Some weeks ago I had a wonderful discussion with Suvrat, who has rapidly uplifted the quality of discussion on geological/earth sciences, paleontology, evolution and whatnot. My own interest in the geological sciences came through an interest in paleontology which comes from a serious interest in and study of evolution. So it is an absolute pleasure to discuss "naive" questions on geology, different type of deposits and beds and fossils with someone who actually knows what he is talking about, and Suvrat is exactly that. For my simple (and sometimes simplistic) questions, Suvrat patiently wrote back in magnificent detail explaining and clarifying broad questions in geology (and research in those areas in India), filling his answers with personal perspective. I thought snippets of the whole thread would be of significant interest to readers of this blog who cannot but have been fascinated by dinosaurs and moving continental plates and changing worlds.
The discussion started when I wrote to him about this discovery of some fossils in India, which showed a prehistoric snake devouring dinosaur eggs. A spectacular finding, it gave a new perspective on snakes millions of years old, and how they evolved over time. Now, the fossils were discovered in Gujarat, in what are called the Lameta Formation beds. These beds were formed over 67 million years ago, in the late Cretaceous era, amongst the oldest such formations still around in south Asia. I knew nothing about this region itself, and in general the state of paleontology and geology in India and other parts of South Asia, and this piqued my interest so I asked Suvrat:
".....are there any parts of south Asia where they've found fossils and deposits from Paleozoic (particularly Cambrian) or even Precambrian eras? I'm guessing, particularly because of the climate (and geology) it might be hard to find remains and fossils from those eras. But is there anything like the Burgess shale in south Asia?........also, parts of China and Mongolia have yielded spectacular remains of Cretaceous as well as Cenozoic stuff. Do you think parts of south Asia (like the Lameta beds) might hold some treasures like those parts? Finds from here might help piece together evolutionary bits, particularly since the Indian subcontinent split off from Gondwanaland somewhere in the mid Cretaceous. So presumably (and if you're very lucky) you could find some really interesting fossils and look and see how they compare with fossils on either side of Gondwanaland and Laurasia, and stuff in between. What do you think?"
To this Suvrat patiently came up with a beautiful bite-sized "dummies" post about Cambrian and pre-Cambrian sediments in India:
".....Throughout much of the Paleozoic the Peninsular Indian continent was part of Gondwanaland, surrounded by what would become Antarctica, Australia, Africa. So there were no marine incursions and no marine sediments were deposited. So (there is) no chance of a Burgess type deposit in S. Asia. There is Cambrian sediment northwards in the Himalayas but that is crumpled and metamorphosed, so if it did contain exceptional fossil beds like Burgess, they have been destroyed.
There is plenty of Precambrian sediment all over the Indian continent. The most promising for animal fossils is the Vindhyan basin. There is Proterozoic sediment there but the Neo-Proterozoic where early animal evolution unfolded is not very well represented and has not yielded too much in terms of animal body fossils. Some tracks and trails have been found but their significance is debated. So there is some scope for further surprises there. This post give a flavor of the controversies regarding the Vindhyans.
As Gondwanaland began to split up the eastern margin of the future Indian continent rifted earlier. Here continental interior basins developed filled by fluvial sediments (a lot of India's coal is from these basins). These contain abundant plant fossils which have Gondwanaland affinities i.e. they are similar to ones found in Antarctica and Australia. So the plant fossil record does tell us about this ancient geography and evolutionary relationships of floral groups. Later the western margin of the Indian continent rifted from Africa and marine basins developed in Rajasthan, Gujarat and M.P. There is a thick Jurassic marine fill and thinner Cretaceous marine sediment. There is Cretaceous sediment is south India on the eastern margin. These deposits have been studied quite extensively and their fossil record is being studied as part of the larger paleo-geographic framework."
