Japanese scientists discover genes that enable type-2 diabetes

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By level1diet

Wednesday, August 6, 2008 -- Japanese researchers at dozens of universities and medical research labs have announced today the discovery today of several previously unknown genes that make humans susceptible to type-2 or adult onset diabetes.

See the report here, in today's edition of The Journal of Clinical Endocrinology & Metabolism at http://jcem.endojournals.org/cgi/content/short/93/8/3136

OBESITY RELATED DIABETES

This kind of diabetes is also called "non insulin dependent diabetes mellitus" or NIDDM by doctors and researchers. Scientists have known for decades that the tendency to develop type-2 diabetes was passed down from parents to their offspring. How the tendency was handed down, whether through merely food and exercise choices or through the DNA, that has been the debate.

Type-2 diabetes is related to obesity, over consumption of food energy and lack of exercise, and usually occurs in adults in their middle years. Recent trends have also showed the disease developing in more and more very obese and inactive children, some as young as 10-12 years old.

WHICH CAME FIRST, THE CHICKEN OR THE EGG?

Because the disease usually shows up in people who are fat and who don't exercise, scientists and physicians have often claimed authoritatively that being fat and not being active caused the disease in the first place. We now know this not to be true... read how we know this below, and what we should do about it.

The minority view

A few scientists, a very small minority, claimed that the cause was 'sensitivity' or 'lack of sensitivity' to various foods -- an inheritable characteristic passed down genetically from mother and father to son and daughter. For proof in those days, they could only cite population studies and family history studies that showed links between diabetes and certain families who either had or didn't have the disease in their family, even though they tended to eat the same diets, and to have similar exercise or activity patterns.

The old diabetes debate

This reasoning was basically the old argument: "Which came first, the chicken or the egg?" Did people get fat, begin to exercise less and develop diabetes because their genes lead them to that lifestyle pattern, or did the lifestyle pattern of totally voluntary overeating and refusal to exercise initiate the disease, in virtual isolation from any pre-existent genetic condition?

What fat people said to their doctors

Millions of fat people who didn't exercise by time they were adults, and who were overeating, sometimes worked up the courage to tell their doctors that "the (genetic) devil made me do it." Most doctors refused to accept this information, explaining to their patients that "all you have to do is push away from the table."

Many population studies seemed to prove the doctors right. Every study consistently showed that people who exercise more and ate less eventually lost weight and improved or even reversed their type-2 diabetes.

So, since reversing overeating and inactivity were the solution, wasn't it logical to assume that they had actually caused the disease in the first place?

Wrong. We now know that type-2 diabetes is caused by genetic factors that make us less efficient fat-burners, even while we are active, but also while at rest. Genes also make us less efficient at creating new beta cells to produce insulin that would help us burn more calories all through the day.

So, does this mean that we should just blame our parents for our obesity and diabetes? Can we simply fold our arms and say, "It's not my fault?"

You'd be right. It's not your fault. Diabetes is caused by genes, even though overeating and lack of exercise does develop early on the road to getting the disease.

But, even though the absolute first cause of diabetes was not your fault, dealing with the disease IS YOUR FAULT. You must take responsibility for doing something about the condition. Read about how... how diabetes starts in children, and what you can do about it below.

New understanding of the actual 'first causes' of type-2 diabetes

The problem with all of the population studies and with the metabolic studies about diabetes was simple.

They never studied the right people.

The never studied babies, infants, toddlers, preschoolers, and preteens. Now we know that it is during those years that pre-diabetes is first evident. New studies have consistently proved that.

And, those preschool aged and preteen children begin to get fat well before they stop exercising as much as kids who don't get fat.

Read that again. Kids who later develop obesity and diabetes tend to get fat before there is any difference or slow-down in their activity levels.

Interesting, huh?

A few scientists back in the 1990's did take a look at children who were prone to get diabetes. Over time, a few studies began to show that in very young children who later tended to develop diabetes, obesity and low resting energy expenditure (low metabolism) PRECEDED the appearance of lack of exercise and other activity. In other words, certain groups of children tending to get fat while they were still very active.

Read the ground-breaking study of Pima Indian children, published in 2002 in the peer-reviewed scientific journal -- the full 10-page report is available online and also as a PDF, free of charge -- PEDIATRICS, August 2002, "Assessing risk factors for obesity between childhood and adolescence: II. Energy metabolism and physical activity." at http://pediatrics.aappublications.org/cgi/content/full/110/2/307

Their Conclusion? Here it is:

"... a decrease in PAL (physical activity level) in free-living conditions seems to follow, not precede, the development of obesity ..."

Doctors ignored this important finding

This revolutionary information fell on deaf ears in the medical world. It seemed to fly in the face of the popular opinion that lack of exercise and simply eating more that we were 'burning up' through activity levels were the main reason, or some argued the only reason that people got fat and eventually developed type-2 diabetes.

Importantly, the scientific study referred to above carefully pointed out that even though kids got fat in the first place before they decreased exercise, when they never responded to the weight gain by increasing their exercise to even higher levels, then they were even more likely to become really obese.

In other words, if these diabetes kids had begun to increase activity as soon as they began to gain weight, so that they were more active that non-diabetes-prone kids who were NOT getting fat, then these diabetes prone kids would decrease their likelihood of ever developing the disease.

But, the sad fact is that these little weight gainers would have to exercise more than the 'normal' non-diabetic-prond kids all around them. Sad but true.

In other words, you may get fat due to genetic or inherited family traits that you can't do anything about. This may happen even while your exercise and total physical activity levels are perfectly normal, at a very young age of 5 or even less. But, if you fail to respond to that initial weight gain by becoming more active, then you will increase the probability of becoming really obese and ultimately diabetic in later years. For many Pima Indians, this obesity develops as early as 10 years old.

Looking for the real first causes of diabetes

Pima Indians are about 4-1/2 times more likely than caucasian Americans to become seriously fat or obese by the age of 10. In 2000, about 13% of all American children were obese at 11 years old, compared to 53% obesity for Pima children of the same age.

The inherited characteristic for diabetes was hotly debated for many years. Some authorities guessed that this may not be really a genetic condition, but was instead merely a cultural, social and habit related phenomenon. They suggested that the main component was really the way parents passed down food choices, exercise patterns, and cooking methods like frying or boiling to their children.

The argument was about nature vs. nurture -- genes vs. behavior.

Today's news from Japan strongly favors nature

The Japanese studied 15 human genes from 1,921 people with type-2 diabetes, and 1,622 'control group' people who did not have diabetes.

Of the 15 studied possible 'gene candidates' for association with NIDDM adult onset diabetes, two of the genes had the strongest associations with diabetes. They were located in places associated with the ability to reproduce for insulin-producing beta cells in the pancreas. Six other genes were found to have slightly less significant associations with the disease, and the other seven genes appeared to have no relation to type-2 diabetes at all.

CONCLUSION

It appears that the trend of research on type-2 diabetes now favors two important lines of thought:

1) The Nature or "Egg" Side -- Obesity-related type-2 diabetes probably starts very early in life, before age 5, and is based largely upon genes that poorly dispose the individual to maintain sufficient populations of healthy beta cells in their pancreas. Poor beta cell functionality leads insufficient insulin production, which results in lower resting metabolic rates, lower energy expenditures while exercising, and weight gain. Ultimately, the increased obesity and resulting further resting metabolic rates and energy expenditures lead to a chain reaction of ever increasing weight gain and decreasing physical activity, accompanied by increased stresses on the pancreas and its beta cells that are producing less and less insulin per beta cell, and further accompanied by a simultaneous increase and lack of response to insulin (called insulin resistance) due to high levels of circulatory free fatty acids and fats inside muscle fibers themselves -- until the individual finally becomes an overt type-2 diabetic.

The entire process evidently all starts due to lack of metabolism, due to genes that due not maintain a high enough population of newly growing or reproduction of beta cell tissues.

2) The Nurture or "Chicken" Side -- a solution to the problem may at least partly lie in responding to early weight gain, even for very young children, by increasing the amount of time they spend moving, playing and in all kinds of activity while shortening the time spent inactive.

For your children

If no response is made as soon as even slightly unusual weight gain is noticed (instead of mere growth, which is normal), then the child will be at risk for serious obesity and diabetes in coming years.

If your child has noticable amounts of body fat and appears to be 'round' -- even while young and apparently active -- take immediate action! A round-faced 2 or 3 year old will usually mean a very obese, diabetic adult.

Decrease their TV time and video, computer or video game playing. Increase their physical activities. Onset of obesity and diabetes CAN be delayed or even prevented, even though your child may be genetically disposed to become a diabetic.

Healthy food doesn't have to be boring

Put your children on a healthy, controlled diet that resembles the 60% high fiber carbs / 25% good fats / 15% low fat proteins as outlined in our Level 1 Anti-inflammatory Diet program we describe below. Make the food presentations exciting and attractive. Keep meals fun with lots of variety and highly contrasted flavors. Involve your kids in the cleaning, cutting, and even the cooking of the healthy foods. Make mealtime an adventure for them. Teach them to understand that good food can be fun food.

