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The hepatic lipase gene (LIPC) is associated with the synthesis of hepatic lipase enzyme (LIPC) which catalyzes the hydrolysis of fat. Hepatic lipase converts intermediate-density lipoprotein (IDL) to low-density lipoprotein (LDL).It is expressed in the liver and in the adrenal glands. Specific alleles of this gene are known to either increase or decrease hepatic lipase levels, and due to linkage disequilibrium, the levels of lipoprotein lipase, which is associated with variations in the plasma HDL levels. People with the T variant of the gene are shown to be associated with higher baseline HDL levels.
| CHIP Version | LIPC SNPs |
| 23andMe (Use your 23andme raw data to know your LIPC Variant) | |
| v1 23andme | Present |
| v2 23andme | Present |
| v3 23andme | Present |
| v4 23andme | Present |
| V5 23andme (current chip) | Present |
| AncestryDNA (Use your ancestry DNA raw data to know your LIPC Variant) | |
| v1 ancestry DNA | Present |
| V2 ancestry DNA (current chip) | Present |
| Family Tree DNA (Use your FTDNA raw data to know your LIPC Variant) | |
| OmniExpress microarray chip | Present |
People with the C variant of the gene were associated with reduction in weight, body fat and visceral fat.
In a study investigating the effects of endurance training on plasma lipoprotein levels, people with the C variant of the gene have been found to be associated with exercise mediated reduction in VLDL and increase in HDL. The benefit of exercise was found to be more in men with CC genotype than women.
In a meta-analysis study conducted on children, boys with the T allele had a higher BMI and higher risk of obesity. In another study, boys with the T variant of the gene were found to be associated with higher HDL level on high fat intake.
In a study conducted to determine gene-nutrient interactions, people with the T variant on a low fat diet (less than 30% of energy from fat) have been shown to be associated with higher HDL levels. In a study conducted to identify how Chinese, Malays and Asian Indians in Singapore were exposed to similar environment but where Asian Indians had three times the rates of myocardial infarction compared to Chinese, found that a complex interplay of environmental and genetic factors gave rise to these ethnic differences. A high fat diet was shown to be associated with higher serum triglyceride and lower HDL-cholesterol concentrations in people with the T variant while those with the C variant were shown to be associated with lower serum triglyceride and higher HDL cholesterol under the same dietary conditions. People with the T variant of the gene may have an impaired adaptation to a high fat diet, increasing the risk for cardiovascular disease.
In a study conducted on the LIPC gene variant and insulin sensitivity, the baseline insulin sensitivity was found to be similar between the gene variants but, upon exercising, people with the C variant were shown to be associated with higher insulin sensitivity. In a similar study, men with the T variant were shown to be associated with an improvement in insulin sensitivity when MUFA and carbohydrate rich are consumed instead of SFA fat. There was no association with women with the T variant and between diet and insulin sensitivity among men and women with the C variant.
| Genotype | Phenotype | Recommendation |
| CC | [Limitation] More likely to have lower baseline HDL [Advantage] More likely to have higher HDL level upon exercising [Advantage] More likely to have higher HDL on high fat diet [Advantage] More Likely to have improvement in insulin sensitivity upon exercising [Limitation] Less Likely to have improvement in insulin sensitivity when on MUFA and Carbohydrate rich diet | Likely increase in HDL upon exercising Including exercise routines is beneficial to HDL levels and insulin sensitivity |
| CT | Slightly improved insulin sensitivity upon exercising | Likely increase in HDL upon exercising Including exercise routines is beneficial to HDL levels and insulin sensitivity |
| TT | [Advantage] More likely to have higher baseline HDL [Limitation] Less likely to have higher HDL level upon exercising [Limitation] More likely to have Lower HDL on high fat diet [Limitation] Less Likely to have improvement in insulin sensitivity upon exercising [Advantage] More Likely to have improvement in insulin sensitivity when on MUFA and Carbohydrate rich diet | Likely increase in HDL level when on MUFA and Carbohydrate rich diet People with this gene variant would benefit from consuming low fat diet and carbohydrate rich diet |
“Nutrigenetics, fitness genetics, health genetics are all nascent but rapidly growing areas within human genetics. The information provided herein is based on preliminary scientific studies and it is to be read and understood in that context.”
DRD2 is a protein-coding gene that is located on chromosome 11.