Coming to the spectacular fossil finds in Gujarat that the paper discusses Suvrat continues "...the Lameta are mostly marginal marine and terrestrial deposits ...the last stage of deposition in western India before the Deccan volcanism. Being terrestrial deposits the fossil record is not as rich as marine sediments since the chances of fossils getting destroyed in terrestrial settings is higher. However as the recent find shows, freakish events like mudslides, floods, river banks caving in and so on can preserve spectacular examples. So while the background rate of fossil preservation is not that good, there is always a chance of a catastrophic event entombing entire horizons.
In a sense we are lucky to have the Lameta at all. These deposits are quite thin, just a few meters of so and would have surely been completely eroded away by now. But the Deccan volcanics over much of Cenozoic have encased them in a protective shell and saved them from destruction. So a Chinese basin type preservation (in the Lameta) is not out of the question. We need to conserve whatever good localities are available for further study. "
His last lines were obviously a red flag for more questions from the ever curious and persistent schoolboy (me). So I asked:
"...........Is anything like that ever likely to happen in India? For all its faults in other spheres, China has done spectacularly not only to preserve its fabulously rich geological basins (which are fossil treasure troves), and has also developed a strong community of Chinese paleontologists and geologists who are making some spectacular contributions to science. Paleontology or geology are hardly significant professions for anyone in India.....it is a "no scope" profession. Similarly, there are so many sites in the US (from the badlands in the Dakotas all the way down south to sites in Oklahoma and Texas) that have not only been reasonably well preserved, but where American geologists and paleontologists have been given unrestricted access and lots of funding to carry out their research. I'm pretty sure a researcher in India will struggle to carry out any field trips in these fields, and the Indian government can sometimes make it very difficult for foreign scientists to carry out field research in India (for various reasons). So how do you see things in India, and where do you see things going towards?"
Suvrat comes up with even more perspective, and ends on an optimistic note:
"........Over in India we have strong social pressures to take up Medicine, Engineering, MBA ...but not pure science and certainly geology ranks lower in the sciences as well. China probably has suffered less of that historically and so plenty of really bright Chinese students take up geology and the result combined with adequate government support is the world class research coming out of their labs. There may be another economic angle to this. Historically, salaries in China were more equitable across all professions (that has changed recently) ..and so a doctor in practice probably did not make that much more than a geologist teaching at a State Univ. In India there always have been great differences in income, based on profession. Geology jobs for long until recent were with the government and salaries modest. On the other hand a doctor or a lawyer or a MBA always made more money. I wrote a post sometime back speculating why Bengali geologists published more in top class research journals in sedimentary geology than other ethnicities in India, outlining some of these issues."
But then there is the key question of site preservation. Most of us know how abysmally historic sites are protected in India. Geologically/Paleontologically spectacular sites unfortunately aren't necessarily breathtakingly beautiful forests or mountains, but are often what look like "waste/fallow land". Secondly, there is a massive construction boom in India which demands both land and material (for bricks, stone etc). All of this obviously encroaches on these lands. Here is Suvrat's perspective on those sites in India:
".....those kinds of geology parks do exist in India but enforcement is non -existent. I have had two bad experiences. One in Jabalpur, coincidentally in the Lameta beds. That was during college a couple of decades ago and the outcrop already showed signs of being worn away by human activities and the threat of encroachment from slums. The second is at Gilbert Hill (Andheri) Mumbai which is a great example of columnar jointing in basalts but also is the de-facto toilet of the surrounding slums. Both sites are officially geology heritage sites but neglected. Recently there was a report on how Jurassic rocks containing fossils from the Rajmahal hills in Jharkhand are being used for construction purposes despite pleas from geologists for protecting at least part of the site. So that awareness and political clout to protect these sites as national monuments and for science just does not exist in India for now." Think about that. A magnificent and rare geological formation right in the middle of Mumbai, which, with some vision could be made into a national monument type public park! But even before that happens, the site may be lost for ever by a city with a voracious appetite.
