Here’s another pop quiz: What’s the most effective way to prevent or reverse diabetes?
- Exercise
- Diet
- Weight Loss
- Avoiding sugar
The answer, surprising to many, is not diet, it is — weight loss! Losing about 5-10% of your body weight seems to have the most impact in reducing your risk of developing diabetes. In fact, every kilogram of weight loss lowers risk by 16%! This was shown in some good studies, especially an article in 2006 from Diabetes Care, called “Effect of Weight Loss with Lifestyle Intervention on Risk of Diabetes”. This study delved deep into the amazing research from one of public health’s most famous programs, the Diabetes Prevention Program, which studied thousands of pre-diabetics over many years. This program released a world-famous study in 2002 showing that aggressive lifestyle changes reduced a pre-diabetic’s chance of developing full-blown diabetes by an astonishing 58%; this was much more effective than the preventive daily pill, called metformin, which reduced risk 31%.
But this initial study didn’t specifically say which part of lifestyle changes was most effective; was it the weight loss, the increased exercise, or a diet overhaul? We found out the answer from this above 2006 follow-up study, which broke down the 2002 data. The main points:
- A 5% weight loss reduced risk 58%
- Second most effective: exercise. Those who met the goal (150 minutes a week of moderate exercise) reduced risk by 44%
- Third most effective: diet changes, especially reducing daily fat to <25% total daily calories
What this should mean for my readers, especially those who have been told they are pre-diabetic, is that you should focus first on losing at least 5% of your weight. Of course, a major component of weight loss involves more exercise and eating less fat, so it’s all connected. But what the data does mean is that if you only focus on exercise but are still gaining weight, or if you’re cutting fat but still not losing weight, then you need to rethink your action plans.
Other great news: the study also shows that those who achieved all three goals (losing >7% weight; exercising >150 minutes a week, and lowering diet fat <25%) lowered their risk of diabetes by over 80%! The figure below from this 2006 study clearly shows step-by-step lowering of risk with all 3 components; the dashed line shows the risk when weight loss is removed as a factor: as you see, there is still an improvement but not nearly as impressive:
I think this is a great study which really helps clarify people’s wellness plans for lifestyle choices. Now, the major question is — how to lose weight? Well, if I could figure that one out and patent it, I’d be rich. Serious weight loss is extremely hard, perhaps even more difficult than quitting smoking. What we do know is that diets do not work — people who repeatedly diet almost always regain weight plus a bit more. Nope, the simple answer, unfortunately, is that we all need to do the hard work of reevaluating our lifestyle; true and sustained weight loss must include diet changes and routine exercise. Don’t forget the golden rule of 150 minutes a week of heart-racing exercise.
Do You Know How Overweight You May Be?
I created a Body Mass Index (BMI) calculator on a previous post here, where you can see which category you fit: normal, overweight, obese, or morbidly obese.
More Information
The web has tons of information for diabetics, but here are a few detailed patient handouts from the UpToDate Patient Information website:
Patient Info on Diabetes Type 2
Patient Info on Diet and Diabetes
Other good bets would be from WebMD.com or the Mayoclinic.com.
Although early risk factors are not set in stone, and current lifestyle makes a difference, one huge risk factor for diabetes (and obesity too) is whether one was formula fed or breastfed as an infant. Breastfeeding has a lifelong protective effect and formula feeding raises the risk substantially.
There are even protective effects for the breastfeeding mother. There are many others, but regarding this discussion, breastfeeding reducing the incidence of Type 2 Diabetes and lowers risk of obesity later on as well for her.
I’d love to cut n paste from some of the documents I have from WABA and The Academy of Breastfeeding Medicine but they are not cooperating and get jumbled up. I did manage to fix up this one citation
“A review of infant feeding practices and childhood chronic diseases shows increased risk for Type I diabetes, celiac disease, some childhood cancers, and inflammatory bowel disease associated with artificial infant feeding. Davisl MK Breastfeeding and chronic disease in childhood and adolescence. North Amer 48:125- 141, 2001”
I just don’t have time to unjumble the other ten or so citations (just about diabetes and weight alone). There are many more, regarding (infant) chronic illness, childhood cancers, mortality (death), dental occlusion (poorly aligned teeth), gastrointestinal infections, pneumonia, nutrient deficiencies, cardiovascular disease and protection against/sensitivity to environmental contaminants. And for the mother, stress management, osteoporosis, breast and ovarian cancer, rheumatoid arthritis.
