I want to start my first article on predictive medicine by introducing myself. My name is Carlos Martín and I am CTO of medmesafe. At the end of this article, which I hope someone other than my friends and family will reach, which would mean that what I am telling you is of some interest, I will leave you my social networks in case you want to contact me.
At the end of spring 2018, after reading so many scientific studies on how obesity affects health, I came to the conclusion that, although I did not feel bad, weighing 141 kg, I had to take measures to avoid that in the future (and it didn’t have to be very far away) began to have health problems. I have to admit that the data that most convinced me to take action after listening to Dr. Dolores Saavedra in a meeting with the scientific and ethics committee of medmesafe was the relationship between obesity and the increased probability of suffering a cancer, a disease that I am terrified of.
On June 5, 2018, I put myself in the hands of Dr. Saavadra, after starting a diet on my own a few months ago: I basically stopped snacking between meals and reduced the amount of my rations, which along with training the basketball with a team of veterans, led me to lose 7 kg without reducing volume (don’t notice it on the belt). Below, you can see what the starting point was:
At that time I started a ketogenic diet controlled by Dr. Saavedra and I underwent a nutrigenetic profile analysis. It is essential to emphasize at this point in the article that no weight loss diet should be followed, and in general for any other purpose, without the supervision of a doctor or nutritionist.
The nutrigenetic profile analysis that I performed is a combination between the genetic analysis of obesity and diabetes and the cardiometabolic genetic analysis. At 141 kg, I was very concerned about whether, in addition to the risk I had taken from obesity, I had a genetic propensity for diabetes and cardiovascular disease.
Thanks to the fact that I carried out this study, I have tools to avoid gaining weight again or, being a purist, gaining fat, especially visceral. During this year I have been publishing information about this analysis and the weight loss process on my social networks, such as this article about the rebound effect that I published on LinkedIn.
In the article “Genetic analysis of obesity and diabetes” by nutritionist Blanca Montoya you can find a detailed explanation of the information provided by this type of analysis. Regarding my analysis and in summary form these are the results of it:
The genetic load in relation to environmental (epigenetic) factors is considered high: 13 of the 21 thrifty polymorphisms are present; of these, the patient is homozygous for 4 and heterozygous for 9 and double heterozygous for two of them.
Regarding the central control of intake, the risk is low (1/3 in heterozygosity).
Regarding thermogenic regulation and lipid metabolism, the genetic risk is high (4/6, two homozygous and two heterozygous).
Regarding the inflammatory process in adipose tissue, the risk is high (3/4 two homozygous and one heterozygous + double heterozygous).
Regarding insulin resistance and predisposition to DM2, the risk is moderate (2/5, one homozygous and another heterozygous).
In relation to cardiovascular risk, the genetic load is high (5/7, one homozygous and four heterozygous).
The following graph visually represents the above quote:
But, what does this mean practically? In this first article I will focus on the proinflammatory process of adipose tissue.
In the section referring to this issue, the report stated:
In this group, the patient presents three thrifty polymorphisms:
The first is in the IL-1B gene (Interleukin 1-Beta gene) in homozygosis. The polymorphism of this gene, in addition to altering immune function, causing low-grade chronic inflammation of adipose tissue (lipoinflammation) has been linked to total fat mass in young people, through the regulation of adipogenesis, food intake, and consumption. energy expenditure. The CC genotype for this polymorphism (as in the present case) has been associated with increased total fat mass and therefore the development of obesity.
The second is located in the IL-1RN gene (Interleukin 1 Receptor antagonist protein gene) in heterozygosis. This gene has been related to increased serum levels of leptin and IL-1RN, which could be the cause of an alteration in the regulation of immune function involving the IL-1 system, which has been associated with the development of obesity. As in the case of other genes, this gene together with the previous one not only add their effects, but they are enhanced by increasing the amount of total fat and the predisposition to immunity.
or resistance associated with obesity (double heterozygous).
The third is found in the IL-6 gene (Interleukin 6 gene) in homozygosis. This gene participates in the inflammatory process of adipose tissue in obesity (low-grade chronic inflammation) and has also been linked to alterations in the lipid profile that accompanies insulin resistance. This lower sensitivity is due to the fact that the activation of the insulin receptor is altered, modifying the cascade of phorylations that are required for its correct function (post-receptor resistance).
It is possible that after reading this it is not clear what the problem is. Ok, just kidding, of course for ordinary mortals in whose group I include myself, it doesn’t make any sense. The explanation of these paragraphs of the report is carried out by the doctor who accompanies us in the genetic analysis process within the medmesafe platform, in my case Dr. Saavedra.
What these 3 paragraphs come to say is that I have some polymorphisms that cause me to store more fat than the population average. Said like this, it seems that it was obvious before doing the analysis, otherwise I would have weighed 141 kg, of which 54.1 kg, at least, were fat and a visceral fat level of 24 (ideally a level close to 6).
But what is the most converted to fat? Especially carbohydrates, Dr. Saavedra explained to me when she gave me the report. The report also states:
Due to the presence of genes that favor low-grade chronic inflammation present in adipose tissue (lipoinflammation), it is recommended to completely avoid dairy products and increase the consumption of foods rich in DHA (oily fish, olive oil, avocado, nuts, etc.). ) as the only source of fat or supplement this essential omega 3 fatty acid.
As there is an ancestral genotype not adapted to current foods, processed foods should be avoided, as well as refined sugars and flours.
These generic recommendations of the report must be specified by a doctor or nutritionist, indicating the correct amounts and appropriate products based on the history of each one of us.
With this information and the change in habits I have managed not to gain weight.
Below, I show you my weight on December 11, 2018, when I reached the minimum weight (and visceral fat index) and finished my weight loss diet and my weight on May 22, the last time I went to revision:
As can be seen in these more than 5 months I have increased (91.8 – 83.9 =) 7.9 kg, where (18.8 – 14.5 =) 4.3 kg are fat and (73.0 – 69.4 =) 3.6 kg of muscle. During this time I have skipped a lot my correct eating habits (I will no longer call it a diet) and increased exercise, although it has made me gain muscle, which is very good, it has not managed to maintain the level of fat, accumulating in the stomach.
And what was I like at 141 kg and how was I at 84 kg? In this image where you can compare the before (August 2017) with the after (January 2019).
I already have the tools to maintain my weight and especially my visceral fat at the correct levels for my health, which allows me to maintain good eating habits and know when I make mistakes and thus remedy them so that it does not happen again.
If you have come this far, I thank you for reading my first article on this blog and I hope to hear your opinion through the blog and social networks.
And as promised is debt, I leave you my social networks: