Distinct success behaviors that characterize long-term weight loss include: frequent self-monitoring and self-weighing, reduced calorie intake, smaller and more frequent meals/snacks throughout the day, increased physical activity, consistently eating breakfast, more frequent at-home meals compared with restaurant and fast-food meals, reducing screen time, and use of portion-controlled meals or meal substitutes.


BAD GENETICS? IS OBESITY GENETIC OR ENVIRONMENTAL SUMMARY

  • Scientists have often debated is obesity genetic or environmentally caused?
  • Genetic and environmental factors of obesity can both contribute to obesity.
  • Much of the information we receive about dieting comes from social media and other resources.
  • Some people don’t gain weight in response to overfeeding, others do gain weight in response to overfeeding. The response is highly variable.
  • Rebound weight gain causes body fat cells to increase in number more than before starting a diet.

DO YOU HAVE A GENETIC DISPOSITION FOR OBESITY?

The primary objective of your diet would be to further determine whether your body composition changes are coming from the right changes in muscle and fat. A well-designed diet should have a lean mass increase or be maintained during a diet while losing body fat. It’s pretty easy to lose weight by just reducing your calories by creating a large calorie deficit, but as a result, you will also lose large amounts of muscle, which wreaks havoc on your metabolism.

Everyone is looking for the quick fix in which you go down this Wizard of Oz path, only to find that the magic diet everyone is looking for is basically just physics. Whether it’s a ketogenic diet, a low-fat, paleo, intermittent fasting, or whatever diet you decide to follow, all diets come down to creating a caloric deficit.

Social media has bombarded viewers which advertisements that claim to eat certain fat-burning foods and ingredients increase calories burned at rest and burn more fat. Detox and slimming teas that burn fat, supplements that block fat absorption from foods, juicing for better health, there is an endless list of scams.

There is no research to support the use of detox diets for weight management or toxin elimination.(1) A case study reported that a woman was admitted to the emergency room for electrolytes dysfunction from a “detox tea” that likely exhibited a diuretic effect.(2)

Is Obesity Genetic or Environmental: Carbs Debate

Advocates of a particular diet as a way of life often demonize foods that lead are claimed to result in fat accumulation, such as bread, pasta, rice, etc. Some of the most popular phrases why people are not losing weight are: “Carbs make you fat.” “Carbs after 6 PM will cause you to become fat” or “I have a slow metabolism.” Others tout the use of fat-burning ingredients.

Some of the most common examples are “drink and consume fat-burning foods” (e.g., pineapple, ginger, onion, avocado, asparagus, celery, chili, broccoli, green tea, garlic, etc.) to lose weight. There is no shortage of misinformation regarding the best diet to lose body fat and gain muscle.

ARE YOU GETTING YOUR INFORMATION FROM CREDIBLE SOURCES?

Today, just about everyone is trying some form of new dieting. The obesity epidemic is not getting improving; in fact, it is getting worse. Based on current global trends, almost 64% of the population will be either obese or overweight by the year 2025, compared to 54% in 2000.(3)

Low Carb, low fat, Carnivore, Paleo, Vegan, Intermittent Fasting, High Protein, Clean Eating, etc., the list of diets is endless in 2022. The top 10 Google searched diets in America in 2021 were ranked from most searched to least searched: Keto Diet, Vegan Diet, Intermittent fasting, Weight Watchers, Vegetarian Diet, Mediterranean Diet, Paleo Diet, Optavia Diet, Dash Diet, and Atkins Diet.

Good sources of information about diets are further complicated by people not knowing the difference between a registered dietician and a nutritionist. A registered dietician is a nutrition expert that has met and completed academic and professional requirements for administering dietary counseling by passing a national board certification.

Is Obesity Genetic or Environmental: Good Information is Essential

A nutritionist has a broad range of credentials and expertise, but in many states, anyone can call themself a nutritionist without any formal education. Many people do not understand the difference between a registered dietician and a nutritionist.(4) With social media growing at a staggering rate, many people are looking on the internet and advice for information about diet, losing fat, and gaining muscle.

