Colon Cancer is the third most deadly cancer worldwide. There were more than 1.4 million cases each year and 694,000 deaths globally. The treatment of colon cancer includes chemotherapy, surgery and radiation therapy. However, advances in diagnosis and treatment leads to development and improvement in survival. Numerous data point out that genetic changes function as vital role in the development of colon and rectal cancer. In which regulatory molecules mRNA affects various molecular and cellular target including cancer cells. That is why, development in research used mRNA as based diagnostic biomarkers for colon cancer in human. Furthermore, certain kind of mRNA used to predict survival in colon cancer patients. As well as a better knowledge of molecular mechanisms and associated gene is important for early diagnosis and treatment.
ULBP2 a novel prognostic biomarker in Colon Cancer
ULBP2 is a potential biomarker in colon cancer survival. Previous study shows that matrix metalloproteinase-9 reveals as an important marker for postoperative prognosis in colorectal cancer patients. Also extracellular matrix plays a vital role in cancer progression in which it provides structural and biochemical support in cells. Despite from all of these, digestion is also considered to have a major role related to cancer preventive activity. Additionally, an in vitro of peptides gastrointestinal digestion can inhibit colon cancer cells proliferation and inflammation. Moreover, recent study showed that up and down regulated mRNAs are largely amass in extracellular matrix and digestion. As a result, it would entails that abnormality of extracellular matrix and digestion takes part in colon cancer progression.
Furthermore, the Wnt signaling pathway gives clinical importance on various diseases including colon cancer. Since alteration of this pathway are mostly observed in colorectal cancer with microsatellite instability. So, inhibiting this pathway might be helpful strategy for targeting chemotherapy-resistance cells. Also drug metabolism determined resistance of colorectal cancer resorcinol-based heat shock protein 90 inhibitors. Therefore, Wnt signaling and drug metabolism are both important pathway enriched by up and down regulated mRNAs.
Prognostic biomarkers are very important and have the power to change the course of disease if only knew beyond prognostic factors. In this research ULBP2 gene that encodes cell surface glycoprotein located at chromosome 6 demonstrates prognostic biomarker for colon cancer. High level of ULBP2 is deemed independent indicator for overall survival and identified as the sole outstanding mRNA.
Source: Prepared by Joan Tura from BMC Biological Research
Volume 51:10 March 29, 2018
Aflatoxins produced by a certain molds that are poisonous carcinogens which grow mostly in soil, hay, decaying plants and grains. It can affect livestock and human as natural contaminants in foods like peanuts and corn meal. There are four types of aflatoxins these are B1, B2, G1 and G2 in which all are teratogenic, carcinogenic and immunosuppressive. Its toxic effect might be due to the generation of free radicals resulting into lipid peroxidation that damage biological system. On the other hand yogurt is produced from the bacterial fermentation of milk. In which bacteria produces lactic acid that acts on milk protein to give yogurt its texture and tart flavor. However, yogurt contains plenty of probiotic bacteria that offer benefits as microflora in the intestines. It also helps boost immune response and suppress carcinogenesis since fermented dairy products contain live lactic acid bacteria.
Selenium-fortified yogurt protects against aflatoxin toxicity
Yogurt has been known as therapeutic to various disorders including lactose intolerance, indigestion, intoxication, gastroenteritis, kidney, liver disorders and cancer. Selenium added to yogurt considered as the basic trace elements vital for normal growth and development in humans and animals. It also acts as anti-oxidant as well as improves nutritional values. Additionally, selenium has both enzymatic and structural functions that protect harmful reactive oxygen and minimized the production of hydrogen peroxide from aflatoxins. Ingestion of aflatoxins leads to weight loss due to the change in digestive enzymes activity that causes malabsorption of nutrients.
Aflatoxins will impair the biosynthesis of protein which results to the degranulation of the endoplasmic reticulum. It also caused liver fibrosis and poses health risk to humans and livestock. In this research , a positive results shows that selenium-fortified yogurt suppress the level of aflatoxins in rats. It also proved that with selenium contents inhibit the activity of enzymes related to carcinogenesis. Since yogurt improves intestinal mucosa and microflora that influence intestinal barrier. These yogurt bacteria inhibit the peroxidation of lipids by foraging reactive oxygen.
