What is Obesity?

It is estimated by 2030 that 1 in 2 adults will be obese (BMI ≥ 30), with 1 in 4 having Class II obesity (BMI ≥ 35).  Populations who will be most affected include women, non-Hispanic black adults, and lower socioeconomic classes. 

Obesity is a chronic, relapsing, multi-factorial, neurobehavioral disease resulting in chronic inflammation. 

Why does excess fat mass (adiposity) matter?  Excess fat mass results in pathogenic adiposity.  Pathogenic adiposity is the combination of sick fat disease (altered endocrine and immune responses) and fat mass disease (abnormal physical forces) resulting in adverse metabolic, biomechanical, and psychosocial health consequences.  Weight loss shouldn’t be about treating the number on the scale but more about preventing the diseases that are a consequence of obesity.

Obesity bias is rampant and results in social, psychological, and medical consequences.  People with obesity are often viewed as weak-willed, lazy, and non-compliant.  Women who are overweight make 15% less on average than their counterparts.  Weight stigma has been shown to increase eating and cortisol levels, as well as decrease exercise and self-regulation.  Unfortunately, weight bias in healthcare often results in avoidance of medical care, mistrust in medical providers, poor communication, and decreased adherence to recommendations. 

Body weight regulation is not as simple as energy in versus energy out.  Energy storage is controlled by hormonal signals that regulate fat storage versus fat burning.  Hunger and appetite are controlled by the brain, gut, adipose (fat) tissue, and pancreas via a multitude of neurochemicals and hormones.  Two of these regulators are ghrelin and leptin.  In simple terms, ghrelin stimulates hunger while leptin stimulates satiety. 

In short, hunger, energy homeostasis, and metabolism are COMPLEX and are dysregulated in obesity.    

What is metabolism?  Metabolism is the process in which nutrients are used to build tissue, regulate body functions, and provide energy.  The largest portion is our basal metabolic rate (BMR).  This is the basic amount of energy required to keep your body running.  Adding to BMR, to calculate total energy expenditure, is thermoregulation, the thermic effect of food, physical activity, and NEAT (non-exercise activity thermogenesis).  An individual’s metabolic rate is affected by numerous variables including genetics, muscle mass, weight, level of fitness, sex, age, and environmental factors such as temperature.

Historically, the human body was built to survive famine, store energy when needed, and respond to acute stress.  When famine (or decreased caloric intake) was detected, the human body was designed to go into survival mode.  This often results in what we term metabolic adaptation.  Metabolic adaptation means the ability of the body to adjust its metabolism for survival.  There are strong biologic forces resisting weight loss, and weak ones resisting weight gain.

Metabolic adaptation contributes to weight gain, or plateau, after weight loss.  As we decrease our caloric intake, our BMR will decrease accordingly.  This results in increased ghrelin (appetite-stimulating hormone) and decreased leptin (appetite-suppressing hormone).  Other agents of satiety (CCK and PYY) are also decreased.  These hormonal adaptations have been noted to persist for greater than a year following severe energy restriction and weight loss. 

Metabolic adaptation is also one of the risks of consecutive dieting.  With each diet, weight loss may be achieved but BMR will also decrease.  While weight often goes back on after the diet, BMR does not increase.  And it will potentially continue to decrease with each ensuing dieting endeavor.

Other, just as equally important, influencers on weight management include sleep, emotions, stress, endocrine, insulin dysregulation, medications, the gut microbiome, environmental stimuli, immune, and genetic/epigenetic expression. 

Eating behaviors, such as binge or emotional eating, are often a result of intrinsic physiologic mechanisms controlled by brain neurotransmitters.  For example, dopamine controls the reward circuit, or addictive quality, of food.  Conscious decisions are driven by its effects.  Dopamine is released even at the sight of food and is strongly triggered by sugar.  In individuals with obesity, down-regulation of dopamine receptors blunts the reward response leading to compulsive overfeeding.

Sleep

Most people underestimate the importance of quality sleep for weight management.  Prolonged sleep restriction of less than 6.5 hours a night has been associated with unhealthy dietary patterns.  This is mainly characterized by increased consumption of food and beverages with a high glycemic index (measurement of the rise in blood glucose after consumption of a particular food). 

Sleep deprivation also results in hormonal imbalances in cortisol, insulin, ghrelin, leptin, and melatonin.

What nutritional elements can affect sleep?  A diet with decreased fiber, increased saturated fat, and processed simple sugars has been shown to prolong sleep latency and decrease slow wave sleep and overall sleep quality.

Individuals with obesity may have GERD and OSA.  Both of which contribute to poor sleep quality.                 

Getting sunshine (to the eyes) earlier in the day not only helps establish an appropriate circadian rhythm, but can also increase production of MSH (melanocyte stimulating hormone).  MSH results in a rise of the hormone CCK, causing satiety.  This partially explains why people feel less hungry during the summertime when outside consistently.                                                                                                                                              

Stress

Psychosocial stress is positively associated with body mass index gain over 5 years.  Stress results in sleep problems, inflammation, decreased immune system functioning, and increased cortisol and catecholamine production. 

Chronically elevated cortisol can lead to insulin resistance, trigger inflammation, and increase fat storage. Cortisol lowers our metabolism, triggers central weight gain, and leads to cravings for sugary/fatty foods due to a rise in insulin. 

Catecholamines, such as adrenaline and noradrenaline, are usually released in a “fight or flight” response and mobilize energy stores. However, with chronic release from stress, catecholamine resistance occurs. This results in a decreased response to these hormones and poor fat mobilization.

Environment

Social ties have been shown to influence weight loss intentions and weight control behaviors, including healthy eating and physical activity. Having friends that are overweight makes an individual 60-70% more likely to be overweight.  This is in comparison to only a 40% increased risk if an individual’s siblings are overweight. 

We also live in an obesogenic food environment where portion sizes are large, foods high in fat, sugar, or sodium are readily accessible and inexpensive, and advertising of these unhealthy foods leads to induced demand.

Genetics/Epigenetics

There are currently over 1000 genes that have been identified that control appetite, weight regulation, and body composition.  While there is likely a strongly genetic component to obesity, in most individuals with obesity, no single genetic cause can be identified. 

In most cases, however, our genes are not our destiny.  Epigenetics is how our environment interacts with our genes to turn them on or off.  This includes MANY aspects of our lives including stress, food, sleep, emotions, adverse childhood events, in utero exposure, physical activity, age, and time in nature.  Interestingly, weight gain itself can change the expression of our genome.

Sex Hormonal Changes

Peri-menopausal hormonal shifts can alter body weight and fat distribution.  On average, 5 pounds of weight are gained during this transitional period, with the range from 3-30 pounds.  Weight gain appears to be inversely associated with starting BMI.  Individuals with a lower BMI tend to gain more.  Increased BMI and visceral (central) adiposity are associated with all-cause mortality.  Menopausal women have 2-4 times higher rates of cardiovascular disease and can also see an increase in blood pressure and LDL cholesterol.  Women also tend to have a loss of lean muscle mass. 

Hormone replacement therapy may not prevent weight gain, but it can minimize central adiposity redistribution, enhance insulin sensitivity, improve cardiovascular health, and preserve muscle mass.

Lower testosterone levels in men can increase central adiposity and weight gain, as well as make it more difficult to lose weight or build muscle mass. In turn, excess central adipose tissue will increase the activity of an enzyme (aromatase) which converts testosterone to estradiol, resulting in a vicious cycle. Estrogen also increases the production of a binding protein (sex hormone binding globulin) that ties up free active testosterone. Stress can also decrease free active testosterone by stealing the precursor cholesterol to make cortisol rather than testosterone.

Physical Activity

Decreased energy expenditure, from lack of physical activity and sedentary behavior, is predictive of weight gain. Low levels of physical activity and recreation are strongly related to weight gain in both men and women.

Physical activity alone, however, has only a small impact on weight loss. 

The Physical Activity Guideline for Americans to prevent weight gain is 150 minutes/week of moderate physical activity.  Unfortunately, to maintain normal body weight, individuals over the age of 40 may need closer to 420/minutes a week!  

Physical activity, however, does decrease the risk of weight gain, after loss, as well as cardiovascular risk.  It also helps preserve skeletal muscle mass with weight loss which will help with BMR. 

Therefore, it is essential in weight maintenance.

It’s many other benefits include improved glucose regulation, lipid levels, blood pressure control, sexual function, and sleep.  It also decreases mood disorders, some cancers, and overall all-cause mortality.

NEAT

Non-exercise activity thermogenesis is energy expended on activities that are not sleeping, eating, or exercise.  This includes fidgeting, standing, walking, and climbing stairs.  Incorporating NEAT can increase energy expenditure as much as 2000 kcal a day!  NEAT also improves insulin resistance and metabolic parameters.  Taking a walk after eating will improve your body’s glucose/insulin response to caloric intake. 

Any amount of physical activity has health benefits.  Move more, sit less!

Gut Microbiome

There are many hypothesized reasons why the gut microbiome plays a role in weight management. 

