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Tuesday, November 10, 2015
Food / Drink ... Health / Nutrition ... Science ...

Here’s another “interesting article” post from me. Yea, yea, I know, people usually do this sort of thing thru Twitter, and do it with a lot fewer words. Seems much more efficient, right? Well maybe, but I try to squeeze all the “juice” that I can out of an interesting article and share it with the world. And that wouldn’t go so well on Twitter. So, here’s another article post for you, this time from the October, 2015 Scientific American (gonna be about science, right?).

This one is called “The Fat Gene”. Sounds like it’s about the question of genetics and obesity — many people claim that obesity is driven largely by genetics and not all that much by eating and exercising habits. Thus, the fact that they are overweight is not their fault. There is some solid evidence for the existence of such “fat genes”, although it remains that for most people, being overweight is driven more by eating and exercise patterns — i.e., too many calories go in, and not enough go out. Although heredity may make it harder for some people than others to maintain a proper weight, in most cases, genes are not destiny with regard to weight.

But the article in question is not about that. Instead, the authors are searching for clues about how modern humans evolved from the great apes and early hominids. Many aspects of our past are written within our genes, and scientists are getting better and better at opening this book and reading it. More and more evidence shows that a gene that regulates uric acid in the body and blood played an important role in distinguishing modern humans from apes. Yes, uric acid, as in “gout”.

It now appears that a mutation in a gene that regulates the production of uric acid (called the “uruicase gene”) happened right at the time when the more generic apes started branching off into differing species. This happened around 18 million years ago, and the resultant species became the orangutan, chimpanzee, gorilla . . . and yes, human. Interestingly, the mutation did not happen to some apes in Africa, where all wild apes are today. Before that time, apes had headed north into southern Europe and western Asia (including Spain and Turkey and Iraq). It was a lot warmer 22 million years ago, and parts of Europe were semi-tropical, just the way that apes like it.

However, over a few million years, things change weather-wise (unlike today, when climate changes over much shorter time-scales, e.g. global warming effects being seen within hundreds and not millions of years). It was getting colder, and the apes, who were designed originally for hot climates, were at a big disadvantage. They didn’t die out from Europe immediately, however; many millennium’s worth of natural selection pressures started to favor those apes whose genes could efficiently store fat. Obviously, the ape that could put on some weight around the belly in the milder years had a better shot at getting through a cold, dry famine period. So, the Euro-ape population increasingly came to possess the “thrifty gene”; this gene did its work by allowing more uric acid to be formed when digesting sweet things. Uric acid works to help the convert sugars into fat.

Unfortunately this had some nasty side-effects such as raising blood pressure and increasing insulin resistance. But hey, back then most apes only consumed a moderate amount of sugar anyway, from whatever fruit they scrounged up. The benefits of putting on the pounds in preparation for the cold and lean years outweighed any problems regarding cardiovascular disease, metabolic problems and diabetes. Hey, hardly any apes lived long enough in the wild to worry about old-age diseases like this.

As it kept on getting colder and colder, the Euro-ape populations shrunk, until by 7 million years ago they were completely gone. Did they just die off? Yes, for the most part; but a handful of them started to migrate south, back toward the land of their distant ancestors. Enough of their progeny survived to re-establish themselves as a viable species in Africa. Actually, though, the tough winter conditions they had been through gave them both mental and physical capabilities that made them a bit better than the other apes who had stayed in the warm jungle or savanna all along. They became the species to beat, the species from which modern humans eventually arose.

So, two interesting points. First off, we sometimes hear it said that every human is ultimately an African. This is probably true, but if you trace where our progenitors had been, then everyone on the planet is also ultimately European !!! When the hominid species later found their way back to Europe (Neanderthals around a quarter million years ago, and modern homo sapies about 50,000 years back), perhaps they experienced a sense of deja vu . . . “you know, it really seems like we’ve been here before”.

Second, and more importantly, this “thrifty fat gene” gives humans increased risk of heart disease and diabetes (and the metabolic syndrome leading up to it). And also obesity, so long as times stay good and famine never strikes. It’s pretty clear that the thrifty gene, and the uric acid that it helps to produce, work in conjunction with the fructose sugar found in fruit. When the only sugar that humans got was from an occasional banana, obesity, heart disease and diabetes weren’t such a big deal. But fast forward to the modern era, when fructose consumption is very high . . . so now you DO have a big problem.

As I discussed recently, over the past 10 years, the notion that fructose (the key component to table sugar) is more damaging than any other carbohydrate has emerged based on preliminary research. A variety of experts pushed back against this idea, claiming that a carb is a carb, and that obesity is entirely a matter of too many calories relative to calorie use. In my opinion, this contention is losing the battle; sugars really are the bad carb. A recent study published by the Mayo Clinic concludes that “added sugar (i.e. sugar added in processed foods including cookies, cakes and soft drinks) is the principal driver of type 2 diabetes and its consequences”.

And now, Scientific American tells us that a study of human evolutionary genetics shows that “as we have added more and more table sugar and high-fructose corn syrup to packaged foods, obesity and diabetes have skyrocketed and average uric acid levels in our blood have increased. By cutting way back on our fructose intake . . . we should be able to protect ourselves from multiple diseases”. Not much doubt is left in my mind. Sugar tastes wonderful, and a VERY little bit of it won’t hurt . . . but get past 5 or 6 total teaspoons a day and it ain’t very good for you (6 teaspoons sounds like a liberal allowance, but that has to include sugar from EVERYTHING, not just soda, candy, cookies and coffee; there’s plenty of sugar in fruit drinks, sauces, catsup, yogurt, milk, most cereals, salad dressings, smoothies, raisins, on and on).

