What Is Metabolic Rate?

Metabolism includes all the chemical reactions that occur in the body to maintain a balance. Metabolism is the combination of various functions in your body. The rate at which these processes occur is termed your metabolic rate. The food you eat is broken down and converted into energy. The breakdown of nutrients present in food and the formation of useful products for energy is metabolism. Your body breaks down nutrients into food and converts them into energy or heat. The extra nutrients are stored as fat for later use.

Metabolism is broadly categorized into:
1. Anabolism - the body utilizes the energy from nutrient breakdown to form complex molecules needed for daily functioning
2. Catabolism - the breakdown of food components or nutrients into simpler form to produce the energy needed for daily functioning

Some people have a faster metabolism than others. It varies from person to person, depending on a lot of factors.

Resting Metabolic Rate, or RMR for short, is the rate at which your body burns energy when at rest. Knowing your RMR will help you understand the energy needed by your body to perform basic life-sustaining functions like breathing, circulating blood, nutrient processing, cell growth, and functioning.

Basal Metabolic Rate (BMR) and RMR are slightly different. BMR is the minimum rate at which your body burns just enough calories to exist. RMR is a good estimate of your BMR.

By knowing your metabolic rate, you understand how many calories you burn and what your calorie intake needs to be to remain fit. It can help you devise a diet and exercise plan to remain healthy, stay fit and perform better.

Metabolic Rate and Exercise

Exercise helps you maintain weight and also can help change your metabolic rate. By building muscle through exercise, you can increase your BMR. The more intense your workout is, the longer your body takes to recover, the metabolism will increase more.

Exercises that increase muscle mass can help increase the resting metabolic rate also. The effect of exercise on metabolic rate increases with an increase in the intensity of the training.

The BMR of an average man is around 7,100 kJ per day, while that of a woman is 5,900 kJ per day. The expenditure of energy is continuous during the day; the rate varies and is found to be at its lowest early in the morning.

Estimating Metabolic Rate

BMR is usually estimated through the Harris-Benedict formula revised in 1990. The formula is gender-specific. You can calculate it on your own. All you need is your weight, height, age, and a little bit of math. The formula is given below.

BMR = (10 × weight in kg) + (6.25 × height in cm) - (5 × age in years) - 161

BMR = (10 × weight in kg) + (6.25 × height in cm) - (5 × age in years) + 5

How Does Genetics Influence Metabolic Rate?

UCP1 Gene

The UCP1gene encodes the uncoupling protein, which plays a role in generating heat by allowing fast substrate oxidation and lower ATP production in brown adipose tissue. It is responsible for adaptation to cold climates. Variants in this gene are associated with metabolism.

*rs1800592 *
rs1800592 is an SNP found in the UCP1 gene. The A allele is associated with a higher metabolic rate and slower weight gain compared to the G allele.

GPR158 Gene

The GPR158 gene encodes a protein called G-protein coupled receptor 158, which is highly expressed in the brain. It is known to influence the risk of obesity in mice. Variants in this gene are found to be associated with energy expenditure.

rs11014566 is an SNP in the GPR158 gene. People with the GG genotype were found to have lower energy expenditure, higher BMI, and higher fat mass compared to people with the AA genotype. This is seen in American Indians.

Non-Genetic Factors That Affect Metabolic Rate

A number of factors other than genetics influences metabolic rate. These include
- Age: Metabolism decreases with age due to gain in fat, loss of muscle, and decrease in physical activity. This means that the metabolic rate will also decrease with age.
- Gender: Generally, men have a faster metabolism than women because they tend to have more lean body mass and testosterone and lesser estrogen.
- Drugs: Nicotine and caffeine tend to increase metabolic rate.
- Body composition: Larger people tend to have a higher RMR. People with more lean muscle tissue and lesser fat have a higher RMR.
- Diet: A balanced diet can help you achieve optimal RMR. Fasting, starving, or crash dieting leads to loss of lean muscle mass and a decrease in RMR.
- Body temperature: Increase in body temperature increases RMR.
- Physical activity: Exercise done regularly increases muscle mass and can increase your RMR also.

Boosting Your Metabolic Rate

Working out can help you stay fit and healthy and increase your metabolism, thereby increasing the resting metabolic rate. Here are a few things that you can do to increase metabolic rate:
- Include plenty of proteins in your meal. It leads to a rise in the thermic effect of food, which is the extra calories needed to digest and absorb the nutrients in food. It also prevents muscle loss due to dieting and increases your metabolism.
- HIIT (High-Intensity Interval Training) workouts involve quick and intense energy bursts. Research shows that it helps boost metabolic rate after training.
- Lifting weights helps build and maintain muscle mass and increase metabolic rate. It also helps combat the drop in metabolism that occurs after weight loss.
- According to a review, resistance training can reduce fat mass and improve lean body mass, resulting in an increase in basal metabolic rate.
- Make sure you get adequate sleep. Sleep deprivation has negative effects on metabolism and is a risk factor for obesity.
- Research shows that drinking coffee can increase your metabolism and promote the burning of fats.


  1. Resting Metabolic Rate is the rate at which your body burns energy when at rest. Knowing your RMR will help you understand the energy needed by your body to perform basic life-sustaining functions like breathing, circulating blood, nutrient processing, cell growth, and functioning.
  2. Training and high-intensity workouts can boost your metabolism and metabolic rate. Exercise also increases muscle mass, which boosts metabolic rate.
  3. Variations in certain genes are found to affect metabolic rate. The AA genotype of SNP rs1800592 found in the UCP1 gene is associated with a higher metabolic rate and slower weight gain. The G allele of SNP rs11014566 found in the GPR158 gene is associated with lower energy expenditure.
  4. Non-genetic factors like age, gender, diet, body temperature, and body composition can lead to changes in your metabolic rate.
  5. Metabolic rate can be increased by increasing the intensity of exercise, lifting weights, resistance training, and eating a protein-packed meal.



What are Omega-3 and Omega-6 Fatty Acids?

Fats are an essential component of your diet, and omega-3, 6, and 9 are important dietary fats. Each of these fatty acids has health benefits when consumed in the right balance. Any imbalance in these fatty acids can result in many health conditions and diseases.

Omega-3 (alpha-linolenic acid) and omega-6 (linoleic acid) fatty acids are polyunsaturated fatty acids. Numbers 3 and 6 in the name of these fatty acids indicate the position of the final double bond in the chemical structure of the fatty acids. They are known as ‘poly’ unsaturated because they have many double bonds. Both omega-3 and omega-6 fatty acids are termed essential acids because our body cannot produce them. They need to be obtained through diet or supplements.

It is important to maintain a balance of omega-3 and omega-6 fatty acids. One must consume more omega-3 than omega-6. A reversed ratio of these fatty acids can result in chronic inflammation and diseases like rheumatoid arthritis, diabetes, atherosclerosis, etc. This occurs because linoleic acid and alpha-linolenic acid compete for metabolism by the enzyme delta-6-desaturase. A higher intake of linoleic acid or omega-6 can reduce the amount of the delta-6-desaturase enzyme left for the metabolism of alpha-linoleic acid or omega-3. This can cause chronic health conditions in the body. Therefore, it is important to maintain a healthy ‘ideal’ ratio of omega-3 and omega-6 fatty acids.

Importance of Omega-3 and Omega-6 Fatty Acids

Both omega-3 and 6-fatty acids are required by our body, and they play different roles. Both these essential fatty acids can be used to produce other fatty acids. They are also required for growth and repair in the body.

Omega- 3 Fatty Acids

Omega-3 fatty acids form an integral part of cell membranes. The omega-3 fatty acid is known to have anti-inflammatory properties, regulates blood pressure, and prevents fatal heart diseases. In fact, studies are focused on studying how omega-3 can protect one from diabetes and some types of cancer.

Omega-6 Fatty Acids

Omega-6 fatty acids are said to provide energy and linoleic acid is the most common omega-6 fatty acid. Excessive consumption of omega-6 can cause increased blood pressure, the formation of blood clots, and increased water retention.

