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  #1   ^
Old Tue, Sep-17-19, 08:41
teaser's Avatar
teaser teaser is offline
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Default height vs diabetes

Quote:
Shorter people are at higher risk of type 2 diabetes, study shows

Short stature is associated with a higher risk of type 2 diabetes, according to a new study in Diabetologia (the journal of the European Association for the Study of Diabetes).Tall stature is associated with a lower risk, with each 10cm difference in height associated with a 41% decreased risk of diabetes in men and a 33% decreased risk in women.

The increased risk in shorter individuals may be due to higher liver fat content and a less favourable profile of cardiometabolic risk factors, say the authors that include Dr Clemens Wittenbecher and Professor Matthias Schulze, of the German Institute of Human Nutrition Potsdam-Rehbruecke, Germany, and colleagues.

Short stature has been linked to higher risk of diabetes in several studies, suggesting that height could be used to predict the risk for the condition. It has been reported that insulin sensitivity and beta cell function are better in taller people. Short stature is related to higher cardiovascular risk, a risk that might in part be mediated by cardiometabolic risk factors relevant to type 2 diabetes -- for example blood pressure, blood fats and inflammation.

This new study used data obtained in the European Prospective Investigation into Cancer and Nutrition (EPIC) -- Potsdam; a study that included 27,548 participants -- 16, 644 women aged between 35 and 65 years and 10,904 men aged between 40 and 65 years -- recruited from the general population of Potsdam, Germany between 1994 and 1998.

A variety of physical data were collected from participants, including body weight, total body height and sitting height (with leg length calculated as the difference between the two), waist circumference and blood pressure. For this study, a sub-cohort of 2,500 participants (approx. 10%) was randomly selected being representative for the full study. Those with diabetes already or lost to follow up were excluded, leaving 2,307 for analysis. In addition, 797 participants of the full cohort who went on to develop type 2 diabetes were included. Of these, an investigation of potential mediating factors was carried out for 2,662 participants (including 2,029 sub-cohort members and 698 diabetes cases).

The study found that the risk of future type 2 diabetes was lower by 41% for men and 33% for women for each 10cm larger height, when adjusted for age, potential lifestyle confounders, education and waist circumference.

The association of height with diabetes risk appeared to be stronger among normal-weight individuals, with an 86% lower risk per 10cm larger height in men, and 67% lower risk per 10cm larger height in women. In overweight/obese individuals, each 10cm larger height was associated with diabetes risk being 36% lower for men and 30% lower for women. The authors say: "This may indicate that a higher diabetes risk with larger waist circumference counteracts beneficial effects related to height, irrespective of whether larger waist circumference is due to growth or due to consuming too many calories."

Larger leg length was associated with a lower risk of diabetes. A slight sex difference was noted -- for men a larger sitting height at the cost of leg length related to increased risk, whilst amongst women both leg length and sitting height contributed to lower risk. The authors suggest that, among boys, growth before puberty, which relates more strongly to leg length, will have a more favourable impact on later diabetes risk than growth during puberty (assuming that truncal bones are the last to stop growing). For girls both growth periods seem to be important.

The authors also calculated to what extent the inverse associations of height and height components with type 2 diabetes risk are explainable by liver fat (measured as Fatty Liver index) and other cardiometabolic risk factors. When the results were adjusted for liver fat content, the men's reduced risk of diabetes per 10cm larger height was 34% (compared with 40% in the overall results), and the women's reduced risk was just 13% compared with 33% in the overall results.

Other biomarkers also affected the results: in men adjustment for glycated haemoglobin (a measure of blood sugar) and blood fats each reduced the risk difference by about 10%. In contrast, among women adjustment for adiponectin (a hormone involved in blood sugar control) (-30%) and C-reactive protein (a marker of inflammation) (-13%) reduced the associations of height with diabetes, in addition to the reductions observed by glycated haemoglobin and blood fats. Taken together, the authors say that a large proportion of the reduced risk attributable to increased height is related to taller people having lower liver fat and a 'healthier' cardiometabolic profile.

The authors say: "Our findings suggest that short people might present with higher cardiometabolic risk factor levels and have higher diabetes risk compared with tall people… These observations corroborate that height is a useful predictive marker for diabetes risk and suggest that monitoring of cardiometabolic risk factors may be more frequently indicated among shorter persons, independent of their body size and composition. Specifically, liver fat contributes to the higher risk among shorter individuals and, because height appears to be largely unmodifiable during adulthood, interventions to reduce liver fat may provide alternative approaches to reduce risk associated with shorter height."

However they add: "Our study also suggests that early interventions to reduce height-related metabolic risk throughout life likely need to focus on determinants of growth in sensitive periods during pregnancy, early childhood, puberty and early adulthood, and should take potential sex-differences into account."

They conclude: "We found an inverse association between height and risk of type 2 diabetes among men and women, which was largely related to leg length among men. Part of this inverse association may be driven by the associations of greater height with lower liver fat content and a more favourable profile of cardiometabolic risk factors, specifically blood fats, adiponectin and C-reactive protein."


https://www.sciencedaily.com/releas...90916182500.htm

I feel like this is one place where portion size should be mentioned. If you're four feet tall versus six feet four, a standard sized chocolate bar becomes a relatively large serving. Even in the context of what's become "standard" for a keto diet, under 20 grams of digestible carbs a day, that's a lot more carbs for somebody who's four feet versus six feet four (and I think could be reasonably scaled down).

Early nutrition might be a factor, malnutrition in pregancy in early life does make rodents more prone to insulin resistance etc., but that still relates to diet later in life, it exacerbates the response to a diet high in both fat and sugar. In animals with stunted growth due to poor nutrition, you get all this bad stuff happening. In animals on the other hand that are just bred to be short, it's common enough to have the opposite, healthier animals with longer life- and health-spans. If you are short and your well-nourished parents, grandparents etc. were short, I doubt very much that there's a problem in you being short as such, except maybe that relative difference in portion sizes for some problem foods.
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  #2   ^
Old Tue, Sep-17-19, 09:49
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Ms Arielle Ms Arielle is online now
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When will "cheetos" be used as a predictor??

Or "cookies"....?
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  #3   ^
Old Tue, Sep-17-19, 10:18
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My first thought was that taller people might have more growth hormone. Secondly, short people could be maxing out their genetic potential, OR had that compromised by malnutrition by relying on sugars and starches too much.

HGF likely involved.
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  #4   ^
Old Tue, Sep-17-19, 10:33
CityGirl8 CityGirl8 is offline
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This just seems ridiculous to me, like increased lemon imports causing decreased highway deaths or other bizarre correlations. I'm sure they'll eventually discover some other cause like poorer nutrition. Like, maybe people who feed their kids lots of pop tarts vs. people who feed their kids eggs for breakfast might have shorter kids.
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  #5   ^
Old Tue, Sep-17-19, 11:28
teaser's Avatar
teaser teaser is offline
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People who are short due to a genetic limitation in growth hormone--as well as animals--tend to have longer lifespans and a resilience versus metabolic disorders rather than the other way around. It's not really clear that an increased level of growth hormone--outside of calorie restriciton or fasting, is all that healthy. And in those cases, there's a stressor that limits growth in the calorie restriction/fasting, the elevation in growth hormone may ameliorate this, but isn't going to result in a taller/longer phenotype.

For a while growth hormone replacement was touted as sort of a fountain of youth, this became less popular when exogenous growth hormone resulted in insulin resistance.
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  #6   ^
Old Tue, Sep-17-19, 12:37
jschwab jschwab is offline
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Quote:
Originally Posted by teaser
People who are short due to a genetic limitation in growth hormone--as well as animals--tend to have longer lifespans and a resilience versus metabolic disorders rather than the other way around. It's not really clear that an increased level of growth hormone--outside of calorie restriciton or fasting, is all that healthy. And in those cases, there's a stressor that limits growth in the calorie restriction/fasting, the elevation in growth hormone may ameliorate this, but isn't going to result in a taller/longer phenotype.

For a while growth hormone replacement was touted as sort of a fountain of youth, this became less popular when exogenous growth hormone resulted in insulin resistance.


I was thinking about that, too. It seemed to me like the obvious answer might lie in ethnic origin? We know some groups of people are more susceptible to developing diabetes and that many of those groups tend to be on the shorter side. They didn't mention controlling for that at all which made me wonder if they are comparing apples to oranges.
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  #7   ^
Old Tue, Sep-17-19, 19:30
Zei Zei is offline
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Quote:
This new study used data obtained in the European Prospective Investigation into Cancer and Nutrition (EPIC) -- Potsdam; a study that included 27,548 participants -- 16, 644 women aged between 35 and 65 years and 10,904 men aged between 40 and 65 years -- recruited from the general population of Potsdam, Germany between 1994 and 1998.
I don't know what the ethnic breakdown is for the population of that particular German city but wonder, since it's a European place and not somewhere like the U.S. full of descendants of various immigrants, if most study participants are ethnic German.
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  #8   ^
Old Tue, Sep-17-19, 19:42
jschwab jschwab is offline
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Quote:
Originally Posted by Zei
I don't know what the ethnic breakdown is for the population of that particular German city but wonder, since it's a European place and not somewhere like the U.S. full of descendants of various immigrants, if most study participants are ethnic German.


I did not notice that part of it! Probably pretty safe then, as the population would be a lot more homogeneous in that one city, regardless of the impact of migration.
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  #9   ^
Old Wed, Sep-18-19, 10:56
CityGirl8 CityGirl8 is offline
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Actually, Germany has lots of immigrants! Currently, its about 10–15% of the population. The guest worker programs that started in the sixties brought in lots of Turkish, Greek, Yugoslav and North Africans, though this was to the former West Germany. Beginning in the 1990s they've had a steady stream of refugees from various wars including Bosnia and more recently Syria, along with continuing economic migrants from Russia and from other places in the EU.

But they mainly tend to go to places in the former West German areas and Potsdam is in former East Germany, so for the sake this study, it was probably a pretty homogenous population.

The older people in the study, however, would have been children during the pre-WWII years, a time of extreme economic deprivation in Germany. The worldwide depression hit Germany worse than it did the U.S. and plenty of people were starving (literally). Then the deprivation of the war years. Given the age spread and years of study recruitment, people in the study could have been born anywhere between 1929 (65 year olds recruited in 1994) and 1963 (35 year olds recruited in 1998).

Those younger people would not have grown up with the same kinds of food deprivation. I wonder what differences there would have been if the study controlled for that?
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  #10   ^
Old Wed, Sep-18-19, 11:19
jschwab jschwab is offline
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Quote:
Originally Posted by CityGirl8
Actually, Germany has lots of immigrants! Currently, its about 10–15% of the population. The guest worker programs that started in the sixties brought in lots of Turkish, Greek, Yugoslav and North Africans, though this was to the former West Germany. Beginning in the 1990s they've had a steady stream of refugees from various wars including Bosnia and more recently Syria, along with continuing economic migrants from Russia and from other places in the EU.

But they mainly tend to go to places in the former West German areas and Potsdam is in former East Germany, so for the sake this study, it was probably a pretty homogenous population.

The older people in the study, however, would have been children during the pre-WWII years, a time of extreme economic deprivation in Germany. The worldwide depression hit Germany worse than it did the U.S. and plenty of people were starving (literally). Then the deprivation of the war years. Given the age spread and years of study recruitment, people in the study could have been born anywhere between 1929 (65 year olds recruited in 1994) and 1963 (35 year olds recruited in 1998).

Those younger people would not have grown up with the same kinds of food deprivation. I wonder what differences there would have been if the study controlled for that?


I am aware! I basically have an MA in German Studies with an emphasis on the east. But those groups are not, to my knowledge, of especially short stature or known for being predisposed to diabetes as, say, indigenous peoples of the Americas are - that is more what I was thinking of. What you are saying about the war years makes a lot of sense with the starvation and then just the stress and trauma, in general.
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  #11   ^
Old Mon, Sep-23-19, 08:34
M Levac M Levac is offline
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Height vs growth hormone.

Diabetes (type 2) is primarily a disorder of hyperglycemia. Growth hormone is potently inhibited by hyperglycemia. It follows therefore that height is affected by hyperglycemia through inhibition of growth hormone.

Since growth hormone acts on all tissues, not just bones, it follows therefore that all tissue growth is affected through the same sequence, resulting in smaller organs and skeletal structure overall, which we can see a model of in the Zucker rats (often cited by Taubes in his lectures).

Consequently, we end up with a system that is rendered less able to dispose of excess dietary carbohydrates, except through excess fat accumulation, where fat tissue acts as a glucose sink by virtue of insulin and by virtue of fat tissue's ability to convert glucose to glycerol (and then triglycerides) for storage. And since the liver is now smaller than normal, and since the liver is the primary site of disposal of excess glucose by conversion to glycogen, this allows the excess dietary carbohydrates to cause blood glucose to rise beyond what is otherwise possible in an adult human who would have grown to normal height/size beforehand.

Conversely, while growth hormone is inhibited by hyperglycemia, insulin is stimulated, which then causes fat tissue growth through the process known as insulin-induced lipohypertrophy (or lipodystrophy, depending on your point of view), where fat tissue grows not merely in overall size, but also in number, i.e. there's more fat cells than otherwise.

The combination of these factors then makes possible the observation of an association between height and diabetes (type 2).

Not necessarily how it actually works, just how I see it.

Last edited by M Levac : Mon, Sep-23-19 at 08:41.
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  #12   ^
Old Mon, Sep-23-19, 08:48
M Levac M Levac is offline
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Quote:
Originally Posted by teaser
People who are short due to a genetic limitation in growth hormone--as well as animals--tend to have longer lifespans and a resilience versus metabolic disorders rather than the other way around. It's not really clear that an increased level of growth hormone--outside of calorie restriciton or fasting, is all that healthy. And in those cases, there's a stressor that limits growth in the calorie restriction/fasting, the elevation in growth hormone may ameliorate this, but isn't going to result in a taller/longer phenotype.

For a while growth hormone replacement was touted as sort of a fountain of youth, this became less popular when exogenous growth hormone resulted in insulin resistance.

...when combined with hyperglycemia, from eating a boatload of carbs. Ironically, trying to avoid insulin resistance by avoiding carbs also fixes the primary demand for exogenous GH, i.e. no inhibition from hyperglycemia.

-edit- Forgot. Never mind that insulin resistance does not exist. To wit, even with diagnosed insulin resistance, eating carbs and pumping out tons of insulin and injecting insulin on top of it, there's still full inhibition of ketogenesis at the liver which can only be done by insulin therefore proves that there's no such thing as insulin resistance. How else could the liver respond to insulin and inhibit ketogenesis but by remaining exquisitely sensitive to it?

-edit again- I won't go through my entire paradigm, but the primary cause of insulin resistance (or of the phenomena we call insulin resistance) is absence of ketones in the blood.

Last edited by M Levac : Mon, Sep-23-19 at 08:56.
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