The image of a universal panacea is increasingly promoted by both health workers and patients contributes to the fact that in 2019 the sale of vitamin D supplements registered a profit of $ 1.1 billion, players in the dietary supplement market expecting this profit to reach $ 1.7 billion in 2025.

And it is “waiting” not “estimating” because in market reports such as“Vitamin D market”, those who might be interested are trained how to educate people to buy more and more.

It’s just that vitamin D is not a magical supplement that wipes away any disease, it is a physiologically active hormone that can spell nothing but side effects when taken without a proven vitamin D deficiency as a leaf in the wind of the pharmaceutical industry.

Sadly, being a dietary supplement, you can be be educated indirectly by the same supplement manufacturers to blame any side effects they might cause on anything and everything else besides them, as these manufacturers are not required by law to demonstrate either that these supplements do what they say they do, nor that these supplements do not have side effects.

When you buy and use dietary supplements you are a “client” not a “patient”, regardless of whether the person who prescribed them to you is a physician or not. Physicians do not have the professional training to prescribe dietary supplements. Nobody has the professional training to prescribe dietary supplements. Dietary supplements are promoted not “prescribed” because dietary supplements are legally defined as “foods” not as “drugs”.

In todays’s hectic life, the hope that you could prevent something, anything, by simply taking a pill instead of the healthy lifestyle you know you should actually have is ever more present – although even on these products’ label is written black on white that they cannot replace a healthy lifestyle.

– Who cares if maybe they cannot?

– Maybe they can.

– Just that the current scientific evidence shows that they mainly cannot.

The efficiency of using vitamin D supplements for the prevention of various diseases ranging from cancer to cardiovascular disease is an assumption unsupported scientific evidence. (1, 2, 3)

Hypovitaminosis D is one of the many consequences of an unhealthy lifestyle, not the cause of illnesses that result from the unhealthy lifestyle you keep trying to hide by taking supplements.

Both hypovitaminosis D and these illnesses are consequences. The cause of these illnesses is the unhealthy lifestyle not the lack of vitamin D. And the cause does not disappear when if you somehow manage to wipe away one of the consequences. Even vitamin D deficiency doesn’t disappear when you take vitamin D supplements if you don’t have the deficiency first.

And, if scientific evidence points to the fact that preventing various diseases by using vitamin D supplements is just a cozy assumption, current scientific evidence shows that the efficacy of using vitamin D supplements to prevent osteoporosis in the absence of vitamin D deficiency is another cozy assumption. (4)

A physician recommending dietary supplements is not practicing medicine, he practice marketing. As cozy, inefficient and unprofessional as when a beautician would recommend artificial tanning devices to achieve an appropriate vitamin D status. (5) And of course we can mock science by inviting evidence based medicine fans to participate in a double blind, randomised, placebo controlled, crossover trial of the parachute. (6)

Regardless of the core profession, dietary supplement promoters are taught how to educate you to feel that you need these products by the pharmaceutical industry, not by independent labs or objective researchers who scientifically prove that vitamin D supplementation of any good to those without a vitamin D deficiency.

Despite the fact that today being popular seems more important than being physiologically correct, vitamin D supplements show no efficacy without deficiency, (7, 8) and osteoporosis prevention is far more complicated than taking some pill.

References

(1) Beveridge, Louise A., et al. “Effect of vitamin D supplementation on markers of vascular function: a systematic review and individual participant meta‐analysis.” Journal of the American Heart Association 7.11 (2018): e008273.

(2) Autier, Philippe, et al. “Effect of vitamin D supplementation on non-skeletal disorders: a systematic review of meta-analyses and randomised trials.” The lancet Diabetes & endocrinology 5.12 (2017): 986-1004.

(3) Manson, JoAnn E., et al. “Vitamin D supplements and prevention of cancer and cardiovascular disease.” New England Journal of Medicine 380.1 (2019): 33-44.

(4) Reid, Ian R., Mark J. Bolland, and Andrew Grey. “Effects of vitamin D supplements on bone mineral density: a systematic review and meta-analysis.” The Lancet 383.9912 (2014): 146-155.

(6) Pierret, Lauranne, et al. “Overview on vitamin D and sunbed use.” Journal of the European Academy of Dermatology and Venereology 33 (2019): 28-33.

(6) Smith, Gordon CS, and Jill P. Pell. “Parachute use to prevent death and major trauma related to gravitational challenge: systematic review of randomised controlled trials.” Bmj 327.7429 (2003): 1459-1461.

(7) Fassio, A., M. Rossini, and D. Gatti. “Vitamin D: no efficacy without deficiency. What’s new?.” Reumatismo 71.2 (2019): 57-61.

(8) Reid, Ian R., and Mark J. Bolland. “Controversies in medicine: the role of calcium and vitamin D supplements in adults.” Medical Journal of Australia (2019).

Articolul Vitamin D supplements – hype and physiology apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

And I wrote “sadly” for two reasons:

1) Because putting the equal sign between health and alkalinity ignores the fact that anyone can instantly become alkaline when they:

• vomit (Mehler & Walsh, 2016)
• have a thermal shock in case of heat stress (Bain et al., 2015)
• have fever (Schuchmann et al., 2011)
• have a stroke (Zöllner et al., 2015)

2) Because the target audience of alkaline water and water alkalizing devices are often cancer patients.

Just that the story about improved health through modifying pH either by alkaline diet either by drinking alkaline water is quite hype.

We know from a long time now that malignant cells that use the Warburg effect (aerobic glycolysis) have an alkaline intracellular pH and an acidic extracellular one – alkalinity helping them to avoid apoptosis, to proliferate and to metastasise (Griffiths, 1991; Harguindey et al., 2005; White et al., 2017).

Some preclinical studies performed on glycolytic malignant cellular lines or on mice with homogeneous glycolytic malignant tumours show that extracellular alkalinity could contribute to destroying these types of malignant cells (Mazzio et al., 2012; Yustisia et al., 2017). Other studies confirm this conclusion, but also show that in the case of malignant cells that do not use the Warburg effect alkalizing the extracellular environment can help them proliferate and metastasise (Wanandi et al., 2017).

The attempt to counteract extracellular acidosis induced by aerobic glycolysis by drinking alkaline water ignores the fact that in vivo tumours are heterogeneous and that malignant cells are highly adaptive (Vlashi et al., 2014; Xie et al., 2014; Obre & Rossignol, 2015) as they can survive by using other metabolic pathways than aerobic glycolysis: the Crabtree effect, (Jones & Thompson, 2009) the reverse Warburg effect (Pavlides et al, 2009), entosis (Lozupone & Fais, 2015) etc.

And a metabolic analysis performed on 740 biopsies from breast cancer patients shows that only 40.3% of the studied tissue samples presented aerobic glycolysis (Choi et al, 2013). We wipe out the fact that even in tumours with the same localisation we cannot simply tell by default that drinking alkaline water associate apoptosis or malignant proliferation and metastasis, we wipe out the fact that 60 is bigger than 40 and we sell assumptions to confuse and desperate patients.