The Dopamine Receptor Gene (DRD2) is associated with the synthesis of DRD2, which is the main receptor for all antipsychotic drugs.
The hormone Dopamine is a neurotransmitter and its secretion is increased during emotional upheavals.
From an evolutionary aspect, this hormone is released in response to some adverse condition, to prepare the body for a flight or fight response.
Under normal circumstances, when dopamine binds to DRD2 receptor, it should lower feelings of hunger and increase satiety.
Specific alleles of the DRD2 gene have been shown to be associated with a lower amount of DRD2 in the brain, which could lead to binge eating or overeating.
Before we look at the function of dopamine receptors, let’s understand what is dopamine.
Dopamine is a very important neurotransmitter and neurohormone in the body, which is responsible for enabling communication between nerve cells in the brain.
Dopamine is also linked with the brain's pleasure and reward system, and also controls movement.
Apart from this, dopamine also plays a role in memory and focus.
Dopamine receptors are important when we talk about certain neurological disorders like Parkinson’s disease.
Dopamine is produced by the substantia nigra in the brain( a part of the basal ganglia) which is responsible for controlling movement.
So, a steady flow of dopamine to these dopamine receptors ensures that controlled bodily movements occur normally.
But, when there is a decrease in dopamine reaching the receptors, movement, controlled movement and motor skills are affected, as we see in case of Parkinson’s disease.
The reverse of this happens in Tourette’s syndrome, where there is an excess of dopamine leading to excessive movements.
Dopamine receptors ensure adequate neurological signaling to allow dopamine to perform its functions and abnormal dopamine receptor signaling results in neuropsychiatric disorders.
These receptors are also the prime target of neurological drugs such as antipsychotics.
There are 5 types of dopamine receptors – DRD1 to DRD5.
It is a member of the D1-like receptor family and is the most abundant dopamine receptor found in the CNS.
The DRD1 receptor is found in the cortex, striatum and the limbic system of the brain, and the cardiovascular system.
It modulates the actions of dopamine receptor D2.
When dopamine binds to the DRD1 receptor, it regulates the growth and development of nerve cells in the brain and influences behavioral responses.
This receptor is a member of the D2-like receptor family and is found in many regions of the brain but has the highest concentration in the basal ganglia.
Since the basal ganglia comprise of structures responsible for motor control and learning, the DRD2 receptor mutations result in diseases such as schizophrenia or disorders like myoclonus dystonia.
Along with the DRD1 receptor, the DRD2 receptor reinforces the effects of drug abuse.
This is a part of the D2-like receptor family-like Drd2 and is mainly present in two regions of the limbic system – the islands of Calleja and nucleus accumbens.
These two areas of the brain are primarily involved in reinforcing pleasure activities and emotions like addiction, laughter, etc.
It has been researched that mutations in this receptor can increase the susceptibility to a hereditary essential tremor 1, which is a type of movement disorder.
It is also a member of the D2-like receptor family and is the receptor that is targeted by medications that are aimed at treating neurological disorders such as Parkinson’s and Schizophrenia.
This receptor is involved in motor coordination and exploratory behavior in humans.
A mutation in the DRD4 receptor can result in attention deficit hyperactivity disorder and dysfunction of the autonomic nervous system.
It is a member of the D1-like receptor family, just like DRD1.
These receptors are present in the limbic system of the brain and have a variety of functions such as long-term memory, smell, emotion, and behavior.
It has been shown that the D5 receptors have a higher affinity than the D1 receptors which means that they bind more easily to dopamine.
The SNP rs1800497 is also known as the Taq1A polymorphism of the dopamine D2 receptor(DRD2).
In a study conducted on obese people, Binge eating disorder and it was found that it was significantly associated with SNP rs1800497 and rs6277 that show enhanced or increased dopamine production.
The presence of the A1 allele is associated with reduced dopamine receptor availability in the brain thereby it was hypothesized that carrying this allele would increase the risk of emotional eating, especially in adolescents.
People with the T variant of the gene were found to be associated with increase in emotional eating behavior.
A recent study conducted on children found that T variant predisposes them to greater energy intake and higher risk of obesity.
Also, the presence of the T variant improves the speed of processing in individuals as compared to those who have the C variant.
The G allele of SNP rs4245150 of the DRD2 gene is associated with an increase in worry and anxiety.
[table “121” not found /]In a study conducted to determine linguistic language learning ability, people with the CC genotype were shown to be associated with better concatenative memory.
Another study conducted on older people, it was found that people with C variant had better associative memory.
A research was conducted to determine the genetic basis of bilingual ability, the T variant was found twice the amount among Spanish-English bilinguals than among only English speaking students.
[table “122” not found /]The different types of D2-like receptors are found in different regions in the brain.
The D2 receptors are in high concentration in:
The D3 receptors are more limited in distribution and are found mainly in the nucleus accumbens of the limbic system.
However, less number of the D3 receptors are found in:
D4 receptors are the least in number in the brain and these are found in moderate levels in:
We often meet people in our social circles who are food-O-holics or are ‘foodies’ as they call themselves.
Most of these people struggle to control themselves when they see food or cannot prevent themselves from overeating.
But, on the other hand, we see some people who know exactly how much they want to eat and stop at a time when they feel they are full. These people avoid overeating.
While it may seem easy to prevent overeating, it is a habit that is difficult to break.
But, can one stop overeating?
Well, of course, you can! Here are a few effective ways to stop overeating:
these include watching TV or browsing through your phone, tablet or computer.
When you are distracted while eating, you tend to focus less on how much you are eating, often leading to excessive eating.
As these can make you feel full soon and yet you haven’t loaded up on excessive amounts of food or calories.
Including whole grains, salads, vegetables, fruits, etc., is a good way to increase the fiber content of your meals.
If you are seriously trying to avoid overeating, there are high chances that you have tried to keep food that you tend to indulge in away from you.
However, this behavior tends to backfire when you fall prey to the temptation and your problem of overeating is still unsolved.
Feel free to balance out the food items you eat and occasional indulgence will do no harm.
When we eat chips from a packaged packet or munch on popcorn from a tub, we tend to binge eat on them without knowing the quantity we are consuming.
The best thing to do in such cases is getting out just the proportioned or measured amounts of food items onto the plate.
Having a set routine for your three meal and snack-time is one of the time-tested methods to prevent overeating.
When you eat your meals regularly, your body knows how much it needs.
When you eat erratically or tend to skip meals, you feel more hungry due to a calorie deficit and this leads to overeating during the next meal.
When you consume foods that are high in proteins such as a high protein breakfast, it tends to lower the hunger causing hormone ghrelin, thereby preventing overeating.
It is also a great idea to consume some yogurt in your breakfast for the same reason.
It is often said that one must eat slowly and each meal should last a minimum of 20 minutes.
This is because this is the time needed by your stomach to convey to your brain that it is now full and that you need to stop eating.
However, in today’s lifestyle, people tend to eat really fast to save on time and get back to work.
This leads to unintentional overeating and we often don’t realize it.
There is no substitute for water.
Consuming more water throughout the day and keeping yourself hydrated also helps you feel less hungry, thereby preventing overeating during mealtimes.
Every now and then we come across diets that promise you weight loss and a healthy lifestyle.
But, these diets are not sustainable and people often fall back into their old lifestyles.
We all feel anxious in our day to day lives, especially in today’s world where we all struggle for something or the other.
It is okay to suffer from anxiety once in a while but in many individuals, it becomes a chronic problem.
Anxiety which is chronic in form has detrimental effects on one’s mind and body and severely impacts the quality of one’s life.
While there are many medications in the market that help reduce or treat this condition, it is best to resort to some natural methods of doing so. Some of these are:
Sleep is the best healer and medicine for our body for this is when our body relaxes completely.
People suffering from anxiety often find it difficult to get good sleep but they can use some tips to improve their sleep duration and quality.
When your mind and body have relaxed enough, you tend to feel the difference in your anxiety levels.
Caffeine causes mental alertness, can make your mind active and can cause nervousness.
So, if you already suffer from anxiety, avoid caffeinated foods and drinks and resort to something more calming and soothing to both your mind and your body.
Alcohol makes teleports you to another world, doesn’t it?
You feel comfortably numb or sedated and it gives you a sense of calmness.
But, the reality is that once the effect of alcohol starts to wear off, anxiety returns, and this time even more strong.
So, it is best to avoid resorting to alcohol and staying completely off it if you suffer from anxiety.
Just like alcohol, many people reach out for a puff when they are most stressed.
But, though the nicotine tends to offer you solace at that moment, in the long term, it tends to push you more towards developing an anxiety disorder.
Though quite a clichéd statement, eating healthy is actually beneficial for reducing your stress levels.