If anyone wants to find the document, it’s called “Risks of Formula Feeding” put out by the World Alliance for Breastfeeding Action and INFACT Canada. Retrieve (two pdf files) at http://www.waba.org .
from my IMVA newsletter (International Medical Veritas Association)
view online here, about Type 2 Diabetes
http://blog.imva.info/medicine/insulin-magnesium-story
“There is a strong relationship between magnesium and insulin action. Magnesium is important for the effectiveness of insulin. A reduction of magnesium in the cells strengthens insulin resistance.[1],[2]
….A new study published in the journal Clinical Nutrition from a team of Brazilian researchers has found that low levels of magnesium worsens the symptoms of type 2 diabetes, as this often results in low levels of insulin and elevated blood sugar. The research indicates that a diabetic’s ability to control blood sugar levels is closely tied to their magnesium levels, as the mineral plays an important role in insulin receptor cells. Another study published in the journal Diabetes, Obesity and Metabolism found that taking oral magnesium supplements helps individuals who have become insulin resistant avoid developing type 2 diabetes. These are just the latest in a long string of studies that the medical establishment and mainstream diabetes organizations continue to ignore……”
Low serum and intracellular magnesium concentrations are associated with insulin resistance, impaired glucose tolerance, and decreased insulin secretion.[3],[4],[5]
…..Insulin resistance and magnesium depletion result in a vicious cycle of worsening insulin resistance and decrease in intracellular Mg(2+) which limits the role of magnesium in vital cellular processes.[7]
view the entire thing at the link above. It’s not blocked in China. Or, sign up for their newsletter or RSS feed here
http://blog.imva.info/
This article
http://healthandenvironmentonline.com/2011/02/21/chemicals-and-diabetes-a-short-history/
was linked to in one of the fantastic yahoo groups I keep up with.
“Chemicals as an emerging risk factor in developing type-2 diabetes: a short history”
(I cut out some parts… see whole thing at link above)
“. obese persons that do not have elevated POPs [persistent organic pollutants such as DDT, PCBs and dioxins. ] are not at elevated risk of diabetes, suggesting that the POPs rather than the obesity per se is responsible for the association. ”
Evidence is emerging that persistent organic pollutants, even at background levels in populations, act in conjunction with obesity to cause type-2 diabetes.
You may be surprised by these words, written by Professor David Carpenter, Director of the Institute for Health and the Environment at the University of Albany, New York, in a review summarising the significance of studies examining a potential role for environmental pollutants in the onset of type-2 diabetes (Carpenter 2008).
In England, approximately 5% of men and 4% of women have been diagnosed with diabetes (Health Survey for England). In some states of the US, as much as 12.7% of the adult population is diagnosed as diabetic (Kaiser State Health Facts). Because many cases of diabetes go undiagnosed, the real incidence rates are thought to be higher.
Diabetes is a group of metabolic diseases in which a person’s blood sugar levels are too high. There are two main types of diabetes. Type-1 diabetes results from the body’s failure to produce insulin. Type-2 diabetes results from cells in the body losing the ability to respond to insulin, and is sometimes combined with insufficient insulin production.
Type-1 diabetes is caused by an autoimmune reaction that results in the destruction of the insulin-producing cells in the pancreas. It tends to develop early in life and is much rarer than type-2 diabetes. Type-2 diabetes becomes more common as people grow older.
Type-2 diabetes is of particular concern because incidence of the condition is increasing at an alarming rate. Although confirmatory data is not yet available, risk projections (Zimmet et al. 2001) have estimated that between 2001 and 2010, global incidence rates could have increased by 46%. North America could see an increase of 23%, Latin America of 44% and Africa of 50%.
There is also evidence that the age of onset for type-2 diabetes is coming down. Mean age at diagnosis in the US decreased from 52.0 to 46.0 years between 1988 and 2000 (Koopman et al. 2005). It was already clear by 2001 that type-2 diabetes was no longer an adult disease, with children as young as eight years old being diagnosed (Brosnan et al. 2001).
Going beyond the established risk factors
The main factors identified as responsible for diabetes are an aging population with a genetic predisposition towards diabetes, combined with changes associated with a so-called “modern” lifestyle such as low physical activity, obesity and eating more foods high in animal fats.
Human epidemiological studies are, however, challenging the completeness of this picture of the causes of the disease: researchers are finding consistent correlations between an elevated risk of type-2 diabetes and the presence in people of persistent organic pollutants (POPs) such as DDT, PCBs and dioxins. An earlier study found that levels of PCBs among subjects with diabetes were 30% higher than in the control subjects (Longnecker et al. 2001).
