October Newsletter
In This Issue
Lower Your Risk of Diabetes
Those Things Will Kill You
Teen BMI and Death
A New Model of Medical Care
Dr. Niedfeldt
Old-fashioned medicine with 21st Century convenience and technology
Quick Links
Join Our List
View my profile on LinkedIn 
Follow me on Twitter



I hope this newsletter finds you and your family well. Watching the changes of the leaves over the last few weeks has been wonderful. I am looking forward to a great weekend as it sounds like we are due for some nice temperatures and maybe one last shot at seeing some color. Good luck to our football teams this weekend especially Homestead and of course the Badgers and Packers. It's a great time of year! 


I really emphasize the power of lifestyle in my newsletters and in my practice. The last few months have shown decreased risk of cancer and heart disease through changes in diet and exercise. This month, we look at risk of diabetes. The first article shows that diet really matters when it comes to diabetes. Those people who improve their diet have lower rates. Those who let their diet slip, have higher rates. Pretty simple, right? Check out the specific recommendations in my commentary. 

I think we all know smoking is bad. But how to smoking-related diseases occur and why? The second article has a likely explanation. Smoking actually causes damage to the DNA in our genes. Pretty scary stuff, huh? Read on to see how to lower your risk of genetic damage if you smoke.  

Does being an overweight teen cause problems in adulthood? The answer is yes. The third article shows significant increased risk of diabetes in overweight teens as they get older. 

Click on the links the the left to check out our web site...

Lower Your Risk of Diabetes
Changes in Diet Quality Affects Diabetes Risk          
This study, from Diabetes Care, shows that changes in diet, both good and bad can affect our risk of developing Type 2 diabetes. The authors followed 124,607 healthy adults without diabetes over 20 years and assessed their diets every 4 years using a scale called the Alternate Healthy Eating Index. A 10% decrease in score was associated with 34% increased risk of diabetes, while an increased score of 10% was associated with an 11% decrease in risk. This finding was independent of weight gain or loss and exercise and shows that diet is an independent risk factor for diabetes.   


  • OBJECTIVE: Recent public health recommendations emphasize adopting a healthful dietary pattern, but evidence is scarce on whether incremental diet quality changes have an impact on long-term diabetes prevention. We aim to evaluate diet quality changes during a 4-year period and subsequent 4-year type 2 diabetes incidence.
  • RESEARCH DESIGN AND METHODS Participants of prospective cohorts, the Nurses' Health Study (NHS), NHS II, and the Health Professionals Follow-up Study, who were free of diabetes at baseline (n = 124,607), were observed for ≥20 years. Diet quality, reflected by the Alternate Healthy Eating Index (AHEI) score, was assessed every 4 years to calculate changes. 
  • RESULTS We documented 9,361 cases of type 2 diabetes during 2,093,416 person-years of follow-up. A >10% decrease in AHEI score over 4 years was associated with a higher subsequent diabetes risk (pooled hazard ratio 1.34 [95% CI 1.23-1.46]) with multiple adjustment, whereas a >10% increase in AHEI score was associated with a lower risk (0.84 [0.78-0.90]). Greater improvement in diet quality was associated with lower diabetes risk across baseline diet quality status (P for trend ≤ 0.001 for low, medium, or high initial diet quality) and baseline BMI (P for trend ≤ 0.01 for BMI <25, 25-29, or 30 kg/m2). Changes in body weight explained 32% (95% CI 24-41) of the association between AHEI changes (per 10% increase) and diabetes risk.
  • CONCLUSIONS Improvement in overall diet quality is associated with a lower risk of type 2 diabetes, whereas deterioration in diet quality is associated with a higher risk. The association between diet quality changes and diabetes risk is only partly explained by body weight changes.


I had an interesting conversation with a nutritionist this week. He made a statement that was blunt but really quite true. Everything you put in your mouth is either making you healthy or making you sick. Those words really ring true after reading this article. As the researchers followed people over 20 years, those who ate a less healthy diet became less healthy. Those who ate more healthy became more healthy, at least as it pertains to diabetes. My readers may remember other studies pointing out the link between healthy diet, heart disease and cancer as well. What's the secret? Eat more vegetables and fruits, legumes, whole grains, omega-3 fatty acids. Eat less sugar sweetened beverages, fruit juice, refined grains, transfatty acids, red/processed meat, salt, and avoid excessive alcohol intake. Although this study found results were independent of activity and weight loss, adding more activity will likely be quite synergistic for overall health. 

