Introduction

American culture places great emphasis on body shape. There is a widely held presumption that “diet plus exercise = looking good.” This premise gives rise to huge expenditures of time and resources in all-too-often frustrating attempts to “get in shape,” but what is not considered is that shape and size may have entirely different biological underpinnings. Many individuals successfully lose weight and significantly reduce body size, only to remain unhappy with their residual shapes.

To a certain degree size may be under one’s control by the intentional modulation of caloric intake and burn, but there is little data to support the idea that even the most stringent efforts can effectively and permanentlychange body configuration or fat distribution. For example, dietary manipulation can affect overall size, but though it may temporarily shrink both waist and hips, it will not necessarily bring about the desired waist-to-hip ratio. Because many Americans believe that body shape can be controlled by behavior, societal judgment is often levied against patients who choose to manipulate their native body contours surgically. Absent evidence that shape is inborn, many continue to struggle for decades, only to fail to reach their goals. Since surgery requested later in life is more complex, and complication rates can be higher, this misconception has ethical implications.

Anatomy and body shape are evaluated routinely by a host of imaging techniques. Medical imaging underwent major expansion in the late twentieth century with the introduction of CAT scan technology, magnetic resonance imaging, and other computer-based modalities. During those same years, however, the advent of digital cameras resulted in a shift in clinical photography to a less scientific “point-and-shoot” mentality, which produced an explosion of case-related patient images that were often published with no consistent standardization of technique. The outcomes of plastic surgery intervention are often evaluated by looking at these less-than-ideal “before and after” snapshots.

Such documentation fails to provide accurate and quantifiable data to support the notion that surgery has effected permanent change, or that the underlying condition could only be changed by surgery in the first place. Fortunately for our future understanding of this complex issue, standardized imaging technologies and software now exist to address long-unanswered questions about the inheritance of body shape and the quantification of surgical results. A new and unique monozygotic mirror-twin model incorporating standardized photographic techniques provides a tool for investigating questions of anatomic development and adult human form.

Anatomic Observations Using a Mirror-Twin Model

Facial skin features historically were thought to stem from a combination of genetic and environmental influences. In the past, to help determine the genetic origin of a facial skin feature, correspondence of surface findings was erroneously sought by comparing the same sides of two twins . More recently, I have used highly standardized photographic techniques and skin surface analysis to address questions of inheritance of anatomic features . With technical insight from Kalev Peekna, I developed a formal digital method to easily account for the phenomenon of mirroring in twins which, though previously ill-defined by science, has been long acknowledged among twins themselves. Anatomic mirroring is the term used to describe the phenomenon that a lesion or anatomic structure on one side of a monozygotic (MZ) twin is found in a similar location on the opposite side of the co-twin (e.g., a mole on twin A’s right cheek can be paired to a mole on twin B’s left cheek). Our technique was therefore developed to definitively and reproducibly diagnose mirroring and allow for its differentiation from simple same-side concordance in order to show the genetic contribution to facial shape .

Figure 1 shows typical concordance of skin features in a pair of MZ twins who exhibit no anatomic mirroring. Correspondence in the skin surface findings in another set of twins can only be appreciated if opposite sides of the face are carefully examined (figure 2).

Figure 1. (Click the magnifier to enlarge image.) Detailed analysis of the same sides of the faces of two concordant, non-mirrored MZ twins reveals striking similarities. These similarities include the same number and configuration of wrinkle creases on both the forehead and brow, nearly identical crow’s feet wrinkle lines with similar branching patterns at the corners of the eyes, similar helical root creases, pre-tragal creases, identical oblique earlobe creases, and a series of skin lesions that appear to have migrated at different rates during early embryonic development, with each feature being more anterior in twin B. None of the findings present on the right sides of the twin faces are present on the left.

Figure 2. (Click the magnifier to enlarge image.) Both twin A (left) and twin B (right) exhibit a polygon of nevi only on opposite cheeks. It is likely that different rates of embryologic tissue transit account for the slight differences in the shapes of the polygonal arrangement in each twin, although both clusters remain within the boundaries of the anatomic region innervated by the second branch of the trigeminal nerve.

New digital addition and subtraction techniques used to analyze highly standardized images of twins can be employed to study facial shape for the presence of anatomic mirroring . As in radiological techniques used for digital subtraction angiography, images of twin faces are overlapped and then digitally subtracted from each other to determine whether anatomic shape was concordant (present on the same side in both twins) or mirrored (present on the right side in one and left side in the other), as are the twins in figures 3 and 4. Analysis of 27 pairs of monozygotic twins showed that 64 percent of male pairs and 23 percent of female pairs exhibited the mirror phenomenon, and that there was no relationship between the mirror phenomenon and the timing of the first split of the egg in either gender . When the appropriate side of the face was analyzed (i.e., either the same or opposite) in these same twins, nearly 100 percent of skin features were found to be present in both twins . In light of these observations, all future studies of anatomic inheritance should control or consider the mirror phenomenon.

Figure 3. (Click the magnifier to enlarge image.) Representative pair of female mirror twins. Twin A and twin B have been digitally overlapped.

Figure 4. (Click the magnifier to enlarge image.) When digitally subtracted from each other, the images from figure 3 show symmetrical “ghosting” consistent with anatomic mirroring of the pair’s skin findings. (Digital subtraction of the images of concordant twins results in an asymmetrical “ghost,” indicating that the inherent asymmetries of the face are concordant and not mirrored.)

In addition, and perhaps more importantly, the above findings bring the role of environmental influence into question. It is illogical to think that random environmental influence could consistently affect only one side of one twin and only one side (for example, just the mirror-opposite side) of another twin in exactly the same way over their entire lifetimes—whether they were raised in the same or different environments. As a result, environmental influence can be eliminated as a variable if mirroring is analyzed and controlled in the twin study population.

Standardized imaging and digital analysis have preliminarily confirmed the presence or absence of mirroring of body form in MZ twin torsos. Figure 5 illustrates the extreme alignment of anatomy when two concordant male MZ twin torsos are digitally added to each other, but the alignment is lost when the photograph of Twin B is horizontally flipped. Digital subtraction has successfully identified concordance or mirroring in all pairs studied to date. It follows that the body shapes of the twin pairs must be inherently similar (concordant) or similar-but-mirrored, regardless of differences in size .

Figure 5. (Click the magnifier to enlarge image.) Left to right: The native state of twin A; the native state of twin B; the digital addition of twin A imposed on twin B, showing near-complete anatomic alignment of the torsos; and, finally, the digital addition of the native state of twin A added to the horizontally flipped image of twin B, showing a dramatic decrease in alignment consistent with a non-mirrored native state.

Measuring Postsurgery Results

The same standardized imaging techniques can also be used to accurately quantify postsurgery results, because photographic variance has been nearly eliminated. In figure 6, the postoperative result has been digitally subtracted from the preoperative baseline anatomic state, providing evidence of shape change which can actually be measured. The same methods could be used to track disease progression (e.g. Cushing disease or HIV-related lipodystrophy), the effects of therapeutic interventions, or changes in body configuration due to aging.

Figure 6. (Click the magnifier to enlarge image.) Standardized digital subtraction analysis (preoperative minus postoperative views) of the surgically imposed shape changes following full-body circumferential reproportioning. This surgery was preceded by weight loss of more than 100 pounds, which had reduced the patient’s size, but had not achieved the patient’s desired shape.

Discussion

The above findings, developed using a MZ twin approach that controls for the “mirror twin” phenomenon, supports the concept that body surface features and body shape are genetically predetermined. Diet and exercise appear to be able to temporarily alter size, but it seems that only surgery, disease, or trauma can permanently alter shape.

This observation has direct implications for twins and non-twins alike who have concerns about skin or body features. Patients who request body contour surgery (the elective alteration of baseline anatomic form) are often counseled to make lifestyle changes to alter their weight (with the presumption that it will change their shape) before surgery is performed. In light of the findings presented above, patients should instead be counseled to adopt healthy diets and exercise routines that can be maintained throughout adulthood, regardless of the effect on weight preoperatively. Surgery should proceed once metabolic steady state is reached and body weight has stabilized, after several months, so the patient can enjoy an improved body configuration without struggling to maintain an unrealistic daily routine. Data on the genetic inheritance of undesired body shapes could help inform future ethical decisions regarding elective surgery.

The broader implication of these photographic and anatomic findings is that the very structure of the “nature vs. nurture” debate as it pertains to body shape must be reconsidered. It is clear that there may be limits to the effect of environment on anatomic shape.

  • Goals of health care/Enhancement
  1. Gedda L. Twins in History and Science. Springfield, IL: Charles C. Thomas; 1961.

  2. Teplica D, Keith D. A study of the mirror symmetry phenomenon in the faces of 100 sets of monozygotic twins, using rigidly standardized photographic techniques and digital analysis. Paper presented at: 10th International Workshop on Multiple Pregnancy; September 5-7, 1996; Zakopane, Poland. Arch Perinat Med. 1996:1(2).

  3. Teplica D, Peekna K. The mirror phenomenon in monozygotic twins. In: Blickstein I, Keith L. Multiple Pregnancy: Epidemiology, Gestation, and Perinatal Outcome. 2nd ed. London: Taylor and Francis; 2005: 277-288.

  4. Teplica D, Derom C, Peekna K, Derom R. Embryological timing in mirror-image twinning . Twin Res Hum Genetics. 2007;10 Suppl:54.

  5. Teplica D. Iconography in twins: a modern photographic perspective. Paper presented at: The 1st World Congress of Twin Pregnancy: A Global Perspective; April 16-18, 2009; Venice, Italy.

The gene that determines where your body fat ends up

Where women’s bodies store fat is governed by a genetic variant that also influences the risk of developing type-2 diabetes, new research has found.

The research, presented at the American Society of Human Genetics, in Baltimore, discovered a gene called KLF14 appears to be a master regulator of how and where fat ends up.

Women with one particular “allele”, or version, of the gene tend to have slimmer hips, while women with another are more “pear-shaped”, the study claimed.

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The gene variant appeared to regulate hundreds of other genes active in fat cells, changing the structure and function of those cells.

“At the whole-body level, these differences between alleles are not associated with changes to overall weight or body mass index, but they do affect women’s hip circumference,” said Kerrin Small, PhD, Head of the Genomics of Regulatory Variation Research Group at King’s College London and lead author on the study.

The research also found women who have a “pear-shaped” body type, carrying more fat on their hips, are significantly less likely to develop type-2 diabetes than those with smaller hips.

Along with regulating body fat, the KLF14 gene also appears to affect people’s sensitivity to insulin, a hormone that regulates blood sugar, Dr Small found.

Type 2 diabetes develops when the body becomes less responsive to insulin, causing levels of both the hormone and blood sugar to soar.

“Looking at the variant we studied, large-scale genome-wide association studies show that women with one allele tend to have larger hips than women with the other one, which would have a protective effect against diabetes,” she said. “Most genes that have been associated with type 2 diabetes are related to the pancreas. What’s different about the KLF14 gene is that it’s expressed in fat tissue.”

Researchers first identified the relationship between the variant KLF14 gene and Type 2 diabetes risk in a large, genome-wide association study of a broad population.

The effect on diabetes risk was initially modest, but when Dr Small focused on a more specific population – women who inherited the gene variant from their mothers – the effect grew.

“These findings have important implications as we move toward more personalised approaches to disease detection and treatment,” Dr Small said.

“If we can identify the genes and protein products involved in diabetes risk, even for a subset of people, we may be able to develop effective treatment and prevention approaches tailored to people in that group.”

A Simple Guide To Body Genetics (And How They Affect Your Health)

How many of you have been here before? You start a new fitness program and you’re completely committed, determined to make this the one that sticks. You buy new sneakers, cute workout clothes, and make your grocery lists religiously.

You get to the gym, sweat a lot, hurt a lot, eat clean, say no to tasty things, and go to sleep feeling accomplished.

But then a few weeks go by and the anxiety starts to creep in. You’re not seeing the changes you want to be seeing and you start to doubt yourself.

Is all the hard work worth it? You look at your mom and sigh as you realize your tummy has the same bulge over your waistband that she does.

Why is your best friend so skinny? Is it because of her skinny mom? You’re 99% sure she’s allergic to sweat and doesn’t know where the gym is so you decide life is not fair.
And then you check yourself because the color green doesn’t suit you.

How Genetics Play a role on Your Body Type

Body genetics are sort of the pink elephant in the room when it comes to health and fitness goals- you don’t want to admit they matter and you don’t want to sound like you’re making excuses. But you constantly find yourself wondering what you do and don’t have control over.

Simply put, the exact influence of genes on your physique is not absolute; we know they play a role but they do not have to be your fate.

If your parents are obese, categorized as having a Body Mass Index (BMI) of > 30, you run a higher risk of developing obesity, meaning there is a genetic predisposition toward being overweight, making weight management a bit more complicated for some.

A great number of studies on genetics have been done on twins, many estimating the heritability of BMI to be 40-70%. We know that a pair of identical twins who share 100 percent of their genes are more likely to have the same BMI as a pair of fraternal twins who share about 50 percent of their genes.

What’s even more telling is that when identical twins have been raised apart in different environments, they still tend to have similar BMIs.
Along with BMI, we see twins having similarities in skinfold thickness, waist:hip ratio, and waist circumference.

The exact mechanism in which we inherit the susceptibility to distribute fat in certain ways is not clear; some studies have made a neuronal connection, while others have concentrated on genes and enzymes specific to fat stores.

