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

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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.

The exposome is defined as the set of non-genetic factors to which we are exposed throughout our lives and which condition our state of health and disease.

The WHO estimates that approximately 25% of diseases are related to these non-genetic factors, which could be avoided. Therefore, it provides extremely valuable information in the design of preventive, diagnostic, and therapeutic strategies in the medicine of the future.

Dr. Débora Nuevo – Neolife Medical Team

What is the EXPOSOME?

The set of traits presented by each individual is what we call phenotype, which is the product of each person’s gene combination (called a genotype) within a given environment.

What we understand as an exposome, a term coined by C. Wild in 2005, is the set of environmental (non-genetic) factors to which each individual is exposed from the moment of conception and which may condition the state of health or disease.

This name encompasses multiple factors, which also vary over time, and which we may group into 3 categories or domains:

• The General External domain includes social, economic, and psychological factors, such as education, climate, psychological stress, and the social or financial situation.
• The Specific External domain includes the influence of infectious agents, chemical and environmental contaminants, radiation, alcohol and tobacco use, profession or occupation and medical treatments.
• The Internal domain refers to metabolism, circulating hormones, microbiota, inflammation, lipid peroxidation, oxidative stress, and aging.

Variability and susceptibility windows of the exposome

In order for non-genetic factors to impact our health, they need to be able to alter biology at different levels (altering the microbiota, interacting in metabolic processes, decompensated the usual cellular pathways…).

That’s why the exposome is especially difficult to cover. Not only because of the variability of its nature but also because it is modified over time, that is, it is dynamic.

Its effect depends on the dose or the level of exposure, as well as the moment in which it occurs, so we are talking about intrapersonal variability.

And this effect does not turn out to be the same in all individuals, with population groups that are more susceptible than others, also leading to interpersonal variability.

On the other hand, it is worth mentioning the existence of windows of susceptibility, which are the specific periods throughout an individual’s life in which they are especially sensitive to certain exposures. An example is the special susceptibility to many factors at early stages of life, which may condition important events in later stages.

How do we study the exposome?

Due to the complexity of the term exposome, the approach must be multidisciplinary and comprehensive.

To obtain the data for the study of the exposome, biomonitoring is the most widely used strategy. There are two types of biomonitoring, which in turn complement each other by providing a more complete picture:

• Human biomonitoring: It consists of collecting biological samples, usually blood or urine. Concentrations of toxics or pollutants and their metabolites are analyzed. Other parameters that are compared to reference values are also measured.
• Environmental biomonitoring: It collects environmental samples that may include food, water, or air, and so their presence and the level of exposure are linked to the environment of the different population groups.

The biomarkers in turn may indicate:

• Exposure, indicating only the presence of a substance,
• Effect, the evidence of biochemical, physiological, or behavioral alterations that are associated with diseases,
• Susceptibility, in relation to the ability to respond to the exposure of a non-genetic factor.

The exposome in health and disease

According to the WHO, among the top 10 causes of death linked to a person’s life environment we find cardiovascular disease, cancer, and respiratory diseases.

Cardiovascular diseases

The role of an individual’s diet on the cardiovascular system is well known. For instance, a diet rich in salt or fat may lead to high blood pressure or dyslipidemia, which in turn are risk factors for atherosclerosis, myocardial infarction, or stroke.

The microbiota is also widely related to the risk of cardiovascular disease. Certain foods and components of the gut flora have been linked to a higher risk of atherosclerosis. An example is L-Carnitine, which is found in meats or dairy products and is metabolized by the gut microbiota generating, among other compounds, N-trimethylamine oxide, which promotes cardiovascular inflammatory processes.

Pollution, noise, or lifestyle habits are also factors that may be avoided and help lower the incidence of cardiovascular disease.

Early identification of these exposure factors and their elimination are key strategies in the development of preventive plans based on each individual’s exposome.

Cancer

Cancer is a multifactorial disease, and a large number of the factors involved are still unknown. However, it seems clear that some non-genetic factors are linked to the development of cancer,

One factor typically linked to skin cancer is exposure to the sun. UV radiation is known to cause mutations in skin cell DNA.

Additionally, some substances, like pesticides, some air pollutants, toxic substances that are present in certain foods or water (e.g. arsenic), as well as others like physical activity or circadian rhythm are also closely linked to skin cancer.

Breast cancer is also influenced by the exposome. Exposure to certain substances, like dichlorodiphenyltrichloroethane (DDT), polycyclic aromatic hydrocarbons (PAH), and heavy metals during certain susceptibility windows (such as the prenatal stage, gestation, or menopause) are strongly linked to the development of this pathology.

Lung cancer has smoking as its main non-genetic risk factor. Between 80 and 90% of lung cancers occur in smokers or former smokers.

Respiratory diseases

Once again, smoking is responsible for chronic respiratory pathologies such as COPD or asthma. Moreover, exposure to cigarette smoke during the prenatal phase also increases the risk of alterations in the fetus’ lung function and the development of diseases.

Allergies and asthma are closely linked to environmental pollutants. Climate change, urban pollution, and biodiversity loss are key to the development of allergies.

Endocrine diseases

The exposome also plays an important part in the development of endocrine pathologies. Some compounds have recently been shown to act as endocrine disruptors by altering hormonal pathways. These molecular compounds have structures that are very similar to some hormones, and through these, they can impersonate them at different steps in the operating pathway.

One example of these endocrine disruptors are the phthalates used as plastics, which are found in PVC, cosmetics, or hygiene and personal care products. These high lipid compounds, once in the bloodstream, may advance to any part of the body. In testes or ovaries, they are able to alter the secretion of hormones and cause fertility problems.

Additionally, an unhealthy diet, a sedentary lifestyle, or specific environmental components may play a key role in the development of DM II.

