Fighting Cancer With Low Carb Atkins Diet?

Fighting cancer with low carb (Atkins) diet: A review on cancer and nutrition and a comparison with recommendations made by the American Cancer society

In recent years, there has been a push for alternative treatments for cancer that focus on lifestyle modification and health improvements rather than relying solely on chemotherapy or surgery. One such alternative treatment is the low carb or Atkins diet. While the Atkins diet was developed as a weight loss plan, it has also been called a “kidney-friendly” diet due to its adherence to a restricted protein intake. Furthermore, while referral guidelines from the American Cancer societies are predominantly standardized around normal type of diets, the structure of the cancer site may require changes in modifying diets.

Initial work on the impact of diet on carcinogenesis has mainly focused on associations with excess calorie intake and body weight. A large body of evidence now supports a link between unsupportive dietary practices and cancer induction. It has been well documented that inactivation of vitamin D plays an important role in cancer growth. These include habitual weight gain, overuse of alcohol in women, air pollution, dyslipidemia, lack of physical activity, obesity, depression, vitamin C deficiency, poor dietary intake, usage of fisetin, elevated homocysteine levels, a tendency for hyperactivation in immunity, predominantly the TH1 response producing type feedback. Although slight variations exist, oxidative stress has also often been found to increase with carcinogen acid exposure in accordance with the intensity of mitochondrial oxidative action. Insufficient hormone-independence of glutathione S-transferases also serves as an important factor in supporting progression to cancer.

Consumption of avoidant nutrients may promote mutagenic damage through unique effective epigenetic regulation altered by dysfunctional gene regulatory mechanisms. It appears that many nongenetic factors undertaken during diet markedly disfavor cells during differentiation as functionably tumorigenic progress. Implications of the metabolic status that affects tumor metabolism are also highlighted while discussing the effects of macronutrients causing both an opposite and divergent impact on biological pathways, especially mitochondria. However, the weight of evidence points towards the fact that the energy composition of a typical American diet carries potential risks amplifying physical interactions that correspond with environmental carcinogens.

Scientific literature suggests that increased impact on risk of carinogenesis is carried on by refined carbohydrates, sugar, or starch products. i.e. products high in fermentable carbohydrate. In a randomization conducted in 229 obese professors, restriction of these has been shown to help contribute to statistically significant decreases in lymphocyte telomere shortening, frequencies of increased blood counts, total serum cholesterol, UA, β-TC, reduction in TG,, homocystine, insulin responses, UACR, AUC, HOMA-IR and, importantly, fewer arrhythmias. Moreover, a paradigm shift in how to integrate complementary principles of exercise, stress management and social support might strengthen adherence to support the implications of highly controlled diets and become the cornerstone of widespread efforts directed to develop preventative interventions for patients diagnosed with cancer. By combining definitive therapy with interconnected lifestyle modifications and concurrent peer support, this opportunity to navigate behavior until the national cancer agenda embarks on achieving optimal prevention and avoiding recurrence.