Besides many mammary malignant cells, also many ovarian cancer cells and prostate cancer cells prefer to use the reverse Warburg effect, the Crabtree effect, entosis or autophagy (Whitaker-Menezes et al., 2011; Schlaepfer et al., 2014; Nieman et al., 2011).

We have no randomised controlled study performed on cancer patients treated with intention to cure to prove that alkaline water contributes to healing cancer or that it prevents this diagnosis – researchers considering that promoting alkaline water is scientifically unjustified in oncological context (Fenton & Huang, 2016).

There is only marketing based on studies performed on cell lines and on laboratory animals that support hypotheses outside the complex malignant metabolic context of heterogeneous tumours developed in vivo in humans.

Of course, anyone can spend their money on whatever they want as most people haven’t enough patience to develop heat shock or a stroke to become more alkaline. Not even in August.

References

Bain AR et al. “Cerebral vascular control and metabolism in heat stress.”Comprehensive Physiology (2015).

Choi J et al. “Metabolic interaction between cancer cells and stromal cells according to breast cancer molecular subtype.” Breast cancer research15.5 (2013): R78.

Fenton TR & Huang T. “Systematic review of the association between dietary acid load, alkaline water and cancer.”BMJ open 6.6 (2016): e010438.

Griffiths JR. “Are cancer cells acidic?” British journal of cancer 64.3 (1991): 425.

Harguindey S et al. “The role of pH dynamics and the Na+/H+ antiporter in the etiopathogenesis and treatment of cancer. Two faces of the same coin—one single nature.” Biochimica et Biophysica Acta (BBA)-Reviews on Cancer1756.1 (2005): 1-24.

Heil DP. “Acid-base balance and hydration status following consumption of mineral-based alkaline bottled water.” J Int Soc Sports Nutr 7.1 (2010): 29.

Jones RG & Thompson CB, 2009. Tumor suppressors and cell metabolism: A recipe for cancer growth. Genes & development, 23(5), 537-548.

Lozupone F & Fais S, 2015. Cancer Cell Cannibalism: A Primeval Option to Survive. Current molecular medicine, 15(9), 836-841.

Mehler PS & Walsh K. “Electrolyte and acid‐base abnormalities associated with purging behaviors.” International Journal of Eating Disorders (2016).

Nieman KM et al. Adipocytes promote ovarian cancer metastasis and provide energy for rapid tumor growth. Nature medicine. 2011;17(11):1498-503.

Obre E & Rossignol R. Emerging concepts in bioenergetics and cancer research: metabolic flexibility, coupling, symbiosis, switch, oxidative tumors, metabolic remodeling, signaling and bioenergetic therapy. The international journal of biochemistry & cell biology. 2015; 59:167-81.

Pavlides S et al, 2009. The reverse Warburg effect: aerobic glycolysis in cancer associated fibroblasts and the tumor stroma. Cell cycle, 8(23), 3984-4001.

Schlaepfer IR et al. Lipid catabolism via CPT1 as a therapeutic target for prostate cancer. Molecular cancer therapeutics. 2014;13(10):2361-71.

Schuchmann S et al. “Respiratory alkalosis in children with febrile seizures.” Epilepsia 52.11 (2011): 1949-1955.

Vlashi E et al. “Metabolic differences in breast cancer stem cells and differentiated progeny.” Breast cancer research and treatment 146.3 (2014): 525-534.

Wanandi SI et al. “Impact of extracellular alkalinization on the survival of human CD24-/CD44+ breast cancer stem cells associated with cellular metabolic shifts.” Brazilian Journal of Medical and Biological Research 50.8 (2017).

White, KA et al. “Cancer cell behaviors mediated by dysregulated pH dynamics at a glance.” J Cell Sci 130.4 (2017): 663-669.

Whitaker-Menezes, Diana, et al. “Hyperactivation of oxidative mitochondrial metabolism in epithelial cancer cells in situ: visualizing the therapeutic effects of metformin in tumor tissue.” Cell cycle 10.23 (2011): 4047-4064.

Xie J et al. “Beyond Warburg effect–dual metabolic nature of cancer cells.” Scientific reports 4 (2014): 4927.

Yustisia I et al. “Effects of extracellular modulation through hypoxia on the glucose metabolism of human breast cancer stem cells.” Journal of Physics: Conference Series. Vol. 884. No. 1. IOP Publishing, 2017.

Zöllner JP et al. “Changes of pH and Energy State in Subacute Human Ischemia Assessed by Multinuclear Magnetic Resonance Spectroscopy.” Stroke 46.2 (2015): 441-446.

Articolul Alkaline water and cancer apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

However, as I encourage all of my patients to be, I also invite you to be skeptical and read – of course, or not – the studies quoted in these articles. And although it is just an invitation to understand that animal protein in general and dairy products in particular are not carcinogenic, please take into consideration that regardless of long-held personal beliefs these foods consumption by patients diagnosed with cancer is helping them achieve better prognosis by supporting the effectiveness of oncology treatment and by counteracting side effects.

Epidemiological studies that analyse the carcinogenicity of meat consumption are made by evaluating the responses given by the respondents in that study compared to those who have declared that they have consumed and those who have declared that they have not consumed meat. There are answers given by some people questioned and believed on their given word. So the results of epidemiological studies:

• don’t show causality, epidemiology studies simply pointing out risk factors for the population questioned within that particular study – Ananth & Schisterman, 2017
• may differ from one study to another, depending on the actual memory and honesty of the individuals questioned in each particular study about what they have consumed in their youth or 1 year ago – a phenomenon long known and called „recall bias“ – Chavarro et al., 2009
• can be easily manipulated by omitting various bias factors, depending on the honesty, financial interests and personal beliefs of the researchers publishing these questionnaire studies – de Abreu Silva & Marcadenti, 2009; Fogelholm, Kanerva & Männistö, 2015

Starting from the fact that epidemiology is based, however, on the honesty of both researchers and study participants, there still remain two semantic issues – generated by the fact that the respondents answer the questions of the epidemiologists by basically reading words in a questionnaire.

1. How do we define the word “cancer”?

In most questionnaires, “cancer” is a diagnosis, but today we know there are countless completely different diseases called “cancer”.

– So eating any type of meat increases the risk of any type of cancer?

