Did you know that our ancestors were nocturnal? They used to stay awake in the night to hunt without worrying about dangerous predators and sleep during the day. Now, our circadian rhythms are lined up with the sun. That's why as soon as the sun sets, our bodies start getting ready for rest, and we end up feeling sleepy.
Circadian rhythms are biological cycles that coordinate essential mental and physical functions, such as sleep and hunger. The circadian clock is regulated by a part of the brain called the Suprachiasmatic Nucleus (SCN).
The circadian clock is also influenced by temperature. When the body temperature drops around the afternoon and late evening, it induces drowsiness and sleep.
Sleep is induced by a hormone called melatonin, which is produced in low-light conditions. Bright light conditions during the day suppress melatonin production and promote wakefulness.
People who work the night shift have disrupted circadian rhythm and have an increased risk for the following conditions:
Working the night shift is carcinogenic to humans, according to multiple studies conducted the world over.
Several studies show that disruption in the night’s sleep can reduce melatonin levels and increase the risk of tumor growth.
Some animal studies have shown that exposure to light at night led to the growth of breast cancer.
The risk of breast cancer among nurses and other night-shift workers seems to be higher than their counterparts who worked day shifts.
A study published in the Journal of National Cancer Institute in 2001 reported that women who work in rotating night shifts for at least three nights per month, along with day shifts, have a moderately high risk of breast cancer.
Further, the risk seems to be higher when the night shifts per week increase!
This increased risk is attributed to the messed-up melatonin levels in the body.
In addition to promoting sleep, melatonin also stops tumor growth and protects against the spread of cancer cells.
When melatonin levels decrease in the body, it results in an imbalance of inflammatory cytokines, increased mutations in the cells, and oxidative damage (due to free radicals).
These events can all trigger cancer development.
A reduction in melatonin also affects estrogen levels, which further increases the risk of breast cancer.
A long duration of shift work throughout the years is associated with estrogen and progesterone-positive tumors.
When the circadian rhythm is altered, it changes the expression of the CLOCK genes. This also influences the production of reproductive hormones.
The Neuronal PAS Domain Protein 2 or NPAS2 gene is the largest circadian gene. It plays a vital role in sleep homeostasis and circadian rhythm regulation.
This gene also regulates the cell cycle and works with certain other genes for repairing DNA. The NPAS2 gene shows a strong association with breast cancer.
rs2305160 (Ala394Thr) is an SNP (Single Nucleotide Polymorphism) in the NPAS2 gene.
Among women with little or no exposure to shift work, the A allele (AA or AG) is associated with a significantly lower risk of breast cancer.
However, among women with AA genotype who had worked >2 years of rotating night shifts, the risk of breast cancer was nearly 3 fold compared to women with the same genotype with <2 years of night shift work.
| Genotype | Implication - > 2 years of rotating night shifts |
| AA (Thr/Thr) | ~3 fold increased risk of breast cancer |
| AG (Thr/Ala) | Slightly increased risk of breast cancer |
| GG (Ala/Ala) | Normal risk of breast cancer |
Use Xcode Life’s Free Gene Tool To Find Out If You Have The Risk Genotype!
RAR-Related Orphan Receptor A or the RORA gene is located on chromosome 15 and regulates genes involved in the body’s circadian rhythm.
rs1482057 is an SNP in the RORA gene. A study published in 2014 showed that SNP rs1482057 was associated with breast cancer in postmenopausal women.
Women who have at least one A allele and had a history of working night shifts in their lifetime had a higher risk of developing breast cancer.
