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.
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.
A research study on the data from Adolescent Brain Cognitive Development (ABCD) Study suggests a relationship between certain regions in the brain and weight gain among children and adolescents. The study explored the relationship between “reward region” and food processing and suggests that this region may predict obesity in children.
Childhood obesity is a serious problem in the United States, putting children and adolescents at risk for poor health. Overweight children are much more likely to become overweight adults unless they adopt and maintain healthier patterns of eating and exercise.
Previous research has identified a region in the brain associated with overeating or unhealthy eating behavior.
Almost all our actions are driven by two things: Necessity and Reward. An activity can be considered a reward when it motivates us or gives us pleasure. Neurons, the brain's fundamental working unit, communicates this "reward" using dopamine, which is popularly known as the "happy hormone."
Incidentally, food-reward is common in animal training routines. An animal is rewarded with a treat when it performs certain actions and this programming of food-reward is routinely used by animal trainers in zoos and entertainment venues and other animal training facilities.
Hedonic hunger describes eating for pleasure than hunger - to enjoy the taste rather than to meet the body's energy needs. This pleasure eating triggers the brain's reward system region, which can lead to overeating - a common cause of obesity.
"The ABCD study or the Adolescent Brain Cognitive Development Study is the largest long-term study of brain development and child health in the United States." The study was done on over 10,000 children from ages 9-10 and was followed up through early adulthood.
Using the data from this study, the researchers attempted to investigate the relationship between the reward system region in the brain (called the nucleus accumbens) and eating behavior by examining 5300 research participants.
It was observed that when 2000 participants returned for a one year follow up, the waist circumference had increased by an average of 2.76 centimeters per participant.
The cell density (number of cells for a given area) in the reward region of the brain was examined using a noninvasive MRI technique.
The MRI revealed changes in the cell density that reflected the increase observed in the waist circumference.
The study speculates that the increase in this cell density can be because of an inflammation caused due to a diet rich in high-fat foods.
The findings essentially tell us that a vicious cycle of pleasure eating leading to changes in brain, in turn leading to overeating and increasing the risk of obesity.
Not all children who carry a few extra pounds can be classified as obese. Weight fluctuations are commonly observed in the growing stage of children. Before you decide on dietary changes for your child based on any weight gain you see, it's best to consult a doctor. The doctor may use growth charts, calculate the BMI and, take a family history, and, if necessary, may order a few tests to outline the issue behind the weight gain.
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
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Carbohydrates are one of the main classes of food. It is the main source of energy for the body. They are a group of organic compounds present in the form of food in cellulose, starch, and sugar. They are called carbohydrates, as they contain hydrogen and oxygen in the same ratio as water (2:1). These are then broken down to release energy.
Due to the association of carbohydrates with weight gain, the carbs may disguise as an enemy to a healthy diet. However, the right kind of carbs in the right amounts can definitely earn a rightful place in your diet.
A healthy weight is an important element of good health. The amount of food you eat and what you eat is important for maintaining a healthy weight.
For years, there was a myth that a low-carb diet is the best way to lose weight, but a growing body of evidence suggests otherwise.
Carbs are sub-divided into three categories depending on the number of sugars present and the nature of the chemical bonds between them.
Although this is the conventional way of classifying carbs, a more pragmatic approach would be to classify them as refined and whole carbs.
Whole carbs include vegetables, legumes, whole fruits, and grains, which are unprocessed and thus have their nutrient content intact.
The stripping of nutrients in refined carbs as a part of processing makes them count as 'empty calories.'
This removal of the nutrients results in rapid absorption and metabolism of these carbohydrates.
This results in spiked sugar levels and unstable energy levels, the latter of which causes “sugar rush” after consuming sugar-rich foods.
The refined or the sugary carbs are simple carbohydrates that the body quickly absorbs.
Their metabolism occurs rapidly, which results in major swings in the blood glucose levels. This induces hormonal and metabolic changes that can promote overeating.
Not all carbohydrates are bad for health.
Unprocessed carbs that are present in vegetables, fruits, and grains are healthy.
Studies reveal that these improve metabolization and help in weight loss.
Another class of carbs, the processed ones, are unhealthy because they lose the fiber during processing and contain no essential nutrients.
Examples of these include white bread, white rice, and the like.
Intake of foods containing processed carbs can result in weight gain and increased risk of type 2 diabetes.
Studies show that high unprocessed carbs in the diet can lead to a craving for more carbs, and people tend to get caught in the vicious cycle.
Thus, making changes to your diet by including more of unprocessed carbs can be a healthy choice.
Studies have shown that there is a link between genetic factors and dietary factors such as weight loss, weight gain, obesity.
Nearly 70% of the world population carries the gene for obesity. This explains why obesity is growing rapidly around the world.
However, people can reverse this gene's effect by exercising and including more protein in their diet.
A study has found an association between the FTO gene and the intake of carbohydrates.
The individuals with the A variant were found to have a higher risk of obesity than ones with the CC wild type.
The FTO gene has a negative association with over-eating.
About 23% of the global population carries a variant in the AMY1 gene, which shows an association with low copy numbers of the gene and reduced ability to digest starch.
70% of people from agricultural populations have an AMY1 copy number variant, which shows an association with better starch digestion and lower risk of obesity when compared to 37% of non-agricultural populations.
The conventional diet plans and workout regimes architected for weight loss need not help everyone achieve their desired goals.
There is a multitude of factors that influence weight loss, including a person’s lifestyle, genetic makeup, and the environment.
Your genes can influence how you metabolize the nutrients you get from your diet. This directly has a role to play in weight gain/loss.
For instance, some people may possess a genetic variant that aids in the faster metabolization of carbohydrates, while others may carry a variant that will help in faster break-down of saturated fats.
You can leverage such genetic information to adopt a practical and personalized weight loss plan.
While genetic tests may not lay out the A-Z of weight loss, it certainly helps you pin the right path for your weight loss journey.
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In the US, around 4.6 percent of the population aged 12 and above are diagnosed with hypothyroidism. It is a condition where the body does not produce enough thyroid hormones. The thyroid is an important regulator for many functions in the body. This butterfly-shaped organ controls blood pressure and, therefore, the efficiency of the digestive system. Since this hormone controls such important processes, it indirectly controls energy regulation and metabolism. Hypothyroidism can be diagnosed through routine blood tests, or after symptoms start to show. The most common cause of this condition is a disease called Hashimoto's.
Since the thyroid hormones are involved in so many functions, there may be many symptoms, and they may be wide-ranging and diverse.
The main symptoms are fatigue, cold intolerance, joint, and muscle pain. The other signs and symptoms are:
If left untreated, this could manifest into more severe symptoms like:
It has been a long-known fact that there is a complex relationship between thyroid, body weight, and metabolism.
Metabolism, determined by measuring the oxygen usage by the body over a specific time, is regulated by the thyroid hormone.
This measurement, when done in rest, accounts for something called ‘basal metabolic rate’ or BMR.
A low BMR may have an association with weight gain in certain cases.
Low thyroid hormone levels is a contributor to low BMR levels, and earlier, this was one of the diagnostic tools for hypothyroidism.
However, a low BMR could be due to an n number of reasons, and thus, it is not an effective measure of diagnosis anymore.
In the case of hypothyroidism, weight gain need not always be due to excess fat in the body.
Accumulation of salt and water being the contributor to weight gain is more plausible here.
Weight gain also depends a lot on the severity of hypothyroidism. In other words, more weight gain may be seen in cases of severe hypothyroidism.
To conclude, if weight gain is the only visible symptom, it’s better to explore the other contributors first before suspecting hypothyroidism.
Firstly, it is important to assess whether you’re at risk for the disorder, for quick diagnosis and treatment.
Early detection and treatment can help manage the complications that emerge if hypothyroidism is left untreated.
Identifying the risk factors also can point in the right direction for losing weight with hypothyroidism.
The TSHR (Thyroid Stimulating Hormone (TSH) Receptor) gene codes for a receptor protein that is found on the membrane of the cells that span across the thyroid gland.
The receptor binds specifically to TSH and plays a pivotal role in thyroid hormone metabolism.
A part of the receptor is outside the thyroid gland cell, and the rest remains in the cell.
The thyroid-stimulating hormone binds to the receptor, which brings about a series of reactions that control the development of the thyroid gland.
TSHR gene mutations can cause congenital hypothyroidism. These mutations change the building blocks that make up the receptor protein.
Moreover, the mutations affect the spread of the receptors across the thyroid gland. Other mutations make the receptors reside completely within the cell or impair the hormone's ability to bind with the receptor.
