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Our genes are a template for how our bodies work. Most people on keto diets tend to consume a high amount of saturated fats. The diet works only when the stored fat is properly broken down and used for energy. Certain variants of the APOA2 gene tend to interfere with this saturated fats metabolism and hence, carriers of such variants may not get the desired benefit from this diet.
There seems to be an endless debate about whether saturated fats are good or bad for your health.
The truth is, all of us need a little bit of fat for some body functions like hormone production or maintenance of cell integrity.
But, what is considered 'too much' for your body is determined by certain gene variants you carry.
Let's explore this concept with a diet that's been constantly gaining popularity for weight loss and prevention and treatment of certain health conditions:
The basis of this diet is ketosis, which refers to the metabolic process in which the body converts stored fats into energy, releasing ketones in the process.
Hence, the conventional keto diet, which calls for high consumption of fats may work only if the stored fat is metabolized efficiently.
Several genes contribute to how your body reacts to saturated fats.
APOA2 gene is one of them that determines how well you tolerate saturated fats and how well you can transport cholesterol.
Depending on the variant of this gene you carry, you may need to modify the keto diet a little bit, in order to maximize its benefits to your body.
From the evolutionary perspective, certain human societies, such as those in the colder northern regions are likely to have subsisted on the large intake of fats for hundreds of generations.
As a result, they could have developed adaptations that enable them to metabolize this macro ingredient in food quite efficiently.
If you have inherited those genes, then your body is better able to cope with fats intake.
APOA2 gene produces a protein apolipoprotein -II, which plays a role in fat metabolism and obesity.
Individuals with the sensitive variant of this gene are more prone to increased BMI (6.8 times greater BMI), waist circumference, and body weight in response to high levels of saturated fat (more than 22g of saturated fats per day).
This was an observation in comparison to the people with the non-sensitive variant of the gene consuming the same amount of saturated fats.
It is vital for the carriers of the sensitive variant to limit their saturated fat intake.
However, there was no difference among individuals with both versions, in terms of weight and BMI when saturated fat intake was low (less than 22g per day).
One possible mechanism that could help explain the above gene-diet interactions is that, the sensitive variant of this gene produces lower levels of the protein, APOA2 (regulates the satiety response), resulting in low satiety and greater appetite among individuals with higher saturated fat intake.
This appetite may preferably be for foods rich in saturated fat and this higher fat intake would lead to greater weight.
Other genes like FTO, PPARG also impact the metabolism of saturated fats.
Carrying even 2-3 variants that affect saturated fats metabolism can pose a challenge to cholesterol control and weight loss.
It is thus vital for such individuals to alter their diet with lesser intake of saturated fatty acids.
Replacing saturated fatty acids with monounsaturated fatty acids (MUFA) and poly-unsaturated fatty acids can be a good start.
Sources of MUFA
Sources of PUFA
Upload your DNA raw data to Xcode Life to know your genetic variants for saturated fat metabolism.
