Dr. Sharma's Obesity Notes

How do people become severely obese? Anyone, who thinks the answer is simply, “by eating too much and not moving enough”, is not only wrong, but is essentially missing the whole point of what it will take to find solutions.

A study by Julia Temple Newhook, Deborah Gregory and Laurie Twells from the Memorial University of Newfoundland, St. John’s, published in the Journal of Social, Behavioral, and Health Sciences, seeks to better understand what causes some people to gain weight.

The researchers conducted extensive interviews with individuals seeking bariatric surgery regarding their perspectives on their histories of weight gain and their explanations for weight gain as well as the emotions surrounding their weight gain experiences.

In today’s post, I would like to touch on what the authors describe as, “important life events”, which in some cases, interestingly enough, begin with being born.

Thus, for many participants, weight gain struggles began in childhood:

“Sam, an unemployed laborer in his 20s, said that he had been big since the age of 9: “It’s hereditary. A lot of people in my family are big.” Deirdre, an educator in her 40s, said, “I have never been slim. I have never been below a size 18, 20. Never. … I don’t remember as a child being small.” She added, “I know that part of it is genetics, because I really do believe that. I have a set of grandparents who were huge … I guess it is my metabolism.”

This is very much in line with my own clinical experience, where patients often describe always having been large for as long as they can remember with bullying and name calling belonging to their earliest childhood memories.

Others, on the other hand, describe a previous slim childhood or adult life, prior to rapid weight gain. In women, the most common life event likely to precipitate irreversible weight gain was pregnancy:

“Annie, a retired caregiver in her 60s, reported that she now weighs over 300 pounds, but recalled, “I only gained weight after I had my daughter … I was 127 pounds when I got pregnant … I went up to 181 and I never went below that after.”

But it was not just the course of pregnancy itself that was held responsible:

“…increased childcare and domestic workloads—that followed. Heidi, a customer service worker in her 30s, explained, “You don’t have the ‘you time’ to do what you need to do to try to take care of yourself a bit better. Everything is your children.”

Another major life event is loss of a dear one:

“Theresa, a retired educator in her 60s, talked about gaining weight after her husband died: “I ate my way through … That was my comfort I didn’t go the gym and I didn’t exercise … grief is strange. I was angry for a long time.”

This observation is also very much in line with the findings in my own practice, where I often see unresolved grief and trauma (emotional, physical or sexual) as a driver of dramatic weight gain. In my experience such negative life experiences can occur at any age (and virtually in anyone) and it is often possible to narrow down the exact temporal relationship between the event and subsequent weight gain.

For some, the life event was “simply” a change in “circumstances”:

“Jennifer, a manager in her 40s, said that when she moved from her rural home to an urban center for university, “I gained 90 pounds in about 9 months. … I was going to school so I wasn’t active at all, and I was eating takeout twice a day for my meals because it was cheap. I ate for free where I worked and I ate deep-fried food for all that time.”

This scenario is likewise not unusual – especially amongst the migrant and immigrant population, where adapting to a new life can often have profound effects on body weight for no reason other than having switched from one environment to another.

And then there was injury and illness:

“Derek, a customer service worker in his 30s, suffered a sports injury in his late teens: “I had a hockey injury, actually, is what started it. … I put on a lot of weight.” He said that his weight gain was exacerbated by a changing lifestyle as he entered the workforce: “Sports stopped. … My weight just ballooned. The only way I know to describe it is it’s like I went to bed being fairly active and in half decent shape and waking up and being 150 to 200 pounds overweight.”

Again, this scenario is not uncommon – I have previously posted on the remarkably high number of former competitive athletes in our bariatric clinic.

While life events were deemed an important contributor to developing severe obesity, this was not all that the interviewees had to offer.

More on other aspects of these investigations in the coming posts.

If certain life events have led to your weight gain – I’d certainly appreciate hearing about them.

AMS
Vancouver, BC

As someone, who sees patients with obesity for a living, I fully recognize the importance of genetic predisposition.