On specific types of cancer, studies indicate that:

1. red or processed meat intake does not associate increased risk of renal cancer – Alexander & Cushing, 2009
2. red meat intake does not associate increased risk of lung cancer – Gnagnarella et al., 2018
3. meat intake is not associated with increased risk of multiple myeloma – Alexander et al., 2007
4. meat intake does not associate an increased risk of prostate cancer – Bylsma & Alexander, 2015
5. meat intake does not associate an increased risk of ovarian cancer – Crane et al., 2013
6. the excessive intake of deli meats like sausage and hamburgers associates an increased risk of breast cancer, not the consumption of red meat in itself – Anderson et al, 2018; Boldo et al., 2018
7. it is questionable if the risk of childhood brain cancer is associated or not with the consumption of sausage, hamburger or hotdogs by pregnant women – Pogoda & Preston-Martin, 2001;Huncharek, 2011; Henshaw & Suk, 2015
8. excessive intake of red meat associates the increased risk of digestive cancers, but this correlation differs from one digestive segment to another:
   • excessive red meat consumption associates an increased risk of esophageal cancer – Salehi et al., 2013
   • the evidence that supports an the increased risk of gastric cancer by eating red meat, sausages or precooked meat – Zhao, Yin & Zhao, 2017
   • there are sufficient epidemiological associations to support the increased risk of colorectal cancer by excessive consumption of red meat (Chan et al., 2011), although some studies point out that association seems to be valid only in distal colon cancer (Larsson et al., 2005; Bernstein et al., 2015)
   • excessive red meat consumption does appear to increase the risk of pancreatic cancer in men, but not in women, and the correlation is inconsistent and only shows related to excessive intake not with normal intake – Zhao et al., 2017
   • meat consumption is not correlated with an increased risk of liver cancer – Fedirko et al., 2013

2. How do we define the word “meat”?

Beef steak, turkey stew, pork meatball soup, grilled lamb, “mici” (a Romanian dish made from minced meat), chicken soup, hotdogs, hamburgers, schnitzels and the famous hot wings flying out of the overly used hot oil directly into the garlic mayonnaise – all are often put comfortably under the same “meat” label.

– But is Angus beef steak as carcinogenic as the hotdogs? 

– Or the Mangalita pork meat as carcinogenic as the hamburger? And what if the hamburger is made of Angus beef? 

– And what about quail, cock or pheasant meat?

The best answer based on „I will tell the truth, the whole truth, and nothing but the truth, so help me God“ is that we simply don’t know. Some giraffes want to see only green in front of their eyes, some ostrich – just sand.

What we know – at large – on specific types of meat is that:

1. “white meat” intake does not increase or associate a moderate decrease in the risk of “cancer” – Kolahdooz et al., 2010; Maragoni et al., 2015; Etemadi et al., 2017
2. “red meat” intake correlates with an increased risk of “cancer” – Domingo and Nadal, 2017

The words “white meat” generally define chicken, turkey or other poultry and fish. And the words “red meat” define generically “processed red meat” and “unprocessed red meat”.

– Now is all the red meat carcinogenic, no matter how little we consume?

First of all, any type of meat may be biologically pink or red depending on how sedentary that particular animal was (visible to the naked eye, looking at the piece of meat on our plate, or visible on the microscope, looking at the number and type of muscle fibres in the meat). Even wild fish has more red meat than farmed fish, simply because it swims more. Defining meat as white or red based on the species is pretty shallow.

Secondly, the words “processed red meat” generically define precooked products made of meat that has already been minced, such as hamburgers, hotdogs, salami, sausages, canned meat, liver pate, and fast food meat products. And the words “unprocessed red meat” generally define home cooked beef, sheep, pork and game meat, industrially unprocessed.

Studies that separate “red processed meat” from “red unprocessed meat” contradict the generic link between “red meat” and “cancer” (Larsson and Orsini, 2013; Anderson et al., 2018).

A systematic analysis published by Carr et al. in 2016 in International Journal of Cancer indicates that unprocessed red meat the normal intake does not increase the risk of cancer, not even in the case of colorectal cancer. This analysis shows that, in order to associate an increased in risk, the consumption of unprocessed red meat must be excessive and that the consumption of pork meat does not involve the increase of risk even when excessive, the risk being increased only by excessive consumption of beef or lamb.

Systematic analyzes that examined the association between the heterocyclic amines, polycyclic aromatic hydrocarbons or benzopyrene, formed in meat during cooking, and the carcinogenic impact of hem iron indicate only poor associations between red and processed meat consumption and increased risk of cancer (Kuratko et al., 2016).

So, the current scientific literature shows that:

1. Generally, moderate “meat” consumption does not associate an increased “cancer” risk.
2. Particularly, the consumption processed meat and the excessive consumption of beef or lamb meat are associated with an increase in the risk of certain types of cancer.

The problem with nutrition these days is that anyone who can chew is a nutritionist undercover, thus at the diametrically opposite pole of those recommending to cancer patients to avoid meat consumption, are the ones recommending to cancer patients to start a ketogenic diet – diet based on keeping carbohydrates intake as low as possible, “low intake” defined solely on the imagination residing within the self-proclaimed nutritionist’s pen. Nope, it’s not Dukan or Atkins, it’s pure Gigica diet, strictly tailored for you with tons of meat meant to starve away cancer.

The studies quoted in this article support the moderate consumption of lightly cooked or boiled meat as part of a healthy diet similar to the Mediterranean diet, not the recommendation of ketogenic diet for cancer patients – a recommendation made by those who elegantly offer illusions to cancer patients, understanding superficially or at all the oncological consequences of this extreme diet.

In my fourth book, I present in detail – with scientific arguments – that the ketogenic diet associates an increased risk of metastasis and recurrence, an increase in tumor aggression and the development of resistance to oncological treatment.

This is based on the current scientific data which:

1. contraindicates ketogenic diet in any patient diagnosed with cancer (Erickson et al., 2017)
2. recommends moderate meat consumption as part of a variety of dairy, cheese, eggs, fish, fruits, vegetables, seeds, grains, whole grains and quality oils (Schwingshackl & Hoffmann, 2014)

Moderate intake of high quality meat cooked the right way, not hotdogs or schnitzels eaten on the run.

Quoted studies

Alexander, Dominik D. et al. “Multiple myeloma: a review of the epidemiologic literature.” International journal of cancer 120.S12 (2007): 40-61.

Alexander, D. D., & Cushing, C. A. (2009). Quantitative assessment of red meat or processed meat consumption and kidney cancer. Cancer detection and prevention, 32(5), 340-351.

Ananth, C. V., & Schisterman, E. F. (2017). Confounding, causality, and confusion: the role of intermediate variables in interpreting observational studies in obstetrics. American journal of obstetrics and gynecology, 217(2), 167.

Anderson, Jana J. et al. “Red and processed meat consumption and breast cancer: UK Biobank cohort study and meta-analysis.” European Journal of Cancer 90 (2018): 73-82.

Bernstein, Adam M. et al. “Processed and unprocessed red meat and risk of colorectal cancer: analysis by tumor location and modification by time.” PloS one 10.8 (2015): e0135959.

Boldo, Elena, et al. “Meat intake, methods and degrees of cooking and breast cancer risk in the MCC-Spain study.” Maturitas 110 (2018): 62-70.