Health Benefits of Omega-3 Fatty Acids:
- Help fight depression
- Promote brain health during pregnancy and right after birth
- Improve vision
- Reduce the risk of heart diseases
- Reduce symptoms of metabolic syndrome
- Help fight inflammation
- Prevent autoimmune diseases
- Reduce inflammation and inflammatory conditions in the body
- God for your joints
- Known to improve sleep
- Reduce the risk of cancer

Health Benefits of Omega-6 Fatty Acids:

Recommended Dietary Intake(RDI)

There are no specific numbers of Recommended Dietary Intake(RDI) of omega-3 fatty acids, but the Adequate Intake of this essential fatty acid as given by the Board of Institute of Medicine is:
- Adult Males: 1.6 g/day
- Adult Females: 1.1 g/day
- Pregnancy: 1.4 g/day
- Lactation: 1.3 g/day

According to the Food and Nutrition Board of the US Institute of Medicine, the Adequate Intake of omega-6 fatty acid for 19-50 years age group is:

How Does Genetics Influence Omega-3 and Omega-6 Levels?

The FADS2 Gene

The FADS2 or the Fatty Acid Desaturase 2 Gene provides instructions for the preparation of the delta-6-desaturase enzyme. Delta-5 and delta-6-desaturase are the enzymes that are part of the slowest step in the production of polyunsaturated omega-3 and omega-6 fatty acids.

rs3834458 is a single nucleotide polymorphism or SNP in the FADS2 gene. The T allele of this SNP plays a role in the reduced activity of delta-6-desaturase. This may lead to higher omega-3 and omega-6 levels in the body.

The MTHFR Gene

Mutations or changes in the MTHFR or methylenetetrahydrofolate reductase gene results in an excessive build-up of homocysteine in the blood and reduces levels of folates and other vitamins.

rs4846052 is an SNP located on chromosome 1 and associated with the _MTHFR _ gene. The different forms or genotypes (TT, CT, and CC) of this SNP were associated with PUFA levels in red blood cells (RBCs). Higher levels of RBC DHA (Docosahexaenoic acid is an omega-3 fatty acid), EPA (Eicosapentaenoic acid is an omega-3 fatty acid), ARA (Arachidonic acid is a polyunsaturated omega-6 fatty acid), and linoleic acid (omega-6 fatty acid) and were observed for the TT genotype versus TC and CC genotypes.

Non-genetic Factors Influencing Omega 3/6 Levels

While the metabolism of these fatty acids is dependent upon genetics, there are few non-genetic factors that affect one’s omega-3 and omega-6 levels in the body.


Since diet is the primary source of omega-3 and omega-6 fatty acids, the levels of these fatty acids and their right ratio is dependent upon the foods consumed by an individual.


Many conditions like pregnancy or other metabolic disorders require an additional supplement of omega-3 and omega-6 to maintain their optimum levels in the blood. Therefore, in these individuals, the supplements influence the levels of omega-3 and omega-6.


Regular exercise and workouts help maintain the right ratio of omega-3 and omega-6 fatty acids in the blood.

Systemic conditions

Many systemic conditions can alter the metabolism of omega-3 and omega-6, thereby affecting their levels in the body.

The Effects Of Inadequate Omega-3 and Omega-6 Levels

Though omega-3 and omega-6 fatty acids are essential, you will be surprised to know that nearly 90% of the population falls short of their target intake. A reduced level of omega-3 and omega-6 fatty acids results in a deficiency. Common deficiency symptoms of these fatty acids include:
- Fatigue
- Changes in skin, hair, and nails
- Decreased concentration and attentive power
- Leg cramps and joint aches
- Changes in the menstrual cycle in women
- An increased risk of cardiovascular diseases
- Feeling low and depressed

Recommendations to Maintain Adequate Levels of Omega-3 and Omega-6

The goal here is to maintain a healthy omega-3/omega-6 ratio. Here are a few recommendations to improve your omega-3 and omega-6 levels:

  1. Consume foods that are rich in omega-3 fatty acids. These include seafood like salmon, mackerel, herring, oysters, sardines, anchovies, and others.
  2. Vegetarian foods that are rich in omega-3 include flax seeds, chia seeds, walnuts, and soya beans.
  3. Avoid vegetable cooking oils that are high in omega-6 fatty acids and can disrupt the ratio with omega-3.
  4. Taking omega-3 fatty nutritional supplements consistently at the same time every day can help you maintain optimum and adequate levels of omega-3 fatty acids.


  1. Omega-3 and omega-6 fatty acids are important for your body and are called essential fats because your body cannot produce them.
  2. Both these fatty acids perform different roles in the body. Omega-3 is found in cell membranes and affects the function of receptors in these cells. Omega-6 is known to provide energy.
  3. For a healthy body, it is essential to maintain a healthy ratio of omega-3 and omega-6 fatty acids. An imbalance in the ratio can give rise to chronic inflammatory diseases.
  4. While there is no recommended dietary intake for omega-3 and omega-6 fatty acids, everyone must get an adequate intake of these essential fatty acids.
  5. There are few genes like FADS2, MTHFR, and PEMT and their SNPs that affect the levels of omega-3 and omega-6 levels in the body.
  6. Both these fatty acids have many health benefits to the body when consumed in optimum quantities.



Emotional Eating: An Introduction

When an individual feels low or encounters negative emotions, the feeling is often accompanied by emptiness. Food is believed to fill that void by providing temporary pleasure and satisfaction. This practice of reaching out to food to suppress or soothe our negative thoughts can be called emotional eating.

Finding comfort in food might seem normal but can lead to several complications if the individual loses control over how much or what he eats.

Conditions like compulsive eating or binge-eating are subtypes of emotional eating. They occur only in extreme cases, wherein the individual bing-eats large portions as opposed to what’s optimum. About 3.5% of women and 2% of men in the US are diagnosed with binge-eating disorder at some point in their life.

So, it is clear that overeating is linked to emotional eating, but there is more to it; mind you, emotional eating is a very broad term. The interplay of foods and moods is extensive. We all enjoy a variety of foods at different time points. When people find themselves in a negative space, they automatically reach out to a candy bar or sugary snack to combat negativity.

But, one can argue that eating indulgent foods can also be triggered during events of happiness, and that is partially true. However, we are more likely to pick grapes over chocolates when in a neutral mood. This is because we often think of the long-term perspective when we are happy and the present/near-term events when we are sad. And, in such times, we tend to indulge in quick pleasures to absolve ourselves of the momentary pain.

What Is The Science Behind Emotional Eating?

Emotional eating is triggered by certain reward systems in the brain. Let’s understand how these psychological factors alter our eating episodes. Motivation (wanting), outcome (liking), memory (learning), habituation (adapting) are the four factors that respond to cues like food, alcohol, drug, money, etc.


Poor food memory is known to alter food consumption levels; sugary or carbohydrate-rich items, especially, tend to impair memory, leading to vicious cycles of overeating. This is because our brain remembers the satiating effects of a particular meal and registers an expectation in the future food intake. This influence in our eating experiences, therefore, plays a role in decision making during mealtime.

Motivation (wanting) and Outcome (liking)

One of the main properties of food is its palatability that produces a sense of pleasure and addiction. Overeating of palatable foods can be triggered by the failure to downregulate the “wanting” and “liking” of the foods we consume.
Coupled with emotional biases, we tend to binge-eat without attending to our “wants” and “likes.” Many research studies suggest that obese people, more often than not, pay little attention to their food cues, while leaner people show a larger bias to their food cues. Their food consumption is a function of eating to satiety; in other words, they eat food only when hungry.

Habituation (Simple Learning)

Appetitive responses to different foods vary and are habituated as they are eaten. It is a simple form of learning that limits the quantity or size of food that we eat. As we consume newer food varieties, we take more than optimum quantities and lose habitation, leading to increased meal sizes and overeating.

Genetics Behind Emotional Eating

DRD2 Gene and Emotional Eating

Dopamine, the ‘happy hormone,’ is an important neurotransmitter crucial for emotional and mental wellbeing. The DRD2 gene encodes the D2 Dopamine receptor. DRD2 variants can affect the D2 receptor activity and result in addictive or reward-dependent behaviors. Individuals carrying this variation run the risk of over-eating disorders as well as obesity. Such individuals consume palatable foods to compensate for the improper functioning of dopamine, especially during emotional times.

rs1800497 is an SNP in the DRD2 gene. It is also known as the TaqIA (or Taq1A) polymorphism. The A1 or the T allele of this SNP is associated with a reduced number of dopamine binding sites in the brain.
According to a study, the presence of even one copy of the A1 or T allele was associated with an increased risk for emotional eating.

