Hi there folks, we hope you had a good Christmas here at the West 12 Health Centre and would like to wish you a Happy New Year. To continue with our previous post we think it would only be fair to explain some of the theories behind the inevitable weight gain we all experience this time of year in particular.
64% of adults in the UK are overweight or obese (BMI >25 and >30 respectively), interestingly though people may fail to recognise their own weight gain over time as well as their weight problems (Ziebland et al, 1996). This is surprising as the physical and psychological risks of excessive weight gain are well documented. It has also been recognized that such risks to health occur with any level of weight gain. Increases of less than five kilograms have been found to be associated with increased disease load, even for those within a healthy BMI range (18.5-25)(Lim, et al., 2008; WHO, 2000).
The easy explanation for weight gain is having too much energy intake from food and not enough burning off of this energy via exercise and physical activity, we all know that. We also know that it must be more complex than that otherwise it wouldn’t be such an issue! For the purposes of this article we will concentrate on early biological factors and briefly, environmental factors that contribute to weight gain.
It is important to begin by stating that a fluctuating body weight is normal for most adults throughout their lives. Even those who appear to maintain a stable weight fluctuate above and below their ‘preferred’ weight. Just like any other system, when there is a change that disturbs one’s weight, the body has mechanisms that attempt to restore our weight to a set value. Clear examples of this are seen in those who have starved or recovered from food shortages post-war (Keys et al, 1950) and in pregnant women, who return to their initial weight post-partum (Garrow, 1974).
One theory that follows this train of thought is the set point theory. It states that each of us has a preferred weight that is genetically programmed in our bodies and is a weight that we would prefer to maintain under normal circumstances. This theory works well with muscle tissue, as after famine or stopping of bodybuilding, lean muscle mass returns to its initial levels. Fat mass however, is less well behaved as it acts as a buffer to store energy for times it may be needed. In order to understand why it is important to understand how our fat develops from an early age to adulthood.
Firstly, we are all built differently genetically and we all inherit different body types and shapes. What we know is that the number of fat cells is a major determinant for the fat mass of adults. The number of fat cells stays constant in adulthood in lean AND obese individuals and is set during childhood and adolescence (Spalding et al, 2008) and this begins with what we inherit.
The likelihood of children being overweight or obese when one or both of their parents is obese is significantly higher. A child with one obese parent has a 50 percent chance of being obese. When both parents are obese, their children have an 80 percent chance of obesity. How much of that is genetic and how much of that is due to our environment is still under discussion (24-77%) (Wardle et al, 2008). A key reason is that overweight/obese parents are more likely to raise their children in an obesogenic (fattening) environment.
Secondly, there are key moments in our childhood where the number and size of our fat cells are determined:
- Ages 0-2 years – A growing child has a huge increase in the number of cells at this age, therefore being overfed or being overweight here increases the number of cells dramatically. This clearly depends on genetics, birth weight, how the mother fed during pregnancy and how much/what the baby is fed etc. Breast fed babies grow at a slower rate than formula fed and this may contribute to weight in later life (Ziegler, 2006). If the mother has conditions during pregnancy, then these may increase the babies likelihood of being overweight. Early life is CRITICAL for healthy development.
- 5-7 years – Adipose Rebound – This is the age where a child’s body fat reaches its lowest point, along with the body mass index (BMI), before it increases. An early rebound (before the age of 5) is associated with an increased risk of overweight and has shown that adult obesity occurs more frequently in children who have early adipose rebound (Rolland-Cachera et al 2006)
- Age 9 -13 years (puberty-adolescence) – Going into puberty is the time when there is more emphasis on an increase in the size of the fat cells that we already have in the body. Too great an increase in the size of these fat cells leads to resistance to insulin. Insulin resistance may be linked to increased cardiovascular risks as well as diabetes. If children reach this age overweight, they have a much higher likelihood of being an overweight or obese adult. Interestingly, girls may be at particular risk for adult obesity if their disease is present or develops during adolescence, and that adolescent-onset obesity in females may herald a lifelong problem (Dietz, 1994). Boys more than girls, appear to deposit fat around the belly (read our first post for more info) and lose fat peripherally as they mature. Increased belly fat in obese adults predicts heart disease, hypertension (high blood pressure), and hyperlipidemia (high level of fat in the blood). These effects contribute to glucose intolerance and type 2 diabetes.
