerbated, particularly affecting the most vulnerable populations and making them more susceptible to different health problems. The authors conclude by recalling that good nutrition is an appropriate and effective strategy that can protect people from disease and epidemics, relieves the burden on the health system, reduces health care spending, and saves lives (3, 4). For this reason, in countries where legislation is more lax and there are fewer controls, governments need to become more involved and establish more quality controls.

Here at Neolife, we wish to convey the important role that nutrition has in human health. Unfortunately, the prevalence of overweight, obesity, and malnutrition is increasing on a global scale, leading to the need for healthy lifestyle habits. Governments must ensure sustainable and safe food policies, prioritizing people’s health condition in order to prevent future diseases that may threaten health systems.

Nutritional education and the adoption of healthy eating habits are fundamental pillars of our comprehensive health program. September is a good month to resume and bring back healthy lifestyle habits (often neglected in the summer months), take charge of our health, and opt for healthy food choices. For this reason, the Neolife team has worked and continues to work on improving services in the nutrition department. We have recently released new monitoring programs and nutritional bonuses with the aim of improving nutrition habits, body composition, and health. For more information, do not hesitate to contact our Medical Assistant in person, by phone, or by e-mail.

BIBLIOGRAPHY

(1) (2020). “Obesity and overweight”. World Health Organization.

URL: https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight

(2) De Luis Román, D.A. Bellido Guerrero, D. García Luna, P.P. Olivera Fuster, G. (2017). “Dietoterapia, nutrición clínica y metabolismo” [Diet therapy, clinical nutrition, and metabolism]. Third edition. Sociedad Española de Endocrinología y Nutrición. Grupo Aula Médica, S.L. Madrid, Spain.

(3) 2020 Global Nutrition Report: Action on equity to end malnutrition. Bristol, UK: Development Initiatives.

URL: https://globalnutritionreport.org/

(4) (2020). “Del hambre al sobrepeso en una misma vida: el nuevo panorama de la nutrición” [From hunger to overweight within the same lifetime: the new nutrition landscape].

URL: https://www.nutrinfo.com/noticias-nutricion/del-hambre-al-sobrepeso-en-una-misma-vida-el-nuevo-panorama-de-la-nutricion-3992

(5) (2017). “70% of supermarkets sell controversial ultra-processed foods”. Food Watch.

URL: https://www.foodwatch.org/nl/persberichten/2017/70-supermarkt-bestaat-uit-omstreden-ultra-processed-foods/

(6) 2020 Global Nutrition Report: Action on equity to end malnutrition. Executive summary. Bristol, UK: Development Initiatives.

URL: https://globalnutritionreport.org/reports/2020-global-nutrition-report/executive-summary/

La entrada From Hunger to Overweight in One Lifetime se publicó primero en Neolife.

The negative effects of excess activation of the mTOR pathway can lead to cancer, insulin resistance, diabetes, Alzheimer’s, etc. Meanwhile, if we always keep it inhibited, we would affect the creation of tissue, muscle, bone, and cell repair – leading to sarcopenia, osteoporosis, weakness… and these are the problems of an over-activation of the AMPk pathway.

In this second part of the articles dedicated to the AMPk and mTOR metabolic pathways, we will try to give some ideas on how to balance these two pathways to get the best out of each of them. At Neolife, we know how to help you with these strategies adapted to your situation and your state of health so that you have an optimal quality of life and state of health.

Dr. Alfonso Galán González – Neolife Medical Team

High-intensity exercise, or exercise at high-intensity intervals, such as HIIT, has been shown to activate the AMPk pathway, while strength (weight) training activates the mTOR pathway.

In this second part of the articles dedicated to the AMPk and mTOR metabolic pathways, we will try to give some ideas on how to balance these two pathways to get the best out of each one.

Scientific interest in them has been increasing in recent years, as shown by the number of articles published in Pubmed when you search for mTOR:

And for AMPk:

We mentioned in the previous article that the negative effects of excess activation of the mTOR pathway can lead to cancer, insulin resistance, diabetes, Alzheimer’s, Parkinson’s, etc. Meanwhile, if we always keep it inhibited, we would affect the creation of tissue, muscle, bone, and cell repair – leading to sarcopenia, osteoporosis, weakness… and these are the problems of an over-activation of the AMPk pathway – mTOR’s “antagonistic” pathway.

Thus, we do not want to develop diabetes, neurodegenerative and cardiovascular diseases, or cancer; however, we also do not want to lose bone mass or muscle mass, which we need in order to have an adequate metabolic rate to promote the burning of fat and glucose.