One must avoid foods that contain too much sugar, artificial sweeteners, flavors and colors, chemicals, dehydrating agents and preservatives.
All these affect one’s mood and temperament and can increase anxiety levels.
The age-old art of meditation removes any negative and disturbing thoughts and helps instill a sense of calmness and peace of the mind.
However, it is easier said than done and this remedy often takes time but has repeatedly shown to reduce anxiety and people.
While slow, fast breathing is seen in cases of anxiety, practicing deep breathing while you meditate can help counter anxiety.
What differentiates those homebodies who love to spend days on end at home and those that have this irking urge to undertake a holiday just a few days after they have returned from a long vacation?
Well, blame it on the DRD4-7R gene that is called as the ‘wanderlust gene’.
This gene codes for increased curiosity and restlessness and is present only in 20% of the population.
When proper history was taken while studying the gene, most people had a history of travel or will to travel.
This gene has also been linked to the first settlers in the continent of Africa who had the courage to migrate farther away from home, thereby spreading across the globe.
A mutant form of this DRD4 gene, the 7r makes people more likely to take risks, explore new places, new food, cultures, new ideas, drugs, and sexual opportunities.
Few scientists also link this DRD4 7r gene with migration.
A few scientists have also linked this behavior that is ‘out of control’ and hints at those people who wish to quit their high paying jobs for a few months of vacation, which is clearly irrational.
However, for a species as vast as humans in terms of genetics, it is unfair and rather difficult to pin down one particular gene for people who travel.
References:
“Nutrigenetics, fitness genetics, health genetics are all nascent but rapidly growing areas within human genetics. The information provided herein is based on preliminary scientific studies and it is to be read and understood in that context.”
Does your 23andme, Ancestry DNA, FTDNA raw data have DRD2 gene variant information?
| CHIP Version | DRD2 SNPs |
| 23andMe (Use your 23andme raw data to know your DRD2 Variant) | |
| v1 23andme | Present |
| v2 23andme | Present |
| v3 23andme | Present |
| v4 23andme | Present |
| V5 23andme (current chip) | Present |
| AncestryDNA (Use your ancestry DNA raw data to know your DRD2 Variant) | |
| v1 ancestry DNA | Present |
| V2 ancestry DNA (current chip) | Present |
| Family Tree DNA (Use your FTDNA raw data to know your DRD2 Variant) | |
| OmniExpress microarray chip | Present |
The Insulin signaling protein type 2 gene (INSIG2) is associated with the synthesis of INSIG2 protein which interacts with transcription factors, activating the synthesis of cholesterol and fatty acids. The variants of the INSIG2 gene have been shown to be associated with body fat accumulation. Specific alleles of this gene are known to either increase or decrease INSIG2 protein levels which are associated with subcutaneous fat accumulation upon exercising.
| CHIP Version | INSIG2 SNPs |
| 23andMe (Use your 23andme raw data to know your INSIG2 Variant) | |
| v1 23andme | Present |
| v2 23andme | Present |
| v3 23andme | Present |
| v4 23andme | Present |
| V5 23andme (current chip) | Present |
| AncestryDNA (Use your ancestry DNA raw data to know your INSIG2 Variant) | |
| v1 ancestry DNA | Present |
| V2 ancestry DNA (current chip) | Present |
| Family Tree DNA (Use your FTDNA raw data to know your INSIG2 Variant) | |
| OmniExpress microarray chip | Present |
In the Framingham Heart Study, people with the C variant of the gene were shown to be associated with obesity, measured in terms of BMI. In a recent similar study conducted on a North Indian population, there was a significant association between INSIG2 gene polymorphism and severe obesity. In another study that analyzed the level of subcutaneous fat, women with the C variant of the gene were shown to be associated with higher levels of baseline subcutaneous fat.
Men with the C variant of the gene were associated with higher gain in subcutaneous fat upon resistance training while men with the G variant showed a loss in subcutaneous fat. In another study, men with the G variant of the allele were shown to be associated with Intramuscular (IMAT) volume in the upper arm after 12 weeks of training than for the subcutaneous fat. In a study on obese children who were on a weight loss program, children with the C variant of the gene were found to lose less weight than children with the G variant.
