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July 20, 2025 7 min read
One of the most dangerous myths about obesity still circulating today is the idea that genetics are the primary cause. Youβll hear people say things like, βI have a slow metabolismβ or βIt runs in my family,β as if body fat is predetermined and unchangeable.Β
While genetics do play a role, obesity is overwhelmingly a result of behavior, lifestyle, and environment.
And seeing that every state in America and all of its territories have an adult obesity rate above 20%, itβs a societal problem that we all need to take responsibility for(1).
To move forward, we need to strip away excuses and understand how body fat is truly regulated. This article explains the biological systems involved in weight gain, how genetics contribute, and why behavior still has the final word in whether someone becomes obese or not.
Before diving into genes and behaviors, we need to address the physiological foundation: energy balance.
Obesity results when energy intake (calories consumed) consistently exceeds energy expenditure (calories burned). The surplus energy is stored in adipose tissue (white fat). This is governed by the First Law of Thermodynamics, which applies to human physiology just as it does to physics.
Energy in vs. energy out might sound oversimplified, but the equation holds.Β
The complexity lies in what influences each side of that equation, and this is where behavior trumps biology.
Genes can affect all three components slightly, but none to the degree that explains modern obesity rates. Nationwide obesity rates have more than tripled since the 1960s(2), so the explosion in obesity over the past 50 years cannot be pinned on genetics, it happened far too quickly for our DNA to evolve.
Data Source: Centers for Disease Control and Prevention, National Center for Health Statistics. Image source: usafacts.org
Itβs true that genetics influence body weight. Twin studies show that BMI has a heritability of around 40β70%(3).
But heritability is not destiny. It reflects variability within populations, but not inevitability for individuals.
For example, a person may be genetically predisposed to higher appetite or lower spontaneous activity (NEAT), but this predisposition only results in obesity if behaviors match those tendencies such as eating hyperpalatable foods, staying sedentary, and ignoring hunger/satiety signals.
Furthermore, monogenic obesity, where a single gene causes extreme weight gain (such as mutations in the leptin or MC4R genes), is extraordinarily rare, affecting less than 1% of obese individuals(4).
So yes, some people are born with a higher βrisk,β but the overwhelming majority become obese due to behavioral and environmental patterns, not broken genes.
If your environment rewards inactivity and makes calorie-dense food cheap and accessible 24/7, the behavioral triggers for overeating become hard to resist.
Think about this: in 1975, obesity rates were under 10% worldwide. Today, over 42% of U.S. adults are obese.Β
All these are behavioral patterns, not genetic shifts. Even people with genetic predispositions can remain lean with the right environment and choices. In fact, research shows that individuals with βobesity genesβ can offset their risk by staying physically active and eating a nutrient-dense diet(5).
Another common myth is that obese individuals have slow metabolisms. Metabolism is the process by which your body converts the food you eat into energy to fuel everything from breathing and digestion to movement and cell repair.
Studies using doubly labeled water, the gold standard for measuring total energy expenditure, show that most obese individuals actually have normal or even higher metabolic rates because larger bodies require more energy to maintain(6).
Metabolism can 'slow down' due to a combination of physiological and behavioral factors, most commonly from losing muscle mass, aging, chronic dieting, or becoming less physically active.
The more accurate scientific term for this is called 'adaptive thermogenesis' and it is the body's built-in energy conservation system.
In other words, your metabolism doesnβt just βslow downβ on its own. It adapts to your habits, muscle mass, and energy intake. The key is to maintain lean mass, stay active, and avoid chronic under-eating.
The good news is that behavior is modifiable. Even modest, consistent changes in physical activity and nutrition can produce powerful results over time.
Strength training isnβt just for bodybuilders, itβs your best tool for long-term fat loss.
Not everyone needs to track calories forever, but building awareness of what and how much you eat every day is criticalΒ at first. Over time your behavioral patterns can shift into autopilot which will allow for more intuitive eating within boundaries. But you need to gain control first. What gets measured gets managed.
For those with significant obesity or behavioral struggles, support from a registered dietitian, licensed therapist, or certified trainer can dramatically improve outcomes.
But the responsibility ultimately falls on you, because nobody can make your food choices for you.
There are millions of people and programs that can show you the way and light the path, but you are the one who must walk it.
This statement is a great analogy that highlights the problem perfectly. Obesity is not a moral failing, nor is it purely genetic. It's a behavioral response to an environment that promotes overeating and inactivity. Your genes may influence your hunger cues, cravings, or activity preferences, but they donβt dictate your actions.
And in training, what you do matters far more than what you're born with. Strength, muscle, fat loss, performance, all of it is built by consistent, intelligent behaviors over time. The path to change is hard, but it is within your control. The first step is to stop outsourcing the blame to your DNA and take control back with action.
Our premier thermogenic fat burner delivers:
When your training, nutrition, and lifestyle are dialed in, SHREDDEDβAF brings the metabolic edge you need to break through plateaus and reach your best physique yet.
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References:
1. https://www.cdc.gov/obesity/data-and-statistics/adult-obesity-prevalence-maps.html
2. https://usafacts.org/articles/obesity-rate-nearly-triples-united-states-over-last-50-years/
3. Maes HH, Neale MC, Eaves LJ (1997). Genetic and environmental factors in relative body weight and human adiposity. Behavior Genetics. https://link.springer.com/article/10.1023/A:1025635913927
4. Farooqi IS, OβRahilly S (2005). Monogenic obesity in humans. Annual Review of Medicine. https://pubmed.ncbi.nlm.nih.gov/15660521/
5. Li S et al. (2010). Physical activity attenuates the genetic predisposition to obesity in 20,000 men and women. Archives of Internal Medicine. https://pubmed.ncbi.nlm.nih.gov/20824172/
6. Pontzer H et al. (2021). Daily energy expenditure through the human life course. Science. https://pubmed.ncbi.nlm.nih.gov/34385400