Below are some of the biochemical markers currently being researched in connection to obesity and weight gain:

Genes, Enzymes, Hormones and their effect on Weight Regulation

FTO gene – a nuclear protein connected to BMI, obesity, and type 2 diabetes.

SCD-1 gene – encodes an enzyme that hinders fat burning and promotes fat storage in muscle.

GIRK-4 gene – a gene possibly associated with food regulation and energy expenditure and has been linked to adult-onset obesity in animal studies.

TPP II enzyme – has been shown to stimulate the formation of new fat cells and has been connected to hunger signaling in animal studies.

TRAP enzyme – has been linked to the formation of new fat cells.
Other genes with >20 studies positively associating them with obesity include the ADRB2 gene, the ADRB3 gene, and the PPARG gene.

Genetics and BOdy Weight: Environment, Race, and Ethnicity

As discouraging and frustrating as your unrelenting fat stores can be, there is the theory of the “Thrifty Genotype” to consider, which proposes that those same genes kept your ancestors alive at one point.

In the hunter-gatherer days, those who were predisposed to storing fat in the absence of adequate energy had higher rates of survival than those without genetic advantage.

Unfortunately, today, it is proposed that those same genes lend to the multiple obesity-associated chronic diseases that lead to some of the top causes of death in the United States.
In other words, thanks for your help genes, but you’re really not helping anymore.

The ethnic background has also definitively been tied to your weight status. In the United States, non-Hispanic blacks have the highest prevalence of obesity (38.1%), followed by Hispanics (31.3%), and non-Hispanic whites (27.1%).
Is there a racial genetic component? Researchers are studying links between race and fat stores. For instance, one study found that people of African ancestry possess three genes that may impact BMI and increase the tendency toward obesity.

On the other hand, we also know that race, ethnicity, and cultural background influence our environment and daily patterns which greatly impact our food and lifestyle choices.

Although the human genome has remained the same, our world is different. Major changes in energy expenditure and food consumption took place with the onset of the Industrial Revolution, the invention of the automobile, and advances in mass-food production.
What does this all mean? It means there is no one answer and we simply need more research.

Genetics and Taste Preferences

How about the foods you choose to eat? Is there a reason you taste soap when you eat cilantro but your siblings pile it sky-high onto their tacos?

Numerous studies show that there is a genetic component to food preferences.

The presence or absence of certain genes has been linked to the preference or aversion of certain foods.
One way genetics influences taste preference is the sensitivity an individual has to bitter compounds in foods: individuals with low taste thresholds for bitter compounds have more food dislikes than those with higher taste thresholds.
The best known of these bitter compounds is PTC, mainly influencing an individual’s preference for certain fruits and vegetables.

Why the variation in our taste preferences? One theory is that the ability to identify and reject bitter substances provided our ancestors with an evolutionary advantage to help identify bitter plant poisons. To avoid death.
Again, thanks to genes, we’re good now.

Genetics and Physical Activity

Ok, now let’s get to the gym. If your mom can pump some serious weight, do you have an upper hand in the gym? If your dad played college ball, does that help your athletic performance?

Twin studies show that up to 90 percent of your baseline muscle strength is hereditary. This is believed to be at least partly due to variations in fiber type.

If you have more slow-twitch (type I) fibers, you may be better able to perform endurance-related activities but have a harder time increasing your muscle mass.

On the other hand, if you have more fast-twitch (type II) fibers, you may build muscle mass more easily but have a tougher time with endurance.
True testing of your muscle fiber constitution requires a muscle biopsy, but if you see an athletic trend in your family, you may be able to figure it out.

How about cardio? Has running always come easy to you while your friends struggle to get past a mile?
Well, you may have more tiny DNA segments called single nucleotide polymorphisms (SNPs). One study showed that individuals who possessed 19 or more improved their cardiovascular fitness three times as much as those with nine or less.

No talented athlete, however, would be half what he or she was without strong bones. They are the foundation that strong muscles are built upon and the framework that determines your mobility. And it’s genetic; bone mineral density (BMD) has a 50-90% heritability rate.

Lean muscle mass, leg extensor strength, and grip strength have all been positively associated with BMD.
But we also know something else. BMD is influenced by good ol’ weight bearing exercise.

Genetics and Body Type

Despite the numerous connections being made between genes and body composition, there have been equally strong connections being made between exercise and body composition.

Exercise can reduce your genetic predisposition of overweight by as much as 40 percent.

Although there is a genetic factor in muscle fiber composition, we know there is an undeniable connection between muscle fiber area and training. Muscle bulk and strength have only a moderate genetic component explaining 30–50% of their growth, leaving the majority to be explained by environmental factors.

This leaves room for physical activity and strength training to improve athleticism, strength, and further increase lean body mass.

Wrapping Up Body Genetics

So what does it all mean? It means that yes, just because obesity runs in your family and you are more prone to a certain body type, it does not mean you have any less control over your own personal actions.

No matter your chromosomal make-up, there is no one gene that can entirely hinder weight loss or muscle growth. These are normal physiological consequences of prolonged daily behaviors such as decreased caloric intake and strength training.

On the flip-side, if you were born with a six-pack, a natural mesomorph, but don’t do the work to maintain this genetic advantage, you too can gain weight and lose lean body mass.

No one is immune to the benefits of a healthy lifestyle or the consequences of lack thereof. If you feel you are struggling more than your friend beside you working the same exact routine, the truth is, you just might be.

But that is all the more reason to turn your attention to the inside, focus on yourself, and create realistic goals and expectations.

It is important to be aware that you are unique and that your body genetics was influenced by Mom and Dad the day you were born, but it is equally important to realize that the decisions you make in young adulthood and beyond are yours alone.

Will your cankles ever go away? Nope. But your belly can. Will your boobs spontaneously go up a cup size? Probably not, but you can put inches on your booty if you work it right.

So look in the mirror, thank your parents, put on your sneakers, and go to the gym. Be the best you can be because that is more than enough.

Diet vs. Genetics: Which One has the Biggest Impact on Weight Management?

Weight loss — the concept of it seems so simple. You know, eat less, move more, or perhaps, eat healthy and move more. But then again, if you’re someone who’s had trouble losing weight in the past, or at least maintaining that weight loss, you may have asked yourself if genetics are to blame.

The prevalence of obesity has become a public health crisis in the United States, with more than 78 million, or one-third, of adults being obese. Obesity increases the risks of comorbidities such as diabetes, cardiovascular disease, and high blood pressure. By developing a healthy diet and increasing physical activity you can reduce body weight and improve metabolic health. Obesity treatment plans, and weight loss plans in general, focus on reducing caloric intake by at least 500 calories a day to induce weight loss of a pound per week.

