Weight Management

Scientists have long known that genes are the software of life, determining what a creature will look like and where the parts go."Genes tell the body where the head goes and where the tail goes, what goes on the front and what goes on the back," explains C. Ronald Kahn of the Harvard Medical School and president of the Joslin Diabetes Center in Boston.No news there. But without looking at you, Kahn can examine a sample of your genes and tell you if you're shaped like an hourglass or a pear and whether you have huge hips or a beer belly."By looking at your genes, we can tell how fat you are and how your body fat will be distributed," Kahn said yesterday."<h2>Fat genes</h2>Some experts have called obesity an epidemic. The condition has been linked to genetics, but many researchers say poor diet and lack of exercise have played a role in the increase of obesity. Some even suspect it could be contagious. But anyone who thinks logically about it can imagine that we might inherit the tendency, just like blue eyes or big noses.Figuring it all out is of great importance, because obese people are at greater risk of diabetes, cardiovascular disease, cancer and more. Specifically, those shaped like apples—with their fat concentrated in the abdomen—are at much higher risk for diabetes.Kahn's team examined the genes in fat around internal organs and under the skin of nearly 200 people thin and fat and in between, as well as in some mice.Three genes—named Tbx15, Gpc4, and HoxA5—express themselves so distinctly that the differences can be used to predict a person's body mass index (BMI) and waist-to-hip ratio."This finding suggests that the expression of these genes could be related to the pathogenesis [production and development] of obesity," said Joslin researcher Stephane Gesta.The results are published in the latest issue of the journal Proceedings of the National Academy of Sciences.<h2>Now what?</h2>The study raises huge questions: Does body shape predict obesity, or is it a result of obesity?"While we don't know yet whether this genetic activity is a cause or an effect of obesity," Gesta said, "these data do suggest that different forms of obesity could be a developmental problem that begins very early in life."And an even bigger one: Can you alter the potentially deadly fate your body shape might suggest is in store?"Now that's the big question," Kahn said.&nbsp;"While we now can predict the fat pattern, we have no magic bullet to alter the outcome. But with these new findings, we have identified potential targets for perhaps one day changing body shape. We don't have drugs to alter the pattern now, but perhaps in the future we will."Source: https://www.livescience.com/4050-genes-predict-body-shape-fatness.html

Figuring it all out is of great importance, because obese people are at greater risk of diabetes, cardiovascular disease, cancer and more. Specifically, those shaped like apples—with their fat concentrated in the abdomen—are at much higher risk for diabetes.

