Aware and Beware @ Health

What does Biotin do to our metabolic activities?

Biotin is a water-soluble B vitamin, also known as Vitamin B7 or Vitamin H. Biotin is an essential micronutrient for mammals that plays a key role in metabolism of fats, carbohydrates and proteins in our body.

How biotin plays its role?

Biotin acts as a covalently bound coenzyme for five carboxylases, those are acetyl-CoA carboxylases 1 and 2, propionyl –CoA carboxylase (PCC), 3-methylcrotonyl-CoA carboxylase (MCC) and pyruvate carboxylase. These are key enzymes in metabolism of fatty acids, amino acids and gluconeogenesis, a metabolic pathway that generates glucose from non-carbohydrate carbon substrates ^{[1, 4,5]}.

DNA studies and gene expression studies suggested that numerous genes are regulated by biotin at the transcriptional and post-transcriptional level. Biotinylation and biotin deficiencies have an impact on turning on or off genes, replication and repair of DNA and response to cell stress.

Biotin structure

Source of Biotin: Food

Human body cannot synthesize Biotin. Most healthy individual get the required biotin from Well-balanced diet. Food rich in Biotin are egg, meat, poultry, Fish, cereals, seeds, Nuts and vegetables. Foods that are super rich in Biotin are   

• egg yolk
• beef liver
• salmon fish
• pork
• sunflower seeds
• sweet potato
• Almonds
• Spinach
• Broccoli

Raw egg white contain Biotin binding protein called avidin, which decreases the bioavailability of Biotin. Cooking the egg prevent this Biotin loss ^[2,4]. It is also found that gut microbes also capable of synthesizing biotin but its contribution to the body is not well known ^[10].

Recommended intake:

It is evident that dietary biotin is 100% bioavailable.

Recommended dietary allowance (RDA) of Biotin is not established yet, due to the insufficient evidence. Recommendation for adequate intake (AI) are based on the average intake of biotin in an apparently healthy population. The AI for biotin is 30 mcg in men, women, and pregnant women who are 19 yrs and older and increases to 35 mcg for lactating women^[2,4].  

 Biotin Deficiency:

Biotin deficiencies are generally very rare to occur. Congenital or genetic biotin deficiency is due to autosomal recessive disorder, which leads to the dysfunction of either holocarboxylase synthase (HLCS) or biotinidase. Holocarboxylase synthetase (HLCS) is a key enzyme that play a pivotal role in biotin-dependent metabolic pathways.  It is found to catalyses the binding of biotin to all 5 carboxylases. HLCS is also to found to participate in gene regulation at the chromatin level.  Biotinidase is an enzyme that catalyse the release of biotin from break-down products of carboxylases and hence its important in biotin recycling ^[1,4,5]. When it occurs within the first 6 weeks of life, it is known as neonatal type and in this deficiency the enzyme holocarboxylase synthetase is absent and patients typically have severe, life threatening conditions. Past 3 months of life, the infantile form predominates and is defined by a biotinidase deficiency.

Acquired biotin deficiency commonly caused by the raw egg consumption. The protein Avidin in raw egg whites bind to biotin tightly thus preventing it from being used by the body. Other reasons for deficiency may be due to taking anticonvulsant medications, such as valproic acid. Alcoholism, pregnancy, prolonged use of antibiotics which affects normal gut flora can also be the causes for acquired biotin deficiency ^[3].

Symptoms of biotin deficiency ^[3]:

Either acquired or congenital, symptoms for Biotin deficiency includes:

• Alopecia
• Eczematous skin rashes
• Seborrheic dermatitis
• Conjunctivitis
• Neurological symptoms occurs at more severe levels, which includes depression, lethargy, hypotonia and seizures. Generally, dermatological manifestation appears first in biotin deficiency and thus it is an important indicator.

Biotin supplementation:

There are no established studies that the healthy human with balanced diet are deficient for biotin. Typical dietary intake of biotin in western population is estimated to be between 35 and 70 mcg/day.

Pharmacological doses of biotin supplementation is being recommended for frank biotin deficiency. It is observe in  individuals who have mutation in HLCS, biotinidase and in people who consumes large amount of raw egg whites ^[3,5].

 Biotin Supplementation for hair and nail growth:

Since Biotin is necessary for keratin production, it is considered important in promoting the Hair and nail growth. Till date there are no clinical trials supporting that biotin supplementation helps in improving the quality of hair and nail growth, but there is a study which showed 18 reported cases of biotin use for hair and nail growth changes the quality. In all cases, patients receiving biotin supplementation had an underlying pathology for poor hair or nail growth. All cases showed evidence of clinical improvement after receiving biotin^[3,6].

As said earlier for acquired and inherited causes of biotin deficiency and for some conditions, such as brittle nail syndrome or uncombable hair syndrome which is characterised by dry, frizzy, straw-coloured or silvery-blond hair, biotin supplementation may help and benefit ^[11,3,6]. However, healthy people need to take doctor advice before taking Biotin supplementation since no trials proves biotin efficacy in healthy individuals.

Toxicity:

As far as reported, there are no toxicities associated with excess biotin intake. Food and Drug Administration (FDA) warning stated that biotin might interfere with laboratory tests leading to incorrect diagnoses. According to the case studies and in vivo studies shows that ingestion of biotin supplement interfere with the results of biotinylated immunoasssays. Thyroid test, endocrine test are some of the test that might be interfered by biotin supplements ^[12,6,3].

Pregnancy and Biotin deficiency:

Pregnancy and lactation increases the demand for the biotin. Studies found that despite of dietary intake, there is a marginal biotin deficiency found in pregnant women. Studies suggest that increase in the biotin intake during pregnancy is likely needed, when there is a marginal biotin deficiency ^[5].

Diabetes and Biotin:

Animal studies suggest that high dose of biotin helps in controlling the diabetes and certain diabetic complications. Further studies are warranted to this association of Diabetes to Biotin.

Take away points:

• Biotin is a water-soluble vitamin, which is essential for metabolism of fats, proteins and carbohydrates.
• Biotin deficiency is very rare, If biotin deficiency occurs,  biotin rich foods helps and biotin supplements has to be taken based on doctor’s advice.

Reference:

1. Teo Soleymani MD, et al. The Infatuation With Biotin Supplementation: Is There Truth Behind Its Rising Popularity? A Comparative Analysis Of Clinical Efficacy Versus Social Popularity. J Drugs Dermatol. 2017;16(5):496-500.
2. https://ods.od.nih.gov/factsheets/Biotin-HealthProfessional/
3. Deepa P. Patel, Shane M. Swink, Leslie Castelo-Soccio, A Review of the Use of Biotin for Hair Loss. Skin Appendage Disord 2017; 3:166–169. DOI: 10.1159/000462981.
4. Zempleni J, Kuroishi T. Biotin. Adv Nutr. 2012;3(2):213-214. Published 2012 Mar 1. doi:10.3945/an.111.001305.
5. Donald M Mock, Biotin: From Nutrition to Therapeutics. J Nutr 2017; 147:1487–92.
6. Jason J. John and Shari R. Lipner, Consumer Perception of Biotin Supplementation. Journal of Cutaneous Medicine and Surgery 2019, Vol. 23(6) 613–616. DOI: 10.1177/1203475419871046.
7. Shari R. Lipner & Richard K. Scher (2018) Biotin for the treatment of nail disease: what is the evidence?, Journal of Dermatological Treatment, 29:4, 411-414, DOI: 10.1080/09546634.2017.1395799 [Pubmed abstract].
8. Jason J John , Victoria Cooley , Shari R Lipner, Assessment of biotin supplementation among patients in an outpatient dermatology clinic. J Am Acad Dermatol 2019 Aug; 81(2):620-621.  doi: 0.1016/j.jaad.2018.12.045. Epub 2019 Jan 8.
9. Rocio Rodriguez-Melendeza, Janos Zemplenia, Regulation of gene expression by biotin_ (Review). Journal of Nutritional Biochemistry 14 (2003) 680–690.
10. Ian Rowland · Glenn Gibson, et al. Gut microbiota functions: metabolism of nutrients and other food components. Eur J Nutr (2018) 57:1–24 DOI 10.1007/s00394-017-1445-8.
11. Pamela Calderon , Nina Otberg, Jerry Shapiro, Uncombable hair syndrome. J Am Acad Dermatol . 2009 Sep;61(3):512-5.  doi: 10.1016/j.jaad.2009.01.006.
12. Mark F. McCarty B.A. In type 1 diabetics, high-dose biotin may compensate for low hepatic insulin exposure, promoting a more normal expression of glycolytic and gluconeogenic enyzymes and thereby aiding glycemic control. Medical Hypotheses 95 (2016) 45–48.
13. US Food and Drug Administration. The FDA warns that biotin may interfere with lab tests: FDA safety communication.  https://www.fda.gov/medicaldevices/safety/alertsandnotices/ucm586505.htm. Accessed September 3, 2018.

