The bacteria in your gut affect blood insulin levels and may influence your chances of developing type 2 diabetes

Developing type 2 diabetes is for a large part influenced by your diet but also genes. However, a recent study has now shown that your gut microorganisms might also play an important role in the risk of developing type 2 diabetes (T2D). The article published in Nature Genetics entitled “Causal relationships among the gut microbiome, short-chain fatty acids (SCFA’s) and metabolic diseases”, claims evidence that bacterial metabolites such as SCFA’s are able to influence insulin levels and increase the risk of getting T2D.

Various studies have suggested that increased SCFA production benefits the host by exerting anti-obesity and antidiabetic effects, however, results of different studies are not always in agreement. Moreover, there is also evidence that increased production of SCFAs in the gut might be related to obesity, due to energy accumulation. Resolving these conflicting findings requires a detailed understanding of the causal relationships between the gut-microbiome and host energy metabolism, and the present study contributes to this.

The authors analyzed data from a large population study based in Groningen (The Netherlands), comprising 952 individuals with known genetic data, as well as information on parameters associated with metabolic traits such as BMI and insulin sensitivity. In addition, data were acquired for the type and the function of the bacteria which were present in the gut of the study participants. Combining this data, the authors tried to answer the question of whether changes in microbiome features causally affect metabolic traits or vice versa?

A technique called Mendelian randomization (MR) which is increasingly accepted to establish cause-effect relationships in the onset of diseases was applied. The primary outcome of the analysis was that host genes influence the production of the SCFA butyrate in the gut, which is associated with improved insulin response in the blood after an oral glucose tolerance test. In addition, abnormalities in the production or absorption of propionate, another SCFA, were causally related to an increased risk of T2D.

So far available data suggest that overweight humans or those with type 2 diabetes may have different microorganisms in their gut compared to healthy people. These microorganisms which are commonly found in healthy people are absent from the T2D patients. Whether the differences in the microbiota between healthy and T2D patients are an effect of the disease development or account for causality is challenging to be answered. With the data from the present study, authors are able to go one step further and demonstrate potential routes by which microorganisms are able to regulate our metabolic status underlying their importance for our wellbeing.

Collectively the present article suggests that production of bacterial SCFA’s play a pivotal role in the regulation of metabolic traits such as blood insulin levels and are associated with the onset of T2D.

Since the study was observational and did not include any T2D patients, confirmation of the results is essential. Follow up studies including T2D patients would be highly informative. With the rising prevalence of obesity in adults, which is reaching epidemic levels, the prevalence of T2D will also continue to rise. In the past years, scientists have mainly focused on the role of human gene data, but this has not led to major breakthroughs. Perhaps knowledge of the microbiome will elucidate molecular mechanisms which can be translated to novel effective treatments for metabolic disorders such as T2D.

REFERENCES
Sanna, S., van Zuydam, N. R., Mahajan, A., Kurilshikov, A., Vila, A. V., Võsa, U., . . . Oosting, M. (2019). Causal relationships among the gut microbiome, short-chain fatty acids and metabolic diseases. Nature genetics, 1.

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Yoga practice has become very popular in the last two centuries. In most western countries, yoga studios are booming. For example, Dutch practitioners are said to spent 325 million euros per year on yoga classes, clothes and events.

In scientific research, yoga and its beneficial effects on physical and mental health, have also become a serious topic of interest. In a previous post, Hannah Kurts had already outlined the positive effects of yoga for several psychiatric disorders (https://newbrainnutrition.com/how-to-help-mental-health-with-yoga/)

Recently, the effects of yoga on cognitive performance and behavioral problems in 5-year old children have been examined. A group of Tunisian researchers offered 5-year old children in kindergarten a 12-week yoga program, regular physical education, or no kind of physical activities.

They found that this kind of kindergarten-based yoga practice, had significant positive effects on visual attention, visuo-motor precision and symptoms of hyperactivity and impulsivity, in comparison to regular physical activities or no physical activities [1].

One might wonder: Quiet and peaceful yoga exercises with a bunch of energetic 5-year olds? How would that even work?

The yoga they offered in this project was a 30-minute routine, instead of a more regular 90-min session: 5 minutes of warming up, doing jogging, jumping, stretching. Next, 15 minutes of the well-known yoga postures, standing, sitting, flexing. Next, 5 minutes of breathing techniques and lastly, 5 minutes of yogic games, to train memory, awareness and creativity. And they practiced only twice a week.

It seems very promising that such a curtailed version of yoga practice can have positive effects on attention, executive functions, and behavioral control, which are all skills that are vital to good academic performance [2][3].

In some European and North-American countries, the idea of school-based yoga practice isn’t so revolutionary anymore. France, Italy, Brazil, and Canada have recognized yoga practice in its school curriculum. Italy seems to be the school-yoga champion: Classroom-based yoga is performed in all Italian schools since 2000 [4].

REFERENCES
[1] Jarraya S, Wagner M, Jarraya M and Engel FA (2019) 12 Weeks of Kindergarten-Based Yoga Practice Increases Visual Attention, Visual-Motor Precision and Decreases Behavior of Inattention and Hyperactivity in 5-Year-Old Children. Front. Psychol. 10:796. doi: 10.3389/fpsyg.2019.00796

[2] Chaya, M. S., Nagendra, H., Selvam, S., Kurpad, A., and Srinivasan, K. (2012). Effect of yoga on cognitive abilities in schoolchildren from a socioeconomically disadvantaged background: a randomized controlled study. J. Altern. Complement. Med. 18, 1161–1167. doi: 10.1089/acm. 2011.0579

[3] Verma, A., Uddhav, S., Ghanshyam Thakur, S., Devarao, D., Ranjit, K., and Bhogal, S. (2014). The effect of yoga practices on cognitive development in rural residential school children in India. Natl. J. Lab. Med. 3, 15–19.

[4] Flak, M. (2003). Recherche Sur Le Yoga Dans L’éducation. 3ème Millénaire: Spiritualité – Connaissance De Soi – Non-Dualité – Méditation, 125. Available at: http://www.rye-yoga.fr/ (accessed July 15, 2018).

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MoBa is short for The Norwegian Mother and Child Cohort Study which is a large pregnancy observational study. During the years 1999-2008 pregnant women in Norway were recruited to the study. The study is conducted by the Norwegian Institute of Public Health. Questionnaires regarding health, diet and environment were sent out to the women during and after pregnancy. Women are sent regular follow-up questionnaires. As the child grows up, the child also completes questionnaires. In addition, the fathers were invited to participate with a questionnaire when their partner was pregnant. Biological samples were also collected from the mother, father and child. Today there are 114 500 children, 95 000 mothers and 75 000 fathers participating in the study.

https://www.fhi.no/en/studies/moba/

The study was set up to gain knowledge about the causes behind serious disease. The study is unique because it gathers information from fetal (in vitro) life and follows the offspring into adulthood. In this manner it is possible to look at early influences and later disease. The study is prospective, which means that information about mothers, fathers and their offspring is registered before a disease has manifested itself. With this design, women are asked questions several times during her pregnancy and do not have to try to remember what she did when looking back at her pregnancy.

MoBa is population-based and became nationwide with 50 participating hospitals in Norway. For more information on the many publications based on MoBa data, visit this link:

https://www.fhi.no/en/studies/moba/for-forskere-artikler/publications/

The participating women in MoBa also filled in a questionnaire about eating habits before and during pregnancy.

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The popularity of yoga practice has risen sharply in recent years. In 2006, already 2.6 million people in Germany practiced yoga regularly (1). The arguments for yoga are widely spread in the population, for example the energy and immune function are increased and back pain, arthritis and stress are relieved (2). For others, the practice of yoga is an important factor in doing something good for themselves, while for others the discipline and control of the body is more in focus.

But, where does yoga come from?
The yoga tradition originates from India, the religion of Buddhism, and has a philosophical background with original roots reaching back over 2000 to 5000 years. The term “yoga” comes from the word “yui”, which has its origin in Sanskrit, a very ancient Indian language, and means “unite”. Accordingly, yoga refers to the union of body, mind and soul (3).

What exactly does a yoga practice involve?
In western countries the focus is especially on the Asana practice, the postures. The postures can be lying, sitting or standing and should be performed as attentively as possible. All Asanas have associated Sanskrit names and also pictorial names such as the Cobra (Bhujangasana) or the down looking dog (Adho Mukha Svanasana). Further essential elements are the breathing techniques (Pranayama), where the breath is consciously directed (e.g. Kapalabathi, alternative breathing) and the meditation (Dhyana), where the mind is consciously directed, by calming down, insight can be attained and a state of deep relaxation can be achieved.

But, can yoga really have a positive effect on mental and physical health?
In view of the study and literature available, YES! A meta-analysis results that yoga is effective as a complementary treatment for psychiatric disorders such as schizophrenia, depression, anxiety, and posttraumatic stress disorder (4).

Yoga can have a positive influence on the reduction of depression symptoms, the reduction of stress and anxiety, and can lead to an increase in self-love, awareness and life satisfaction (5, 6). On the physiological level, the results can also be found in the reduction of the stress hormone cortisol (7).

In the case of anxiety disorders, relaxation is a central component of yoga practice. Clients lack confidence, courage and stability, so that autogenic training, progressive muscle relaxation and deep relaxation can be beneficial.

In the presence of eating disorders, yoga can make an important contribution to increasing body satisfaction, awareness and receptivity as well as reducing self-objectivity and psychological symptoms (8). Prevention programs with concentration on yoga appear promising, as body satisfaction and social self-concept have been increased and bulimic symptoms reduced.

Conclusion: The integration into the health system for prevention and complementary therapy seems to be reasonable and as Mind Body Therapy, integrated into the treatment concept, positive effects on mental health can be achieved. In addition to body awareness, yoga concentrates on personal awareness and self-love and has an effect on the emotional, mental, cognitive and physical body levels. The yoga classes can be specifically adapted to the needs of the participants and can be set up in a disorder-specific way.

Advantages of yoga as a complementary therapy:
– Lower costs
– At the same time positive effect on the body
– No side effects
– Preventive and therapeutic support
– Less time required
– New contacts

What do you need to consider?
1. Choice of Yoga-Studio (atmosphere, costs, course offers)
2. Yoga teacher (e.g. education of teacher, authentic)
3. Yoga style (discover your preference, adapt to your daily state, examples follow)

– Vinyasa = flowing asanas, activating, breath and asanas in harmony
– Hatha = origin, breathing exercises, meditation, gentle asanas
– Ashtanga = powerful, always constant flowing sequences, condition
– Yin = relaxing, longer lasting asanas, calm, passive
– Acro Yoga = combination of acrobatics and yoga
– Kundalini = spiritual, mantras singing, meditation, energies

REFERENCES

  1. Klatte, R., Pabst, S., Beelmann, A. & Rosendahl, J. S. (2016). The efficacy of body-oriented yoga in mental disorders. Deutsches Arzteblatt international, 113 (20), 359. https://doi.org/10.3238/arztebl.2016.0195.
  2. Cramer, H., Ward, L., Steel, A., Lauche, R., Dobos, G. & Zhang, Y. (2016). Prevalence, Patterns, and Predictors of Yoga Use: Results of a U.S. Nationally Representative Survey. American journal of preventive medicine, 50 (2), 230–235.
  3. Jaquemart, P. & Elkefi, S. (1995). Yoga als Therapie. Lehrbuch für die Arzt und Naturheilpraxis. Augsburg: Weltbild Verlag.
  4. Cabral P, Meyer HB, Ames D. (2011). Effectiveness of yoga therapy as a complementary treatment for major psychiatric disorders: A meta-analysis. Prim Care Companion CNS Disord. 2011;13:pii: PCC10r01068.
  5. Ponte, S. B., Lino, C., Tavares, B., Amaral, B., Bettencourt, A. L., Nunes, T. et al. (2019). Yoga in primary health care. A quasi-experimental study to access the effects on quality of life and psychological distress. Complementary therapies in clinical practice, 34, 1–7. https://doi.org/10.1016/j.ctcp.2018.10.012
  6. Snaith, N., Schultz, T., Proeve, M. & Rasmussen, P. (2018). Mindfulness, self-compassion, anxiety and depression measures in South Australian yoga participants: implications for designing a yoga intervention. Complementary therapies in clinical practice, 32, 92–99. https://doi.org/10.1016/j.ctcp.2018.05.009
  7. Bershadsky, S., Trumpfheller, L., Kimble, H. B., Pipaloff, D. & Yim, I. S. (2014). The effect of prenatal Hatha yoga on affect, cortisol and depressive symptoms. Complementary therapies in clinical practice, 20 (2), 106–113. https://doi.org/10.1016/j.ctcp.2014.01.002
  8. Neumark-Sztainer, D. (2014). Yoga and eating disorders: is there a place for yoga in the prevention and treatment of eating disorders and disordered eating behaviours? Advances in eating disorders (Abingdon, England ), 2 (2), 136 145. https://doi.org/10.1080/21662630.2013.862369

 

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Why do some people have a higher craving for carbohydrate-rich and junk-food than others? Why are weight-loss programs more effective in some individuals than others? And why are some people more physically active?

The dopamine system in the brain plays an important role in regulating how much you eat and whether or not you gain weight. When this system does not function optimally, people have a higher craving for junk-food, lower physical activity, and unsuccessful body weight control.

There are two mechanisms that determine food-related behaviour.

The more direct, homeostatic, mechanism constantly surveys the body’s energetic needs and holds them actively in balance. That is homeo-stasis.

The second non-homeostatic mechanism determines the way humans, and other animals, react to food: how willingly and often they will consume it again, and whether they feel anticipation or craving for it.

These behaviours are both largely regulated by the neurotransmitter dopamine, a chemical that conveys information in the brain. Once released by one nerve cell it binds to a receptor, a large molecule on the surface of the adjacent nerve cell, thus changing its functioning. A major component in eating-related behaviour is the dopaminergic D2 receptor (DRD2) that is most abundantly localized in striatum, a brain region activated by food anticipation and consumption1.

The function of the dopaminergic system affects eating and weight-related problems in four ways.

First, in some people, the dopamine system reacts more vigorously in response to food.

Second, this response leads to increased eating and possibly obesity.

Third, overeating and obesity lead to less efficient dopaminergic signaling.

Fourth, this lower dopaminergic signal needs to be compensated by more intense behaviour e.g., more eating2.

For example, in people with lower levels of dopamine D2 receptor, cravings for carbohydrate-rich food and junk-food are more prevalent3,4.

Besides eating-related behaviour, dopamine also affects health/obesity via voluntary physical activity, creating a vicious circle: obesity leads to weaker dopaminergic signal, especially lower levels of DRD2 receptor, and this, in turn, leads to decreased exercise and motivation for physical activity5–7.

Furthermore, individuals with lower levels of DRD2 receptors may benefit less from long-term weight loss programs and are less effective in weight maintenance8,9. Thus, dopamine affects body weight via choice of foods, physical activity, and body weight reduction efficacy. Despite the reasons for food-cravings, part of the solution is acknowledging and managing these impulses. Conscious action towards weight-reduction will lead to less pronounced food-cravings, which in turn leads to favourable solution of weight related problems10.

REFERENCES
1. Wise, R.A. Philos Trans R Soc Lond B Biol Sci 361, 1149–1158 (2006).
2. Alonso-Alonso, M. et al. Nutrition reviews 73, 296–307 (2015).
3. Lek, F.-Y., Ong, H.-H. & Say, Y.-H. Asia Pac J Clin Nutr 27, 707–717 (2018).
4. Yeh, J. et al. Asia Pac J Clin Nutr 25, 424–429 (2016).
5. Kravitz, A.V., O’Neal, T.J. & Friend, D.M. Front Hum Neurosci 10, 514–514 (2016).
6. Matikainen-Ankney, B.A. & Kravitz, A.V. Ann N Y Acad Sci 1428, 221–239 (2018).
7. Ruegsegger, G.N. & Booth, F.W. Front Endocrinol 8, 109–109 (2017).
8. Roth, C.L., Hinney, A., Schur, E.A., Elfers, C.T. & Reinehr, T. BMC Pediatr 13, 197–197 (2013).
9. Winkler, J.K. et al. Nutrition 28, 996–1001 (2012).
10. Smithson, E.F. & Hill, A.J. Eur J Clin Nutr 71, 625 (2016).

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We, human beings in Western society, make over 200 food choices each day (1). That’s a lot! Fortunately (or, according to others, unfortunately), we don’t actually have to think about each and every one of them, or at least not consciously. If our food choices are not so much a conscious decision, then how do we make them? A lot has been written about external factors influencing our food choices, for instance, alluring displays in supermarkets or the availability of unhealthy foods in our day-by-day environment. In this blog, I will address the potential role of genetics on food choices: to what extent do our genes determine what we eat?

Eating behaviours are complex, i.e. they are very diverse and influenced by many different factors. When we investigate complex behaviours, we are unlikely to find simple explanations. In other words: we do not expect to find one gene that makes me prefer pizza margarita over pizza fungi, nor will we find a single gene responsible for my triple-chocolate ice cream consumption. There are, however, some instances in which specific genes have relatively simple and straightforward effects on our food choices. This is the case when genetic variants code for food sensitivities.

A famous example is the LCT gene (or, more precisely, the C>T change at 13910 bases upstream of the LCT gene in the 13th intron of the MCM6 gene). The LCT gene codes for lactase persistence, or lactose tolerance after childhood. Worldwide, the majority of people (and most other mammals, for that matter) no longer tolerate dairy products after childhood. For them, consuming milk products causes nausea, bloating and cramping within 2-3 hours. As a result, they will soon learn not to consume dairy products. Those who have the lactase persistence gene, however, don’t have any problems digesting dairy products and, thus, are more likely to consume them (2). Geographical region is important here: while in Northern European countries such as the UK and Finland, 90-100% of people tolerate dairy products, in South-East Asia and Australia this number is close to 0% (3).

A similar situation seems to occur for genes coding for certain taste receptors on the tongue. The TAS2R38 gene, for instance, makes some people extremely sensitive to bitter taste. This, of course, will cause them to avoid bitter foods such as cruciferous vegetables (4). A recent study has even identified a small number of genes that together cause people to either love or hate marmite (5)! Another gene variant (CYP1A1), coding for caffeine clearance from the body, causes carriers to drink less or more coffee and tea (6).

Thus, when food sensitivities are involved, food choices can be driven by specific genes. Most food choices, however, have very little to do with food sensitivities and are much more complex. Pizza Margarita or Pizza Funghi? Triple-chocolate ice cream today or maybe tomorrow? While for such complex food choices there is no single gene responsible, our genetic make-up still does have influence. Typically, for complex behaviours, many different genes can be identified. While each gene individually contributes only a little bit, together they can actually have quite an effect on your food choices. For instance, a recent study identified seven genetic variants each having a small effect on carbohydrate intake. Taken together, genes explained 8% of the variation in carbohydrate intake between individuals (7).

In conclusion: while some genetic variants have rather drastic effects on our food choices, by giving us a physical adverse reaction to certain foods, there are only few of them. Most of our food choices are much more complex. These are influenced by multiple genes at the same time, and even together these genes have only limited influence.

REFERENCES
1. Wansink, B., & Sobal, J. (2007). Mindless eating: The 200 daily food decisions we overlook. Environment and Behavior, 39(1), 106-123. doi: 10.1177/0013916506295573

2. Szilagyi, A. (2015). Adaptation to Lactose in Lactase Non Persistent People: Effects on Intolerance and the Relationship between Dairy Food Consumption and Evolution of Diseases. Nutrients, 7(8):6751-79. doi: 10.3390/nu7085309

3. Itan, Y., Jones, B.L., Ingram, C.J.E., Swallow, D.M. & Thomas, M.G. (2010). A worldwide correlation of lactase persistence phenotype and genotypes. BMC Evol Biol, 10:36. doi: 10.1186/1471-2148-10-36

4. Feeney, E., O’Brien, S., Scannell, A., Markey, A. & Gibney, E.R. (2011). Genetic variation in taste perception: does it have a role in healthy eating? Proc Nutr Soc, 70(1):135-43. doi: 10.1017/S0029665110003976.

5. Roos, T.R., Kulemin, N.A., Ahmetov, I.I., Lasarow, A. & Grimaldi, K. (2017). Genome-Wide Association Studies Identify 15 Genetic Markers Associated with Marmite Taste Preference. BioRxiv (preprint). doi: 10.1101/185629

6. Josse, A.R., Da Costa, L.A., Campos, H. & El-Sohemy, A. (2012). Associations between polymorphisms in the AHR and CYP1A1-CYP1A2 gene regions and habitual caffeine consumption. Am J Clin Nutr, 96(3):665-71. doi: 10.3945/ajcn.112.038794.

7. Meddens, S.F.W., de Vlaming, R., Bowers, P., Burik, C.A.P., Karlsson Linnér, R., Lee, C., et al. (2018). Genomic analysis of diet composition finds novel loci and associations with health and lifestyle. BioRxiv (preprint). doi: 10.1101/383406

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