In 2006 Professor Duk-Hee Lee of the School of Medicine at Kyungpook National University, Korea, pushed the hypothesis further. On the basis of her own research finding “unusually strong” associations between POPs exposure and diabetes (Lee et al. 2006a), Lee speculated that obesity may not be sufficient for developing type-2 diabetes but, in addition, exposure to POPs was necessary to initiate the disease (Lee et al. 2006b). These levels could be as low as the background levels to which everyone is already exposed.
Because Lee’s epidemiological research at the time was only cross-sectional, however, she could not at that time draw any conclusions about the direction of causation: either elevated POPs levels caused diabetes in obese people, or obese people with diabetes metabolised POPs differently leading to elevated levels of the chemicals in their body. Which it was, Lee could not say. Indeed, before 2006 not one single prospective study had been carried out to test whether or not body burden of POPs was associated with type-2 diabetes.
Since 2006 three studies have confirmed the direction of causation, showing that POPs exposure in obese people causes type-2 diabetes, rather than the other way around. These are a study conducted by the U.S. Centers for Disease Control and Prevention, which found people with the highest levels of exposure to six POPs were 38 times more likely to have diabetes than those with the lowest exposure (Turyk et al. 2009), a study by Lee herself (Lee et al. 2010) and a further study of Swedish women (Rignell-Hydbom et al. 2009).
The need to reduce POPs exposure in food
Lee’s 2010 study is arguably the most provocative. Besides providing evidence that type-2 diabetes is caused by more factors than obesity alone, if correct then her findings have two profound implications: firstly, that current type-2 diabetes epidemiology may be badly confounded by POPs exposure; and secondly, that extremely low concentrations of pollutants are sufficient to initiate diabetes in obese people.
The implications are related because Lee found that exposure to background levels of POPs is sufficient to substantially raise the risk of diabetes. “The problem is the doses are so low that the control groups used in the epidemiological studies are already being exposed to levels of POPs which significantly increase the risk of developing diabetes,” explains Carpenter.
This would mean that current epidemiology which associates obesity with type-2 diabetes is not able to rule out a causal role for POPs. Instead, it can only tell us that obesity raises risk in conjunction with whatever factors (such as POPs exposure) occur simultaneously in obese people. If such a role could be confirmed, it would amount to a significant breakthrough in understanding the causes of diabetes and mark out a clear course of action.
Carpenter believes that heritage contaminants such as PCBs are still present at extraordinarily high levels, even though they were banned as long as 40 years ago, and points to food as the major source of exposure.
POPs such as PCBs, flame retardants and dioxins are recirculated in commercial food production through animal feed, as animals and fish are fed animal and fish fats to accelerate growth. Fish oils and fish meals are the animal feeds most heavily contaminated with dioxin, followed by animal fats, according to the EU Feeding Fats Safety research project.
As a result, animal foods contribute 80% to total human dioxin exposure and are the primary route for dioxin into food systems. As a result the EU is currently funding research into reducing POPs load in animal feed. There is already evidence that switching to purified feed can reduce POPs levels in salmon by 51-82% (Berntssen et al. 2010), while switching to non-animal feeds would likely be even more effective in reducing human exposure to POPs.
Absence of medical attention
The precise extent of the contribution of POPs to diabetes is not yet known. However, Carpenter says: “There aren’t any very good explanations for the marked increase in diabetes, except it is paralleled by the rise in obesity. If one accepts that obesity is not the only risk factor, then the [.] emerging issue of chemicals that might promote diabetes or obesity looks interesting. ”
Given the pressure rising rates of diabetes are already exerting on healthcare, coupled with the looming threat of an aging population for which this problem is only likely to get worse, one could ask why the issue is not yet widely discussed?
“In general it is very hard to get this sort of thing published in the medical literature,” says Carpenter. “The clinical community needs to understand there are about 12 compelling studies in the area.”
For now, Lee’s two papers from 2006 are almost the only ones published in medical journals; most studies looking at the issue are published in environmental health journals, and these do not have wide readership among the medical community.
“Most physicians are so busy treating patients they don’t give a thought to what might have caused diabetes; they think someone who has diabetes has just not exercised and has eaten too much,” says Carpenter, who has a medical degree himself. “They have no understanding of the role of these chemical exposures: education about chemicals as potential causes of diabetes for physicians is absolutely critical.”
Several recent studies are once again showing links to PHTHALATE chemical exposure (most likely in personal care products) having a role in diabetes. Google diabetes phthalates ncbi and some recent studies will come up (2010, 2011, June 2012)