But Suvrat ends with on an optimistic note. " ..........the good news is that geology salaries are going up. A lot of private companies in mining and petroleum are setting up shop and geologists make a good income both in production and in R and D. Add to that because of environmental concerns and groundwater in particular the need for good geology expertise is being recognized. So "saving the earth" or "save India from climate change" may be a good theme to use to educate people about the importance of geology and chip away at the age old social reluctance to see geology as a top profession and encourage bright young students to pursue it as a career."
I share some of Suvrat's optimism in that private stake holders (including big oil) have made some spectacular finds in geology, and have often worked to protect it. But will it happen in India, or will those geological and paleontological scientific treasures be lost even before they are found and studied?
Saturday, April 17, 2010
Thursday, April 01, 2010
Eating high fructose corn syrup makes Yogi bear.......
.......fatter than the average bear.
Apologies for that awful title that I couldn't resist.
If you are fond of sweets, chocolates, candy, cookies and ice cream, and have ever read the label for the ingredients, you must have noticed one of them, called high fructose corn syrup (HFCS). You might have wondered about it a little, or just thought that fructose is sweet like glucose, and gone on with your indulgence. HFCS has now largely replaced table sugar (or sucrose) as the main sweetener in most confectioneries sold in most stores. A huge reason for this has been the easy availability of the vast quantities of corn grown in the US, from which high fructose corn syrup is extracted, making it cheaper than sucrose. While there has been speculation for a while (and increasing correlative data) suggesting that HFCS may increase obesity or other health problems related to sugar, much of this has been decried by the food industry.
However, the data is slowly shifting towards the adverse health effects of HFCS. A recent paper in Pharmacology Biochemistry and behavior (Bocarsly et al, http://dx.doi.org/10.1016/j.pbb.2010.02.012) now suggests that HFCS causes the characteristics of obesity, from increases in body weight to increased triglycerides in the blood.
Let's take a look at what this study shows.
The researchers studied the effects of HFCS in captive rats. Their experiments were simple. They fed groups male or female rats, either normal rat chow, or rat food mixed with sucrose (sugar), or rat food mixed with equal amounts (and calories) of HFCS (and each sample size was ten rats). They varied their experiment so that the rats could eat HFCS with every meal, or HFCS was provided only for 12 hours during the day. They carried out these studies over a short time frame (two months) as well as a longer time frame (6 months). Here is the rationale behind this experiment. The experiment not only tested if HFCS could cause increase in weight, but compared it directly with consuming table sugar, sucrose. Now sucrose is a compound that is made of one molecule of glucose and one molecule of fructose. So when sucrose is broken down, it breaks down to fructose and glucose. Secondly, the process by which glucose and fructose are broken down are similar, and the amount of energy they each can release is the same. HFCS has around 55% fructose and 45% glucose. So the food industry has always claimed that using sucrose, or using an equivalent amount of fructose would be biologically very similar. However, when rats were fed either regular food, or food + sucrose, or food + HFCS, the results were quite different.
Here is what the experiment unambiguously revealed.
The male rats fed HCFS gained more weight than mice fed with regular chow or chow supplemented with sugar even over a two month period. Over a six month period, this weight gain in male rats was very significant when compared with rats eating regular chow. In male rats, after 6 months of these diets, the rats on HFCS weighed on average a 100g more than rats fed on regular food. Female rats also gained weight eating HFCS, but at a lower rate than males. After a 7 month duration on these diets, the rats fed with normal food weighed 177% over baseline. However, the rats with continuous access to HFCS were ~200% heavier than baseline. There were a few other interesting observations, indicative of the effects of HFCS on obesity. In both male and female rats, the increase in body weight was accompanied by an increase in actual abdominal body fat, as well as increased triglycerides. So if the same effects hold for humans, the weight gain would primarily be around the abdominal region.