Bylsma, L. C., & Alexander, D. D. (2015). A review and meta-analysis of prospective studies of red and processed meat, meat cooking methods, heme iron, heterocyclic amines and prostate cancer. Nutrition journal, 14(1), 125.

Carr, Prudence R. et al. “Meat subtypes and their association with colorectal cancer: Systematic review and meta‐analysis.” International journal of cancer 138.2 (2016): 293-302.

Chan, Doris SM et al. “Red and processed meat and colorectal cancer incidence: meta-analysis of prospective studies.” PloS one 6.6 (2011): e20456.

Chavarro, Jorge E. et al. “Validity of adolescent diet recall 48 years later.” American journal of epidemiology 170.12 (2009): 1563-1570.

Crane, Tracy E. et al. “Dietary intake and ovarian cancer risk: a systematic review.” Cancer Epidemiology and Prevention Biomarkers (2013): cebp-0515.

de Abreu Silva, Erlon Oliveira, and Aline Marcadenti. “Higher red meat intake may be a marker of risk, not a risk factor itself.” Archives of internal medicine 169.16 (2009): 1538-1539.

Domingo, J. L., & Nadal, M. (2017). Carcinogenicity of consumption of red meat and processed meat: A review of scientific news since the IARC decision. Food and Chemical Toxicology, 105, 256-261.

Erickson, N. et al. “Systematic review: isocaloric ketogenic dietary regimes for cancer patients.” Medical Oncology 34.5 (2017): 72.

Etemadi, Arash et al. “Mortality from different causes associated with meat, heme iron, nitrates, and nitrites in the NIH-AARP Diet and Health Study: population based cohort study.” bmj 357 (2017): j1957.

Fogelholm, M., Kanerva, N., & Männistö, S. (2015). Association between red and processed meat consumption and chronic diseases: the confounding role of other dietary factors. European journal of clinical nutrition, 69(9), 1060.

Gnagnarella, Patrizia et al. “Carcinogenicity of High Consumption of Meat and Lung Cancer Risk Among Non-Smokers: A Comprehensive Meta-Analysis.” Nutrition and cancer 70.1 (2018): 1-13.

Fedirko, V. et al. “Consumption of fish and meats and risk of hepatocellular carcinoma: the European Prospective Investigation into Cancer and Nutrition (EPIC).” Annals of oncology 24.8 (2013): 2166-2173.

Henshaw, D. L., & Suk, W. A. (2015). Diet, transplacental carcinogenesis, and risk to children.

Huncharek, Michael. “Maternal Dietary Intake of N-Nitroso Compounds from Cured Meat and the Risk of Pediatric Brain Tumors.” Handbook of Behavior, Food and Nutrition. Springer, New York, NY, 2011. 1817-1831.

Kolahdooz, Fariba et al. “Meat, fish, and ovarian cancer risk: results from 2 Australian case-control studies, a systematic review, and meta-analysis–.” The American journal of clinical nutrition 91.6 (2010): 1752-1763.

Kuratko, Connye et al. “Systematic Reviews of Current Literature Fail to Establish Dietary Benzo [a] pyrene, Heterocyclic Aromatic Amines, or Heme Iron as Mechanisms Linking Red and Processed Meat Consumption with Cancer Risk.” The FASEB Journal 30.1 Supplement (2016): 1167-5.

Marangoni, Franca, et al. “Role of poultry meat in a balanced diet aimed at maintaining health and wellbeing: an Italian consensus document.” Food & nutrition research 59.1 (2015): 27606.

Larsson, Susanna C., et al. “Red meat consumption and risk of cancers of the proximal colon, distal colon and rectum: the Swedish Mammography Cohort.” International journal of cancer113.5 (2005): 829-834.

Larsson, S. C., & Orsini, N. (2013). Red meat and processed meat consumption and all-cause mortality: a meta-analysis. American journal of epidemiology, 179(3), 282-289.

Pogoda, J. M., & Preston-Martin, S. (2001). Maternal cured meat consumption during pregnancy and risk of paediatric brain tumour in offspring: potentially harmful levels of intake. Public health nutrition, 4(2), 183-189.

Salehi, Maryam et al. “Meat, fish, and esophageal cancer risk: a systematic review and dose-response meta-analysis.” Nutrition reviews 71.5 (2013): 257-267.

Schwingshackl, L., & Hoffmann, G. (2014). Adherence to Mediterranean diet and risk of cancer: A systematic review and meta‐analysis of observational studies. International journal of cancer, 135(8), 1884-1897.

Zhao, Zhanwei et al. “Association between consumption of red and processed meat and pancreatic cancer risk: a systematic review and meta-analysis.” Clinical Gastroenterology and Hepatology 15.4 (2017): 486-493.

Zhao, Z., Yin, Z., & Zhao, Q. (2017). Red and processed meat consumption and gastric cancer risk: A systematic review and meta-analysis. Oncotarget, 8(18), 30563.

Articolul Is meat carcinogenic? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

Among other side effects reported by patients during antiestrogenic treatment, the main complain is muscle and joint pain. And among other side effects reported by patients during statins treatment, the main complain is also muscle and joint pain. So – at least because of this shared side effect that can be co-amplified when both treatments are administrated simultaneously – we should first ask the question:

– Can ER+ breast cancer patients take statins during antiestrogenic treatment?

But first, let`s start with a far more important question:

– Can breast cancer patients take statins?

Of course, anyone can take a pill – the second question refering to statins’ carcinogenity and long term safety when administred to breast cancer patients and not to the kinetic ability to swallow a pill.

Epidemiological studies state that statins administration does not increase the risk of cancer – Browning si Martin, 2007. But we don’t have randomised controlled trials that prove statins safety for breast cancer patients.

All we have is a multitude of epidemiological studies with head-to-head contradictory results:

– statins administration in people without cancer:

• is not associated with increased risk of breast cancer – Cauley et al., 2006
• is not associated with decreased risk of breast cancer –  Undela, Srikanth and Bansal, 2012
• is associated with increased risk of breast cancer – McDougall et al., 2013
• is associated with decreased risk of triple negative breast cancer – Kumar et al., 2008
• is not associated with decreased risk of triple negative breast cancer – Woditschka et al., 2010

– statins administration in breast cancer patients:

• is associated with a decreased risk of recurrence – Kwan et al., 2008
• is not associated with a decreased risk of recurrence – Nickels et al., 2013
• is associated with a decreased risk of breast cancer mortality – Murtola et al., 2014
• is not associated with a decreased risk of breast cancer mortality – Smith et al., 2016

Despite these contradictory results, one of the systematic reviews of the epidemiological studies on breast cancer and statins connection concluded that statins administration appears to be safe and potentially beneficial for breast cancer patients  (Manthravadi, Shrestha si Madhusudhana, 2016).

So, one: Epidemiological studies – in English, studies that do not prove causality but just raise questions about possible risk factors that should be further tested in randomised controlled trials – claim that statins seem to be safe from an oncological point of view when administered to breast cancer patients, even though we don’t know if this epidemiological hypothesis is true or not.

But – even though statins are among the most sold medications on the planet – paradoxically, the systematic review don by Ravnskov et al. in 2016 shows that people over 60 years of age with high LDL-cholesterol levels leave as much or more than people with low LDL-cholesterol levels.

So, two: The fact that lowering cholesterol by administering statins has a beneficial clinical impact is a generalization not a certainty.

And we know that statins administration side effects associate the main sarcopenic obesity causes:

• sarcopenia (gradual loss of muscle mass) – Wilke et al., 2007 ; Prado et al., 2011
• hyperinsulinism and insulin resistance – Goldstein and Mascitelli, 2013; Aiman, Najmi and Khan, 2014

So, three: Statins administration to breast cancer patients can indirectly increase the risk of obesity.

And breast cancer patients’ obesity increases the risks of metastasis, recurrence and mortality.

References

Aiman, U., Najmi, A., & Khan, R. A. (2014). Statin induced diabetes and its clinical implications. Journal of pharmacology & pharmacotherapeutics, 5(3), 181.

Browning, D. R., & Martin, R. M. (2007). Statins and risk of cancer: a systematic review and metaanalysis. International journal of cancer, 120(4), 833-843.

Cauley, Jane A., et al. “Statin use and breast cancer: prospective results from the Women’s Health Initiative.” Journal of the National Cancer Institute 98.10 (2006): 700-707.

Goldstein, M. R., & Mascitelli, L. (2013). Do statins cause diabetes?. Current diabetes reports, 13(3), 381-390.

Kumar, Anjali S., et al. “Estrogen Receptor–Negative Breast Cancer Is Less Likely to Arise among Lipophilic Statin Users.” Cancer Epidemiology and Prevention Biomarkers 17.5 (2008): 1028-1033.

Manthravadi, S., Shrestha, A., & Madhusudhana, S. (2016). Impact of statin use on cancer recurrence and mortality in breast cancer: A systematic review and meta‐analysis. International journal of cancer, 139(6), 1281-1288.

McDougall, J.A., Malone, K.E., Daling, J.R., Cushing-Haugen, K.L., Porter, P.L. and Li, C.I. (2013) Long-Term Statin Use and Risk of Ductal and Lobular Breast Cancer among Women 55 to 74 Years of Age. Cancer Epidemiology, Biomarkers & Prevention, 22, 1529-1537.

Murtola, Teemu J., et al. “Statin use and breast cancer survival: a nationwide cohort study from Finland.” PloS one 9.10 (2014): e110231.

Nickels, Stefan, et al. “Mortality and recurrence risk in relation to the use of lipid-lowering drugs in a prospective breast cancer patient cohort.” PloS one 8.9 (2013): e75088.

Prado, Carla MM, et al. “Two faces of drug therapy in cancer: drug-related lean tissue loss and its adverse consequences to survival and toxicity.” Current Opinion in Clinical Nutrition & Metabolic Care14.3 (2011): 250-254.

Ravnskov, Uffe, et al. “Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review.” BMJ open 6.6 (2016): e010401.

Smith, Amelia, et al. “De novo post-diagnosis statin use, breast cancer-specific and overall mortality in women with stage I-III breast cancer.” (2016): 592.

Undela, Krishna, Vallakatla Srikanth, and Dipika Bansal. “Statin use and risk of breast cancer: a meta-analysis of observational studies.” Breast cancer research and treatment 135.1 (2012): 261-269.

Wilke, R.A., Lin, D.W., Roden, D.M., Watkins, P.B., Flockhart, D., Zineh, I., Giacomini, K.M. and Krauss, R.M. (2007) Identifying Genetic Risk Factors for Serious Adverse Drug Reactions: Current Progress and Challenges. Nature S. Moonindranath, H. L. Shen 29 Reviews: Drug Discovery, 6, 904-916

Woditschka, Stephan, et al. “Lipophilic statin use and risk of breast cancer subtypes.” Cancer Epidemiology and Prevention Biomarkers(2010): cebp-0524.

Articolul Can breast cancer patients take statins? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

Although the word „cancer“ covers a multitude of localisations, loco-regional or distance disorders, immunohistochemistry and genetic mutations – and therefore completely different evolutions and treatments from one patient to another, even for patients with the same localisation – pseudo-oncology sells all sorts of panacea good for any type of cancer one might have.

We do not know what happens long-term to the patient who is using complementary-integrative “medicine” because these systems are not legally required to monitor patients long-term. By law, such pseudo-oncology products and strategies can be sold based on the supposition that they are safe. The safety is not tested or addressed in any way, it is assumed.

– Still, can we put the equal sign between tumour disappearance and cancer cure?

Scientifically, the disappearance of the tumour is called “complete pathological response” – and in allopathic medicine can be obtained surgically or by chemotherapy.

The hypothesis that tumour disappearance means cancer cure has been contradicted for decades by the fact that the surgical removal of the tumour does not necessarily mean that the cancer is cured (Haagensen et al., 1951).

Also, if surgical removal of cancer does not necessarily mean healing, the same is true sometimes in the case of tumour disappearance by chemotherapy (Cortazar et al., 2014).

For example, we know that patients with triple-negative breast cancer or HER2+ often respond very well to chemotherapy given immediately after diagnosis, obtaining tumor disappearance before surgery (therapeutic response called “pathologic complete response”), and that such response can sometimes be obtained even in multicenter tumours (Ataseven et al., 2015).

And according to the current scientific data we also know that the surgical intervention remains important even after obtaining pathologic complete response to neoadjuvant chemotherapy. (Ring et al., 2003; Clouth et al., 2007; Daveau et al., 2011).

So, the complete disappearance of the tumour does not mean curing cancer, we know that for a long time, and we do not hide under the carpet that we know.

The honest treatment efficiency evaluation is the essential difference between complementary-integrative “medicine” and allopathic medicine.

In spite of the various personal examples quoted and promoted as proof that you can naturally cure your own cancer without oncological treatment, based on the available scientific data:

• the ketogenic diet is not recommended for any patient with cancer diagnosis (Erickson et al., 2017)
• administration of various dietary supplements during chemotherapy is associated with decreased survival (Smith et al., 2016)
• vitamin C administration does not have antitumoral effect, even at huge doses of 70, 90 or 110 g/m2 administered intravenously (Hooffer et al., 2008)
• antioxidants administration during oncological treatment is contraindicated (Seifield et al., 2003)
• antioxidants may increase the metastasis risk (Herraiz et al., 2016)

Unlike complementary-integrative medicine, oncology is based on the objective treatment efficiency evaluation:

• in the short-term – the periodic evaluation of the pathological response is essential for each patient’s treatment individualisation
• in the long-term – the regular clinical and imagistic evaluation are essential for the early diagnosis of any possible metastasis or recurrence that might occur after treatment even in the case of patients that actually obtained pathologic complete response

So, if you are an oncological patient and you are tempted to try a “miracle” that “cured” another person’s cancer “naturally”, ask yourself at least these three questions:

1. Has the cured cancer been objectively evaluated in an imagistic, histopathological or clinical way? Or the disappearance of the tumour is simply assumed based on the fact that the patient “feels better”?
2. Compared to you, did the person have the same cancer location, the same type of cancer and the same number of tumours?
3. Compared to you, did the person have the same lymph node or the same metastases?
4. Compared to you, did that person have the same age, same sex and identical family history?
5. Compared to you, did the person suffer from the same diseases other than cancer?
6. Compared to you, did that person gained or lose weight after diagnosis?
7. Do you know what happened to that person after 10, 15 – or at least 5 years?

