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The methylenetetrahydrofolate reductase (MTHFR) mutation report provides information about the common polymorphisms in the MTHFR gene, which are associated with increased levels of homocysteine in the blood.
MTHFR is a gene that codes for the enzyme called methylenetetrahydrofolate reductase (MTHFR). This enzyme is responsible for the conversion of inactive folate to active folate. A variation in this gene in some people can disrupt this conversion and lead to various health problems.
Some signs of MTHFR polymorphisms are cardiovascular and thromboembolic diseases, anxiety, bipolar disorder, colon cancer, and chronic pain.
Not all MTHFR gene variations are associated with significant MTHFR enzyme activity. There are two important MTHFR SNPs, rs1801133 and rs1801131, associated with the MTHFR enzyme activity. These variations affect approximately 1 in 4 people significantly and about 1 in 2 people mildly.
Information about the variant of these two highly significant genes is present in the table titled “Prominent MTHFR SNPs.”
The MTHFR enzyme activity is provided as a bar diagram below the table titled Prominent MTHFR SNPs. It is based on the two prominent SNPs.
Apart from the two important MTHFR SNPs, there are other variations in the MTHFR gene which are associated, in varying degrees, with MTHFR enzyme activity. Information about these SNPs is included in the table titled “Other MTHFR SNPs.”
The presence of a large number of homozygous (2 risk variants- red color) of high ranking SNPs may be associated with lower enzymatic activity and higher homocysteine levels.
Certain SNPs are found to have a higher impact, and variations in these SNPs may have a greater impact on health. The ‘Rank’ is indicated as ‘high,’ ‘medium, and ‘low’ depending on the potential impact. Please bear in mind that the Rank is a theoretical value and not experimentally verified.
The column ‘normal’ (e.g., C) is the variant associated with normal enzyme activity, while the column ‘risk’ (A) is the variant associated with reduced enzyme activity. ‘Geno’ refers to your genotype.
Disclaimer: As always, please bear in mind that human traits are a result of complex interactions between multiple genes and multiple environmental factors. The findings presented in this report are of a preliminary nature and are not considered clinically- or medically- actionable.
For years, diets called for the elimination of fats, urging us to move towards low-fat alternatives. While, like any other nutrient, overdoing fats can lead to weight gain, cutting out dietary fats need not necessarily result in weight loss. Replacing bad fats (trans fats, saturated fats) with good fats (mono and poly-unsaturated fats) comes with benefits that extend beyond weight loss. This article covers everything there is to know about incorporating monounsaturated fats in your diet.
Fats are an important component of any meal as they help in absorbing fat-soluble vitamins and minerals.
They also store energy within the body, protect vital organs, and help in muscle movement.
Fats are chains of carbon and hydrogen, and depending on the length of these chains and the arrangement of these atoms, they are classified into different types of fats.
The “mono” in monounsaturated fats represents the single double bond that is found in its chemical structure.
Owing to this chemical structure, monounsaturated fats are often liquid at room temperature.
Anthropologists claim that the diet of early humans was more similar to that of modern chimpanzees. They consumed fruits, vegetables, leaves, flowers, and meat. It is believed that meat was first consumed about 2.6 million years ago.
However, our early ancestors engaged in scavenging food rather than hunting. They consumed the edible portions of flesh that were left behind by the predator. Jesicca Thompson, an anthropologist from Yale University, says that the early humans consumed bone marrow stuck in between the bones of the dead animal rather than the “meat.” The marrows are rich in fat content. Thompson claims that it was around this time that humans started adding fat-rich food to their diet.
Modern-day diet has monounsaturated fats in vegetable and seed oils. A study confirmed that the first use of vegetable oil, particularly olive oil, was seen around 8000 years ago in the Middle East. But it was in the 1600s when people started making oil from vegetables.
The 1800s saw the widespread use of vegetable oil as the commonly used whale oil became expensive. In the process of making affordable soaps using cottonseed oil, two industrialists in Cincinnati took the opportunity to introduce it in the food industry. In a few years, animal fats were replaced by vegetable cooking oils, and we can still find them in our kitchens today.
Studies observed that people from the Middle East or the Mediterranean countries had a lower risk of heart diseases, despite consuming a fat-rich diet. Further investigation showed that their diet included olive oil and other seed oils as their main source of fat and not animal fat. This could mean that the health benefits come from unsaturated fats rather than saturated fats from animals.
A study consisting of around 840,000 adults aged 4-30 years found that the consumption of monounsaturated fats reduced the risk of heart disease by 12%, compared to the control group (little to no monounsaturated fats consumption)
Monounsaturated fats improve overall health by:
Sources of monounsaturated fats are olive oil, peanut oil, avocados, nuts, safflower, and sunflower oils.
Weight gain is caused when the calories consumed are greater than the calories burnt.
All fats provide the same amount of energy, which is about nine calories per gram.
Based on your lifestyle and your basal metabolic rate, including the right amount of fat in your diet, can help with weight management.
Even though weight gain/loss is a simple equation of calories in and out, the quality of the food you eat as part of your diet is very important.Some studies have shown that if calorie intake remains the same, diets high in MUFAs lead to weight loss and could even be more effective than a high-carb diet.
It is recommended to use monounsaturated fats as a replacement to saturated or trans-fats as much as possible.
The 2015 Dietary Guidelines for Americans suggest that fats should be limited to 25 to 30% of the total daily calories; this includes all types of fats.
This gene is involved in the control of fat metabolism (break down) and insulin sensitivity (how well your body responds to insulin) in the body.
Changes in this gene directly affect anti-diabetic, anti-atherogenic (preventing fatty deposit formation), and anti-inflammatory activities.
The gene codes for a protein called the adiponectin, that is involved in aids fatty acid breakdown. Higher the adiponectin levels, more efficient the fatty acid breakdown.
Decreased adiponectin levels are thought to play a central role in obesity and type 2 diabetes.
Changes in lifestyle, such as incorporating exercise and a following balanced diet, that result in weight loss, can lead to an increase in adiponectin concentration and increase insulin sensitivity.
A study found that a variation rs17300539 in the ADIPOQ gene can lead to a difference in blood adiponectin levels.
Individuals with a G allele have lower blood adiponectin levels when compared to those with an A allele. Carriers of the A allele (AA/AG), therefore, had lower weight, BMI, waist, and hip circumferences.
While considering the monounsaturated fats intake of greater than 13% of the total energy intake, the A allele carriers had a considerably lower BMI compared to GG carriers.
This shows a relationship between the effect of a gene on monounsaturated fats intake and weight.
NR1D1, also known as Rev-ErbA alpha, is present in the liver, skeletal muscles, adipose (fat) tissues, and the brain in mammals.
Adipogenesis is the process by which adipocytes, or fat cells are formed.
Rev-ErbA alpha includes adipogenesis and could be a potential target for novel anti-obesity treatments.
A study analyzed the association between NR1D1, monounsaturated fats intake, and weight in North American and Mediterranean populations.
People with the AA and AG types had a lower waist circumference and a decreased risk for obesity than people with the GG type.
The A allele occurrence was also significantly low in the ‘abdominally obese’ group.
There was also a significant interaction for obesity with NR1D1 and monounsaturated fats intake in the Mediterranean population.
Individuals with the A allele had higher protection against obesity with diets rich in monounsaturated fats. (>55% of total fat).
PPARG is a gene predominantly present in adipose tissue. It plays a role in adipocyte differentiation (converting one type of cell to another), regulating glucose levels, and insulin signal transduction (communication between two cells).
A change in this gene has been studied to play a role in increased sensitivity to insulin and a more favorable lipid profile.
A study recruited overweight subjects between the ages of 20-65 years in southeastern Spain.
They analyzed the subjects as they underwent a treatment program for obesity.
This included analyzing the diets and the number of calories expended during exercise.
They found a gene-diet interaction between PPARG and monounsaturated fats intake.
People who had the G allele (CG/GG) were significantly less obese than those with the C allele (CC) - when monounsaturated fats intake was high (>56% of total fat).
This difference disappeared in low monounsaturated fats diets.
Overall, in each case, diets with high monounsaturated fats intake (>55% of total fat) resulted in a greater weight loss in individuals.
Most foods have a combination of all types of fats. Foods and oils that have a higher percentage of MUFA are:
Fats are a necessary component in a balanced diet. However, not all types of fats are healthy. While saturated fats are the ‘bad fats,’ the unsaturated fats are ‘good fats.’ Monounsaturated fats or MUFAs are fats joined by a single bond. They help reduce the risk of health conditions like diabetes and cancer. They also enhance insulin sensitivity and, therefore, play a role in weight management. Several genes ADIPOQ, NR1D1, and PPARG, mediate how your body responded to MUFAs in terms of weight gain. People with certain types of these genes tend to benefit more from MUFA consumption in terms of weight loss and can include more MUFA-rich foods in their diets. Some food sources of MUFAs include avocados, olive oil, peanuts, and eggs. Even though MUFAs are present in certain animal sources like red meat, their benefits are negated by the saturated fats in them.
There are many different types of genetic tests that are used for a range of applications, from ancestry analysis to diagnosing clinical conditions like Alzheimer’s. The type of genetic test to be performed is based on your reason for testing. Each type of test differs in the information it can provide, the amount of data obtained from it, its cost, accuracy, and even the sample used for the test (saliva, blood, hair, etc.).
Genetic testing is used to identify the changes in your DNA sequences, also known as mutations or variations.
As a simple example- if the word “APPLE” were a gene sequence, it will be spelled correctly in the majority of people; however, you may carry a “variation” of this gene that is spelled as “APBLE.”
Biologically speaking, many of these changes are harmless, meaning small spelling variations do not alter the individual’s health. However, some variations are harmful or advantageous to varying degrees.
The analysis of your DNA data reveals what variations are present in your DNA and their effects on your health.
The genotyping test is one of the most inexpensive tests available in the market. This test is also very popular among consumers since it is widely marketed by many direct to consumer (DTC) genetic companies like 23andme and AncestryDNA to perform ancestry and health analysis.
Genotyping reveals the differences in a sample DNA sequence by comparing it with the reference DNA sequence.
As a simple example, if A-P-P-L-E is the reference gene sequence, and the sample sequence is A-P-B-L-E, genotyping tests will be able to detect the P→ B change. This kind of change in a single letter is called a single nucleotide polymorphism (SNP). Your genome contains around 4-5 million SNPs that may be unique to you.
Most SNPs do not have any significant health implications; however, some of these differences may be indicative of the development of certain health conditions or certain unique traits related to your health and wellness. They can be advantageous or disadvantageous to various degrees. These DNA variants or genotypes may act alone or in concert with a few to several hundred other DNA variants to create a health impact.
Genotyping has a broad range of applications, including ancestry, pharmacogenomics (ADME), fingerprinting, clinical and health conditions, and lifestyle and wellness traits. Though generally, genotyping is not the test of choice for health or clinical applications.
A note on genotyping:
Genetic tests based on the genotyping chip method have an accuracy of more than 99% when performed using standardized protocols in certified labs. However, even the less than 1% inaccuracy amounts to a few hundred variants, some of which can be important. Typically, genotyping tests are not used for clinical or diagnostic purposes.
The full human genome is 3 GB in size. You can imagine a book with chapters, pages, paras, and sentences which is 3 GB in size. Your clinician may only be interested in para two on page 100 in chapter 3 because it is relevant to the condition he/she is treating you for. He will order a test for your known as targeted sequencing, which is designed to read specific segments of the DNA. This test is much cheaper than reading the whole genome and has a significantly shorter turnaround time.
Targeted sequencing is typically used for:
Though the genome is 3 GB in size, much of it is filled with pages that scientists don’t yet understand the meaning of. Approximately 98% of the genome is not yet understood. The 2% that scientists do understand is known as the exome. Many people prefer to go for a test that reveals the information in their entire exome- this is known as Whole-Exome Sequencing (WES).
Exome sequencing is typically used for:
If you prefer to have your whole genome analyzed, a Whole-Genome Sequencing (WGS) test is what would be performed for this purpose.
Whole-genome sequencing is typically used for:
The accuracy of sequencing tests depends on what is known as ‘Coverage.’ Coverage, also termed as ‘sequencing depth,’ refers to the number of times the DNA sample gets sequenced. Essentially, the higher the number, the higher the accuracy.
| Technique | Cost | Site | Coverage | Data Size(depends on coverage) |
| Targeted sequencing | $300-$1000 | The specific region of interest | 200-1000x | 100 MB–5 GB |
| WES | $500 - $2000 | Exome | 150-200x | 5 GB–20 GB |
| WGS | $1000 - $3000 | Genome | 30-60x | 60 GB–350 GB |
Before choosing a genetic test, it’s important to keep in mind a few points:
Recently, DTC genetic tests have become very popular due to a combination of reasons:
The cost of genetic testing in general has been decreasing primarily due to technological advancements and increasing consumer demand.
Over the last few years, the self-testing trend has gained popularity due to an increase in self-awareness and self-monitoring.
This trend is facilitated by self-learning over the internet and other media and the availability of low cost internet-connected wearable devices enabling us to understand our bodies better.
Personalization in various aspects of health and well-being. We are at the end of the one-size-fits-all era.
We understand that carbohydrates are not equally bad for everybody, fat does not always cause high cholesterol levels, and COVID-19 does not affect everyone the same way.
Genetics enables us to understand our uniqueness in several aspects of life.
Ancestry testing is the largest segment in DTC genetic testing. People love understanding where their ancestors came from- their genetic genealogy.
Not only that, The DNA data also allows people to discover their biological parents, siblings and other relatives through a variety of online services!
If you have received DTC genetic reports from one of many sources available, you may have come across the following:
There could be several reasons for this:
Some examples of mismatch between self-observation and your genetic results:
> You have been drinking milk all your life without complaints, but your genetic test results indicate that you are lactose intolerant.
> Your genetic results indicate that your are NOT gluten intolerant, however, you have issues consuming gluten.
The above are but a few examples of how there might be a mismatch between your genetic results and your own observations about yourself.
Regardless of the reasons below, please remember that your observations or your physicians/healthcare professional’s assessment of your health overrules the findings of the genetic test report.
In other words, your consumer genetic test report is always secondary to other assessments.
Genetics is about probability. Having a variant only increases the likelihood that the association may be true for you, but it's not certain. It’s very much possible that other genetic and non-genetic factors overcome the association.
Regardless of what your fitness goals may be, aerobic capacity is an important metric to focus on. It determines how well your body can utilize oxygen. Simply put, the better the aerobic capacity, the longer you will be able to sustain exercises. Aerobic training not only helps achieve peak fitness but also improves cardiac health and respiratory functions. An individual's genetic makeup can determine up to 50% of their aerobic capacity by influencing factors such as antioxidant production, heart functioning, etc. The analysis of such genes and their variants can give a clearer idea of the kind of training you need to take on to achieve maximum results.
Aerobic capacity (AC) is the maximum amount of oxygen consumed while performing intense activities that involve large muscle groups.
It is also a measure of how effectively the heart and the lungs get oxygen to the muscles. Hence, improving your aerobic capacity can directly result in more efficient use of oxygen by the body.
The other term which is used to describe aerobic capacity is vO2 max.
However, the vO2 max also takes into consideration the individual's body weight.
One of the best ways to estimate your cardiovascular fitness is by calculating your Aerobic Capacity.
If you are in a fitness center, one of the following two techniques can be used to measure your AC
A simpler and less accurate way of measurement is a walk/run test.
This requires walking/running at the maximum speed you can and measuring your heart rate at the end of it.
With this measurement, you can use one of the many online calculators that are available to check your Aerobic Capacity.
For instance, Rockport walk test is one such calculator that requires the input of your heart rate, time of the run/walk, and your weight to calculate your Aerobic Capacity.
Genes majorly control a lot of factors that have an association with the fitness levels of an individual.
According to a study in 2016, 155 genetic markers were found to be associated with better athletic performance, 93 of which were endurance-related markers, and the other 62 were power/strength related markers.
Polymorphisms of ACE, ADRB, ACTN3, PPARGC1A were one of the first genetic markers found to be associated with athletic performance.
There's another famous exercise genetics study conducted by a consortium of five universities in the United States and Canada revealed astonishing variation in the aerobic capacity amongst the 481 participants.
The study subjected its participants to identical stationary-bicycle training regimens with three workouts per week of increasing intensity under strict control in the lab.
The results
These can be attributed to the variants of genes like NRF1, NRF2, VEGF, PPARA, etc. that an individual carries.
The nuclear respiratory factor (NRF2) gene influences the vo2 max. NRF2 regulates the expression of antioxidant proteins and thus can influence the oxygen uptake.
| Genotype | Implication |
|---|---|
| AA | 57.5 % higher training response |
| CC | Normal training response |
Some genes affect a few secondary traits that exert influence on aerobic capacity.
For example, genetic variations in VEGF in the gene influence heart structure, size, and function. These have an impact on the stroke volume which is an important determinant of aerobic performance.
| Genotype | Implication |
|---|---|
| GG | Reduced aerobic performance |
| CC | Normal aerobic performance |
Genetics is only 50% of the fitness story.
The rest wires down to other factors like your lifestyle, your eating habits, and your training.
Getting at least 150 minutes of moderate aerobic exercise, or 75 minutes of vigorous activity each week is vital to ensure a longer healthier life
Augmenting your aerobic capacity can result in better blood and oxygen flow to muscles.
Therefore, this promotes faster recovery between sets and improves your flexibility.
Aerobic exercises include walking, running, cycling, swimming, and almost every other cardio workout.
When aerobic exercises are performed, your heart is trained to deliver more oxygen in a said span of time, and at the same time, your muscles are trained to utilize the oxygen delivered more efficiently.
To improve your aerobic capacity, it is important to understand how your body builds endurance.
It depends on the following three things:
When you train to increase all the above-mentioned variables, naturally the amount of blood and oxygen, reaching your muscles increase.
This, in turn, has a positive effect on your overall athletic performance.
Aerobic training usually, targets large muscle groups of your body that boost your heart rate for longer periods of time.