There remain some limitations in this study. The dramatic increases in body weight as well as abdominal fat was observed in rats that had food + HFCS available continuously. In female rats that had access to HFCS only for 12 hours during the day (for a long duration) did not show those dramatic weight increases. However, male rats even with controlled access to HFCS showed this increase in abdominal fat accumulation. Since we care about human consumption of HFCS, does human consumption of HFCS reflect tightly controlled access to it, or a constant availability of HFCS with any meal? Secondly, there will be some differences in the rates of metabolism of glucose and fructose between humans and rats. However, the broad processes of absorption and breakdown of these nutrients are very similar in us and in rats, so it is quite likely that this general phenomenon will hold true in humans. But doing these experiments in humans (where a long term study could be five or ten years) would be extremely difficult to control. Secondly, the experiments were done in rats kept in cages in a laboratory. One could argue that there is clearly nothing in common between laboratory rats and humans. These rats exercise very little and are largely sedentary. They don't run around as much as they should, are already somewhat obese even before feeding on HFCS, and have fairly unlimited access to food and can eat whenever they want to, and as much as they want to in one sitting. Surely that can't be the way humans live. Oh but wait a minute!
The authors in their discussion speculate on why HFCS might cause increased body weight gain when compared to regular food or even food supplemented with an equivalent amount of sucrose, but their discussion only briefly touches on aspects of sugar metabolism that could explain this. So I'll elaborate a little more, and add some of my own speculation based on how these sugars are metabolized. In short, it all comes down to the body's way to regulate sugar levels, sense how much is there, and feedback to control the effects of these sugars.
Firstly, glucose and fructose are absorbed very differently. Glucose is absorbed early in the small intestine, while fructose is absorbed later. But the big difference comes in how and where the two sugars, as well as sucrose itself are metabolized. Sucrose has to be broken down in the stomach into glucose and fructose before it can be used. Glucose can be used by just about every cell in the body through a process called glycolysis, to break it down into usable energy. The process of glucose breakdown is a very tightly regulated process called glycolysis. In this process, a key regulatory step happens when glucose is converted to another sugar called fructose-6-phosphate, and then to another sugar called fructose-1,6-bisphosphate, which is then broken down into triglycerides and then energy. Now, the enzyme that does this conversion to fructose-1,6-bisphosphate is called phosphofructokinase and it is highly and exquisitely regulated by multiple inputs, including other co-factors as well as other modifications. This allows the cell to tightly and precisely control how much glucose is broken down. Fructose however is broken down not in all cells but largely only in the liver through a process called fructolysis. Here, instead of fructose being converted to fructose-6-phosphate, and then being tighly regulated in its conversion to 1,6-bisphosphate and later triglycerides, it is converted into a similar (but biologically very different) sugar called fructose-1-phosphate. This small change in the position of that single phosphate group makes a huge difference biologically, since the breakdown of this sugar into triglycerides happens very quickly and easily, and is not tightly controlled by many inputs. The result of this is that fructose is very rapidly and easily broken down into triglycerides which can then be used for energy, or be converted into glycogen or fats for storage. While the eventual outcome of glucose and fructose is similar, the way the two are regulated and controlled is very different. In other words, the body has much more control over how fast glucose is broken down, but far less control over fructose breaking down.
So this phenomenon, combined with the fact that HFCS has over 55% fructose, and 45% glucose means that the body is dealing with a much higher ratio of fructose to glucose when compared with just plain old table sugar (sucrose). The difference is small over a few meals, but over a long period of time, this adds up to quite a lot. Also, what this difference in circulating glucose (that is regulated and not tightly broken down) does is change the way the body responds to feeding. Glucose controls insulin release, which in turn controls a hormone called leptin, which controls apetite and satiety in the brain. Now, this small but continuous difference in fructose/glucose ratios (comparing HFCS to sucrose) alters how much circulating glucose remains in the blood, which can alter leptin levels as well as leptin sensitivity, and this finally alters the brain's ability to be satiated after a meal. Over time, HFCS could change the satiety achieved by eating, and also finally alter eating patterns. All this put together could cause the increase in body weight seen over time.