Conversely, women having the CC genotype and working night shifts showed a decreased risk of breast cancer.
| Genotype | Implication |
| AA | Increased breast cancer risk on night shift work |
| AC | Increased breast cancer risk on night shift work |
| CC | Decreased breast cancer risk on night shift work |
Cryptochrome circadian regulator 2 or the CRY2 gene gives instructions to produce a protein involved in regulating the body’s circadian rhythm.
rs2292912 is an SNP in the CRY2 gene, located on chromosome 11. Night shift working increased the risk of breast cancer in women who carried the CG genotype of rs2292912 SNP.
| Genotype | Implication |
| CG | Increased breast cancer risk on night shift work |
| GG | Decreased breast cancer risk on night shift work |
| CC | Decreased breast cancer risk on night shift work |
Since working night shift hours increases the risk of breast cancer in women, one of the most effective ways to lessen this risk is to reduce working night shifts.
Switching with a colleague’s shift, alternating your night shifts with day shifts, or switching jobs can be a few ways by which you can reduce your night shift hours.
Apart from disrupting the sleep-wake cycle, disturbed sleep or poor quality of sleep in people who work night shifts can increase their risk for breast cancer.
So, if you are working a night shift, ensure you get your 7-8 hours of sleep every day. If you have trouble sleeping, consult your doctor about supplements that can help you catch up on your daily sleep.
People working the night shift must try and reduce other risk factors of breast cancer.
A healthy diet with lots of fruits, limited alcohol consumption and smoking, adequate physical activity, and reduced exposure to harmful chemicals can help reduce breast cancer risk.
Regular exercising comes with a range of health benefits, one of which is reduced risk for developing breast cancer. Many studies conducted over the last 20 years have consistently reported a lower risk of breast cancer among women engaging in regular physical activity.
However, the exact mechanism behind this is unclear. Being active may lower estrogen levels in the body. Studies have shown that women with lower blood estrogen levels have a lower risk of breast cancer than women with higher levels.
Adipose tissue is the primary source of estrogen in postmenopausal women. So, reducing body fat with exercise can lower estrogen production and significantly reduce breast cancer risk in postmenopausal women.
In addition, exercise also reduces inflammation in the body, strengthens the immune system, decreases insulin resistance, and reduces oxidative stress – all of which are risk factors for breast cancer development.
A study published in The Journal of the American Medical Association in 2005 reported that physical activity after breast cancer diagnosis might reduce the risk of death due to the disease.
Women who performed physical activity equivalent to walking for 3 to 5 hours per week at an average pace benefited the most.
The study also reported that physical activity after breast cancer diagnosis reduced the chances of recurrence and improved the quality of life in these women.
The primary reason cited for the reduced risk is the low levels of circulating estrogen.
A study conducted in 2015 reported that weight loss by exercise resulted in an increase in lean mass, greater fitness, and a positive effect on the serum sex hormone levels due to greater loss of body fat.
These effects have been associated with a decreased risk of postmenopausal breast cancer.
A systematic review analysis was conducted and published in 2019, wherein researchers studied 38 cohort studies published between 1994 and 2017 comprising 68,416 breast cancer cases.
The researchers observed that the risk for breast cancer was significantly lower in people with exposure to physical activity longer than a year but less than five years, followed by those who had a lifetime exposure to physical activity.
In a study published in 2014, the authors found that breast cancer and colorectal cancer survivors, who increased their physical activity before or after their cancer diagnosis, showed a decreased mortality risk compared with those who were inactive or did not change their physical activity levels.
5-methyltetrahydrofolate-homocysteine methyltransferase reductase or MTRR gene gives instructions for producing the enzyme methionine synthase reductase, which is required for the normal functioning of enzyme methionine synthase.
Certain changes in the MTRR gene can induce insulin resistance, thereby making the cells unresponsive to insulin. This can result in type 2 diabetes.
Previous studies reported the association of this genetic change with lung and colorectal cancers, but not with breast cancer.
A 2019 study examined the effect of genetically driven insulin resistance on breast cancer risk.