The exposome and the aging process

Aging is a natural and physiological process,

At the molecular level, it results in genomic instability, wear and shortening of telomeres, and a series of epigenetic changes that lead to an alteration in mitochondrial function and cellular senescence.

However, we don’t all age the same way. Aging is a biologically complex process, involving genetic and environmental factors. It is the exposome that is responsible for making a difference towards healthy aging with a similar genetic component. Some non-genetic factors have been associated with the maintenance of telomeres which is a great measure in the assessment of aging.

Pollution, smoking, obesity, and poor sleep quality are known to have a negative effect on the telomere length,

And so, the study of the influence of the exposome on cellular aging may be the key to the medicine of the future and to achieving a healthy aging process.

BIBLIOGRAFÍA

(1) Rappaport SM, Barupal DK, Wishart D, Vineis P, Scalbert A. The blood exposome and its role in discovering causes of disease. Environ Health Perspect. 2014;122(8):769-774. doi:10.1289/ ehp.1308015

(2) Wild CP. The exposome: From concept to utility. Int J Epidemiol. 2012;41(1):24-32. doi:10.1093/ije/ dyr236

(3) Olea N, Casas M, Castaño A, Mendiola J, Vrijheid M. Informe Anticipando. Exposoma. Fundación Instituto Roche. 2020. institutoroche.es

(4) https://www.vidasostenible.org/que-es-el-exposoma/

La entrada The Exposome and the Medicine of the Future se publicó primero en Neolife.

One study showed that men, black people, and older patients were more likely to catch COVID, while those taking melatonin, paroxetine, or carvedilol were less likely to do so.

In diseases with a high degree of inflammation, melatonin use is very promising, as it lowers circulating cytokine levels. Melatonin has also been shown to be beneficial in patients who have suffered a heart attack, or those with cardiomyopathy, hypertensive heart disease, and pulmonary hypertension.

Dr. Alfonso Galán González – Neolife Medical Team

SThere is a hypothesis that has been proposed that the RAS suffers two blows that lead to the progression of COVID-19 disease in patients with a history of inflammation.

The first would come from the low-grade inflammation associated with diseases that cause chronic inflammation, and the second blow is caused by COVID. This may explain the higher mortality rate in patients with this type of pathology.

In these blog posts, we have often referred to this incredible molecule (here), and we’ve even mentioned how beneficial it is in coronavirus disease (here).

This time, we will delve deeper (even at the molecular level) into what makes melatonin have these effects, presenting the research that supports these findings.

What are the effects of melatonin that may help us combat COVID-19?

They are summarized in this chart:

In this first part, we will talk about its antiviral, anti-inflammatory, antioxidant, chronobiotic, and immunomodulatory effects, leaving the rest, together with an explanation of the studies currently underway, for a second blog post.

ANTIVIRAL EFFECT

SARS-CoV-2 enters the pulmonary epithelial cells and others through the ACE2 receptor.

The glycoprotein spike on the surface of the virus is bound to the ACE2 receptor (angiotensin-converting enzyme 2); after membrane fusion, the viral RNA genome is released into the cytoplasm and results in two polyproteins that are split by the SARS-CoV-2 main protease, which results in the replication-transcription complex.

Melatonin has been shown to inhibit the virus protease more effectively than other ligands.

Another way in which it may regulate infection is by binding and inhibiting calmodulin, which regulates the expression and retention of ACE2 in the cell membrane.

One study showed that men, black people, and older patients were more likely to catch COVID, while those taking melatonin, paroxetine, or carvedilol were less likely to do so.

The relationship between COVID and melatonin and the Renin-Angiotensin System (RAS) goes somewhat further. In general, RAS induces inflammation, high blood pressure, vasoconstriction, fibrosis, and proliferation via the ACE2/angiotensin II/AT1R axis and the opposite effects via the ACE2/angiotensin (1-7)/MAS axis.

The RAS is activated by chronic inflammation in cancer, diabetes, high blood pressure, and obesity. SARS-CoV-2 induces the internalization and detachment of ACE2, which leads to the inactivation of the ACE2 / angiotensin (1-7) / MAS axis.

And so, there is a hypothesis that has been proposed that the RAS suffers two blows that lead to the progression of COVID-19 disease in patients with a history of inflammation. The first would come from the low-grade inflammation associated with these diseases that activate the ACE/angiotensin II/AT1R axis, and the second blow is triggered by COVID, as it renders the ACE2/angiotensin (1-7)/MAS axis inactive. This may explain the higher mortality rate in patients with this type of pathology.

Melatonin is an effective angiotensin II activation inhibitor and facilitates the action of angiotensin (1-7), thus acting on both “blows”.

Anti-inflammatory/Immunoregulatory Effect

Immunoregulation

T cells are the most advanced cells in our immune system. For a somewhat more complete explanation of how our immune system works, please read this blog post.

For the purposes of this blog post, we will mention a few types of white blood cells (a fundamental cell of the adaptive immune system). There are T helper cells (Th cells), also known as CD4+ cells, that include Th1, Th2, Th17, and T regulators (Treg) (CD4+ CD 25+).

Despite the complexity of the immune system, the fundamentals of its functioning are based on 3 white blood cell populations, the Th1, the Treg, and the Th17. Th cells activate Treg, inhibit Th17, and promote antigen-independent cytotoxicity by inducing the evolution of NK (Natural Killer) cells from our innate immune system into natural killer cells that are activated by lymphokines. Their actions are usually mediated by the secretion of IL-2, the main growth factor for white blood cells.

The relationships between these subtypes of white blood cells are markers for the main diseases suffered by human beings. And so:

• A low ratio of Th1 to Treg is typical in advanced neoplasia.
• A higher ratio of Th17 to Treg is typical in autoimmune diseases… and acute respiratory distress induced by coronavirus.