Genes Predict Body Shape and Fatness

Trò chuyện cùng Quang Trần về chạy Ultra Trail (chạy bộ siêu đường dài trên địa hình rừng núi nắng lạnh thất thường; gần đây nhất là quãng đường 246km ở Spartathlon tại Hy Lạp), chúng ta ít nhiều có cảm giác: ước gì mình cũng được tham gia những cuộc đua đầy thách thức như thế…<img src="https://api.genetica.asia/storage/zRtKeNkT5yKGkvPrsTDiaEJwCoxjSj78GoHH8aZl.jpeg">Dòng startus trên Facebook cá nhân của chàng trai sinh năm 1989 có đoạn viết: “Giờ này năm ngoái, tôi nhìn Sơn Trà qua cửa kính máy bay cùng với bao tâm trạng. Tạm biệt 3 năm ở Đà Nẵng thân thương để đến với Sài Gòn đầy năng động và hứa hẹn. Để rồi mở ra một năm bước ngoặt của cuộc đời, trải qua nhiều thành công lẫn tiếc nuối”.Nói vậy dễ nhận tưởng Trần Duy Quang (tức Quang Trần) là người Đà Nẵng. Nhưng không phải vậy, anh sinh ra và lớn lên ở Bình Định, có một thời gian đến Đà Nẵng làm việc và gắn bó nơi đây, nhất là với đường chạy địa hình qua Trạm ra đa, đỉnh Bàn Cờ, Cây đa ngàn năm… và tiếp nối là con đường ven biển.Trở lại với cuộc hẹn, khi tôi liên lạc thì Quang Trần đang ở Hy Lạp chuẩn bị tham dự giải Spartathlon. Spartathlon là một trong những giải chạy Ultra Trail khắc nghiệt nhất thế giới. Các VĐV dự giải sẽ phải chạy không ngừng nghỉ suốt 36 giờ, xuyên qua đất nước Hy Lạp, xuất phát từ thủ đô Athens và về đích tại chân bức tượng Leonidas, tại Sparta.Hành trình dài 246,8km được thiết kế theo dấu chân của người lính huyền thoại Pheidippides. Trong số 400 người được phép tham gia thì Quang Trần là người Việt Nam duy nhất. Hóng tin từ trang Facebook cá nhân của anh, và thấy hình ảnh anh băng về đích với lá cờ đỏ sao vàng mà lòng đầy mến phục. Spartathlon không chỉ là một cuộc đua, nó là cuộc chiến của bản thân mỗi người chạy.“Trên đường hướng về Sparta giữa cái nắng chói chang của Hy Lạp, chỉ còn vỏn vẹn 1 cái full marathon nữa (cách đích 42km) là tôi sẽ kết thúc hành trình đầy thử thách này. Trong 200km tôi chạy cùng một anh người CH Czech dáng người cao to cơ bắp, cứ chạy được 15-20m thì anh lại ngẩng mặt lên nhìn về phía trước và đi bộ vài bước. Cổ anh vươn dài như để kéo cả cơ thể rệu rã ấy tiến về phía trước, mắt hướng thẳng về quãng đường xa xăm, khuôn mặt nhăn nhó hằn đầy đau đớn. Rồi anh lại cúi mặt xuống đất và tiếp tục chạy 15-20m, lại ngẩng mặt lên đi bộ vài bước... Một động tác đơn điệu, nhàm chán được anh lặp đi lặp lại trong nỗi đau tột cùng của thể xác, nó kéo dài như thế suốt hơn 1 ngày.“Đến lúc đó tôi mới cảm nhận được hết sự kiên định, lì lợm, quyết tâm, và kỷ luật của những người chạy cự ly dài”, Quang Trần kể lại và thừa nhận đó cũng là hình ảnh của chính anh.Kỷ niệm về Spartathlon Hy Lạp với Quang Trần còn nhiều lắm, như việc anh may mắn được đội Bỉ giúp rất nhiều trong khi chạy. Đội chạy này còn tặng Quang Trần áo đấu có ký tên của các thành viên. Đặc biệt có ông Paul Beckers là một huyền thoại của Bỉ, ông về hạng 2 Spartathlon năm 1992, lúc anh chỉ mới 3 tuổi. Năm 2003, ông vô địch thế giới chạy 24 giờ liên tục với 270km. Còn với bản thân anh, không từ ngữ nào lột tả hết cảm giác chiến thắng bản thân và hiện thực hóa ước mơ ghi tên Việt Nam trên đường chạy marathon quốc tế.