It’s true that we inherit eye color, hair, skin, body-type and more from our parents, and for the most part, we can’t change these traits. But what about our weight? For many years, scientist believed that set point — our body-to-fat ratio within a 10- to 15-pound weight range that optimizes our chances of survival — was something inherited that we couldn’t influence.

But in the past few decades it has become clear that the set point isn’t entirely predestined and unchanging. In fact, your set point is also governed by your environment, even from the time you are growing in utero. In a 2010 article on the set point theory, German scientists wrote: “Searching for the genetic background of excess weight gain in a world of abundance is misleading since the possible biological control is widely overshadowed by the effect of the environment. ” And our environment includes our lifestyle choices and eating habits.

Good news! Your food talks to your genes carrots

Today there’s an entire field of research called nutrigenomics, or “nutritional genomics,” investigating the effects nutrients have upon genes in both disease and health.

The information our genes receive from our food can be a powerful way to “convince” them to respond in ways that are healthy — and it’s not so much about how much we eat (although obviously, overeating isn’t going to help anyone) than about what we eat.

The reason it may feel like we can’t change our set point weight is that our bodies like stability — and our metabolism defends the set point by slowing down or speeding up when our weight approaches the outer limits of our set point’s range.

So how can you change your environment to reprogram your weight? Follow our tips for optimizing metabolic rate and consider one more factor: your emotional health.

We’ve always known intuitively that laughter is the best medicine, but before now we haven’t really grasped why. Studies of laughter therapy in type 2 diabetics showed that as many as 23 different genes were altered as a byproduct of laughter. Not only that, but the activity of several blood enzymes and their precursors changed as well, in ways that were beneficial toward preventing a range of metabolic imbalances.

So one of the ways that we can send positive signals to our genes, cells, and proteins is by cultivating positive emotions. At the same time, addressing sources of negative emotions — particularly trauma from our past that is a continual source of sadness, guilt, shame, or anger — can reduce the flow of negative messages to our genes and cells. (For further guidance, we suggest reading Dr. Candace Pert’s Molecules of Emotions.)

You can influence your set point

It’s so important that women realize that we can communicate with our genes and get at least some of them to change their behavior. Our genes receive messages all the time through our nutritional choices and the patterns of our emotions, whether we realize it or not. Our Weight Loss Resistance Package helps you take care of your nutrition, your emotions, exercise, and stress, to help influence your set point and make lasting changes in your body. But keep in mind that influencing set point doesn’t happen all at once. If you are trying to lose a large amount of weight, we suggest doing this in increments and letting the body have time to stabilize in between periods of losing the weight. To make lasting changes, our set point needs time to rebalance. We’re always here to help.

References

1Abrass, C. 2004. Overview: Obesity: What does it have to do with kidney disease? J. Am. Soc. Nephrol., 15 (11), 2768–2772. URL: http://jasn.asnjournals.org/cgi/content/full/15/11/2768 (accessed 03.20.2009)

2 Müller, M., et al. 2010. Is there evidence for a set point that regulates human body weight? F1000 Med. Rep., 2, 59. URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2990627/?tool=pubmed (accessed 10.05.2011).

3 Gibbs, W. 1996. Interview with Rudolph L. Liebel. URL: http://www.sciam.com/article.cfm?id=interview-with-rudolph-l&page=1 (accessed 03.20.2009).

4 Hayashi, K., et al. 2006. Laughter regulates gene expression in patients with type 2 diabetes. Psychother. Psychosom., 75 (1), 62–65. URL (abstract): http://www.ncbi.nlm.nih.gov/pubmed/16361876 (accessed 03.20.2009).

Hori, M., et al. 2009. Positive emotion-specific changes in the gene expression profile of tickled rats. Mol. Med. Rep., 2 (2), 157–161. URL: http://www.spandidos-publications.com/mmr/2/2/157 (accessed 03.20.2009).

5 Hayashi, K., et al. 2007. Laughter modulates prorenin receptor gene expression in patients with type 2 diabetes. J. Psychosom. Res., 62 (6), 703–706. URL: http://www.ncbi.nlm.nih.gov/pubmed/17540229 (accessed 03.20.2009).

Hayashi, K., et al. 2007. Laughter up-regulates the genes related to NK cell activity in diabetes. Biomed. Res., 28 (6), 281–285. URL (PDF): http://www.jstage.jst.go.jp/article/biomedres/28/6/281/_pdf (accessed 03.20.2009).

Nasir, U., et al. 2005. Laughter therapy modulates the parameters of renin-angiotensin system in patients with type 2 diabetes. Int. J. Mol. Med., 16 (6), 1077–1081. URL: http://www.ncbi.nlm.nih.gov/pubmed/16273289 (accessed 03.20.2009).

References for text box:

Minieri, M., & Di Nardo, P. 2007. Nutrients: the environmental regulation of cardiovascular gene expression. Genes Nutr., 2 (2), 163–168. URL: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=18850172 (accessed 03.20.2009).

Berdanier, C. 2006. Mitochondrial gene expression: influence of nutrients and hormones. Exper. Biol. Med., 231 (10), 1593–1601. URL: http://www.ebmonline.org/cgi/content/full/231/10/1593 (accessed 03.20.2009).

Schuster, G.U. 2006. Nutrients and gene expression. In Kaput J., Rodriguez R.L., eds. Nutritional Genomics. John Wiley & Sons, Inc.

Walker, W., & Blackburn, G. 2004. Symposium introduction: Nutrition and gene regulation. J. Nutr., 134 (9), 2434S–2436S. URL: http://jn.nutrition.org/cgi/content/full/134/9/2434S (accessed 03.20.2009).

Clarke, S., & Abraham, S. 1992. Gene expression: Nutrient control of pre-and posttranscriptional events. FASEB J., 6 (13), 3146-3152. URL (abstract): http://www.ncbi.nlm.nih.gov/pubmed/1397836 (accessed 03.20.2009).