Why Wait Until The New Year? How to Use Integrated Genetics Now for Patient Success in 2021 

Are your patients waiting until January 1stto improve their diet? Especially this year, its easy for patients to talk themselves into December feasts of sugary, high-fat foods that are nutrient-poor, inflammatory, and may lead to weight gain and metabolic dysregulation.

Instead of starting the new year feeling tired, inflamed and overweight, how can you help your patients kick off 2021 feeling clear, light and full of energy? 

Let us look at how you can use integrated genetics to make personalized dietary recommendations that match patients’ metabolic gene codings, curb food cravings, increase satiety and maintain a healthy weight.

Why Eating for Your Genes Matters

Losing weight is the classic New Year’s Resolution. Do these complaints sound familiar? 

  • I’ve tried all the latest diets – why don’t they work? 
  • I feel like I’m constantly losing then re-gaining the same 10 pounds.

69% of patients follow the latest dietary trends yet obesity rates continue to rise. The problem is that a “trendy diet” may not be ideal for their genetics and may even have adverse affects, causing weight gain instead of weight loss along with feelings of sickness or malaise. 

Its time to change the conversation from “Will Keto help me lose weight?” to “What is the best diet for my genes?”

Genetics accounts for up to 70% of our metabolism and body weight!This has huge implications for the effectiveness of our dietary treatment recommendations and patient compliance. Our genes dictate how quickly our metabolism burns through our food. This affects how much food we need, as well as the protein-fat-carb ratio.

Not eating according to our own personal genetics can cause a litany of ill effects on the body including actually slowingmetabolism and promoting food cravings – the kind that are impossible to ignore, and continually drive us back to the cupboard in food-foraging mode!

Why Willpower Only Takes Us So Far

Our genetic makeup determines how satisfied we feel after a meal. Do we receive satiety messages that prevent us from eating more? Or do we continue to get hunger messages that drive us back to the fridge even though we feel uncomfortably full?

Gone are the days of one-size-fits-all diets. Trying to adhere to one of those diets is exactly why your patients need to ‘go on another diet’ every year, proclaiming that this is the year they will finally ‘stick with it.’ 

But until we change our brain’s biochemistry, willpower will only take us so far. Willpower alone will never boost our metabolism. Knowing your patients’ metabolic and dietary gene coding and altering their expression accordingly is the key to giving patients power over their metabolism, thoughts about food and eating behaviour. 

Genes that Affect Hunger and Satiety 

The FTO Gene

FTO (a.k.a. the “fatso” gene), regulates production of the 3 main hormones controlling hunger, satiety and metabolism; Ghrelin Leptin and Adiponectin.

Individuals that carry a risk allele (heterozygote or variant) have:

  • Increased production (and decreased postprandial suppression) of Ghrelin, the “hunger hormone”.
  • Reduced leptin sensitivity (leptin resistance).
  • Decreased Adiponectin.
  • Increased white fat adipogenesis through its effect on IRX-3 and IRX-5.
  • Slower metabolism secondary to leptin resistance, decreased adiponectin and less brown fat.
  • Impaired fat burning.

Overall, in large-scale multiple population studies, the FTO risk allele accounts for an overall 1% increase in the body mass index (BMI) and a 22% increased risk of obesity, independentof diet and exercise. However, the effect is significantly worse if an FTO-A individual consumes a low protein, high saturatedfat or high calorie diet. In an example of nutritional epigenetics, the influence of the A allele is greatly enhanced with such nutrition. In a striking illustration of this effect, the FTO A-allele has a prevalence of over 75% in some African populations yet the incidence of obesity and diabetes is extremely low as a result of their low-fat diet. Africans living in the US and consuming a typical western high saturated fat diet have a similar prevalence of FTO-A, but much higher BMI and type 2 diabetes risk.Knowing your patient’s FTO status is vital when planning their diet.

The Role of Visual Cues

A 2018 study3found evidence that allelic variants in the FTO gene raise obesity risk through impaired central nervous system satiety processing, thereby increasing food intake. Individuals carrying high-risk FTO alleles:

  • Had higher postprandial activation by visual cues of calorically dense foods in brain regions involved in satiety perception
  • Reported less post-meal satiety
  • Rated calorically dense, “fattening” foods as more appealing
  • Ate more total calories at a buffet meal 


ADIPOQ genes code for adiponectin production. This hormone plays a significant role in the regulation of blood glucose and insulin.  It significantly increases fatty acid oxidationand has a profound effect on the storage and use of fat as an energy source. Research indicates that it prevents the development of metabolic syndrome disorders such as diabetes.

There are 2 main ADIPOQ SNPs.

·      ADIPOQ rs17366568 codes for the production of adiponectin during weight loss.

·      ADIPOQ rs17300539 codes for the production of adiponectin during weight maintenance.

I look at both of these SNPs as they have a profound influence on individuals during andafter a diet. The lower adiponectin production associated with risk alleles results in:

  • Slower rate of weight loss
  • Unstable blood sugars, insulin levels
  • More food cravings
  • Regaining weight more easily after weight loss (the “Yo-yo” dieter)

The Role of Stress

The epigenetic effect of diet and stress on ADIPOQ gene expression is significant. Both a high fat diet and chronic stress individually decrease adiponectin production through inhibition of ADIPOQ transcription. However, when combined, the effect is overpowering and is a factor important to consider in any diet2.

The MC4R Gene

The MC4R gene codes for the Melanocortin-4 receptor, which has a central role in satiety and control of food intake. Variations in this gene represent the most common form of monogenic obesity because a defect or variance in this gene results in fewer MC4R receptors and thus decreased function. When there are not enough receptors available, the “stop eating” signal is impaired, and individuals never get the message to stop seeking out food.

The MC4R rs17782313 risk allele is associated with:

  • An 8% increase in obesity. Each risk allele increases BMI by 0.22 units.
  • Increased body weight by up to 43% independent of diet and exercise and increased BMI by 0.44 units.
  • Decreased satiety. Increased appetite and snacking, especially with foods high in saturated fat.
  • Strong association with emotional and stress-related overeating.
  • Weight gain on antidepressants and antipsychotics.
  • Increased insulin resistance and a 14% increase in risk for type-2 diabetes.

Treatment for individuals carrying the risk allele uses dietary modifications such as intermittent fasting but effective management needs some important supplements.

The Stress Genes

We saw above how stress impacts the ADIPOQ gene. It also affects numerous other metabolic genes including MC4R. In one study4looking at the association of the variant MC4R C-allele with obesity, once adjusted for other variables, the results indicated that those individuals with high stress levels had a stronger association with higher BMI and preferential intake of processed and fat-dense foods over fruits and vegetables. The authors concluded that the interaction of stress and the variant allele of MC4R altered energy intake and eating behavior to an extent that exceeded that of the variant allele alone. The coding for genes such as ADRB2, NR3C2 and FKBP5 impacts the way an individual responds to stress. Accounting for these is essential when personalizing a diet and supplement plan for your patients.


Protein, fat and carbohydrate

Low fat, high fat, low carb, protein rich? Dietary choices are endless and every new diet changes the ratios of these 3 macronutrients. So what balance is right for your patient? Again, genetics gives us the answers. Understanding how your patient handles these foods allows the perfect proportions to be recommended, promoting healthy weight and avoiding side effects.


FTO is the key gene for protein. Risk allele carriers need substantially more protein than those with the normal allele. Exercise frequency should be included in the evaluation as this has an epigenetic effect on the FTO gene. Getting too much protein leads to inflammation and weight gain.


Is keto is the best way to lose weight? Only for a select few! Anyone who starts a ketogenic diet will lose weight initially due to cutting out refined foods and sugar. That’s great for anyone. But the high saturated fat in a keto diet can easily increase inflammation, cholesterol and weight depending on how you code for your FTO, APOA2 and FABP2 genes. APOA2 individuals with the risk allele have been shown in multiple populations to be at a significantly increased risk of obesity when they ingest more than 22 grams of saturated fat per day. In a study on FTO in the journal Metabolism from 20091found that risk allele carriers that ate a diet containing 53 grams or more of saturated fat per day had lower HDL to total cholesterol ratios, higher cholesterol, LDL’s and triglycerides and higher levels of insulin resistance. The bottom line, diets like keto are great for some people but potentially harmful for others.


Not everyone does well on a low-carb diet! Knowing your patient’s coding for genes like GIPR, TCF7L2 and IRS1 gives you valuable information on how much and how frequently they can have carbs with their meal. Individuals with normal alleles tolerate carbs well and actually feel fatigued and unhealthy when they restrict them. For those with risk alleles, choosing the correct carb balance is not only important for weight, metabolism and energy but has profound implications on long-term risk of conditions such as type-2 diabetes. For example, the risk allele of TCF7L2 increases population-attributable risk of diabetes by 16-21%. Heterozygous individuals have a relative risk of 1.45 while the homozygous genotype confers a relative risk of 2.41.

Intermittent Fasting

I.F. is popular and has great research supporting its benefits with regard to weight and health. But is it right for everyone? Certainly not in my practise. Some individuals feel weak, have headaches, low energy and poor concentration. Many actually lose too much weight. Looking at FTO, MC4R and ADIPOQ coding gives an excellent guide to who should be including I.F. as part of their dietary plan.


Using Integrated Genetics to Curb Cravings and Balance Metabolism

When it comes to achieving healthy weight, making dietary and supplement recommendations is tough. There are numerous choices and most of the time it’s hit or miss, a process of trial and error. BUT knowing how your patients code for these metabolic genes takes the guess work out of your plan. You can avoid giving advice that might increase cravings, make them feel unhealthy and actually increase their weight. Eating the wrong foods in the wrong ratios or even at the wrong times can result in poor compliance, increased inflammation and rapid weight regain as well as potentially harmful long-term health effects. Avoid this pitfall by using integrated genetics.

How the GeneRX Report Can Help

My GeneRX reportuses algorithms based on my years of clinical experience and research into genetics. It seamlessly analyses and integrates all of these genes, and provides you with an easy-to-read report with detailed dietary, supplement and lifestyle recommendations. 

2021 is almost here.  Why wait till January? Be proactive and get started now! Use GeneRxto help your patients boost their metabolism, keep the weight off, and find the personalized diet that leaves them feeling healthy and satisfied?

Want to see the full report? I break it all down for you in this short video

Ready to get started? Learn how easy it is to create an account, upload a file and edit a report HERE

Want to learn more about metabolic and dietary genes?

In our latest book Fix Your Genes to Fit Your Jeans, my husband Dr. Stephen Reed, MD and I take deep dive into the value of genetic analysis in understanding individual nutritional, metabolic and hormonal strengths and weaknesses. Here’s what health care practitioners are saying:

“As a practitioner this book has added incredible value to my practice. It outlines the most important genes for weight management, how to clinically recognize them and EXACTLY how to treat them through diet, exercise and specific foods. My clients are reporting the relief they feel when reading this book to learn it wasn’t a character default but genetic factors that controlled their metabolism. Having used the protocols in this book, I can say they are 100% what people need.”

  1. Chamberlain A., 2009. “Ala54Thr polymorphism of the fatty acid binding protein 2 gene and saturated fat intake in relation to lipid levels and insulin resistance: the Coronary Artery Risk Development in Young Adults (CARDIA) study”. Metabolism. 58(9): 1222-8.
  • De Oliviera et al.2011.High-fat diet and glucocorticoid treatment cause hyperglycemia associated with adiponectin receptor alteration.” Lipids in Health and Disease.10:11
  • Melhorn SJ, Askren MK, Chung WK, Kratz M, Bosch TA, Tyagi V, Webb MF, De Leon MRB, Grabowski TJ, Leibel RL, Schur EA. FTO genotype impacts food intake and corticolimbic activation. Am J Clin Nutr. 2018 Feb 1;107(2):145-154. doi: 10.1093/ajcn/nqx029. PMID: 29529147; PMCID: PMC6454473.
  • Park S. et al. 2016. “Interactions with the MC4R rs17782313 variant, mental stress and energy intake and the risk of obesity in Genome Epidemiology Study.” Nutrition & Metabolism.13: 38.