I know I wrote more than 3 questions. But there are so many differences even between two people with exactly the same immunohistochemical type of cancer that I can still write so many other questions.

Cocaine is also natural and it has side effects.

The tumour disappearance should be monitored long, loong, looong time to be able to say that patient is cured – which is why the clinical and radiological controls that are regularly performed long-term after cancer disappearance are absolutely essential.

Quoted studies

Ataseven, Beyhan, et al. “Impact of multifocal or multicentric disease on surgery and locoregional, distant and overall survival of 6,134 breast cancer patients treated with neoadjuvant chemotherapy.” Annals of surgical oncology 22.4 (2015): 1118-1127.

Clouth, B., et al. “The surgical management of patients who achieve a complete pathological response after primary chemotherapy for locally advanced breast cancer.” European Journal of Surgical Oncology (EJSO) 33.8 (2007): 961-966.

Cortazar, Patricia, et al. “Pathological complete response and long-term clinical benefit in breast cancer: the CTNeoBC pooled analysis.” The Lancet 384.9938 (2014): 164-172.

Daveau, Caroline, et al. “Is radiotherapy an option for early breast cancers with complete clinical response after neoadjuvant chemotherapy?.” International Journal of Radiation Oncology* Biology* Physics 79.5 (2011): 1452-1459.

Erickson, N., et al. “Systematic review: isocaloric ketogenic dietary regimes for cancer patients.” Medical Oncology 34.5 (2017): 72.

Haagensen, C. D., and Arthur Purdy Stout. “Carcinoma of the breast. III. Results of treatment, 1935-1942.” Annals of surgery 134.2 (1951): 151.

Herraiz, Cecilia, Eva Crosas-Molist, and Victoria Sanz-Moreno. “Reactive oxygen species and tumor dissemination: Allies no longer.” Molecular & cellular oncology 3.2 (2016): e1127313.

Hoffer, L. J., et al. “Phase I clinical trial of iv ascorbic acid in advanced malignancy.” Annals of Oncology 19.11 (2008): 1969-1974.

Ring, Alistair, et al. “Is surgery necessary after complete clinical remission following neoadjuvant chemotherapy for early breast cancer?.” Journal of clinical oncology 21.24 (2003): 4540-4545.

Seifried, Harold E., et al. “The antioxidant conundrum in cancer.” Cancer Research 63.15 (2003): 4295-4298.

Smith, Peter J., et al. “Complementary and alternative medicine use by patients receiving curative‐intent chemotherapy.” Asia‐Pacific Journal of Clinical Oncology 12.3 (2016): 265-274.

Articolul What does it mean to be cured of cancer? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

But the intracytoplasmic ROS level determines whether the cell progresses in the cell replication cycle or not, lower levels leading to cell cycle progression while higher ones leading to cell cycle arrest and cell death (Cairns, Harris and Mak, 2011).

Also, studies show that malignant cells have a higher tolerance for ROS than normal cells – Szatrowski and Nathan, 1991. So, to impede malignant cells survival and proliferation we need a higher level of intracytoplasmic ROS level.

And although vitamin C can act both as a pro-oxidant and antioxidant depending on the dosage, we do not know if the clinic impact of vitamin C administration is beneficial for patients with curable cancers during active oncology treatment and not during palliative care (Schumacker, 2006; Grasso et al., 2014).

Active oncology treatment with intention to cure makes the difference in what a cancer patient can or cannot take, and while there still are chances of healing antioxidants administration can decrease treatment efficacy.  

Up to now, no randomised controlled trial has proven that vitamin C has a beneficial impact in cancer patients without metastasis during chemotherapy or  radiotherapy done with intention to cure, the only benefits being increased quality of life and decreased palliative treatment toxicity in terminal cancer patients – Unlu et al., 2015; Li, Zhang and Tang, 2016

All studies showing antioxidants administration benefits are either case studies, animal studies, cell studies, studies done on incurable cancer patients or observational studies on cancer risk factors. Still the scientific interest is high, many researchers trying to prove that the improved quality of life or the decreased toxicity could be beneficial also for patients during active treatment and not only during palliation.

For instance, some researchers say cancer patients have vitamin C deficiency and therefore supplementing it would stimulate immune system and increase the quality of life of the patients, without separating either patients during active treatment from patients during palliation  or the many types of cancer.

– But what cancer patients have vitamin C deficiency?

And although many naturopaths or complementary medicine practitioners would say “all”, the study that led to this popular assumption only analysed 50 terminal cancer patients of which only 15 had low vitamin C levels. Can we just delete the other 35 and extrapolate that “cancer patients have vitamin C deficiency”? – Maryland et al., 2005

The time of diagnosis is essential when it comes to antioxidants intake impact, and there are 3 distinct periods of time:

1. before diagnosis – cancer prevention – when daily moderate intake of antioxidants naturally found in fruits, vegetables, raw seeds, legumes, lean meat, fish, whole dairy and eggs contributes up to a point to a decreased cancer risk
2. early stage diagnosis – active oncology treatement with intention to cure – when oncology nutrition is strictly personalised based on malignant metabolism, tumour localisation, treatment stage and patient comorbidities. And I would like to underline that we cannot cure cancer through nutrition, be it oral or iv, and that during active oncology treatment the main goal is treatment efficacy and not decreased treatment toxicity or increased quality of life.  During active treatment we have no proof that antioxidants have any beneficial impact on treatment efficacy.
3. late stage diagnosis or when the disease has advanced and it reached an incurable stage – palliation – when the main goals are decreased treatment toxicity or increased quality of life. And this is the only period of time when antioxidants might be useful.

Some researchers go as far as to say that the only moment when cancer patients can be administrated antioxidants without decreasing healing chances is during scientific trials – Wilson et al., 2014

Even the chemotherapy with which vitamin C is compared by complementary / integrative medicine practitioners is palliative chemotherapy not curative active treatment. – Gourgou-Bourgade et al., 2012

Chemotherapy side effects are very popular and thickly underlined by these practitioners, but most don’t also mention alternative treatments side effects because their providers are not obliged by law to prove neither their efficacy nor their safety. And of course “they are natural thus they don’t have side effects”. Cocaine is also natural.

Malignant cellular biology is extremely complex. There is a huge difference between destroying some malignant cells in a Petri dish and destroying a self-born and grown tumour in a living organism.

To understand the difference between destroying some malignant cells in a Petri dish and destroying a self-born and grown tumour in a living organism imagine trying to destroy a wasp nest.

The fact that we catch some wasps in a jar and we kill them with substance X does not mean that the whole nest will be destroyed:

• the nest might have such a complex internal structure that some wasps might not come in contact with substance X, otherwise effective if contact would occur;
• the wasps we killed in the jar with substance X might be of different age or specie than the wasps in the nest;
• and some wasps might not be in the nest when we administered the substance, thus being able to go and build another nest elsewhere.

Cancer is a heterogenous mass of cells in different stages of cell cycle able not to die. And avoiding apoptosis is very complicated, involving a whole lot of genetic modifications that make malignant cells unpredictable and very adaptable.

Assuming that vitamin C is beneficial simply because it is an antioxidant or because it might act as a pro-oxidant sounds logic and natural, and low cost, and low importance because of the supposed lack of side effects, but up to now it is just a potentially risky assumption.

– Then why it is given intravenously in high doses in some centres even alongside neoadjuvant chemotherapy, treatment also widely practiced by many naturopaths or other integrative/complementary medicine practitioners?

Maybe because 40 years ago the Nobel laureate for chemistry Linus Pauling argued that high-dose vitamin C heals or prevents cancer, the same as 400 years ago the Pope used to say that the Earth was flat. So you should had been completely out of the box to even think it is round.

– What made Pauling sustain with such vehemence vitamin C for cancer treatment?

In the ’70 Pauling and Cameron published two apparently randomised controlled studies in which they managed to highly increase the survival of terminal cancer patients to whom they administered intravenously at first and orally thereafter high doses of vitamin C – Pauling and Cameron, 1976; Pauling and Cameron, 1978

But dr. William DeWys – the head of research at US National Cancer Institute at the time – has severely criticised the validity of these studies results (Cabanillas, 2010) because:

1. the study has been restrospective and not randomised
2. and because around 20% of the patients retrospectively selected to be included in the control arm died just few days after they have been considered incurable, dr. DeWys arguing that this led to an artificially increased survival time for the vitamin C group.

Then, in 1981, Murata et al. published a study with similar retrospective design – study widely quoted at the proof that Pauling and Cameron were actually right.  – Murata, Morishige and Yamaguchi, 1981

But neither Pauling and Cameron’s studies nor Murata’s were randomised controlled trials, but restrospective ones without causal value. And what we also need to underline is that:

• all 3 studies were done on terminal cancer patients with diverse forms of cancer
• most patients died anyway within less than a year, so randomised or not, vitamin C for sure did not cure them

The hypothesis that curing cancer is as easy, simple and natural as vitamin C administration was later on contradicted by the very death of Pauling himself – who died of lung cancer in 1994 despite administering 18 g vitamin C daily.  So in his case, taking vitamin C did not prevent cancer, and did not help him cure cancer after diagnosis.

Unlike these retrospective studies, the 2 randomised controlled studies done at Mayo Clinic showed that a daily oral administration of 10g of vitamin C is of no benefit for cancer patients – Creagan et al., 1979, Moertel et al., 1985.

But the results of these studies have been disputed based on vitamin C pharmacokinetics, vitamin C supporters arguing that the antitumor effect can be obtained only through intravenous administration. – Padayatty et al., 2004

But, even for intravenous administration there are at least 3 more but:

1. despite the fact that the RDI for vitamin C is 60 mg, the supposed antitumor effect is not obtained even at doses as high as 70 g/m² administred intravenously – Hoffer et al., 2008; Stephenson et al., 2013
2. vitamin C administration can decrease oncology treatment efficacy:
   • antioxidants can decrease chemotherapy and radiotherapy efficacy – Bairati et al., 2005; Lawenda et al., 2008; Heaney et al., 2008
   • vitamin C inhibits the antitumor effect of bortezomib in patients with multiple myeloma or lymphoma – Perrone et al., 2009
3. Vitamin C does have side effects – beside gastrointestinal discomfort (diarrhea, bloating) vitamin C administration can:
   • increase iron absorption – being contraindicated in patients with hemochromatosis – Stotts and Bacon, 2017
   • increase the risk of renal oxalates lithiasis in men – being contraindicated in patients with a history of oxalic nephropathy or renal insufficiency – Massey et al., 2005; Ferraro et al., 2016
   • have a prothrombotic and procoagulant impact – being contraindicated in patients with cardiovascular disease at risk of thrombosis – Kim et al., 2015; Mohammed et al., 2017

Vitamin C is not as pink as pseudo-oncology industry would like patients to believe and the fight against cancer is far more complicated than simply taking vitamins.

In final stages, during palliative care, decreasing treatment toxicity and increasing quality of life are primary.

But during active oncology treatment for curable cancer we want the patient to feel good or we want the patient to be cured?

References

Bairati, Isabelle, et al. “Randomized trial of antioxidant vitamins to prevent acute adverse effects of radiation therapy in head and neck cancer patients.” Journal of clinical oncology 23.24 (2005): 5805-5813.

Cabanillas, Fernando. “Vitamin C and cancer: what can we conclude-1,609 patients and 33 years later.” PR Health Sci J29.3 (2010): 215-217.

Cairns, Rob A., Isaac S. Harris, and Tak W. Mak. “Regulation of cancer cell metabolism.” Nature Reviews Cancer 11.2 (2011): 85-95.

Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: prolongation of survival times in terminal human cancer. Proc Natl Acad Sci U S A 1976; 73 (10): 3685–3689.

Cameron E, Pauling L. Supplemental ascorbate in the supportive treatment of cancer: reevaluation of prolongation of survival times in terminal human cancer. Proc Natl Acad Sci U S A 1978; 75 (9): 4538–4542.

Gourgou-Bourgade, Sophie, et al. “Impact of FOLFIRINOX compared with gemcitabine on quality of life in patients with metastatic pancreatic cancer: results from the PRODIGE 4/ACCORD 11 randomized trial.” Journal of clinical oncology31.1 (2012): 23-29.

Grasso, Carole, et al. “Pharmacological doses of daily ascorbate protect tumors from radiation damage after a single dose of radiation in an intracranial mouse glioma model.” Frontiers in oncology 4 (2014).

Ferraro, Pietro Manuel, et al. “Total, dietary, and supplemental vitamin C intake and risk of incident kidney stones.” American Journal of Kidney Diseases 67.3 (2016): 400-407.

Heaney, Mark L., et al. “Vitamin C antagonizes the cytotoxic effects of antineoplastic drugs.” Cancer research 68.19 (2008): 8031-8038.