A survey of models found some alarming relationships between their beliefs about food and their practices of weight loss. 62% had a negative body image, 69% were trying to lose weight from a fad diet, and their nutritional status was below normal values. Based on the fad diet, most of the models believed in consuming drinks that are believed to eliminate fat (slimming products such as shakers, slimming tea, and fibrous drinks) as much as 57.6% and dietary methods by consuming one type of food only (carbohydrates, protein alone, or fruit and vegetables only) with a percentage of 55.7%.(5)

There is an endless debate on social media about diet superiority. If a person claims you are not losing weight because you don’t follow a particular diet, X is a red flag. Some will advocate that they have research studies to validate their claims and cherry-pick studies (i.e., only promote studies that justify their cause while ignoring conflicting data) to justify their beliefs about why they should follow a diet. All diets work by creating a caloric deficit! The diet that you should follow is the one that works best for you. It may be keto, a modified carbohydrate diet, or low fat.

BAD GENETICS? IS OBESITY GENETIC OR ENVIRONMENTAL?

The diet that works best for you should be the one you can follow for a prolonged period of time. If you can only stick to a diet for a few weeks, then what’s the point of following a plan that is not sustainable? The goal of any diet should be long-term adherence. Nearly 22 years ago, an article titled “Popular Diets: A Scientific Review” by Freedman and Kennedy concluded that all popular diets and diets recommended by governmental and non-governmental organizations result in weight loss by caloric restriction. However, it is important to note that weight loss is not the same as weight maintenance.(6)  They further concluded,

“The American public needs to be told (and believe) that diets are not followed for 8 days, 8 weeks, or 8 months, but rather form the basis of everyday food choices throughout their life.”

-Freedman and Kennedy. Obesity Research, 2001

bad genetics weight loss dna test genetic disposition genetically dispositioned the thrifty gene theory suggests thatGENES OR ENVIRONMENT CAUSING OBESITY?

IS OBESITY GENETIC OR ENVIRONMENTAL: IS BELLY FAT GENETIC

Can I see myself following this diet for the next year? Successful weight loss is an intentional loss of at least 10% maintained over one year.(7) Distinct success behaviors that characterize long-term weight loss include: frequent self-monitoring and self-weighing, reduced calorie intake, smaller and more frequent meals/snacks throughout the day, increased physical activity, consistently eating breakfast, more frequent at-home meals compared with restaurant and fast-food meals, reducing screen time, and use of portion-controlled meals or meal substitutes. (8, 9)

GENES OR ENVIRONMENT CAUSING OBESITY?

The obesity epidemic is increasing, and it is not because of carbohydrates, as many claim. The obesity epidemic continues to increase because of a society of excess calories, insufficient physical activity, insufficient sleep, etc. Many widely accept that obesity develops from a complex interaction between genetic susceptibility and exposure to an obesogenic environment. World-famous obesity expert Dr. George Bray has written about the complex interaction between genes and the obesogenic environment one lives in. Dr. Bray was famously quoted saying, ‘Genes load the gun, the environment pulls the trigger.’(10) An interesting study found that a personalized diet that was individual traits was not better for weight loss than a standardized diet.

Obesity is not simply a lifestyle choice; rather, it results from a complex interaction between genetic susceptibility and exposure to an environment that encourages positive energy balance.(11) Environmental factors that may promote obesity include low physical activity, poor diet, excess alcohol consumption, socioeconomic factors, etc.

People are not overeating because they are hungry but overeating because of boredom, pleasure, anxiety, etc.(12) People are eating for the ”food reward” and “pleasure” of eating rather than the caloric value.

IS OBESITY GENETIC OR ENVIRONMENTAL: WHAT CAN WE LEARN FROM OVERFEEDING STUDIES

The view of obesity has changed over the decades from the simplistic view that being overweight was strictly due to a lack of willpower and that weight loss was entirely due to a person being lazy and lacking willpower. Obesity results from several a combination of genetics, social, and environmental factors. It has been estimated that body fat distribution has a strong genetic component, with ~60% of body fat being genetically determined even after adjusting for BMI.(13)

Weight loss is regulated by many physiological mechanisms that resist further weight loss. For example, patients with severe obesity were placed on a low-calorie diet for ten weeks and then followed up for 52 weeks. During the weight-loss period, several hormones involved in appetite regulation (i.e., increased hunger) were increased. One year after initial weight reduction, levels of the hormones that stimulate appetite that encourages weight regain after diet-induced weight loss do not revert to the levels recorded before weight loss.(14) This suggests that weight regain has a strong physiological basis and is not just people returning to their old habits.