This is indeed a far stronger determinant for shape and size than most people suspect (the heritability of body fat is about the same as that of body height!).

For clinicians, taking a good family history can often pose a problem, not least because of time limitations.

So this is how I ask my patients about their family history of obesity:

“If I brought your whole family together for a family photograph, would you stand out because of your size or would you fit right in there?”

No one has ever been offended by this question and the information is not only useful but opens a whole avenue of possible discussion.

Often, I will follow the question with, “Who else stands out?” and “Would this picture have looked different when you were younger?”

There are obviously a number of scenarios that emerge from such questions:

For example, my patient can respond that she definitely stands out, always has, as everyone else in her family is “skinny”.

Or, my patient can tell me that she not only fits in well (on her dad’s side) and in fact is not even the biggest (compared to her two sisters”).

My experience has taught me that there are often many subtle clues in how patients will answer these questions.

I have seen patients, who suffered through skinny moms, who were themselves paranoid about weight gain and deeply disappointed in the fact that they had an “obese” offspring – you can imagine what this does to self-esteem and eating behaviour in the kid.

I have seen patients, who had an obese father, who insisted that you always eat up and grow up to be “big and strong” – the “bigger” the “stronger”.

I have seen patients, who had obese older siblings and always feared that one day they would be that big – resulting in significantly pathological eating behaviour and a compulsive obsession about “healthy” eating.

Thus, discussing this imaginary family picture can open the discussion to many aspects – not just of genetics but discussions about family dynamics, eating behaviours, body image issues, and countless other topics that I need to understand in order to fully appreciate the context and belief system in which my patients makes decisions about their health behaviours and expectations.

Clearly, even just a mental picture can be worth a thousand words.

AMS
Edmonton, Alberta

Perhaps one of the most frustrating experiences encountered by patients trying to lose weight, is the variation in weight loss between individuals. Thus, it is not uncommon to see one person easily shedding the pounds, while another, with similar or even greater effort, making little progress.

While, as clinicians it may be tempting to simply blame this on “non-compliance”, a paper by Adriana Moleres and colleagues from the University of Navarra, Pamplona, Spain, published in the FASEB Journal, suggestions that a significant part of this variable response may be attributable to differences in DNA methylation.

As readers may know, methylation of DNA is an important epigenetic phenomenon, whereby certain genes are turned on or off (often forever). These epigenetic changes tend to happen during certain times in human development, including early fetal development and adolescence.

In the current study, Moleres and colleagues compared DNA methylation between adolescent high and low responders to a 10 week multidisciplinary weight loss program.

Using methylation microarrays, the researchers identified five regions located in or near AQP9, DUSP22, HIPK3, TNNT1, and TNNI3 genes that showed significantly differnt methylation levels between high and low responders. Interestingly, the AQP9 and HIPK3 genes have previously been associated with obesity or weight-loss responses.

They were also able to calculate a methylation score that was significantly associated with changes in weight, BMI-SDS, and body fat mass loss after the treatment.

While it is difficult to determine the actual functional effect or mechanisms underlying these epigenetic DNA variations, the findings do point to a “biological” reason that may determine weight loss response to diet and lifestyle interventions.

As I’ve said before, in weight management, one size does not fit all.

AMS
Edmonton, AB

Moleres A, Campión J, Milagro FI, Marcos A, Campoy C, Garagorri JM, Gómez-Martínez S, Martínez JA, Azcona-Sanjulián MC, Martí A, & on behalf of the EVASYON Study Group (2013). Differential DNA methylation patterns between high and low responders to a weight loss intervention in overweight or obese adolescents: the EVASYON study. FASEB journal : official publication of the Federation of American Societies for Experimental Biology PMID: 23475851

Now that we have discussed the myths and presumptions, it is time to turn to what the authors of the New England Journal of Medicine paper consider to be “facts”.

These are statements about obesity, which the authors consider facts because there is sufficient evidence to consider them empirically proven.

