Monday, March 22, 2010

Obesity & Heredity, Part 2: You Are What Your Parents Ate

Stephan Guyenet at Whole Health Source wrote a brilliant blog series a few months back, called “The Body Fat Setpoint,” in which he describes the mechanisms behind an individual's ability to maintain a  very specific weight.  No matter how much a person overeats and how much weight is gained, his or her body is simply primed to be at this “setpoint” and will “defend” it diligently through natural fat regulation mechanisms.  Stephan references a study where:

They overfed lean and modestly overweight volunteers 50% more calories than they naturally consume … After 6 weeks of massive overfeeding, both lean and overweight subjects gained an average of 10 lb (4.6 kg) of fat mass and 6.6 lb (3 kg) of lean mass...  Following overfeeding, subjects were allowed to eat however much they wanted for 6 weeks. Both lean and overweight volunteers promptly lost 6.2 of the 10 lb they had gained in fat mass (61% of fat gained), and 1.5 of the 6.6 lb they had gained in lean mass (23%).  

To me, the most interesting aspect regarding human overfeeding studies like this is that, once the overfeeding period has ended, the participants return to their original weight without dieting.  As Stephan indicates, this means that our bodies have the inherent ability to maintain our “normal weight.”  Refer to the post I wrote on tribal fattening practices and the fact that the fattened women who refuse to overeat their real foods diet return to a healthy weight in short order.  Normal weight, however, appears to be different for every individual. For example, when a person has a normal weight – a setpoint – that, by all standards, can be seen as obese, we are left with the question of just why in the heck this is happening.  Why does the body insist on remaining in such a biologically abnormal state?

Many scientists and researchers claim that leptin – a hormone which regulates appetite – plays a key role in obesity, as many people who are overweight exhibit low levels of the hormone.  Much research has been conducted on the validity of this theory and it is now recognized that leptin resistance – in which the body can no longer can recognize when it has had enough food – is what enables a person to eat more than they need, thus leading to obesity and keeping that person obese.  And, surprise, surprise: artificial fructose is a prime culprit in leptin resistance because fructose doesn't stimulate leptin (or insulin for that matter).  No stimulation, no appetite regulation.

Skinny Jeans & Skinny Genes

Okay, so leptin appears to play a role in weight maintenance.  That's all fine and good, but why can some people eat and drink whatever they want -- including artificial fructose -- without affecting their body composition while some people become obese?  This is where I believe heredity comes into play.  Depending on what stage of degeneration a person is in – first, second, or third generation of processed food consumption, let's say, and/or what a person's mother ate while pregnant with him/her – obesity can be more or less of a potential complication.

In my case, for example, my mother wasn't overweight when I was in the woom and neither of my parents are overweight now.  This is despite consuming a lot of high-fructose corn syrup and omega-6 vegetable oils for much of their lives.  I was raised on this typical industrial diet and never experienced issues of overweight as a child, and I have no issues now.  At age 18, I altered my diet and cut out processed foods, which is how I eat now, eight years later.  But my older brother, now age 29, has continued to eat our childhood foods without gaining significant weight.  Other health problems aside, my family has no weight issues.  Is there something about us genetically that is behind all of this?  I think it's a strong possibility.  And maybe this is because, like Don Gorske, we may have a closer-to-pure hereditity.  We are not yet degenerated to the point where the disease of obesity has set in.

In contrast, I know of a few childhood friends (two brothers) who now appear to be on the receiving end of metabolic discord through familial degeneration.  In their twenties now, they are both experiencing weight problems.  They also drink a lot of beer and don't seem to have the best diet in the world.  Observing their parents, the mother has been overweight for at least half of her life (including several years before becoming pregnant) and the father has always been slim, despite drinking a lot of beer and not having the best diet in the world just like his sons.  Why is dad slim while having very similar dietary habits to his overweight sons?  Are his genetics more pure and less degenerated – less overall processed food consumption – than the mother's genes, which appear to have a hereditary predisposition to being overweight?  This may be the case, and it would explain the weight issues of the two sons, as they would inherit half of their mother's genes.        