Those Things Will Kill You
Smoking causes permanent changes in genes

Smoking is a major cause of deaths in the United States and has been shown to cause increased heart disease, cancer, lung disease, diabetes and strokes. When people quit smoking their heart rate and blood pressure begins to normalize. However, although the risk of death due to smoking-related causes is reduced, it does not return to baseline, even years later. This study, from the journal Circulation, explores the reasons for this and found permanent changes to the DNA patterns in the genes linked to smoking-related diseases in people who have smoked which may explain these findings. 
  • Background: DNA methylation leaves a long-term signature of smoking exposure and is one potential mechanism by which tobacco exposure predisposes to adverse health outcomes, such as cancers, osteoporosis, lung, and cardiovascular disorders.
  • Methods and Results: To comprehensively determine the association between cigarette smoking and DNA methylation, we conducted a meta-analysis of genome-wide DNA methylation assessed using the Illumina BeadChip 450K array on 15,907 blood-derived DNA samples from participants in 16 cohorts (including 2,433 current, 6,518 former, and 6,956 never smokers). Comparing current versus never smokers, 2,623 cytosine-phosphate-guanine sites (CpGs), annotated to 1,405 genes, were statistically significantly differentially methylated at Bonferroni threshold of P<1×10−7 (18,760 CpGs at false discovery rate <0.05). Genes annotated to these CpGs were enriched for associations with several smoking-related traits in genome-wide studies including pulmonary function, cancers, inflammatory diseases, and heart disease. Comparing former versus never smokers, 185 of the CpGs that differed between current and never smokers were significant P<1×10−7 (2,623 CpGs at false discovery rate <0.05), indicating a pattern of persistent altered methylation, with attenuation, after smoking cessation. Transcriptomic integration identified effects on gene expression at many differentially methylated CpGs.    
  • Conclusions: Cigarette smoking has a broad impact on genome-wide methylation that, at many loci, persists many years after smoking cessation. Many of the differentially methylated genes were novel genes with respect to biological effects of smoking and might represent therapeutic targets for prevention or treatment of tobacco-related diseases. Methylation at these sites could also serve as sensitive and stable biomarkers of lifetime exposure to tobacco smoke.                         
In normal cells, DNA methylation patterns are stable and orderly to maintain cell functions. Disruption of these patterns can result in altered tissue function and resultant disease. In this study of over 16,000 patients, the researchers found that smokers had 18,670 differentially methylated DNA sites related to 6,720 genes as compared to never smokers. These genes are those related to smoking-related diseases including lung cancer, heart disease, strokes, diabetes and emphysema. There was also a significant dose effect, meaning the more (and longer) one smoked, the worse the changes to the genes. The good news is that 5 years after smoking cessation, most, but not all of these sites did normalize. The bottom line is that the less you smoke (or have smoked) the better. If you are smoking, stop now. Let your genes heal. 
Teen BMI and Death
Adolescent BMI predicts mortality from diabetes
sleeping obese kid
Being an overweight teenager has been shown to predict diabetes mortality later in life. This very large study published in Diabetes Care, reviewed the BMI values of 2,294,139 teens (average age 17) and found that teens with BMI in the 85th to 94th percentile had 8 times the risk of death and those over the 95th percentile had 17 times the risk of death as compared to teens below the 50 percentile. 
  • OBJECTIVE: The sequelae of increasing childhood obesity are of major concern. We assessed the association of BMI in late adolescence with diabetes mortality in midlife.
  • RESEARCH DESIGN AND METHODS The BMI values of 2,294,139 Israeli adolescents (age 17.4 ± 0.3 years), measured between 1967 and 2010, were grouped by US Centers for Disease Control and Prevention age/sex percentiles and by ordinary BMI values. The outcome, obtained by linkage with official national records, was death attributed to diabetes mellitus (DM) as the underlying cause. Cox proportional hazards models were applied.
  • RESULTS During 42,297,007 person-years of follow-up (median, 18.4 years; range <1-44 years) there were 481 deaths from DM (mean age at death, 50.6 ± 6.6 years). There was a graded increase in DM mortality evident from the 25th to the 49th BMI percentile group onward and from a BMI of 20.0-22.4 kg/m2 onward. Overweight (85th to 94th percentiles) and obesity (the 95th percentile or higher), compared with the 5th to 24th percentiles, were associated with hazard ratios (HRs) of 8.0 (95% CI 5.7-11.3) and 17.2 (11.9-24.8) for DM mortality, respectively, after adjusting for sex, age, birth year, height, and sociodemographic variables. The HR for the 50th through 74th percentiles was 1.6 (95% CI 1.1-2.3). Findings persisted in a series of sensitivity analyses. The estimated population-attributable fraction for DM mortality, 31.2% (95% CI 26.6-36.1%) for the 1967-1977 prevalence of overweight and obesity at age 17, rose to a projected 52.1% (95% CI 46.4-57.4%) for the 2012-2014 prevalence.
  • CONCLUSIONS Adolescent BMI, including values within the currently accepted "normal" range, strongly predicts DM mortality up to the seventh decade. The increasing prevalence of childhood and adolescent overweight and obesity points to a substantially increased future adult DM burden.
This study is very concerning. This study reviewed records of people going back all the way to 1967. Even teens who are over the 50th percentile are at 60% increased risk. 
We have an epidemic of obesity in our teens and indeed, the authors found risk increasing in the later groups studied. What this means in the long-term is that we are looking at an epidemic of diabetes related deaths and complications from diabetes unless we make dramatic changes in our diets and exercise programs (makes the first article pretty timely as well). It appears our children are less active than ever and have diets that are worse than ever. Unless we embrace the idea of food being our medicine, we will have a lot more people taking drug company produced medicine. 

Thank you for taking the time to read through this newsletter. I hope you have found this information useful as we work together to optimize your health. 


Last month we found that a healthy diet and exercise was beneficial for heart disease and colon cancer. This month, it's good to prevent diabetes. It is especially important to get this through to our teens. Being overweight as a teen seems to have some life-long increased risks. 

I think we all know smoking is bad for you. Now we know why, it is actually changing your genes and making you more prone to many chronic diseases. While you can reverse much of this after a few years after stopping, some of the changes are permanent. As always, it's best to never start. 


As always, if you have questions about anything in this newsletter or have topics you would like me to address, please feel free to contact me by email, phone, or just stop by! 

To Your Good Health,
Mark Niedfeldt, M.D.