Therefore, consumption of nuts infected with aflatoxins caused toxicity mainly at the kidney and liver. But intake of selenium-fortified yogurt can definitely suppress against aflatoxins toxicity. In general, application of probiotic bacteria and selenium is vital and viable therapeutic approach to improve safety in food industry. Indeed, it is recommended to eat fresh nuts to avoid aflatoxins along with selenium-fortified yogurt to lessen its toxicity.
Source: Prepared by Joan Tura from BMC Agriculture and Food Security
Volume 7:21, June 2018
Breast cancer is the occurrence of lumps or thickening of the surrounding tissues of the breast mostly in women. Yet it also occurs rarely in men. It leads to the changes in shape and appearance of the breast. As well as the changes of skin like peeling, scaling and crusting of the surrounding nipples. Nowadays, extensive support for breast cancer awareness has helped generate advances in treatment and diagnosis. In which survival rates increased while the death rates continuously declining. Due to some factors such as personalized approach for treatment, early detection and have better knowledge of the disease. In this particular research a tumor-infiltrating lymphocytes has been evaluated to convey prognostic information of the breast cancer metastases. Assess its levels, immune composition and ligand expression in metastatic lesions.
Tumor-infiltrating lymphocytes as an Immunogenicity of Breast cancer
Evidences suggest the potential of tumor-infiltrating lymphocytes as biomarker in breast cancer metastatic stage. Even at onset of disease it proves as prognostic biomarker in human epidermal growth factor receptor positive with breast cancer. 94 patients have been studied retrospectively with metastatic breast cancer. Younger women showed significant lowered tumor-infiltrating lymphocytes compared to older patients above 50 years of age. Generally tumor-infiltrating lymphocytes are low but have been recognized significantly at high level with patients having this disease. Moreover, previous reports indicate that at secondary or recurrence of disease a lower tumor-infiltrating lymphocytes level occurs.
Analysis of the characteristics of tumor immune infiltrate differs across metastatic sites. It also suggests that cutaneous tissues might harbor permissive immune microenvironment for tumor growth. In which immune heterogeneity across metastatic sites need to be explored because it is relevant in treatment and immunotherapy. Other factors that are significant to tumor-infiltrating lymphocytes composition are those patients treated with multiple lines of chemotherapy. Indeed, heavily pretreated patients might have an impaired antitumor cytotoxic activity of the immune system.
Therefore, tumor-infiltrating lymphocytes showed strong prognostic value in breast cancer patients. Further examinations of its relevance as biomarker reflect a general activation of the immune system. Thus, it indicates that tumor-infiltrating lymphocytes is a simple method that effectively appreciates the immune activation status of tissue negative tumor. Certainly, given the availability of standardized method of the assessment, this immune marker is technically simple and clinically reliable. Finally, tumor-infiltrating lymphocytes provide novel hypothesis-generating data with regards to immune composition and complex interplay with breast cancer metastatic setting.
Source: Prepared by Joan Tura from Springer BMC Breast Cancer Research
Volume 20:62, 22 June 2018
Pancreatic cancer started at the tissue of the pancreas – an organ in the abdomen that lies behind the lower stomach. Pancreas releases hormones that helps in maintaining the sugar level in the blood and assist in digestion. Pancreatic cancer is hardly detected at early stage and it is recorded as third deadliest cancer in the United States. Some of its symptom includes weight loss, diabetes, jaundice, blood clots, depression and fatigue. However, it is usually characterized at late stage that has been already metastasized. Current therapy of this disease involves adjuvant chemotherapy, surgical resection and radiotherapy. Yet despite of the advancement of the clinical management and therapy the outcome remains unsatisfactory to the patients. So, this novel research of prognostic biomarker helps pancreatic cancer treatment to maximize survival and avoid toxicity.
miRNAs as Prognostic Biomarkers for Pancreatic Cancer
Due to poor prognosis of pancreatic cancer early detection methods have been developed. To have an effective treatment options as well as the importance of critical biomarkers. However, miRNAs shows significance for early detection and diagnosis. It divulges to have great potentials as prognostic biomarkers in pancreatic cancer. miRNAs are small non-coding RNA with 18-22 nucleotides in length that have been known to be associated with tumorigenesis. It is also linked to apoptosis, cell cycle control, proliferation, chemoresistance, metastasis and invasion. This miRNAs modulates key targets and pathways in signaling as well as its unusual expression are associated with chemoresistance.