Of course, there will be people unsatisfied with these data. But the data is suggestive, and this idea is compelling.
Miriam E. Bocarslya, Elyse S. Powella, , Nicole M. Avenaa, and Bartley G. Hoebel (2010).
High-fructose corn syrup causes characteristics of obesity in rats: Increased body weight, body fat and triglyceride levels Pharmacology Biochemistry and Behavior
Apologies for that awful title that I couldn't resist.
If you are fond of sweets, chocolates, candy, cookies and ice cream, and have ever read the label for the ingredients, you must have noticed one of them, called high fructose corn syrup (HFCS). You might have wondered about it a little, or just thought that fructose is sweet like glucose, and gone on with your indulgence. HFCS has now largely replaced table sugar (or sucrose) as the main sweetener in most confectioneries sold in most stores. A huge reason for this has been the easy availability of the vast quantities of corn grown in the US, from which high fructose corn syrup is extracted, making it cheaper than sucrose. While there has been speculation for a while (and increasing correlative data) suggesting that HFCS may increase obesity or other health problems related to sugar, much of this has been decried by the food industry.
However, the data is slowly shifting towards the adverse health effects of HFCS. A recent paper in Pharmacology Biochemistry and behavior (Bocarsly et al, http://dx.doi.org/10.1016/j.pbb.2010.02.012) now suggests that HFCS causes the characteristics of obesity, from increases in body weight to increased triglycerides in the blood.
Let's take a look at what this study shows.
The researchers studied the effects of HFCS in captive rats. Their experiments were simple. They fed groups male or female rats, either normal rat chow, or rat food mixed with sucrose (sugar), or rat food mixed with equal amounts (and calories) of HFCS (and each sample size was ten rats). They varied their experiment so that the rats could eat HFCS with every meal, or HFCS was provided only for 12 hours during the day. They carried out these studies over a short time frame (two months) as well as a longer time frame (6 months). Here is the rationale behind this experiment. The experiment not only tested if HFCS could cause increase in weight, but compared it directly with consuming table sugar, sucrose. Now sucrose is a compound that is made of one molecule of glucose and one molecule of fructose. So when sucrose is broken down, it breaks down to fructose and glucose. Secondly, the process by which glucose and fructose are broken down are similar, and the amount of energy they each can release is the same. HFCS has around 55% fructose and 45% glucose. So the food industry has always claimed that using sucrose, or using an equivalent amount of fructose would be biologically very similar. However, when rats were fed either regular food, or food + sucrose, or food + HFCS, the results were quite different.
Here is what the experiment unambiguously revealed.
The male rats fed HCFS gained more weight than mice fed with regular chow or chow supplemented with sugar even over a two month period. Over a six month period, this weight gain in male rats was very significant when compared with rats eating regular chow. In male rats, after 6 months of these diets, the rats on HFCS weighed on average a 100g more than rats fed on regular food. Female rats also gained weight eating HFCS, but at a lower rate than males. After a 7 month duration on these diets, the rats fed with normal food weighed 177% over baseline. However, the rats with continuous access to HFCS were ~200% heavier than baseline. There were a few other interesting observations, indicative of the effects of HFCS on obesity. In both male and female rats, the increase in body weight was accompanied by an increase in actual abdominal body fat, as well as increased triglycerides. So if the same effects hold for humans, the weight gain would primarily be around the abdominal region.