So that’s the interesting article review for today . . . an interesting story about a cold-weather gene mutation in some ancient apes that changed the world and helped to form the bodies that we inhabit . . . for both better and for worse.

◊   posted by Jim G @ 8:05 pm      
 
 


  1. Jim, When it comes right down to it, probably this comment will be a disagreement with the article more than anything else in what follows. Furthermore, I’m not sure I actually understand fully what this article is saying. Is it saying that a “fat gene” causes some people to gain weight and lack of such gene causes others not to gain weight? Is it saying that the change in weather that took place over millions of year caused a mutation affecting uric acid . . . that then lead to gout which somehow caused weight gain when the weather got colder? Something about this article seems to be something like I sometimes think of my own thinking – start with one thing, roam on all over the place, and end up with some tangent that likely makes no sense. (I recognize this impulse as I’m only too guilty of such myself.) Then again, maybe I just missed the idea completely and am not smart enough to “get it”. Could be.

    Basically, when it comes to gaining/losing weight, I have always found the rule is: If I want to lose weight, I should stop eating (so much); if I need to gain weight (ha!), I should eat more. Simple. And basically I think it is just that simple. Sure one might eat more and then exercise the calories off the next day; but in the end it boils down to eat–—gain weight; stop eating—–lose weight.

    There likely are some other contributors to gaining weight for some individuals. It’s often seemed to me that appetite is somewhat like a thermostat: In some people it may be, by gene(s), set higher than in others. If the “thermostat” is set higher, it takes more food for the person to recognize that one should stop eating; thus for such individuals it may be easier to gain weight and harder to lose it.

    As to the whole “uric acid” mutation business, I find it difficult to connect that to weight gain. I *could* see that weight gain would be a benefit when individuals went to colder climates: Adding fat to the body would aid in staying warmer. Those who have pets always know when it’s going to either get cold or warm up by how the pets eat. Warmer weather: Appetite tends to be reduced. Colder weather: Pets can’t seem to get enough to eat. Seems pretty simple and it makes sense.

    I certainly can understand the point about famine: The more weight one has the longer one will live in a famine. However, oddly enough, I remember some years ago reading a book about WWII where people were starving due to the war. Surprisingly, the book indicated that people who weighed more, actually were obese, wanted to eat more regardless of how much food was available for all. People went so far as to steal food from those who were already near starvation, which made me think of the “thermostat” idea that continued to function even to the point of taking food from starving people even when one had extra weight that could sustain one.

    Another question about this article is: If one talks “mutation”, doesn’t one suppose that change happens quickly? “Millions of years” seem to me to be more of an “evolution thing” than a “mutation thing”.

    As to the “fat gene” causing obesity, heart disease, diabetes, etc.: Perhaps. But I wonder what consideration was given to such things as smoking, drug taking, and other such addictions. An “addiction gene” often seems to make more sense to me when it comes to obesity: Considering the desire for food to the point of overeating excessively with all the other addictions. A “little” of most things will not cause serious harm to the body in most cases (except poisons); but a “lot” of most things can cause problems of one kind or another in a great many cases.

    Then too, I’ve entered my 82nd year and have consistently eaten a dessert after every meal in my life (well, at least as far back as I can remember; after 40 or 50 years one tends to forget and put other things in the place of what has been forgotten). I’m 100% sure I’ve eaten way too much sugar, according to the “standards” of what one should eat. Yet, somehow or other I’ve made it this far – and been surprised and wondered why those much younger than I have died when I’m still here. It might be I may be at the end and there is not too much farther for me to go; but

    Somewhere in all this I think the “fat gene” is perhaps someone’s idea for a good dissertation—along with so many of the other ideas of what and how to eat, what’s good for one to eat and what’s not good for one to eat.

    And while I’m roaming in my thinking about this topic, I often think that much of our culture is based on being “thin” as beauty. However, in some countries being “fat” is considered desirable as it indicates a show of wealth—a person has enough money to actually buy food and gain weight. Much of how one looks, especially when it comes to weight is a cultural thing as I think about it.

    (And as a side issue here, I cannot resist this: It’s my opinion that the tendency to exert pressure on new mothers to lose the “baby weight” very quickly after giving birth will ultimately be a harmful thing for women. Again here is a cultural thing: an idea of how women *should* look. Doctors say: “It takes 9 months to put on the weight; it should take 9 months to lose the weight.”)

    I might also say that it might be a really dull world if everybody weighed just precisely the right weight he/she should weigh. Maybe a few “fat genes” add to the variety of individuals, much like all the other variations individuals have. A variety of individuals is much more interesting than everybody looking alike. Again, this is simply my approach to this topic; and I could very well be totally wrong. Yet, I do not think this article has the answer to the problem of people being fat either.

    I’ve roamed all over the place in this comment, much like my criticism of the article; so I’ve likely had no good argument regarding that point.

    However, I’d still like someone to set up a good study on food as an addiction and/or a study of a “thermostat”-type something in the body that acts as an indicator of when someone has had enough to eat in the eating process. Maybe the two ideas are the same; maybe they are different. That’s another study that may be useful (well, as I see it). MCS

    Comment by Mary S. — November 13, 2015 @ 3:42 pm

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