In a study conducted on Japanese women, the C variant of the gene was shown to have a protective effect on the progression of hypercholesterolemia when on a high fat diet. On an initial analysis in another study, women with the C variant of the gene showed a lower prevalence for hypercholesterolemia.
| Genotype | Phenotype | Recommendation |
| CC | [Limitation] More likely to have higher BMI [Limitation] More likely to have higher subcutaneous fat upon resistance training [Advantage] Less likely to have hypercholesterolemia (Women) | Likely increase in subcutaneous fat upon strength training Including fitness programs, other than strength training might be more beneficial Additional effort may be required to lose weight when compared to people with the G variant |
| CG | Moderate BMI and subcutaneous fat accumulation upon exercising | Likely increase in subcutaneous fat upon strength training Including fitness programs, other than strength training might be more beneficial Additional effort may be required to lose weight when compared to people with the G variant |
| GG | [Advantage] More likely to have lower BMI [Advantage] More likely to have lower subcutaneous fat upon exercising [Limitation] More Likely to have hypercholesterolemia(women) | Likely lower subcutaneous fat upon exercising Strength training has not been shown to be associated with increase in subcutaneous fat upon exercising. There is an increase in Intramuscular volume on training, which may benefit bodybuilders |
“Nutrigenetics, fitness genetics, health genetics are all nascent but rapidly growing areas within human genetics. The information provided herein is based on preliminary scientific studies and it is to be read and understood in that context.”
A healthy weight is maintained during a state of energy balance- when the energy intake of an individual matches the energy expenditure. Weight can accrue over a long period of time if the intake is higher than expenditure. Besides intake and expenditure, other factors such as age, basal metabolism, hormonal imbalance, and genetics also influence weight gain or weight loss.
Many humans have inherited genetic adaptations, which evolved to mitigate the ancestral exposure to cycles of feast and famine. Hence, the human body is very good at storing excess energy as fat and reluctant to lose valuable stores (fat) of energy. This is the basis of the ‘thrifty gene’ hypothesis, which explains why people easily put on weight on an excess calorie diet and find it very hard to lose it.
The heritability associated with energy intake among children is found to be between 47-69%. Twin studies showed that there was a genetic influence on the type of food consumed, along with satiety and food cue response.
There are many genes that have been shown to be associated with obesity and energy intake. Of particular significance is the FTO gene. Studies have shown that certain variants of this gene were associated with increased energy intake and increased hunger. Individuals with the abnormal FTO gene weigh at least 3kgs more than individuals who have the normal copy of the gene.
Individuals with an abnormal copy of the FTO gene eat more frequently, with a tendency to prefer calorie-dense foods and larger portions of food. People with the highest risk variant should exert portion control and eat a lot of food rich in fiber which would help quell the hunger. They should also consider frequent snacking in small quantities of low calorie, high protein, and high fiber foods to counteract the perpetual hunger they may be experiencing to maintain a stable glycemic index and stable levels of hunger and satiety hormones.
A hormone that plays a key role in satiety is ghrelin. Ghrelin is responsible for ‘hunger pangs’ as it signals the brain to eat. After a meal, the level of ghrelin is lowered and levels of another hormone, Leptin, are elevated resulting in a feeling of fullness. In an individual with the high risk variant of the FTO gene, the level of ghrelin remains high even after a meal, re
sulting in over eating. In such individuals, exercise has been shown to restore the level of ghrelin to normal levels.
Individuals with the abnormal FTO gene should be encouraged to follow a regular exercise pattern which will aid in lowering ghrelin levels and provide better satiety response.
Another important gene that affects meal size and meal choice but not meal frequency is MC4R. When the energy levels drop in our body, the hunger center sends signals that inhibit MC4R and there is an increase in appetite. When the stomach is full after eating, satiety signals are sent by the satiety center that stimulates the MC4R to send signals to stop eating.
Overeating that is induced by distress, emotional eating, leads to binge eating which is highly prevalent in adults who are binge eaters or obese. Binge eating disorder is due to hypersensitivity to reward which results in overeating. The tendency to overeat or binge eat can be determined relatively strongly by analyzing the dopamine D2 receptor gene.
Dopamine is a neurotransmitter and its secretion is increased during emotional upheavals. From an evolutionary aspect, this hormone is released in response to some adverse condition, to prepare the body for a flight or fight response. Under normal circumstances, when dopamine binds to the DRD2 receptor, it should lower feelings of hunger and increase satiety. However, mutations in the DRD2 gene lead to a lower amount of DRD2 in the brain, which could lead to binge eating or overeating.