When it comes to dieters, most dieters regain half to all of their original weight within three to five years. However, it’s considered a great achievement if one can even manage to maintain 5 to 10% of their weight loss. Keeping at least 3% of the original weight off is considered weight maintenance.

Your ability to lose, gain or maintain your weight is dependent on genetic, environmental, and behavioral factors. But how much of a role does genetics play in weight loss versus eating a healthy diet? Is there any truth to genetics playing a substantial role in your ability to lose weight to improve health and overall body composition? Or is diet the driving factor?

That extra pouch around your stomach had to come from somewhere, right? Your weight problems during childhood weren’t simply inherited from your parents, correct?

Well, maybe not. Maybe it’s genetics. Maybe it’s diet. Or, maybe it’s a little bit of both.

Genetics and Weight Loss

Genetics play an interesting role in body composition, especially when it comes to body fat. Your body is designed to store fat in certain places, depending on gender, age, and of course, your family genes. If you’re a woman, naturally, you’ll likely carry more fat than men since fat plays a large role in the process of reproduction. Essential fat values for men and women are 3 percent and 8 to 12 percent, respectively. Genes, however, will determine if women will carry this body fat around the hips and thighs as opposed to storing fat in the upper body. Men, on the other hand, tend to carry fat in the abdomen but can also carry fat in other places; the storage of fat, regardless of gender, can play a significant role in influencing health risks.

Could genetics cause your body to have a set body composition? Set point theory suggests that there is a specific weight range that your body may prefer. This is thought to contribute to the likelihood of weight regain following a diet. Set point theory also suggests that this ideal weight range can be genetically altered by diet or environmental factors. In light of this, one article questions if the consumption of Western diets, diets that are large in portion size and typically high-calorie, camouflages the body’s normal weight regulation.

A review published in Maturitas provides evidence that central adiposity, fatness around the abdominal area, is inherited, even after BMI has been accounted for. The researchers also stated genetics influence gender-specific body fat distribution, and DNA variants affect the maintenance and deposition of body fat, as well as body shape. So while genetics can play a role in determining your body composition, are there certain genes calling the shots? Let’s dive deeper.

The Fat Gene vs. Skinny Genes

One of these genes, FTO also known as the fatso gene, is a gene variant associated with the likeliness of fatness and is the common subject of research determining the role of genetics in body fat composition and obesity. FTO accounts for approximately 1 percent of BMI heritability and is heavily involved in food intake regulation. Research has also shown the FTO gene variant is linked with increased total energy intake and is also associated with childhood obesity.

According to a study published by BMJ, those who carry the FTO gene weigh, on average, 6.61 pounds (3 kg) more and are 1.7 times more likely to be obese than those who don’t carry the trait.

The BMJ research reviewed 8 studies involving 9,563 subjects to determine if FTO was a reliable predictor of obesity-related outcomes in randomized weight loss trials.

However, the study showed the FTO gene didn’t affect any changes in adiposity. In fact, those who were predisposed to obesity due to the carriage of the FTO gene responded equally well to weight loss interventions. An important note to consider is that changes in dietary and exercise habits counteract FTO’s effect on obesity.

Another study published by PLoS One investigated the effects of the fatso gene on various abdominal and peripheral fatness phenotypes and obesity-related traits in middle-aged men. The results showed a minor association between FTO and general fatness and body fat distribution.

These studies imply that genetics make a large contribution to where we store fat rather, but don’t necessarily cause us to pack on pounds.

At this point, you may be asking yourself if there’s evidence of people who are predisposed to being skinny? The answer is yes, but don’t get too excited, this hereditary trait isn’t like winning the genetic lottery. A study published in Nature identified chromosome 16 as having links to body weight. Deletion, or the removal of one of the two copies of this chromosome in each cell, is commonly linked to obesity, autism, intellectual disabilities, and an increased risk of seizure. In adults, the duplicate copies of chromosome 16 are 8.3 times more likely of being clinically underweight, which doesn’t necessarily translate to having a healthy body composition.

Does Genetics Restrict a Healthy Diet?

Researchers conducted a randomized clinical trial to determine the effects of a healthy low-fat diet compared to a healthy low-carb diet on body weight change and questioned if genetics modified those effects. The 12-month study focused on implementing reduced calorie diets that were sustainable and focused on the quality of the foods within them.

Based on our earlier discussion and what was explained about the impact genetics have on weight loss, can you guess what the major findings of the study were?

Well, both groups lost a similar amount of weight with the healthy low-fat diet group lost 11.7 pounds (5.3 kg) and the low-carb diet lost 13.2 pounds (6 kg) over 12 months. Bringing in genetics, of the 481 participants who completed the trial, 244 people had a low-fat genotype and 180 had a low-carbohydrate genotype.Though it may seem like a genetic predisposition to respond better to different foods may influence results, there was no significant diet-genotype interaction. In other words, genotype pattern wasn’t associated with the effects of weight loss, but the impact of caloric restriction likely was.

So, should I just cut calories?

Though weight loss is simplified as calories out > calories in, remember that weight loss is more complex than that. An important aspect of diet to learn in regards to its effects on your body composition is the thermic effect of food. Also known as diet-induced thermogenesis, thermic effect describes the amount of expended energy above the resting metabolic rate it takes to digest food. For instance, protein carries a higher thermic effect compared to carbohydrates or fat. In other words, we burn more calories when we have higher protein content in our meals.

It may not only be what we eat but how we eat that contributes to the thermic effect of food. One study found that eating more quickly may reduce the thermic effects of food. This means that not only what you are eating matters, but how you eat it does, as well. When we eat too quickly, we chew less. By doing so, we may decrease the activation of important mechanisms in our nervous system that contribute to the digestion process.

Does this mean that we should just turn to eating high amounts of protein really slowly? Of course not, a well-balanced diet is important in weight loss. Organizations such as the American Heart Association and the American Diabetes Association say finding the best diet plan for you incorporates an array of fruits, vegetables, whole grains, and low-fat dairy. Yet it is controlled portion sizes that are key for not only losing weight but also preventing serious chronic illnesses such as diabetes, heart disease, and stroke.

So, we can see that in some cases, genetics can influence our weight and body composition but chances are, unless you’re a carrier for an extra or deleted chromosome 16 and your doctors say you have issues maintaining a healthy weight, genetics aren’t keeping you from losing weight.

Something else may be and that thing is, you guessed it —

Diet.

Going Beyond Diet to Increase Fat Loss

A combination of a healthy diet and exercise is the most effective strategy to decreasing fat while increasing muscle. A regimen of weight training and cardiovascular (aerobic) exercise can improve muscular endurance, increase Skeletal Muscle Mass, and decrease overall Body Fat Mass by increasing fat oxidation, especially during high-intensity workouts.