In conclusion, these mutations don’t allow the receptor to interact with the hormone efficiently.
When the receptor is unable to interact with the hormone, the hormone production is not stimulated.
This makes the body compensate for the lack of stimulation.
The gland either overproduces the hormone, and functions as normal, or severely under produces the hormone, causing hypothyroidism.
Mutations in the TSH receptor gene result in resistance to TSH, and therefore, a reduction in thyroid hormone production.
Mutations in TSHR may also cause thyroid hypoplasia, that is, an underdevelopment of the thyroid organ.
Firstly, the patient is assessed for symptoms like fatigue, dry skin, constipation, and weight gain.
Above all, the family's and the individual's medical histories are assessed for any previous condition like goiter or any other thyroid problem.
There are increasing reports that correlate the prevalence of thyroid autoimmunity and glycogen storage disease (GSD).
GSD is a condition where stored glucose reserves (stored as glycogen) cannot be degraded efficiently in the body.
Blood tests are the easiest way to diagnose hypothyroidism.
Usually, the levels of TSH and thyroxine are checked.
An underactive thyroid gland would produce high levels of TSH and low levels of thyroxine.
This is because the body is putting in extra efforts to produce the thyroid hormone.
The most common way to treat this condition involves the use of a synthetic thyroid hormone, levothyroxine.
This is an oral medication that reverses the signs and symptoms of the disorder.
Six to eight weeks after the medication, doctors recheck the TSH levels.
Excessive amounts of the hormone can cause increased appetite, insomnia, heart palpitations, and shakiness.
Other medication that you’re taking, as it can affect how the synthetic hormone work, and therefore, it is important to mention them.
This includes diabetes, antidepressants, estrogen, warfarin, heart medication, and supplements like magnesium, aluminum, iron, or soy.
Other treatments include diet supplements, surgery, and herbal remedies.
With regard to diet, it is important to note that conventional weight loss diets need not help in losing weight with hypothyroidism.
Make sure you eat the correct amount of calories that match your BMR as well as your physical activity levels.
Eating too little can slow down metabolism to the extent that any weight loss effort would be sabotaged.
Try to stick to a consistent meal plan and preferably stick to small but frequent meals.
Calorie counting, or keeping a food journal would help in understanding what foods you tend to eat more of, and this can provide an overview of your diet.
Thyroid patients experience tend to constipation and slow metabolism. So losing weight with hypothyroidism can be challenging.
Typically, diets consist of fiber-rich foods to aid in weight loss.
The following have a significant impact on the diet of a thyroid patient:
These components are essential in maintaining an anti-inflammatory diet.
This helps to calm the immune system and reduce excessive inflammation.
This diet also reduces the pressure on the liver and allows the body to metabolize the nutrients efficiently.
Although an underactive thyroid gland is associated with significant weight gain, treating the root cause with supplementing synthetic thyroid hormones does not aid in significant weight loss in patients.
In a study conducted by the American Thyroid Association, the synthetic thyroid hormone, levothyroxine, aided in losing weight in only half the volunteers with hypothyroidism.
The basis for natural remedies for hypothyroidism includes focusing on a balanced diet, curbing stress, and incorporate missing nutrients.
An optimal diet plan for patients with hypothyroidism has been explained in the section above.
Other supplements that can be added are as follows:
Low thyroid hormones affect the body's vitamin B levels.
Taking vitamin B supplements can help tackle the fatigue that the body faces.
Foods that are rich in this vitamin are peas, beans, sesame seeds, tuna, milk, and eggs.
Adding probiotics to your diet can help maintain live, helpful bacteria in the gut- preventing serious conditions like chronic diarrhea.
In its raw form, it helps in the optimal functioning of the thyroid gland.
This helps in losing weight, increasing metabolism, and balancing body temperature.
It helps in maintaining a balanced production of hormones in the body.
It helps in removing body toxins and regulate body fat.
A deficiency of vitamin D can lead to thyroid problems.
Ensure that you get at least 15 minutes of sunlight daily for optimal vitamin D production.
Foods that are rich in this vitamin are mackerel, orange juice, egg yolks, and dairy products.
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What if you learned of a magic pill that could boost your metabolism, aid your weight loss program, help you feel full, increase your lifespan, reduce your risk of diabetes, cancer, and heart diseases while controlling your cholesterol? You'd probably jump on it without thinking twice. Well, you don't need a drug to get these things in their real sense. Not when we can suggest a single ingredient that covers it all - Fiber.