Several studies have been done evaluating the role heredity may play in obesity.  The most compelling subset of these studies are those that include data from adopted children, their adoptive parents, and their biological parents.  Here's an abstract from one of these of these studies, called “Genetic contributions to human fatness: an adoption study:”

A strong relationship was found between the degree of fatness of biologic mothers and that of their adult offspring who had been separated from their mothers at birth and adopted during the first year of life. This relationship persisted even after age, height, and possible confounding environmental factors were controlled. There was little evidence for either selective placement on the basis of parental fatness or gene-environment interaction. There was no relationship between the degree of fatness of adoptive parents and that of the adoptees.

It's interesting that the weight of the child was directly affected by the weight of the biological mother and is not affected by the environment of the adoptive home.  This supports my theory on the two sons who I described above.  There is, however, one glaring confounding factor in all of this talk about obesity and heredity, and that is the increasing consumption of high-fructose corn syrup in the last 30 years.  This amazingly effective human fattener was not significant in the industrialized diet until 1980, when Coca-Cola officially began adding this biochemically engineered sweetener to its popular soft drink.  This also happens to be the time when obesity levels really began to take off.  Check out the graph below from the paper, “High-fructose corn syrup in beverages may play a role in the epidemic of obesity:”


So does that mean that heredity may not be as important as diet in the development of obesity?  Not necessarily.  I believe the two go hand-in-hand and, as I said earlier, it's possible that it is heredity and the diet of the mother which determines susceptibility to the effects of HFCS or other processed foods.

So what lesson have we learned here?  Well, there's still a lot of questions, but I think we can safely say that some people have more difficulty with weight than others, and that reason may not necessarily be connected to dietary choices in all cases.  Rather, there are several lifetimes of degeneration that may be influencing each individuals propensity to gain – and keep on – the fat.

For solutions to inherited susceptibility to obesity, I refer you back to Stephan, who I think provides some good advice.  As far as my recommendations, the best change anyone can make in their diet to make a difference in health, and perhaps body composition, is to simply eliminate the four nasties: artificial fructose, gluten, trans fats, and vegetable oils.  Eat real food.  And please, please, please raise your children on real foods so they don't have the same health difficulties that many of us adults have!  

16 comments:

Beth@WeightMaven said...

Have you read about Pottenger's cats? His work has been criticized for a variety of (legitimate) reasons, but I still find the concept interesting -- nutritional deficiencies are progressive. Later generations suffer from more problems than did their parents.

So maybe it's not just genetics that may predispose someone to obesity like eye color is passed along, but it's also the stage of "disease" in your family.

Then again, perhaps it's just as simple as prenatal factors, especially diet of the mother.

Go figure. In my generation, our mothers smoked and drank booze. But maybe drinking soda and eating McDs might be more problematic!

Ryan Koch @ Health Matters to Me said...

Hi Beth,

Yes, I've read Pottenger's cats -- what a fascinating study! While it has its flaws, it is certainly thought-provoking in the sense that it shows how degeneration happens and how regeneration happens. If I remember correctly, it takes four generations to fully regain optimal genetic development. I wonder if that's goes for humans as well ...

I agree with your other points about disease stages and prenatal factors, as these things also are closely connected with epigenetics (how lifestyle and environment can change our genes).

Anonymous said...

Ryan, I don't under your distinction, using "artificial" in front of fructose. Clarification?

Ryan Koch @ Health Matters to Me said...

Anonymous,

I can understand how that phrasing would be confusing. What I mean by "artificial fructose" is the kind of fructose that is biochemically engineered. In order to make certain kinds of sweeteners, like HFCS and crystalline fructose, certain enzymes are used to alter the original products significantly. I see this as an artificial way of creating a food, as the sugars are broken down into very unnatural and isolated components -- then they are mixed back together to achieve whatever ratio is desired (usually 55:45, fructose:glucose for HFCS).

While a refined sweetener like sugar is, at the least, a nutrient displacer in the diet, enzymatically engineered fructose has known detrimental health effects, such as obesity, diabetes, liver damage, and the like.

Hope that clears things up.

Anonymous said...

Thanks Ryan. I think I understand you to be saying artificial fructose is particularly harmful, but you're not saying real sugar (ex: honey) is not necessarily good for us.

I'm a new reader, and have just begun to dig through the archives. So far, so good!