### ADIPOQ Gene and Emotional Eating
Adiponectin is a 247-amino acid peptide that circulates in large amounts in plasma. The adipocytes (fat cells) play a crucial role in multiple functions like anti-inflammation, cardioprotection, etc., and it is known to regulate energy homeostasis and feeding behavior. Altered circulating adiponectin levels can lead to human eating disorders such as anorexia nervosa or bulimia nervosa (binge eating). Not only does it alter the eating cycles, but it is also observed to have effects on the psychological functioning and emotional health of humans.

rs1501299 is an SNP in the ADIPOQ gene. It is also annotated as c.276G>T.
A study analyzed the emotional eating behavior in young Nigerian adults. It was found that the T-allele in rs1501299 was associated with a decreased risk for emotional eating in the codominant condition - that is, GT when compared to GG and TT types.

Non-genetic Contributors To Emotional Eating

Basically, any negative emotion is a contributor to emotional eating.
- Can be a symptom of atypical depression
- Uncontrolled stress can trigger the release of cortisol hormone, which can amp up your appetite
- An inability to express your emotions can lead to you stuffing them down. This can lead to uncomfortable feelings that may make you combat them with food.
- Childhood habits of being rewarded with foods like ice cream when on good behavior often get carried over to adulthood.
- Overindulging in food can often happen when others around you also overeat. This is often seen in social gatherings.

Recommendations To Overcome Emotional Eating

By not indulging in the ‘trigger emotions,’ even the most painful situations can be handled with ease. Following these tips can help reduce those curveballs and curb your intentions of excessive eating:

Practice mindful eating
When we feed our emotions with food, we do so in a quick manner to bulldoze through the pain, but we can certainly regulate that feeling by consciously judging our own decisions just seconds before eating. So, slow down, savor your food, and practice mindful eating.

Daily exercise
Make daily exercise part of the routine because physical activities can do wonders to your body and mind and act as a powerful stress-buster. Getting into a habit of exercising can help balance out your emotional triggers.

Avoid binge-eating while working
This often becomes a habit whereby people eat mindlessly while working or watching movies, and this can disrupt your attention towards the type or quantity of food that you consume. Over time, it is easy to get habituated to eating without a conscious mind. Avoid doing this to regulate eating habits.

Connect with important people
Connecting with people that are positive and are mindful can help you become more watchful of your eating habits.

Lower the intake of sugary substances
These high carbs, sugary foods can impair the hypothalamus’s function in encoding memory based on foods, leading to either improper eating or binge-eating in the subsequent intakes.

Make time for relaxation
To decompress and unwind, break from responsibilities, and relax; this can awaken you from your daily hustle and stress.


  1. The practice of reaching out to food to suppress or soothe our negative thoughts is called emotional eating. Conditions like compulsive eating or binge-eating are subtypes of emotional eating and occur only in extreme cases.
  2. Emotional eating is triggered by certain reward systems in the brain. The psychological factors that alter our eating episodes are motivation (wanting), outcome (liking), memory (learning), and habituation (adapting); they determine how a cue like food, alcohol, drug, money, etc., is perceived.
  3. Some genes like DRD2 and ADIPOQ influence eating behavior by modulating reward and pleasure responses in the brain. Certain variants in these genes have been associated with an increased risk for emotional eating.
  4. Non-genetic causes of emotional eating include stress, anxiety, food-related cues, childhood habits, social influences, etc.
  5. Mindful eating with an attentional bias is primal in curbing overeating. Coupled with healthy lifestyle habits and exercises, one can manage emotions and effectively regulate eating habits.



What Is Homocysteine?

Unlike most amino acids, homocysteine is a harmful amino acid that is not involved in protein synthesis. It is usually formed in the body.

This harmful amino acid is converted into either cysteine or methionine, amino acids that are safe for the body. There are different interdependent pathways involved in the conversion of homocysteine. B complex vitamins are involved in these pathways.

The normal range of homocysteine levels in the blood is less than 15 micromoles per liter (mcmol/L) of blood. Some people have higher levels of homocysteine, and this leads to hyperhomocysteinemia. High levels of homocysteine are further divided into three categories
- Moderate: 15-30 mcmol/L
- Intermediate: 30-100 mcmol/L
- Severe: Levels greater than 100 mcmol/L

High levels of homocysteine are linked to an increased risk of heart disease and certain vitamin deficiencies.

Complications of Hyperhomocysteinemia

Elevated levels of homocysteine in the blood are harmful to the body. This condition is termed hyperhomocysteinemia.

According to a review published in 2017 in the journal Nutrition and Metabolism, higher homocysteine levels may be a risk factor for developing certain conditions like heart disease or nutritional deficiencies.

A study reported that higher levels of homocysteine and folate deficiency are positively associated with an overall risk of developing cancer with little effect on the type of cancer.

Hyperhomocysteinemia has also been linked to osteoporosis and the progression of bone disease.

Other potential conditions associated with hyperhomocysteinemia include dementia, stroke, atherosclerosis, blood clot formation, heart attack, hypothyroidism, and epilepsy.

Higher homocysteine levels have also been positively associated with an increased risk of all-cause mortality.

Genetics and Homocysteine Levels

A family history of hyperhomocysteinemia can increase your risk of the condition. Some of the genes needed for the breakdown of homocysteine are mentioned below.


The MTHFR gene contains instructions for the production of an enzyme known as methylenetetrahydrofolate reductase. This enzyme is involved in the processing of amino acids through the MTHFR pathway. In this pathway, a compound known as 5,10-methylenetetrahydrofolate is converted into 5-methyltetrahydrofolate, which is the active form of vitamin B9. This conversion is needed for the conversion of homocysteine into methionine. Changes (or variations) in this gene can affect enzyme activity and homocysteine levels.

rs1801133is a well-known single-nucleotide polymorphism or SNP found in the MTHFR gene. There are three forms (or genotypes) of this SNP:
- TT - 10-20% efficiency of folic acid processing, higher levels of homocysteine, lower levels of vitamin B12 and folate.
- CT - 65% efficiency of folic acid processing
- CC - highest efficiency of folic acid processing
People with the CC genotype are found to have normal homocysteine levels.

MTR Gene

The MTR gene contains instructions for the production of the enzyme methionine synthase. This enzyme is needed for the conversion of homocysteine into methionine. This enzyme requires a form of vitamin B12 to function properly.

rs2275565 is an SNP found in the MTR gene. The T allele is found to be the risk allele and is associated with higher levels of homocysteine.


The BHMT gene contains instructions for the production of an enzyme known as Betaine-Homocysteine S-Methyltransferase. This enzyme is needed for the conversion of homocysteine into methionine.

rs3733890 is an SNP found in the BHMT gene. The A allele is found to be the risk allele and plays a role in elevated homocysteine levels.

Non-Genetic Factors That Influence Homocysteine Levels

Vitamin deficiency
Vitamin B6, vitamin B12, and folate deficiency are the common causes of high homocysteine levels. These vitamins are involved in the pathways responsible for the conversion of homocysteine into safer amino acids, methionine and cysteine.

Other underlying health conditions
Kidney disease, psoriasis, Crohn’s disease, and low thyroid hormone levels can lead to high levels of homocysteine.

Studies show that smoking can lead to higher levels of homocysteine.

Chronic alcohol consumption is found to increase homocysteine levels and reduce vitamin B levels.

Levels of homocysteine may also increase with age. A study reported that homocysteine levels were higher in patients above 65 years of age.

Certain medications including antihypertensive, lipid-lowering, antidiabetic, and drugs used to treat people at high risk of cardiovascular disease may raise homocysteine levels.

Symptoms of Hyperhomocysteinemia

The symptoms vary from person to person and maybe very minimal in certain cases. Symptoms are more prevalent in children when compared to adults. The symptoms usually depend on the underlying vitamin deficiency that results in higher homocysteine levels. Common symptoms include:
- Fatigue
- Pale skin
- Weakness
- Dizziness
- Soreness


If you have been diagnosed with a vitamin deficiency causing an increase in homocysteine levels, change your diet to include rich sources of vitamin B and folic acid.

Folate-rich foods include:
- Legumes
- Kidney beans, soybeans
- Egg
- Leafy greens, asparagus, broccoli, root vegetables
- Citrus fruits, papaya, avocado, banana
- Salmon, beef liver
- Nuts and seed
- Fortified breakfast cereals

Vitamin B6-rich foods include:
- Peanuts
- Chicken, turkey
- Soya beans
- Bananas
- Potatoes
- Fortified breakfast cereals

Vitamin B12-rich foods include:
- Dairy products
- Organ meat
- Fortified breakfast cereals
- Eggs
- Fish

Doctors may also recommend supplements to meet your vitamin needs.

If people have hyperhomocysteinemia as a result of an underlying health condition, treatment is focused on managing that condition.

Testing for Homocysteine Levels

A simple blood test is usually recommended to test for homocysteine levels in the blood. Blood tests can detect any vitamin deficiencies that you might have. Based on the results, your doctor may recommend additional tests to find the underlying cause.


  1. Homocysteine is a harmful amino acid that is not involved in protein synthesis. This amino acid is converted into methionine and cysteine, useful and safe amino acids in the body through different interdependent pathways.
  2. The normal range of homocysteine levels in the blood is less than 15 micromoles per liter (mcmol/L) of blood. Higher levels of homocysteine lead to hyperhomocysteinemia. This condition is associated with a risk of cardiovascular diseases, bone disease, and hypothyroidism.
  3. The symptoms of hyperhomocysteinemia are usually caused by underlying vitamin deficiencies. Symptoms are more prominent in children compared to adults. A simple blood test is used to detect homocysteine levels and vitamin deficiencies.
  4. The T allele of SNP rs1801133 found in the MTHFR gene is linked to higher homocysteine levels and lower efficiency of the MTHFR enzyme. The T allele of SNP rs2275565 found in the MTR gene and the A allele of SNP rs3733890 found in the BHMT gene are associated with higher homocysteine levels.
  5. Vitamin B6, vitamin B12, and folate deficiency, other underlying health conditions, smoking, alcohol consumption, age, and certain medication are linked to higher levels of homocysteine.
  6. Including rich sources of vitamins in your diet and treating the underlying health condition can help manage high levels of homocysteine.



Consider the following scenarios,

The above scenarios and several more like these illustrate that when it comes to diet and nutrition, personalized is the way to go - because each individual is different according to their genetic makeup. Thanks to the new science of nutrigenetics, everyone now has access to their genetic information.

Our genes play a role in how the nutrients in the food are broken down, absorbed, metabolized, and excreted. And except for identical twins, no two people have the exact same genetic makeup. Just like how people are different in the way they look- all the way down to the fingerprints, their metabolism of various foods is also different. 

In this article, we will look at some examples of the differences among individuals when it comes to food metabolism.

MCM6 gene produces Lactase enzyme to digest Lactose in milk

One common and famous example is that of lactose intolerance. Lactose, the sugar in milk, is metabolized by the lactase enzyme. Only 30% of the world population, particularly northern Europeans, can digest lactose. About 70% of the world population, including much of the Asian population, cannot metabolize lactose in milk. They appear to have less/no lactase enzyme. 4 genetic mutations have been associated with this. These mutations are seen in the MCM6 gene, the regulator of another gene called LCT, which produces the lactase enzyme. 

HLA-DQ gene affects Gluten Sensitivity

Gluten-free is all the rage these days. However, unless you are gluten-sensitive, you may not benefit from a gluten-free diet, according to research. Much has been written about gluten intolerance; however, most mainstream articles do not focus on the genetic aspect, which is the basis of gluten intolerance. The HLA gene family, involved in immune reactions, is implicated in gluten intolerance. HLA-DQ2 and HLA-DQ8 especially are the bad guys here. In a study conducted to assess the genetic influence on gluten intolerance, nearly all the patients with celiac disease (a severe form of gluten intolerance) had the risk allele in the HLA-DQ2 and the HLA-DQ8 genes. The absence of the same was found in 100% of people without celiac disease.  

VDR gene influences our Vitamin D requirements

Vitamin D can be produced by the skin cells when exposed to sunlight. However, darker-skinned individuals produce less vitamin D than light-skinned individuals. This is because melanin blocks UV light. The amount of melanin that one produces is genetically determined. Whatever vitamin D does get generated still has to be transported inside the cells by vitamin D receptors. Depending upon the genetics of the individual, the vitamin D requirements are different. 

MTHFR gene impacts folate requirements and Neural tube defects

According to the CDC, 3000 pregnancies are affected by Neural Tube Defects (NTD) in the US every year. Further, NTD seems to be more prevalent in Hispanic women than non-Hispanic women in the US. Hispanic women have higher rates of neural tube defects than non-Hispanic women in the United States. Hispanic individuals also are more likely to have folate (vitamin B9) deficiency than non-Hispanic whites and non-Hispanic blacks. Coincidence? We think not! MTHFR stands for methylenetetrahydrofolate reductase and is produced by the MTHFR gene. This enzyme is responsible for converting inactive to active vitamin B9/folate. Mutations in this gene can reduce the amount of enzyme and, thus, the folate produced. And folate deficiency in pregnancy can cause NTDs. Folic acid supplements have been a big game-changer in the prevention of NTDs in pregnancy. 

BCMO gene affects the conversion of Beta-Carotene to Vitamin A

Vitamin A is not produced in the body. It is obtained from plant sources as carotenoids and from animal sources as retinal - both are forms of vitamin A. Beta-carotenoids are the inactive form of vitamin A and need to be converted to the active form inside the body. The BCO1 or BCMO1 gene does the trick here. BCO1/BCMO1 stands for Beta Carotene Oxygenase or Monooxygenase1. This gene contains instructions for the production of a protein with the same name. This protein converts the inactive form of vitamin A (beta-carotene) to the active form, retinoic acid.  But, about 45 percent of the population carries at least one change in the gene that reduces BCMO1 enzyme activity, resulting in significantly impaired ability to convert beta-carotene into retinal. Depending on which combination of the changes someone inherits, beta-carotene conversion can be nearly 70 percent lower than its normal efficiency. Knowing about your BCMO1 gene can help you supplement your diet accordingly to avoid vitamin A deficiency.

PEMT gene variant can lead to Choline Deficiency

Choline is kind of a late bloomer. It was only declared an essential nutrient by the Institute of Medicine in 1998. Thus, it needs to be supplemented through diet. While choline deficiency is rare, it can be harmful, especially for the liver. Non-alcoholic fatty liver disease or NAFLD is a common liver disorder associated with choline deficiency. The PEMT gene contains instructions for producing an enzyme called Phosphatidylethanolamine N-Methyltransferase (PEMT). PEMT is involved in the breakdown of a product to produce phosphatidylcholine (PC). The PC is further broken down into choline. An interesting thing to note here is that estrogen hormone is required for activating this gene. In fact, according to a study, Eighty percent of the women who carried this change in both the copies of the PEMT gene manifested signs of choline depletion - liver and muscle damage. 

CYP1A2 gene impacts how much caffeine you can handle 

Caffeine is our best friend for when we need to pull off those pesky all-nighters and when we need to get through a snoozy zoom meeting. While you may be able to chug down 5 cups of coffee a day, your friend may lose it after a cup and end up sleepless that night. Why is it that caffeine has affected your friend differently? Some people have a change in their CYP1A2, or caffeine metabolizing gene, that may result in an improper breakdown of caffeine, leading to nasty caffeine jitters. Caffeine also has a twin in the body, called adenosine. Adenosine is a sleep-inducer. It goes and binds to its receptor to push our body into rest mode and make us sleep. Caffeine, the evil twin, mimics adenosine and takes up its spot, warding off sleep. Changes in CYP1A2 and ADORA2A (produces adenosine receptors) genes can modulate how much caffeine we can safely consume without experiencing sleep disturbances. 

The FTO (Fat Mass and Obesity gene) influences weight gain tendency

There appears to be no universal pattern of weight loss. While one gains a lot of weight on a high-carb diet, the other seems to enjoy pretzels for breakfast, lunch, and dinner without gaining a pound. While as puzzling as this may seem, genetics seems to provide some clarity here. Carbohydrates seem to interact with a gene called FTO, which produces fat mass and obesity-associated protein. In some people, carbs over-activate this gene, making them want to reach out to more sugary foods, making them gain weight. Proteins also interact with this gene but seem to have the opposite effect. It suppresses hunger, appetite, and promotes satiety - more in some than others. 