Despite all the fantastic health benefits of fiber, researchers still point out that not many people are maximizing its full potential. Of course, that's expected because most people lack the knowledge of the amazing things that fiber can do in the body. To this effect, this article focuses on the benefits of microfiber, with particular interest on their potential to help in weight loss.
Fiber is often divided into different categories, with each category differing in their nutrigenomics. The most popular categories of fiber include insoluble fiber, soluble fiber, and prebiotic fiber.
This is a type of fiber that does not mix with water.
It acts majorly as a bulking agent, helping to form stool and pass it through the guts.
It has proven to be useful in treating constipation.
On the other hand, this category of fiber mixes with water to form viscous gel-like substances that are capable of slowing down how fast the stomach can release digested food to the gut.
Researchers confirm that eating enough soluble fiber reduces belly fat and the prevention of further add-up.
The last type of fiber is the prebiotic fiber that feeds the friendly bacteria present in your gut.
This helps the gut bacteria to produce nutrients for your colon cells, leading to a healthier digestive system.
Facts and research have always pointed out that fiber can help anyone lose weight, even if they don't make other adjustments to their diet.
First, fiber is super-filling, leaving your stomach with little space to eat other high-fat foods.
Besides, the digestive process of fiber is relatively slower compared to sugar and simple starches.
There are several other ways they help to reduce weight, and it's been proven repeatedly.
In fact, dieters who were told to get at least 30 grams of fiber per day without any other dietary parameters lost a significant amount of weight.
Fiber is not just high for keeping your weight and appetite in check; it is also great for your heart-health and can help reduce the risk of diabetes.
There are loads of other benefits that we will discuss as this article progresses.
When it comes to weight loss, fiber's the best choice as it encourages the diversity of gut bacteria.
It's important to know that there are already over 100 trillion helpful bacteria that live in your lower gut.
Such bacteria are harmless, sharing a mutually beneficial relationship with humans.
Since soluble fiber helps to improve gut bacteria, it's a no-brainer that it will help to reduce belly fat.
Most people have always been curious about how fiber helps in weight reduction. Here, let's review some of the ways it works.
It is no surprise that fiber is a powerful natural suppressant of appetite. This keeps you from regularly reaching out for junk.
It is important to know that soluble fiber makes it more likely for you to reduce your intake of calories by suppressing your appetite. This would, in turn, help you lose weight.
There are tons of theories regarding how fiber helps for the reduction of appetite.
However, the most popular one is that it helps regulate hormones involved in controlling appetite.
However, another theory suggests that fiber can aid in appetite reduction by slowing the movement of food through the gut.
Even though everyone can benefit from consuming a fiber-rich diet, the effects of such a diet can vary from person to person.
Some people can lose a considerable amount of weight from this diet, while for others, dropping a few kilos might take a while.
This is because our genetic variations influence how our body responds to different nutrients present in the diet.
Let us take the FTO gene, for example. We've heard several questions about how the FTO gene influences weight loss and weight gain.
The FTO gene, short for FTO alpha-ketoglutarate dependent dioxygenase, located on chromosome 16, is mainly associated with the body-mass index, obesity, and type II diabetes.
A recent study pointed to an association between a particular variation in the FTO gene and carbohydrate intake, with individuals having a certain variant more susceptible to obesity than if they carried the original C allele (normal variant).
We've also seen several other studies establishing a direct relationship between a T to A transition and an increase in BMI.
Over time, a significant association between another variation and dietary fiber intake was noticed.
The research study has, in fact, reported that individuals carrying the AA genotype exhibited lower waist circumference than the T allele carriers on a high fiber diet.
When on a high-fiber diet, people carrying the AA genotype tend to experience more weight loss than the other genotypes.
However, the A allele carriers, are also at a higher risk for obesity when physically inactive for prolonged periods of time.
Fiber-rich food can result in weight loss by increasing the feeling of fullness, thus leading to reduced calorie intake.
Since your genotype favors higher weight loss on fiber intake, you can include more fiber-rich foods in your diet.
Some natural sources of fiber include Broccoli, Lentils, Kidney Beans, Bananas, Barley, Almonds, Carrots, Dates, etc.
Since your genotype also puts you at a higher risk for obesity when physically inactive, ensure to include some light exercises in your routine.