“Anh thấy đấy, khi vượt qua hàng trăm km ở cuộc đua, ở điểm đích tên mình được xướng lên, tên quốc gia mình được hô vang giữa bạn bè hàng trăm quốc gia, chính là những ký ức mà người chạy Ultra Trail nào cũng ghi mãi trong lòng với niềm tự hào”, Quang Trần nói với ánh mắt ánh lên niềm hãnh diện.Qua rất nhiều giải, từ trong nước đến quốc tế, nhưng câu chuyện bắt đầu chạy bộ như thế nào với Quang Trần vẫn như mới diễn ra. Quang Trần nhớ lại: Vào năm 2014, khi còn ở Biên Hòa, mình chạy chơi vài vòng công viên xả stress. Không hiểu sao càng chạy càng mê, cứ muốn tiếp tục luyện tập. Rồi lần lượt mình tham gia các giải 42km, 100km, 160km… và mới đây là giải chạy khó nhằn nhất từ trước đến giờ - Spartathlon 246,8km.Quang Trần tâm sự, chạy bộ đã giúp anh rất nhiều ở quãng thời gian từ Đà Nẵng chuyển vào TPHCM sinh sống, giúp anh kiên trì vượt qua những khó khăn ban đầu để ở lại nơi đây. Hiện nay, anh làm việc ở Genetica, một công ty chuyên phân tích gene: “Việc làm hiện nay của tôi cũng khá thú vị, đó là giới thiệu những kết quả phân tích gene cho những người đến đây tìm hiểu, khai phá sức mạnh của cơ thể, đặc biệt là những người chơi thể thao, từ đó có những lời khuyên cho những ai muốn tiếp tục khai phá sức mạnh, điểm nổi trội của bản thân”Trở lại với dòng status kỷ niệm trên Facebook của anh, đó là dịp anh thăm lại Sơn Trà (Đà Nẵng) vào một ngày mưa với khung cảnh quen thuộc. Sơn Trà đi cùng với giấc mơ Ultra Trail của anh, từ khi mới chớm nghĩ, đến lúc gắn bó tập luyện rồi hoàn thành đường đua. Nó như người bạn thân cùng trải qua bao cảm xúc mỗi ngày.Dù đi đâu, Quang Trần cũng nghĩ về Đà Nẵng, “về Đà Nẵng chỉ để được chạy Sơn Trà thôi!” như nơi đây là cội nguồn cung cấp nguồn năng lượng cho các cuộc đua Ultra Trail trên khắp thế giới. Lý do vì sao anh yêu mến Đà Nẵng như vậy, tôi không hỏi và cứ để Quang Trần cất giữ như nguồn dưỡng khí của riêng anh!&nbsp;<blockquote>"Được cơ hội đến nhiều vùng đất xa xôi trên thế giới mà trước đây mình từng ao ước đặt chân đến, và có được nhiều trải nghiệm đáng nhớ trên các cung đường chạy. Những điều đó giúp tôi luôn nhắc nhở bản thân mình phải luôn giữ đam mê, nỗ lực và kiên định. Vì điều tồi tệ nhất của nỗ lực là thành công sẽ đến muộn một chút mà thôi và cũng là nhắc nhở mình không quên những người đã giúp đỡ cho những ước mơ của mình. Có lúc là tiền, có lúc là những chiếc bánh giàu chất dinh dưỡng, những tin nhắn động viên… tất cả chất chứa niềm tin yêu của mọi người gởi gắm qua từng chuyến đi"</blockquote>Quang TrầnNguồn: https://thethao.sggp.org.vn/chay-de-duoc-nghe-xuong-ten-to-quoc-644616.html