The researchers identified a Single Nucleotide Polymorphism (SNP) rs13188458 in the MTRR gene. It was found that, in a group of physically inactive people, those with the T allele of this SNP had a greater risk for abnormally high insulin levels (hyperinsulinemia) and breast cancer than people with the G allele.
| Allele | Implication |
| T | Higher risk for hyperinsulinemia and breast cancer when physically inactive |
| G | Normal risk for hyperinsulinemia and breast cancer when physically inactive |
ERCC Excision Repair 4, Endonuclease Catalytic Subunit or ERCC4 plays an essential role in repairing damaged DNA. A defect in this gene has been associated with Xeroderma pigmentosa, a skin condition.
A meta-analysis done in 2011 revealed an association between ERCC4 and breast cancer risk. rs1800067 is an SNP in the ERCC4 gene.
Postmenopausal women with the GG genotype of this SNP who engaged in >9.23 hours of recreational physical activity per week experienced statistically significant reductions in breast cancer risk.
| Genotype | Implication |
| GG | Significant reduction in breast cancer risk with exercise |
| AG | Modest reduction in breast cancer risk with exercise |
| AA | Normal risk of breast cancer with exercise |
The MLH1 or MutL homolog 1 gene is a part of MMR or mismatch repair set of genes. It repairs damaged DNA by replacing the portion containing the errors with the corrected sequence.
rs1799977 is an SNP in the MLH1 gene. Women with the G allele of this SNP who were active during the postmenopausal years experienced significant breast cancer risk reductions.
| Allele | Implication |
| G | Significant reduction in breast cancer risk with physical activity in postmenopausal women |
| A | Normal breast cancer risk with physical activity in postmenopausal women |
Researchers have observed that postmenopausal women who exercise for at least 300 minutes per week can successfully reduce their body fat compared to those who spent half that time.
Even 2.5 hours of brisk walking per week can reduce breast cancer by as much as 18%!
If you are in a dilemma about how to begin your exercise, here are some handy and effective tips to help you exercise the right way to keep breast cancer at bay:
Phase 3 of detoxification is the final step of the detoxification process in the body and involves the elimination of the toxins from the body. As this phase is actively involved in transporting waste out of the cells and eventually the body, this phase of detoxification is called the antiporter phase.
Phase 3 is performed by transporting proteins that help move the processed toxins to urine via the kidneys or feces via the intestines.
Elimination is the end goal of phase 3 of detoxification. Some lifestyle factors that lead to poor elimination of waste from the body include:
The enzymes that regulate phase 3 of the detoxification process allow toxins to move across cellular barriers in the liver, gastrointestinal system, kidneys, and the blood-brain barrier.
The p-Glycoprotein family of proteins is an important antiporter found in the small intestine. They enable toxins to move from the cells into the gut. The blood-brain protein is another protein found in the kidneys, liver, and the blood-brain barrier and regulates phase 3 of detoxification.
Two groups of proteins primarily involved in phase 3 of the detoxification process include the ATP-Binding Cassette Transporters (ABCs) and Solute Carriers (SLC10s). SLC10A1 and SLC10A2 play an important role in phase 3 of detoxification by participating in the production, absorption, and excretion of bile salts.
The ABCB1 gene is also called the MultiDrug Resistance 1 (MDR1) or the P-Glycoprotein (P-GP). It gives instructions to produce an important ATP-dependent Phase 3 antiporter protein responsible for transporting various xenobiotics, drugs, lipids, and other exogenous and endogenous toxins out of cells for excretion.
Solute Carrier proteins are responsible for transporting solutes, including toxins, across the cell membranes, for elimination. While most SLC10 proteins are responsible for transporting bile acids, steroidal hormones, drugs, and other products, a few members of this family do not participate in the transport of bile acids.
Secretion and proper flow of bile are important for an effective detoxification process. Bile helps remove endogenous and exogenous toxins from the intestines. Impaired bile flow can result in a build-up of toxins in the body. Some substances that are eliminated through bile are:
Bile also performs other functions that are important for phase 3 detoxification.