Anti-inflammatory

The main pathophysiological mechanism of SARS-CoV-2 infection is upward regulation of pro-inflammatory cytokines induced by the activation of neutrophils, macrophages, and mast cells. They increase IL-1, IL-6, and IL-17, C-reactive protein, and TNF alpha.

Melatonin exerts its anti-inflammatory effects through various mechanisms:

• One of these is the Sirtuin 1 mechanism, which prevents macrophages from becoming the pro-inflammatory type.
• It suppresses NF-kB activity.
• It stimulates the production of Nrf2 in studies of heart and liver protection.
• It reduces pro-inflammatory CK (TNF-alpha, IL-1, IL-6, IL-8, and IL-17) and increases anti-inflammatory ones such as IL-10.

Even though all these terms are too scientific, the charts helps us understand them, and it’s interesting to see the mechanism through which they exert their effects.

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And so, the charts below show how doses of 60 mg of melatonin inhibit the production of pro-inflammatory cytokines.

And increases the anti-inflammatory kind.

Coronavirus infection accumulates hyper-inflammatory monocytes and macrophages in the lower respiratory tract, where they play a key role in determining whether the disease will be severe. Infected monocytes and macrophages change their metabolism from oxidative phosphorylation in the mitochondria to glycolysis in the cytoplasm, generating reactive oxygen species; these monocytes that obtain their energy in this way produce more cytokines, causing the destruction of T cells and alveolar cells, thus aggravating the infection.

Melatonin converts these macrophages with modified metabolism back into M2 anti-inflammatory macrophages that use oxidative phosphorylation.

Antioxidant Effect

In both the cytoplasm and nucleus, melatonin has important antioxidant effects and purifies free radicals. These effects are achieved in 3 ways:

• Melatonin eliminates free radicals.
• Melatonin is metabolized into compounds with great antioxidant power.
• It is a direct antioxidant that stimulates the synthesis of antioxidant enzymes and inhibits pro-oxidants.
• It enhances the effects of other antioxidants such as Vitamin C.

As shown in this graphic, there is an intimate relationship, a kind of “vicious circle”, between the production of Reactive Oxygen Species (ROS) and free radicals and inflammation.

One feeds the other and vice versa. In diseases with a high degree of inflammation, melatonin use is very promising, as it lowers circulating cytokine levels. This has been documented in patients with DM2, periodontal disease, and severe multiple sclerosis, as well as in acute inflammation, such as surgical stress, cerebral or coronary reperfusion.

Generally speaking, these effects are achieved with doses that are higher than those used for a chronobiotic effect (2-3 times, of about 100-300 mg).

SEPSIS

Clinical data for COVID-19 disease show us that these patients are at higher risk of sepsis and heart failure.

Melatonin improves the septic shock by inhibiting the NLRP3 pathway, called inflammasome. What is this? The inflammasome is a complex that promotes the maturation of pro-inflammatory cytokines such as IL-1o and IL-18. The inflammasome is responsible for the activation of inflammatory processes, and there is evidence that shows it induces cellular pyroptosis, a highly inflammatory form of scheduled lytic cell death that occurs most often after infection with intracellular pathogens.

Melatonin has been shown, in rodents, to improve kidney, myocardial and liver damage in cases of sepsis, and in human neonatal sepsis, it improves clinical evolution.

In the study represented in these graphs, it was shown to increase the average lifespan of mice with peritonitis.

Melatonin has also been shown to be beneficial in patients who have suffered a heart attack, or those with cardiomyopathy, hypertensive heart disease, and pulmonary hypertension.

In critical patients, even those admitted to ICU, deep sedation increases long-term mortality. The use of melatonin in these patients lowers the use of sedation, pain, agitation, anxiety, and improves sleep quality.

A study of 10 patients admitted to the hospital with COVID-related pneumonia and poor prognostic risk factors administered melatonin, between 36 and 73 mg daily, along with standard treatment. Benefits were observed in all clinical variables (symptoms, regression of pulmonary infiltrates, inflammation markers), as well as in the need for ventilation, total hospitalization time, and final result (death vs recovery).

Another current article in the “preprint” phase shows data from 791 patients who required intubation from severe COVID lung disease and retrospectively analyses which treatments improved prognosis. Melatonin was the only treatment significantly associated with a better evolution.

Chronobiotic Effect

This refers to molecules that affect the physiological regulation of the body clock and specifically those capable of recovering unsynchronized circadian rhythms or preventing this from happening.

The elderly population is not only more susceptible to coronavirus infection but is more likely to have circadian rhythms that are altered by several causes, such as melatonin levels that decrease with age or an increase in stress from social isolation. The deregulation of circadian rhythms is believed to be involved in multiple pathologies suffered in the elderly, especially cardiovascular and neurodegenerative diseases.

It is worth noting that our immune system shows a significant circadian rhythmicity. Therefore, at the start of the day’s activity, there is greater expression of pro-inflammatory CK such as IL-1, IL-6 and IL-12 as well as macrophagic and leukocyte activity that leads to possible tissue damage. By contrast, anti-inflammatory mediators and other growth and angiogenesis factors are increased in the resting phase. As for immune cells; CD4 and CD8 activity against viral antigens reach their maximum levels in the resting phase, while cytotoxic activity of NK cells is more severe in the early hours of activity.

Indeed, these patterns may be altered in older people and should be taken into account when administering immunomodulators or anti-inflammatory drugs.

Delirium

Cases of delirium are found in 50% of hospitalized older patients and 80% of those in critical condition who require mechanical ventilation. Melatonin use is associated with lower ICU stay, lower prevalence of delirium, and improved sleep quality.

In COVID-19 disease, 15% of hospitalized patients have some degree of impaired of consciousness, from drowsiness to coma. Melatonin should be considered an effective agent for improving sleep and minimizing administration of BZD and antipsychotics.

With this, we end this first part of how melatonin may improve COVID disease. I hope it wasn’t too complicated to understand. I recommend you stay tuned for Part 2, which is very interesting, as well, and which provides insights into how its use is being integrated into the different fields and medical specialties.

BIBLIOGRAFÍA

(1) Gurwitz, D. Angiotensin receptor blockers as tentative SARS-CoV-2 therapeutics. Drug Dev. Res. 2020, 81, 537–540.

(2) Hardeland, R. Melatonin and inflammation—Story of a double-edged blade. J. Pineal Res. 2018, 65, e12525.

(3) Xia, Y.; Chen, S.; Zeng, S.; Zhao, Y.; Zhu, C.; Deng, B.; Zhu, G.; Yin, Y.; Wang, W.; Hardeland, R.; et al. Melatonin in macrophage biology: Current understanding and future perspectives. J. Pineal Res. 2019, 66, e12547.

(4) Sánchez-López, A.L.; Ortiz, G.G.; Pacheco-Moises, F.P.; Mireles-Ramírez, M.A.; Bitzer-Quintero, O.K.; Delgado-Lara, D.L.C.; Ramírez-Jirano, L.J.; Velázquez-Brizuela, I.E. Efficacy of Melatonin on Serum Pro-inflammatory Cytokines and Oxidative Stress Markers in Relapsing Remitting Multiple Sclerosis. Arch. Med. Res. 2018, 49, 391–398

(5) Gitto, E.; Reiter, R.J.; Amodio, A.; Romeo, C.; Cuzzocrea, E.; Sabatino, G.; Buonocore, G.; Cordaro, V.; Trimarchi, G.; Barberi, I. Early indicators of chronic lung disease in preterm infants with respiratory distress syndrome and their inhibition by melatonin. J. Pineal Res. 2004, 36, 250–255.

(6) Gitto, E.; Karbownik, M.; Reiter, R.J.; Xian Tan, D.; Cuzzocrea, S.; Chiurazzi, P.; Cordaro, S.; Corona, G.; Trimarchi, G.; Barberi, I. Effects of melatonin treatment in septic newborns. Pediatr. Res. 2001, 50, 756–760.

(7) Castillo, R.R.; Quizon, G.R.A.; Juco, M.J.M.; Roman, A.D.E.; De Leon, D.G.; Punzalan, F.E.R.; Guingon, R.B.L.; Morales, D.D.; Tan, D.-X.; Reiter, R.J. Melatonin as adjuvant treatment for coronavirus disease 2019 pneumonia patients requiring hospitalization (MAC-19 PRO): A case series. Melatonin Res. 2020, 3, 297–310

(8) Ramlall, V.; Zucker, J.; Tatonetti, N. Melatonin is significantly associated with survival of intubated COVID-19 patients. medRxiv 2020

(9) Chellappa, S.L.; Vujovic, N.; Williams, J.S.; Scheer, F.A.J.L. Impact of Circadian Disruption on Cardiovascular Function and Disease. Trends Endocrinol. Metab. 2019, 30, 767–779.

(10) Zambrelli, E.; Canevini, M.; Gambini, O.; D’Agostino, A. Delirium and sleep disturbances in COVID–19: A possible role for melatonin in hospitalized patients? Sleep Med. 2020, 70, 111.

La entrada Melatonin in the Time of the Pandemic. Part 1 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.

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 impact of coronavirus (or COVID-19) on the population can continue for a fairly long period of time. The symptomatology that we describe in the first part of this article (cough, difficulty breathing, weakness, headache, digestive problems, etc.) can persist well beyond 12 weeks. This is a clinical condition that has come to be called Subacute Coronavirus Disease, or Long COVID.

On many occasions, these patients which are not in the acute phase (or “danger phase”) are considered to be “cured.” However, all the symptomatology that they present at different levels makes it difficult for them to resume their normal life, or at least under usual conditions and/or normal performance levels. Therefore, at Neolife we believe it is important to provide treatment and support to facilitate, as much as we can, a recovery that is as complete and as quick as possible.

Dr. Débora Nuevo Ejeda – Neolife Medical Team

But… what do we consider a “normal recovery?”

Patients admitted to the hospital after a coronavirus-related pneumonia may present difficulties in recovery and said recovery may have a longer duration than usual. However, normally within 12-14 weeks the symptoms have improved. In any case, everything depends on the severity of the disease, existing comorbidities, and the fragility of the patient.

The evolution considered as “normal” that we can expect is as follows:

• At 4 weeks, muscle pain, chest pain, and expectoration are usually significantly reduced.
• Between 4 and 6 weeks, the cough and trouble breathing usually improve.
• After 3 months, most symptoms have disappeared but asthenia (or weakness) may persist.
• At 6 months, it is usual for the entire disease to have been resolved — unless the patient presents complications.

For all those patients who continue to present symptoms after a time that is considered as “normal,” we will try to offer an explanation, support, and treatment to favor optimal recovery.

Management of respiratory symptoms

The Society of Thoracic Medicine defines chronic cough as a persistent cough for more than 8 weeks. Until that time, and unless there are signs of serious infection or other complications such as pleuritic pain, cough should be managed with respiratory exercises and appropriate medication when necessary (such as PPIs when reflux is suspected).

Dyspnoea (or difficulty breathing) may be common after a coronavirus respiratory infection. Severe respiratory distress is uncommon in non-hospitalized patients; however, if it occurs, it requires a preferred referral to emergency or specialized medical services.

Both dyspnea and cough can improve significantly with breathing exercises.

A pulse oximeter is very useful for monitoring symptoms and recovery after COVID-19.

Hypoxia reflects a problem with the diffusion of oxygen and is one of the typical symptoms of respiratory problems associated with coronavirus. This hypoxia can be asymptomatic (also called silent hypoxia) or manifest as an increase in respiratory work or be a reflection of an associated secondary pathology such as bacterial pneumonia or pulmonary thromboembolism.

Monitoring of oxygen saturation for 3-5 days may be especially useful in patients who continue with dyspnea after the acute phase. In some cases, a desaturation test is also recommended in those patients who suffer from dyspnea with exertion or despite having basal oxygen saturations above 95%. This test consists of measuring saturation at rest and after walking 40 steps over a flat surface and sitting and getting up as quickly as possible for 1 minute. A 3% fall in saturation is considered abnormal and must be studied.

Saturations between 94-98% are considered normal, and saturations below 92% may require oxygen therapy.

If recovery is spontaneous, in about 6 weeks no rehabilitation programs are needed. Patients who have had lung damage can benefit greatly from this restorative treatment, defined as a multifaceted intervention based on a personalized assessment and treatment that includes training and behavior modification to improve the physical and psychological condition of these patients with respiratory disease. This may include videos programs, tele-assistance, etc.

Asthenia (weakness)

The severe asthenia (or weakness) that some patients describe with Long COVID is reminiscent of the chronic fatigue described after SARS, MERS, and other pneumonias.

There is no evidence of the usefulness of drug or non-drug therapy to reverse this fatigue.

Additional causes such as deficiencies of certain vitamins, minerals, and/or trace elements that favor the feeling of weakness should be investigated. A hormonal study can also be of great help. The stress of coronavirus infection can alter some hormonal axes.

As for exercise, a gradual return to normal life is recommended. There is controversy about the impact of exercise on chronic fatigue. It is recommended to start exercise gradually and stop it if the patient has fever, dyspnea, severe asthenia, or significant muscle pain.

A physical therapist’s guidelines for restarting physical exercise can be critical in order to do so in the most beneficial way possible.

Cardiovascular complications and their management

Probably 20% of patients admitted have significant cardiac complications and an even greater percentage have cardiological involvement without being aware of it.

These cardiopulmonary complications include myocarditis, pericarditis, infarction, arrhythmias, and pulmonary thromboembolism. They can appear during an active acute COVID infection or weeks later, during the so-called Long COVID disease. They are more common in patients who already have some type of cardiovascular disease. Several pathophysiological mechanisms have been proposed to explain their development, such as viral infiltration, an inflammatory process with microthrombosis, and poor regulation of ACE-2 receptors.

• Chest pain:

Chest pain is quite common in Long COVID. The main difficulty that arises is to differentiate between musculoskeletal (or mechanical) pain and specific chest pain. Diagnosis should be approached in the same way as any chest pain: by reviewing the complete medical history with all previous conditions, by looking at cardiovascular risk factors, and with a thorough physical examination. If there are doubts, the patient should be referred to a specialist for specific tests (ECG, cardiac MRI, echocardiogram, etc.) and relevant treatment.

Treatment of mechanical pain consists of analgesics and anti-inflammatory drugs as needed.

• Pulmonary thromboembolism:

As is well known by now, COVID 19 is considered a proinflammatory state and a state of hypercoagibility with an increased risk of thrombotic phenomena.

Most hospitalized patients receive anticoagulation treatment during their hospital stay or in the ICU. However, post-COVID anticoagulation recommendations vary greatly. A large proportion of patients with moderate or severe disease also receive an anticoagulation regimen that covers at least 10 days after hospital discharge. The duration of treatment with heparin will also vary depending on the degree of mobility the patient has. Those more limited patients will need longer treatments, since immobilization is also a risk factor for thrombosis.

If they are diagnosed with a thrombotic episode, it is treated following the usual guidelines and controls.

• Ventricular dysfunction:

Systolic dysfunction and heart failure after COVID should be managed following conventional guidelines. Intense cardiovascular exercise should be avoided during the first 3 months, especially after myocarditis or pericarditis. These patients should be periodically checked by the specialist.

Again, guidance and follow-up from a physiotherapist is essential in these patients when resuming exercise.

Digestive involvement

The digestive system is one of the systems most commonly affected by the coronavirus. Many patients have diarrhea, nausea, vomiting, epigastric pain, etc. These conditions especially tend to last long. Thus, it is not strange that patients continue to present intestinal transit alterations and abdominal discomfort many weeks after acute infection. This also leads to malabsorption and deficiency of proteins, minerals, and some vitamins.

It is necessary to investigate a potential bacterial overgrowth made stronger by the infection itself and the antibiotic and corticosteroid treatment used in the management thereof. The alteration of the intestinal flora that this causes perpetuates the problem.

Repopulating the intestinal flora with probiotics, making specific dietary changes, and supplementing the deficits caused can favor recovery and the improvement of symptoms.

Neurological involvement

Complications like stroke, vertigo, encephalitis, and neuropathies have been described during or after an acute COVID infection, although they are uncommon. If suspected, they should be evaluated by a neurologist.

Other more nonspecific symptoms which tend to appear with dyspnea and cough are headache, dizziness, and confusion and they should equally be managed in a conventional way. Other added causes that can chronify the condition should be investigated, such as vitamin deficiency (suboptimal vitamin D or low levels of B vitamins), iron deficiency, etc. They should be treated symptomatically when necessary, with specific analgesics and supplements.

• Anosmia and ageusia: loss of smell and taste

4 out of 10 patients experience loss of smell and/or taste. While patients with irreversible loss of smell are not yet known and it is normal to recover said sense in 2 weeks, there are patients who after 8 weeks are still unable to distinguish certain odors.

Young patients and those with milder forms of the disease who do not require hospital admission are most affected by this loss.

There are various olfactory training techniques, rehabilitation of the sense and olfactory memory, that can be guided by professionals and help a lot to recover these senses.

Mental health and wellbeing

There is much talk about the consequences that COVID is having on mental health; stress, anxiety, and other alterations stemming from the breakdown of routine, loneliness, isolation, and social exclusion. There have also been increased sleep problems and the appearance of post-traumatic stress disorder, especially in healthcare personnel and caregivers. Psychological support can be of great help. Using scales like the ones we routinely use in our clinic can also be a great support to assess the magnitude of the problem.

Many papers are now focused on studying the benefits of melatonin on these conditions, both because of its role regulating chronobiotic agents and because of its high anti-oxidant power.

As we have seen, Subacute Coronavirus Disease or Long COVID can encompass many symptoms that significantly limit the quality of life of the patients affected. Identifying issues and providing support and treatment are critical to reducing the impact of COVID over the medium and long term.

BIBLIOGRAPHY

(1) Geddes L. Why strange and debilitating coronavirus symptoms can last for months. New Scientist. https://www.newscientist.com/article/mg24632881-400-why-strange-and-debilitatingcoronavirus-symptoms-can-last-for-months/.

(2) …Gemelli Against COVID-19 Post-Acute Care Study Group. Post-COVID-19 global health strategies: the need for an interdisciplinary approach. Aging Clin Exp Res 2020;doi: 10.1007/s40520-020-01616-x. pmid: 32529595

(3) Phillips M, Turner-Stokes L, Wade D, et al. Rehabilitation in the wake of Covid-19—A phoenix from the ashes. British Society of Rehabilitation Medicine, 2020. https://www.bsrm.org.uk/downloads/covid-19bsrmissue1-published-27-4-2020.pdf.

(4) Assaf G, Davis H, McCorkell L, et al. An analysis of the prolonged COVID-19 symptoms survey by Patient-Led Research Team. Patient Led Research, 2020. https://patientresearchcovid19.com/.

(5) Callard F. Very, very mild: Covid-19 symptoms and illness classification. Somatosphere 2020; https://somatosphere.net/2020/mild-covid.html/.

(6) Garner P. Covid-19 at 14 weeks—phantom speed cameras, unknown limits, and harsh penalties. BMJ Opinion [blog]. 2020; https://blogs.bmj.com/bmj/2020/06/23/paul-garner-covid-19-at-14- weeks-phantom-speed-cameras-unknown-limits-and-harsh-penalties/.

(7) COVID Symptom Study. How long does COVID-19 last? Kings College London, 2020. https://covid19.joinzoe.com/post/covid-long-term?fbclid=IwAR1RxIcmmdL-EFjh_aI-.

La entrada Management of Subacute Coronavirus Disease, or Long COVID 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.

Overweight and obesity have been linked to an increased incidence of lung diseases, such as asthma, chronic obstructive pulmonary disease (COPD), or sleep apnea syndrome. Recent research links this pathology with severe forms of COVID-19, increasing the health risk of worsening the disease.

The natural history of chronic noncommunicable diseases, such as obesity, is the result of the combination of genetic factors, a sedentary life, and unhealthy eating. A new study published in the prestigious scientific journal The Lancet has called overweight and obesity the main risk and severity factor in the COVID-19 process.

Tania Mesa – Director of Neolife Nutrition and Nursing Unit

Excess fat is associated with an inflammatory state that may be increased by infection with the virus.

Obesity and all chronic noncommunicable diseases represent the true global pandemic. Cases of obesity have almost tripled between 1975 and 2016 worldwide. Overall, about 13% of the world’s adult population (11% of men and 15% of women) were obese in 2016 (1). The new SARS-CoV-2 coronavirus, which produces the disease known as COVID-19, continues to expand rapidly around the world. This is a respiratory virus that has been shown to be transmitted quite easily and puts this group of people at greater risk.

The Spanish Society for the Study of Obesity (SEEDO) states that almost half of the Spanish population, subjected to several weeks of lockdown, has experienced an increase in their average weight during this period of time (2). The results of his recently published survey indicate that 44% of the population claims to have gained weight during lockdown and, the majority, 73%, report a weight gain range of between 1 and 3 kilos. Half of the population surveyed in the SEEDO study was unaware that obesity worsens the prognosis of those who have COVID-19 (2).

Increasingly, we have data that point to overweight and obesity as factors linked to a poor prognosis in patients infected with COVID-19. Older age is the main indicator of mortality, but COVID-19 disease affects all ages. Recently, a clear inverse correlation between age and body mass index (BMI) has been shown, in which people admitted to the hospital were more likely to be obese and suffer acute forms of the novel coronavirus disease (3. 4). In a report by the UK’s Intensive Care National Audit and Research Centre (ICNARC), which includes 2,621 patients in intensive care units (ICUs) with COVID-19, 30.7% had a BMI of 30-40, and 7% was higher than 40. With regard to prognosis, the chance of survival was higher in patients with a BMI that was lower than 30 (5).

A new review published by the Mayo Foundation for Medical Education and Research shows that respiratory infections are more common in overweight patients. Obesity is associated with a decrease in respiratory reserve volume and functional capacity of the respiratory system. Generally, the obese patient has a higher number of pro-inflammatory cytokines (proteins responsible for intercellular communication) associated with excess fat tissue. Subjects with obesity therefore present a pro-inflammatory environment and COVID-19 is expected to further exacerbate inflammation by exposing them to higher levels of circulating inflammatory molecules compared to thin subjects (Figure 1). This situation results in metabolic dysfunction, which may lead to dyslipidemia, insulin resistance, cardiovascular disease, high blood pressure, and type 2 diabetes (6. 7).

Another common feature in obesity is vitamin D deficiency, which increases the risk of infections and impairs immune response. By contrast, vitamin D supplements may prevent respiratory infections through various immunoregulatory functions, including decreased production of pro-inflammatory cytokines, reducing the risk of pneumonia. Vitamin D deficiency may be involved in the link between obesity and increased susceptibility to complications and mortality due to COVID-19 (7, 8). It should be noted that alterations in the gut microbiota are common in obese subjects and some protocols for the treatment of COVID-19 include the use of probiotics to maintain the balance of bacterial populations and thus strengthen the immune system (8).

The Massachusetts General Hospital points out that obesity is not a risk factor for becoming infected with COVID-19. However, obese patients are more likely to require intensive care for COVID-19 (9). A characteristic complication of obesity is hypoventilation syndrome, where excess fatty tissue from the chest wall makes it difficult for obese patients to breathe deep and completely. They point out that this combination increases the severity of symptoms in those who develop COVID-19.

Obesity is a chronic disease that requires treatment. A new study published in The Lancet magazine reminds us of the importance of acquiring healthy lifestyle habits. They emphasize that this is a good time to start taking steps towards losing 5% to 10% of your body weight if you are obese (10). Regarding diet, a normal protein low-calorie diet that is low on carbohydrates and fats may be a promising strategy for losing weight and improving health; however, the patient’s profile and condition should always be considered.

In short, there are several biological mechanisms by which COVID-19 disease may affect people with obesity to a greater extent. The treatment of obesity requires a multidisciplinary vision, since it is a complex and multifactorial disease, in which an important component is the balance between energy intake and expenditure, but there are also other contributing factors, such as food availability, age, gender, genetics, metabolism, and physical activity. It is important to note that there are other environments to consider, such as home quarantines, isolation by areas or neighborhoods, isolation due to close contact with patients with COVID-19, etc., as we have recently witnessed. Therefore, it is important for us to be aware of all these factors and to remember the data and information on the increase in body weight during the lockdown suffered in March.

Performing a global assessment, interpreting information, establishing treatment strategies, identifying modifiable factors, and individualizing treatment is what we do here at Neolife, thanks to our team of healthcare professionals and the great success stories we’ve obtained. Treatment should be initiated with the recommendation of lifestyle changes, which requires nutritional intervention, cognitive behavioral therapy, and specific exercise prescription, associated with the pharmacological treatment of obesity and its complications.

BIBLIOGRAPHY

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

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

(2) SEEDO. (2020). “Un 44% de los españoles aumentaron de peso durante el confinamiento” [44% of Spaniards gained weight during lockdown]. Spanish Society for the Study of Obesity.

URL:https://www.seedo.es/images/site/notasprensa/NP_Un_44_de_espan%C3%9Eoles_ha_au

mentado_de_peso_durante_el_confinamiento_Ok.pdf

(3) Simmonnet, A. et al. (2020). “High prevalence of obesity in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) requiring invasive mechanical ventilation”. Obesity. Vol. 28(7):1195-1199.

URL: https://pubmed.ncbi.nlm.nih.gov/32271993/

(4) Bellido G., D. (2020). “Obesidad y Covid-19. La relación cada vez más consistente” [Obesity and COVID-19: An increasingly consistent relationship]. Hospital Universitario de Ferrol. Spain.

URL: https://www.foroactua.com/wp-content/uploads/2020/05/Qu%C3%A9-consecuencias-tiene-la-obesidad-cuando-aparece-el-Covid.pdf

(5) Fernández B., E. (2020). “Obesidad” [Obesity]. Píldora Científica. Revista Española de Salud Pública.

URL:https://www.mscbs.gob.es/biblioPublic/publicaciones/recursos_propios/resp/revista_cdrom/

Suplementos/Pildoras/pildora14_obesidad.pdf

(6) Sanchis-Gomar, F. et al. “Obesity and outcomes in COVID-19: when an epidemic and pandemic collide”. Mayo Clinic. Vol. 95(7): 1445-1454.

URL:https://www.sciencedirect.com/science/article/pii/S0025619620304778

(7) Chiappetta, S. et al. (2020). “COVID-19 and the role of chronic inflammation in patients with obesity”. International Journal of Obesity. Vol. 44, 1790-1792.

URL:https://www.nature.com/articles/s41366-020-0597-4

(8) Petrova, D. et al. (2020). “La obesidad como factor de riesgo en personas con COVID-19: posibles mecanismos e implicaciones” [Obesity as a risk factor in people with COVID-19: possible mechanisms and implications]. Atención Primaria. Vol. 52(7):496-500.

URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7247450/pdf/main.pdf

(9) Fitch, A. & Hutter, M. (2020). “Understanding links between COVID-19 and obesity”. Massachusetts General Hospital.

URL: https://www.massgeneral.org/digestive/weight-center/understanding-links-between-covid-19-and-obesity

(10) Rubino, F. et al. (2020). “Bariatric and metabolic surgery during and after the COVID-19 pandemic: DSS recommendations for management of surgical candidates and postoperative patients and prioritization of access to surgery”.

URL:https://www.thelancet.com/journals/landia/article/PIIS2213-8587(20)30157-1/fulltext

La entrada Obesity in the Crosshairs of COVID-19 se publicó primero en Neolife.

Fatty liver disease comprises a broad group of liver conditions, ranging from simple liver steatosis to steatohepatitis, fibrosis, and even cirrhosis.

Age and obesity increase its prevalence and there is a strong association with metabolic syndrome and increased cardiovascular mortality and malignant diseases. When should you suspect it? How is it diagnosed? How do we prevent it or even reverse it?

Dr. Débora Nuevo – Neolife Medical Team

When should you suspect it?

In patients where liver steatosis is suspected, an initial assessment is recommended through a complete anamnesis or medical history, a full physical examination, and some complementary tests.

1. Medical history:

The patient should be asked the following questions, and an alert should be raised if he or she presents:

• Alcohol intake of more than 20 mg/day in women or more than 30 mg/day in men
• History of hepatitis C and/or B virus infection
• Personal history or family history of diabetes, high blood pressure, and/or cardiovascular disease

2. Physical examination, attention should be paid to the following findings:

• Body Mass Index > 25
• Waist circumference > 102 cm in men or > 88 cm in women
• Significant changes in body weight

3. Complementary tests, monitoring parameters such as:

• Liver enzymes (GOT, GPT, GGT)
• Fasting blood sugar test, HBA1, insulin, HOMA index
• Complete blood count
• Total cholesterol, HDL. triglycerides, and uric acid

How is it diagnosed?

There are different methods for formulating a diagnosis, both noninvasive (like blood tests and a variety of imaging techniques) and invasive methods, like a liver biopsy.

Laboratory data:

• The GPT value has sometimes been used as a screening method for diagnosis. It may be elevated, though it does not usually double or triple the lab’s reference value.
• The relationship between the GOT and GPT, a GOT/GPT ratio > 0.8, allows us to suspect stages of advanced steatosis.
• Elevated liver enzymes and proteins like GGT, alpha-2-macoglobulin, haptoglobin, apolipoprotein A, and TIMP1 should be noted, though none of them is a specific marker.
• High levels of ferritin may also act as predictors of fibrosis.
• Pro-inflammatory cytokines, like TNF alfa and Interleukin 6 (IL-6) may be elevated compared to other patients with fatty liver disease without inflammation.

Imaging tests:

• Abdominal ultrasound: the most commonly used imaging test. It is safe, non-invasive, accessible, low cost, and quite accurate in terms of diagnosis. A fatty liver without steatosis shows a homogeneous echostructure similar to the renal cortex and spleen. A fatty liver has greater echogenicity (it is brighter) due to the accumulation of fat vacuoles within the cells. There are four grades of liver steatosis as seen in an ultrasound: grade 0, without steatosis; grade 1, mild; grade 2, moderate; and grade 4, severe. The sensitivity to detect steatosis is about 93% the more fat there is.
  
• CT scan: a very accurate way to diagnose grade 2 and 3 steatosis, but not to detect grade 1. The attenuation of the liver parenchyma in the CT scan may be altered by other factors like excess iron and glycogen.
• Magnetic resonance imaging: the most sensitive imaging method for detecting an increase in liver fat. It can detect steatosis with only 3% fat content. The only drawback is that it is somewhat more expensive and less readily available than ultrasound.
• Fibroscan or transient elastography: performed with ultrasonographic pulse. It can detect cirrhosis with high accuracy, but its accuracy is lower in stages with less fibrosis.

Invasive tests: A liver biopsy is the best method for diagnosing, classifying, and predicting the evolution of liver steatosis. However, it is an invasive method, not without possible complications, so it should be reserved for patients with high risk of advanced fibrosis to rule out other causes of steatosis or fibrosis.

How can we prevent and/or treat it?

There is currently no specific treatment for fatty liver disease. The goal, both to prevent it and to treat it once diagnosed, is to control risk factors.

• Weight control: in patients with obesity or overweight it is recommended that they lose 10% of the initial weight in the first 6 months (between half a kilo and one kilo a week).
• A diet rich in polyunsaturated fatty acids and low in saturated fats, with antioxidants, fiber, fruits, and vegetables.
• Exercise for at least 30 minutes a day.
• Maintaining optimal cholesterol and glucose levels.
• No smoking and avoiding alcohol.

Some pharmacological measures, such as oral hypoglycemic medications and statins are sometimes also necessary. Medications that aid weight loss, such as orlistat, which inhibits fat absorption, can be quite useful in these patients.

Additionally, there are other therapies under study, such as probiotics that decrease bacterial translocation and decrease levels of TNF Alpha and IL6, among others, lessening liver damage.

Melatonin and Omega 3 fatty acid supplements have also been studied with very good results in lowering the amount of fat and liver damage.

BIBLIOGRAPHY

(1) Aller R, et al. Documento de consenso. Manejo de la enfermedad hepática grasa no alcohólica (EHGNA) [Management of nonalcoholic fatty liver disease (NAFLD)]. Guía de práctica clínica. Gastroenterol Hepatol. 2018. https://doi.org/10.1016/j.gastrohep.2017.12.003

(2) European Association for the Study of the Liver (EASL); European Association for the Study of Diabetes (EASD); European Association for the Study of Obesity (EASO). EASL-EASD-EASO Clinical Practice Guidelines for the management of nonalcoholic fatty liver disease. J Hepatol. 2016;64:1388—402. 2.

(3) Rinella ME. Nonalcoholic fatty liver disease. A systematic review. JAMA. 2015;313:2263—73. 3. Loomba R, Sanyal AJ. The global NAFLD

(4) Nobili V, Alisi A, Raponi M. Pediatric non-alcoholic fatty liver disease: Preventive and therapeutic value of lifestyle.

(5) Elizabeth Hernández-Pérez, Plácido Enrique León García, Norma Edith López-Díazguerrero, Fernando Rivera-Cabrera, Elizabeth del Ángel Benítez. Hígado graso y esteatohepatitis no alcohólica: patogénesis y tratamiento [Fatty liver and nonalcoholic steatohepatitis: pathogenesis and treatment].

(6) Liver steatosis and nonalcoholic steatohepatitis: from pathogenesis to therapy. Medwave2016 Sep;16(8):e6535 doi: 10.5867/medwave.2016.08.6535

La entrada Fatty Liver: the New Epidemic of the 21st Century? Part II 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.