One of the most controversial questions in the integrative oncology field is whether cancer patients should avoid whey protein. Some people contend that dairy products may increase the growth of cancer cells since they contain amino acids and growth factors. Dairy products do contain a molecule called insulin-like growth factor (IGF-1), which has the same activity as the naturally produced human form. As a clinician I recommend that patients avoid any foods that will up-regulate growth factors since that may contribute to the growth of cancer cells.1 So, as part of an anti-cancer diet it would be prudent to avoid
Type 2 Diabetes Mellitus (T2DM) is a condition characterized by poor blood sugar control and insulin resistance. These excess sugars can cause damage to many of the proteins in the body and ultimately damage vital organs such as the kidneys, eyes, and nervous system. Sadly, T2DM affects almost 10% of the entire North American population and up to 25% of the elderly population (aged 65 or older). It is also one of the leading causes of death in North America.
Although T2DM is largely a disease resulting from poor dietary choices and sedentary activity, many people do not realize that there are more factors at play. Here are some other considerations surrounding T2DM that may surprise you:
Environmental Chemical Exposure:
Environmental chemical exposure has been shown to play a role in insulin regulation and blood sugar control. For example, a dose-response relationship has been found between low-level exposure to persistent organic pollutants (POP’s) and the prevalence of diabetes. POP’s are chemicals that do not easily breakdown and bioaccumulate within the environment and potentially in the body. Examples of such compounds include polychlorinated biphenols (PCBs) found in plastics and DDT found in mosquito repellants. Interestingly, it has been found that obesity does not seem to increase the risk for T2DM in those with very low levels of POP’s. This implies that part of the increasing T2DM risk found in overweight individuals is because of excess storage of POP’s within the adipose tissue, leading to insulin and blood glucose disruption. Pesticide exposure has also been linked with an increased risk of pregnancy-related diabetes, just as air pollutants and exposure to phthalates found in plastics have been found to increase the risk of T2DM.
Gamma-glutamyltransferase (GGT) is a liver enzyme that is often used as a marker for liver damage in alcoholics. However, few people know that it can also be used as a non-specific marker for chemical exposure, indicating that more toxic exposure leads to elevated GGT levels. It has been shown that individuals with a GGT level greater than 50 U/L have about a 26-fold increase in diabetes risk vs individuals with GGT levels below 10 U/L. Perhaps GGT should be used as a screening marker in pre-diabetic individuals?
Poor Gut Bacteria:
An altered microflora has been implicated in those with T2DM, showing an alteration in the levels of specific bacteria when compared to those without T2DM. Specifically, a higher ratio of bacteroidetes to firmicutes has been demonstrated with higher levels of Bacillus and Lactobacillus species. Animal studies have shown that the administration of prebiotics can improve metabolic control (such as insulin resistance) just as antibiotic administration in diabetic subjects can improve blood sugar regulation. This suggests that an imbalance in gut bacteria may need to be addressed in diabetic individuals.
Of course, there is still much to learn about the complex relationship between gut bacteria and the development or progression of T2DM. It is known that poor diet can solely be responsible for changes in the composition of the microflora, meaning that perhaps the altered microflora is a result of poor dietary choices and not an independent risk factor for T2DM. More research is clearly needed in this area.
Although genetics cannot be entirely to blame for the development of T2DM, they do play a strong role in predisposing an individual to the condition. For example, if one of your parents has T2DM then you have a 40% risk of developing the condition yourself. If both parents have T2DM, your risk jumps to 70%. These findings are supported by the fact that identical twins have a 70% concordance rate of both developing T2DM. These statistics provide strong evidence for the role of epigenetics in diabetes, meaning that genetic predispositions will only be realized under specific environmental triggers. In other words, poor diet and lifestyle can “turn on” specific genes that cause T2DM, but the presence of the gene itself does not guarantee the disease.
Evidence exists to show that high levels of stress can contribute to the onset of T2DM. Moreover, it is well-known that stress can elevate blood sugar levels in those already diagnosed with T2DM and stressful events can destabilize blood sugars for hours afterwards. The mechanisms for both of these circumstances are not concrete but there are many likely factors at play. First of all, the activation of the hypothalamus-pituitary-adrenal (HPA) axis leads to a rise in cortisol and subsequently blood sugars. At the same time, this can lead to an increase in adipose deposition which directly contributes to insulin resistance.
In conclusion, it is important to remember that the body and mind are complex entities affected by many dynamic factors. The environment that surrounds us greatly impacts our health. For those with T2DM, remember not only to focus on regular exercise and a low-carbohydrate, well-balanced diet, but also living a clean and well-balanced lifestyle.
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Bianchi C, et al. Serum gamma-glutamyltransferase levels are related to insulin sensitivity and secretion in subjects with abnormal glucose regulation. Diabetes Metab Res Rev. 2010 Mar;;26(3):181-6
Lee DH et al. A strong dose-response relation between serum concentrations of persistent organic pollutants and diabetes: results from the National Health and Examination Survey 1999-2002. Diabetes Care. 2006 Jul;29(7):1638-44.
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Kirsty Brown et al. Diet-Induced Dysbiosis of the Intestinal Microbiota and the Effects on Immunity and Disease. Nutrients. 2012 Aug; 4(8): 1095–1119.
Larsen N et al. Gut microbiota in human adults with type 2 diabetes differs from non-diabetic adults. PLoS One. 2010 Feb 5; 5(2):e9085.
Rashmi B. Prasad and Leif Groop. Genetics of Type 2 Diabetes—Pitfalls and Possibilities. Genes (Basel). 2015 Mar; 6(1): 87–123
Cathy Lloyd et al. Stress and Diabetes: A Review of the Links Diabetes Spectrum Apr 2005, 18 (2) 121-127; DOI: 10.2337/diaspect.18.2.121
Mooy JM, De Vries H, Grootenhuis PA, Bouter LM, Heine RJ: Major stressful life events in relation to prevalence of undetected type 2 diabetes. Diabetes Care 23:197 –201, 2000