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Table of Contents
Introduction
Our genetic background can have a significant impact on what we can eat, how much we should eat, and how our bodies respond to different foods.
However, it’s important to remember that genetics is just one factor that influences our diet, and other factors such as cultural and environmental factors also play a significant role.
Some shortcuts and simplifications that tend to justify everything on genetic grounds have also led to the promotion of diets such as the “paleo” diet for the wrong reasons.
For these reasons, I summarise below what we know so far of the fascinating way our DNA can or cannot influence what we eat.
The many ways in which genetics can influence our diet
Our genetic makeup can influence what we can eat in several ways.
First of all, our taste receptors play a vital role in determining what we like to eat. Some people have genes that make them more sensitive to certain tastes, such as bitterness, which may make certain foods unpalatable to them.
Certain food allergies, such as peanut or shellfish allergies, have also a genetic component, and, therefore, if one or both of your parents have a food allergy, you may be more likely to have it as well.
Our genes can also influence how hungry we feel and how satisfied we are after a meal. Some people have a genetic predisposition to overeating, which can lead to obesity and other health problems.
Finally, our genes can also influence how our bodies metabolize certain nutrients. The most famous example is the intolerance to lactose. This intolerance is caused by a genetic variation that makes it difficult for some people to process lactose.
Lactose intolerance is caused by a genetic mutation
As indicated above, lactose intolerance is caused by the body’s inability to digest lactose, a sugar found in milk and other dairy products. The inability to digest lactose is due to a deficiency of the enzyme lactase, which is needed to break down lactose into simpler sugars that can be absorbed by the body.
Lactase is produced in the small intestine and is present in the lining of the intestine as well as in the intestinal fluid. Lactose is normally broken down into glucose and galactose by lactase, which are then absorbed into the bloodstream and used for energy.
In people with lactose intolerance, the lactase enzyme is either absent or present in insufficient amounts, so lactose is not broken down and remains in the intestine. The undigested lactose then passes into the large intestine, where it is fermented by bacteria. This fermentation produces gases, such as hydrogen, methane, and carbon dioxide, which can cause bloating, flatulence, and diarrhoea.
Lactase deficiency is caused by mutations in a gene called LCT, which provides instructions for making the lactase enzyme. There are different variations of the LCT gene that are associated with lactase persistence (the ability to digest lactose) or lactase non-persistence (lactose intolerance).
People with lactase persistence have a variation in the LCT gene that allows the lactase enzyme to continue to be produced into adulthood, whereas people with lactase non-persistence have a variation that leads to a decrease in lactase production after weaning.
How genetic variations influence hunger and satiety
Several genes have been found to be associated with hunger and satiety including the melanocortin-4 receptor (MC4R), FTO, the dopamine D2 receptor (DRD2) and the leptin receptor (LEPR).
MC4R plays a crucial role in regulating appetite and energy balance. Variations in this gene have been linked to both obesity and anorexia. People with mutations in the MC4R gene may have an increased appetite and a reduced feeling of fullness after a meal, leading to overeating and weight gain.
FTO has been associated with obesity and increased food intake. Studies have shown that variations in the FTO gene can affect levels of the hunger hormone ghrelin and the satiety hormone leptin, which can lead to increased appetite and reduced feelings of fullness.
DRD2 has been linked to food reward and addiction. Variations in this gene can affect the response to dopamine, a neurotransmitter that plays a role in regulating food intake and reward. People with certain variations in the DRD2 gene may have a reduced response to dopamine, leading to an increased desire for high-fat and high-sugar foods.
LEPR is involved in the regulation of appetite and energy balance. Variations in this gene can affect the sensitivity to the satiety hormone leptin, leading to increased appetite and reduced feelings of fullness.
Overall, these examples demonstrate how genetic variations can influence hunger and satiety by affecting the regulation of appetite-related hormones and neurotransmitters. However, it’s important to note that genetics is just one factor that influences hunger and satiety, and environmental factors such as diet and lifestyle also play a significant role.
Epigenetic mechanisms can also influence hunger and satiety
Recent studies have shown that some epigenetic mechanisms can also influence these processes.
Epigenetic mechanisms refer to changes in gene expression that are not caused by changes in the DNA sequence itself, but rather by modifications to the DNA molecule or to the proteins that package the DNA. These modifications can alter the accessibility of genes, which can affect their expression and ultimately influence physiological processes.
One example of an epigenetic mechanism that can influence hunger is DNA methylation, which involves the addition of a methyl group to a cytosine nucleotide in the DNA molecule. DNA methylation can alter the accessibility of genes, leading to changes in their expression.
Several studies have found that DNA methylation in genes related to appetite and energy regulation can influence hunger and satiety. For example, DNA methylation in the POMC and leptin genes, which are involved in appetite regulation, were associated with changes in hunger and satiety in response to a meal.
A drastic reduction in caloric intake, which usually occurs when people try to lose weight quickly, is associated with DNA methylation of these genes. This DNA methylation will be maintained long after an individual has stopped dieting and returned to normal caloric intake. Therefore, with the control mechanism for hunger and food intake silenced, this individual will tend to eat more and regain weight.
In another article, I explain in more detail why people who follow a low-calorie diet most often gain weight in the long term.
The content of our gut is influenced by our genetic background
There is growing evidence to suggest that our gut microbiome is influenced by our genetics, as well as environmental factors such as diet, medication use, and lifestyle factors. However, the interaction between all these factors is complex and requires more research to be fully understood.
Nevertheless, several studies have shown that there is a heritable component to the gut microbiome, with family members sharing similar microbial profiles. Additionally, specific genetic variations have been identified that are associated with differences in gut microbial composition and diversity.
For example, genetic variations in the FUT2 gene, which is involved in the production of certain types of sugars in the gut, were associated with differences in the composition of the gut microbiome.
Other studies have identified genetic variants that are associated with differences in the expression of genes involved in immune system function, which can in turn impact the composition and function of the gut microbiome.
Currently, there is no standardized approach for determining which probiotic-rich foods may be most beneficial for an individual, as the effectiveness of these foods can vary depending on a variety of factors, including the individual’s gut microbiome, diet, and overall health status.
This is one of the reasons why professionals should not recommend taking probiotic supplements except in very specific cases, as we have seen in another article.
What is the Paleo diet?
The “paleo” diet refers to a dietary approach that is based on the types of foods that were consumed by early humans during the Palaeolithic era, which ended around 10,000 years ago. The idea behind the paleo diet is that our bodies are best adapted to the types of foods that were available to early humans, such as meat, fish, vegetables, fruits, and nuts.
The paleo diet typically excludes foods that were not available during the Palaeolithic era, such as grains, legumes, and dairy products. Some versions of the paleo diet also exclude processed foods and sugar.
The paleo diet has been popularized as a way to promote weight loss, improve blood sugar control, and reduce inflammation in the body. However, the scientific evidence supporting these claims is mixed, and there is some debate among nutrition experts about the long-term health effects of following a paleo diet.
Paleo diet and genetic assumption challenged by gut microbiota importance
The idea behind the paleo diet is indeed based on the assumption that humans have not evolved to consume foods that were introduced after the Palaeolithic era. However, the scientific understanding of the role of the gut microbiota in human health has shed new light on the relationship between our diet and our biology.
While the paleo diet may exclude certain types of foods that are associated with negative health outcomes, such as processed foods and refined sugars, it may not necessarily reflect the diversity of foods that are beneficial for our gut microbiota. The gut microbiota plays an important role in breaking down and digesting a wide range of foods, including those that were not part of the Palaeolithic diet, such as legumes and dairy products.
In fact, research has shown that a diverse diet that includes a variety of plant-based foods, rather than a strict adherence to a specific set of foods, is more beneficial for promoting a healthy gut microbiota and, consequently, to maintain our overall health.
While our genetics may not have changed much over the past 10,000 years, the genetic makeup of our gut microbiota can change relatively quickly in response to changes in diet. This means that if the paleo diet is based on the idea of eating like our ancient ancestors, it does not consider the ability of our gut microbiota to change and adapt to a new environment and the food available.
In other words, our gut flora is adapted to what we eat today, not to what our ancestors ate thousands of years ago.