The shopping list is ready and you are at the supermarket to pick and choose the essentials for the month. Though you might be doing it on a weekend there isn’t much leisure time to shop at your desired pace. In such situations, it would be extremely helpful if the nutrition labels present in the pack is color-coded for quicker understanding, isn’t it? Nutrition labels on food products help us choose between various products and restrict our consumption of foods that’s high in fats, sugars and salt. The information provided is for 100 grams or per portion of the food and nowadays, due to increased interest in choosing healthier food options food manufacturers are highlighting fat, salt, sugar and energy content on the front of the packaging along with reference intake values. Some of these nutrition labels use colour codes such as red, amber and green and this helps us decode the fat, salt and sugar content of the food in a glance.
This color-coded labelling is also called as ‘traffic light’ labelling that has been proposed as a public health intervention to minimize obesity risk by attending to the dietary intake of individuals. These occur as a part of the front-of-pack (FOP) nutrition rating systems that clearly detail the calories and nutrients present within the food pack. We already have studies that have given a green signal to traffic light food labelling as an excellent initiative to fight against obesity and a modelling study in Australia found it to be a cost-effective method for preventing obesity. Studies of summary indicator FOP systems show that this system is in fact efficient enough to promote healthier product reformulations by manufacturers-this was seen in Canadian manufacturers where they successfully reduced sodium in foods by 80-150 grams. There are different studies that show that sodium, fat and sugar consumption could be reduced if individuals replaced their regular foods with those that follow the FOP system criteria.
Canadian Study on Replacing ‘Red’ Label Foods with Healthier Options: A Nutrition Analysis
Fat, energy, sodium and sugar intake of Canadian adults were calculated using data from the Canadian Community Health Survey, Cycle 2.2 Nutrition (CCHS 2.2)- a national survey that’s aimed at providing authentic data regarding food and nutrients intake of Canadians. The CCHS 2.2 included a sample of 35,107 individuals aged 0 years and above whose food and nutrients intake was calculated through a 24-hour dietary recall. The present research primary included Canadian adults aged 19 years and above, excluded pregnant and breastfeeding women and also those whose food intake data was not available. The different foods consumed by individuals were color-coded in red, amber or green depending on the criteria for food and drinks described in the UK’s ‘Guide to Creating a Front of Pack (FoP) Nutrition Label for Pre-packaged Products Sold Through Retail Outlets’. This was used as the measure to compare against the fat, sodium and sugar intake of foods and drinks.
Those foods that had red color codes were replaced with similar foods that did not have the code for any of the nutrients. Whenever possible, the original food was replaced by the same food from a different brand that provided a healthier option and every effort was taken to ensure that the replaced food was as good as the original choice. For instance, lean ground beef was replaced with extra lean ground beef. There were also instances where some foods were replaced by the same foods but prepared in a much more nutritious manner. But when replacement was not possible the foods were not replaced.
Totally, Canadian adults consumed 5655 unique foods and 495 unique beverages and it was found that 52% foods and 13% beverages contained at least one nutrient that qualified for a red traffic light. On analysis, it was seen that sodium was the nutrient associated with most (27%) red traffic lights while sugar was the nutrient that was least (14%) associated. For beverages, sugars was the nutrient that was mostly (10%) linked to red traffic lights while sodium and fats were least associated (2%). Though replacements for all foods were not possible, the percentage of foods and beverages that qualified for at least one red traffic light dropped to 40% and 2% respectively.
The traffic light food labelling helped Canadian adults reduce their overall intake of energy, total fat, saturated fat and sodium compared to baseline-calorie intake reduced by 5%, total fat by 13%, saturated fat by 14% and sodium by 6% among Canadians. Men reaped maximum benefits as they consumed 122 fewer calories, 12 g less total fat, 4 g less saturated fat and 199 mg less sodium under this food labelling model. The only nutrient that did not show considerable change was sugar. It was amazing to find that total intake of calories and fat were reduced to below recommended Daily Values and this included women’s total intake of saturated fats as well. This study shows that the traffic light labelling system has a positive impact on the individuals’ total nutrient and calorie intake decreasing the consumption of fats, sugars and sodium.
Sustenance of Dietary Changes Possible with Traffic Light Diet
The Massachusetts General Hospital (MGH) studied the nutrient intake of their employees implementing the traffic light diet in their hospital cafeteria with simple ‘traffic-light’ symbols-the program was devised such that green labels indicated healthiest foods, yellow labels indicated less healthy foods and red labels the least healthy ones based on positive and negative criteria. Details whether the main ingredient was fruit, vegetable, whole grain and likewise with the amount of saturated fat was also mentioned. The food habits of 5,695 employees were tracked via the purchases made once after the labels were added and once again after product-placement changes made healthier choices accessible. This analysis remained in place for 2 years.
