Connecting the Dots: Genomics for Mood & Weight Management

Connecting the Dots: Genomics for Mood & Weight Management

Connecting the dots: genomics for mood & weight management

Why do some people seem unaffected by – or even able to thrive under – stress, while others suffer from depression, anxiety, or turn to unhealthy coping strategies like overeating?

While no one factor can explain these differences entirely, emerging research about genetic variations can provide a big clue. Understanding the link between genetic variations and the behaviors that drive harmful coping strategies can not only answer why your patients are struggling – it can help you better support them.

Today I want to share how some of the most common variations impact food and mood – and how you can put this information to use in your practice, even if you haven’t worked with genomics before.

The big 5: Common genetic variants to know

While there are millions of SNPs (Single Nucleotide Polymorphisms), five common stand out as having an outsize impact on mood and weight when a patient has a risk variant: MTHFR, COMT, DRD2 (dopamine receptors), TPH2 (serotonin) neurotransmitter, and FTO variants.

MTHFR plays a role in activating folate. Folate is critical for the conversion of several precursors into the neurotransmitters that they’re supposed to become, such as dopamine, with the help of other co-factors like zinc and vitamin B6.

COMT is responsible for clearing dopamine, detoxing estrogen, and clearing other catecholamines.

DRD2 is the dopamine receptor, and variations in it can impact a patient’s biological access to the neurotransmitter dopamine.

TPH2 influences how well serotonin is made from tryptophan.

FTO is like a “shut off valve” for hunger. People with variants in this gene may struggle to feel full or satisfied with food. This is because the FTO variant influences the balance between the metabolic hormones ghrelin and leptin. These patients with the FTO variant may also burn fat slower since FTO influences the metabolic hormone adiponectin.

Now, let’s take a look at how variants in each of these genes can impact executive functioning, mood, and weight.

MTHFR vulnerabilities make it hard to recover

Do you have patients struggling with addiction, or unable to recover from depression or other chronic psychiatric conditions? A vulnerability in the MTHFR (C6772) SNP is often a factor. For people with this variant, prevention may be the best medicine. (To learn more, check out Dr. James Greenbatt’s Psychiatry Redefined Depression Course here).

MTHFR and other methylation SNPs can be found in the PureGenomics Vitamins, Minerals, and Omega 3s category.

In times of increased stress, or a traumatic experience it’s important to retest important key unique elements that have a genetic variant, such as BCMO1 (Vit A) and GC, CYP2R1, DHCR7 (Vit D SNPs) according to Dr. Samuel Yanuck. If levels are low, supplement accordingly. These SNPs are also found in the Vitamin/Mineral/Omega 3s category with MTHFR.

COMT variant impacts executive functioning

COMT wild type Val/Val typically performs well under pressure. However, since these patients’ COMT is fully functioning, they may degrade their dopamine too efficiently and lack biological access, leading to a struggle with focus. Slowing down dopamine clearance with something like Rhodiola Rosea can be helpful. The DRD2 SNPs will give you insight if the patient can even efficiently use the dopamine that wasn’t clear by their wild-type COMT.

A patient with COMT met/met double risk variant (homozygous) has enough dopamine hanging around, however, a good question and insight to have are how well are they utilizing the dopamine by referencing the DRD2 SNPs.

A patient with this COMT met/met may struggle with anxiousness, insomnia, and hyper-focus when under increased stress since this genetic variant can’t clear catecholamines.  COMT met/met suffers under pressure and their executive functioning can fall apart. These patients may need extra magnesium or lithium orotate, or adenosyl hydroxy B12 under stress.

DRD2 can starve the brain of dopamine

DRD2, which is the dopamine receptor, is susceptible to a very common variation that affects its ability to function. That means even with plenty of dopamine being made, the brain can’t adequately respond because the receptor isn’t working properly.

To explain this to patients, I say that dopamine is like a key that is supposed to open a lock. If the lock isn’t there, the key is useless. The key is dopamine and the lock is the DRD2 dopamine receptors.

When thinking about Dopamine bioavailability, it’s advisable to reference both COMT and DRD2 genetic variations. Again, COMT is how well dopamine is cleared and the DRD2 receptors are how well this important reward-seeking neurotransmitter is utilized.

For more on dopamine, check out this webinar with Dr. Kelly Heim.

TPH2 can block the path to serotonin

Serotonin is well-known as contributing to feelings of well-being and happiness. The neurotransmitter SNP TPH2 can prevent the conversion of tryptophan into serotonin.

Supplementing appropriately can help patients with the conversion from tryptophan to serotonin, as long as the practitioner knows about the variant.

Because of their effect on serotonin and dopamine, TPH2 and DRD2 neurotransmitter genetic variations play a major role in mood, food cravings, appetite, and satiety issues.

Food addictions and genetics

Taking a look at what foods patients crave can also hint at what genetic variants they might have that are being expressed. For example, cravings for chocolate and sweets point to a need for L-Tryptophan to help have biological access to serotonin. In that case, I would reference the patient’s TPH2 variant.

If they crave high-fat, salty foods like chips, popcorn, french fries, cheese, and wine they may be seeking L-Tyrosine for a dopamine hit, therefore, it’s advisable to reference the patient’s DRD2 SNPs

If the patient also has the FTO variant that stops satiety, they might turn to these cravings over and over again to try and feel better. It quickly becomes a vicious cycle. The good news is these genetic vulnerabilities can be supported with amino acid supplementation to help patients break the food addiction cycle. Exercise also can help boost these neurotransmitter levels. Jumping Jacks anyone?

FTO variants make people hungry all the time & burn fat slower

Patients who struggle with overeating may have a common variant for FTO. This variant diminishes satiety and increases appetite. So if the patient has the FTO variant, and they are always hungry plus have variants in the DRD2 or TPH2 SNPs, it’s easy to see why patients can get stuck in unhealthy eating habits. Patients often think it’s a lack of willpower. I think it’s a patient’s vulnerabilities being expressed that are communication they may need higher amounts of nutrients to restore optimal function.

FTO also dictates how much protein is needed. Those with A-allele variants need more protein to experience satiety. Those with T-allele variants have a faster metabolism and require less protein.

The good news is genetics does not have to be the patient’s destiny. Those patients, like myself, with this FTO variant, can achieve satiety and even lose weight by eating a higher-protein diet and reducing saturated fats. But if they drop the higher protein diet, they often gain the weight back. (This was demonstrated by a study in which patients with the A-allele had greater reductions in food cravings at six months than those without the variant.)

Ready to start using genomics in your practice?

As you can see, there is so much to be gained from the study of genomics. Even better – the field is advancing rapidly and more information is quickly becoming available. The time to integrate this clinical decision-making tool into your practice is now.

I recommend PureGenomics. They have really made “genomics, simplified” by providing enhanced reporting that clearly illustrates each SNP, its scientific rating, and which to prioritize for action.

Like many other genomic interpretation platforms, PureGenomics used the red, yellow, green color code classification, After PureGenomics launched PureGenomics 2.0 in May 2020, the platform now uses the more accurate alleles classification. Listen to Dr. Nathan Morris explain why PureGenomics moved away from the color genotype classification here. And download the Genotype Classification Reference Sheet here to assist you in the transition from color classification to alleles.

If you’d like guidance and support on introducing genomics to your practice, take 30 minutes for a free PureGenomics Welcome Call with me. I’ll help you narrow down exactly how genomics could support your practice and the first steps you’ll need to take to get started.

P.S. Interested in learning more about genetic variants and weight?

Friday, July 3, 2020, listen to Episode #6 of Good Medicine On the Go with guest Dr. Penny Kendall-Reed. This episode takes the appetite and satiety conversation a step further. Dr. Penny shares the genetic variants practitioners need to know that have a profound effect on the two metabolic hormones, ghrelin and leptin and what that means for appetite and satiety symptoms and weight management. Follow the podcast to be notified when new episodes are available. And tell a Friend!

Nutrigenomics Coaching

Providers: Have you been learning nutrigenomics yet you feel hesitant to integrate this tool into patient care?

Patients and Parents: Are you ready to learn how to work with your body to build health and resiliency?

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