What is Microbiome:

Currently human microbiome is one of the extensively researched area. Studies exploring the interactions between the human body and microbes residing in it are still in its nascent stage.

Microbiome represents the genome of the microorganisms in a particular environment. Human body contains trillions of microorganism that includes viruses, fungi, protozoa and predominantly bacteria.

The surprising fact here is, compared to the number of human genes, which is approximately 20000-25000, the genes of the total microorganism that resides in the human body, is approximately 200 times more. These microorganisms are vital for maintaining the human health.

Microbes in the human body balance the host’s fitness, phenotype, immune system, nutrition, etc. Microbial imbalance is associated with various diseases such as autoimmune disorders, inflammatory bowel disease, diabetes, allergies, asthma or even cancer.

Gut Microbiome:

When we look into the microbiome of the gut, approximately 100 trillion microorganisms exist in the human gastrointestinal tract ^[1].

Microbial diversity in the whole body is very important especially in the gut. Lower the diversity higher the chance of dysbiosis (microbial imbalance) that leads to many diseases like metabolic disorder, autoimmune disorder, obesity etc.

 The composition of gut microbiota is commonly quantified using DNA

sequencing methods, such as next generation sequencing of 16S ribosomal RNA genes or whole genome shotgun sequencing and analysing their miocrobiome.

Metabolic products of the microbiota are also measurable in stool and serum using metabolomic methods ^[1]

Role of Gut microbiota:

We all have a common question that what these microorganism resides in our gut do to our health?

Studies proved that it contributes to the biosynthesis of vitamins and essential amino acids; it generates important metabolic by-products from dietary components left undigested by the small intestine. Short chain fatty acid (SCFA) by-products such

as butyrate, propionate, and acetate act as a major energy source for intestinal epithelial cells which strengthen the mucosal barrier ^[3].

Metabolite contributed by gut microbiota and their respective function ^[9]:

Metabolite	Respective Function
Short-chain fatty acids (SCFA) e.g., Acetate, butyrate, propionate, hexanoate, valerate	Regulate host metabolic pathways via G-protein-coupled receptor GPR41 or GPR43 -mediated signalling.   Energy homeostasis; synthesis of glucagon-like peptide 1 (GLP-1); Increase leptin production. Improve glucose tolerance and insulin sensitivity.   Potent histone deacetylase (HDAC) inhibitor – regulation of intestinal cell proliferation.   Intestinal gluconeogenesis, lipogenesis, suppression of fasting-induced adipose factor Fiaf (lipoprotein lipase inhibitor) in intestinal epithelium.   Immunomodulatory effect, activate dendritic cells, gut immunity.
Indole Derivatives E.g., Indole, indoxyl sulfate, indole-3-propionic acid (IPA)	IPA as powerful antioxidant, inhibitor of amyloid-beta fibril formation, and exhibits neuroprotective and cytoprotective effects against a variety of oxidotoxins.   IPA regulates intestinal barrier function via the xenobiotic sensor, pregnane X receptor (PXR), in which it reduces intestinal inflammation (downregulates enterocyte pro-inflammatory cytokines TNF-a), and regulate intestinal permeability and mucosal integrity (upregulates junctional protein-coding mRNAs).
Bile acid metabolites: E.g., Deoxycholic acid (DCA), lithocholic acid (LCA)	Bile acid metabolites: E.g., Deoxycholic acid (DCA), lithocholic acid (LCA).   Activate host nuclear receptors and cell signaling pathways: regulation of bile acid, cholesterol, glucose, lipid, and energy metabolism.   Exhibit antimicrobial effects.
Choline metabolites: E.g., Choline, trimethylamine N-oxide (TMAO) and betaine	Modulate lipid metabolism and glucose homeostasis.   Contribute to non-alcoholic fatty liver disease and cardiovascular disease
Phenolic derivatives:   E.g., 4-OH phenylacetic acid, equol, urolithins, enterolactone, enterodiol, 8-prenylnaringenin, 2-(3,4-dihydroxyphenyl)acetic acid, 3-(4-hydroxyphenyl)propionic acid, 5-(3,4-dihydroxyphenyl)valeric acid	Antimicrobial effects: repress pathogenic microbes, influence gut microbiota composition, maintenance of intestinal health.   Protective effect against oxidative stress. Estrogen-modulating effect.   Platelet aggregation inhibition effect.   Urolithin exhibits anti-inflammatory and cancer chemopreventive effects.
Vitamins:   E.g., Thiamine (B1 B6), pantothenic acid (B5), biotin (B7), folate (B11–B9), cobalamin (B12), and menaquinone (K2)	Energy production, red blood cell formation, as enzymatic cofactor for diverse biochemical reactions.   DNA replication, repair and methylation, regulating cell proliferation.   Production of nucleotides, vitamins and amino acids
Polyamines:   E.g., putrescine, spermidine, and spermine	Sustain high proliferation rate of Intestinal epithelial cells.   Dysregulated polyamine metabolism possibly enhances cancer development.   Enhance intestinal barrier integrity and function via stimulating synthesis of intercellular junction proteins   r[occludin, zonula occludens-1 (ZO-1), E-cadherin].   Enhance maturation of intestinal and systemic adaptive immune system.   Spermine inhibits pro-inflammatory M1 macrophage activation.

Source of the table: Zhi Y. Kho and Sunil K. Lal*, The Human Gut Microbiome – A Potential Controller of Wellness and Disease.

Contribution for the intestinal immunity

Germ-free mice studies  suggest that the microbiota directly promote local intestinal immunity through their effects on toll-like receptor (TLR) expression, antigen presenting cells, differentiated T cells, and lymphoid follicles  as well as by affecting systemic immunity through increased splenic CD4+T cells and systemic antibody expression ^[3]

Another study suggest that tight regulation of Treg/TH17 balance by healthy host-gut microbiota interactions are critical to prevent aberrant immuneinflammatory response ^[9]. 

 Is it true that a programmed diet will help in maintaining a balanced Microbiome in our Gut?

Though Gut microbiome is inheritable (genetic or epigenetic), it is not a fixed trait. External lifestyle factors such as diet, exercise drugs etc., influence and shape the gut microbiome.

Diet is the major influencing factor on the function and composition of the Gut microbiome, which eventually influence the metabolic response of the host to the diet. These are two distinct concepts.

This table gives details on few gut microbes commonly affected by diet and their physiological effects ^[3]