Weight gain, although not completely determined by genetics, plays a role in a person’s susceptibility to gain weight. Overfeeding studies have shown that some people are resistant to weight gain while in a caloric surplus, whereas others are more susceptible to gaining weight.(15) In the classic 70s, overfeeding study of prisoners at Vermont State Prison for ten weeks. Only a few prisoners were able to gain weight. The prisoners were eating as much as 10,000 calories per day.(16) This suggests that some people are resistant to weight gain with overfeeding, whereas others are more prone to gaining weight.

THE THRIFTY GENE THEORY SUGGESTS THAT OBESITY HELPED US SURVIVE FAMINES.

Our genes have not changed since prehistoric times, and during former hunter-gatherer times, despite some saying that our genes have changed to predispose us to obesity. The thrifty genes hypothesis was developed to infer that obesity was a positive adaptation to help ancient man survive. The thrifty gene theory suggests that during times of food scarcity, individuals with enhanced ability to store body fat (due to thrifty genes) would survive for longer periods, conferring greater reproductive success. (17) This theory suggests that storing body fat is helpful for our species to thrive. Although famines rarely exist in western society, our genes have not changed, predisposing people to obesity.

Drifty Genotype Hypothesis

Other scientists have proposed the drifty genotype hypothesis in which the lack of predators from the use of fire, weapons, and social behavior led to sedentary behavior, which increased obesity. (18) Another theory is that obesity is increasing chronic stress, causing increased comfort food consumption. (19)Then there is the lazy-thrifty versus peppy thrifty hypothesis, obesity in some (i.e., lazy-thrifty) results from genotypes resulting in less physical activity and overeating.

Contrary to this, some genotypes have a greater affinity for physical activity, excess food consumption, and optimal storage of nutrients. Both types of ‘thriftiness’ store fat through efficient food processing or increased appetite. (20)

Whatever theory you agree with, they all involve excess calorie consumption leading to excess body fat, whether from decreased activity or increased calories consumed. Although dairy products, cereals, refined sugars, refined vegetable oils, and alcohol make up 72.1% of the total daily energy consumed by all people in the United States, these types of foods would have contributed little or none of the energy in the typical early man’s diet.(21)

TIPS TO LOSE WEIGHT

The meager success of diets has led to many new pharmaceutical companies developing drugs to treat obesity. The current drugs on the market were developed to treat obesity thru the following mechanisms:

1.) reducing appetite and therefore reducing energy intake,

2.) increasing energy expenditure to burn more calories, and

3.) reducing calorie absorption. (22)

It should be mentioned that all these have had little success in reducing obesity long term. Many had to be withdrawn from the market due to side effects. Check out the latest weight loss drug study Semaglutide when they stopped taking the drug.

IS OBESITY GENETIC OR ENVIRONMENTAL: ROLLER COASTER DIETING

Whether you lose weight short-term is irrelevant if you only put the weight back on in the following month. Weight loss followed by weight regain is often referred to as Yo-Yo Dieting or Roller Coaster Dieting, in which a person loses and gains weight every few months. The facts are downright scary! Even if a person achieves successful weight loss, 80% of people who had successful weight loss will not maintain that weight loss for 12 months, and more than half of what they lose within two years. (23)

Repeated weight loss attempts have caused many to give up and stop dieting. Rebound weight gain makes your weight go up, but it also makes you fatter than when you started. Rebound weight gain causes body fat cells to increase in number more than before starting dieting. (24) As you will learn, our bodies don’t like losing weight; they do everything possible to preserve our current weight. When weight loss occurs, the human body sets off a cascade of events to regain weight as fast as possible.

The body’s self-defense mechanism says, “I lost a lot of weight because of a food shortage. I have to prepare myself for the next time this happens so that I will create more fat cells just in case this happens again to protect myself.” Obesity is associated with undesirable health conditions, such as cardiovascular disease, diabetes, hypertension, and sleep disorders. Obesity has been found to reduce the lifespan in men by 22% and in women by 13%. (25)

IS OBESITY GENETIC OR ENVIRONMENTAL: HEALTHY OBESE?

Some claim to be healthy obese in which they are overweight but do not suffer any metabolic complications such as hypertension, diabetes, elevated blood lipids, etc. In a recent study, researchers compared healthy obese (i.e., metabolically healthy with no hypertension, diabetes, elevated blood lipids, etc.) to unhealthy obese (i.e., had hypertension, diabetes, etc.) people over 11 years.

At the end of the study, compared to healthy weight controls, those classified as healthy obese were more likely to develop health issues later. Healthy obese were 4.3 times more likely to have type 2 diabetes; 18% more likely to suffer a heart attack or stroke; 76% more likely to develop heart failure; 28% more likely to have a respiratory disease; and 19% more likely to have COPD. Worse yet, for those considered healthy at the start of the study, a third became metabolically unhealthy within three to five years. (26) The author concluded that using the term healthy obese is misleading and should be avoided.

Fat loss is hard! Your body fights you to stop losing body fat and encourages future weight gain. One would think that it would be a simple process because we have so many fat cells. A lean adult has 35 billion adipocytes, totaling 130,000 kcal of stored energy. An extremely obese adult can have 140 billion, totaling 1 million kcal stored energy. (27) The longest-ever medically supervised starvation period in history was 382 days, in which a 27-year-old man went from 455 pounds to 180 pounds. (28) Once calories are reduced, our bodies send off a cascade of events to increase appetite, slow fat metabolism, and reduce energy expenditure. Your body’s fat thermostat, a hormone called leptin, drops and slows the number of calories you burn.

Leptin

Leptin is a powerful regulator of appetite; when fat cells shrink and less leptin is secreted, it signals to the brain to increase appetite. (29) Leptin concentrations are controlled by body fat and food availability. (30) Appetite plays a larger role in controlling fat loss than metabolism. It has been found that for every 20-30 kcal per day increase, appetite will increase by about 100 kcal per day above the prior weight loss. (31)

The popularity of diet documentaries has fueled the use of certain diets. Vegan diets have also grown in popularity with the Netflix Game Changers documentary. All these diets will work as long as you are in a caloric deficit. The media loves to print articles such as, “Man loses 25 pounds eating at McDonald’s every day!” Well, it’s simple, if you are in a caloric deficit, you will lose weight no matter what you eat. Weight loss should not be the primary goal. A well-balanced diet should retain muscle mass while losing body fat.

IS OBESITY GENETIC OR ENVIRONMENTAL KEY POINTS

  • Genetic and environmental factors of obesity can both contribute to obesity.
  • Much of the information we receive about dieting comes from social media and other resources.
  • Some people don’t gain weight in response to overfeeding, others do gain weight in response to overfeeding. The response is highly variable.
  • Rebound weight gain causes body fat cells to increase in number more than before starting a diet.
 

REFERENCES

1.         Klein AV, Kiat H. Detox diets for toxin elimination and weight management: a critical review of the evidence. J Hum Nutr Diet. 2015;28(6):675-86.

2.         Gillett G, Shivakumar N, James A, Salmon J. Acute Severe Hyponatremia Following Use of “Detox Tea”. Cureus. 2021;13(3):e14184-e.

3.         Cecchini M. Use of healthcare services and expenditure in the US in 2025: The effect of obesity and morbid obesity. PloS one. 2018;13(11):e0206703-e.

4.         Veloce D, Fisher M, O’Connor C, Hartman B, Horne JR. The Ontario Public Does Not Understand the Difference Between Registered Dietitians and Unregulated “Nutritionists”: Results from a Cross-Sectional Mixed Methods Study. Healthc Policy. 2020;16(2):111-27.

5.         Vidianinggar M, Mahmudiono T, Atmaka D. Fad Diets, Body Image, Nutritional Status, and Nutritional Adequacy of Female Models in Malang City. Journal of Nutrition and Metabolism. 2021;2021:8868450.