The taste receptors gene influence what tastes we like and dislike

Who wouldn’t love a delicious cheese platter? The smooth, creamy texture of the cheese is nothing less than a party in your mouth. This palatability of cheese is all thanks to the high-fat content in it. While some can enjoy a good amount of high-fat foods, for others, it’s a big no-no. By now, you may already know the reason behind this difference. Genetics, of course; the ApoE gene, in particular. It produces the APOE protein, which metabolizes and clears out fats and cholesterol from the body. A type of ApoE gene called ApoE2 is associated with slower cholesterol metabolism. This results in lower cholesterol levels in the blood. A high-fat, low-carb diet is beneficial for people carrying this variant. Another type, ApoE4, metabolizes and releases cholesterol very fast, the blood cholesterol levels increase. A high-fat diet becomes the E4’s enemy here. 

The ACE gene influences blood pressure response to salt

Sodium, to date, remains the most important dietary factor that contributes to hypertension. The sodium content in the diet that could result in blood pressure spikes differ amongst different people - that is, different people have different salt sensitivity. The ACE gene modulates how sodium regulates your blood pressure. There are two types of ACE gene: The I type and the D type. The I type is associated with lower sensitivity to salt and hence a lower risk for hypertension. The D type, also called the risk type, on the other hand, is associated with a higher sensitivity to salt and a higher risk for hypertension. Over 50% of Africans and Caucasians and about 40% of Asians carry the D type of the ACE gene. 


The above are just a few examples of how genes influence how we respond to various foods we consume. What is good for some may not be for others. Dietary strategies have to be tailored for the individual taking into account several factors, including lifestyle, current health, occupation and importantly, genetics. Genes and big players when it comes to how your body responds to the nutrients in your diet. Certain changes in these genes can put you at risk for nutritional deficiencies, food intolerances, and health conditions like obesity. The good news is that the effects of these genes are not set in stone and can be manipulated by making the necessary changes in your diet and lifestyle. We also now have the technology to learn more about these “nutrition-genes,” which can help you gain some insight on what diet is optimal for your body.

Want to know more about incorporating genetics into your diet? Get in touch with us.

Vitamin B2: An Introduction

Vitamin B2, also called riboflavin, is an essential nutrient needed for human health. It is one of the eight B vitamins. All the B vitamins are important for good health. Vitamin B2 is a water-soluble vitamin. Being a water-soluble vitamin, it can be excreted out of the body easily. Your body only stores a small amount of riboflavin, and hence, you need to include riboflavin in your diet every day.

Vitamin B2 and Health

Vitamin B2 plays a role in
- Maintaining tissues
- Energy metabolism
- Secretion of mucus that prevents dryness induced oil secretion that leads to acne
- Absorption of zinc, which is essential for the skin
- Maintaining the structural integrity of the skin
- Protects cells from oxidative damage
- Maintenance of red blood cells
- Keeping the skin healthy

Recommended Daily Intake of Vitamin B2

The recommended daily intake of vitamin B2 is as follows:
For adults
1.3 mg for healthy men
1.1 mg for healthy women
1.4 mg for pregnant women
1.6 mg for lactating women

For children
0.3 mg for infants up to 6 months
0.4 mg for infants between 6-12 months
0.5 mg for 1-3-year-old children
0.6 mg for 4-8-year-old children
0.9 mg for 9-13-year-old children
1.3 mg for 14-18-year-old males
1.0 mg for 14-18-year-old females

The Influence of Genetics On Vitamin B2 Levels

People of certain genetic types may need more vitamin B2 due to the inefficient transport in their bodies. Certain genes can help determine your risk for vitamin deficiency.


The MTHFR gene produces an enzyme called methylenetetrahydrofolate reductase. This enzyme is involved in the methylation cycle. MTHFR activates 5, 10-methylene TetraHydroFolate(THF) to 5-methyl THF, and this is needed for the conversion of homocysteine to methionine.

This protein is also involved in the conversion of folate to SAMe, which is involved in the methylation of DNA as it is the universal methylation donor. The methylation cycle is essential for various functions in the body.

Vitamin B2 is involved in the metabolism of homocysteine along with Vitamin B1. Vitamin B2 deficiency can lead to high levels of homocysteine, which is a harmful amino acid.

rs1801133 is a single nucleotide polymorphism or SNP found in the MTFHR gene.It is also referred to as C677T. The T allele decreases enzyme activity, with only a 10-20% efficiency in folate processing and leads to high levels of 0f homocysteine in the body.

Non-Genetic Factors that Influence Vitamin B2 levels

Vitamin B2 deficiency is not very common in the US as most of the food items like milk and whole-grain cereals, which are widely consumed, contain good levels of vitamin B2.

Impact of Vitamin B2 Deficiency

Vitamin B2 deficiency can lead to
- Cracked lips
- Itching of skin
- Scrotal Dermatitis
- Inflammation of mouth lining
- Inflammation of the tongue
- Scaly skin
- Hair loss
- Reproductive problems

Non-Genetic Factors that Influence Vitamin B2 levels

How to Manage Your Vitamin B2 Intake?

Certain food items contain vitamin B2. These include:
- Eggs
- Kidney and liver meat, lean meats
- Green vegetables like broccoli and spinach
- Cereals, grains, and bread
- Milk and yogurt
- Lima beans and peas
- Avocados
- Artichokes
- Nuts

Riboflavin is water-soluble. While cooking food, especially boiling, vitamin content may reduce. Make sure to include a daily supply of vitamin B2 rich foods to keep your skin healthy. A balanced diet is always important to keep your skin and other parts of the body healthy.

Your doctor may prescribe certain vitamin B2 supplements to overcome your deficiency apart from your diet.


  1. Vitamin B2 is an essential nutrient needed for the body. As it is a water-soluble vitamin, it cannot be easily stored in the body. It needs to be supplemented through diet.
  2. Vitamin B2 plays a major role in keeping the skin healthy, maintaining its structural integrity, secretion of mucus to prevent acne due to dryness, and other functions in the body also.
  3. The T allele of rs1801133, an SNP found in the MTHFR gene, leads to higher homocysteine and folate levels because of decreased enzyme activity. Vitamin B2 deficiency is linked to higher levels of homocysteine in the blood.
  4. Pregnant women, older adults, and people with certain conditions are at a higher risk of Vitamin B2 deficiency. A poor diet can also lead to deficiency.
  5. A balanced diet with a rich source of vitamins can help reduce the risk of deficiency and keep your skin healthy.



What is Cilantro?

Cilantro is a herb popularly used in cooking. The names cilantro and coriander are commonly used interchangeably. Both cilantro and coriander come from the same plant species, Coriandrum sativum. The nutrient profiles of the plant and seed are different.

In North America, cilantro refers to the leaves and stem, while coriander refers to the seeds. In other countries like India, coriander refers to the leaves and stem, and the seeds are called coriander seeds. Cilantro is the Spanish word for coriander.

Cilantro has a fragrant, citrusy flavor. The coriander seeds have a warm, spicy, earthy aroma with a hint of citrus. It is usually paired with cumin and used as a base ingredient for making spice mixes.

What is Cilantro Taste Aversion?

Even though cilantro is properly used in several cuisines all over the world, some people do not like the taste of it. They find the taste soapy and revolting. This is termed as Cilantro Taste Aversion.

Even the famous American chef, Julia Child, did not have a liking for cilantro. She said the best way to deal with it in food is to pick it up and throw it on the floor.

Cilantro contains several aldehydes. Aldehydes taste soapy in nature. People with cilantro taste aversion perceive the taste of these aldehydes found in cilantro.

The number of people with this aversion is less in Central America and India, where this herb is very popular. Nearly 20% of the East Asian population are found to experience the soapy-taste of cilantro.

Why do some people hate the taste of cilantro but others don’t?
The answer to this question lies in genes.

Genetics and Cilantro Taste Aversion

Cilantro taste preference can be explained by genetics. The olfactory receptors influence our sense of smell, which directly alters our taste perception. Variations in olfactory-receptor genes can affect the way we perceive the taste of certain food items.

OR6A2 Gene

The OR6A2 gene is an olfactory-receptor gene. It carries instructions for the production of Olfactory Receptor Family 6 Subfamily A Member 2 protein. This protein has a high-binding affinity to soapy-flavored aldehydes like the ones found in cilantro. Individuals with an aversion to the taste of cilantro are found to have a variation in this gene.

rs72921001 is a single nucleotide polymorphism or SNP in the OR6A2 gene. Individuals with the A allele of this gene are at a lower risk of detecting a soapy taste.