Our family gave up gluten and it was one of the best things we've done. We resisted the temptation to replace the gluten with a ton of GF processed foods, and we are trying very hard to eat real food. We are in the kitchen....a lot.

Anonymous said...

I wrote:

"I think I understand you to be saying artificial fructose is particularly harmful, but you're not saying real sugar (ex: honey) is not necessarily good for us."

Sorry about the typo...

...but you're not saying real sugar (ex: honey) is neccessarily good for us.

Ryan Koch @ Health Matters to Me said...

Right. HFCS and other forms of artificial fructose are bad news. And while real sugar and honey are not necessities in the human diet, I don't think there's any problem with consuming them. There's not really any research out there that I know of showing unrefined sugar and honey to be detrimental to health. Although eaten in large quantities, it's possible that they could be for the simple reason that they displace other much-needed nutrients in the diet. In other words, if you eat more honey, you might eat less meat, milk, and butter.

Stephan at Whole Health Source posted a paleo diet study a while back where the participants actually ate quite a bit of honey and still saw major health improvements. Refer to his post here and the study here.

That's great that you and your family cut out gluten. I think this simple change would benefit a lot of us immuno-comprimised moderns.

Glad to hear that you're enjoying the blog!

Anonymous said...

Ryan wrote:

"Many scientists and researchers claim that leptin – a hormone which regulates appetite – plays a key role in obesity, as many people who are overweight exhibit low levels of the hormone. Much research has been conducted on the validity of this theory and it is now recognized that leptin resistance – in which the body can no longer can recognize when it has had enough food – is what enables a person to eat more than they need, thus leading to obesity and keeping that person obese."


If leptin resistance causes a person to overeat, doesn't that just bring us back to "fat people eat too much"? It seems to me there has to be more going on at the cellular level, which is broken.

Swede said...

Two words clear this up:

mitochondrial DNA...

This is the eugenic expression, the phenotype that is transferred between generations, based on the mother's health.

"unlike nuclear DNA which is equally inherited from both father and mother, mtDNA is inherited only from the mother, because all our mitochondria are descended from those in our mother's egg cells."

This is a unique genetic transfer that is related to the mother. I suspect it has to do with the fact that (obviously) the female's health is relative to the offspring's health because she can reflect biological availability of nutrients.

Scott

Ryan Koch @ Health Matters to Me said...

Anonymous,

You're right, it does bring us back to "fat people eat too much." As far as I understand, leptin is the mechanism that allows overeating to happen and keeps some overweight people at their heavier weight. It's not that they eat too much, they just eat enough to keep their weight stable. Leptin resistance goes hand-in-hand with insulin-resistance -- which is certainly damage at the cellular level -- and can play a role in how the body stores and accumulates fat.

There are multiple facets to obesity, and a lot of it starts because of the increasingly unnatural diet people are eating. And a lot of it starts, as this series suggests, because of heredity and generations of poor diet.

Swede,

Nice. Thanks for adding that. Makes a lot of sense as to why my childhood friends took on the body tendencies of their mother but not their father. The more I look into the obesity-heredity connection, the more I understand information like this.

Another big thing is epigenetics, which can implicate the father in addition to the mother in terms of what we do or do not inherit. That post is coming soon.

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Eva said...

I think we need to watch making an overemphasis on weight. My mother has a bit of fat on her at 73 years old. Whereas my boss's wife at the same age looks trim and healthy. People assume the trim woman to be healthy but she actually has raging blood glucose problems that are not in good control. She is often very sick, often having too high bg and many times having collapsed from too low bg, plus other problems. Whereas my mother is very healthy and spry and was just the other day mixing cement in the wheelbarrow by herself in order to fix some holes along the fence line. Body weight is not the only sign of health and many thin people are in fact more frail and sick than many fat people. Some people think fat gain is actually a protective measure against metabolic syndrome and although correlated, is not the cause at all. That would indicate that those who can't get fat despite poor diet might be at greater risk for more dangerous levels of metabolic syndrome.

vitamin c said...

Both of my parents now are obese but during their younger years they have the same body built like mine, a thin body. I want to believe that it is hereditary because whatever food and vitamins I take, still I'm having a hard time gaining weight.

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