In terms of chemotherapeutic treatment of pancreatic cancer miRNAs elevated expression inhibits the anti-tumor activity. miRNAs is related to gemcitabine resistance by inhibiting tumor suppressor gene phosphatase and tensin homologue thereby activating the PI3K/AKT pathway. It is also showed that miRNAs expression correlates with prolong overall survival benefits from chemotherapeutic treatment. Additionally, down regulation of miRNAs is responsible for progression of various malignancies including pancreas, breast, prostate, lung and liver cancer. It contains anti-cancer role via modulating targets implicated in cell cycle, apoptosis and DNA repair.
Therefore, it is clear that pancreatic cancer utilizes various mechanisms to maintain a highly resistant phenotype. miRNAs epigenetic controls allow cells to quickly adapt to the genotoxic stress caused by chemotherapy. It is also quickly modulates the mRNA translation in pancreatic cancer cells in response to chemotherapeutic treatment. As a result, various kinds of miRNAs showed great potentials as prognostic biomarkers in pancreatic cancer. Optimistically, these biomarkers will form a solid foundation to have better clinical treatment strategies.To avoid toxicity and enhance the survival rate benefits.
Source: Prepared by Joan Tura from Springer BMC Biomarkers Research
Volume 6:18, 2018
Amidst the battle for supremacy, our army of immune cells relentlessly wages war against various pathogens, especially superbug bacteria. Despite the pool of ample winnings, our body still experiences defeat from time to time. We succumb to diseases as the war reels its favor towards the tenacious pathogens. Of course, we cannot allow our immune defense to be utterly defeated. Otherwise, we’d be dead. As bacteria advance by taking over much space and nutrients inside our body, we get external help through antimicrobial chemicals that scientists continue to contrive. Unfortunately, antibiotic resistance has surfaced and turned certain strains of bacteria into a superbug – one that has become resistant to the effects of antibiotics.
Chemical warfare prior to the rise of a superbug
Antimicrobial chemicals, particularly antibiotics, came into existence as chemicals that were strategically designed and produced with the intent of killing pesky bacteria. In 1928, penicillin was discovered, which led to its use as the first natural antibiotic capable of undermining a spectrum of bacteria, if not by killing, by inhibiting their growth. Its role as a wonder drug against various bacteria caused Alexander Fleming to receive a duly recognition by winning a Nobel prize award for its discovery. Soon, more antibacterial agents came up to our defense. Antibiotics, such as penicillin and cephalosporin, destroy bacterial cell wall whereas polymyxins target bacterial cell membrane. Rifamycin, quinolones, sulfonamides, and the likes interfere with the enzymes essential to bacteria. Once again, we gained an upper hand.
Bacteria resisting: the rise of a superbug
While we thought we finally came up with a powerful weapon, the bacteria conjured up an amazing strategy to work in their favour — antibiotic resistance. Some of them started to morph. They evolved and mutated into new strains referred to as superbug. They became capable of resisting the drugs’ antimicrobial effects. One of their strategies is to produce β-lactamases that destroy the structure of β-lactam antibiotics (e.g. penicillin and cephalosporin). The bacteria that evolved into superbug organisms did not just live; they thrived. They multiplied and passed on to the next generation the features that could withstand a number of antibiotics.
DNA uptake by superbug bacteria
Apart from the vertical gene transfer of genes, antibiotic resistance could also be transferred through horizontal gene transfer. It is a mechanism whereby genes are taken up or transposed from one species to another, and one of the possible explanations for the rise of superbug bacteria. DNA uptake by a bacterial cell was captured for the first time in a video by a team of scientists from Indiana University. In the video1, it shows how a bacterial cell takes up DNA fragments from dead bacterial cells through its pilus. Like a harpoon, the pilus was used by the bacterium, Vibrio cholera, to catch and reel a stray DNA fragment, and then bring it inside the bacterial cell via the same pore on its cell wall. It, then, incorporates the DNA into its own genome. Accordingly, this is probably one of the mechanisms for a bacterium to turn into a superbug.
First video evidence of DNA uptake by Vibrio cholera.