The best way to deal with the soapy taste of cilantro is to avoid using it in meals or picking it out of your plate as Julia Child said.

Certain other ways to deal with this include

Some restaurants use a mix of parsley, tarragon, and dill. Lime of lemon zest can be used to substitute for the bright, citrusy flavor of cilantro. Carrot tops, mint, basil, or Thai basil are also used in certain dishes.

Microgreens are becoming increasingly popular. Micro cilantro tastes less soapy than mature cilantro leaves. Coriander seeds may also have a more palatable flavor compared to cilantro.

Crushing cilantro may help eliminate the soapy-tasting aldehydes. Using cilantro in chutneys and sauces dampens the soapy flavor and can help you get used to the herb.


  1. Cilantro is a herb commonly used in several cuisines around the world. Generally, cilantro has a fresh, fragrant, and citrusy flavor. Cilantro generally refers to the leaves and stem of the plant, while coriander refers to the seeds.
  2. Certain people do not have a liking for cilantro. It tastes like soap to them. This is because they taste the aldehydes present in this herb. The aldehydes give it a soapy taste that is perceived by certain people.
  3. Cilantro taste aversion is linked to a change in the OR6A2 gene. This is an olfactory receptor gene. Olfactory receptors are responsible for the sense of smell which affects taste also.
  4. People who do not like the taste of cilantro are found to have the CC genotype of SNP rs72921001 found in the OR6A2 gene. Carries of the A allele are at a lower risk of detecting this soapy taste.
  5. The best way to deal with this taste aversion is to avoid the herb. You can also use other herbs as substitutes while cooking.



What Is Adiponectin?

Adiponectin is a protein hormone secreted primarily by adipocytes or fat cells. Adipocytes are found in the adipose tissue. Certain other cell types in the muscle and brain can also produce this hormone.

This hormone plays a role in the metabolism of lipids and glucose. Adiponectin also influences the body’s response to insulin and can reduce cholesterol buildup in the arteries and inflammation.

Reference Range for Adiponectin Levels

The reference range for adiponectin levels is based on the Body Mass Index.
1. BMI <25 - Males: 4-26 mcg/mL and females: 5-37 mcg/mL
2. BMI 25-30 - Males: 4-20 mcg/mL and females: 5-28 mcg/mL
3. BMI >30 - Males: 2-20 mcg/mL and females: 4-22 mcg/mL

Genetics and Adiponectin Levels

Research shows that genetic changes can affect adiponectin levels. A few of the genes influencing adiponectin levels are described below.


The ADIPOQ gene carries instructions to produce the protein hormone, adiponectin. Variants or changes in this gene affect adiponectin levels.

rs17366568 is a single-nucleotide polymorphism or SNP found in the ADIPOQ gene.People with the A allele were found to have lower adiponectin levels.

rs6773957 is an SNP in the ADIPOQ gene. People with the G allele were found to have lower levels of adiponectin, and people with the A allele were found to have higher levels of adiponectin.

PAPD4 Gene

The PAPD4 gene carries instructions for the production of a protein known as PAP-Associated Domain-Containing Protein 4. This protein is an RNA polymerase.

rs13358260 is an SNP in the PAPD4 gene. The C allele is found to affect serum adiponectin levels.

KCNK9 Gene

The KCNK9 gene carries instructions for the production of a protein called TASK3. This protein is a potassium channel and is involved in the transport of potassium ions in and out of cells.

rs2468677 is an SNP in the KCNK9 gene. The G allele is found to affect serum adiponectin levels.

Non-Genetic Factors That Influence Adiponectin Levels

Serum adiponectin levels were found to be higher in females.

Health conditions
People with certain health conditions like obesity, diabetes, or higher risk of cardiovascular diseases are found to have lower levels of adiponectin.

Certain diets containing carbohydrate-rich foods, soy protein, fish oil, and linoleic acid can affect adiponectin levels.

Low Levels of Adiponectin

Hypoadiponectinemia is a clinical term that refers to low levels of adiponectin in the body. Lower levels of adiponectin are found in people with obesity, insulin resistance, type 2 diabetes, and cardiovascular diseases.

Lower levels have also been found in people with Non-Alcoholic Fatty Liver Disease(NAFLD).

Studies show that lower levels of adiponectin are related to visceral fat accumulation.

Visceral fat is a type of fat found in the body. Also known as belly fat, it is stored in the abdominal region and around all the major organs like the liver, kidneys, intestines, pancreas, and heart. Accumulation of visceral fat can increase the risk of developing insulin resistance, diabetes, heart disease, low levels of HDL cholesterol (good cholesterol), high blood pressure, and even some cancers.

High Levels of Adiponectin

Studies show that higher levels of adiponectin have a protective effect and lower the risk of type 2 diabetes and heart disease.
Higher levels of adiponectin also promote the synthesis of good cholesterol, HDL cholesterol in the body.

Further research is being done on using this hormone as a therapeutic target to treat people with obesity and diabetes.

A review published in the international journal of inflammation reported that higher levels of adiponectin are found in cases of heart failure, hypertension, and chronic inflammatory autoimmune diseases like SLE, type 1 diabetes, and rheumatoid arthritis.


Changing your diet to follow a healthy and balanced diet is a means of managing adiponectin levels.
- Monounsaturated fats such as fish oil, avocados, olive oil, omega-3 can boost adiponectin levels.
- Make sure you include enough sources of dietary fiber in your meal.
- People who regularly consume caffeine are found to have higher adiponectin levels.
- Curcumin, found in turmeric, can boost adiponectin levels.
- Moderate consumption of ethanol-containing beverages is found to increase adiponectin levels depending on the type of beverage and gender.
- Resveratrol, a compound found in grapes, stimulates the production of adiponectin.
- Zinc supplementation can also restore adiponectin levels to normal in patients with type 2 diabetes.
- A study shows that limiting consumption of carbohydrates to dinner time can increase adiponectin levels and lower the risk for diabetes and cardiovascular disease.

Include exercising in your daily routine at least three times a week. Moderate exercise can help keep your body healthy and increase adiponectin levels.

Testing for Adiponectin Levels

Adiponectin levels are determined using a blood test. Levels in the blood are measured using a method called ELISA (Enzyme-Linked Immunosorbent Assay). ELISA is a plate-based assay technique in which antibodies are usually used to detect the target molecule, such as proteins.

Your doctor may ask you to test for adiponectin levels as a biomarker for certain metabolic disorders like type 2 diabetes.


  1. Adiponectin is a protein hormone secreted primarily by adipocytes or fat cells. It is mainly known for fat-burning. This hormone plays a role in the metabolism of lipids and glucose. It also influences the body’s response to insulin and can reduce cholesterol buildup in the arteries and inflammation.
  2. Hypoadiponectinemia is a clinical term that refers to low levels of adiponectin in the body. Lower levels of adiponectin are found in people with visceral fat accumulation, obesity, insulin resistance, type 2 diabetes, and cardiovascular diseases.
  3. Higher levels of adiponectin promote the synthesis of good cholesterol and are found to lower the risk of diabetes and heart disease in certain cases.
  4. Adiponectin levels in the blood are measured by using a method called ELISA.
  5. Changes in some genes influence adiponectin levels. People with the A allele of SNP rs17366568 found in the ADIPOQ _ gene are found to have lower adiponectin levels. Changes in the _PAPD4 and KCNK9 gene also affect adiponectin levels.
  6. Gender, certain health conditions, and diet also affect adiponectin levels.
  7. Dietary changes and regular moderate exercise can help manage adiponectin levels.



What Is Body Mass Index?

Body mass index or (BMI) is an indicator of your body fat, which is calculated based on your height and weight.
This number is used to classify individuals into different groups – optimum weight, underweight, overweight, or obese.
BMI can be used as a screening test rather than a diagnostic test.
Several factors, such as age, sex, disease, genetics, and lifestyle, affect BMI measurements, and thus, normative standards must be applied for specific groups and individuals.

Both high and low BMI can cause health issues. BMI has proven to be a very useful tool to screen for weight problems in both adults and children. However, it does come with a few caveats:
1. BMI does not furnish information such as the mass of fat in different regions of the body.
2. BMI tends to overestimate the amount of body fat in people who are very muscular - that is, it does not differentiate between lean body mass and body fat mass.
3. BMI may also underestimate the amount of body fat in older adults and other people who have lost muscle mass.