The gut microbiota is involved in many metabolic pathways, as well as energy extraction and storage.  Certain gut bacteria also have greater caloric extraction abilities. 

Short chain fatty acids (SCFAs), metabolites of healthy gut microbiota, are intricately involved in energy balance and nutrient sensing.  SCFA signaling generally improves energy utilization by increasing expenditure, as well as insulin sensitivity. 

The gut microbiome interfaces with several appetite hormones and is part of the gut-brain axis.  The gut-brain axis is a two-way thoroughfare for communication between the brain and the gastrointestinal system. Specific chemosensory cells are influenced by the gut microbiome, and their metabolites, resulting in chemical and hormonal communication with the brain and other organs.

Energy-dense foods (rich in saturated fat and simple sugars) alter energy homeostasis through a change in the gut microbiome.  This occurs by decreasing diversity, increasing the abundance of pathogens, and altering the hormones and microbial components involved in signaling.  The “Western diet” ultimately leads to overstimulation of the sensing pathways resulting in hyperphagia and obesity.  Saturated fats impair the enteric detection of glucose while simple sugars affect the hedonic and homeostatic brain circuits related to glucose sensing.  Consumption of ultra-processed food changes the gut microbiome resulting in increased absorption of calories. 

Nutrition

No single nutritional intervention works for everyone.  In the battle of diets or eating plans, different people gain and lose weight on every single one.

Everyone should focus on nutrient-dense foods and avoid ultra-processed ones. The emulsifiers in ultra-processed foods strip the lining of the gut. This limits the gut’s ability to detect food and send signals to the brain for satiety, resulting in increased intake of food. The hidden sugars in ultra-processed foods also send a signal to the brain via the vagus nerve triggering dopamine activation and the desire to eat even more.

Increase healthy protein consumption.  Protein exerts an increased thermic effect on food, helps maintain lean mass, and increases satiety.  While the recommended dietary allowance of protein (RDA) is a minimum of 0.8 grams of protein/kg/day, this need is variable depending on age, body composition, physiological state, sex, weight loss, and level of physical activity. 

Decrease simple sugars and foods with a high glycemic index.  Insulin, which rises with blood glucose, promotes storage of fat, and prevents breakdown.  Nutritional therapy that lowers insulin levels may decrease fat deposition and improve metabolic syndrome. 

This is likely the premise behind intermittent fasting for weight loss. Unfortunately, intermittent fasting is no longer intermittent if it’s being done every day.  Eventually the body will change its hormonal responses to a fast to preserve itself (again back to metabolic adaptation).  Intermittent fasting also places a large stress on the body and can increase cortisol.  Chronically elevated cortisol can lead to insulin resistance, trigger inflammation, and increase fat storage.

Complex carbohydrates increase satiety.

Decrease saturated fats.  For adults, there is no other required function in the body for saturated fat except as an energy source.  Increase mono and polyunsaturated fats such as fish, olive oil, nuts, seeds, and avocados.

Increase fiber.  This increases satiety and decreases caloric intake.  It also results in increased SCFA production.

The order in which you eat may help in blunting your glucose/insulin response.  Eating carbohydrates after fiber and protein often slows the sugar rise.

Certain foods/supplements may cause a release of the hormone CCK, causing satiety.  These include omega-3 fatty acids, CLA (conjugated linoleic acid), and glutamine.  Glutamine can also decrease sugar cravings for some individuals.

Yerba mata tea increases leptin and other appetite-suppressing hormones.  While it also contains electrolytes, it does contain higher levels of caffeine than other teas.

Don’t drink your calories.  Added sugars in drinks are empty calories.  Should you substitute with high-intensity sweeteners?  Probably not.  There is good evidence to show that artificial sweeteners can increase cravings for food and sugar.  They also potentially worsen insulin resistance and alter the gut microbiome. 

 It’s not just the quantity, but the quality of the food.

What helps us be successful with preventing weight regain?  Successful people from the National Weight Control Registry Data do the following:

·        98% modified their food intake (changed their eating habits)

·        78% eat breakfast every day

·        75% weigh themselves at least once a week

·        62% watch less than 10 hours of TV per week

·        90% exercise, on average, about 1 hour per day

·        Maintainers expend on average 2000 kcal/week in physical activity

 

Weight loss is not a destination.  It’s a lifestyle.

Successful weight loss is often slower than you expect.  Plateaus are common.  There are physiologic drives to restore “lost” energy stores.  Maintaining weight loss is difficult without an intervention plan.  Obesity is a chronic disease, and the disease of obesity is incurable but manageable.   

It’s not all about willpower and you are not alone.  Work with a trained obesity medicine provider to find what is right for you. 

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