Được cơ hội đến nhiều vùng đất xa xôi trên thế giới mà trước đây mình từng ao ước đặt chân đến, và có được nhiều trải nghiệm đáng nhớ trên các cung đường chạy.

Chạy... để được nghe xướng tên Tổ quốc!

Race walkers on a low-carbohydrate, high-fat ketogenic diet showed early signs indicative of bone loss. A low-carbohydrate, high-fat ketogenic diet could alter bone health in athletes, according to a thought-provoking new study of elite race walkers and their skeletons. The study, one of the first to track athletes during several weeks of intense training, finds that those following a ketogenic diet developed early signs indicative of bone loss.The study adds to the considerable existing evidence that how we eat can affect how exercise affects us. It also raises concerns about possible, long-term health impacts from popular diet plans, including a high-fat, ketogenic diet.<img src="https://api.genetica.asia/storage/Vdb0vvhJChQzVIltFK1Eh0bOWaf5tynBSYTzBvy7.jpeg"><h2>THE LINK BETWEEN THE KETOGENIC DIET AND OSTEOPOROSIS</h2>Anyone interested in health, wellness, weight loss, exercise, food or best seller lists is familiar, by now, with ketogenic diets. Known more familiarly as keto diets, they are extremely low-carbohydrate, high-fat regimens, with as much as 90 percent of daily calories coming from fats.Ketogenic diets, if followed scrupulously, reshape how our bodies fuel themselves. Because carbohydrates can be rapidly metabolized, our bodies typically turn to them first for energy, whether the carbohydrates come from our diets or stored sources in our muscles and livers.But if people follow a low-carbohydrate, ketogenic diet, they soon burn through their stored carbohydrates and their bodies start relying on fat for energy. The fat must be broken down first, however, and, as part of that process, the liver creates substances known as ketone bodies that can be converted into energy.Ketogenic diets are popular now — as they have been off and on in the past — among people hoping to lose weight, control blood sugar or otherwise regulate their health. Some athletes also follow the diet, hoping that it will improve performance, since fat, as fuel, is ample, slow-burning and long-lasting.Some studies have suggested, though, that low-carbohydrate, high-fat diets might change bone metabolism. Children with epilepsy who use the keto diet to control their condition tend to have low bone density, for instance. And in athletes, going for a day or two without carbohydrates can change some blood markers related to bone health.But no experiments had tracked bone metabolism in competitive athletes on ketogenic diets for longer periods of time. So, for the new study, which was published in January in Frontiers in Endocrinology, researchers in Australia decided to ask a group of world-class race walkers if they could fiddle with their food for a few weeks.Thirty of the athletes, all of whom were about to embark on intense training for upcoming world championships and other competitions, agreed. The athletes then sorted themselves into two groups, based on whether they were willing to try a keto diet or not.About half said that they were and subsequently began a strict low-carbohydrate, high-fat routine. The other men and women continued with a high-carbohydrate diet. Everyone’s meals were matched in terms of how many calories, relative to body weight, they ate.Before the diets kicked off, though, the researchers drew blood from the athletes before and after a workout, to establish their baseline bone health and other markers of their health and fitness. (The experiment was designed to look at many elements of the ketogenic diet in sports.)Bone is an active tissue, constantly breaking down slightly and remodeling itself in response to the demands we place on it. Knowing this, the researchers checked for the levels of specific substances in the athletes’ blood known to be associated with bone breakdown, rebuilding and overall metabolism.Then the athletes embarked on three and a half weeks of intense training, while eating mostly fat or mostly carbs. Afterward, the researchers again drew their blood and rechecked the markers of bone health.They found differences. The markers of bone breakdown were higher now among the athletes on the keto diet than at the start of the study, while those indicating bone formation and overall metabolism were lower. These same markers were generally unchanged in the high-carb athletes. The athletes on the ketogenic diet, in other words, showed signs of impaired bone health.How their bones might have been affected by their eating is still unclear, says Louise Burke, the head of sports nutrition at the Australian Institute of Sport in Canberra and one of the lead authors of the new study.“We believe that the keto diet may affect bone metabolism due to the downstream effects of low-carbohydrate availability on certain hormones, along with other factors,” she says. But more study, of course, is needed.The researchers also did not look directly at changes, if any, in the athletes’ bone density or follow them beyond three and a half weeks. Whether any worrisome effects on bone health would linger, intensify or disappear after a longer period of high-fat eating remains unknown, as does the question of whether those of us who are not world-class race walkers would be similarly affected, if we work out while eschewing carbs.But the study does remind us that the interplay of nutrition and exercise is intricate and we do not yet fully understand its implications for our health.Dr. Burke and her colleagues plan to study the longer-term effects of ketogenic diets and exercise in future studies.By Gretchen Reynolds Resource: https://www.nytimes.com/2020/02/05/well/move/could-a-keto-diet-be-bad-for-athletes-bones.html&nbsp;

But if people follow a low-carbohydrate, ketogenic diet, they soon burn through their stored carbohydrates and their bodies start relying on fat for energy. The fat must be broken down first, however, and, as part of that process, the liver creates substances known as ketone bodies that can be converted into energy.

Could a Keto Diet Be Bad For Athletes' bones?

A father’s genetic code influences the weight of a baby at birth, according to a new study led by the UCL Institute of Child Health (ICH).The findings suggest that genes inherited from the mother and father regulate a baby’s growth at different times during the pregnancy, to ensure a successful birth as well as the mother’s survival.Fetal growth is an important area of research which takes into account the future health of babies. Normal fetal growth depends on the successful nutrient exchange between the mother and the fetus via the placenta. When this critical balance is impaired, it can result in a small for gestational age (SGA) baby. Low birth weight is a well-known risk factor for Type 2 diabetes and cardiovascular problems in later life.One group of growth genes of particular interest are the imprinted genes inherited from one’s parents - if the paternal one is expressed, the maternal one is imprinted (silenced) and vice versa. The “parental conflict hypothesis” suggests that expression of the father’s genes enhances a baby’s growth, improving the success of the paternal genome to be passed on. In contrast, the mother’s genome limits fetal growth, distributing equal resources to each of her offspring, whilst ensuring her own survival post-birth allowing her to reproduce again.The study, published in the journal PLOS ONE, looked at the relationship between birth weight and the paternally expressed Insulin-like growth factor 2 (IGF2) early in gestation, where IGF2 is a key hormone regulating growth in the womb. Researchers studied this gene in chorionic villus samples taken from women in the first term of their pregnancy, looking for correlations between the gene’s expression and the baby’s subsequent birth weight.Expression of the paternal IGF2 gene was linked to an increase in birth weight, with one relative expression unit being equivalent to a rise in birth weight of 63 g (around two per cent, given an average birth weight of 3 kg). IGF2 expression was found to be lower in SGA neonates.Professor Gudrun Moore, lead author at the UCL Institute of Child Health, says: “Most of us will think of both the mother’s and father’s genes as having an equal influence on birth weight, but this does not appear to be the case. Our study suggests that the two parental genomes may be acting at different times during the pregnancy in order to control the baby’s size. Whilst greater fetal growth appears to be promoted by the father’s genes early on, it must still require careful regulation by the mother to ensure a successful birth.&nbsp;“Understanding the genetic basis of fetal growth is of critical importance in the prevention and monitoring of small and low weight babies. Checking the expression of the paternal IGF2 gene in the first trimester, potentially in the mother’s blood, could help to act as a predictor of how the baby will grow later in the pregnancy. An early growth biomarker could be invaluable in helping to monitor ‘at risk’ pregnancies”.&nbsp;Full report: https://www.gosh.nhs.uk/news/latest-press-releases/2014-press-release-archive/father-s-gene-linked-baby-s-birth-weight