Life in industrialized society almost inevitably leads us to an excess of mTOR activation, as we have plenty of food, we can eat as many times a day as we want (always maintaining high sugar levels with the consequent release of insulin), and we have sedentary jobs not needing to undertake physical activity to get our food. As we have seen, these are the things that inhibit AMPk pathway activation and that may be the cause of the increase in metabolic diseases in recent decades. Obviously, if we think about how the first humans lived, we can see that inevitably there was an alternation between exercise and rest, between eating and fasting…

Currently, we could say that we have to “simulate” all of that in order to improve our state of health and get the benefits of both metabolic pathways while avoiding the negative effects at the same time.

I hope I have been able to convey that neither of the pathways is good or bad; it is a balance between the two that will lead us to greater longevity, a life free of disease, to avoid the loss of muscle mass and bone mass, etc.

How do we balance both pathways?

Alluding to the 4 fundamental pillars of treatment of Age Management Medicine and of Neolife (which we can expand to many more, but for educational and practical purposes we will reduce to 4) which are nutrition, exercise, supplementation, and hormonal balance, we will briefly explain what can be done.

• Nutritional strategies:

The intermittent fasting that we hear about everywhere and about which we have written on our blog on other occasions is a simple technique that will activate the AMPk pathway. We recommend fasts of at least 12h to bring about activation (usual and moderately bearable strategies go up to 14-16h). From that time, the glycogen of the liver already begins to mobilize itself, glucose and insulin in blood lower, and the secretion of hormones increases – such as cortisol, adrenaline, noradrenaline, growth hormone,– as well as the biogenesis of more mitochondria to optimize energy gathering and production.

Meals should preferably be low in carbohydrates and have a low or medium glycemic index (this measures how fast and how many carbohydrates in a food get into the blood in the form of glucose). In order to activate the mTOR pathway after training, to take advantage of the conditions when the workout is over and promote muscle development, it is important for food to be rich in proteins and carbohydrates and for it to have a high glycemic load (white rice, potatoes, pasta, etc.).

• Training strategies:

As we have already mentioned, high-intensity exercise, or exercise at high-intensity intervals, such as HIIT, has been shown to activate the AMPk pathway, while strength (weight) training activates the mTOR pathway. We recommend alternating both forms of training throughout your weekly exercise routine to promote – on the one hand – carbohydrate metabolism, energy collection, fat burning, and mitochondrial biosynthesis, and – on the other – muscle development. We must stop to think here about how intimately related the two pathways are, despite their “antagonistic ” effects. As we develop more muscle, we will have more peripheral insulin receptors, which will favor AMPk action in terms of improving insulin resistance; and those muscles that are more developed because of mTOR activation will be more efficient when producing energy because they have higher mitochondrial density thanks to the activation of the AMPk pathway.

• Supplements:

There are several supplements that help us to activate these pathways in addition to the drugs already mentioned like metformin for the AMPk pathway and rapamycin for the mTOR pathway.

Alpha-lipoic acid, resveratrol, quercetin, EGCG from green tea, berberine, turmeric, anthocyanins from blueberries, zinc, carnitine, virgin olive oil, fish oil (omega 3), ginseng, cinnamon, astragalus, Coenzyme Q10, red rice yeast, and apigenin all activate the AMPk pathway.

As for activating the mTOR pathway, it is a good idea to use amino acids such as leucine, whey protein, and hydrolyzed carbohydrates, which lead to an insulin peak that activates this pathway during strength training. Testosterone also activates the mTOR pathway (Basualto-Alarcón C et al. 2013).

With this we hope to have given you a bit of a better understanding of these important metabolic pathways and how to use them to your benefit. At Neolife, we know how to help you with these strategies adapted to your situation and your state of health so that you have an optimal quality of life and state of health.

BIBLIOGRAPHY

(1) Thomson DM. The Role of AMPK in the Regulation of Skeletal Muscle Size, Hypertrophy, and Regeneration. Int J Mol Sci. 2018;19(10):3125. Published 2018 Oct 11. doi:10.3390/ijms19103125

(2) Lin SC, Hardie DG. AMPK: Sensing Glucose as well as Cellular Energy Status. Cell Metab. 2018;27(2):299‐313. doi:10.1016/j.cmet.2017.10.009

(3) Ciccarese F, Zulato E, Indraccolo S. LKB1/AMPK Pathway and Drug Response in Cancer: A Therapeutic Perspective. Oxid Med Cell Longev. 2019;2019:8730816. Published 2019 Oct 31. doi:10.1155/2019/8730816

(4) Wang Z, Wang N, Liu P, Xie X. AMPK and Cancer. Exp Suppl. 2016;107:203‐226. doi:10.1007/978-3-319-43589-3_9

(5) Saxton RA, Sabatini DM. mTOR Signaling in Growth, Metabolism, and Disease [published correction appears in Cell. 2017 Apr 6;169(2):361-371]. Cell. 2017;168(6):960‐976. doi:10.1016/j.cell.2017.02.004