6.         Freedman MR, King J, Kennedy E. Executive Summary. Obesity Research. 2001;9(S3):1S-5S.

7.         Spreckley M, Seidell J, Halberstadt J. Perspectives into the experience of successful, substantial long-term weight-loss maintenance: a systematic review. International Journal of Qualitative Studies on Health and Well-being. 2021;16(1):1862481.

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9.         Wing RR, Phelan S. Long-term weight loss maintenance. Am J Clin Nutr. 2005;82(1 Suppl):222S-5S.

10.       GA. B. Contemporary diagnosis and management of obesity. Newtown, PA: Handbooks in Health Care. 1998.

11.       Jackson SE, Llewellyn CH, Smith L. The obesity epidemic – Nature via nurture: A narrative review of high-income countries. SAGE Open Medicine. 2020;8:205031212091826.

12.       Decarie-Spain L, Kanoski SE. Ghrelin and Glucagon-Like Peptide-1: A Gut-Brain Axis Battle for Food Reward. Nutrients. 2021;13(3).

13.       Schleinitz D, Böttcher Y, Blüher M, Kovacs P. The genetics of fat distribution. Diabetologia. 2014;57(7):1276-86.

14.       Sumithran P, Prendergast LA, Delbridge E, Purcell K, Shulkes A, Kriketos A, et al. Long-Term Persistence of Hormonal Adaptations to Weight Loss. New England Journal of Medicine. 2011;365(17):1597-604.

15.       Rynders CA, Pereira RI, Bergouignan A, Kealey EH, Bessesen DH. Associations Among Dietary Fat Oxidation Responses to Overfeeding and Weight Gain in Obesity-Prone and Resistant Adults. Obesity (Silver Spring, Md). 2018;26(11):1758-66.

16.       Sims EA, Horton ES. Endocrine and metabolic adaptation to obesity and starvation. Am J Clin Nutr. 1968;21(12):1455-70.

17.       Thrifty genotype rendered detrimental by progress? Lancet. 1989;2(8667):839-40.

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18.       Speakman JR. A nonadaptive scenario explaining the genetic predisposition to obesity: the “predation release” hypothesis. Cell Metab. 2007;6(1):5-12.

19.       Dallman MF, Pecoraro N, Akana SF, La Fleur SE, Gomez F, Houshyar H, et al. Chronic stress and obesity: a new view of “comfort food”. Proc Natl Acad Sci U S A. 2003;100(20):11696-701.

20.       Reddon H, Patel Y, Turcotte M, Pigeyre M, Meyre D. Revisiting the evolutionary origins of obesity: lazy versus peppy-thrifty genotype hypothesis. Obes Rev. 2018;19(11):1525-43.

21.       Cordain L, Miller JB, Eaton SB, Mann N, Holt SH, Speth JD. Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. The American Journal of Clinical Nutrition. 2000;71(3):682-92.

22.       Tak YJ, Lee SY. Long-Term Efficacy and Safety of Anti-Obesity Treatment: Where Do We Stand? Curr Obes Rep. 2021;10(1):14-30.

23.       Hall KD, Kahan S. Maintenance of Lost Weight and Long-Term Management of Obesity. Medical Clinics of North America. 2018;102(1):183-97.

24.       Arner E, Westermark PO, Spalding KL, Britton T, Ryden M, Frisen J, et al. Adipocyte turnover: relevance to human adipose tissue morphology. Diabetes. 2010;59(1):105-9.

25.       Fontaine KR, Redden DT, Wang C, Westfall AO, Allison DB. Years of life lost due to obesity. JAMA. 2003;289(2):187-93.

26.       Zhou Z, Macpherson J, Gray SR, Gill JMR, Welsh P, Celis-Morales C, et al. Are people with metabolically healthy obesity really healthy? A prospective cohort study of 381,363 UK Biobank participants. Diabetologia. 2021;64(9):1963-72.

27.       Hirsch J, Knittle JL. Cellularity of obese and nonobese human adipose tissue. Fed Proc. 1970;29(4):1516-21.

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