For adults who are already diabetic or obese and pre-diabetic

Eat a natural, healthy diet consisting largely of fresh, high fiber colorful vegetables, fruit, whole nuts, olive oils or coconut oils, wild fish or non-grain-fed meat, skinless turkey, chicken and beans, legumes and roots.

Spice it up with red pepper, ginger, turmeric yellow curry, cinnamon, anise, brown tea, green tea, and other strong spices (except salt).

Minimize or avoid dietary dangers like omega-6 vegetable cooking oils, trans-fats, sat-fats, salt, sugars, especially fructose sugars.

Avoid processed or packaged foods with ingredients you can't control or evaluate well.

Take a good quality pure fish oil, magnesium citrate, fiber powder, vitamins gamma-E and alpha-E and ester-C, and borage oil. We explain how much and when to take these supplements on our site.

Then get plenty of exercise, at least 45 minutes/day of low impact cycling, walking, swimming, rowing, etc.

To find out more about the healthy diet described above, visit our Level1Diet.com web-site, which has 1.5 million pages about health, and which provides easy to understand lists of foods to avoid, foods to eat, supplements to take and easy exercise tips.

Chemically stained beta cells viewed through a microscope.
Chemically stained beta cells viewed through a microscope.
Expanded-view drawing showing a gene related to a human chromosome from human DNA.
Expanded-view drawing showing a gene related to a human chromosome from human DNA.
Shows where the pancrease gland sits next to the human intestines.
Shows where the pancrease gland sits next to the human intestines.
Drawing of insulin producing beta cells in the pancreas gland showing insuline entering blood stream.
Drawing of insulin producing beta cells in the pancreas gland showing insuline entering blood stream.

Comments

marisuewrites profile image

marisuewrites 3 years ago

This is excellent information and well laid out, Tom.  The progress in research is promising, and if we can help ourselves out by making early improvements in the way we eat...what a healthier life the next generations can live!  The drawings are interesting!  I'm glad you stay up on the latest news to bring to people.

Where was all this help years ago ?  This has been a long time coming.  It effects millions of people...maybe more -- it could have save mom's eyesight! 

Great report! I like your chicken and egg descriptions...makes it easy to understand!

level1diet profile image

level1diet Hub Author 3 years ago

Thanks, marisuewrites!

Aya Katz profile image

Aya Katz Level 4 Commenter 3 years ago

Very good hub! I've always suspected that the tendency to gain weight through low resting metabolic rate was what got certain people in trouble in the first place.

level1diet profile image

level1diet Hub Author 3 years ago

Aya Katz -- Thanks for your support. We need to rid ourselves of the GUILT and SHAME associated with being fat. Once we do, we can begin to rationally respond the actual problem and take responsibility for doing something about it.

Guilt and shame make us run away from the problem. We stop taking photos of ourself. We take down all the mirrors in our house. We become depressed and don't go out in public too often. We avoid negative feedback we would get from others as often as we can.

I'm going to write another essay, or maybe even a book someday about this problem, something like FAT? IT'S NOT YOUR FAULT, BUT WHAT YOU CAN DO ABOUT IT.

I've personally made that journey, losing almost 100 pounds, a story I tell on my diet site.

Look for a hub on the topic soon here, and a longer essay leading to the book on my Level1diet.com pages.

Aya Katz profile image

Aya Katz Level 4 Commenter 3 years ago

I've added a link to this article on my new hubpage

http://hubpages.com/hub/What-Isnt-Poison

level1diet profile image

level1diet Hub Author 3 years ago

Thanks Aya Katz for the kudos and for the link and also for your nice explanation and summary of the point I made here. Great work. I'm a fan!

proton66 profile image

proton66 Level 1 Commenter 15 months ago

Of course, having diabetes type II is associated with improper dieting and irregular exercising.

Regarding genes causing problems, it would makes sense if you're referring to type I and being obese but it has nothing to do with the lack of insulin production. Beta cells are designed to produce and release insulin hormones which work in conjunction with GLUT4 found in the adipose cells. Having a shortage or almost no insulin comes from beta cells inflammation caused by the immune system going against itself. See (Autoimmune diseases linked to abnormal K+ channel expression in double-negative CD4-- and CD8-- T cells, Eur J. Immunol, Cahalan MD, Chandy GK, Grissmer S., 1990, 20: 747-751.)

Unfortunately, most medications used today do not focus on the source. Most increase sensitivity of the adipose cells for improved glucose storage yet induce hypoglycemia as well. Go figure.

andrebreynolds profile image

andrebreynolds 7 months ago

Very informative hub.

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