Results showed that the purchases of red-labelled foods decreased while the proportion of green-labelled foods purchased increased. Such kind of labelling paved way for greater calorie reduction over the two-year period with the red-labelled foods contributing to major calorie reduction. On the whole, besides reducing total calorie intake the employees were also eating nutritious foods that contribute towards their total calorie intake. Some employees even lost up to 2 kg over time. This is not a weight loss program but one that aims at achieving a steady weight maintenance by individuals instead of allowing them to gain weight. This might be a good start for reversing the obesity epidemic. Organizations conduct wellness programs that help improve well-being of employees but such programs happen only for a short period. But this kind of an intervention is a continuing affair where people are exposed to it daily at work and in the long run it becomes a lifestyle practice. The traffic light labels could be implemented in all workplaces as employees love to eat well but don’t have enough time to read and decide. In such scenarios, the labelling helps them realize when they are about to make an unhealthy food choice and motivate them to choose a better option.
Green, Amber & Red: What Do Each of the Colours Stand For?
The colour codes depict whether a product is high (red), medium (amber) or low (green) in saturated fats, fat, salt and sugar and the total energy provided by it. Going by the color codes helps you choose the right food. For instance, if you would like to go for a veg roll read the color codes to decipher the nutrient content:
Green: If the label is mostly green this is a clear indication that the food is low in that nutrient (fat, sodium or sugar) and you are about to make a great choice.
Amber: This is an indication that the product is neither low nor high in that nutrient and it is always ok to eat foods that have amber on the labels any time.
Red: This is not a declaration to avoid such foods totally but a warning sign that they are high in fats, sugar and sodium. It is always recommended to decrease consumption of red-labelled foods and if you wish to have them, eat them as rarely as possible in minimal quantities.
Traffic-light Labels Could Reduce Population Intakes of Calories, Total Fats, Saturated Fats and Sodium: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5300258/pdf/pone.0171188.pdf
Traffic Light Food Labels Reduce Calories Purchased in Hospital Cafeteria: https://www.sciencedaily.com/releases/2019/07/190710134014.htm
Helping You Eat Well: https://www.nutrition.org.uk/healthyliving/helpingyoueatwell/324-labels.html?start=3
An unmarried man is an eligible bachelor even during his late 30s or 40s while women don’t find themselves a suitable groom as easy as men once they cross early 30s as the society fears that a woman’s reproduction capability and the strength to bear a child decreases as she grows old. We even fear that the child might be born with disorders and complications. The health of the lady remained the sole priority even before conception to ensure a healthy baby but as our knowledge base is expanding, we seem to accept the fact that men play a vital role too. Their health before conception has a greater say in the healthy outcome of the offspring.
The dad’s age too is being considered as a risk factor for the offspring’s health. Advanced paternal age (APA) at conception has been linked to numerous negative outcomes such as low academic achievement, hyperactivity and suicide. Maternal and paternal age is linked to neurodevelopmental disorders and more prominently enhancing the risk of autism spectrum disorder (ASD). Men who father a child at an older age increase the risk of congenital disorders such as Apert syndrome, craniosynostosis, situs inversus, syndactyly, cleft lip or cleft palate and hydrocephalus. The major reason quoted behind the occurrence of diseases such as ASD and schizophrenia is the prevalence of the increased risk of mutations that occur in the germline of the dads. Hence, getting to understand the relationship between paternal age and ASD can help in shedding light on the biological pathways resulting in ASD.
Advanced Paternal Age Increases ASD Risk in Offspring
Associating paternal age with ASD risk started as early as during the 1970s and the study elaborated here is a population-based cohort study to test this theory. It includes a total of 3,78,891 individuals born during 6 consecutive years of whom only 3,18,506 of them had data on paternal age at birth. Information on maternal age at birth was obtained for 1,32,271 people using paternal age data.
Paternal age was categorized into four groups: 15-29 years, 30-39 years, 40-49 years and above 50 years. Results for age was presented in terms of a 10-year increase in paternal age. Maternal age too was divided into 3 groups corresponding to paternal age categories: 15-29 years, 30-39 years and above 40 years. Results showed that the risk of ASD was around 8.4 cases per 10000 persons. It was observed that the risk of ASD increased with increase in paternal age. There were no signs of ASD risk in offspring of the youngest fathers as fathers younger than 20 years had no offspring with ASD. The risk of ASD almost doubled in men who were 10 years older.
Researchers propose that this increase in risk of ASD with increasing age could be due to mutagenesis which was initially called as the ‘copy error’ hypothesis by Penrose according to which new mutations could arise, propagate and accumulate in successive generations of sperm-producing cells. These might be chromosomal abnormalities that could possibly link paternal age with autism. Another reason could be imprinting-a form of gene regulation where the gene expression depends on whether the allele was inherited from the male or female parent in the previous generation. Imprinted genes that are paternally expressed silence maternal gene expression. Only one parental allele is expressed while the other remains silent due to DNA methylation. While the methylation pattern is maintained in somatic cells it is erased and re-established late in spermatogenesis for paternally imprinted genes, a process that could become impaired as age advances-this stands to be considered in the case of autism.
Effect of Paternal Age in Neurodevelopmental Disorders
We repeatedly research and talk about the link between APA and ASD as autism is more common these days that earlier but it was schizophrenia that was the first neuropsychiatric disorder that was linked to APA. Various studies showed that the risk of the disorder increased with paternal age increase though the risk degree differed between the studies. Risk for the disorder was already high for offspring of fathers in their mid-to-late 30s increasing as the paternal age increased. Those in their 40s during conception were at a 2-3 times increased risk of becoming a dad to a schizophrenic child compared to those in their 20s during conception. The link between APA and autism was reported first by Reichenberg et al. The risk with increase in age was on similar lines as for schizophrenia-greater risk in those aged mid-30s and above during conception.
Those studies focusing on the transgenerational persistence of APA-autism link showed conflicting results that the age of the maternal grandmother and maternal grandfather was linked to a higher risk of autism. Sullivan et al. reported that family history of schizophrenia and bipolar disorder was a risk factor for autism. Likewise, the presence of autism during early stages of life increases the risk of schizophrenia development during later stages. The reasons behind this link is usually attributed to genetic factors or genetic mutations in paternal gamates that arise as a consequence of ageing. The behaviour of men delaying fatherhood generally includes social withdrawal and social aloofness that’s greatly related to a higher genetic risk for autism or schizophrenia. Kids born to men with genetic variation are at an increased risk of such disorders irrespective of the father’s conception age. Though a study by Nilsen et al. showed that men who fathered their first child at an advanced age were surrounded by health problems and risky health behaviours other studies did not find any link between behavioural traits and paternal age.
We have numerous debates surrounding the inherited vs de novo effects of APA. Comparison effects of delayed fatherhood and advancing paternal age many studies support that it’s delayed fatherhood that’s increasingly linked to risk of schizophrenia. But a study by Hultman et al. showed that the child with the disorder is generally born later in the father’s life showing that age-dependent factors and not men’s stable traits affect its prevalence. All of the published animal studies show that advanced paternal age at conception is related to behavioural changes relevant to autism and schizophrenia.
An infant is born unto this world with around 60-80 genetic mutations but these are enhanced to a greater degree in individuals with autism and schizophrenia. Genetic mutations that multiply as the paternal age increases affect the APA effect to a greater extent. Research shows that mutation rates double every 16.5 years expressing the risks associated with delayed fatherhood from the age of 25 to 40. Age-related increase in genetic mutations is larger in male than in female by almost 3-fold times and most of the genetic mutations in offspring are primarily from the father.
Selfish Spermatogonial Selection
According to this hypothesis, stem cells with mutations at certain loci gain selective advantage over non-mutated spermatogonial stem cells expanding clonally and becoming prominent in the germline. Activating mutations involved in receptor tyrosine kinase pathway enhance growth processes leading to abnormal proliferation of spermatogonial stem cells that carry these mutations via a process called oncogenesis. The disease phenotypes linked to the mutations make it unlikely for the mutations to be passed over multiple generations making it mostly unsuccessful for extrapolating the hypothesis for complex disorders like autism and schizophrenia. A study by Goriely et al. showed that the genes that were responsible for the selfish behaviour of spermatogonial stem cells belong to the RTK/RAS/MAPK pathway-one of the molecular modules that’s rich in deleterious variants in neurodevelopmental disorders. It is a common opinion among researchers that analysing the selfish selection hypothesis plays an integral role in triggering genetic mutation origins of APA effects.
APA and neuropsychiatric disorders also change based on epigenetic effects -the epigenetic markers regulate gene expression in offspring showing that paternally acquired factors affecting the offspring go beyond those proposed by the genome sequence alone.
DNA Methylation: This is the commonly studied epigenetic modification playing integral role in gene regulation. DNA methylation marks are stable, modification acquired are maintained in daughter cells accumulating over paternal lifespan in a similar fashion as de novo genetic mutation. It is to be noted that epigenetic programming occurs twice during fertilization-once before birth in embryonic primordial germ cells and then followed by establishment of new methylation patterns that’s different in male and female embryos. The programming once again occurs at fertilization. Ageing brings about changes in epigenetics and DNA methylation levels help in predicting chronological age of humans. It was Malaspina in 2001 who first proposed that age-related epigenetic modifications mediated APA effects. But, age-related disruption of normal DNA methylation in gametes cannot account for the father-to-offspring transmission of the APA effect. Even before the blastocyst stage paternal methylation marks are erased with only those in the imprinted regions remaining in the embryo’s somatic cells. So, the time frame within which paternally acquired non-imprinted DNA methylation marks could affect offspring development is scarce.
Genomic Imprinting: Imprinting is a complex phenomenon where differential DNA methylation in paternal gametes is linked to monoallelic gene expression in offspring. These imprints are seen in parental germline, inherited after fertilization, erased in fetal germline and later re-established in the offspring. The imprinting regions regulate gene expression which are found in both sexes and autosomal chromosomes characterized by age- and tissue-specific expression patterns. They also play a vital role in early development regulating placental formation and functioning and also early brain development.
The parental imprints in the germline could be present in the somatic offspring cells conveying the message that imprinted genes could be involved in mediating APA effects. Various studies have shown a number of neurodevelopmental disorders (such as Prader-Willi syndrome or Angelman syndrome) that have resulted as an outcome of errors in imprinting. But we have no research in humans that supports the theory that imprinting errors affect APA effect. It is hence seen that inherited and de novo factors contribute to epidemiological observations. But the evidence does not suggest that older men should refrain from having a child. There is a low occurrence rate of these disorders at baseline and a 5-fold increase in odds ratio even under a strong de novo effect gives us a low probability that the offspring will suffer from autism or schizophrenia due to a high paternal age.
Studying the Effects of Paternal Age on Twins
The present study uses a population-based sample of twins (Twins Early Development Study [TEDS]) to test the effect of paternal age on offspring behaviour. A study by Lundstrom et al. proved that the effects of APA was observed in the offspring only when he/she was around 9 years. Sample size from the TEDS study-of more than 15000 twin pairs-were collected. These individuals were assessed of their social functioning skills at age 4, 7, 9, 14 and 16 respectively.
Social development was measured using parent’s (mostly mothers) rating of the Strengths and Difficulties Questionnaire (SDQ) that helped in analysing both good and problematic aspects of childhood behaviour between 4 and 16 years. The questionnaire mainly focused on five subdomains including conduct problems, emotional symptoms, hyperactivity, peer problems and prosocial behaviour. The effect of paternal age on all five subdomains was checked through five questions scored from 0 to 2 such that the maximum score possible for the subdomain was 10. Contrary to other domains, high scores in the prosocial domain indicated less problematic behaviour.
Results showed that there was a significant link between paternal age and differences in social development in the general population with no effect on behaviour domains. Some kids born to older fathers find it difficult in social settings and the challenges they face increase as they get older. Genetic influence on social development is most pronounced on offspring of the oldest group of fathers.
Advancing Paternal Age and Autism: https://jamanetwork.com/journals/jamapsychiatry/fullarticle/668208
Advanced Paternal Age Effects in Neurodevelopmental Disorders-Review of Potential Underlying Mechanisms: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5299396/pdf/tp2016294a.pdf
Paternal Age Alters Social Development in Offspring: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5409803/
Movies are not spicy without a villain and life too seems to be bland when it goes on and on without some challenges to dethrone. So is the connection between free radicals and antioxidants. Our body is our recluse from which we garner energy for day-to-day functioning of all activities. This energy is acquired from the food that we eat. Free radicals are produced as a consequence of metabolic steps when food is converted into energy, as a result of normal cellular function and also as part of natural physiological process of all living beings. They might also be derived from external sources such as exposure to X-rays, ozone, cigarette smoking and industrial chemicals. There is a continuous formation of free radicals happening in our body as a result of enzymatic and nonenzymatic reactions. Until their production is normal there is no harm caused from them but once overproduction happens, they can become dangerous to even basic processes needed to keep individuals alive. In order to avoid such damages, the cells also produce free radical scavengers known as antioxidants.
Free Radicals & Antioxidants
Free radicals are molecules that contain one or many unpaired electrons in their outer orbit which become highly unstable when they try to react with other molecules to attain molecular stability. In this outreach, the free radical robs other molecules of their electrons creating a chain reaction leading to the damage of DNA and protein breakdown. But it is essential to known that not all free radicals are harmful and there are some of them which help to wipe out invading pathogenic microbes to protect the body’s defense mechanism. In science, we use the terms reactive oxygen species (ROS) and reactive nitrogen species (RNS) to describe free radicals and other non-radical reactive derivatives.
The human body has its own tactical ways for self-defence. It has an excellent antioxidant network that plays the defense role helping to neutralize free radicals and maintain homeostasis. But the defense mechanism doesn’t work in favour of the individual all the time where an imbalance between free radical production and antioxidant defense is possible. Such imbalance leads to what we call ‘oxidative stress’. This oxidative stress is considered to be the starting point for the origin of numerous diseases, development of ageing and the onset of health problems such as arthritis, cardiovascular and neurodegenerative diseases, inflammation and cancer. Oxidative stress is also possible due to poor diet or disease. Nowadays, we read numerous articles that suggest the consumption of various foods for antioxidant benefits but there are also questions raised whether performance of exercise can alleviate the effects of free radicals.
Exercise & its Effect on Free Radicals
Physical activity has been proposed as a solution to remove the harmful effects caused by free radicals on the human body. Various studies these days show evidence that ROS are generated during exercise but physical activity helps in improving antioxidant defense. Physical activity is different from exercise. We define physical activity as some body movement produced by skeletal muscles resulting in energy consumption and examples include everyday life activities and exercises such as walking and cycling. Moderate exercise and an active lifestyle have been proposed as good ways to reduce oxidative stress. It finally depends on the exercise duration, intensity, fitness condition and nutritional status as to whether the reactive species are helpful or harmful. On the other hand, we also have research showing that exercise-induced free radical production promotes insulin sensitivity in humans thereby acting as a catalyst for type 2 diabetes prevention.
Regular practise of moderate-intensity exercise helps to stay away from oxidative stress while acute bodily exercises can cause oxidative stress and increase the production of free radicals. Overperformance of exercise increases the amount of reactive and nitrogen species which increase ROS production and RNS might cause imbalance among RONS and antioxidants. Hence, exercise-an activity that must benefit the body-becomes the cause for exhaustion and injury.
Effect of Low-intensity Exercise on Antioxidants & Oxidative Stress
The study included 2 groups: one group of low-intensity exercise performers (EXG) and another one performing no exercises called the control group (CG) with each group consisting of 20 participants. Low-intensity exercise is that which gets you to about 40-50% of your maximum heart rate (MHR) such as jogging and walking. Those individuals above the age of 30, suffering from chronic diseases or taking long-term medications were excluded from the study. Blood samples of all the participants were collected and antioxidant capacity of the samples was estimated using the Benzie and strain method.
A comparison between the two groups was made regarding body mass index (BMI), alanine transferase (ALT), alkaline phosphate (ALP), aspartate (AST) and FRAP. Significant difference in BMI values was found in both groups with BMI of CG less than the BMI of EXG. ALT of CG was less than that of EXG; ALP of CG was high than the ALP of EXG; AST of CG was less than the AST of EXG. The study concluded that low-intensity exercise had no effect on liver enzymes but improved blood life quality by reducing various health problems related to oxidative damage of cells and muscles fatigue.
Physical Activity Improves Antioxidant Capacity in Individuals with Type 2 Diabetes Mellitus
We have numerous evidences pointing to the fact that free radicals and oxidative stress contribute towards Type 2 diabetes mellitus (T2DM) and its related complications. Some of the causes of oxidative stress during diabetes include overproduction of ROS by mitochondria and nonenzymatic glycation. Physical activity or exercise helps to improve insulin resistance by improving insulin action and vascular function while decreasing ROS generation. Animal studies were conducted to bring about the effect of exercise on T2DM. Regular and moderate-intensity aerobic exercise that consisted of 12 weeks of swimming was conducted for both diabetic and lean rats which were between 8 and 20 weeks of age. The animals performed the exercise in a cylindrical tank that contained water in a controlled temperature. The animals were placed in the tank everyday at the same time. While the duration was for 15 min/d initially it was increased to 60 min/d by the end of the first week and the schedule was followed thrice every week. The sedentary rats were placed in similar containers where the swimming session was held for all the 60 min to ensure that rats in both groups underwent the same amount of stress. The research team observed an amelioration of insulin resistance and diabetic dysmetabolism. A decrease in systolic and mean blood pressure and heart rate, decrease in oxidative stress and increase in NO production was observed.
