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  #1   ^
Old Tue, Sep-24-19, 03:03
Demi's Avatar
Demi Demi is offline
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Default Today's obesity epidemic may have been caused by childhood sugar intake decades ago

Quote:
From Science Daily

Today's obesity epidemic may have been caused by childhood sugar intake decades ago

Current obesity rates in adults in the United States could be the result of dietary changes that took place decades ago, according to a new study published by researchers at the University of Tennessee, Knoxville.

"While most public health studies focus on current behaviors and diets, we took a novel approach and looked at how the diets we consumed in our childhood affect obesity levels now that we are adults," said Alex Bentley, head of UT's Department of Anthropology and lead researcher of the study, which was published in Economics and Human Biology.

Consumption of excess sugar, particularly in sugar-sweetened beverages, is a known contributor to both childhood and adult obesity. Many population health studies have identified sugar as a major factor in the obesity epidemic. One problem with this theory, however, has been that sugar consumption in the US began to decline in the late 1990s while obesity rates continued to rise well into the 2010s.

That increase shows in the numbers: By 2016, nearly 40 percent of all adults in the US -- a little over 93 million people -- were affected by obesity.

In Tennessee alone, the adult obesity rate more than tripled, from about 11 percent in 1990 to almost 35 percent in 2016. By 2017, however, obesity in Tennessee had fallen 2 percent from the previous year.

If high-sugar diets in childhood have long-lasting effects, the changes we see now in adult obesity rates may have started with diets decades ago, when those adults were children.

"Since the 1970s, many available infant foods have been extremely high in sugar," said Hillary Fouts, coauthor of the study and cultural anthropologist and professor in the UT Department of Child and Family Studies. "Other independent studies in medicine and nutrition have suggested that sugar consumption during pregnancy can cause an increase in fat cells in children," she added.

"Up to this point, no studies had explicitly explored the temporal delay between increased sugar consumption and rising obesity rates," says Damian Ruck, postdoctoral research fellow in the Department of Anthropology and coauthor of the study. To address the problem, the authors modeled the increase in US adult obesity since the 1990s as a legacy of the increased excess sugar consumption measured among children in the 1970s and 1980s.

The researchers tested their model using national obesity data collected between 2004 and 1990 by the Centers for Disease Control and Prevention. They compared those obesity rates with annual sugar consumption since 1970 using the median per capita rates issued by the US Department of Agriculture.

The model also roughly captures how obesity rates vary by age group among children and teenagers.

"Our results suggest that the dietary habits learned by children 30 or 40 years ago could explain the adult obesity crisis that emerged years later," said Ruck.

A large portion of the sugar increase before 2000 was from high fructose corn syrup (HFCS), which after 1970 quickly become the main sweetener in soft drinks and a common ingredient in processed foods. At peak sugar consumption, in 1999, each person in the US consumed on average around 60 pounds of HFCS per year and more than 400 calories per day in total excess sugars.

US sugar consumption has declined since 2000. "If 2016 turns out to be the peak in the obesity rate," Bentley added, "that is coincidentally one generation after the peak in excess sugar consumption."

The researchers are planning to continue their studies in the area by exploring the effect of sugar-sweetened beverages. "This is important because obesity disproportionately affects the poor," said Bentley.

In a paper published in Palgrave Communications in 2018, Bentley and his colleagues found that the relationship between low income and high rates of obesity became noticeable on a national scale in the early 1990s. The 2018 study shows that the correlation between household income and obesity rate has grown steadily, from virtually no correlation in 1990 to a very strong correlation by 2016.

Journal Reference:
R. Alexander Bentley, Damian J. Ruck, Hillary N. Fouts. U.S. obesity as delayed effect of excess sugar. Economics & Human Biology, 2019; 100818 DOI: 10.1016/j.ehb.2019.100818


https://www.sciencedaily.com/releas...90923164534.htm
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  #2   ^
Old Tue, Sep-24-19, 04:41
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GRB5111 GRB5111 is offline
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It makes sense that a lag effect occurred between the time of peak sugar consumption and the visible results of obesity and poor health. The epigenetic influence on subsequent generations being prone to obesity is also plausible. I'd add inexpensive sugar-sweetened cereals, healthy whole grains, as a major contributor as well.
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  #3   ^
Old Tue, Sep-24-19, 07:31
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NewRuth NewRuth is offline
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Quote:
"Up to this point, no studies had explicitly explored the temporal delay between increased sugar consumption and rising obesity rates," says Damian Ruck, postdoctoral research fellow in the Department of Anthropology and coauthor of the study. To address the problem, the authors modeled the increase in US adult obesity since the 1990s as a legacy of the increased excess sugar consumption measured among children in the 1970s and 1980s.



Maybe the "temporal delay between increased sugar consumption and rising obesity rates" is because it isn't only sugar consumption contributing to obesity. Heart-healthy-wholegrains, policies skewing diets away from fat and protein, increased omega-6 consumption, increased antibiotic use all have reasonable evidence that they contribute to obesity.

Modeling is just fancy data manipulation. You know the answer you're looking for and you keep doing the math until you get it.
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Old Tue, Sep-24-19, 09:35
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Ms Arielle Ms Arielle is online now
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Quote:
I'd add inexpensive sugar-sweetened cereals, healthy whole grains, as a major contributor as well.