It is clear to see childhood is very important for the development of weight gain in adults. The environment (including diet) in which children are raised is just as important, if not more important than the genetics we gain from our parents. A large responsibility therefore rests on the parents, who of course are feeding their children but cannot be held solely responsible. Schools and government etc must also attempt to educate parents and society in general about the importance of good nutrition throughout childhood (and life in general) as it clearly impacts adulthood and therefore society as a whole in the future. Overweight and obesity is costing the UK nearly £50 billion a year when taking into account all the problems related with being overweight or obese…£50 billion…
Back to the subject, children raised in an environment where they are exposed to being overweight or obese is known as an obesogenic environment. It is defined as “an environment that promotes gaining weight and one that is not conducive to weight loss” within the home or workplace (Swinburn et al, 1999). This environment leads to a vicious cycle in children/adolescents who gain excessive weight because they have:
- Low physical activity level
- Insulin resistance
- More fat cells produced
- Hormone problems causing increased hunger
- Lower self-esteem
- Poorer sleep – disrupting appetite further and increasing fatigue
- Socioeconomic disadvantage – reduced social and economic opportunities, increased discrimination in workplace, health care etc
It is easy to see how this can become a constant vicious cycle that is very hard to break out of and is one that often continues through to adulthood. It is a complex issue that is misunderstood, with public response often being ‘stop being so lazy’ or ‘exercise more and go on a diet,’ when the truth is that it is not as simple as that for many of us. For more, have a read of this great article on the subject:
Some suggest that the environment is now overriding genetics. This is seen especially when these ethnic groups (African and South Asian) enter western society and show high increases in their BMI due to the high fat, sugar and dense food combined with lower levels of physical activity. South Asians have a lower healthy BMI and waist circumference size due to their ethnicity.
Now to throw a spanner in the works – Epigenetics. I realise this is probably a term most people haven’t come across so we will try to make the explanation more understandable without all the scientific jargon.
Not until quite recently was it thought that everyone’s DNA was hardwired.That we all got a mix of genes of some sort from our parents and that nothing we ever do in our lifetime will alter our DNA and that it would be passed on unchanged to our children. However, with epigenetics, we now know that just having a gene for something (like obesity) doesn’t mean that it will be expressed.
Epigenetics looks at how our environment and external influences can affect our gene activity WITHOUT changing our actual DNA. It suggests that our lifestyle choices and diet at ANY AGE can change how our genes are expressed and therefore change our observable characteristics like physical appearance, physiology, behaviour etc.
The most famous of these epigenetics studies is called Avon Longitudinal Study of Parents and Children, which has monitored 14,500 families since the early 1990s. The on going study has found that:
- the lifespan of grandchildren seemed to be influenced by their paternal grandfathers’ access to food, particularly during the grandfather’s slow growth period – that is between the ages of 9 and 12 before they reached puberty. Children tended to live longer if their grandfather had endured food scarcity during this particular time of life.
- Additionally, grandsons of grandmothers who smoked, even if their mothers didn’t, were bigger.
- Meanwhile, that men who had started smoking before they were 11 had sons who were more likely to be obese by the time they were teenagers.
Therefore, the message is – whatever we do not only affects our lives but the health, behaviours etc of our future generations. The positive is that we can affect our gene expression and can change no matter what we inherit. So for all of you sitting there cursing your parents and your grandparents for certain traits, there is always hope and possibility to change, no matter your circumstances, especially weight gain…and there is no better time to start than now.
Well…that was a bit of a marathon, we know, we know…well done for getting this far, we hope you enjoyed our second post. Look out for another soon and have a great start to the New Year.
West 12 Health
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Dietz WH. (1994). Critical periods in childhood for the development of obesity. Am J Clin Nutr. . 59 (5), 955-959.
Garrow, J. Energy balance and obesity in man. New York: American Elsevier, 1974.
Keys, A., Brožek, J., Henschel, A., Mickelsen, O., & Taylor, H. L., The Biology of Human Starvation (2 volumes), University of Minnesota Press, 1950.
Lim, S. S., Norman, R. J., Clifton, P. M., & Noakes, M. (2008). Losing weight through lifestyle modification: A focus on young women. In A. B. Turley & G. C. Hofmann (Eds.), Life style and health research progress (pp. 155-181). Hauppauge, NY: Nova Biomedical Books; US
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