Impaired bile flow can result in a build-up of toxins in the body, leading to diseases. Here are some ways to improve bile flow:
An important part of the detoxification process, especially phase 3, is the elimination of toxic metals. There are 23 heavy metals that are harmful to human health – antimony, arsenic, bismuth, cadmium, cerium, chromium, cobalt, copper, gallium, gold, iron, lead, manganese, mercury, nickel, platinum, silver, tellurium, tin, thallium, uranium, vanadium, and zinc (in excess). Occupational exposure and rising pollution levels in residential areas are major contributors to metal toxicity.
These heavy metals increase the production of free radicals that cause oxidative stresses in the cells of the specific organs. When the cells in these organs are overwhelmed by oxidative stress, they begin to function abnormally and cause diseases.
Fasting allows the body to rest, break down food better, and function efficiently. In the short term, fasting helps to increase the metabolic rate. Fasting also helps toxin removal from the cells more efficiently by releasing certain enzymes involved in the detoxification process.
Exercise alone cannot detoxify the body, but along with a healthy lifestyle, it enhances the functioning of various organs like the liver, kidneys, lungs, immune system, and intestines to improve detoxification. A study conducted in Sweden reported that exercising releases the various stored toxins from the cells into the blood, making it easy to eliminate them.
1. Phase 3 of detoxification is the final step of detoxification and aims to eliminate the toxins from the body.
2. This phase is regulated by a few groups of enzymes, primarily the p-Glycoprotein family of proteins.
3. ABCB1, SLC10A1, and SLC10A2 genes have an important role to play in regulating phase 3 of detoxification.
4. Bile production and flow are vital for an effective detoxification process as it eliminates bilirubin, metals and maintains cholesterol balance in the body.
5. Phase 3 of detoxification is also vital for preventing metal toxicity.
6. We can maintain healthy detoxification by following a healthy lifestyle, avoiding toxic foods and toxins in the environment, fasting, and regular exercising.
The phase 1 detoxification process transforms toxins, drugs, and other harmful substances in the body into active forms. The active forms are more toxic and have to be quickly removed to avoid damage to the body.
This is done by phase 2 detoxification. This phase is called the conjugation phase. Conjugation is the process of joining two things together. In phase 2 detoxification, the active compounds from phase 1 are modified to lower the toxicity and make them water-soluble for easy elimination from the body.
The phase 2 detoxification stage is very important in protecting the cells from cancer-causing chemicals (carcinogens).
There are six different pathways in phase 2 detoxification that are aided by different enzymes. All these pathways need to work harmoniously for efficient detoxification. The conjugated products are sent to phase 3 detoxification and are finally eliminated.
Glutathione conjugation is a pathway that uses glutathione to neutralize toxins. Glutathione is a type of antioxidant that helps prevent cell damage and oxidative stress. The Glutathione S-transferases (GSTs) are a group of enzymes that help combine glutathione with active toxin elements.
The conjugation makes the toxins water-soluble and makes it easy to remove them from the body.
GSTs helps detoxify the following:
GSTs are distributed throughout the body in the liver, kidneys, brain, spleen, intestines, lungs, and skeletal muscles.
Proteins: Amino acids are the bases of glutathiones. Lowered levels of protein intake may alter amino acid levels in the body and lead to reduced ability to produce glutathione.
Omega-3 fatty acids: Inflammation in the body reduces glutathione supply. Omega-3 fatty acids can help reduce chronic inflammation. Include omega-3 rich foods like fatty fish, nuts and seeds, avocados, and fish oil in your food.
Vitamins: Vitamins B, C, and E are all important to produce and maintain glutathione activity in the body.
Amino acids are building blocks of proteins. Some of the amino acids can attach themselves to toxins and make them water-soluble and easy for excretion.
Two enzymes help with amino acid conjugation - Acyl-CoA synthetases and Acyl-CoA amino acid N-acyltransferases.
A common amino acid - glycine, helps in removing toxic benzoate from the body. Benzoate is a very common preservative used in foods.
Protein: Food sources like meat, seafood, poultry, eggs, and dairy products are rich sources of proteins. They help improve amino acid levels in the body.
Amino acid supplements: Amino acid supplements are a mix of essential amino acids in the right quantities and help improve amino acid levels in the body.
Methylation is the process of substituting one atom in a substance by a methyl group. In this pathway, a methyl group is added to toxins to make them biologically less active to help transport them out. This pathway uses the Methyltransferases (MT) enzyme group for conjugation.
There are many MT enzymes, but the most important ones are the Thiopurine S-methyltransferase (TPMT) and the Catechol-O-methyltransferase (COMT).
TPMT helps in the methylation of heterocyclic sulfhydryl compounds like thiopurines (immunosuppressive drugs).
COMT helps in the methylation of neurotransmitters like dopamine, epinephrine, and norepinephrine. There are two forms of COMT. The membrane-bound catechol-O-methyltransferase (MB-COMT) is produced by the brain's nerve cells. The shorter version called the soluble catechol-O-methyltransferase (S-COMT) helps send out excess hormones in the body.
Also Read: COMT Gene Influences Worrier And Warrior Personality
Folate: Folate is a methyl donor and helps make methyltransferases (MT). Foods like legumes, dark leafy greens, beetroots, and cruciferous vegetables are rich in folate.
Choline: Choline is an essential nutrient that acts as a methyl donor and helps in the methylation process. Foods like red meat, eggs, seafood, whole grains, legumes, and dairy products are choline-rich.
Vitamins B2, B6, and B12: - These three vitamins play a role in methyl metabolism and help act as methyl donors. Foods like dairy, liver and kidney, shellfish, dark green vegetables, and red meat are rich sources of B vitamins.
Sulfonation is the process of attaching sulfates to toxins to neutralize them. In sulfonation, sulfotransferase enzymes (SULTs) transform various steroids, peptides, vitamin D, serotonin, and catecholamines (neurotransmitters) in the body. SULTs also help remove the following toxins from the body.
Retinoic acid (Vitamin A): Vitamin A can induce (promote the production of) SULT enzyme in the body. Food sources like liver, fish, eggs, dairy products, fruits, and vegetables like apples, asparagus, and carrots are rich in vitamin A.
Caffeine: Certain studies show that caffeine sources like coffee, tea, green tea, and cocoa can increase SULT activity.
In acetylation, the N-terminal acetyltransferases (NATs) enzymes make use of acetyl CoA to attach themselves to the toxins. NATs are responsible for removing different types of carcinogens (cancer-causing agents) present in food and the environment. These also are responsible for removing excess folate from the body.
There are two NAT enzymes - NAT1 and NAT2 that are important parts of acetylation.
Quercetin: Quercetin is a natural flavonoid found in various fruits and vegetables like cherry tomatoes, broccoli, blueberries, kale, and apples. A small study found that consuming 500 mg of quercetin a day helps improve NAT enzyme levels.
The glucuronidation pathway is the most important one of phase 2 detoxification. This pathway uses the help of the UDP-glucuronosyltransferases (UGTs) enzymes.
UGT enzymes metabolize up to 70% of all drugs in the body.
UGTs help in the elimination of the following toxins and hormones.
- Cruciferous vegetables: Cruciferous vegetables like cabbage, cauliflower, Brussel sprouts, and broccoli help increase UGT enzymes
- Lycopene: Lycopene is a type of carotenoid that has antioxidant properties. It helps increase UGT enzymes. Some sources of lycopene include pink and red-colored fruits and vegetables like watermelons, pink grapefruits, and tomatoes.
- Ellagic acid: Ellagic acid is a type of natural antioxidant that increases UGT enzymes. Foods like pomegranate, berries, blackcurrants, and walnuts are rich sources of ellagic acid.
- Ferulic acid: Ferulic acid is another antioxidant that increases UGT enzymes. Foods like broccoli, carrots, parsnip, olives, berries, and roasted coffee are rich in ferulic acid.
1. The phase 2 detoxification stage is called the conjugation phase. The toxins transformed in phase 1 are made "less dangerous" to the body in phase 2.
2.There are six pathways in this phase 2 detoxification. - Glutathione Conjugation, Amino Acid Conjugation, Methylation, Sulfonation, Acetylation, and Glucuronidation.
3. The glutathione conjugation pathway makes use of Glutathione S-transferase (GSTs) enzymes to make toxins water-soluble and less active.
4. The amino acid conjugation pathway makes use of amino acids to combine with toxins and makes them easier to send out of the body.
5. The Methylation pathway adds a methyl group to the toxins and makes them biologically less active.
6. The Sulfonation pathway attaches sulfates to toxins to neutralize them.
7. In the Acetylation pathway, the N-terminal acetyltransferases (NATs) enzymes are used to remove different carcinogens that enter the body through food.
8. The glucuronidation pathway is one of the most important phase 2 detoxification pathways. This uses UDP-glucuronosyltransferases (UGTs) enzymes to remove a wide range of toxins from the body.
Excess body weight is responsible for about 11% of cancers in women and 5% of men. Did you know that the risk for postmenopausal breast cancer is 1.5 times higher in overweight women and 2 times higher in women with obesity? Let’s understand more about how obesity contributes to breast cancer risk.
Being overweight or obese increases the risk for breast cancer, especially in postmenopausal women. Your Body Mass Index (BMI) determines if you have a healthy weight, are overweight, or are obese.
A BMI between 18 and 24.9 is considered healthy. A BMI between 25 and 29.9 means that you are overweight. If your BMI is higher than 30, it could indicate obesity.
Women with a BMI over 25 are at an increased risk of developing breast cancer than those with a healthy weight. In addition, this risk is exceptionally high after menopause. Being overweight or obese also increases the risk of breast cancer recurrence.
The exact link between increased weight and breast cancer risk is complicated and multifactorial. The high risk appears to be connected to the estrogen production by the fat cells.
In premenopausal women, estrogen is mainly produced by the ovaries. However, in postmenopausal women, adipose tissues or fat tissues is the main source of estrogen production.
The number of fat cells is higher in overweight or obese women. This results in increased estrogen production, which is a risk factor for breast cancer development. This is especially of significance for Hormone-Receptive breast cancers that develop and grow on exposure to estrogen.
It has been found that women who are obese after menopause are at a 30% higher risk of developing breast cancer. Gaining more than 22 pounds after menopause can increase the risk of breast cancer by 18%.
Studies report an association between obesity and a lower risk of Estrogen-Receptor Positive (ER-Positive) breast cancer but a higher risk of ER-negative and Triple-negative breast cancer in premenopausal obese women.
In addition, a study from the Breast Cancer Surveillance Consortium database showed that obesity is associated with an increased risk for Inflammatory Breast Cancer (IBC) in premenopausal women.
The Million Women Study followed 1.2 million UK women ages 50 to 64 years for a mean of 5.4 years. Out of these, 45,037 women had breast cancer. The study identified a nearly 30% higher risk of developing postmenopausal breast cancer with obesity.
A meta-analysis of 34 studies reported that the risk of postmenopausal breast cancer increases with every 5kg/m2 increase in BMI.
Obesity affects the prognosis and survival rate of breast cancer patients. A recent study found that obese women with breast cancer experienced an 11% decrease in overall survival rate, irrespective of their menopausal status.
Besides breast cancer, obesity is a risk factor for type 2 diabetes and heart diseases - the latter seems to be the leading cause of mortality in women with early-stage breast cancer.
It has also been observed that obese women with breast cancer are more likely to experience complications during surgery and radiation.
In addition, systemic chemotherapy and endocrine therapy for treating breast cancer are less effective in obese women, further reducing prognosis and survival rate.
Breast cancer-specific mortality among obese women is 1.3 times higher compared to women with a normal BMI.
The mortality rate in obese women is also dependent upon the type and characteristics of the tumor. For example, obese women with Luminal A and Luminal B breast cancer were 1.8 and 2.2 times more likely to die from cancer than normal-weight women.
However, obesity was not associated with breast cancer-specific mortality among women with HER2- and triple-negative tumors.
BRCA1 Interacting Helicase 1 (BRIP1) is located on chromosome 17 and, along with the BRCA1 gene, helps repair any damage to the DNA. It is also responsible for maintaining chromosomal stability.
rs16945628 is a Single Nucleotide Polymorphism (SNP) in the BRIP1 gene. The TT genotype of this SNP is associated with an increased risk of breast cancer in women with a BMI of ≧25 kg/m2.
Insulin-like Growth Factor Binding Protein 3 or IGFBP3 gene is located on chromosome 7 and participates in cell growth, multiplication, and differentiation, and cancer development in the breast tissue.
rs2854744 is an SNP in the IGFBP3 gene linked to the risk of breast cancer. The CC genotype of this gene significantly increases the risk of breast cancer compared to the AA genotype. This increase was found to be more pronounced in older women.
Studies also showed that women carrying the AC+CC genotypes of the IGFBP3 gene had a larger tumor size in the breast.
Obesity is a critical non-genetic risk factor for breast cancer.
Other factors that increase breast cancer risk in obese women are:
According to a 2019 study, sustained weight loss is associated with lower breast cancer risk for women aged 50 years and older.
The researchers looked at 180,885 women from 10 studies. The women's weights were recorded 3 times over a period of 10 years; once when they enrolled and once every 5 years.
Weight changes of 2 kilograms or less (about 4.4 lbs) were counted as stable.
The study reported the following*:
*Compared with those whose weight was stable.
The study did not include women on postmenopausal hormone therapy, and the results were more prominent in obese or overweight women.
Despite this, the study suggests that even a modest amount of sustained weight loss can lower your breast cancer risk and improve survival rate, if diagnosed with breast cancer.
Diet is as important to mental health as it is to physical health. Previous studies have reported that the "traditional" dietary pattern, loaded with vegetable oil, meat, salt, and organ meat, is associated with increased odds of anxiety and depression in women. A recent study by researchers at the Ruhr-University Bochum and University of Duisburg, Germany, has reported higher depression scores among vegetarians than non-vegetarians.
Depression is a common yet serious mental condition that negatively impacts how you feel, the way you think and act. Depression occurs as a result of a combination of social, psychological, and biological factors.
Some of the common symptoms of depression are :
Depression susceptibility is related to diet both directly and indirectly. Unhealthy eating patterns can cause mood swings. When you stick to a healthy diet, you are setting yourself up for fewer mood fluctuations.
In particular, sugar is considered a major culprit. When consumed in higher quantities, it causes a temporary spike in 'feel-good' hormones like dopamine, which is not good for your health. In addition, the fleeting sugar rush followed by a crash is terrible for your mood.
A German research team conducted a meta-analysis on depression and vegetarian diet.
Meta-analysis refers to a procedure where the information collected from different experiments (with the same objective) is put together and studied. This combines the results of multiple studies to form a conclusion.
The analysis included data from 49,889 participants, of which 8,057 were vegetarians, and 41,832 were non-vegetarians. The large sample size makes this a robust study.
The researchers observed a higher depression score among vegetarians when compared to the non-vegetarians. But there was no causal relationship observed between them. That is, there was no proof that a vegetarian diet directly causes depressive moods. Depression didn't seem to increase a person's chance of adopting a vegetarian diet either.
This study, however, showed that it might be more likely that people switch to a vegetarian diet after developing mental health issues. The researchers cite three possible reasons for this:
