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Rates Of Diabetes I And II Are Rapidly Rising In Young Children And Teens

haidut

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I posted recently the rather sad finding that colon cancer rates have doubled in young people. Colon cancer is one of the cancers considered solidly an "old person" cancer and one with strong genetic component (like most cancers according to the FDA).
Breaking News: Colorectal Cancer Rates In Young People Have Doubled

The study above obviously rules out genetics or even obesity as causes of this increase, but some responses I got from doctors over email were along the lines of "it's just one condition, so we can't rule out genes yet". Well, now we can add both types of diabetes as another condition affecting vast swaths of people globally to the list of conditions likely not ruled by genes. Diabetes is perhaps the most common chronic disease in developed nations worldwide, so if it is not genetic then to me the message is even stronger than the one provided by the colon cancer study.
According to the study below rates of both types of diabetes are rapidly rising in children and teens - a group of people who should be among the healthiest (if not the healthiest) of all age groups. The risk of developing both diabetes I and II are thought to be heavily influenced by genes, and diabetes II is also though to be influenced by advancing age. So, the rapidly rising rates in children and teens are ruling out the genetic explanation as the authors themselves say in the actual study.
I wonder how many other serious conditions have to become a "disease of the young" before the genetic fallacy is finally abandoned...

MMS: Error
Rates of new diagnosed cases of type 1 and type 2 diabetes on the rise among children, teens

"...Rates of new diagnosed cases of type 1 and type 2 diabetes are increasing among youth in the United States, according to a report, Incidence Trends of Type 1 and Type 2 Diabetes among Youths, 2002-2012(link is external), published today in the New England Journal of Medicine. In the United States, 29.1 million people are living with diagnosed or undiagnosed diabetes, and about 208,000 people younger than 20 years are living with diagnosed diabetes."

"...“Because of the early age of onset and longer diabetes duration, youth are at risk for developing diabetes related complications at a younger age. This profoundly lessens their quality of life, shortens their life expectancy, and increases health care costs,” said Giuseppina Imperatore, M.D., Ph.D., epidemiologist in CDC’s Division of Diabetes Translation, National Center for Chronic Disease Prevention and Health Promotion. The study results reflect the nation’s first and only ongoing assessment of trends in type 1 and type 2 diabetes among youth and help identify how the epidemic is changing over time in Americans under the age of 20 years."
 

jaa

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As someone who thinks genetics play a role in just about all things human, what position are you arguing against? The weak one (100% genetics 0% environment) or the strong one (genetics and environment play a role)? Most people subscribe to the latter view and anything else seems pretty unreasonable to me.
 

haidut

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As someone who thinks genetics play a role in just about all things human, what position are you arguing against? The weak one (100% genetics 0% environment) or the strong one (genetics and environment play a role)? Most people subscribe to the latter view and anything else seems pretty unreasonable to me.

I think you have them reversed - the strong one is about 100% due to genetics. I actually do not subscribe to any genetic theory for majority of conditions, not even the weak one. I think the weak version is just an attempt to keep the genetic hypothesis of pathology alive despite absolute lack of evidence of therapy. About 50 years ago the strong genetic position was the dominant one in medicine and now after half a century of abject failure to produce anything of note, the weak one was introduced as a compromise.
The failure of the genome | Jonathan Latham
The Selfish Gene: The Broken Promises of the Human Genome Project
http://www.nytimes.com/2010/06/13/health/research/13genome.html?pagewanted=all&_r=0

There are indeed some diseases with a heavy genetic component like phenylketonuria and maybe hemophilia, but things like diabetes, cancer, CVD, etc are straight up environmental. Just because something is inherited does not make it genetic. As I mentioned in a few other posts, a person's health at birth is the weighted average of the lifelong health of his/her parents, grandparents, and great-grandparents, with the health of the mother during pregnancy accounting for about 70% of that weighted average. The longer the person lives the more their own life adds to the weighted average. But as far as genes being responsible for common conditions like diabetes, cancer, Alzheimer, etc - this is quite obviously bunk. Epigenetic heritability of disease predisposition - yes. But genetic determination of disease or its predisposition - hell no.
The Neo-Darwinian Theory Of Evolution Is Incomplete Without Lamarck
Genes do NOT matter (much)

I think the term epigenetic should be dropped altogether. It was coined to ensure the continued presence and primary role of genes in the discourse (and future budget/funding) on top which somehow the secondary role of environmental activation or silencing of genes is bolted. But the very term reveals the belief that it is still genes that control the fate of the organism while the environment plays an unpredictable and decisively secondary "trigger" role. This needs to end, the idea of genes responsible for disease is dead with the exception of a few conditions that are indeed genetic and easily diagnosable at birth.
 
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In the United States, 29.1 million people are living with diagnosed or undiagnosed diabetes, and about 208,000 people younger than 20 years are living with diagnosed diabetes.

They don't specify how much is type 1 vs. type 2 in that sentence.

The two diseases should never even be talked about in the same sentence. In fact, the two diseases shouldn't even share the same word of "diabetes."

The two diseases are completely different from each other.