Calculating Your BMI

To calculate the BMI using the metric system, you need to divide your weight (in kilograms) by the square of your height (in meters):
WEIGHT(Kg) / [HEIGHT(meters)]^2

Since height is usually measured in centimeters, the formula can be written as:
[WEIGHT(Kg) / HEIGHT (cm)/ HEIGHT(cm)] x 10,000

To calculate the BMI in the English system, the formula is:
WEIGHT(lb) / [HEIGHT(in)]^2 x 703

Before the BMI calculation, the weight needs to be converted into decimal values in case it is given in terms of ounces.

BMI Categorization

In order to calculate an individual’s BMI, his/her weight(in kgs) must be divided by the square of his/her height(in meters).
Based on the above-mentioned calculation, individuals are categorized as:
- <18.5: Underweight
- 18.5 to 25: Normal
- 25 to 30: Overweight
- 30 or higher: Obese

Based on BMI, obese individuals are further classified as:
- 30 to 35: Mild obesity
- 35 to 40: Moderate obesity
- 40 or higher: Extreme or severe obesity

BMI in Children

Unlike in the case of adults, BMI measurements during childhood and adolescence take age and sex into consideration. The BMI is calculated the same way by measuring height and weight. This is then plotted on a sex and age-specific chart. This will indicate whether the child’s weight is within a healthy range.
- Below the 5th percentile: Underweight
- 5th percentile to less than the 85th percentile: Healthy weight
- 85th to less than the 95th percentile: Overweight
- Equal to or greater than the 95th percentile: Obesity

How Does Genetics Influence Your BMI?

FTO Gene and BMI

FTO or Fat mass and obesity-associated gene, as the name suggests, is linked to body weight. It contains instructions for producing a protein known as alpha-ketoglutarate-dependent dioxygenase FTO.
The FTO gene is one of the most researched genes for obesity.

rs9939609 is an SNP in the FTO gene. It has been linked to an increase in total body fat levels. According to a study conducted, the presence of the AA allele in this SNP has been shown to contribute to obesity and increased BMI, irrespective of how the adipose (fat) tissue distribution is.
Factors influencing an individual’s BMI, like insulin sensitivity and plasma cholesterol levels, are also associated with the SNP rs9939609.

BDNF Gene and BMI

The BDNF gene contains instructions to produce the protein by Brain-Derived Neurotrophic Factor. This protein is found in the brain and spinal cord. It is especially found in the regions of the brain that control eating, drinking, and body weight. Hence, this protein influences all of these functions.

rs6265, also known as Val66Met, is a Single Nucleotide Polymorphism (SNP) in the BDNF gene. A study carried out a detailed examination of eating behavior in persons with different Val66Met types (Val-Val or GG, Val-Met or AG, and Met-Met or AA). It was discovered that people who have the Met-Met (AA) type had a lower BMI than those with the Val-Met (AG) or the Val-Val (GG) genotype.

Non-genetic Factors That Influences Your BMI

Certain factors can predispose you to a higher BMI. The good news is that most of these factors are modifiable and can be worked around to achieve the ideal BMI.


Adults who have a normal BMI often start to gain weight in young adulthood and continue to gain weight until they are ages 60 to 65. In addition, children who have obesity are more likely to have obesity as adults.


Women are likely to accumulate fat near their hips and buttock areas. Men build up fat around their abdomen (belly) region.
Women tend to build up fat in their hips and buttocks. Extra fat, particularly if it is around the abdomen, may put people at risk of health problems even if they have a normal weight.


In American adults, the prevalence of obesity is the highest in African Americans, followed by Hispanics/Latinos, then Caucasians. This is true for men and women.


Needless to say, dietary habits influence your body weight. High-calorie and high-sugar foods increase your risk for overweight and obesity.

Other factors that influence your BMI include your levels of physical activity, your work environment, and your family habits and culture.

Effects of High BMI

High BMI and obesity can increase the risk of many chronic health conditions, including:
- High blood pressure
- Type 2 diabetes
- Liver disease
- Osteoarthritis
- Cardiovascular disease
- Musculoskeletal problems

Effects of Low BMI

Being underweight and have insufficient fat in your body can also lead to health complications like:
- Anemia
- Malnutrition
- Bone loss and osteoporosis
- Decreased immune function

BMI May Not Be The Best Indicator Of Obesity?

One of the prime reasons for this is that BMI doesn’t differentiate between muscle and fat.
It may not be accurate, especially if you are in one of the following groups:

Athletes: Athletes tend to have higher bone mass and lean muscle mass. As a result, they may have higher BMI.
But this increased lean muscle mass can actually be healthy as it helps boost metabolism and prevent heart diseases and diabetes.

Pregnant or breastfeeding women: Most of the weight gain during pregnancy is to provide nourishment for the growing fetus and is usually not an indication of bad health or obesity.

Older people: In people who are 65 or older, a BMI of less than 23 is associated with health risks. The ideal BMI for this age group is considered to be 27.

Alternative Ways To Measure Body Fat
- Waist circumference
- Waist to height ratio
- Body fat percentage
- Waist to hip ratio


  1. Body Mass Index or BMI is a value that is derived by measuring a person’s height and weight. It could be an indicator of whether a person’s weight is healthy.
  2. A BMI reading of >30 could indicate overweight, and <18.5 could indicate underweight.
  3. BMI in children is also measured using height and weight. This is plotted on a chart specific for age and sex and then analyzed.
  4. Your genes influence your BMI by modulating several weight-related factors. FTO is one such gene, which has been widely studied for obesity.
  5. Other factors like age (early adulthood to 60 years), sex (women are at higher risk), and ethnicity (African Americans have a higher risk) also increase obesity risk.
  6. Both higher and lower BMI can be harmful to health. High BMI has been associated with health conditions like obesity and type 2 diabetes. Lower BMI can increase your risk for bone loss and anemia.
  7. BMI need not always be the best indicator of obesity. This is because it doesn’t differentiate between lean muscle mass and fat. So, BMI may not be a useful tool for athletes, pregnant women, and older people.
  8. Maintaining your calorie intake and calorie expended can help you maintain a healthy weight.



Nicotine Dependence: Introduction

Nicotine is a nitrogen-containing chemical and is a highly addictive substance. It is mainly found in tobacco and is primarily consumed by inhaling the smoke of tobacco cigarettes. Nicotine produces ‘pleasurable and pleasing’ effects on the brain. With regular smoking, you tend to get used to these positive feelings. Going without a smoke can make you experience unwanted effects - this indicates nicotine dependence.

According to the CDC, smoking is the leading cause of preventable death in the U.S. A study even suggests the smoking is responsible for 1 in every 5 deaths in the U.S..

## Symptoms of Nicotine Dependence
The symptoms vary amongst individuals and also differ based on the level of dependence. Some signs to watch out for include:
- A history of at least one unsuccessful attempt to quit smoking
- Withdrawal symptoms like irritability, mood swings, insomnia, restlessness, increased hunger, and anxiety
- Social withdrawal - an unwillingness to participate in any activities or go to any places that discourage smoking.

Causes Of Nicotine Dependence

The addictive quality of nicotine is what causes nicotine dependence. Nicotine triggers the release of the happy hormone, dopamine. This pleasure response is what smokers chase after. Smoking also increases the heart rate, which in turn boosts the noradrenaline hormone. The increased hormone levels enhance mood and concentration.

People who smoke nicotine start craving the dopamine rush. When they abstain from smoking for a few hours, the hormone levels start to drop, and they start to experience undesired effects like irritability and anxiety.

Brief History of Nicotine/Tobacco Usage

Nicotiana tabacum is the type of nicotine found in tobacco plants. The tobacco plant has been used for its medicinal benefits for at least 200 years.

“It is thought that Christopher Columbus, while exploring America for the first time, discovered tobacco.

Using tobacco for smoking started and spread rapidly over the 1600s. When it was introduced in Europe, some saw its medicinal purpose, while others viewed it as a toxic, addictive substance.

Tobacco usage exploded when cigarette-making machines were introduced in the 1880s. Only in 1964, a study established a link between smoking and heart and lung cancer was published. 30 years later, in 1994, the U.S. FDA recognized nicotine as a drug with addictive properties. Finally, only in 2009, the Supreme Court granted the FDA control to establish some nicotine regulations.

The Role of Genetics In Nicotine Dependence

A person may have smoked cigarettes in his youth and would’ve had no trouble stopping it after. Another person may enjoy recreational smoke but not feel the need to smoke a few every day. Yet another person continues to smoke a pack a day and cannot seem to quit this habit.

So, what contributes to these differences in smoking patterns? Why are the pleasure-inducing effects of nicotine evident in some and not in others?

Some studies have revealed that the differences in response to nicotine can be attributed to changes in some genes involved in the production of receptors to which nicotine binds to.

Let’s dilute this further. Nicotine has a similar structure to the neurotransmitter, acetylcholine. Acetylcholine is known to influence memory, arousal, attention, and mood. Nicotine binds to a type of acetylcholine receptors called the nicotine acetylcholine receptors or nAch. nAch receptor has 5 subunits. These subunits are produced by certain genes. Any changes in these genes can alter the structure of the subunits, which in turn can alter the nAch structure. These alterations modify how you respond to nicotine.

CHRNA5 Gene and Nicotine Dependence

The CHRNA5 gene contains instructions for producing the α5 subunit of the nAch receptor. Certain changes or mutations in this gene alter the α5 subunit and makes the nAch receptor channels more/less sensitive to nicotine.

rs16969968 is an SNP in the CHRNA5 gene. It influences the pleasurable effects of nicotine. The A allele has been associated with “enhanced pleasurable responses” to a person’s first cigarette. The A allele carriers are at an increased risk for nicotine addiction, compared to the G allele carriers.

Interestingly, the A allele has also been associated with lower risk for cocaine dependence!

CHRNB3 Gene and Nicotine Dependence

The CHRNB3 gene contains instructions for producing the β3 subunit of the nAch receptor. This gene has been identified to predispose an individual to nicotine addiction.

rs10958726 is an SNP in the CHRNB3 gene. The T allele of this SNP has been associated with increased risk of nicotine dependence.

Several other genes like CHRNG, CHRNA4, CYP2B6, and FMO also influence the risk of nicotine dependence.

Non-genetic Contributors To Nicotine Dependence

Age: According to a study, the chances of developing nicotine dependence is higher when the age of onset of smoking is before 21, especially between 18-20 years.
Peers: People who grow up with smoking parents or spend more time around friends who smoke are more likely to get into the habit of smoking and may eventually develop nicotine addiction.
Substance usage: People who consume alcohol or drugs are more likely to become nicotine dependent. The reverse relationship is also true! In fact, according to a study conducted to evaluate concurrent use of alcohol and cigarettes, approximately one-third of current drinkers smoked, whereas approximately 95 percent of current smokers used alcohol.
Mental illness: People with mental troubles like depression, PTSD, or schizophrenia are more likely to be smokers than other people. A study that looked at depression and nicotine dependence from adolescence to young adulthood concluded that depression is a prominent risk factor for nicotine dependence, and the adolescent and youth population exhibiting depression symptoms constitute an important group that requires smoking intervention.
Mental illness: People with mental troubles like depression, PTSD, or schizophrenia are more likely to be smokers than other people. A study that looked at depression and nicotine dependence from adolescence to young adulthood concluded that depression is a prominent risk factor for nicotine dependence, and the adolescent and youth population exhibiting depression symptoms constitute an important group that requires smoking intervention.

Effects of Nicotine Dependence

Using tobacco can lead to grave health complications. Nicotine dependence has been tied to increased risk of various health conditions.

Lung and Other Cancers

Tobacco smoking, to date, remains the most established contributor to lung carcinogenesis or lung cancer. Recent studies suggest that nicotine, in small quantities, accelerates cell growth and in large quantities becomes toxic to cells. Nicotine also decreases the levels of CHK2, a protein that acts as a tumor suppressor. Further, it lowers the effects of anti-cancer treatments. Smoking contributes to 30% of all deaths due to cancer!

Chronic Obstructive Pulmonary Disease (COPD)

Cigarette smoking remains the leading cause of COPD in the U.S. A CDC analysis revealed that the prevalence of COPD in adults was 15.2% among current cigarette smokers, compared to 2.8% among adults who never smoked!

Heart and Other Circulatory System Complications

Smoking causes damage to the heart and blood vessels. It also alters your blood chemistry, contributing to plaque build-up. In the U.S., smoking accounted for 33% of all deaths caused due to cardiovascular diseases.


Research shows that nicotine influences the activity of pancreas. The usage of nicotine leads to decreased production of insulin by the pancreas. Thus, the blood sugar levels are poorly regulated, leading to diabetes. Smokers with diabetes may require higher doses of insulin to keep their blood sugar levels in check.

Pregnancy Complications

Tobacco smoking during pregnancy increases the risk of both morbidities and mortality of newborns. Nicotine damages the developing lungs and brain of the fetus. Common birth defects caused due to nicotine are cleft lip and cleft palate. Nicotine Replacement Therapy (NRT) has been suggested for pregnant women who are unable to quit smoking. However, the safety of NRT to the developing fetus has not been well-documented yet.

Nicotine Withdrawal

Nicotine withdrawal is the set of symptoms one experiences upon stopping tobacco usage. It can start as early as 30 minutes from the last usage. The range and severity of symptoms can depend on how long the person has been smoking and how often they have smoked. Some symptoms include:
- Increased craving for nicotine
- Increased hunger and appetite
- Mood swings
- Sweating
- Nausea and vomiting
- Tingling feelings in hands and feet
- Headaches
- Anxiety
- Depression
- Difficulty in concentrating
- Insomnia

Recommendations To Overcome Nicotine Dependence

Owing to the withdrawal symptoms, quitting smoking can be very challenging. The following are the basics of any de-addiction program which can help you overcome nicotine addiction.
- Staying away from triggers
- Support of friends and family
- Other support groups
- Web-based programs

There are also other specific ways that can help you gradually become nicotine-independent.

Nicotine Replacement Therapy (NRT)

It is the process of administering the nicotine that your brain demands in a safer way by avoiding all the other harmful substances present in cigarettes. This also provides relief from the withdrawal symptoms. NRT supplies lower doses of nicotine at slower rates. Some of the commonly available NRTs include:
- Nicotine gums
- Nicotine patches
- Nicotine nasal spray
- Nicotine inhaler
- Nicotine lozenges
All of these are generally available over the counter and do not require prescriptions.


There are certain medications available that do not contain nicotine but are designed to produce the same effects of nicotine on the brain. They help decrease cravings and alleviate other withdrawal symptoms. Some examples of these medications include Chantix and Zyban.

Important note
In 2009, the FDA mandated the makers of such medications to put a black box, warning the users about the possible dangerous psychological effects, including agitation, depression, and suicidal thoughts.

Cognitive Behavioral Therapy (CBT)

CBT trains smokers to cope with the symptoms of withdrawal. CBT has known to achieve twice the success rate when it comes to quitting smoking (compared to people who didn’t receive CBT).


  1. Nicotine dependence is usually seen in the form of tobacco/cigarette smoking addiction. It is caused due to the pleasure-inducing property of nicotine that releases dopamine in the brain.
  2. Upon regular smoking, a person can get used to this ‘dopamine rush’ and, when abstained from smoking, can experience unwanted side effects related to the drop in hormonal levels.
  3. Nicotine’s structure resembles that of acetylcholine’s and hence goes and binds the to acetylcholine receptors known as nAch receptors.
  4. The genes that contribute to the production of these receptors influence how you respond to nicotine or the effects produced by nicotine on your body.
  5. CHRNA5 is a gene that forms a subunit of the nAch receptor. The A allele of rs16969968 SNP present in this gene increases the risk for nicotine addiction.
  6. Other factors that influence nicotine dependence risk include age, smoking habits of peers, substance abuse, and mental illnesses.
  7. Nicotine usage has been linked to numerous health conditions, including cancer, especially lung cancer, COPD, diabetes, heart diseases, and pregnancy complications.
  8. Nicotine withdrawal is the set of symptoms seen when a person tries to quit his nicotine habit. These symptoms can pose a real challenge to stay away from nicotine.
  9. Nicotine replacement therapy or NRT is commonly recommended for people who are trying to quit smoking. Other than NRTs, cognitive behavioral therapy, counseling, support groups can also help break out of nicotine dependence.



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