Here are some simple exercises that can make you feel great all day.
T allele carriers may not experience a significant weight loss on fiber intake.
A lesser reduction in BMI on high fiber intake was noticed in the TT genotype in comparison to the AA genotype.
While ensuring adequate fiber intake, consumption of other weight loss-friendly foods can also help.
After several studies on the effect of fiber from food, researchers have concluded that the benefits of fiber from supplements cannot equal that of food fiber.
Plus, getting fiber from supplements might mean missing out on essential vitamins, minerals, and other nutrients present in fiber-rich food.
However, people who may have certain dietary restrictions like gluten intolerance may need to turn to fiber supplements to get the daily recommended dose.
Having talked so much about fiber for weight loss, and how the DNA diet affects your journey towards achieving the perfect body structure, it's also important that we suggest some dietary sources of fiber.
Bear in mind that most fiber-rich foods contain both soluble and insoluble fiber. Some popular fiber-rich foods include:
There you have it now. We've reviewed everything you'll need to know about fiber and weight loss.
We've also made recommendations on foods with high fiber content. With the average fiber requirements for your body per day pegged between 25 to 30 grams, it lies on you to find what fits your body and stick to it.
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The Fat Mass and Obesity gene (FTO) is associated with the synthesis of the FTO enzyme, also known as the alpha ketoglutarate dependent dioxygenase. FTO gene expression has been shown to be upregulated in the hypothalamus of the brain after food deprivation, which is associated with increased consumption of high calorie foods. There are 3 SNPs that we analyze in association with weight management and carbohydrates, fiber, protein or saturated fat intake- rs9939609, rs8050136 and rs11076023.
In a review study, children with the A variant of the gene were shown to be associated with greater intake of biscuits when compared with children with the T variant (rs9939609). Adults with the A variant (rs9939609) were also shown to have altered post prandial satiety (feeling of being full) levels. In a similar study conducted to identify the association between post prandial satiety and rs9939609, people with the A variant of the fat gene were found to be associated with low sensation of feeling full after a meal.
Loss Of Control Over Eating
In a study conducted on 289 youth, people with the A variant (rs9939609) of the gene had a greater tendency to eat more fat than people with the T variant (rs9939609), with 37.4% of people with the A variant reporting loss of control over eating when compared with 18.8% of people with the T variant. Subsequently, the study showed that people with the A variant of the gene had a significantly greater body mass index.
TV advertisement and overeating
TV advertisements could also induce people to overeat, but the extent of overeating is shown to be associated with the fat gene variant carried by the individual. A study was conducted on 200 children post lunch, involving screening of a 34 minute television program, which also included food advertisements and toy advertisements. Children with the A variant (rs9939609) of the gene consumed significantly more snacks when they were exposed to food advertisements.
In a study conducted on 1618 people from an Asian Indian population, people with the A variant (rs8050136) of the gene had a 2.46% higher risk of obesity when compared to people with the C variant among people on a high carbohydrate diet. In the same study, it was found that among people who were inactive, people with the A variant were found to be associated with 1.89 times increased risk for obesity.
In the study on 1618 people from an Asian population, people with the A variant (rs11076023) of the gene were shown to be associated with 1.62cm lower waist circumference than people with the T variant of the gene.
In a study conducted to identify the association between fat intake, FTO genotype (rs9939609) and body fat percentage, people with the T variant did not show an increase in body fat percentage with increase in fat intake, but people with the A variant were shown to be associated with increased body fat percentage with increased fat intake.
In a study conducted on 4839 men and women on a high fat diet, people with the A variant (rs9939609) were shown to be associated with higher BMI and were twice as likely to be obese when compared with people with the T variant.
In a study conducted on 737 overweight adults, people with the A variant of the gene (rs9939609) were shown to be associated with a reduced food craving on a hypo-caloric and a high protein diet.