Of course type 2 is on the rise because so many people are getting fat. Type 2 is caused by becoming fat. Type 2 is completely curable.

The burden of proof is on you to show me the lean people with "type 2." Show me the lean people with diabetic retinopathy and amputated toes and feet.

Type 1 is extremely rare.

Diabetes Needs To Be Renamed

.
 
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haidut

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They don't specify how much is type 1 vs. type 2 in that sentence.

The two diseases should never even be talked about in the same sentence. In fact, the two diseases shouldn't even share the same word of "diabetes."

The two diseases are completely different form each other.

Of course type two is on the rise because so many people are getting fat. Type 2 is caused by becoming fat. Type 2 is completely curable.

Type 1 is extremely rare.

Diabetes Needs To Be Renamed

.

Noted. So what do you think explains the rising incidence of type 1? The actual study does break them down. I will find the quote and post it here.
 
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Noted. So what do you think explains the rising incidence of type 1? The actual study does break them down. I will find the quote and post it here.

If it's truly type 1, no insulin at all being produced by the pancreas, or also not enough insulin, both instances which should also be separated, it's probably due to environmental toxins destroying the beta cells and it can also be genetic in the sense that more people are being born with genetic defects that cause beta cell issues.

.
 
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haidut

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If it's truly type 1, no insulin at all being produced by the pancreas, or also not enough insulin, both instances which should also be separated, it's probably due to environmental toxins destroying the beta cells and it can also be genetic in the sense that more people are being born with genetic defects that causes beta cell issues.

.

Yes, but why are the rates of type I increasing if it is genetic? I guess it comes down to that environmental toxin, but is there any evidence so far implicating a gene that this toxin somehow activates/silences?
 

Tarmander

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Type 1 diabetes incidence is definitely increasing from everything I have read, which needs an explanation. The traditional explanation is that the immune system goes crazy and attacks the beta cells, killing them. I read a new theory the other day that flips the cause around and instead says that the immune system is functioning just fine, but the beta cells malfunction and send out a distress call that they are in need of death, and the immune system complies.

I was helping with a local diabetes walk coming up here where I live, and it is being done on an Indian reservation. They have children as young as 6 who are type 2 diabetics, which is insane, as well as adults in their 20s going on dialysis from diabetes complications. I would say the different incidences of disease between different ethnic groups does support some kind of epigenetic model. However it would be difficult to isolate all the factors given the history of stress certain groups have gone through. Perhaps this is a case of support for the theory about stress having multi generational effects.
 

haidut

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Type 1 diabetes incidence is definitely increasing from everything I have read, which needs an explanation. The traditional explanation is that the immune system goes crazy and attacks the beta cells, killing them. I read a new theory the other day that flips the cause around and instead says that the immune system is functioning just fine, but the beta cells malfunction and send out a distress call that they are in need of death, and the immune system complies.

I was helping with a local diabetes walk coming up here where I live, and it is being done on an Indian reservation. They have children as young as 6 who are type 2 diabetics, which is insane, as well as adults in their 20s going on dialysis from diabetes complications. I would say the different incidences of disease between different ethnic groups does support some kind of epigenetic model. However it would be difficult to isolate all the factors given the history of stress certain groups have gone through. Perhaps this is a case of support for the theory about stress having multi generational effects.

Incidence for all autoimmune conditions is rising, especially in the young. When pretty much all chronic, degenerative conditions increase like and in young people who should be the most resilient (i.e. living longer increasing vulnerability argument) that the argument that somehow genes are responsible is...well, irresponsible.
 

Tarmander

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Incidence for all autoimmune conditions is rising, especially in the young. When pretty much all chronic, degenerative conditions increase like and in young people who should be the most resilient (i.e. living longer increasing vulnerability argument) that the argument that somehow genes are responsible is...well, irresponsible.

What I was saying is that genes are related to how strongly something affects the person. Alcohol use is a good example where Europeans seem to tolerate it quite well where as other ethnic groups who do not have a history of fermenting sugars do not.

So for this example, somehow the Native Americans are suffering at much higher levels then other ethnic groups.
 

zztr

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The idea that modern dysgenic trends play some role in increasing disease rates is highly believable. Many people with poor health are having four and more children. We're perhaps four generations into this modern phenomenon.

It's not a simple as saying there are genes for disease. There's the matter of mutation load.
 

tankasnowgod

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As someone who thinks genetics play a role in just about all things human, what position are you arguing against? The weak one (100% genetics 0% environment) or the strong one (genetics and environment play a role)? Most people subscribe to the latter view and anything else seems pretty unreasonable to me.

As someone who thinks that genetics play a role, what kind of evidence can you offer? Specifically, which SNPs carry which mutations which would influence the development of Type 1 or 2 diabetes?

An example of a disease that has a well established genetic component is hemochromatosis. Mutations of C282Y, H65D and S63C are found on SNPs
rs1800562, rs1799945, and i3002468. But those mutations don't directly cause the disease, they simply cause the body to load iron at a higher rate. Excess iron is what causes problems, and if iron is removed from the body (by chealators, loss of blood, or other factors), the disease never truly develops in genetically susceptible individuals. At the same time, people exposed to excess iron (like iron workers, smokers, athletes that use iron supplements for "iron doping") can develop the disease, even if they don't have the genetic mutations.