Bacteria	Physiological changes	Associated disease states
Bifidobacterium spp.	SCFA production; improve gut mucosal barrier; lower intestinal LPS levels	Reduced abundance in obesity
Lactobacillus spp.	SCFA production; anti-inflammatory and anti-cancer activities	Attenuate IBD
Bacteroides spp.	Activate CD4 + T cells	Increased abundance in IBD
Alistipes spp.		Reported in tissue from acute appendicitis and perirectal and brain abscesses
Bilophila spp.	Promote pro-inflammatory TH1 immunity	B. wadsworthia observed in colitis, perforated and gangrenous appendicitis, liver and soft tissue abscesses, cholecystitis, FG, empyema, osteomyelitis, and HS
Clostridium spp.	Promote generation of TH17 cells	Several spp. are pathogenic causing tetanus, botulism, gas gangrene, or pseudomembranous colitis
Roseburia spp.	SCFA production	Reduced abundance in IBD
Eubacterium spp.	SCFA production; form beneficial phenolic acids	Reduced abundance in IBD
Enterococcus spp.		Several spp. are pathogenic causing UTI, endocarditis, or bacteremia
Faecalibacterium prausnitzii	SCFA production; anti-inflammatory effects	Reduced abundance in IBD and obesity
Akkermansia muciniphila	Anti-inflammatory effects	Reduced abundance in IBD, obesity, and psoriatic arthritis
Escherichia coli	TLR-activation	Increased abundance in IBD gastroenteritis, UTI, and meningitis
Helicobacter pylori		Gastritis; ulcers; mucosal associated lymphoid tissue (MALT) cancers
Streptococcus spp.		Some spp. are pathogenic causing meningitis, pneumonia, and endocarditis

Source of the table: Singh et al, Influence of diet on the gut microbiome and implications for human health. J Transl Med (2017) 15:73.

Microbiota-targeted diets:

Studies on overweight and obese people has shown that lower bacterial diversity (dysbiosis) plays a role in the development and progression of obesity. Lower bacterial diversity has also been observed in people with inflammatory bowel disease, psoriatic arthritis, type 1 diabetes, atopic eczema, coeliac disease, type 2 diabetes, and arterial stiffness, than in healthy controls. In Crohn’s disease, smokers have even lower gut microbiome.

Reduced gut microbiome diversity seems to be associated with various diseases, which indicates that species rich gut ecosystem is more robust against environmental influences, and diversity seems to be a generally good indicator of a “healthy gut.” ^[1]

Animal studies shows that artificial sweeteners such as sucralose, aspartame, and saccharin disrupts the balance and diversity of gut microbiota. Food additives, such as emulsifiers also found to affect the gut microbiome in animals.

Key points based on the previous Diet-microbiome interaction are probiotics or dietary fibre has a beneficial effect on Gut microbiome, which could potentially reduce obesity. Drugs, food ingredients, antibiotics, and pesticides could all have adverse effects on the gut microbiota.

Examples of foods, nutrients, and dietary patterns that influence human health linked to their effect on the gut microbiota

Dietary element	Effect on gut Microbiome	Effect on health outcomes mediated by gut microbiome
Low FODMAP (fermentable oligosaccharides, Disaccharides, monosaccharides and polyols) diet	Low FODMAP diet increased Actinobacteria; high FODMAP diet decreased abundance of bacteria involved in gas consumption	Reduced symptoms of irritable bowel syndrome
Cheese	Increased Bifidobacteria, which are known for their positive health benefits to their host through their metabolic activities. Decrease in Bacteroides and Clostridia, some strains of which are associated with intestinal infections	Potential protection against pathogens.Increased production of Short chain fatty acids (SCFA) and reduced production of Trimethylamine N-oxide.
Fibre and prebiotics	Increased microbiota diversity and short chain fatty acid (SCFA)  production	Reduced type 2 diabetes and cardiovascular disease
Artificial sweeteners	Overgrowth of Proteobacteria and Escherichia coli. Bacteroides, Clostridia, and total aerobic bacteria were significantly lower, and faecal pH was significantly higher	Induced glucose tolerance
Poly phenols (ex. From tea, coffee, berries and vegetables such as artichokes, olives and asparagus)	Increased intestinal barrier protectors (Bifidobacteria and Lactobacillus), butyrate producing bacteria (Faecalibacterium prausnitzii and Roseburia) and Bacteroides vulgatus and Akkermansia muciniphila. Decreased lipopolysaccharide producers (E coli and Enterobacter cloacae)	Gut micro-organisms alter polyphenol bioavailability resulting in reduction of metabolic syndrome markers and cardiovascular risk markers
vegan	Very modest differences in composition and diversity in humans and strong differences in metabolomic profile compared with omnivore diet in humans.	Some studies show benefit of vegetarian over omnivore diet, others fail to find a difference

Source of the table:  Ana M Valdes and colleagues, Role of the gut microbiota in nutrition and health. BMJ 2018; 361:j2179.