In a study conducted on 2577 Korean study participants, it was found that people with the A variant (rs9939609) of the fat gene were associated with increased risk for obesity and, thereby, an increased risk for diabetes. In a similar study conducted on 4,189 Han Chinese individuals, people with the A variant of rs9939609 and A variant of rs8050136 were shown to be associated with type 2 diabetes and obesity in the Asian population.
|CHIP Version||FTO SNPs|
|23andMe (Use your 23andme raw data to know your FTO Variant)|
|V5 23andme (current chip)||Present|
|AncestryDNA (Use your ancestry DNA raw data to know your FTO Variant)|
|v1 ancestry DNA||Present|
|V2 ancestry DNA (current chip)||Present|
|Family Tree DNA (Use your FTDNA raw data to know your FTO Variant)|
|OmniExpress microarray chip||Present|
|AA||[Limitation] More likely to have higher risk for obesity. [Limitation] More likely to have higher fat percentage on a high fat diet [Limitation] More likely to have higher BMI on a high fat diet [Limitation] More Likely to have loss of control eating episodes [Limitation] More Likely to have higher risk for type 2 diabetes [Advantage] More likely to have lower food craving on a high protein diet||A common fat gene myth is that people with this variant are doomed to remain overweight or obese, however, practicing mindful eating and consciously avoiding increased consumption of high fatty food could help in better weight management For people with this variant of the fat gene weight loss can be achieved by balancing food intake with appropriate exercises A high protein diet may be beneficial as it reduces food craving. So foods that turn off fat genes are foods that are rich in protein. Spirulina is a rich source of protein and helps improve satiety|
|AT||Moderate risk for obesity|
|TT||[Advantage] More likely to have lower risk for obesity. [Advantage] Less likely to have higher fat percentage on a high fat diet [Advantage] Less likely to have increased BMI on a high fat diet [Advantage] Less Likely to have loss of control eating episodes [Advantage] Less Likely to have higher risk for type 2 diabetes [Limitation] Less likely to have lower food craving on a high protein diet||Ensure a healthy balance between food intake and exercises|
|AA||[Limitation] More likely to have increased risk for obesity. [Limitation] More Likely to have higher risk for type 2 diabetes||Ensure a healthy balance between food intake and exercises|
|AC||Moderate risk for obesity||Though the risk for obesity is lower, practise healthy eating practices and ensure sufficient physical activity|
|CC||[Advantage] More likely to have lower risk for obesity. [Advantage] Less Likely to have higher risk for type 2 diabetes||Though the risk for obesity is lower, practise healthy eating practices and ensure sufficient physical activity|
|AA||[Advantage] More likely to have lower waist circumference on a high fiber diet||Consume a fibre rich diet to ensure better weight maintenance Fibre rich foods include black beans, lima beans, broccoli, artichoke and brussels sprouts|
|AT||Moderate waist circumference on a high fiber diet||A fiber rich diet may not considerably lower weight but it helps in bowel movements and in controlling blood sugar levels|
|TT||[Limitation] More likely to have higher waist circumference than people with the A variant on a high fiber diet||A fiber rich diet may not considerably lower weight but it helps in bowel movements and in controlling blood sugar levels|
“Nutrigenetics, fitness genetics, health genetics are all nascent but rapidly growing areas within human genetics. The information provided herein is based on preliminary scientific studies and it is to be read and understood in that context.”
The hepatic lipase gene (LIPC) is associated with the synthesis of hepatic lipase enzyme (LIPC) which catalyzes the hydrolysis of fat. Hepatic lipase converts intermediate-density lipoprotein (IDL) to low-density lipoprotein (LDL).It is expressed in the liver and in the adrenal glands. Specific alleles of this gene are known to either increase or decrease hepatic lipase levels, and due to linkage disequilibrium, the levels of lipoprotein lipase, which is associated with variations in the plasma HDL levels. People with the T variant of the gene are shown to be associated with higher baseline HDL levels.
|CHIP Version||LIPC SNPs|
|23andMe (Use your 23andme raw data to know your LIPC Variant)|
|V5 23andme (current chip)||Present|
|AncestryDNA (Use your ancestry DNA raw data to know your LIPC Variant)|
|v1 ancestry DNA||Present|
|V2 ancestry DNA (current chip)||Present|
|Family Tree DNA (Use your FTDNA raw data to know your LIPC Variant)|
|OmniExpress microarray chip||Present|
People with the C variant of the gene were associated with reduction in weight, body fat and visceral fat.
In a study investigating the effects of endurance training on plasma lipoprotein levels, people with the C variant of the gene have been found to be associated with exercise mediated reduction in VLDL and increase in HDL. The benefit of exercise was found to be more in men with CC genotype than women.
In a meta-analysis study conducted on children, boys with the T allele had a higher BMI and higher risk of obesity. In another study, boys with the T variant of the gene were found to be associated with higher HDL level on high fat intake.
In a study conducted to determine gene-nutrient interactions, people with the T variant on a low fat diet (less than 30% of energy from fat) have been shown to be associated with higher HDL levels. In a study conducted to identify how Chinese, Malays and Asian Indians in Singapore were exposed to similar environment but where Asian Indians had three times the rates of myocardial infarction compared to Chinese, found that a complex interplay of environmental and genetic factors gave rise to these ethnic differences. A high fat diet was shown to be associated with higher serum triglyceride and lower HDL-cholesterol concentrations in people with the T variant while those with the C variant were shown to be associated with lower serum triglyceride and higher HDL cholesterol under the same dietary conditions. People with the T variant of the gene may have an impaired adaptation to a high fat diet, increasing the risk for cardiovascular disease.
In a study conducted on the LIPC gene variant and insulin sensitivity, the baseline insulin sensitivity was found to be similar between the gene variants but, upon exercising, people with the C variant were shown to be associated with higher insulin sensitivity. In a similar study, men with the T variant were shown to be associated with an improvement in insulin sensitivity when MUFA and carbohydrate rich are consumed instead of SFA fat. There was no association with women with the T variant and between diet and insulin sensitivity among men and women with the C variant.
|CC||[Limitation] More likely to have lower baseline HDL [Advantage] More likely to have higher HDL level upon exercising [Advantage] More likely to have higher HDL on high fat diet [Advantage] More Likely to have improvement in insulin sensitivity upon exercising [Limitation] Less Likely to have improvement in insulin sensitivity when on MUFA and Carbohydrate rich diet||Likely increase in HDL upon exercising Including exercise routines is beneficial to HDL levels and insulin sensitivity|
|CT||Slightly improved insulin sensitivity upon exercising||Likely increase in HDL upon exercising Including exercise routines is beneficial to HDL levels and insulin sensitivity|
|TT||[Advantage] More likely to have higher baseline HDL [Limitation] Less likely to have higher HDL level upon exercising [Limitation] More likely to have Lower HDL on high fat diet [Limitation] Less Likely to have improvement in insulin sensitivity upon exercising [Advantage] More Likely to have improvement in insulin sensitivity when on MUFA and Carbohydrate rich diet||Likely increase in HDL level when on MUFA and Carbohydrate rich diet People with this gene variant would benefit from consuming low fat diet and carbohydrate rich diet|
“Nutrigenetics, fitness genetics, health genetics are all nascent but rapidly growing areas within human genetics. The information provided herein is based on preliminary scientific studies and it is to be read and understood in that context.”
[idea]In the last few decades, the nutritional dogma has been about emphasising small & frequent meals throughout the day. Recent research shows that those who eat less are generally healthier, with improved metabolic health, cognition and live longer than those who eat more. Intermittent fasting is based on the principle of alternating between periods of eating and fasting. Intermittent Fasting is practiced in several ways including periodic multi day fasts to skipping a meal or two on certain days of the week. Most of us already fast every day, while we sleep. Simply extending this fast is referred to as Intermittent fasting. One way of doing this is by having your first meal at noon and last meal at 8 p.m in the evening, thus going on an 18 hours fast every day.[/idea]
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From an evolutionary perspective, fasting and food deprivation is one of the factors that could have attributed to the optimal performance of the human brain. Evolution favoured the selection pressure of those individuals who were adept in acquiring food from the limited food sources. Recent research demonstrates the beneficial effect of intermittent fasting and vigorous exercise on brain health. The fact is, until recently, humans did not have guaranteed food supply and may have had to struggle to obtain food for survival. During the course of thousands of years, we have developed the “genetic” ability to use calories wisely and to survive for periods of time without food. This genetic ability is what enables “slow” calorie burning and calorie storage for long periods of time in most people. This is why most people have a tendency to become obese upon consuming excessive food. Our bodies were not built in an environment of excessive food, rather the lack of it.
From that point of view, “simulated” fasting acts to prime the body to a state of calorie deficit, which has been shown by many studies to have several beneficial effects, some of which are listed above. Intermittent Fasting can be performed in a number of ways and it is controversial whether one way is better than others. In some forms, some foods are allowed while some others advise complete fasting. The duration and timings also differ. Given this, one can experiment with a schedule that works best for them. Some suggestions are given below.