I think promoters of the genetic argument need to start producing specific instances like the above, that can either be verified or falsified. Otherwise, claiming that diseases have a "genetic component" is pretty much meaningless.
 

tankasnowgod

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The idea that modern dysgenic trends play some role in increasing disease rates is highly believable. Many people with poor health are having four and more children. We're perhaps four generations into this modern phenomenon.

It's not a simple as saying there are genes for disease. There's the matter of mutation load.

Why is that any more believable than the environmental argument? We are about 8-9 generations past the industrial revolution, and dealing with higher heavy metal and other toxin loads than previous humans. How is mutation load testable? Is that more important than, say, mercury load? Pufa load? Iron load?
 

haidut

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What I was saying is that genes are related to how strongly something affects the person. Alcohol use is a good example where Europeans seem to tolerate it quite well where as other ethnic groups who do not have a history of fermenting sugars do not.

So for this example, somehow the Native Americans are suffering at much higher levels then other ethnic groups.

Yes, but how to we measure that vulnerability? Without discovering the genes for those specific vulnerabilities we cannot say anything definitively and btw those genes are not likely to ever be found judging from the last 50 years of intensive search. So, saying genes affect our vulnerability but without being able to point out which ones and by how much is violating Occam's Razor rule.
 

haidut

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The idea that modern dysgenic trends play some role in increasing disease rates is highly believable. Many people with poor health are having four and more children. We're perhaps four generations into this modern phenomenon.

It's not a simple as saying there are genes for disease. There's the matter of mutation load.

The argument for poor people having more children is certainly true. But like I mentioned, heritability does not imply genetic causes. You can inherit poor health from your parents epigenetically. For instance if you parents had CVD but your other ancestors (as far as you can check) did not then you also have a high chance of getting CVD. How do we separate epigenetic from genetic heritability and influence? I don't automatically dislike genes as explanation, I am simply saying that when I ask a geneticist which genes are possibly causally linked to CVD I am being told flatly "none so far". So, without specific examples for suspect genes there is nothing to test and falsify/confirm. It's just an extra variable that adds nothing to the hypothesis.
 

haidut

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I think promoters of the genetic argument need to start producing specific instances like the above, that can either be verified or falsified. Otherwise, claiming that diseases have a "genetic component" is pretty much meaningless

Exactly, thanks for bringing this up. It adds complexity without explaining anything. So, violates the Occam Razor rule and also cannot be really be falsified.
 

zztr

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when I ask a geneticist which genes are possibly causally linked to CVD

Well the mutation load argument is different than saying "which genes." It's more like poor fit and finish on a new vehicle dragging down performance. There's a decent amount of research on this, can't say I'm super familiar.
 

Constatine

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Well the mutation load argument is different than saying "which genes." It's more like poor fit and finish on a new vehicle dragging down performance. There's a decent amount of research on this, can't say I'm super familiar.
Such arguments seem like a cover up for a lack of evidence. Can mutation load be separated from poor nutrition and general damage to an organism? Genes are altered and damaged based on environmental factors, when the health of an organism is poor through generations there will be gene damage, but the gene damage is not the cause of the poor health.
 

jaa

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As someone who thinks that genetics play a role, what kind of evidence can you offer? Specifically, which SNPs carry which mutations which would influence the development of Type 1 or 2 diabetes?

An example of a disease that has a well established genetic component is hemochromatosis. Mutations of C282Y, H65D and S63C are found on SNPs
rs1800562, rs1799945, and i3002468. But those mutations don't directly cause the disease, they simply cause the body to load iron at a higher rate. Excess iron is what causes problems, and if iron is removed from the body (by chealators, loss of blood, or other factors), the disease never truly develops in genetically susceptible individuals. At the same time, people exposed to excess iron (like iron workers, smokers, athletes that use iron supplements for "iron doping") can develop the disease, even if they don't have the genetic mutations.

I think promoters of the genetic argument need to start producing specific instances like the above, that can either be verified or falsified. Otherwise, claiming that diseases have a "genetic component" is pretty much meaningless.

That's a great example that explains the effects of both genetics and environment and has given me a better mental model for these things. Thanks!

I think part of the issue is one side or the other is arguing for an ultimate cause. Taking your example, if no interventions are used, a person with a certain genetic disposition will develop hemochromatosis.

The person arguing for the environmental factors would say something like "Yes, but for any disease chalked up to genetics there is a theoretical intervention* that does not manipulate genes and still cures the disease. And it all comes down to environment anyway because look at what happens to people who are exposed to high levels of iron without the genetic predisposition."

To which the person in favour of the gene's eye view can say "Yes, but for any disease chalked up to the environment there is a theoretical intervention* that only manipulates genes and still cures the disease."

I agree distinctions are starting to sound pretty meaningless at this point. Though I hope that should clarify my position.

*At least in all but the most extreme cases
 
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