Antioxidants came to the defense of animals with T2DM in yet another study by Nishida et al. which reported increased Cu/Zn-SOD protein production as a result of low-intensity exercise in contrast with increased Mn-SOD after moderate-intensity exercise. Studies from other researchers on a six-month moderate-intensity aerobic exercise training showed decrease in lipid peroxidation, increase in GSH and catalase activity in T2DM and obese individuals. Oliveira et al. compared the effects of 12 weeks of training on 3 different exercises (aerobic, strength and combined training) on T2DM male and female human participants showing that aerobic training program provided important upregulation in antioxidant enzymes and increased NO bioavailability which helps to minimize oxidative stress and chronic complications of diabetes.
Hence, regular and moderate exercise can have antioxidant and anti-inflammatory effect in individuals with type 2 diabetes.
Both aerobic and anaerobic exercise can produce free radicals but oxidative stress always doesn’t occur because ROS production is dependent on the exercise intensity. While high ROS production due to acute exercise performance is harmful to the immune system chronic exercise produces physiological adaptations that can empower a person’s antioxidant system.
Regular Physical Exercise as a Strategy to Improve Antioxidant & Anti-inflammatory Status: Benefits in Type 2 Diabetes Mellitus: https://www.hindawi.com/journals/omcl/2012/741545/
Oxidants, Antioxidants & the Beneficial Roles of Exercise-induced Production o Reactive Species: https://www.hindawi.com/journals/omcl/2012/756132/
Is Exercise the Best Antioxidant Supplement? https://www.unm.edu/~lkravitz/Article%20folder/Antioxidants.pdf
Impact of Low-intensity Exercise on Liver Enzymes and Antioxidants Systems of the Body: https://www.unm.edu/~lkravitz/Article%20folder/Antioxidants.pdf
Obesity rates have become unjustifiable with more than 40% of adult population staying overweight and more than 14% of children existing in the obesity zone. Inappropriate environmental, biological and psychological factors have resulted in a situation where obesity rates have tripled since 1975. We have moved past the fact that adult obesity rates are inappropriately high and now researchers are mainly focusing on childhood obesity rates. 10% of the global population is obese and almost 15% of kids between 2 and 5 years old are obese. We have multiple research on the effect of early life factors and its effect on childhood obesity. Its also known that maternal and paternal obesity increase the risk of obesity in the offspring and most excess weight in childhood are gained during the preschool years. Some of the evident examples come from some of the most developed nations-U.S. has 69% adults and 32% kids either in the obese or overweight range; Western Europe exbibits some of the highest obesity/overweight rates and data from the ‘National Child Measurement programme’ (NCMP) shows that more than one in five kids in England are now obese/overweight by the time they are enrolled in primary school and the rates increase further to one in three by the age of 6. To make things worse, 8% of infants and toddlers display weight ranges above 95th percentile in the U.S.A. This is indeed a nightmare as obesity/overweight that’s prevalent in these tender years is sure to linger past adolescence and well into adulthood.
Staying above recommended weight ranges since childhood puts the kid at a potential risk for comorbid conditions such as diabetes, cardiovascular problem and even cancer. We have a good number of research done on the risk factors of obesity during childhood years such as children’s eating habits, infant feeding practices and television viewing but what we need exactly is to understand the factors present in both parents and offspring that promote obesity across early life stages (right from preconception through prenatal period to infancy to the tender age of 2). Though researchers focus on risk of obesity through childhood and adolescent years we have evidence showing that the foundation for inappropriate weight gain is laid in early years of life by actions and interactions that can have biological and behavioural consequences. Such influences on obesity and risks for it are linked across generations-from parent to child. An understanding of various processes and sewing them together in the right order helps us focus on the generation link that’s evident.
The intrauterine environment shapes the trajectory of weight gain and after birth the teachings of parents and families combined with the socioeconomic environment has greater impact on the weight trajectories of infants and toddlers. Obesity rates of kids greatly vary depending on where they live.
