Why Am I Always Hungry? The Answer Can Lie In Your Genes

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I meet individuals in my clinical practice who eat healthily, are dedicated to eating the right foods prepared the right ways. They don't necessarily drink alcohol. They exercise daily or regularly, and yet they struggle with their weight and they always have. They reluctantly ask, “Why am I always hungry?”

Outsides may judge these individuals as not trying hard enough or that they’re binge eating. Some may think they're eating behind closed doors.

I've even heard clinicians argue that people who can't lose weight aren't telling the truth.

But the reality is that many of these people are biochemically fitter than those who appear normal weight and healthy.

This leads to the questions:

Why do some people struggle with weight balance or weight loss and others don't?

Why do some people experience what we call “weight loss resistance”?

Why are some people always hungry?


Weight is more than simply “calories in equals calories out”

What is it that differentiates one person’s ability to balance and maintain their weight from the next person?

In my training as a dietitian, I was taught that “calories in equals calories out.” So if you balance what you eat (calories in) with your activity, energy expenditure or the rate at which you burn calories (calories out), then you will always return to weight balance. I think some still repeat this equation.

What I see genetically is that this simplistic energy balance equation does not work for many people. It doesn't matter what they do, they can't efficiently or effectively shift their weight. Or if they do, it just takes so much longer, even though they're eating well and exercising as diligently as the next person.

What we now know is the role that genes play in weight balance, and how genes influence hunger and satiety. Let’s dig into this a little more.

“A lot of things impact our weight and many of them are not obvious.”


How Genes Can Affect Your Weight

Variations in genes can alter

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  • Your hunger and satiety cues (they can change your perception of when you feel hungry and when you feel full)

  • How you perceive taste and flavor

  • The efficiency and effectiveness of how you access energy stored in your cells for burning. Some of us are very efficient energy burners. Some of us are not

  • How your body stores energy (thermogenesis).

  • Your metabolic rate

  • The efficiency and effectiveness of exercise

So you see, there are a lot of dynamics at play. Your genes have a hand in all of them!

Depending on your unique gene blueprint, it can be very easy for some people to maintain or lose weight. For other people, the struggle is real. Like pushing a rock uphill. And for some people, losing or maintaining a healthy weight is complicated by genes that alter their hunger and satiety cues.

So let’s talk about how some of your genes influence your feelings of hunger and fullness (satiety).


Genes, hunger and satiety

There’s an unruly cluster of genes that influence, or “play tricks,” with our hunger and satiety cues. Think of them as troublemakers because they can trick us into feeling hungry when we're really not. And they won’t shut off our “munchies” when we're actually really full.

Hunger turned on and “it's time to stop eating” turned off.

Backwards messages from faulty genes can lead to overeating. It can happen to the most mindful of eaters. It may lead to those second helpings, larger portions and absent-minded snacking, even though we're actually full. It’s a gene trick. that we may not be aware of. It’s hard to stop eating when there’s no shut off valve.

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This is not about willpower either. With faulty genes, individuals literally may not know that they’re overeating or over-snacking. They're not conscious of this. We know through the literature, particularly with children, the shutoff is just not there.

“What's important, when we understand how these genes play tricks on us, is that it’s not about willpower.”

This being said, it’s important to separate emotional or stress-induced over-eating from genetically-influenced eating. How do we know if genes are at play? Genetic testing.


Genes that impact why you are always hungry

I work with a lot of people who come to me for reasons that have nothing to do with weight at all; it is another complex health issue that they’re looking to solve. But when I look at the area of their genetic report that reflects hunger, satiety and weight balance, I often see a pattern of genes that suggest a propensity to snacking or craving foods.

When I see these patterns on a report, I’ll ask the individual whether they feel as if they’re constantly looking for food or are always hungry. About 60 percent of individuals say they didn't want to tell anyone, but they always thought it was their imagination. They say they can eat, and then eat again in two hours because they feel hungry again. I tell them it is not their imagination, it's actually their genes at play.

So which genes are we talking about here? MC4R, FTO, LEPR, and DRD2. 