Some of the commonly recommended aerobic exercises include
Some of the aerobic exercises that you can do at home include:
If you are already not inspired to take up aerobics, take a look at the benefits you can acquire from aerobic training.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4114002/
https://www.ncbi.nlm.nih.gov/pubmed/17357964
https://www.ncbi.nlm.nih.gov/pubmed/25729143
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Ever wondered how some people run multi-million dollar companies along with a gazillion other philanthropic work? Read on to understand more about entrepreneurship potential and the debate about its source of origin.
From selling cupcakes to running a multi-million dollar biggie, entrepreneurs form a diverse spectrum.
Any business idea, transformed into a business model to serve customers/clients fall under entrepreneurship.
But most of them, who run big or small successful businesses have some highly similar qualities.
It takes more than just an idea to be a successful entrepreneur.
The first "light bulb" moment is only a start to a snowball of those to follow. Initially, setting up an idea means having to act as five different roles in one.
Granted we have a lot of resources online, but to gather the motivation and humility to be able to understand and learn new things and then adapt that into your idea of a business model, takes quite some time.
So, first and foremost, patience is key.
And most definitely, you would have to disable ‘autoplay’ on youtube, too bad Netflix doesn't let you do that!
Understanding a market gap and tapping into that potential is extremely important with new ideas.
Your cupcakes might taste out of the world delicious, but what is the customers’ incentive to buy them, if they can find great cupcakes (tried and tested) from Costco?
What if you add a factor of customization, say you provide the customers icing essentials to make it their own?
That might make it interesting.
Understanding what the customers need and delivering, is one of the most crucial components of entrepreneurship.
When American computer scientist, Paul Graham was asked what are the most important things to remember to become a successful entrepreneur, he said, surrounding yourself with good, efficient people, finding the best market-product fit and spending as little money as possible.
These frame a 3-step activation for your success account. If either of them fails to happen, it could be significantly hard to create a successful empire.
A successful entrepreneur in one of his books talks about how running a startup is like juggling.
It creates an illusion that you’re balancing three balls mid-air but in reality, a juggler focuses on one ball to balance the rest.
This is how entrepreneurs deal with multitasking.
By prioritizing the right task at the right time. It is crucial to identify the most important problem and solve that first.
“Most of us spend too much time on what is urgent and not enough time on what is important.”
Stephen R. Covey
It’s all about smart working
Hard Work is not the only key to success. Many entrepreneurs have seen success in hiring people who do smart work.
"Hire a lazy person to do a difficult job they will find an easy way to do it"
Bill Gates
Entrepreneurs have to be constantly driven to work towards success.
All successful entrepreneurs have their dull days and depressing mornings.
They too get distracted with the sweet smell of freshly sprinkled earth or a fresh batch of cookies.
It’s about how they bring their attention back to work, which is admirable.
A famous tech expert, Aytekin Tank says finding this grit, to keep up with a goal for a lifetime comes from endless motivation and learning to overcome resistance.
Coming up with routines that get our body and mind prepped to do a task could make a significant difference.
Love is not the only kinda north star we need.
Having a life vision and mission for a company helps with clear growth and better focus towards the end goal.
In this ever-changing world, be it Twitter or LinkedIn there is a 200-300 character limit to say what you have in mind.
It’s highly crucial to stay focused and walk towards your north star.
It’s common to see entrepreneurs sound profound and knowledgeable.
But the successful ones are almost always curious to understand more.
This constant need to understand and reinvent helps with rapid growth as the approach would be customer-centric instead of it being driven by trends based on market competition.
Despite the common assumption that reading about entrepreneurship doesn't help you become one, it is important to read and understand experiences to avoid common mistakes and be exposed to different business models.
Of course, we are no Bill Gates who can read about 750 words per minute and follow that with a 90% retention rate but we sure can try!
It’s not uncommon to see nepotism in the Business world.
Even The President of the United States, Donald Trump took over his father’s company, and now, his sons run the Trump empire.
There are endless debates on how businesses run successfully for generations.
Though arguably, it’s a matter of convenience to pass on power to our kin, studies suggest that genetics could contribute a fair share to why they run successfully.
Here’s some complex math for you:
Behavior patterns = Complex
Genetics = Complex
Behavioral Genetics = ? (haha, complex math)
Behavioral Genetics is barely black and white.
It’s hard to figure out what shade of grey we are looking at (we might need Christian’s help on that one!).
Since behavior entails what you are and what you see, it involves a great deal of both environmental factors and multiple genes that contribute to one trait of ours.
In the recent past, there has been emerging research conducted on such grey areas of behavioral science.
Thanks to all the mass observations about business tycoons, entrepreneurship has been one such potential studied.
Most genetic research, to resolve debates of behavior, always conducts studies on twins.
Their high similarity in genetic makeup leads to more conclusive results than in general human studies.
Studies have shown that 30 to 35% of the entrepreneurial traits could be attributed to heritability.
Though this implies that environmental factors contribute to the rest of the major 70%, 1/3rd of the fraction is a significant number to make or break, in this fast-paced world.
Nonetheless, having a genetic predisposition only increases the likelihood of becoming a successful entrepreneur, but that has to coincide with various other environmental factors and maybe a few tik-tok videos to make it big in this world.
As organizational behavior is a higher-order function, genes that are related to it often are responsible for very brainy activities.
Brain activities control the release of different brain chemicals like neurotransmitters and these activities are controlled by different genes responsible for their action.
For example, Serotonin levels can contribute to the attitude of ‘taking chances’.
This would help you be less risk-averse which is beneficial for an entrepreneur.
As we are all humans and the genetic outline is pretty much the same, we often find different variations of one particular gene.
These range from the tiniest of a change at a nucleotide level (the fundamental unit of the DNA structure) called Single Nucleotide Polymorphisms (SNPs) to big structural variations where chunks of the DNA are cut out, duplicated, etc.
These are often causes of genetic diseases.
But SNPs are the most common type of variation known to human beings.
The outcome of the variations depends on the extent of its influence in the gene.
The functions of the gene could be altered, like structuring a protein or if it is a regulatory gene, it might affect that function.
Some of these variations could make us susceptible to different traits.
This applies in case of behavioral traits too.
Now, these different variations make us susceptible to traits that are common in successful entrepreneurs, it increases our likelihood of becoming one, too.
The likelihood increase would take place only with the possession of the uncommon variation, often referred to as the minor allele.
A major study conducted to understand the genetic influences in self-employment discovered SNPs in the gene RNF144B, indicating an increased probability of being self-employed.
The minor allele T, of an SNP in this gene, has an association with an increased probability of being self-employed.
| TT Genotype | Increased probability of being self-employed |
| CC Genotype | Normal entrepreneurship skills |
The SNPs of the SV2C gene was also part of the study with two different variations. RNF144B is a gene that codes for a structural protein.
SV2C on the other hand codes for brain transport proteins called synaptic vesicles. So the range of the involvement of these genes is extremely varied.
| AA Genotype | Increased probability of being self-employed |
| GG Genotype | Normal entrepreneurship skills |
Several other genes also have an association with entrepreneurship potential.
To quote an example from Scott Shane’s best-seller:
Born Entrepreneurs, Born Leaders: How Your Genes Affect Your Work Life
Some people might have a version of a gene that increases their odds of making large financial bets, but the influence of this gene on risk-taking might only be manifest in high-pressure, short-time-to-make-a-decision situations, such as currency trading operations.
Thus, the gene might not influence managers’ decisions to gamble billions of dollars on new technologies after months of careful evaluation, but it might affect traders’ choices to bet billions of dollars on currencies in a few seconds on foreign exchange markets.
This also helps us understand how there are no binaries with these behavioral traits.
However, the genetic predisposition only increases the likelihood of your entrepreneurship potential.
If the person who is good with big financial bets never explores a career in a Wall street set-up, he would never discover his potential.
The rest of the environmental factors HAVE to coincide to create a successful entrepreneur.
This could be as fundamental as having the means to source capital for the implementation of the business idea.
Entrepreneurship potential still has many unknowns we are yet to explore.
But we have to understand and acknowledge that various factors are contributing to an entrepreneur’s success.
Be it genetic or environmental, it is a life-long journey of being best at what you do.
Being successful in any field takes some serious perseverance and commitment.
So, regardless of the origin of our instincts, let’s try to be good at what we do!
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Our body is fueled everyday by different nutrients – some that are required in larger quantities while others in lesser, and few in traces amounts. Some nutrients form structural components of our cells whereas, there are others that participate or regulate various functions and processes in the body. One such trace mineral, and an essential one too, is copper.
Our body needs minerals for various physiological processes.
While some minerals are needed in larger quantities like sodium, calcium, and potassium, some like copper are essential trace minerals that are vital for survival.
Copper is found in all body cells and plays an important role in the formation of blood vessels, maintenance of the nervous, and the immune system.
Our body has about 2 mg of copper per kilogram of body mass.
Though copper is found in all parts of the body, organs like the liver, kidney, heart, and the brain have it in higher quantities.
As mentioned earlier, our body needs copper for plenty of activities. These include:
Intake of less than the Required Dietary Allowance (RDA) of copper can lead to copper deficiency whereas, taking in more than the RDA can lead to copper toxicity, both of which can be harmful.
For adolescents and adults, the RDA is about 900 mcg per day.
Any intake above 10,000 mcg or 10 mg per day can be toxic.
The copper requirement of the body changes with age, gender, and conditions like pregnancy.
| Age | Male | Female | Pregnancy | Lactation |
|---|---|---|---|---|
| 0-12 months | 200 mcg | 200 mcg | ||
| 1-3 years | 340 mcg | 340 mcg | ||
| 4-8 years | 440 mcg | 440 mcg | ||
| 9-13 years | 700 mcg | 700 mcg | ||
| 14-18 years | 890 mcg | 890 mcg | 1000mcg | 1000 mcg |
| 19+ years | 900 mcg | 900 mcg | 1300 mcg | 1300 mcg |
Copper deficiency can occur due to diet, nutritional deficiencies, or digestive issues resulting from surgeries or other conditions.
These are called acquired copper deficiencies.
Another type of copper deficiency is inherited copper deficiency that is genetic in origin.
Surgeries like bariatric surgery, gastrectomy, upper GI tract surgery, and other stomach surgeries result in copper deficiency.
Inherited copper deficiency is rare and affects one in every 1,00,000 births.
The gene causing this condition is inherited in an X-linked recessive manner and runs in families.
The SELENBP1 is located on chromosome 1 and is a part of the selenium-binding protein family.
Selenium is an essential mineral and is known for its anticarcinogenic properties and a deficiency of it can result in neurologic diseases.
The protein encoded by the SELENBP1 gene is said to play a selenium-dependent role a ubiquitination/deubiquitination-mediated protein degradation.
One of the phenotypes for the SELENNP1 gene is serum copper measurement.
The presence of the G allele in this SNP causes a decreased absorption of copper resulting in an increased risk of developing a copper deficiency.
The SMIM1 gene or Small Integral Member Protein 1 is located on chromosome 1 and codes for a small, conserved protein that takes in part in the formation of red blood cells.
The A allele of the SNP rs1175550 is associated with serum copper measurement.
The main problem with copper deficiency is that it is hard to diagnose as its symptoms are very similar to other nutritional deficiencies such as vitamin B12 deficiency.
Since low copper levels in the body can affect a person’s immunity, it is important to identify it in time.
Clinical symptoms of copper deficiency include:
Copper deficiency can also be recognized hematologically as it presents with a triad of anemia, neutropenia, and thrombocytopenia (rare).
Copper deficiency is usually not the first thing that is diagnosed when one presents with symptoms as many nutritional deficiencies present with similar clinical symptoms.
However, your doctor may suspect copper deficiency if you have a history of any of the following:
If your doctor suspects a copper deficiency, he/she may order a blood test for detecting plasma copper levels.
However, one must note that this is not a conclusive test for copper deficiency as many other factors can cause a false elevation of blood copper levels.
The first step in the treatment of copper deficiency is identifying the cause and removing or treating it.
For example, if the copper deficiency is due to excess zinc supplements, your doctor will reduce the zinc supplements to allow more absorption of copper.
Many a time, doctors prescribe copper supplements to make up for the deficiency of the mineral.
Common copper supplements include copper sulfate, copper gluconate, and copper chloride.
It can take about 4 to 12 weeks to treat a copper deficiency.
Taking 2 mg of copper per day can help restore normal copper levels in a deficient individual.
However, the exact dosage is determined by a doctor after evaluating other health and lifestyle factors.
In the case of individuals who cannot take oral copper supplements, they may be put on IV copper treatment.
Along with copper supplements, consuming copper-rich foods can really help.
Copper is an essential mineral for the body but it is also a trace mineral which means that our body needs a very little amount of copper to function.
However, many people suffer from a deficiency of this mineral that can result in complications over a period of time.
Some people who require copper supplements include:
However, care must be taken to consult with your doctor before taking copper supplements as copper toxicity can be as harmful to the body as copper deficiency.
Apart from this, people who have had surgery such as bariatric surgery, gastrectomy, or those who suffer from GI tract diseases such as IBS, celiac disease, etc., also need supplements as they are more likely to have copper deficiency due to the poor absorption.
There are certain rules to follow when taking copper supplements. We know that zinc interferes with copper supplements and so, avoid taking both zinc and copper supplements at the same time.
Fix two different times for both supplements and stick to these times every day.
Ideally, take your copper supplement at least two hours after taking your zinc supplements for maximum absorption.
Copper supplements can cause stomach irritation and acidity, and hence, copper supplements can be taken with meals can help reduce irritation.
Many people who take antacids may need higher dosages of copper supplements as antacids interfere with the absorption of copper.
Copper supplements can cause side effects and the common ones are:
There are symptoms of overdose that one must watch out for and avoid:-
Apart from supplements, diet plays an important role in restoring normal copper levels in the body.
To treat copper deficiency and maintain optimum copper levels in the body, some copper-rich foods that you can include in your diet are:
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https://ods.od.nih.gov/factsheets/Copper-HealthProfessional/#en3
https://www.genecards.org/cgi-bin/carddisp.pl?gene=SELENBP1
https://www.snpedia.com/index.php/Rs2769264
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3766178/
https://www.genecards.org/cgi-bin/carddisp.pl?gene=SMIM1&keywords=SMIM1
Ever wondered how going off carbs for a couple of days almost always shows instant results? Thank all the glycogen stored in your body. But some people have trouble storing this entity as we do, disrupting their chance to live a typical life. Let’s peak into what actually happens with Glycogen Storage Disease.
Metabolism is a biological process that breaks down the food we eat and provides energy to keep us alive.
In some cases, different key stakeholders in this process fail to fulfill their duty.
There is a spectrum of conditions that fall under the umbrella of Glycogen Storage Disease (GSD), which cause such trouble.
Since it did not have any popular awareness challenge go viral (bring back the ice buckets!) and fortunately is a rare condition, it hasn’t had too much light thrown on it.
According to the reports, the incidence rates appear to be 1 in 100,000.
As the symptoms set out at an early age, Glycogen Storage Disease appears to affect the little ones more than the adults.
Our body uses glycogen, a complex sugar compound, as a fundamental storing unit of energy. Metabolizing glycogen, to break it down into glucose, provides the instant energy we need. As we need to conserve some of this energy, these glucose molecules are combined back into glycogen. This is used as a reservoir to tap into when there is a lack of energy supply. Different parts of the muscles and the liver act as storage units for glycogen.
For this process to take place, some special proteins called enzymes (biocatalysts) aid the formation and deformation of glycogen.
When these enzymes don't function optimally, it leads to a spectrum of diseases.
This could lead to a range of different symptoms depending on the type of diseases.
The types are classified based on the enzyme which is at fault. It starts from GSD1 and runs up until GSD 15.
The types 1 to 4 cover almost 90% of the reported cases, with sub-type of GSD1 - GSD 1a, aka Von Gierke Disease being most common.
As the condition affects the necessity of food metabolism, symptoms start to show 3 to 4 months after birth.
The cause of Glycogen Storage Disease is genetic.
The gene that is responsible for the malfunction of the enzyme can pass on from the parent generation to the next, making it hereditary.
But the child will express symptoms of the associated GSD, only when both parents possess a defective gene.
Every human gets their 23 chromosomes from each parent.
Genes that are subunits to chromosomes have one trait, which is dominant and other recessive (some exceptions, of course).
The level of expression marks the difference between them.
Now, for the expression of a recessive trait, both parents must pass on their recessive versions of traits.
The Mendelian world calls this an autosomal recessive condition.
A random process selects the gene to be passed down to the next generation.
In the case of autosomal recessive conditions, there is a 25% chance of occurrence.
If just one parent passes it on, then the child will remain healthy but acts as a carrier of the gene.
Carriers could potentially pass it on to the coming generations.
We obtain glucose from the diet we eat.
Glycogenin is an enzyme that is responsible for cutting down this glucose into short fragments.
Another enzyme, glycogen synthase, helps in the conversion of glucose into Glycogen.
Now, some branching enzymes add branches to Glycogen, which the liver then stores as a reservoir of energy.
When we fast or there is a need for muscle contraction, the body taps into the said reservoir.
The process of breakdown involves four enzymes.
Glycogen Phosphorylase and glycogen debranching enzymes help in unraveling the molecule to release glucose and expend energy.
Another method of breaking it down involves enzymes such as a-glucosidase and Glucose-6-phosphatase.
Every action in our body is instructed by the beautifully wound helix, DNA.
As these enzymes correspond to specific genes, any defect in this gene will directly translate into the enzyme’s action.
Take the example of the most common type of GSD - GSD type 1a.
One of the enzyme genes involved in breaking down glycogen is Glucose-6-phosphatase. G6PC and SLC37A4 genes code for this enzyme.
As genes code for proteins and proteins like enzymes carry out the function, an error in the gene structure or function will lead to a collapse of the entire system.
A good analogy would be a loose brick in a building that could make it fall into pieces. Geneticists call these errors, mutations. As these ‘errors’ have been major contributors in the history of evolution, they have been beneficial in many ways.