Individuals who carry the abnormal gene should consciously avoid overeating when feeling distressed or should store healthy snacks to eat at times of distress. Another study showed that deficits in the dopamine D2 receptor led mice to be inactive, which in turn lead to weight gain. Therefore, people with an abnormal gene should consciously stay active.
Regulating energy intake can moderate susceptibility to weight gain and obesity and is essential for people with a higher propensity to gain weight. Interventions that promote self-regulation of energy intake have the potential to control weight gain and also encourage healthy dietary habits. When designing intervention strategies, it is important to understand the genetic aspects involved as nearly 30% of obese individuals underreport their energy intake. The most effective way to fight obesity is through calorie restriction or lowering energy intake. People who carry abnormal genes for energy intake should follow mindful eating to ensure a balance in energy homeostasis.
Individuals who carry the abnormal gene should consciously avoid overeating when feeling distressed or should store healthy snacks to eat at times of distress. Another study showed that deficits in the dopamine D2 receptor led mice to be inactive, which in turn lead to weight gain. Therefore, people with an abnormal gene should consciously stay active.
Regulating energy intake can moderate susceptibility to weight gain and obesity and is essential for people with a higher propensity to gain weight. Interventions that promote self-regulation of energy intake have the potential to control weight gain and also encourage healthy dietary habits. When designing intervention strategies, it is important to understand the genetic aspects involved as nearly 30% of obese individuals underreport their energy intake. The most effective way to fight obesity is through calorie restriction or lowering energy intake. People who carry abnormal genes for energy intake should follow mindful eating to ensure a balance in energy homeostasis.
Find out which variations of these genes you carry and more at www.xcode.life
Nutrigenetics, fitness genetics, health genetics are all nascent but rapidly growing areas within human genetics. The information provided herein is to be read and understood in that context.
Weight loss struggles are an increasing phenomenon world over with the majority of people aspiring to achieve a slim body either for aesthetic reasons or good health. However, in recent years, obesity has increased dramatically in many parts of the world with India ranking third in the world’s most obese countries. According to a study, ‘Global, regional, and national prevalence of overweight and obesity in children and adults during 1980–2013:a systematic analysis for the Global Burden of Disease Study 2013’, India accounts for 15% of the world’s obese population along with China.
With the rise in obesity, there has also been a significant rise in metabolic diseases associated with obesity such as diabetes, hypertension and heart disease. India has been particularly hard hit with rates of diabetes reaching as much as 20% of the population in some parts of the country. Even though accounting for only 20% of the world’s population, India shoulders 60% world heart disease burden. Studies claim that 40% - 70% of obesity is influenced by genetic predisposition, with environmental elements accounting for the rest. As alarming as this is, there is hope for change. Several scientific studies indicate that the prevention of metabolic conditions by lifestyle modifications such as healthy diet and exercise are far more effective than clinical treatment for these conditions at a later stage.
| With over 50% of obesity being attributed to genetics, obesity can be an inherited condition. Studies find that the risk for obesity is 2-8 times higher for a person with a family history as opposed to a person with no family history of obesity. The FTO gene, also commonly known as the obese gene, is considered to be highly contributory to obesity in individuals. People carrying this gene are found to have a 70% higher chance of being obese than non-carriers. Other genes such as MC4R, INSIG, TCF7L2, LEP, IRS, have also been found to contribute to this condition. However, this does not necessitate a certainty of obesity in carriers. Studies have found that corrective lifestyle measures can alleviate obesity even in people with a genetic predisposition. |
Apart from genetics, a variety of environmental factors have also contributed to this rapid increase in obesity. The most prominent of them being unhealthy food choices and decreased physical activity. The increase in access to junk and processed food has led to unhealthy snacking and food habits. Home-cooked meals are maybe visited once a day with the remaining meals consisting of take-outs or packaged food. In addition, a sedentary lifestyle with minimum to nil physical activity greatly adds to the rise of this condition. Another factor for concern is the lack of regular sleep patterns. Working night shifts and staying up late hours in the night have also shown to contribute to an increasing waistline.
Weight management through standard diets or weight loss plan is a key strategy to reduce the risk or more effectively manage metabolic diseases.
However, the vast majority of weight loss solutions either do not work or work temporarily as they are not sustainable over the long term. The global weight loss industry is estimated to be around USD 600 billion. However, a recent 10-year study by King’s College London determined that an overwhelming 99% of people attempting to lose or maintain weight loss will fail in the long run, indicating that the vast majority of the money spent on weight loss treatments is wasted.