However, a combination of weight training and aerobic exercise doesn’t necessarily lead to greater losses of body fat or increases in muscle mass. Researchers conducted an 8-month study on 119 sedentary, overweight, or obese adults and split them into three workout groups — resistance training, aerobic training, and a combination of the two.

The aerobic training group and the aerobic + resistance training groups lost more total body mass and fat mass than those in the resistance-alone training group, while the resistance training group and combination group, increased their Lean Body Mass more than the aerobic-only group. But, the combination group didn’t significantly reduce fat mass or overall body mass compared to aerobic training alone.

For the record, it should be stressed again that both types of workouts have their advantages and the types of exercises you choose should be dependent on your health and body composition goals. What’s most important is that to avoid blaming genetics for your lack of progress, improving your diet and adding in a variety of exercise will help you achieve your goals much more effectively.

Which One is More Impactful on Weight and Body Composition?

Based on the evidence provided in this article, though genetics play a small role in weight management and body composition, it’s clear diet has the biggest impact on weight and body composition. Understanding the roles nutrition and exercise play in your fitness goals is more important than wondering if you’re having trouble with weight loss because of hereditary factors.

If anything, the only influences your family has on your attempts to live healthier are the beliefs and attitudes towards healthy food and exercise they’ve instilled in you. In other words, you’ve inherited their behaviors towards health and wellness, which can be changed by forming new healthy habits.

So, no more blaming your weight or body composition on your mother, father, or great-aunt, who was overweight for most of her life. Sure, you may be predisposed to carrying a few extra pounds around your waist, but your body composition is up to you, your dietary habits, and your exercise habits.

Take a look at your environment, including the people you’re around all of the time. Ask yourself how changing one aspect of your surroundings can support your health and wellness goals.

If weight loss and improving your body composition is important to you, start with your diet. No diet is one-size fits all and there’s no magic bullet to developing healthier eating habits. However, as the research shows above, you’re more likely to lose those pounds by eating a healthy diet.

And if for whatever reason, you’re not convinced by now — think of it this way, all of the credit from the results yielded from your hard work of eating a healthy, balanced diet and exercising regularly goes to you and no one else.

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T’ara is a Nutrition Education graduate from American University who is passionate about mindful eating, diabetes management and living healthy through healthy cooking. She is the founder of Cooking to a T, a blog dedicated to making healthy, homemade and delicious food and blogging about living with type 2 diabetes.

The amount and quality of food and not a person’s genetics will lead to weight loss, a US study has found.

It has been suggested that variations in genetic makeup make it easier for some people to lose weight than others on certain diets.

To test this theory researchers at Stanford University conducted a randomised control trial involving 609 overweight adults, who all underwent genetic and insulin testing before being randomly assigned to either a low-fat or low-carb diet for 12 months.

Gene analyses identified variations linked with how the body processes fats or carbohydrates. But weight loss averaged around 5kg to 6kg at follow-up regardless of genes, insulin levels or diet type.

What seemed to make a difference was healthy eating, researchers said.

Participants who ate the most vegetables and consumed the fewest processed foods, sugary drinks and unhealthy fats lost the most weight.

Prof Lennert Veerman from the School of Medicine at Griffith University in Queensland said the study showed there was probably no such thing as a diet right for a particular genetic make-up.

“We eat to fill our stomach and, if that’s with vegetables, we tend to lose weight, whereas if it’s with chocolate or French fries, flushed down with a soda, we gain weight,” Veerman said.
The study was published Tuesday in the Journal of the American Medical Association.

Participants had 22 health education classes during the study and were encouraged to be physically active but the focus was on what they ate.

They were advised to choose high-quality foods but were not given suggested calorie limits nor were they provided with specific foods. Results are based on what they reported eating.

Fat intake in the low-fat group averaged 57 grams during the study versus 87 grams beforehand, while carb intake in the low-carb group averaged 132 grams versus 247 grams previously.

Both groups reduced their daily calorie intake by an average of about 500 calories.

The leading Australian nutritionist Dr Rosemary Stanton, from the school of medical sciences at the University of New South Wales, said the “excellent” study highlighted the importance of eating plenty of vegetables.

Stanton advises people to seek professional help to choose quality foods because the macronutrient content of of a diet “does not really matter”.

“Some previous studies that have damned carbohydrates have not taken note of the foods that supplied it,” Stanton said. “For example, lentils and lollies are both ‘carbs’ but one is a nutrient-dense high quality food while the other is junk. Simply calling them ‘carbs’ does not provide this vital distinction.”

While most diets worked, the real challenge was sticking with them, Veerman said.

“Instead of ‘going on a diet’ it would be better to find new, healthier habits,” he said.

You Can Actually Override Your “Fat” Genes—Here’s How

If you’re like many fit women, you’ve worked your butt off (or some other fill-in-the-blank trouble spots), but your belly fat seems to stick around no matter how well you eat or how hard you sweat. It’s incredibly frustrating, so what’s the deal? Genetics is a big factor: Studies of twins and families show that the amount of ab fat each person carries is inherited-roughly 30 to 70 percent of the total variation in waist size from person to person is attributable to genetics-and that apple-shaped physiques are more likely to be passed down than other body types.

“You can inherit abdominal-fat-risk gene variations from your mother or your father or from both,” says epidemiology professor Lu Qi, M.D., Ph.D., the director of the Tulane University Obesity Research Center. Inheriting these genes from one parent elevates your odds of living with belly bulge, but if you get socked with a lot of genes from both sides, you may be at an even greater risk for belly pudge that won’t easily budge. (Did you know you can do an at-home DNA test to find out if you have the gene?)

More than a couple of genes affect abdominal fat. There are 49 to be exact, according to a recent study in the journal Nature. Nineteen of these genes have a stronger effect in women, which suggests that genes may be influenced by hormones, says Kari North, Ph.D., a professor of epidemi­ology at the University of North Carolina at Chapel Hill’s Carolina Center for Genome Studies. One major player in the belly ­fat game is cortisol, which you most likely know as the hormone triggered by stress.

“Chronic exposure to cortisol can result in a complete shift in body shape, around middle and thin arms and legs, even if you’re not genetically predisposed to that physique,” says Shawn Talbott, Ph.D., the author of The Cortisol Connection. Here’s why: When you’re under stress your body cranks out cortisol, which springs fat from fat stores and dumps it into the bloodstream to give the liver and other organs energy for the fight-or-flight reaction. Any fat that isn’t used for energy gets redeposited in fat stores, primarily in the abdomen.

Whether you have an apple shape because you were born with it or because stress has messed with your waistline, it may trigger unhealthy eating habits that can make it even tougher to shed ab. Researchers at Drexel University found that in women, an increase in the percentage of body fat stored in the abdomen was linked to a 53 percent increase in the likelihood of developing out­ of ­control bingeing over a two­ year period, whereas total body fat was not associated with disordered eating. Researchers think that high percentages of ab fat may interfere with hunger and satiety messages sent to the brain, which can lead to overindulging.