As one may expect, “conclusive” evidence can only come from experimental studies (ideally, consistent findings from several well-designed randomised controlled trials, which constitute the highest level of evidence). Thus, it should come as no surprise that most of the facts identified by the authors pertain to issues that lend themselves to examination in such trials.

Obesity Fact #1 is that,

“Although genetic factors play a large role, heritability is not destiny; calculations show that moderate environmental changes can promote as much weight loss as the most efficacious pharmaceutical agents available.”

This fact is based on several studies that have shown that it is indeed possible to “modulate” genetic risk by changes to the environment (i.e. diet and exercise).

This finding is neither new nor limited to obesity. After all, even severe monogenic inborn errors of metabolism (like phenylketonuria) respond to changes in the environment (like elimination of phenylalanine in the diet).

However, it is important to remember that achieving lower weights for someone with a strong genetic disposition for obesity will always be so much harder than for someone without that genetic risk.

Thus, while environmental changes, which affect everyone, can perhaps reduce the average weight in a population, they will still leave the biggest people the biggest (albeit at a lower weight).

Just how big and feasible such environmental changes would need to be to significantly reduce obesity will remain to be seen.

At the individual level we have a fair idea that, for some people, this effort is likely to be substantial (readers may recall the recent series on Mark, Julie, Gertrude and Janice).

At an individual level there is certainly no doubt that some people are going to have to work much harder at trying to lose weight or keeping it off than others – so much at least, will always be destiny.

AMS
Edmonton, AB

Continuing this series, we now turn our attention to obesity presumption #2 from the New England Journal of Medicine paper on obesity myths, presumptions and facts.

Remember, that the authors define presumptions as commonly held beliefs that are yet unproven.

Presumption #2 is stated as,

“Early childhood is the period during which we learn exercise and eating habits that influence our weight throughout life.”

The notion behind this presumption is the fact that body weight indexes, eating behaviors, and preferences that are present in early childhood are correlated with those later in life.

Note the word “correlated” in the above sentence – as we all know, correlation is not causation!

As a father of three grown children, each of who turned out wonderfully different, I can attest to the fact that certain behavioural traits and patterns do persist into adult life – but that is not the question.

The question is, whether or not my parental influence (or anyone else’s) had anything to do with this.

As readers may be well aware, there is a vast body of credible literature that describes the uncanny similarities between genetically identical twins (including those separated at birth) compared to non-identical twins (including those raised together).

Call me a sceptic if you may, but while I have my own doubts on what role great parents may play in shaping their kids behaviours and preferences, I have absolutely no doubt at all that poor parenting can damage those behaviours and preferences once and for all.

Thus, while I have no idea how to make a kid with no musical talent love to play a musical instrument, I have no doubt at all, that I could get any kid (talent or no talent) to hate it.

Similarly, while I have no idea how to make a kid with no interest in sports to show interest, I have no doubt that I can get even the most enthusiastic athletic kid to drop out of phys-ed.

Along these lines, while I have no idea how to instil healthy eating habits and a healthy self-image in a kid, I for sure know how to destroy any desire for healthy foods and shatter any self-image for life.

Thus, while parents may spend a lot of time and effort on schlepping the horse to water, there is little they can do make to actually make it drink – certainly no amount of persuasion, reasoning, or physical harm will have the desired effect. At best, it will come to fear and perhaps shy away from water only to wither away from thirst. While dragging the horse to water provides opportunity, ultimately, it will be the horse who decides whether or not it actually needs a drink.

I think that preferences (including those for foods and activity) are more genetic than we like to think and that if anything, parental modelling (do as I do not as I say) and support are the best we can offer.

I have yet to see orthorexic nutritional coddling translate into anything other than an adult with an unhealthy relationship and preoccupation with food – unfortunately, I have heard far too many stories of how the parental food police (whether qualitative or quantitative) resulted in little more than in “food rebellion”, especially as those kids turn into teenagers and assert their new-found independence.

So if you asked me about parental influences in early childhood – Positive influence? Perhaps – Negative influence? Absolutely!

AMS
Edmonton, AB