Variants in these genes can influence body weight by altering satiety mechanisms. In other words, they promote cravings, mindless snacking or searching for food because of constant hunger. All of this can result in overeating and weight gain. Now some people can have variants in the aforementioned genes, eat and eat and have no problems losing or maintaining their weight. This is because genetically, they are effective energy burners. Lucky them. Other individuals, do not have the same genetic jewels so overeating is problematic.

From the group of four genes mentioned above, I find that LEPR and DRD2 are the biggest trouble-makers in the hunger and satiety arena, so I’ll focus on these two in this article. Come with me.


LEPR

The gene LEPR is associated with leptin. Leptin is a hormone that binds to receptors on your cells and acts as a shutoff valve for your hunger cues. It flips the switch and says, “OK, you're not hungry anymore. Good to go. Don't need to eat anymore.”

People who have gene variants on LEPR produce leptin that doesn't effectively or efficiently bind to the receptors. This means you shut down the communication to the brain saying that you've eaten enough and you are always hungry.

Dr. Dan Stickler, CEO of The Apeiron Center was a bariatric surgeon in his earlier medical career . He said that in performing many bariatric surgeries his team noticed that some people, in spite of the surgery, would gain weight. And it wasn't because they weren't adhering to the food advice.

Through his research, Dan learned that the culprit in weight regain among his patients wasn't specifically the LEPR gene, rather its sibling or “partner in crime”—the ghrelin gene (GHSR). The ghrelin gene initiates your hunger cues. It turned out that a common observation among people with weight regain after bariatric their grehlin gene was in the “on” position, leaving them unable to turn off. or turn down their hunger cues. The faulty (disruptive!) grehlin gene helped Dan’s team discover one of the reasons why some people had different outcomes to bariatric surgery.


DRD2

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The DRD2 gene is a dopamine-related gene. Dopamine is associated with reward and euphoria. A defect in dopamine-binding receptors leads to some individuals constantly searching around looking for a “high” or feel-good reward, because that’s what dopamine does! It’s the same feeling you get after a good workout, or when you've eaten a great meal or, during these pandemic times, when you were able to see your loved ones again.

That kind of rushing, gushing, warm feeling is a dopamine high.

Specific to hunger and satiety, DRD2 amplifies that need for a reward or a high. Variants in the DRD2 gene can alter communication between the gut and the brain so that the brain gets the repetitive message, “Keep on eating; you're still hungry. You’re not full yet.“


How to work with genes that always make you hungry

So how do you work with these “upside down” genes that always keep you hungry, seeking out food, and don’t tell your brain when you’re full and satisfied?

1 - Eat mindfully

The first thing is to pay attention to when you eat and why you're eating. In other words, eat mindfully. Be aware of when and why you're eating in the first place. If eating is stress or emotionally-induced, you’ll want to work on first. Stress and emotions can drive overeating regardless of whether your genes are acting up or not.


2 - Choose slower-digesting food

Certain foods stick around in your stomach longer because they’re more slowly digested. By choosing these foods, the stomach is extended or distended longer, which means those grehlin receptors in the stomach receive the “I’m full” signal and are less likely to message your brain to keep eating!

Foods that are digested more slowly are rich in fiber, protein and some fat. Protein and fat stick around longer. Carbohydrates don't. If you're snacking on carbs, which are often some of the yummy foods, will disappear from your stomach faster. And guess what? Your genes are going to kick on to say, “OK, I’m hungry. What can I eat next?” So think of fiber-rich legumes and whole grains (if you eat grains), but always include protein and fat to slow things down.


3 - Time-restricted eating

Take advantage of time-restricted eating. Time-restricted eating mean eating within a specific window of time during the day and not about restricting food.

A time-restricted eating approach means eating during a consistent period (or window) of time every day. You may start with a 16 hour eating window and then reduce that window to 14 hours, then 12 hours and then 10 hours. Some people eat all their meals within eight hours.

Reducing your eating window reduces both the digestive burden on your body and your need for insulin. While insulin helps to regulate your blood sugar, it also happily shuttles any excess energy into fat storage. By restricting your eating window, you can keep insulin out of the fat storage business!

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  • Time restricted eating also allows your body to “sort out the trash.”

  • Late at night, say between midnight and 2:00 o’clock in the morning when you are sleeping, your body goes through a process called autophagy

  • The process of autophagy is akin to recycling. It looks at the fragments of what you've been eating and what the body has been using to repair your cells and DNA and separates useful material that can be recycled from the stuff that needs to go to the dump. So your body might recycle amino acids that can be strung back together to create a protein, but put a tag on defective, damaged or toxic molecules that can go to the dump (AKA be excreted).

  • Your body sorts recyclables from the trash, while you're asleep. If you're eating at 10, 11, 12 o'clock at night, your body can’t do the sorting because you diverted its attention to digestion. You essentially derail the trash service. Excess trash in your body is as unsightly as excess trash in your neighborhood!


4 - Help your energy plan with vitamins and minerals

If you want to get the best “Return On Ingestion (R.O.I), give your body the right vitamins and minerals to assist in energy extraction.

What does this have to do with always being hungry you might ask?

If you have “faulty” or “defective” genes that have you dashing to the refrigerator or calling for take out all the time, at least give your body the right vitamins and minerals so that it can extract energy efficiently for you.

Food intake without the right energy extraction tools means you're creating a big food garbage dump versus an energy plant.

Help your energy plant with B vitamins. Your body takes molecules from fat and carbohydrate and feeds them into the Krebs cycle. The Krebs cycle transforms these molecules and feeds them into the electron transport chain (ETC) where the base unit of energy for your body is produced. That energy unit is called ATP. You can't produce energy without your B vitamins period.

Fire up your energy plant

Target these food groups for your B’s

  • Nuts, seeds, legumes, and seaweed.

  • B-rich nuts include peanuts, walnuts, almonds and pistachios. Also Brazil nuts, which are the best source of selenium on the planet too.

  • B-rich seeds, target sunflower, pumpkin and chia seeds

  • B-rich legumes, shoot for garbanzo beans or chickpeas, lentils and also soy beans (whole soybeans or edamame).

  • Seaweed or sea plants, are among the most nutritionally-robust foods you can buy, and yes B-rich!

  • One exception is vitamin B12. If you're plant-focused, look to nutritional yeast. Animal and seafood naturally contain B12

  • The Genomic Kitchen’s Ingredient Toolbox includes B vitamin-rich foods.


Key Take-Aways

  • Genes can influence hunger and satiety, altering signals to the brain.

  • These signals can override satiety cues, prompting snacking and food-seeking behaviors that can result in overeating.

  • Variants in the DRD2 gene can enhance the sense of hunger, further inducing food-seeking for reward.

  • Working with these genes include awareness, choosing foods that delay emptying of the stomach to trick grehlin receptors into registering fullness.

  • Using an intermittent fasting strategy to restrict the eating window and reduce insulin secretion which promotes fat storage.

  • Genes are not predictive or diagnostic. Just because you have gene variants that might promote over-eating, does not mean that they are active or have this influence in you.

    To learn more about gene testing or to discover your unique gene blueprint, contact us at The Genomic Kitchen.


References

Romer AL, Su Kang M, Nikolova YS, Gearhardt AN, Hariri AR. Dopamine genetic risk is related to food addiction and body mass through reduced reward-related ventral striatum activity. Appetite. 2019 Feb 1;133:24-31. doi: 10.1016/j.appet.2018.09.010. https://pubmed.ncbi.nlm.nih.gov/30296504/

Carpenter CL, Wong AM, Li Z, Noble EP, Heber D. Association of dopamine D2 receptor and leptin receptor genes with clinically severe obesity. Obesity (Silver Spring). 2013;21(9):E467-E473. doi:10.1002/oby.20202. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7081169/

Glick D, Barth S, Macleod KF. Autophagy: cellular and molecular mechanisms. J Pathol. 2010;221(1):3-12. doi:10.1002/path.2697. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2990190/