As much as that vicious cycle makes it sound as if get­ ting rid of ab fat is a lost cause, it’s not and there’s hope. You just have to be more strategic about how you attack the prob­lem than the woman with the at abs on the treadmill next to you who’s probably genetically blessed. Working out will reduce stress (which in turn decreases cortisol) and improve cortisol sensitivity, meaning you secrete less cortisol whenever you are anxious and that your level of the hormone returns to normal more quickly, Talbott says. And a 30-­year study on pairs of twins published in the International Journal of Obesity found that physically active subjects (who exercised 30 minutes a day) had a waist circumference that was 3.3 inches smaller than their inactive twins, indicating that exercise can help mitigate genetic influences.

“Those at high genetic risk for abdomi­nal fat can still shed it through exercise; it may just be a more challenging and lengthier pro­cess than it is for someone with less genetic risk,” says Yann Klimentidis, Ph.D., an assistant professor of epidemiology and biostatistics at the University of Arizona’s Mel and Enid Zuckerman College of Public Health, who has conducted research on the subject. Many experts agree, saying that chang­ing your routine and going harder may be the key to finally losing your pooch. Here are two proven approaches to doing just that; work them both into your week to double­team ab flab and make a fat­belly breakthrough.

High-intensity interval training

HIIT works to trim you in two ways: It specifically helps to burn off the flab covering your abs, and when it includes the right strength moves, it can simultan­eously firm the muscles them­ selves. The point is to do a lot of reps at a high intensity (at about 80 percent of your maximum effort) and to go heavy on ab-specific exercises.

“Circuits of moves like seated band rows paired with reverse plank holds, plank shoulder taps paired with side plank holds, and burpees paired with high plank holds are effective for losing abdominal fat,” says Cassandra Forsythe, Ph.D., R.D.N., the author of The New Rules of Lifting for Women. Do each pair of moves for 20 seconds total (10 seconds per move), taking a 10-second break between sets, and then repeat the whole circuit eight to 10 times. (Or try our HIIT-filled 30-day bodyweight challenge to get started.) If you’re doing moves with weights, “they should be heavy, but not so heavy that you can’t lift them 12 to 15 times at a pretty fast pace,” Forsythe says.

Cinching core work

To strengthen and cinch in your middle, train your core, not just your abs, every other day. For a quick 360-degree blitz, try doing the Pilates “hundred” combined with the Ab Series of 5 (single-leg stretch, double- leg stretch, single-straight-leg stretch, double-straight-leg stretch, and criss-cross) in quick succession without stop- ping, suggests Pilates instructor Kit Rich, the creator of Fit by Kit with Lucy Activewear. (Try videos for these and other Pilates ab classics.)

“This series works every core muscle, including the deep, notoriously hard-to-reach transverse abdominis,” Rich says. Or rather than stick with just Pilates, mix it up with other disciplines. Forsythe suggests four types of core workouts: core endurance, like planks and balance exercises that you hold for 20 to 60 seconds; core strength, including weighted Russian twists and leg raises; core power, such as medicine ball slams

and wall throws; and complete core, including dead lifts and Supermans, which get the small spinal erector muscles in on the action. Incorporate two types of core exercises every time you work out, and make sure to hit all four categories each week. “This ab regimen assures that you work your core from every angle and position,” Forsythe says. Bye-bye, Spanx!

  • By By Lesley Rotchford

Overweight Calculator

This calculator can be used to calculate your overweight status.

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Related: Body Fat Calculator | Calorie Calculator | Ideal Weight Calculator

What Is Being Overweight and Obesity?

Overweight refers to increased body weight in relation to height beyond the accepted standard. The standard has been defined by the medical profession on the basis of a variety of reference percentiles based on body mass index (BMI) in various populations. A widely used set of reference BMI values is that developed by three doctors (Must A, Dallal GE, and Dietz WH ‐ Reference Data for Obesity, 1991) which is based on the sample from the first National Health and Nutrition Examination Survey (NHANES I).

Becoming overweight may or may not be due to increases in body fat. It may also be due to an increase in lean muscle. For example, professional athletes or military personnel may be very lean and muscular, with very little body fat, yet they may weigh more than others of the same height. While they may qualify as overweight due to their large muscle mass, they are not necessarily fat.

Obesity is defined as an excessively high amount of body fat or adipose tissue in relation to lean body mass. Being obese means that body fat is now beyond an accepted standard for your height.

Currently, 34 percent of Americans are overweight and a separate 34 percent are obese, according to the Center for Disease Control and Prevention in Atlanta.

Genetics Matter, But Don’t Tell the Whole Story

There is a clear genetic tendency for obesity. But only for a relatively small percentage of the population. There is also a genetic tendency to becoming overweight, but this is less clearly defined.

Genetics don’t tell the whole story, however. “Genes are not destiny,” states the Harvard School of Public Health in a recent study.

For example, studies show that some of us have a genetic tendency to gain weight while eating fried foods, while others can consume all the fries they want to without gaining much weight.

In 2008, for example, a group of scientists demonstrated that physical activity offsets the effects of one obesity-promoting gene, a common variant of FTO. The study, in which 17,058 Danish men and women took part, found that people who carried the obesity-promoting gene, and who were inactive, had higher BMIs than people without the gene variant who were inactive. Having a genetic predisposition to obesity did not seem to matter, however, for people who were active: Their BMIs were no higher or lower than those of people who did not have the obesity gene.

Physical Activity Makes the Difference

It adds up to this: Physical activity gets energy out and helps keep you at a healthy weight, regardless of your genetic inheritance.

The best way to avoid being fat forever is to not get too fat in the first place. The latest research shows that, once you’ve been heavy and lost weight, you have to eat less and exercise more to simply maintain your body at a new, lower weight than would someone at the same height and weight who has never been heavy — essentially dieting for the rest of your life just to break even.

It Helps to Never Gain Too Much Weight

This is because the very act of losing weight places your body in a metabolically disadvantaged state — for how long, nobody is sure. Therefore, you need fewer calories simply to stay thinner, even if you’re not trying to lose. There’s a penalty to pay for having been overweight, experts say.

A study, published in the New England Journal of Medicine, suggests that if a person loses 10 percent of his or her body weight — going from, for example, 150 pounds to 135 pounds — there is a long-lasting change in the levels of hunger-controlling hormones which will make her crave food. The body seeks to defend that formerly heavier weight you got to, and it has vigorous mechanisms to achieve that, the study shows. As soon as you drop your guard, the weight creeps back on because your metabolism is not working as efficiently. That’s why losing a great deal of weight and keeping it off happens so infrequently.