Dietary intervention and the Gut Microbiota                  

Three main categories of dietary interventions have been studied so far in precision nutrition-microbiome studies:

Role of Microbiota in response to fibre intervention, response to energy restriction and excess intervention, Response to bioactives, fermented products, and other dietary components.

However, the studies could not clearly conclude how specific certain microbiome features are associated with certain metabolic responses or dietary factors.

When we look into the precision nutrition field, it is still in its infancy. Although many studies are being carried out, precision nutrition and the role of the gut microbiome are still not clear and comprehensive.

Extensive research are going on to understand the interaction between gut microbiome and the diet, among those to mention, the effects of prior dietary practices and metabolic flexibility on gut microbiome is still an important area to be explored. This flexibility may be influenced by factors such as physical activity, age, other associated diseases etc. Other life style factors such as contribution of genetic, epigenetic factor on the diet-microbiome interactions should also be considered.^[12]

Though this research area is very intricate, we hope the precision nutrition and the microbiome targeted diet prescription comes true soon.

References:

1. Ana M Valdes and colleagues, Role of the gut microbiota in nutrition and health. BMJ 2018; 361:j2179.
2. Christopher L. Gentile and Tiffany L. Weir, The gut microbiota at the intersection of diet and human health. Science 362 (6416), 776-780.
3. Singh et al, Influence of diet on the gut microbiome and implications for human health. J Transl Med (2017) 15:73.
4. Lloyd-Price et al, The healthy human microbiome. Genome Medicine (2016) 8:51.
5. Chua et al. Temporal changes in gut microbiota profile in children with acute lymphoblastic leukemia prior to commencement-, during-, and post-cessation of chemotherapy. BMC Cancer (2020) 20:151.
6. Gijs den Besten, Karen van Eunen, et al. The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism. Journal of Lipid Research Volume 54, 2013.
7. Lloyd-Price et al. The healthy human microbiome. Genome Medicine (2016) 8:51.
8. Johnson AJ, Zheng JJ, Kang JW, Saboe A, Knights D and Zivkovic AM (2020) A Guide to Diet-Microbiome Study Design. Front. Nutr. 7:79. doi: 10.3389/fnut.2020.00079.
9. Zhi Y. Kho and Sunil K. Lal*, The Human Gut Microbiome – A Potential Controller of Wellness and Disease (2018). Front. Microbiol. 9:1835. doi: 10.3389/fmicb.2018.01835.
10. Riley L. Hughes* A Review of the Role of the Gut Microbiome in Personalized Sports Nutrition (2020). Front. Nutr. 6:191. doi: 10.3389/fnut.2019.00191.
11. Hughes RL, Marco ML, Hughes JP, Keim NL, Kable ME. The role of the  gut microbiome in predicting response to diet and the development of recision nutrition models—Part I: overview of current methods. Adv Nutr. (2019). 10:953–78. doi: 10.1093/advances/nmz022.  
12. Hughes RL, Kable ME, Marco M, Keim NL. The role of the gut microbiome in predicting response to diet and the development of precision nutrition models. Part II: results. Adv Nutr. (2019) 10:979–98. doi: 10.1093/advances/nmz049.

Can we trick and change our brain chemicals to our wish?? The answer is yes.

Social laughing or even faking a smile can make this happen! Laughter can change the brain chemicals in a desired manner, which will be great for our mood enhancement and health.

“Even a Fake laughter brings amazing changes in your body” 

In order to use this boon that we have got, there are lot of research on the laughter are going on! As an alternative to various therapies to relive stress, boosting immunity, enhancing the overall mental and physical health for the old as well as the young population, laughter therapies are advised.

Two types of laughter that we are going see here are

• Spontaneous (Genuine)
• Simulated/self-induced laughter.

Spontaneous laughter also called as Duchenne laughter is triggered by a stimulus for example, by a joke or any humor. However, the stimulated laughter also called as Non-Duchenne laughter is defined as a laughter induced by oneself consciously without any stimuli, in a controlled environment.