One group of growth genes of particular interest are the imprinted genes inherited from one’s parents - if the paternal one is expressed, the maternal one is imprinted (silenced) and vice versa

Father’s gene linked to baby’s birth weight

Short sleep duration increases expression of genetic risks for high body mass index.Toss out another old wives' tale: Sleeping too much does not make you fat. Quite the opposite, according to a new study examining sleep and body mass index (BMI) in twins, which found that sleeping more than nine hours a night may actually suppress genetic influences on body weight.The study looked at 1,088 pairs of twins and found that sleeping less than seven hours a night was associated with both increased BMI and greater genetic influences on BMI. Previous research has shown that genetic influences include things like glucose metabolism, energy use, fatty acid storage and satiety. In this study, the heritability of BMI was twice as high for the short sleepers than for twins who slept longer than nine hours a night."The results suggest that shorter sleep provides a more permissive environment for the expression of obesity related genes," said principal investigator Nathaniel Watson, MD, MSc, of the University of Washington. "Or it may be that extended sleep is protective by suppressing expression of obesity genes."Watson and colleagues determined that for twins sleeping less than seven hours, genetic influences accounted for 70 percent of the differences in BMI, with common environment accounting for just 4 percent and unique environment 26 percent. For twins averaging more than nine hours of sleep, genetic factors were attributed to 32 percent of weight variations, with common environment accounting for 51 percent and unique environment 17 percent.More research is needed, Watson said, but these preliminary results may suggest that behavioral weight loss measures would be most effective when genetic drivers of body weight are mitigated through sleep extension.Reference: https://www.sleepfoundation.org/articles/longer-sleep-times-may-counteract-genetic-factors-related-weight-gain

Toss out another old wives' tale: Sleeping too much does not make you fat. Quite the opposite, according to a new study examining sleep and body mass index (BMI) in twins, which found that sleeping more than nine hours a night may actually suppress genetic influences on body weight.

Longer Sleep Times May Counteract Genetic Factors Related to Weight Gain

Genes influence every aspect of human physiology, development, and adaptation. Obesity is no exception. Yet relatively little is known regarding the specific genes that contribute to obesity and the scale of so-called “genetic environment interactions” the complex interplay between our genetic makeup and our life experiences.A 2014 study found that consumption of fried food could interact with genes related to obesity, underscoring the importance of reducing fried food consumption in individuals genetically predisposed to obesity. The search for human obesity genes began several decades ago.Emerging research has also begun to identify the genetic underpinnings of so-called “common” obesity, which is influenced by dozens, if not hundreds, of genes. In addition, research into the relationship between certain foods and obesity is shedding more light on the interaction between diet, genes, and obesity.<h2>Rare Forms of Obesity Caused by Mutations in a Single Gene (Monogenic Obesity)</h2>Several rare forms of obesity result from spontaneous mutations in single genes, so-called monogenic mutations. Such mutations have been discovered in genes that play essential roles in appetite control, food intake, and energy homeostasis-primarily, in genes that code for the hormone leptin, the leptin receptor, pro-opiomelanocortin, and the melanocortin-4 receptor, among others.Obesity is also a hallmark of several genetic syndromes caused by mutation or chromosomal abnormalities, such as Prader–Willi and Bardet-Biedl syndromes. In these syndromes, obesity is often accompanied by mental retardation, reproductive anomalies, or other problems<h2>“Common Obesity” Caused by Mutations in Multiple Genes</h2>In the 21st century, obesity is a health problem affecting rich and poor, educated and uneducated. Body fat level varies from person to person, however, and some people have always tended to carry a bit more body fat than others. Some studies of large populations suggest that this variation in our susceptibility to obesity has a genetic component. But rather than being controlled by a single gene, susceptibility to common obesity is thought to be affected by many genes (polygenic).In 2007, researchers using genome-wide association studies identified the first obesity-related gene variants in the so-called “fat mass and obesity-associated” (FTO) gene on chromosome 16. These gene variants are fairly common, and people who carry one have a 20 to 30 percent higher risk of obesity than people who do not.&nbsp;Most people probably have some genetic predisposition to obesity, depending on their family history and ethnicity. Moving from genetic predisposition to obesity itself generally requires some change in diet, lifestyle, or other environmental factors.&nbsp;<h2>The Bottom Line: Healthy Environments and Lifestyles Can Counteract Gene-Related Risks</h2>Having a better understanding of the genetic contributions to obesity-especially common obesity-and gene-environment interactions will generate a better understanding of the causal pathways that lead to obesity. Such information could someday yield promising strategies for obesity prevention and treatment. But it’s important to remember that overall, the contribution of genes to obesity risk is small, while the contribution of our toxic food and activity environment is huge. As one scientist wrote, “Genes may co-determine who becomes obese, but our environment determines how many become obese.” That’s why obesity prevention efforts must focus on changing our environment to make healthy choices easier choices, for all.Reference: https://www.hsph.harvard.edu/obesity-prevention-source/obesity-causes/genes-and-obesity/

﻿Emerging research has also begun to identify the genetic underpinnings of so-called “common” obesity, which is influenced by dozens, if not hundreds, of genes.

Obesity-Promoting Genes in an Obesity-Promoting World

The World Health Organization (WHO) defines malnutrition as “deficiencies, excesses, or imbalances in a person’s intake of energy and/or nutrients”. The malnourished children are also more likely to have delays in neurocognitive development, vaccine failure, and susceptibility to infection. Despite malnutrition being a major global health problem, we do not yet understand the pathogenesis of this complex disorder. Although lack of food is a major contributor to childhood malnutrition, it is not the sole cause. The mother’s prenatal nutritional status, enteric infections, and intestinal inflammation also contribute to the risk of childhood malnutrition and recovery. Besides, there is another potential risk factor, host and maternal genetics, that may play a role in the risk of malnutrition via several biological pathways. Understanding the genetic risks of malnutrition may help to identify ideal targets for intervention and treatment of malnutrition.The gut microbiota sustains trillions of microbes and viruses that can be altered by diet and can then affect the metabolic output for an individual. In twin studies of children through three years of age from rural villages in Malawi, twin pairs with acute, moderate, or severe malnutrition had less mature gut microbiomes. In the discordant twin pairs, the twin with malnutrition had a microbiome similar to those of children with malnutrition, despite receiving the same well- controlled diet. This well-designed twin study confirmed that poor diet is not the only risk factor of malnutrition and that the interaction of these pathogens with the gut of the developing child, possibly controlled by genetic variation, may create a biological environment that inhibits the child’s growth.Macronutrient (protein, carbohydrate, and fat) intake is a relatively stable measurement that relates directly to dietary intake. However, there is large interindividual variation, and the heritability ranges from 11% to 65%. The researchers identified a significant single-nucleotide polymorphism (SNP) near the FGF21 locus associated with decreased protein intake, increased carbohydrate intake, and decreased fat intake after adjusting for body mass index (BMI). They also identified a variant in the FTO gene associated with total percentage of carbohydrate intake and a variant near the TANK gene associated with decreased fat intake, increased carbohydrate intake, and marginally decreased protein intake. The identification of these putative nutrition-associated genes in even well-nourished research populations underscores the complexity of nutrition and draws attention to the idea that genetics may influence macronutrient intake and thus directly affect malnutrition.Genetic studies of micronutrients in serum or blood, including trace elements like zinc, have also identified genes that control or regulate these nutrients. These genes may be ideal targets for the design of therapeutics that could enhance micronutrient uptake and reduce malnutrition. Zinc absorption in the gut requires transporters for uptake and then release into the circulation, and zinc deficiency leads to oxidative stress and decreased intracellular signaling.Additionally, studies of vitamin A or serum retinol have identified SNPs in two genes, RBP4 and TTR, that are involved in retinol transport. Vitamin A, like zinc, has many roles and has been associated with multiple disease outcomes beyond malnutrition. If we can identify gene targets or pathways for supplementation, we may be able to ameliorate some of the underlying malnutrition outside of just diet and non therapeutic interventions.A principal risk factor for malnutrition is diarrheal disease. Most children present with diarrhea—enteric inflammation that may be caused by viruses, bacteria, or parasites—at least once in the first few years of life. Advances in water and sanitation have prevented many acute diarrheal episodes in the developed world. A meta-analysis of genome-wide association studies of diarrheal disease in young children identified the FUT2 locus, which is involved in histo-blood group antigen production, as associated with diarrheal disease.Specifically, it identified the putative causal allele W154X (at rs601338), which may explain disease or disease severity in healthy children of European ancestry. Identifying genes that are associated with diarrhea may suggest biological mechanisms for susceptibility that induce the downstream effect of diarrhea, malnutrition.&nbsp;A potential unifying mechanism of malnutrition is EED, a chronic inflammatory condition of the gut with malabsorption accompanied by systemic inflammation. It is thought to be caused by repeated or chronic enteric infections in infants living in unsanitary conditions. Genome-wide association studies of gut inflammation, specifically inflammatory bowel disease and celiac disease, may also provide insight into the genetics of malnutrition through systemic and enteric inflammation. Celiac disease is a T cell–mediated autoimmune disease that results in enteropathy of the gut and leads to villous flattening in affected individuals. Celiac disease pathology is triggered by gluten, which is present in wheat, barley, and rye, and the phenotype is heterogeneous in both presentation and progression. Removal of dietary gluten reverses this pathology. Celiac disease has a strong genetic component, with a sibling recurrence risk of 20–60 and 45 genetic loci identified; 6 polymorphisms have been identified within the major histocompatibility complex. Interestingly, celiac disease and EED share a similar histology, with atrophy of the villi and lymphocytic infiltration. The clinical and pathological overlap of these two diseases may indicate a shared genetic component that is triggered by environmental assaults from either food or pathogens.It is key to recognize that we observe an outcome of malnutrition as classified by stunting, wasting, or micronutrient deficiencies, but there are multiple pathways to reach this outcome. Thus, we must approach the complexity of malnutrition with multiple prongs, and genetic and genomic studies may assist in breaking down the risk alleles for diarrhea, enteric infections, inflammation, malabsorption, nutrient deficiency, and more.Full report here: https://www.annualreviews.org/doi/pdf/10.1146/annurev-genom-083117-021340

Although lack of food is a major contributor to childhood malnutrition, it is not the sole cause.

Suy dinh dưỡng ở trẻ em có di truyền không?

Does Malnutrition Have A Genetic Component?

The gene variant became more common in humans after cooking and farming became widespread, and might now help people avoid diabetes, according to the findings published in eLife."We found that people differ in how efficiently their bodies can manage blood sugar levels, resulting from an evolutionary process that seems to have been brought about by changing diets," said the study's lead author, Professor Frances Brodsky, Director of UCL Biosciences.The researchers were investigating the CLTCL1 gene, which directs production of the CHC22 protein that plays a key role in regulating a glucose transporter in our fat and muscle cells.After people eat, the hormone insulin reacts to higher levels of blood glucose by releasing the transporter to remove glucose from the blood, taking it into muscle and fat tissue. Between meals, with the help of the CHC22 protein, the glucose transporter remains inside muscle and fat so that some blood sugar will continue to circulate.The research team, consisting of specialists in population genetics, evolutionary biology, ancient DNA and cell biology, analyzed human genomes as well as those of 61 other species, to understand how the gene producing CHC22 has varied throughout evolutionary history.In humans, by looking at the genomes of 2,504 people from the global 1000 Genomes Project, they found that almost half of the people in many ethnic groups have a variant of CHC22 that is produced by a mutated gene, which became more common as people developed cooking and farming.The researchers also looked at genomes of ancient humans, and found that the newer variant is more common in ancient and modern farming populations than in hunter-gatherers, suggesting that increased consumption of carbohydrates could have been the selective force driving the genetic adaptation.By studying cells, the researchers found that the newer CHC22 variant is less effective at keeping the glucose transporter inside muscle and fat between meals, meaning the transporter can more readily clear glucose out of the blood. People with the newer variant will therefore have lower blood sugar."The older version of this genetic variant likely would have been helpful to our ancestors as it would have helped maintain higher levels of blood sugar during periods of fasting, in times when we didn't have such easy access to carbohydrates, and this would have helped us evolve our large brains," said first author Dr Matteo Fumagalli, who began the study at UCL before moving to Imperial College London."In more recent years, with our high-carb diets that often provide us too much sugar, the newer variant may be advantageous," Dr Fumagalli added.The researchers say that while this genetic variant does not play a direct role in the development of diabetes, having the older variant may make people more likely to develop diabetes, and it may also exacerbate insulin resistance involved in diabetes."People with the older variant may need to be more careful of their carb intake, but more research is needed to understand how the genetic variant we found can impact our physiology," added Professor Brodsky.Reference: https://www.sciencedaily.com/releases/2019/06/190604084857.htm

The researchers were investigating the CLTCL1 gene, which directs production of the CHC22 protein that plays a key role in regulating a glucose transporter in our fat and muscle cells.

Gene mutation evolved to cope with modern high-sugar diets

What should we eat? Answers abound in the media, all of which rely on their interpretation of recent medical literature to come up with recommendations for the healthiest diet. But what if you could answer this question at a molecular level -- what if you could find out how our genes respond to the foods we eat, and what this does to the cellular processes that make us healthy -- or not?<h2>How our genes respond to the foods we eat</h2>How does food affect gene expression? NTNU researchers Ingerid Arbo and Hans-Richard Brattbakk have fed slightly overweight people different diets, and studied the effect of this on gene expression.&nbsp;This study has found that a diet with 65% carbohydrates, causes a number of classes of genes to work overtime. This affects not only the genes that cause inflammation in the body, but also genes associated with development of cardiovascular disease, some cancers, dementia, and type 2 diabetes -- all the major lifestyle-related diseases.&nbsp;Moreover, "both low-carb and high-carb diets are wrong," says Berit Johansen, a professor of biology at NTNU. "But a low-carb diet is closer to the right diet. A healthy diet shouldn't be made up of more than one-third carbohydrates (up to 40 percent of calories) in each meal, otherwise we stimulate our genes to initiate the activity that creates inflammation in the body." This is not the kind of inflammation that you would experience as pain or an illness, but instead it is as if you are battling a chronic light flu-like condition. Your skin is slightly redder, your body stores more water, you feel warmer, and you're not on top mentally. Scientists call this metabolic inflammation.In addition, some clusters of genes that stood out as overactive are linked to the most common lifestyle diseases. Genes that are involved in type 2 diabetes, cardiovascular disease, Alzheimer's disease and some forms of cancer respond to diet, and are up-regulated, or activated, by a carbohydrate-rich diet. It can be said that diet is the key to controlling our personal genetic susceptibility to disease.&nbsp;In choosing what we eat, we choose whether we will provide our genes the weapons that cause disease. The immune system operates as if it is the body's surveillance authority and police. When we consume too many carbohydrates and the body is triggered to react, the immune system mobilizes its strength, as if the body were being invaded by bacteria or viruses. Furthermore, the fat/protein trap is just as bad as the carbohydrate trap. Eating several small and medium-sized meals throughout the day is important. Don't skip breakfast and don't skip dinner. One-third of every meal should be carbohydrates, one-third protein and one-third fat. That's the recipe for keeping inflammatory and other disease-enhancing genes in check.Reference: https://www.sciencedaily.com/releases/2011/09/110919073845.htm &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;

How does food affect gene expression? NTNU researchers Ingerid Arbo and Hans-Richard Brattbakk have fed slightly overweight people different diets, and studied the effect of this on gene expression.

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