There remain some limitations in this study. The dramatic increases in body weight as well as abdominal fat was observed in rats that had food + HFCS available continuously. In female rats that had access to HFCS only for 12 hours during the day (for a long duration) did not show those dramatic weight increases. However, male rats even with controlled access to HFCS showed this increase in abdominal fat accumulation. Since we care about human consumption of HFCS, does human consumption of HFCS reflect tightly controlled access to it, or a constant availability of HFCS with any meal? Secondly, there will be some differences in the rates of metabolism of glucose and fructose between humans and rats. However, the broad processes of absorption and breakdown of these nutrients are very similar in us and in rats, so it is quite likely that this general phenomenon will hold true in humans. But doing these experiments in humans (where a long term study could be five or ten years) would be extremely difficult to control. Secondly, the experiments were done in rats kept in cages in a laboratory. One could argue that there is clearly nothing in common between laboratory rats and humans. These rats exercise very little and are largely sedentary. They don't run around as much as they should, are already somewhat obese even before feeding on HFCS, and have fairly unlimited access to food and can eat whenever they want to, and as much as they want to in one sitting. Surely that can't be the way humans live. Oh but wait a minute!
The authors in their discussion speculate on why HFCS might cause increased body weight gain when compared to regular food or even food supplemented with an equivalent amount of sucrose, but their discussion only briefly touches on aspects of sugar metabolism that could explain this. So I'll elaborate a little more, and add some of my own speculation based on how these sugars are metabolized. In short, it all comes down to the body's way to regulate sugar levels, sense how much is there, and feedback to control the effects of these sugars.
Firstly, glucose and fructose are absorbed very differently. Glucose is absorbed early in the small intestine, while fructose is absorbed later. But the big difference comes in how and where the two sugars, as well as sucrose itself are metabolized. Sucrose has to be broken down in the stomach into glucose and fructose before it can be used. Glucose can be used by just about every cell in the body through a process called glycolysis, to break it down into usable energy. The process of glucose breakdown is a very tightly regulated process called glycolysis. In this process, a key regulatory step happens when glucose is converted to another sugar called fructose-6-phosphate, and then to another sugar called fructose-1,6-bisphosphate, which is then broken down into triglycerides and then energy. Now, the enzyme that does this conversion to fructose-1,6-bisphosphate is called phosphofructokinase and it is highly and exquisitely regulated by multiple inputs, including other co-factors as well as other modifications. This allows the cell to tightly and precisely control how much glucose is broken down. Fructose however is broken down not in all cells but largely only in the liver through a process called fructolysis. Here, instead of fructose being converted to fructose-6-phosphate, and then being tighly regulated in its conversion to 1,6-bisphosphate and later triglycerides, it is converted into a similar (but biologically very different) sugar called fructose-1-phosphate. This small change in the position of that single phosphate group makes a huge difference biologically, since the breakdown of this sugar into triglycerides happens very quickly and easily, and is not tightly controlled by many inputs. The result of this is that fructose is very rapidly and easily broken down into triglycerides which can then be used for energy, or be converted into glycogen or fats for storage. While the eventual outcome of glucose and fructose is similar, the way the two are regulated and controlled is very different. In other words, the body has much more control over how fast glucose is broken down, but far less control over fructose breaking down.
So this phenomenon, combined with the fact that HFCS has over 55% fructose, and 45% glucose means that the body is dealing with a much higher ratio of fructose to glucose when compared with just plain old table sugar (sucrose). The difference is small over a few meals, but over a long period of time, this adds up to quite a lot. Also, what this difference in circulating glucose (that is regulated and not tightly broken down) does is change the way the body responds to feeding. Glucose controls insulin release, which in turn controls a hormone called leptin, which controls apetite and satiety in the brain. Now, this small but continuous difference in fructose/glucose ratios (comparing HFCS to sucrose) alters how much circulating glucose remains in the blood, which can alter leptin levels as well as leptin sensitivity, and this finally alters the brain's ability to be satiated after a meal. Over time, HFCS could change the satiety achieved by eating, and also finally alter eating patterns. All this put together could cause the increase in body weight seen over time.
Of course, there will be people unsatisfied with these data. But the data is suggestive, and this idea is compelling.
Miriam E. Bocarslya, Elyse S. Powella, , Nicole M. Avenaa, and Bartley G. Hoebel (2010).
High-fructose corn syrup causes characteristics of obesity in rats: Increased body weight, body fat and triglyceride levels Pharmacology Biochemistry and Behavior
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