Seeds of Obesity Sown Even Before Deciding to Plant
Preconception: The risk of obesity in the next generation starts even before conceiving. Until sometime back most studies focused on maternal influence of obesity on the offspring but recently even the paternal involvement in determining offspring’s health has now been taken into consideration.
The major factors affecting offspring include a mother’s birth weight, obesity and nutritional status throughout her life. Pre-pregnancy obesity rates have steadily increased since the last decade to the present one and statistics show that mothers who are overweight/obese before pregnancy are at an increased risk of having children who are large for gestational age at birth compared to their normal weight counterparts. A study by Whitaker et al. showed that maternal obesity during the first trimester of pregnancy doubled the risk of childhood obesity at 2 years of age. Fathers affect embryonic development through genetic and epigenetic mechanisms. Epigenetic changes affect the fetus’ metabolism which is primarily due to variations in the dad’s diet. This shows that paternal lifestyle behaviour definitely puts future kids at risk of obesity and obesity-related outcomes. These epigenetic changes could even be inherited by the developing sperm. All this clearly show one thing-the world that’s been monopolizing the attention to women who plan to conceive must also consider the health of men. A number of suggestions have been proposed for women in their reproductive years right from nutritional guidance to weight management. They are advised to take supplements that include multivitamins and folate to avoid deficiencies such as neural tube defects and likewise. A survey showed that 77% women opted for enrolling in a program that promoted effective lifestyle intervention before conceiving and this shows that women are on the right track. Men should also be encouraged to take care of their health. Actually, both men and women must be motivated to stay within normal weight ranges right from adolescence to help the future generation to stay at a minimal risk of obesity.
Prenatal influence: The environment affects us in many a way. Environmental exposure and timing of exposure to different factors within the environments produce interactions that are biologically seeded in the developing child. Epigenetic influence do exist and the gene sequence cannot be modified but we can indeed change the gene expression in response to environmental cues. For instance, changes to the placenta made as a result of maternal stressors or nutritional status prevails as the mediator between the developing child and the environment. This prevails as the trailer for the fetus before the main picture is shown (when the fetus then becomes a newborn). The fetus becomes adapted to epigenetic changes which then regulate behaviour, obesity and glucose tolerance. But when the fetus is small for gestational age during development or there was restricted intrauterine growth the growing newborn is at a greater risk of suffering during later stages in life.
When metabolic pathways, hormonal signalling and glucose metabolisms change by a greater margin during pregnancy it increases the risk of larger birth size and higher percentage of body fat at birth. The gut bacteria also play a critical role as researchers have come up with differences in the microbiome of overweight individuals compared to normal-weight people. The same is also seen in pregnant women and hence, might be transferred to the child too (as the child gets the microbiome composition from mother during birth through the birth canal and it’s also affected by the mode of delivery) thereby resulting in intergenerational transfer of obesity.
Maternal Lifestyle: Time and again gynaecologists insist on a healthy maternal weight gain and lifestyle behaviours to deliver a healthy offspring. Eating, physical activity and smoking levels during pregnancy have a strong impact on the risk of obesity for the fetus developing inside the mother’s womb. Besides preconception obesity gestational weight gain (GWG) changes the pregnant woman’s metabolism leading to higher risk for dyslipidaemia, glucose intolerance and insulin resistance. Such GWG leads to a greater percentage of offspring born with higher birth weight, increased body fat during the neonatal period and greater adiposity all though childhood and adulthood as well. All this is due to increased nutrition transfer from overnourished mothers to the developing fetus.
Moms pass on food likes and dislikes to the developing fetus. The food that she consumes, her tastes and smelling traits that are present during fetal development strongly influence a child’s preferences for food and flavour. Now we can understand why our little ones love sweets, hate certain vegetables and relish certain foods more than others. Performing physical activity regularly during pregnancy helps the woman deliver infants that are smaller than the ones born to women who don’t exercise. Different studies come up with different results and hence reviews are inconclusive. Another important factor affecting fetal weight is smoking status of the pregnant woman. Smoking, both maternal and paternal, during the prenatal period is strongly linked to obesity development in the offspring during childhood and adulthood.