Unfortunately, not in the case of Glycogen Storage Diseases.
So, when there is a mutation in this gene, glucose-6-phosphatase does not play its role and leads to the build-up of Glycogen and fat.
We know, too much of anything is toxic. Hence, the accumulation of Glycogen and fat hinders the function of organs like liver and kidney.
In the case of type 3 Cori disease/Forbes disease, a distinct part of the gene, called Exon3, carries two mutations that cause the debranching enzyme to malfunction.
As a debranching enzyme is responsible for the decomposition of Glycogen, it leads to toxic accumulation.
Andersen disease (type 4) affects the GBE1 gene that codes for glycogen branching enzyme leading to large amounts of abnormal Glycogen accumulated, causing severe conditions like liver cirrhosis, which is ‘doctor’ for scarring.
Types 1, 3, and 4 are far more common in comparison to other types.
Most often, all different types have a combination of some common symptoms in varying intensities.
As the age of onset is rather young in the case of Glycogen Storage Diseases, doctors generally ask the parents about symptoms showcased by their child and call for relevant tests.
Blood tests and MRI/ultrasound scans are routine. In some cases, a biopsy of a suspected organ might be required for confirmatory diagnosis.
Genetic testing has evolved over time and is performed to confirm the diagnosis.
This is extremely helpful in the case of couples who have observed a family history of Glycogen Storage Disease.
Seeking genetic counseling before planning a family will help provide a clearer picture of the chance of occurrence in their case.
Carrier testing for at-risk family members and prenatal diagnosis have led to significant changes in family planning.
The treatment options are specific to the type of GSD diagnosed with the patient.
Generally, it includes major dietary restrictions.
Uncooked corn starch can be a good feed to children over two years of age, as corn starch can promise a slow release of glucose.
This is fed in small portions throughout the day.
For type 1, elimination of food which is high in lactose and fructose is advised (that's pretty much everything tasty, from mozzarella to maple syrup).
Allopurinol is prescribed if there is a risk of kidney stones or gout, as it reduces the levels of uric acid in the blood.
Some extreme cases like the type 4 of GSD could require liver transplant depending on the extent of the condition.
When the patient is prone to frequent muscle cramps during exercise, a high protein diet is advised.
In some cases, the intake of glucose and fructose is advised. And of course, as their muscles are now more susceptible to damage, over-exhausting the body is a big No-No.
Unfortunately, prevention is barely an option.
As this is a genetic condition, the only way of prevention is to ‘not pass on the genes’.
Parents can seek genetic counseling to check if both carry the defective gene as it takes two to tango in this case.
But we have come a long way with the prognosis of the condition.
The unawareness of the disease’s details led medical researchers to believe GSD to be a fatal condition until the early ’70s.
People now live long and normal lives with significant dietary shifts.
This barely seems like a change in the millennial world of Keto and Atkins!
Speaking of Keto and Atkins, Glycogen is the secret quarterback in the low-carb diet game.
Glycogen storage and weight loss have a strange love story.
A typical healthy liver in an individual can hold up to 400 grams of glycogen and muscle cells, about 100 grams.
As glycogen and water co-exist in a 1:3 ratio, there are 3 grams of water present for every gram of glycogen.
This is the real reason behind the initial weight loss observed when any sort of low-carb diet is practiced.
It would rather be ideal for comparing body fat percentage or keeping track of monthly weight changes, for getting a better measure of body change as opposed to this initial quick loss of weight.
The body stores about 1500-2000 calories of Glycogen typically.
With a low-carb diet, the body uses this up and has little or no reservoir of energy. Possibly dehydrated.
This can lead to a constant state of fatigue in some extreme cases that could potentially damage the liver as it would be exposed to undue stress.
So we should be cautious when we make such lifestyle changes and always seek professional guidance.
In the case of sportsmen, a low-carb diet could lead to quick use of the stored Glycogen, especially the ones stored in the muscles.
This leads to a case of muscle fatigue and, in extreme cases, will lead to a phenomenon known as “hitting the wall”. Glycogen is also brain food.
So severe lack of Glycogen leads to cognitive symptoms like confusion, disorientation when you have a “bonk” during exercise.
Though there is cutting current edge research to discover new enzyme replacement therapies and gene therapies, this spectrum of diseases affects many lives.
But once again, we are hopeful that genomics will save the day!
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146814/ - Ozen H. (2007). Glycogen storage diseases: new perspectives. World journal of gastroenterology, 13(18), 2541–2553. https://doi.org/10.3748/wjg.v13.i18.2541
https://www.tandfonline.com/doi/full/10.3109/01913123.2011.601404 - Hicks J, Wartchow E, Mierau G. Glycogen storage diseases: a brief review and update on clinical features, genetic abnormalities, pathologic features, and treatment. Ultrastruct Pathol. 2011;35(5):183‐196. doi:10.3109/01913123.2011.601404
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(04)16986-9/fulltext Astrup, A., Meinert Larsen, T., & Harper, A. (2004). Atkins and other low-carbohydrate diets: hoax or an effective tool for weight loss?. Lancet (London, England), 364(9437), 897–899. https://doi.org/10.1016/S0140-6736(04)16986-9
https://onlinelibrary.wiley.com/doi/abs/10.1038/icb.2015.109 - Gleeson M. (2016). Immunological aspects of sport nutrition. Immunology and cell biology, 94(2), 117–123. https://doi.org/10.1038/icb.2015.109
Our genes are a template for how our bodies work. Most people on keto diets tend to consume a high amount of saturated fats. The diet works only when the stored fat is properly broken down and used for energy. Certain variants of the APOA2 gene tend to interfere with this saturated fats metabolism and hence, carriers of such variants may not get the desired benefit from this diet.
There seems to be an endless debate about whether saturated fats are good or bad for your health.
The truth is, all of us need a little bit of fat for some body functions like hormone production or maintenance of cell integrity.
But, what is considered 'too much' for your body is determined by certain gene variants you carry.
Let's explore this concept with a diet that's been constantly gaining popularity for weight loss and prevention and treatment of certain health conditions:
The basis of this diet is ketosis, which refers to the metabolic process in which the body converts stored fats into energy, releasing ketones in the process.
