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The IL1B gene encodes interleukin 1b, a crucial inflammatory cytokine that impacts metabolism and weight control. Read this post to learn about the surprising link between this gene and obesity.
The IL1B gene is responsible for producing interleukin 1-beta (IL-1b), one of the chief inflammatory cytokines. IL-1b acts as an “alarm signal” from white blood cells (macrophages, monocytes, and neutrophils) in response to cell stress or damage [R, R, R, R].
This signal triggers the production and release of many other pro-inflammatory compounds. Thus, cytokines in the IL-1 family — including IL-1b — play a central role in both acute and chronic inflammation [R, R, R, R].
SNPs in the IL1B gene correlate with a range of inflammation-related disorders, such as:
Studies have been investigating the link between inflammation, metabolic disorders, and obesity. Not surprisingly, IL-1b emerged as a crucial factor in this field, too [R, R].
IL1B encodes interleukin 1b, a critical inflammatory cytokine in autoimmunity, cancer, heart disease, and more. It’s one of the factors that connect inflammation and metabolic health.
Scientists have noticed that mice lacking the IL-1 family of cytokines are more prone to obesity. On the other hand, animals with enhanced IL-1 activity burn more fat, which makes them resistant to weight gain [R, R].
These findings seem contradictory, given that obesity is a pro-inflammatory state. Researchers dug deeper to reveal the exact mechanisms and suggested a surprising role of IL-1b in the brain: it appears to improve leptin signaling. Low IL-1b levels may contribute to leptin resistance [R, R].
Leptin is a crucial hormone that suppresses appetite and stimulates energy expenditure. Over-secretion leads to leptin resistance, a condition in which leptin loses the above functions [R].
Besides the central effect (in the brain), IL-1b may act directly on the fat tissue to release leptin and reduce the size of fat cells [R].
However, being an inflammatory cytokine, IL-1b has its dark metabolic side. It’s one of the primary cytokines involved in diabetes development. Patients with metabolic syndrome have elevated IL-1b, too [R, R].
IL-1b may stimulate fat burning by improving leptin sensitivity in the brain and fat tissue. On the other hand, it causes inflammation and plays a role in diabetes and metabolic syndrome.
One SNP in the IL1B gene, rs1143634, has shown a clear association with obesity and fat mass across different ages and ethnic groups.
Among 1,068 young Swedish men, those carrying the “GG” genotype had higher total fat mass and more fat in their arms, legs, and trunks. They also had slightly higher body mass index (BMI), likely due to differences in body fat [R].
In a trial of 880 older European (Caucasian) descendants, the “GG” genotype correlated with 34% higher rates of obesity [R].
Two studies of 438 Korean women observed up to five times lower frequency of the “A” allele among those who were overweight and obese [R, R].
Another IL1B SNP, rs1143627, showed a potential link with obesity. Among 3,014 Swedish elderly men, the “GG” genotype was associated with increased fat mass. However, other studies failed to confirm the association or yielded conflicting results [R, R, R].
The “GG” genotype at rs1143634 correlates with higher body fat and obesity rates across different ages and ethnic groups. Rs1143627 might have the same effect, but the evidence is weak.
Surprisingly, this SNP showed the opposite effect on waist circumference, a measure of abdominal obesity.
Among 556 Australian patients with heart disease, those with the “AA” genotype had 4 cm higher waist circumference compared with the “GG” carriers. The link was significant only in obese subjects, in which the difference was 6.1 cm for these two genotypes [R].
The “AA” allele was also slightly associated with metabolic syndrome [R].
Sounds weird? Keep reading to get a precise explanation for these seemingly conflicting results.
The “AA” genotype at rs1143634 may be associated with metabolic syndrome and higher waist circumference in obese people.
As mentioned, IL-1b may support fat burning but also contribute to inflammation and metabolic syndrome.
In test tubes, the “AA” genotype at rs1143634 enhanced IL-1b production up to four times, which may explain the beneficial effects of the “A” allele on fat loss. Swedish men with the “G” allele had higher leptin levels, indicating potential leptin resistance [R, R, R].
On the other hand, the “A” allele was associated with higher CRP and fibrinogen levels, the primary markers of inflammation. That may explain the opposite effect on waist circumference and metabolic syndrome in obese people [R, R].
Simply put, rs1143634 impacts IL-1b levels and follows its opposing effects on fat loss and metabolic health.
The “A” allele at rs1143634 increases IL-1b levels, which may be beneficial for fat loss but also contribute to inflammation and metabolic syndrome.
Note: In some papers, you may see “C>T” as the two possible alleles for these SNPs. Unlike us at SelfDecode, some studies report on a negative DNA strand, and their “C>T” equals our “G>A”.
Primary SNP:
IL1B rs1143634
Population Frequency: About 40% of European descendants carry one copy and 55% carry both copies of the “G” allele. This allele is even more common in African and East Asian populations, where 77% and 96% of people carry both copies, respectively.
Other important SNP:
IL1B rs1143627
Population Frequency: About 12% of European descendants carry the “GG” genotype. This genotype is more common in East Asian (24%) and African (40%) populations.
Physical exercise and long-term fitness may protect against leptin resistance [R, R, R].
Resistance training is probably the best strategy to lose weight. In addition to promoting fat burning, it boosts other beneficial hormones and components that suppress appetite, improve mental health, and more. These include:
Aerobic exercise (walking, running, swimming, etc.) has also caused significant reductions in belly fat in multiple studies [R, R].
Regular exercise helps prevent leptin resistance and improve weight loss.
Impaired circadian rhythm may contribute to leptin resistance and thus worsen the impact of your variant [R].
Research over the past few decades has recognized the importance of circadian biology in obesity, energy balance, and metabolism [R].
A disrupted circadian rhythm may be why shift workers seem to be at an increased risk of obesity [R].
In one trial, restful sleep in non-obese individuals (8+ of uninterrupted sleep) normalized leptin levels. On the other hand, sleep deprivation can decrease leptin and increase appetite [R, R].
Short sleep duration correlated with weight gain in several studies. Scientists suggest that poor sleep may increase hunger and cravings [R, R, R, R, R].
Improve your sleep quality to lessen the impact of IL1B and boost metabolic health and weight control.
Increased protein intake can improve leptin sensitivity and reduce appetite, which is crucial for people with rs1143634-G [R, R].
Research suggests that getting more calories from protein may support weight loss, metabolism, and satiety (fullness) [R, R, R].
Healthy foods rich in protein include [R]:
Increased protein intake may improve leptin sensitivity and help you shed extra pounds.
In animals, the consumption of polyphenol-rich fruits and vegetables prevented leptin resistance [R].
Vegetables are rich in soluble fiber, which may support weight loss. Fiber gets broken down by probiotic bacteria to produce butyrate, a fatty acid with potential weight-loss effects in preclinical research [R, R, R, R].
Polyphenols from various fruits, such as blueberries and apples, led to lower weight in animal studies [R, R].
Polyphenol-rich fruits and vegetables may prevent leptin resistance and support weight loss, but clinical evidence is lacking.
According to animal studies, some probiotic supplements may improve obesity-induced leptin resistance [R].
L. gasseri significantly decreased BMI and total and belly fat in 210 healthy Japanese adults. The authors underlined that constant consumption of this probiotic might be required to maintain the effect. This strain showed promising fat-burning properties in two more clinical trials [R, R, R].
In a clinical trial of 125 obese adults, L. rhamnosus induced weight and fat loss [R].
Humans with more B. animalis in their microbiome have lower BMIs. Daily ingestion of milk containing this strain significantly reduced BMI, total cholesterol, LDL, and inflammatory markers in a clinical trial on 51 people with metabolic syndrome [R, R, R].
Read this post to learn more about the effects of probiotics on weight loss.
Probiotic supplementation may improve leptin resistance. Strains such as L. gasseri, L. rhamnosus, and B. animalis have shown the most promising results for weight loss.
In studies on obese animals, Garcinia cambogia extract enhanced glucose metabolism and leptin signaling [R, R, R].
In a clinical trial on 99 obese men, it lowered BMI and belly fat when combined with a weight-loss drug (orlistat) [R].
Garcinia reduced body weight and fat mass in many clinical trials, ranging from 21 to 100 overweight and obese subjects [R, R, R, R, R, R].
In a 2011 review of 12 studies, Garcinia extract caused a weight loss of about 2 pounds (0.88 kg) over several weeks [R].
Garcinia cambogia extract may counteract your variant by improving leptin resistance. It supported weight loss in many smaller clinical trials.
Aleksa received his MS in Pharmacy from the University of Belgrade, his master thesis focusing on protein sources in plant-based diets.
Aleksa is passionate about herbal pharmacy, nutrition, and functional medicine. He found a way to merge his two biggest passions—writing and health—and use them for noble purposes. His mission is to bridge the gap between science and everyday life, helping readers improve their health and feel better.
The information on this website has not been evaluated by the Food & Drug Administration or any other official medical body. This information is presented for educational purposes only, and may not be used to diagnose or treat any illness or disease.
Also keep in mind that the “Risk Score” presented in this post is based only on a select number of SNPs, and therefore only represents a small portion of your total risk as an individual. Furthermore, these analyses are based primarily on associational studies, which do not necessarily imply causation. Finally, many other (non-genetic) factors can also play a significant role in the development of a disease or health condition — therefore, carrying any of the risk-associated genotypes discussed in this post does not necessarily mean you are at increased risk of developing a major health condition.
Always consult your doctor before acting on any information or recommendations discussed in this post — especially if you are pregnant, nursing, taking medication, or have been officially diagnosed with a medical condition.
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