Diabetes & PCa "protection".

[pjoshea13]

New study below.

This post follows on from a Yahoo thread, where I suggested that burnout of the beta cells in the pacreas is responsible for reduced risk of PCa in diabetics.

"Persons with type 1 diabetes were identified from five nationwide diabetes registers: Australia (2000-2008), Denmark (1995-2014), Finland (1972-2012), Scotland (1995-2012) and Sweden (1987-2012)."

Increased risk (men):

+23% for stomach

+30% for kidney

+53% for pancreas

+100% for liver

Reduced risk:

-44% for PCa

Other studies have noted that protection is stronger with time since diagnosis of diabetes. In fact, one U.S. study found that protection only begins ~1 year after diagnosis, so the 44% reduction would likely be much higher if newer cases were excluded.

I continue to be amazed that this type of study seems not to have been turned into advice to men. Obviously, not advice to become diabetic, but rather to restore insulin sensitivity.

Insulin resistance occurs when the body is challenged by chronic glucose spikes. The pancreas responds by pumping out more insulin. Insulin is a PCa growth factor.

Fasting glucose is a clue that insulin resistance exists. The reference range is 70-100 mg/dL, but 85-100 is unsafe, IMO.

A surrogate measure of insulin resistance is the triglycerides:HDL cholesterol ratio, with 1:1 being ideal IMO.

High carb/low fat diets promoted by Dean Ornish increase triglycerides, & a >3:1 ratio is not uncommon.

Addressing insulin issues might have a dramatic effect on PCa risk, but could be much more important after a PCa diagnosis. Again, IMO.

{How many urologists/oncologists read the Diabetologia journal, do you think?}

-Patrick

ncbi.nlm.nih.gov/pubmed/269...

Diabetologia. 2016 Feb 29. [Epub ahead of print]

Cancer incidence in persons with type 1 diabetes: a five-country study of 9,000 cancers in type 1 diabetic individuals.

Carstensen B1, Read SH2, Friis S3, Sund R4, Keskimäki I5, Svensson AM6, Ljung R7, Wild SH8, Kerssens JJ9, Harding JL10, Magliano DJ10, Gudbjörnsdottir S6; Diabetes and Cancer Research Consortium.

Author information

1Steno Diabetes Centre, Gentofte, Denmark.

2Usher Institute of Population Health Sciences & Informatics, University of Edinburgh, Teviot Place, Edinburgh, EH8 9AG, Scotland, UK. [e-mail].

3Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen, Denmark.

4Centre for Research Methods, Department of Social Research, University of Helsinki, Helsinki, Finland.

5Division of Health and Social Services, National Institute for Health and Welfare, Helsinki, Finland.

6Department of Medicine, Sahlgrenska University Hospital, University of Gothenburg, Gothenburg, Sweden.

7Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

8Usher Institute of Population Health Sciences & Informatics, University of Edinburgh, Teviot Place, Edinburgh, EH8 9AG, Scotland, UK.

9Information Services, NHS National Services Scotland, Edinburgh, Scotland, UK.

10Department of Clinical Diabetes and Epidemiology, Baker IDI Heart and Diabetes Institute, Melbourne, Australia.

Abstract

AIMS/HYPOTHESIS:

An excess cancer incidence of 20-25% has been identified among persons with diabetes, most of whom have type 2 diabetes. We aimed to describe the association between type 1 diabetes and cancer incidence.

METHODS:

Persons with type 1 diabetes were identified from five nationwide diabetes registers: Australia (2000-2008), Denmark (1995-2014), Finland (1972-2012), Scotland (1995-2012) and Sweden (1987-2012). Linkage to national cancer registries provided the numbers of incident cancers in people with type 1 diabetes and in the general population. We used Poisson models with adjustment for age and date of follow up to estimate hazard ratios for total and site-specific cancers.

RESULTS:

A total of 9,149 cancers occurred among persons with type 1 diabetes in 3.9 million person-years. The median age at cancer diagnosis was 51.1 years (interquartile range 43.5-59.5). The hazard ratios (HRs) (95% CIs) associated with type 1 diabetes for all cancers combined were 1.01 (0.98, 1.04) among men and 1.07 (1.04, 1.10) among women. HRs were increased for cancer of the stomach (men, HR 1.23 [1.04, 1.46]; women, HR 1.78 [1.49, 2.13]), liver (men, HR 2.00 [1.67, 2.40]; women, HR 1.55 [1.14, 2.10]), pancreas (men, HR 1.53 [1.30, 1.79]; women, HR 1.25 [1.02,1.53]), endometrium (HR 1.42 [1.27, 1.58]) and kidney (men, HR 1.30 [1.12, 1.49]; women, HR 1.47 [1.23, 1.77]). Reduced HRs were found for cancer of the prostate (HR 0.56 [0.51, 0.61]) and breast (HR 0.90 [0.85, 0.94]). HRs declined with increasing diabetes duration.

CONCLUSION:

Type 1 diabetes was associated with differences in the risk of several common cancers; the strength of these associations varied with the duration of diabetes.

KEYWORDS:

Cancer incidence; Cancer rate ratio; Cancer subtypes; Diabetes duration

PMID: 26924393 [PubMed - as supplied by publisher]

[pjoshea13]

I am so used to reading about the protection of adult-onset diabetes, that I didn't realize that the study was for type 1 diabetes. My comment about protection only starting a year after diagnosis is therefore irrelevant.

-Patrick