(6) Bertoldo MJ, Faure M, Dupont J, Froment P. AMPK: a master energy regulator for gonadal function. Front Neurosci. 2015;9:235. Published 2015 Jul 14. doi:10.3389/fnins.2015.00235

(7) Jeon SM. Regulation and function of AMPK in physiology and diseases. Exp Mol Med. 2016;48(7):e245. Published 2016 Jul 15. doi:10.1038/emm.2016.81

(8) Xu J, Ji J, Yan XH. Cross-talk between AMPK and mTOR in regulating energy balance. Crit Rev Food Sci Nutr. 2012;52(5):373‐381. doi:10.1080/10408398.2010.500245

(9) Johnson SC, Rabinovitch PS, Kaeberlein M. mTOR is a key modulator of ageing and age-related disease. Nature. 2013;493(7432):338‐345. doi:10.1038/nature11861

(10) Kim J, Yang G, Kim Y, Kim J, Ha J. AMPK activators: mechanisms of action and physiological activities. Exp Mol Med. 2016;48(4):e224. Published 2016 Apr 1. doi:10.1038/emm.2016.16

(11) Basualto-Alarcón C, Jorquera G, Altamirano F, Jaimovich E, Estrada M. Testosterone signals through mTOR and androgen receptor to induce muscle hypertrophy. Med Sci Sports Exerc. 2013;45(9):1712‐1720. doi:10.1249/MSS.0b013e31828cf5f3

La entrada mTOR and AMPk – the two sides of metabolism that you need to be familiar with and balance. Part II se publicó primero en Neolife.

The Mediterranean diet was listed as one of the items on the UNESCO Representative List of the Intangible Cultural Heritage of Humanity in 2010. Thus, the Mediterranean diet is the ideal model for eating habits that prevent chronic diseases.

There is increasingly more proof that demonstrates the beneficial effects of the Mediterranean diet on cardiac insufficiency, both in terms of it progression and mortality rate. The study of prolonged adherence to this type of eating habit periodically yields new, positive results for human health and, consequently, for preventing diseases.

Alejandro Monzó – Neolife Nutrition and Nursing Unit

The Mediterranean diet includes different compounds that favorably modulate the relative expression of certain genes.

The main characteristics of a Mediterranean diet include an abundance of foods of plant origin, virgin olive oil as the main source of fat, consumption of fish and poultry in low or moderate amounts, a relatively low intake of red meats and moderate consumption of wine, normally with meals (Figure 1) (1).

Amongst the healthy properties of the Mediterranean diet, we can note that it is a balanced, varied diet that supplies an adequate amount of nutrients. It is low in saturated fat and high in monounsaturated fatty acids, complex carbohydrates, and dietary fiber. What most makes the Mediterranean diet stand out is the type of fat that it is characterized by (olive oil, fish, and nuts), the proportions of main nutrients (cereals and vegetables as the main dishes and meats or similar as side dishes), and its richness in micronutrients, originating from the use of fresh, local, seasonal vegetable products, as well as aromatic herbs and seasonings. It also features a high antioxidant load and other beneficial substances of plant origin (1,2).

It is a diet that has been sufficiently proven as palatable, possible, sustainable, and respectful of biodiversity. Public health strategies should encourage populations to adopt healthy eating habits like the Mediterranean diet to ensure healthier populations and protect the environment. The great historical past of the Mediterranean diet and the long tradition of its use without evidence of adverse effects makes it very promising for public health (1,2,3).

According to current evidence, the Mediterranean diet is a dietary approach that is recommended to prevent chronic diseases, includingcardiovascular diseases, type 2 diabetes, and certain types of cancer. The beneficial mechanisms of following this type of diet include the reduction of blood lipids and inflammatory and oxidative stress markers, as well as an improvement in insulin sensitivity, endothelial function, and antithrombotic function (4). These effects may be explained by the bioactive ingredients contained in the foods that make up the Mediterranean diet, such as polyphenols, monounsaturated and polyunsaturated fatty acids, vitamins, minerals, and dietary fiber (4, 5).

The PREDIMED Study (Prevention with the Mediterranean Diet Study) is a randomized controlled clinical trial aimed at assessing the possible effects of two nutritional interventions involving the traditional Mediterranean diet on the risk of major cardiovascular complications (3, 5). After 5 years of follow-up, it was shown that, compared with a low-fat diet, the Mediterranean diet (without calorie restriction and enriched with extra virgin olive oil or nuts) reduced the incidence of cardiovascular complications in a sample of nearly 7,500 participants of advanced age with high cardiometabolic risk by 30%. This study represents the highest level of scientific evidence of primary prevention of cardiovascular disease with a dietary pattern so far. In addition, it has been shown that a 2-point increase in adherence to the Mediterranean diet significantly reduces mortality and/or cancer incidence by 6%. In the PREDIMED study, it was shown that the two combined Mediterranean diet groups had less risk of developing breast cancer than the control group (2).