Numerous systemic reviews and meta-analysis of data show that maternal pre-pregnancy weight gain is linked to an increased risk of overweight/obesity in the offspring, children born to moms after weight loss were only at a 35% risk of overweight/obesity compared to 60% risk in kids born to moms who remained obese, according to a study. A recent systemic review showed that 19 of 21 studies supported increased risk of childhood overweight in kids when moms experienced GWG. Kids of women who gained excessive weight during pregnancy were at a 4-times higher risk of being overweight at age 3 compared to kids whose mothers gained inadequate weight according to a study by Oken et al. A population-based cohort study proved that compared to infants of women who gained 8-10 kg of weight during pregnancy those of women who gained more than 23 kg were about 2.5 kg heavier at birth.
Factors Affecting Obesity Risk Up to 2 Years of Age: Infant birth weight is a strong determining factor of obesity/overweight risk in the child. Kids born either too small or big for gestational age are at an increased risk of overweight, obesity, metabolic disorders and cardiovascular diseases. The birth weight of the child is determined by the maternal weight at conception and GWG. As in adults, infants too should gain a definite weight in a definite period and accelerated weight gain occurring during the first 4 months of life are related to obesity at 7 years of age and a 60% increase in risk if weight gain happens within the first 2 years of life. but the reason behind rapid weight gain during this period is due to genetic factors, epigenetic processes, differences in placental leptin levels and the infant’s gut microbiome composition.
Infant-feeding habits: Kids depend on their parents for making the right decisions up to a certain age and food habits are one of those. What and how much food parents feed their infants directly affect the weight gain and obesity risks of child during later stages in life. There are not any recommended dietary guidelines for kids younger than 2 years of age to help parents and caregivers choose the right portions and foods to feed the kids. Infants are blessed with the knowledge to know how much to eat, when to eat and when they are full. They self-regulate their needs even while breastfeeding choosing how much to drink how often. That’s why infants fed on formula by parents gain more weight maybe due to the amount and pattern of feeding and so do infants who start weaning early in life. The child’s ability to self-regulate narrows down when it is dominated more and more by parental intervention.
Sometimes, parents feeding practices also depend on the child’s food choices which is affected greatly by its exposure to sweet and sour taste during prenatal exposure to the mother’s diet but they can be modified by repeated exposure to certain foods by the parents. Some parents also use feeding as a mechanism to soothe infants and such practices lead to unintentional weight gain in kids. Our lifestyle and sedentary behaviour also hold greater influence on obesity risks. The present world encourages the use of car seats and strollers that make the children idle, exposure to television starts right from their 3rd month sometimes and many suffer from lack of sleep due to increased screen time. A prospective cohort study on more than 900 infants showed that those who slept for less than 12 hours doubled their odds of becoming overweight by age 3 compared to others. An infant’s birth weight and rapid weight gain during the first months of life are clear cut indicators of future obesity risk. Hence, it does show that the way parents and caretakers feed infants and the steps that they take to engage children do affect the risk of long-term weight gain in these little ones.
In recent years, more attention has been focused on interventions targeting parents and modifiable risk factors that prevent obesity and promote healthy growth in the first 1000 days of life. Lifestyle and nutrition practices followed through life-before conception, time spent in utero and the following months after birth greatly affect the child’s weight at birth, during childhood and well into adulthood. Women who take care before conceiving, while pregnant and even after childbirth have greater chances of giving birth to and nurturing kids who are at a minimum risk of obesity in life. Nutritional interventions by parents, the steps they take to ensure kids’ exposure to healthy food and their participation in physical activity plans with the children do indeed help in making the kids as healthy as possible. It would be beneficial for both the kid and the mother when the woman strives for a healthy weight before pregnancy, abstains from smoking, strives for a normal weight gain during pregnancy, breastfeeds unless there is some health issue linked and takes care that infants get the desired sleep time during the first few years of life.
Preventing Obesity Across Generations: Evidence for Early Life Intervention: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5305001/
Prevention of Overweight & Obesity in Early Life: https://www.cambridge.org/core/journals/proceedings-of-the-nutrition-society/article/prevention-of-overweight-and-obesity-in-early-life/F9BB50517A0A0F9D4F542276A30926D5/core-reader
The Effect of Early Life Factors & Early Interventions on Childhood Overweight & Obesity: https://www.cambridge.org/core/journals/proceedings-of-the-nutrition-society/article/prevention-of-overweight-and-obesity-in-early-life/F9BB50517A0A0F9D4F542276A30926D5/core-reader
Preventing Childhood Obesity: Early Life Messages & Epidemiology: https://onlinelibrary.wiley.com/doi/full/10.1111/nbu.12277
Prenatal & Early Life Influences: https://www.hsph.harvard.edu/obesity-prevention-source/obesity-causes/prenatal-postnatal-obesity/
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