This just replaces the sugar reduction. So Im not expecting a change in obesity in future generations due to limiting daily sugar intake.
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Old Tue, Sep-24-19, 10:40
CityGirl8 CityGirl8 is offline
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So often I see studies like this and I'm shocked that they're saying no one has studied it before. I've long assumed this was the case and fairly settled science--at least within the low carb community. Obviously not within the heart-healthy-whole-grains-CICO crowd. But I did assume there was at least some science behind it. There have been studies that show that when mother experience gestational diabetes their children are more likely to be obese, I believe, so it's pretty easy to go from there. Also, the idea that if you eat too much sugar for a long time (you know starting in childhood) that 20 or 30 years of that is going to make you fat.

But if this is what it takes to convince people, then it's good we have studies like this.
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  #6   ^
Old Wed, Sep-25-19, 05:52
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WereBear WereBear is offline
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Quote:
Originally Posted by CityGirl8
So often I see studies like this and I'm shocked that they're saying no one has studied it before. I've long assumed this was the case and fairly settled science--at least within the low carb community. Obviously not within the heart-healthy-whole-grains-CICO crowd.


Because grant applications who explored any sugar connection were turned down because they challenged "settled science"? For decades?
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Old Wed, Sep-25-19, 21:14
M Levac M Levac is offline
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Quote:
If high-sugar diets in childhood have long-lasting effects

Reminds me of another idea. If only we can stick with this diet for a month, it's gonna have long-lasting effects, then we can just go back to our regular diet. That's the wrong idea, isn't it.

The correct idea is flow rate. The flow rate of fat into fat tissue vs the flow rate of fat out of fat tissue. Sincce it's a flow rate, it's an on-going thing, not merely some fire-and-forget one-time permanent action with long-lasting effect. The flow rate must be acted on continuously, just like when we're trying to fill a leaky bucket.

On the other hand, since we're talking childhood, it's entirely possible to act during that period and expect long-lasting effects, as we can observe from certain deficiencies that affect growth in various ways (growth hormone deficiency for example), and then observe the effect in adulthood as shorter height, smaller organs, and smaller skeletal structure overall. Is this what's going on here?

Quote:
"Other independent studies in medicine and nutrition have suggested that sugar consumption during pregnancy can cause an increase in fat cells in children," she added.

"Up to this point, no studies had explicitly explored the temporal delay between increased sugar consumption and rising obesity rates,"

That's not entirely true. We are aware of a phenomenon called insulin-induced lipohypertrophy (or lipodystrophy), where the number of fat cells increases due to long-term hyperinsulinemia. We are also aware that this particular growth results in a different type of fat tissue in some way that responds specifically to a recently developed drug (still in testing phase yet) called Adipotide, which acts on certain cells to cause apoptosis, which then causes fat cells to asphyxiate due to lack of blood and oxygen, thereby reducing overall fat tissue mass locally.

Additionally, we are aware of generational epigenetics, where first, something acts on the parent to cause some disorder, the parent then reproduces offspring and "transmits" (in quotes because it's not exactly like an infection or something, though we can't rule out infections per se) the disorder to the offspring, and where second, this offspring is also then exposed to the same primary cause which produced the disorder in the parent, thereby exacerbating the disorder further in the offspring.

The point is it's been studied, but not necessarily this new idea of temporal delay. The causality here is on-going, not delayed. This means the amplitude of the effect is proportional to the length of action, the longer the action the bigger the effect. It is also proportional to the strength of the action, the higher the insulin the bigger the effect. This is exacerbated further when we're dealing with generational epigenetics.

Finally, the idea here is about table sugar, not all sugars. So when we're looking at a substance that's part of a class of substances whose actions are similar or identical, we must also consider the whole class of substances, not merely one of. I suppose we could find this trick with other substances as well, such as derivatives (I'm thinking ergot derivatives, with pergolide and cabergoline) where we blame one (pergolide) for the benefit of another (cabergoline), typically in the context of drug patents which expire (the patent on pergolide has long expired, while the patent on cabergoline is still in effect, correct me if I'm wrong).

The point is that when we look at associations, we'll find there isn't one when looking merely at one of rather than the whole class of substances.
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  #8   ^
Old Thu, Sep-26-19, 00:28
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Dalesbred Dalesbred is offline
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I also wonder about the effect of antibiotics, which appear to be given more freely to children “just in case”, and the impact these might have on a developing gut biome; if gut bacteria start off out of whack it would be harder to develop an optimal mix. And fecal transplants have proved how important a good mix is in maintaining a healthy weight.
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  #9   ^
Old Thu, Sep-26-19, 10:11
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Little Me Little Me is offline
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Quote:
A large portion of the sugar increase before 2000 was from high fructose corn syrup (HFCS), which after 1970 quickly become the main sweetener in soft drinks and a common ingredient in processed foods. At peak sugar consumption, in 1999, each person in the US consumed on average around 60 pounds of HFCS per year and more than 400 calories per day in total excess sugars.

I would also add the Fat Free Snacks business that started in the 80s.
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