A key reason for failure is a one size fits all approach. Diet plans are standardised on a few core ideas such as high protein, high fats or low carbs, and are extended to as many customers as possible to maximise the market reach. Here, it is assumed that everyone’s body is the same on the inside and hence the same recommendations should work for all. This assumption turns out to be misguided. Genetics impacts all aspects of our lives including how we metabolize foods. Some people are capable of eating all they can and are able burn off the calories, while some people struggle to manage their desired weight despite their best attempts. This is because the underlying genetics is different for all individuals. So far, the tools to understand an individual’s genetics were unavailable. However, over the last decade, with significant advancements in science and technology, these tools are now both available and affordable.
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In a recent study by Stanford University, people who followed a diet program tailored to their genetics were shown to lose as much as 2.5 times the amount of weight compared to people who followed a “standard” diet advice. Understanding one’s genetic profile can help individuals understand their body type and tailor their diets to foods best suited to them. A healthcare professional can use insights from the genetic test to then create a personalized diet to help individuals optimize their metabolism, and achieve their weight objectives, while reducing associated health risks.
Weight loss doesn’t just make one look and feel good, but greatly improves the day-to-day quality of life too. Energy levels, mood, temperament, immune system – all get a boost while reducing the risks for several health and metabolic conditions. In fact, healthy lifestyle choices have also found to help control certain conditions like Type 2 diabetes, PCOS and other lifestyle diseases. Not just for the obese or sedentary, proactive individuals should also consider undergoing a genetic test to understand their body’s unique metabolic profile to customise weight management program as per their lifestyle and genetics.
However, it is important to note that genetic testing can guide your effort correctly, but not replace it. Focussing on the overall nature of sustainable weight loss, Dr. M. Lakdawalla of CODS (Centre for Obesity and Digestive Surgery) India, says, “While genes do play some role in causing a predisposition to obesity, I would not say that they are entirely to blame. A paper published by Harvard's TH Chan School of Public Health states that ‘Active adults who carried the obesity-promoting gene had a 30 percent lower risk of obesity than inactive adults who carried the gene’. Worldwide, we have seen an increase in obesity over the past 30 years - it cannot entirely be put down to genetics. There are several factors that play a role - unhealthy lifestyles, rising stress levels, physical inactivity, rise in conditions such as diabetes, etc.”
Genetics is not just about physical differences among individuals. IT influences all aspects of human physiology and impacts several aspects of our health including, how our body responds to fats, carbohydrates, proteins, gluten, lactose, salt, and vitamins. This understanding will continue to grow by leaps and bounds in the years ahead. One thing is for certain, that the era of "standard" diets, nutrition, and medication is over. Evidence from several scientific studies indicates that what we consume as food and medicine need to be tailored to the individual's genetic type.
[idea]In the last few decades, the nutritional dogma has been about emphasising small & frequent meals throughout the day. Recent research shows that those who eat less are generally healthier, with improved metabolic health, cognition and live longer than those who eat more. Intermittent fasting is based on the principle of alternating between periods of eating and fasting. Intermittent Fasting is practiced in several ways including periodic multi day fasts to skipping a meal or two on certain days of the week. Most of us already fast every day, while we sleep. Simply extending this fast is referred to as Intermittent fasting. One way of doing this is by having your first meal at noon and last meal at 8 p.m in the evening, thus going on an 18 hours fast every day.[/idea]
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From an evolutionary perspective, fasting and food deprivation is one of the factors that could have attributed to the optimal performance of the human brain. Evolution favoured the selection pressure of those individuals who were adept in acquiring food from the limited food sources. Recent research demonstrates the beneficial effect of intermittent fasting and vigorous exercise on brain health. The fact is, until recently, humans did not have guaranteed food supply and may have had to struggle to obtain food for survival. During the course of thousands of years, we have developed the “genetic” ability to use calories wisely and to survive for periods of time without food. This genetic ability is what enables “slow” calorie burning and calorie storage for long periods of time in most people. This is why most people have a tendency to become obese upon consuming excessive food. Our bodies were not built in an environment of excessive food, rather the lack of it.
From that point of view, “simulated” fasting acts to prime the body to a state of calorie deficit, which has been shown by many studies to have several beneficial effects, some of which are listed above. Intermittent Fasting can be performed in a number of ways and it is controversial whether one way is better than others. In some forms, some foods are allowed while some others advise complete fasting. The duration and timings also differ. Given this, one can experiment with a schedule that works best for them. Some suggestions are given below.
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Diabetes is the most challenging health problem of the 21st century with India being the diabetic capital of the world. More than 65 million Indians are affected from type 2 diabetes and the number is expected to double in the next 20 years. The most shocking news is that 270 million Indians are below the poverty line and yet there is an increase in the diabetic peak. Unlike other health conditions, diabetes does not seem to be inherited in a simple pattern, it is twisted and complicated with a combination of genetic make-up and environmental factors. Yet, most people are born with higher susceptibility to develop type 2 diabetes. According to ADA, the risk of developing type 2 diabetes is:
Type 2 diabetes is mainly caused by an interaction between our genetic makeup and our unhealthy lifestyle choices. Type 2 diabetes is a polygenic disorder where numerous genes have been identified as risk factors. The variation in genes confers some impairment in insulin secretion, utilization, and glucose & lipid homeostasis. If you have type 2 diabetes your body does not use insulin properly. This is called insulin resistance. At first, your pancreas will produce extra insulin to make up for it but, over a period of time, it cannot make enough insulin to keep the blood glucose at normal levels.
The root cause of type 2 diabetes is obesity. It runs down the family as they tend to have a similar lifestyle and eating pattern. Obesity is 80% correlated with diabetes. If you have a family history of obesity it becomes difficult to figure out if your diabetes is mainly caused due to lifestyle factors or genetic variations. It is natural that sedentary parents tend to have sedentary children and their unhealthy eating habits are passed on to the next generation. However, studies have shown that in obese individuals, by losing even 4 kg of the body weight, can reduce the risk of developing type 2 diabetes.
Here are 5 alternative healthy foods to knock out type 2 diabetes:
It’s never too late to start caring for yourself and Xcode provides products and services based on metabolic and fitness genotyping. Even if you carry a genetic risk variant, you can still minimize your risk by understanding your genetics and choosing the right food and lifestyle options that are compatible with your genetic makeup. So take action today to prevent and knock out diabetes.
SNP or Single Nucleotide Polymorphism can simply be termed as copying error made by cells during the process of making new cells wherein a ‘wrong’ nucleotide is present in the DNA sequence in the place of a ‘correct’ nucleotide. For e.g., let’s assume that the normal sequence of a particular section of DNA in humans is AATGCT. A SNP is when the sequence becomes AATGCA, where the last letter (nucleotide) instead of ‘T’ is replaced with ‘A’. These copying errors are like typographical errors which lead to variations in the DNA. These typos in DNA might affect protein function and structure, when present within genes that form these proteins. These variations in the DNA are the root cause for majority of health conditions, differences in response to drugs or diseases etc.
SNPs can be associated with lifestyle related conditions like diabetes, obesity and stroke. These SNPs also contribute to difference in food metabolism e.g. lactose intolerance.
With over 30 million people diagnosed to be diabetic, India is well on its way to becoming the diabetes capital of the world!
Diabetes mellitus is a metabolic disorder that occurs when the body cannot regulate the production or usage of insulin. Insulin is a hormone that converts sugar, starches, and other food into energy. This energy is either used immediately or stored as fat or glycogen. In a diabetic, the body does not produce enough insulin to move the sugar into cells, and the sugar gets accumulated in the blood.
Type 2 diabetes occurs later in life and hence is referred to as adult-onset diabetes. In type 2 diabetes, the muscle and fat cells in the body become resistant to insulin which causes the pancreas to make more insulin. As long as the pancreas continues to produce insulin to overcome this resistance, blood glucose levels remain normal. However, after several years the resistance of the cells continues to increase and the pancreas begins to produce lesser insulin. This result in hyperglycemia (abnormally high levels of sugar in the blood) and the symptoms of type 2 diabetes start manifesting. Type 2 diabetes is most often seen in obese or overweight people and the elderly.
Type 2 diabetes is asymptomatic in the majority of the cases over a long period of time. If symptoms do occur, they include fatigue, increased hunger (polyphagia), frequent urination (polyuria) and increased thirst (polydipsia), blurred vision, erectile dysfunction, and poor wound healing.
Genes have a role in glucose metabolism, and genetic variations within these genes affect their function, thereby increasing the risk for type 2 diabetes.