Hence, the conventional keto diet, which calls for high consumption of fats may work only if the stored fat is metabolized efficiently.
Several genes contribute to how your body reacts to saturated fats.
APOA2 gene is one of them that determines how well you tolerate saturated fats and how well you can transport cholesterol.
Depending on the variant of this gene you carry, you may need to modify the keto diet a little bit, in order to maximize its benefits to your body.
From the evolutionary perspective, certain human societies, such as those in the colder northern regions are likely to have subsisted on the large intake of fats for hundreds of generations.
As a result, they could have developed adaptations that enable them to metabolize this macro ingredient in food quite efficiently.
If you have inherited those genes, then your body is better able to cope with fats intake.
APOA2 gene produces a protein apolipoprotein -II, which plays a role in fat metabolism and obesity.
Individuals with the sensitive variant of this gene are more prone to increased BMI (6.8 times greater BMI), waist circumference, and body weight in response to high levels of saturated fat (more than 22g of saturated fats per day).
This was an observation in comparison to the people with the non-sensitive variant of the gene consuming the same amount of saturated fats.
It is vital for the carriers of the sensitive variant to limit their saturated fat intake.
However, there was no difference among individuals with both versions, in terms of weight and BMI when saturated fat intake was low (less than 22g per day).
One possible mechanism that could help explain the above gene-diet interactions is that, the sensitive variant of this gene produces lower levels of the protein, APOA2 (regulates the satiety response), resulting in low satiety and greater appetite among individuals with higher saturated fat intake.
This appetite may preferably be for foods rich in saturated fat and this higher fat intake would lead to greater weight.
Other genes like FTO, PPARG also impact the metabolism of saturated fats.
Carrying even 2-3 variants that affect saturated fats metabolism can pose a challenge to cholesterol control and weight loss.
It is thus vital for such individuals to alter their diet with lesser intake of saturated fatty acids.
Replacing saturated fatty acids with monounsaturated fatty acids (MUFA) and poly-unsaturated fatty acids can be a good start.
Sources of MUFA
Sources of PUFA
Upload your DNA raw data to Xcode Life to know your genetic variants for saturated fat metabolism.
25% to 50% of people who reported to hospitals in China with coronavirus in December 2019, had hypertension or other comorbidities like diabetes, cancer, or heart conditions. In Italy, 75% of COVID-related deaths included hypertensives. Hypertension and severe COVID symptoms have a genetic connection. But how interlinked are they? Read on to find out more!
The clinical and epidemiological features of COVID-19 have been under constant study and several research studies have been published about it over the last several weeks.
A lot of focus is on the comorbidities that have an association with COVID, in particular.
The most common comorbidities in one report were hypertension (30%), diabetes (19%), and coronary heart disease (8%).
ACE inhibitors, which are used to treat hypertension, have been researched to increase the ACE2 receptor expression, to which the coronavirus binds to.
But, it is important to note that none of these can be declared as a 'cause' of COVID since these are more prevalent in the elders, who appear to be at an increased risk for COVID.
However, blood pressure control is extremely important to reduce the impact of COVID in your body.
The coronavirus appears to affect any individual despite factors like their age or gender.
However, recent research reveals that some people tend to have more severe symptoms, in comparison to others who may experience mild symptoms or be completely asymptomatic.
Some genetic factors tend to influence how the virus enters your body, and consequently, how the virus affects you as well.
There is a wide acceptance amongst the scientific community that there is a genetic risk factor that causes severe symptoms in some individuals, while rendering other asymptomatic.
One such disease that scientists have researched is hypertension.
The limited studies on this reveal that the novel coronavirus latches on to the human protein ACE2 receptors and gains entry into the lungs.
Hypertensive individuals are prescribed Angiotensin-Converting Enzyme(ACE) inhibitors, and some studies have shown that these medications increase the number of ACE receptors, thereby increasing the portals for entry of the virus.
There are, however, opposing theories with a few groups of scientists saying that the ACE2 can actually protect the lungs from a very severe infection of 2019- nCov.
A very common health condition that is prevalent today is hypertension or abnormally high blood pressure.
A blood pressure level of 120/80mm Hg is considered normal, and having blood pressure equal to or higher than 130/80 mm Hg is called hypertension, in an otherwise healthy individual.
Though a common condition today, hypertension runs in families, and therefore, genetics and heredity may play a major role in determining the disease risk.
Individuals who have hypertensive parents tend to have an increased risk of developing the condition. However, how the exact inheritance of this condition is still unknown.
Many Genome-Wide studies have been conducted to study the influence of genes on the development of hypertension.
Around 280 genetic variants have been found that are said to increase the risk of hypertension and other associated conditions such as coronary artery disease.
Some genes that have a significant role to play in the development of hypertension are –
With the currently available studies, it has been observed that there are many genes that play a role in the pathophysiology of hypertension. It is highly unlikely that just one or two will emerge as the leading genes associated with the condition.
Now it is as simple as just following 3 simple steps to identify your risk for hypertension using your DNA raw data.
So far, it is quite evident that hypertension is high-risk comorbidity that results in severe symptoms if affected by COVID.
Pneumonia is one of the most common complications in severe cases.
In a hypertensive individual, high blood pressure damages the blood vessels and arteries. Therefore, it results in reduced blood flow to the heart.
As a result, your heart needs to work extra hard to pump blood, so it reaches all parts of your body.
When this happens over a period of time, it results in the weakening of the heart muscles.
The same effect can occur when there is hypercholesterinemia occurs together with hypertension.
Most common symptoms to look out for if you suspect a COVID infection include:
As a hypertensive individual, you need to take extra care to reduce your chances of contracting COVID. Here are some guidelines that you need to follow:
https://www.cebm.net/covid-19/coronaviruses-a-general-introduction/
https://academic.oup.com/eurheartj/article/38/29/2309/3852720
https://jasn.asnjournals.org/content/13/suppl_3/S155
https://academic.oup.com/ajh/article/33/5/373/5816609
https://pubmed.ncbi.nlm.nih.gov/24842388/
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