Why do so many of us get so fat? the answer appears obvious. “The fundamental cause of obesity and overweight,” the World Health Organization says, “is an energy imbalance between calories consumed and calories expended.” Put simply, we either eat too much or are too sedentary, or both. By this logic, any excess of calories—whether from protein, carbohydrate or fat (the three main components, or “macronutrients,” in food)—will inevitably pack on the pounds. So the solution is also obvious: eat less, exercise more.

The reason to question this conventional thinking is equally self-evident. The eat less/move more prescription has been widely disseminated for 40 years, and yet the prevalence of obesity, or the accumulation of unhealthy amounts of body fat, has climbed to unprecedented levels. Today more than a third of Americans are considered obese—more than twice the proportion of 40 years ago. Worldwide, more than half a billion people are now obese.

Besides getting fatter, we are also developing more metabolic disorders, such as type 2 diabetes, which is marked by hormonal abnormalities in the processing and storage of nutrients and is far more common in obese individuals than in lean ones.

The dissonance of an ever worsening problem despite a seemingly well-accepted solution suggests two possibilities. One, our understanding of why people get fat is correct, but those who are obese—for genetic, environmental or behavioral reasons—are unable or unwilling to heal themselves. Two, our understanding is wrong and hence so is the ubiquitous advice about how to make things better.

If the second option is true, then maybe what makes us fat is not an energy imbalance but something more akin to a hormonal defect, an idea embraced by European researchers prior to World War II. If so, the prime suspect or environmental trigger of this defect would be the quantity and quality of the carbohydrates we consume. Under this scenario, one fundamental error we have made in our thinking about obesity is to assume that the energy content of foods—whether avocado, steak, bread or soda—is what makes them fattening, not the effects that these foods, carbohydrates in particular, have on the hormones that regulate fat accumulation.

Given how often researchers refer to obesity as a disorder of the energy balance, one might assume that the concept had been rigorously tested decades ago. But a proper scientific vetting never actually happened. The experiments were too difficult, if not too expensive, to do correctly. And investigators typically thought the answer was obvious—we eat too much—and so the experiments were not worth the effort. As a result, the scientific underpinning of the most critical health issue of our era—the burgeoning rates of obesity and diabetes and their complications—remains very much an open question.

After a decade of studying the science and its history, I am convinced that meaningful progress against obesity will come only if we rethink and rigorously test our understanding of its cause. Last year, with Peter Attia, a former surgeon and cancer researcher, I co-founded a nonprofit organization, the Nutrition Science Initiative (NuSI), to address this lack of definitive evidence. With support from the Laura and John Arnold Foundation in Houston, Tex., we have recruited independent scientists to design and carry out the experiments that will meticulously test the competing hypotheses of obesity (and by extension, weight gain). The Arnold Foundation has committed to fund up to 60 percent of NuSI’s current research budget and three years of operating expenses for a total of $40 million. The investigators will follow the evidence wherever it leads. If all works out as planned, we could have unambiguous evidence about the biological cause of obesity in the next half a dozen years.

The Hormone Hypothesis
To understand what makes the hormone hypothesis of obesity so intriguing, it helps to grasp where the energy-balance hypothesis falls short. The idea that obesity is caused by consuming more calories than we expend supposedly stems from the first law of thermodynamics, which merely states that energy can neither be created nor destroyed. As applied to biology, it means that energy consumed by an organism has to be either converted to a useful form (metabolized), excreted or stored. Thus, if we take in more calories than we expend or excrete, the excess has to be stored, which means that we get fatter and heavier. So far, so obvious. But this law tells us nothing about why we take in more calories than we expend, nor does it tell us why the excess gets stored as fat. And it is these “why” questions that need to be answered.

Specifically, why do fat cells accumulate fat molecules to excess? This is a biological question, not a physics one. Why are those fat molecules not metabolized instead to generate energy or heat? And why do fat cells take up excessive fat in some areas of the body but not others? Saying that they do so because excess calories are consumed is not a meaningful answer.

Answering these questions leads to consideration of the role that hormones—insulin, in particular—play in stimulating fat accumulation in different cells. Insulin is secreted in response to a type of carbohydrate called glucose. When the amount of glucose rises in the blood—as happens after eating a carbohydrate-rich meal—the pancreas secretes more insulin, which works to keep the blood glucose level from getting dangerously high. Insulin tells muscle, organ and even fat cells to take up the glucose and use it for fuel. It also tells fat cells to store fat—including fat from the meal—for later use. As long as insulin levels remain high, fat cells retain fat, and the other cells preferentially burn glucose (and not fat) for energy.

The main dietary sources of glucose are starches, grains and sugars. (In the absence of carbohydrates, the liver will synthesize glucose from protein.) The more easily digestible the carbohydrates, the greater and quicker the rise in blood glucose. (Fiber and fat in foods slow the process.) Thus, a diet rich in refined grains and starches will prompt greater insulin secretion than a diet that is not. Sugars—such as sucrose and high-fructose corn syrup—may play a key role because they also contain significant amounts of a carbohydrate called fructose, which is metabolized mostly by liver cells. Though not definitive, research suggests that high amounts of fructose may be an important cause of “insulin resistance.” When cells are insulin-resistant, more insulin is required to control blood glucose. The result, according to the hormone hypothesis, is an ever greater proportion of the day that insulin in the blood is elevated, causing fat to accumulate in fat cells rather than being used to fuel the body. As little as 10 or 20 calories stored as excess fat each day can lead over decades to obesity.

The hormone hypothesis suggests that the only way to prevent this downward spiral from happening, and to reverse it when it does, is to avoid the sugars and carbohydrates that work to raise insulin levels. Then the body will naturally tap its store of fat to burn for fuel. The switch from carbohydrate burning to fat burning, so the logic goes, might occur even if the total number of calories consumed remains unchanged. Cells burn the fat because hormones are effectively telling them to do so; the body’s energy expenditure increases as a result. To lose excess body fat, according to this view, carbohydrates must be restricted and replaced, ideally with fat, which does not stimulate insulin secretion.

This alternative hypothesis of obesity implies that the ongoing worldwide epidemics of obesity and type 2 diabetes (which stems to great extent from insulin resistance) are largely driven by the grains and sugars in our diets. It also implies that the first step in solving these crises is to avoid sugars and limit consumption of starchy vegetables and grains, not worrying about how much we are eating and exercising.

Forgotten History
Conventional wisdom did not always favor the energy-imbalance hypothesis that prevails today. Until World War II, the leading authorities on obesity (and most medical disciplines) worked in Europe and had concluded that obesity was, like any other growth disorder, caused by a hormonal and regulatory defect. Something was amiss, they believed, with the hormones and enzymes that influence the storage of fat in fat cells.

Gustav von Bergmann, a German internist, developed the original hypothesis more than a century ago. (Today the highest honor bestowed by the German Society of Internal Medicine is the Gustav von Bergmann Medal.) Bergmann evoked the term “lipophilia”—love of fat—to describe the affinity of different body tissues for amassing fat. Just as we grow hair in some places and not others, we store fat in some places and not others, and this “lipophilic tendency,” he assumed, must be regulated by physiological factors.

The lipophilia concept vanished after World War II with the replacement of German with English as the scientific lingua franca. Meanwhile the technologies needed to understand the regulation of fat accumulation in fat cells and thus the biological basis of obesity—specifically, techniques to accurately measure fatty acids and hormone levels in the blood—were not invented until the late 1950s.

By the mid-1960s it was clear that insulin was the primary hormone regulating fat accumulation, but by then obesity was effectively considered an eating disorder to be treated by inducing or coercing obese subjects to eat fewer calories. Once studies linked the amount of cholesterol in the blood to the risk of heart disease and nutritionists targeted saturated fat as the primary dietary evil, authorities began recommending low-fat, high-carbohydrate diets. The idea that carbohydrates could cause obesity (or diabetes or heart disease) was swept aside.

Still, a few working physicians embraced the carbohydrate/insulin hypothesis and wrote diet books claiming that fat people could lose weight eating as much as they wanted, so long as they avoided carbohydrates. Because the most influential experts believed that people got fat to begin with precisely because they ate as much as they wanted, these diet books were perceived as con jobs. The most famous of these authors, Robert C. Atkins, did not help the cause by contending that saturated fat could be eaten to the heart’s delight—lobster Newburg, double cheeseburgers—so long as carbohydrates were avoided—a suggestion that many considered tantamount to medical malpractice.

Rigorous Experiments
In the past 20 years significant evidence has accumulated to suggest that these diet doctors may have been right, that the hormone hypothesis is a viable explanation for why we get fat and that insulin resistance, driven perhaps by the sugars in the diet, is a fundamental defect not just in type 2 diabetes but in heart disease and even cancer. This makes rigorous testing of the roles of carbohydrates and insulin critically important. Because the ultimate goal is to identify the environmental triggers of obesity, experiments should, ideally, be directed at elucidating the processes that lead to the accumulation of excess fat. But obesity can take decades to develop, so any month-to-month fat gains may be too small to detect. Thus, the first step that NuSI-funded researchers will take is to test the competing hypotheses on weight loss, which can happen relatively quickly. These first results will then help determine what future experiments are needed to further clarify the mechanisms at work and which of these hypotheses is correct.

A key initial experiment will be carried out jointly by researchers at Columbia University, the National Institutes of Health, the Florida Hospital–Sanford-Burnham Translational Research Institute in Orlando, and the Pennington Biomedical Research Center in Baton Rouge, La. In this pilot study, 16 overweight and obese participants will be housed throughout the experiment in research facilities to ensure accurate assessments of calorie consumption and energy expenditure. In stage one, the participants will be fed a diet similar to that of the average American—50 percent carbohydrates (15 percent sugar), 35 percent fat and 15 percent protein. Researchers will carefully manipulate the calories consumed until it is clear the participants are neither gaining nor losing fat. In other words, the calories they take in will match the calories they expend, as measured in a device called a metabolic chamber. For stage two, the subjects will be fed a diet of precisely the same number of calories they had been consuming—distributed over the same number of meals and snacks—but the composition will change dramatically.

The total carbohydrate content of the new diet will be exceedingly low—on the order of 5 percent, which translates to only the carbohydrates that occur naturally in meat, fish, fowl, eggs, cheese, animal fat and vegetable oil, along with servings of green leafy vegetables. The protein content of this diet will match that of the diet the subjects ate initially—15 percent of calories. The remainder—80 percent of calories—will consist of fat from these real food sources. The idea is not to test whether this diet is healthy or sustainable for a lifetime but to use it to lower insulin levels by the greatest amount in the shortest time.

Meaningful scientific experiments ideally set up a situation in which competing hypotheses make different predictions about what will happen. In this case, if fat accumulation is primarily driven by an energy imbalance, these subjects should neither lose nor gain weight because they will be eating precisely as many calories as they are expending. Such a result would support the conventional wisdom—that a calorie is a calorie whether it comes from fat, carbohydrate or protein. If, on the other hand, the macronutrient composition affects fat accumulation, then these subjects should lose both weight and fat on the carbohydrate-restricted regime and their energy expenditure should increase, supporting the idea that a calorie of carbohydrate is more fattening than one from protein or fat, presumably because of the effect on insulin.

One drawback to this rigorous scientific approach is that it cannot be rushed without making unacceptable compromises. Even this pilot study will take the better part of a year. The more ambitious follow-up trials will probably take another three years. As we raise more funds, we hope to support more testing—including a closer look at the role that particular sugars and macronutrients have on other disorders, such as diabetes, cancer and neurological conditions. None of these experiments will be easy, but they are doable.

One ultimate goal is to assure the general public that whatever dietary advice it receives—for weight loss, overall health and prevention of obesity—is based on rigorous science, not preconceptions or blind consensus. Obesity and type 2 diabetes are not only serious burdens to afflicted individuals but are overwhelming our health care system and likely our economy as well. We desperately need the kind of unambiguous evidence that the NuSi experiments are designed to generate if we are going to combat and prevent these disorders.

Why is my belly continuing to get bigger despite the fact I’m not gaining weight or eating as much?

I think i’m eligible to answer this as I’ve been through the same situation.

May 2016: While in college, I was 60 kgs(underweight), skinny, flat bellied (indistinct 6 pack). I used to workout quite a bit which included push ups, pull ups, crunches, planks and 3 km running. My diet included mess food which was compulsory to survive,lots of fruits, banana especially and little to no junk food.

As a result I was fit and had very little body fat.

Time went by, left college in may 2016. Came back home.

2017: Exercises started becoming irregular.

Intake of fruits decreased and junk food increased a bit.

Gradually, exercises became a thing of the past.

Belly fat began to accumulate slowly and by the time I realised this, it was not too late.

As I did not indulge in workouts I’d very little diet just to feed my stomach. My diet was now half of what I used to devour in college.

All this while, I gained only 3–4 kg weight and a significant amount of belly and waist fat.

I always had the urge to lose that loyal belly fat but I wasn’t motivated enough to accomplish it.

Dec 2017: I was 63 kgs, Finally controlled my diet, began to drink lots of water, started exercises to lose belly fat and I expect to see results in a month or two.

Lesson learnt: Fat accumulates in the body because of inactivity and you may not gain so much weight but fats will be visible. Control on diet is the most important aspect of staying fit. Exercises should continue for ever.

Hope you’ve had your little dose of motivation and you won’t lose anything on losing your belly fat. 🙂

Note:This answer should not be reproduced anywhere else.

Fat belly girl weight gain

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