Likewise, the PREDIMED Diabetes study showed that prolonged adherence to the Mediterranean diet (without caloric restriction, rich in monounsaturated fat and bioactive polyphenols) significantly reduced the risk of type 2 diabetes in people with high cardiometabolic risk (2). Additionally, a meta-analysis of 50 studies with 534,906 participants, including type 2 diabetics, demonstrated the benefits of the Mediterranean diet on different aspects of metabolic syndrome (6): the waist circumference (-0.42 cm), HDL cholesterol (+ 1.117 mg/dl), triglycerides (-6.14 mg/dl), systolic and diastolic blood pressure (-2.35 and at 1.58 mmHg, respectively).

Other results show that the Mediterranean diet is associated with better cognitive function, with lower risk of cognitive impairment, and with lower risk of general dementia and Alzheimer’s disease – although it is not possible to establish a cause-effect relationship (2). In the great Nurses’ Health Study, the Mediterranean diet was associated with greater telomere length (telomeres are repetitive sequences at the end of chromosomes that are linked to a greater longevity). In the PREDIMEDstudy, this effect was only obtained in women (2).

It is worth mentioning a new study carried out by experts from Harvard University (7). A metabolic signature has been identified that can assess an individual’s adherence and metabolic response to the Mediterranean diet and help predict the future risk of developing cardiovascular disease. This signature consists of 67 metabolites (molecules produced by metabolic processes that circulate through the bloodstream and can be measured through a blood sample) and allows researchers to determine which people are more adherent to the Mediterranean diet and, also, their metabolic response to said type of diet. Thus, the metabolic signature could be an objective tool for the scientific community, as it reflects the metabolic response of individuals to diet and the risk of cardiovascular disease. Therefore, scientists note that it has great potential to help establish personalized diets in the future.

As a conclusion, the Mediterranean diet is a valuable cultural asset that represents much more than just a basis for nutrition. It is a healthy and balanced lifestyle that includes recipes, ways of cooking, celebrations, customs, typical local and seasonal products, as well as various human activities.  It has proven to bring great benefits for human health and, currently, is under study in different pieces of research that, undoubtedly, will yield new and promising data in the future. According to the World Health Organization (WHO), the Mediterranean diet is the most recommendable way to eat in order to have a good quality of life and prevent chronic diseases that are so present nowadays – and these are key objectives in the global health program that characterize Neolife.

BIBLIOGRAPHY

(1) Fundación Dieta Mediterránea. (2010). “La pirámide de la Dieta Mediterránea: un estilo de vida actual”.

URL: https://dietamediterranea.com/nutricion-saludable-ejercicio-fisico/

(2) De Luis Román, D.A. Bellido Guerrero, D. García Luna, P.P. Olivera Fuster, G. (2017). “Dietoterapia, nutrición clínica y metabolismo”. Third edition. Sociedad Española de Endocrinología y Nutrición. Grupo Aula Médica, S.L. Madrid, Spain.

(3) Salas-Salvadó J. & Mena-Sánchez G. (2017). “El gran ensayo de campo nutricional PREDIMED”. Nutr Clin Med. Vol. 11(1): 1-8.

URL: https://www.aulamedica.es/nutricionclinicamedicina/pdf/5046.pdf

(4) Schwingshackl, L. et al. (2019). “Mediterranean diet and health status: active ingredients and pharmacological mechanisms”. British Jorunal of Pharmacology.

URL: https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1111/bph.14778

(5) Estruch R. et al. (2013). “Primary prevention of cardiovascular Disease with a Mediterranean diet”. N Engl J Med 368:1270-90.

URL: https://www.nejm.org/doi/full/10.1056/NEJMoa1200303

(6) Kastorini, C-M. et al. (2011). “The effect of Mediterranean Diet on metabolic syndrome and its components: a meta-analysis of 50 studies and 534,906 individuals”. J Am Coll Cardiol. Vol. 57(11):1299-313.

URL: https://pubmed.ncbi.nlm.nih.gov/21392646/

(7) Li J. et al. (2020). “The Mediterranean diet, plasma metabolome, and cardiovascular disease risk”. European Heart Journal, ehaa209.

URL:https://academic.oup.com/eurheartj/advance-article-abstract/doi/10.1093/eurheartj/ehaa209/5836100?redirectedFrom=fulltext

La entrada The Mediterranean Diet: A Healthy Eating Model se publicó primero en Neolife.