 Do Spontaneous (Duchenne laughter) and self-induced laughter (Non-Duchenne laughter) bring different effects on the body?

Yes. According to the neuroimaging study, these two laughter uses two different neuronal pathways ^[1]

Distinction between spontaneous versus self-induced/simulated laughter remains an important area for exploring in the research field ^[3,5]

Boosting immunity, Pain tolerance level and reliving stress:

A study suggest that spontaneous laughter increases natural killer cell activity, IgM, IgG and other leukocytes which obviously have a positive effect on immunity. ^[1]

Spontaneous laughter increases the endorphin levels, high levels of CNS endorphins will be associated with an elevated pain threshold. Endorphins are a class of endogenous opioid peptides produced in the central nervous system (CNS) that functions as neurotransmitters and it also has analgesic properties. It also play a central role in social bonding. Especially Beta-endorphins helps in cushioning the human against physiological and psychological stress ^[3].

Social laughter (Duchenne):

 Spontaneous or Duchenne laughter is intensely social and contagious. The effects of social laughter are enormous than we imagine.

A study published in Journal of Neuroscience (2017), says social laughter helps in maintaining social bonding between human. Social laughter increases pleasurable sensations and triggered endogenous opioid release in thalamus, caudate nucleus, and anterior insula of the brain. ^[7]

Faking a laugh

Now we wonder what happens when we are faking a laughter and what their benefits are.

Even a physical act of laughing gives a positive physiological and chemical response to the body as in the case of Stimulated/self-induced laughter even without humor, which helps to combat the depression as effectively as spontaneous laughter. ^[3,5]

In 2018 a small study was conducted on the effect of laughter therapy in older people. It shows that laughter therapy intervention significantly reduced the systolic blood pressure and heart rate. There was also a significant increase in plasma concentration of serotonin and a significant decrease in salivary concentration of chromogranin A. So laughter therapy proves to subside the depression and improve the quality of life ^[4]

Benefits of laughing  1. Increase immunity 2. Increases Pain tolerance level 3. Reduces the psychological and physiological stress 4. Increases social bonding in human 5. Increase the sense of well being 6. Combat depression 7. Help to improve the overall health and quality of life (QOL) especially in the old age population tremendously where heavy exercises are difficult to increase endorphins

Laughter as a therapy

When we see on laughter therapy, the methods used other than humor are clapping, vocalizing laughter like sounds, dancing.

Laughter yoga is an important form of Laughter inducing therapy without using humor which are usually done in groups. They used to do clapping, laughter exercises, yoga exercises, breathing and relaxation exercises in general. ^[5]

To conclude, “Laughter is a best medicine” either if it is a Genuine or a fake, It creates a good positive effect on our body.

Reference:

1. Dexter Louie, BA, Karolina Brook, MD, and Elizabeth Frates, MD. The Laughter Prescription: A Tool for Lifestyle Medicine. Am J Lifestyle Med. 2016 Jul-Aug; 10(4): 262–267.
2. JongEun Yim, Therapeutic Benefits of Laughter in Mental Health: A Theoretical Review. Tohoku J. Exp. Med., 2016, 239, 243-249.
3. R. I. M. Dunbar et al. Social laughter is correlated with an elevated pain threshold. Proc. R. Soc. B (2012) 279, 1161–1167. doi:10.1098/rspb.2011.1373.
4. Yoshikawa Y, Ohmaki E, Kawahata H, et al. Beneficial effect of laughter therapy on physiological and psychological function in elders. Nursing Open. 2019; 6:93–99.
5. C. Natalie van der Wal, Robin N. Kok, et al. Laughter-inducing therapies: Systematic review and meta-analysis. Social Science & Medicine 232 (2019) 473–488.
6. Mary Payne Bennett and Cecile Lengacher. Humor and Laughter May Influence Health: III. Laughter and Health Outcomes. eCAM 2008;5(1)37–40.
7. Manninen, Lauri Tuominen, et al. Social Laughter Triggers Endogenous Opioid Release in Humans. The Journal of Neuroscience, June 21, 2017 • 37(25):6125– 6131.