(Video credit: Ankur Dalia, Indiana University, uploaded on YouTube by Group IU Biology News)
A researcher from the team, Courtney Ellison, recounted, “The size of the hole in the outer membrane is almost the exact width of a DNA helix bent in half… If there weren’t a pilus to guide it, the chance the DNA would hit the pore at just the right angle to pass into the cell is basically zero.” It appears that the pilus takes a crucial role in horizontal gene transfer. If left to chance the DNA fragment would not easily get inside the cell since the pore was too small for it to fit. Through horizontal gene transfer, those that were once sensitive to the antibiotic could later become superbug bacteria as well. As Ankur Dalia, another researcher from the same team, pointed out, “Horizontal gene transfer is an important way that antibiotic resistance moves between bacterial species….” The video that the research team captured for the first time could explain how antibiotic resistance can be acquired from one superbug bacterial species to another.
The battle is far from over. The antibiotic resistance already raised global concerns as it has rendered certain antibiotics ineffective. Pathogenic superbug bacteria have successfully armed themselves with genes that could neutralize antibiotic effects. Fortunately, scientists do not waver in determining the strategies that superbug bacteria exploit. The recent discovery of the way by which bacteria employ to make them antibiotic-resistant superbug strains could lead to better therapeutic strikes that could counter them, hopefully, with ample success.
— written by Maria Victoria Gonzaga
1 Indiana University. (2018). IU scientists watch bacteria ‘harpoon’ DNA to speed their evolution. Retrieved from https://news.iu.edu/stories/2018/06/iub/releases/11-scientists-watch-bacteria-harpoon-dna-to-speed-their-evolution.html
When someone says “I could die of a broken heart…”, chances are, that person may be truly risking life from a broken heart – a condition referred to as broken heart syndrome. The emotional agony can be likened to a physical pain. Apparently, it was only recently that it gained stalwart attention from researchers as they began to probe the pathobiology behind a broken heart syndrome.
Broken heart syndrome – overview
Hearing stories of a person in severe emotional distraught from a loved one’s death and then died not long after is not uncommon. How much of losing a loved one, a gut-wrenching rejection, or an austere betrayal could lead to death no longer surprise us. Deep sorrow certainly takes a toll. Death is inevitable but dying from a broken heart syndrome is something that is treatable and preventable, thus, is escapable. Inopportunely, the pathobiological aspect of a broken heart syndrome has not been fully unmasked. What is known about it so far is the fact that severe emotional stress is capable of triggering the transient weakening of the heart muscle, turning the latter fatally dysfunctional.
Pathology of Broken heart syndrome
The medical term for broken heart syndrome is takotsubo cardiomyopathy. The condition was first described in Japan in 19901 and the name is derived from”takotsubo“, which when translated means an “octopus trap“. It is so because the left ventricle of the heart of a person with broken heart syndrome is shaped like a contraption pot used for catching octopuses. Its apex balloons or bulges out while its base remains as is. As a result, the heart with temporarily enlarged apical ventricle cannot function as it should. Consequently, blood is not pumped properly and this leads to angina (chest pain) and shortness of breath, which are symptoms typical of a heart attack. Because of this, broken heart syndrome can be easily mistaken as a heart attack. The difference lies in the arteries. A true heart attack is due to an occlusion in the artery. In broken heart syndrome, arteries are not obstructed. Also, the ventricle is only temporary dysfunctional and therefore may normalize again if given enough time to rest and recuperate.
Biology of a broken heart syndrome
Unraveling the mysteries of broken heart syndrome is a recent biological pursuit. Consequently, the precise mechanism is not yet clear. Experts presume a surge in adrenaline and other stress hormones since the condition is often associated with emotional stressful events (n.b. it has also been reported to happen during euphoric events, e.g. winning a lottery). The overwhelming presence of these hormones might have stunned the heart and triggered structural changes in the myocytes and/or the coronary blood vessels.2 In a study published in Psychoneuroendocrinology, researchers found that bereaved individuals have higher levels of pro-inflammatory cytokines.3
A person who went through a broken heart syndrome and survived it could attest how the struggle had been real. Having to go through an intensely stressful event could plausibly cloud one’s drive and enthusiasm for life. Research on the pathobiology behind broken heart syndrome is understandably new, and as such inadequate for now.
— written by Maria Victoria Gonzaga
1 Akashi, Y.J., Nef, H.M,, Möllmann, H., & Ueyama, T. (2010). “Stress cardiomyopathy”. Annu. Rev. Med. 61: 271–86. Doi:10.1146/annurev.med.041908.191750
2 Harvard Women’s Health Watch. (2018). Takotsubo cardiomyopathy (broken-heart syndrome). Retrieved from https://www.health.harvard.edu/heart-health/takotsubo-cardiomyopathy-broken-heart-syndrome.
3 Fagundes, C.P., Murdock, K.W., LeRoy, A., Baameur, F., Thayer, J.F., & Heijnen, C. (2018). Spousal bereavement is associated with more pronounced ex vivo cytokine production and lower heart rate variability: Mechanisms underlying cardiovascular risk? Psychoneuroendocrinology 93:65-71. doi: 10.1016/j.psyneuen.2018.04.010.
Respiratory failure is an outcome from inadequate gas exchange wherein arterial oxygen and carbon dioxide not at normal levels. A drop of oxygen is called hypoxemia while the rise in arterial carbon dioxide is hypercapnia. Respiratory failure includes abnormal blood gases, increased of breathing and increased respiratory rate. In obstetric patients a complicated conditions occurs resulting to various complications and several physiological changes. That is why risk of complication in pregnancy with respiratory failure considered challenge for positive maternal and neonatal outcomes.
Causes in Maternal Respiratory failure
The main causes of respiratory failure were postpartum hemorrhage, peripartum period, preeclampsia and pneumonia during pregnancy. In which the oxygen reserve impairment during pregnancy causes fast desaturation leading to fetal hypoxia. Many of the patients showed improvement after delivery in partial pressure of arterial oxygen. But some exhibited high incidence of neonatal respiratory distress syndrome. Neonatal complications were commonly caused by sepsis and meconium aspiration syndrome as well as impairment in neurological development.
Acute respiratory distress syndrome is classified as mild to severe injuries from aspiration, trauma and multiple transfusions. It is also a condition of newborn having dyspnea with cyanosis that is often related to surfactant deficiency. However, preterm infant retinas showed incomplete retinal vascularization. On the other hand obstetric patients showed 74% having maternal respiratory failure complications while 25.4% to non-obstetric patients.
Indeed, early delivery might improve maternal oxygenation and reduce mortality rate. However maternal respiratory failure may not always improve after the delivery wherein deleterious sepsis and lung injury persist after delivery. Additionally a detailed examination is needed to follow up the neonates in the future. Using the risk categories whether normal, questionable and abnormal, if the mental developmental index is <70 then the neonates are suspected to have mental retardation.
Source: Prepared by Joan Tura from Journal of the Formosan Medical Association
Volume 117, Issue 5, May 2018, Pages 413-420
Leptospirosis is a corkscrew shaped that is known as one of the most widespread bacterial zoonoses in the world. Symptoms range from mild flu to severe multi-organ failure and fatal pulmonary hemorrhagic syndrome. In which the key factors of these diseases are from stray animals, poor sanitation, rodents, heavy rainfall and flooding. Many regions have been increasingly exposed to leptospirosis infection due to climate change, global warming, poverty and high urban density. Rodents are the main animal reservoir in urban settings mainly involved in pathogenic transmission. Moreover, a high prevalence in rodent population occurs in major cities such as in Baltimore, Tokyo and Copenhagen. In Italy sporadic cases of leptospirosis have been often related to river flooding. This study focused on molecular survey of rodents in the city of Palermo, Italy.
Human leptospirosis cases
Two cases in 2009 of leptospirosis in Palermo during spring and fall seasons and there were 22 locations monitored. A rodent is the main reservoir for leptospirosis related to heavy rainfall and flooding in urban streets and riverbanks. During street floods individual were potentially in contact with water contaminated by infected rodent urine. So, the risk of infection is high but because of good hygienic conditions and economic wellness severe symptoms is rare. It is also possible that periodic exposures to serovars leave the immune competent population more resistant to infection. Other cases also in Northern Italy an elderly woman has a fatal infection after river flooding occurs.
Based on molecular testing leptospirosis are positive in all species of wild rodents living in almost all areas in the city. Mice and rats are the natural source for this pathogenic infection. The main common problem in Palermo, Italy is the urban street floods from heavy rains and waste accumulation. In which the city is represented by almost ten thousand stray dogs feeding on garbage. Previously, a patient was in contact with contaminated water in street flood after violent cloudburst. Waste collection also is one of the problem in Palermo that eventually facilitates the increased of rodent population.
High prevalence of leptospirosis occurs in mild wet climate, flooding of urban streets and socio-economic problems. Other Italian cities has presence of simultaneous risk factors for leptospirosis, and thus, a major concern from this underestimated zoonosis should be considered by public health authorities and clinicians particularly for elderly and immune-compromised individuals. However, severe symptomatic cases are referred to hospitals and the true prevalence of infection is probably not evaluated.
Source: Prepared by Joan Tura from Journal of Infection and Public Health
Volume 11, Issue 2, March–April 2018, Pages 209-214
Essential fatty acids, such as omega-3 and omega-6, are fatty acids that are polyunsaturated due to the multiple double bonds in their biochemical structure. As a fatty acid, they are basically a hydrocarbon chain with a carboxylic acid on one end and a methyl group on the other end. The methyl end of the chain is referred to as “omega”. Thus, omega-3 and omega-6 fatty acids got their names based on where the first double bond between two carbon molecules occurs from the methyl end of the hydrocarbon chain. This means omega-3 fatty acid is the essential fatty acid whose first double bond occurs between the third and the fourth carbon molecules whereas the omega-6 fatty acid is one in which the first double bond is between the sixth and the seventh carbon molecules.1, 2
Why essential fatty acids are essential
Essential fatty acids, particularly omega-3 and omega-6, are labeled as essential because we need them for various biological processes but our body is not equipped to produce them. We lack desaturase enzymes, which catalyze the insertion of double bonds distinctive of omega-3 and omega-6. We can only obtain these essential fatty acids by consuming food containing them. Some of the good sources are fish, seeds, bananas, nuts, and vegetable oils. In humans, α-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) are the three most notable omega-3 fatty acids whereas linoleic acid (LA) is one of the most important forms of omega-6 fatty acids.1, 2 However, how much of the essential fatty acids we need daily varies according to what our body requires. Our body needs them in an amount based on several confounding factors. Some of the factors to consider are physical activity and the time of the year.3
Biological importance of essential fatty acids omega-3 and omega-6
The essential fatty acids, omega-3 and omega-6, are important in the diet because of their various biological roles. The biochemical processes in which they take a part of are mostly associated with the regulation of the inflammatory responses of the body. For instance, they form the precursors to prostaglandins, thromboxane, leukotrienes, lipoxins, and resolvins. The essential fatty acids are also involved in cell signaling, e.g. by modulating lipid rafts in cell membranes. Furthermore, the essential fatty acids, and their metabolites, have been found to: (1) modulate the activities of angiotensin-converting and HMG-CoA reductase enzymes, (2) act as nitric oxide enhancers, (3) serve as β-blockers, (4) enhance diuresis, (5) enhance insulin action, (6) enhance insulin action, and (7) function as anti-atherosclerotic molecules.4
Essential fatty acids: the omega-6: omega-3 ratio
Too much of anything, no matter how good they are for health, can turn out bad. The essential fatty acids omega-3 and omega-6 can turn against us especially when taken in wrong proportions. They are unsaturated fats and therefore they are tagged as the healthy fats since they are “good for the heart”. Omega-3 fatty acids, most especially, have been associated with increasing high density lipoprotein (HDL, the good cholesterol) while decreasing low density lipoprotein (LDL, “the bad cholesterol”). However, a great disparity between the amount of omega-6 and omega-3 in the diet could be detrimental to health. Too much omega-6 while too little of omega-3 in the diet has been linked to increased risk to chronic inflammation and cancers such as breast, prostate, and colorectal. In contrast, more omega-3 fatty acids than omega-6 promoted anti-inflammation and decreased risk to cancer.3, 5
No consensus has been reached yet as to the proper omega-6: omega-3 fatty acid ratio. However, researchers recommend the ratio from 1:1 or 2:1 to 5:1 of omega-6 fatty acid to omega-3 fatty acid.5 More studies in this regard are needed. A healthy ratio of these essential fatty acids appears to be a key to proper biological functions and decreased risk to certain life-threatening health conditions.
— written by Maria Victoria Gonzaga
1 “Omega-3 fatty acid”. (n.d.). Biology-Online Dictionary. Retrieved from https://biology-online.org/dictionary/Omega-3_fatty_acid
2 “Omega-6 fatty acid”. (n.d.). Biology-Online Dictionary. Retrieved from https://biology-online.org/dictionary/Omega-6_fatty_acid
3 DiPasquale, D. (2011). “Everything About Fat”. Sott.net. Retrieved from https://www.sott.net/article/230686-Everything-About-Fat
4 Das, U. N. (2006). Biological significance of essential fatty acids. J Assoc Physicians India. 54:309-19. https://pdfs.semanticscholar.org/ff75/7e0dbe0a14fc2810ba52b833a5682b02b09e.pdf
5 Huerta-Yépez, S., Tirado-Rodriguez, A. B., & Hankinson, O. (2016). Role of diets rich in omega-3 and omega-6 in the development of cancer. Bol Med Hosp Infant Mex. 73(6):446-456. doi: 10.1016/j.bmhimx.2016.11.001.
Intermittent fasting recently gained popularity as an alternative way to keep one’s weight in check. Its basic tenets, though, go against what we had been previously told – to never skip a meal, especially breakfast. We have been accustomed to eating “like a king” as soon as we wake up to prepare the body for the toils and turmoils of the day. Intermittent fasting, though, says that it is alright to put that first meal off until you reach the time window for “feasting”.
Intermittent fasting – overview
Intermittent fasting promises profound health benefits. Accordingly, it can slow down aging, boosts immune defense, and help shed the extra weight.1 All the health benefits are seized if it is done properly. Intermittent fasting is a cycle between a fasting period and a non-fasting period. It may be done in two ways: whole-day fasting and time-restricted eating. Whole-day fasting is the more stringent form. It entails a 24-hour fasting done twice a week (5:2 plan) or every other day (1:1 plan). Time-restricted eating is a daily cyclic period of 16 hours of fasting and 8 hours of non-fasting. The periods are flexible. The pattern can be 12:12 (i.e. equal periods of fasting and non-fasting) or 23:1 (wherein the non-fasting period is set for only one hour). There are no restrictions as to the amount and the kinds of food to eat although consumption of healthy food within the recommended amounts during the non-fasting period is ideal.
Intermittent fasting – recent studies
Kim and others conducted a research on mice and they found that intermittent fasting helped to kick-start the metabolism and to burn fat by generating body heat in mice. Further, they found that during the fasting period there was an increase in the expression of vascular growth factor, a biochemical essential in angiogenesis and in activating the anti-inflammatory macrophages in white adipose tissue.2 Intermittent fasting may also help improve the ability of intestinal stem cells to regenerate as observed in a study in both aged and young mice by MIT biologists. Accordingly, it seems to have induced a metabolic switch in the intestinal stem cells causing the cells to preferably break down fatty acids instead of glucose.3 These are just some of the studies implicating the potential benefits of intermittent fasting, such as body fat reduction, adipose thermogenesis, metabolic homeostasis, and the preferential utilization of fat-derived ketone bodies and free fatty acids as energy sources via ketogenesis.4
Intermittent fasting – is it for all?
In spite of the purported health benefits of intermittent fasting, this weight loss modality is not recommended for all. Instead of being beneficial, it may be detrimental to the health of those who are immunocompromised and underweight. 4 Thus, consulting a physician should be the initial step. The extent of the positive effects may also differ from one individual to another. Despite the various studies highlighting the health benefits of intermittent fasting, they were done mostly on rodent models. Therefore, further studies are required to validate such promising results in humans.
Unless substantial studies to corroborate the health benefits of intermittent fasting are presented, a window of doubt remains. If in time intermittent fasting proves to be beneficial it would still lead to further queries, e.g. which fasting cycle is the ideal. Also, the effects may vary between young and older people, or between men and women especially when hormones are taken into account. Thus, similar to other weight loss modalities, it is possible that intermittent fasting may work for some people but not for all.
— written by Maria Victoria Gonzaga
1Cohut, M. (2018). Intermittent fasting may have ‘profound health benefits’. Retrieved from https://www.medicalnewstoday.com/articles/321690.php
2 Kim, K.H., Kim, Y.H., Son, J.E., Lee, J.H., Kim, S., et al. (2017). Intermittent fasting promotes adipose thermogenesis and metabolic homeostasis via VEGF-mediated alternative activation of macrophage. Cell Research, 27: 1309-1326. https://www.nature.com/articles/cr2017126′>10.1038/cr.2017.126
3 Trafton, A. (2018). Fasting boosts stem cells’ regenerative capacity. Retrieved from http://news.mit.edu/2018/fasting-boosts-stem-cells-regenerative-capacity-0503
4 Longo, V. D., & Mattson, M. P. (2014). Fasting: Molecular Mechanisms and Clinical Applications. Cell Metabolism, 19 (2), 181–192. http://doi.org/10.1016/j.cmet.2013.12.008