Hoffer, L. J., et al. “Phase I clinical trial of iv ascorbic acid in advanced malignancy.” Annals of Oncology (2008): mdn377.

Jacobs, Carmel, et al. “Is there a role for oral or intravenous ascorbate (vitamin C) in treating patients with cancer? A systematic review.” The oncologist 20.2 (2015): 210-223.

Kim, Keunyoung, et al. “High-Dose Vitamin C Injection to Cancer Patients May Promote Thrombosis Through Procoagulant Activation of Erythrocytes.” Toxicological Sciences 147.2 (2015): 350-359.

Lawenda, Brian D., et al. “Should supplemental antioxidant administration be avoided during chemotherapy and radiation therapy?” Journal of the national cancer institute 100.11 (2008): 773-783.

Li, F., Zhang, L., & Tang, S. C. (2016). Revisiting vitamin C in cancer therapy: Is “C” for cure, or just wishful thinking?.

Massey, Linda K., Michael Liebman, and Susan A. Kynast-Gales. “Ascorbate increases human oxaluria and kidney stone risk.” The Journal of nutrition 135.7 (2005): 1673-1677.

Mayland, Catriona R., Michael I. Bennett, and Keith Allan. “Vitamin C deficiency in cancer patients.” Palliative medicine19.1 (2005): 17-20.

Mohammed, Bassem M., et al. “Impact of high dose vitamin C on platelet function.” World journal of critical care medicine 6.1 (2017): 37.

Murata, A., F. Morishige, and H. Yamaguchi. “Prolongation of survival times of terminal cancer patients by administration of large doses of ascorbate.” International journal for vitamin and nutrition research. Supplement= Internationale Zeitschrift fur Vitamin-und Ernahrungsforschung. Supplement 23 (1981): 103-113.

Padayatty SJ, Sun H, Wang Y et al. Vitamin C pharmacokinetics: implications for oral and intravenous use. Ann Intern Med 2004; 140 (7): 533–537.

Perrone, G., et al. “Ascorbic acid inhibits antitumor activity of bortezomib in vivo.” Leukemia 23.9 (2009): 1679-1686.

Stephenson, Christopher M., et al. “Phase I clinical trial to evaluate the safety, tolerability, and pharmacokinetics of high-dose intravenous ascorbic acid in patients with advanced cancer.” Cancer chemotherapy and pharmacology 72.1 (2013): 139-146.

Stotts, Matthew J., and Bruce R. Bacon. “Metabolic and Genetic Liver Diseases: Hemochromatosis.” Liver Disorders. Springer International Publishing, 2017. 339-353.

Szatrowski, T. P., & Nathan, C. F. (1991). Production of large amounts of hydrogen peroxide by human tumor cells. Cancer research, 51(3), 794-798.

Schumacker, P. T. (2006). Reactive oxygen species in cancer cells: live by the sword, die by the sword. Cancer cell, 10(3), 175-176.

Unlu, A., Kirca, O., Ozdogan, M., & Nayır, E. (2015). Journal of Oncological Science.

Wilson, Michelle K., et al. “Review of high‐dose intravenous vitamin C as an anticancer agent.” Asia‐Pacific Journal of Clinical Oncology 10.1 (2014): 22-37.

Articolul Vitamin C for cancer patients? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

1. Decreased basal metabolic rate

The only part of the metabolic rate that we can influence without making ourselves ill is the energy used by our skeletal muscles that contracts 24h in a row to maintain body tonus. The higher the active muscle mass percentage, the higher the metabolic rate; and vice versa – the metabolic rate decreases through muscle mass loss (sarcopenia).¹

Sarcopenia is mainly associated with aging, but it also develops in about 25% of breast cancer patients, both in those who lose weight and in those who gain weight during chemotherapy, being conclusive for chemotherapy toxicity.^{2, 3}

During breast cancer chemotherapy, besides the increased muscular catabolism generated by the decreased estrogen,⁴ the muscle mass is gradually lost through the sedentariness and inadequate intake of protein to sustain muscle mass.⁵ 

Many breast cancer patients have an inadequate protein intake either due to decreased appetite,⁶ either to the fact that they completely exclude meat and/ or dairy products from their diet based on common beliefs associated with cancer.⁷

Yet plant foods completely lack B12 vitamin, and have either an imbalanced, insufficient or unusable content essential nutrients and micronutrients.^{8, 9} And besides dysphagia, balance disorders, and osteoporosis, the decreased basal metabolic rate is causing:

• An increase in the body fat percentage – in patients who don’t overeat;¹⁰
• An increase in the body fat percentage, aggravated sarcopenia, and further decreased basal metabolic rate – in patients who overeat.^{11, 12}

Also, studies prove that being sedentary decreases the basal metabolic rate of the breast cancer patients because it deregulates the balance between muscle protein degradation and synthesis. Thus, breast cancer patients can actively fight the metabolic decrease caused by sarcopenia through proper protein intake and through resistance training.

Anaerobic exercise (either isometric or isokinetic using only the body weight as a resistance) can improve muscle protein turn-over in favor of synthesis.¹³ The result is a maintained muscle mass and basal metabolic rate if the patient has not developed sarcopenia yet, or a gradual increase in the active muscle mass if the patients already has some degree of sarcopenia (which can happen in old patients who developed sarcopenia due to aging ± due to chemotherapy).¹⁴

So, practicing minimal daily resistance training exercises – even in hospital settings – can maintain or improve metabolism.

1. Decreased ability to perceive satiety

Many breast cancer patients develop dyslipidemia during chemotherapy, or are already dyslipidemic at the start of the treatment. During the treatment, dyslipidemia is caused:

• Either by the decreased intestinal absorbability of disaccharides paralleled by an intestinal hyperpermeability for undigested proteins generating dysbiosis which leads to an increased lipolysis;^{15, 16}
• Either by too low appetite (unintentional starvation);¹⁷
• Either by the overeating foods high in carbohydrates.¹⁸

But, no matter the mechanism, dyslipidemia causes leptin resistance decreasing the patient ability to perceive satiety and generating hedonic hunger, sometimes even soon after eating a full meal.^{19, 20}

Studies prove that many breast cancer patients without prior diabetes develop muscle insulin resistance during treatment.²³ Insulin resistance is the survival mechanism used when the patient is either:

• limiting too much her food intake;²¹
• or when she is overeating foods too high in carbohydrates and too low in proteins.²²

Insulin is stimulating the secretion of the satiety hormone leptin, and hyperinsulinemia is generating such an increase in leptin secretion that the hypothalamic neurons within the satiety nervous center become unresponsive to leptin. This practically creates the loss of control over the eaten amount of food and a paradoxical hunger state very soon after eating.

In consequence, breast cancer patients lose control over their eating behavior both when they eat too little and when they eat too much:

• When the patient overeats or when she eats regardless of physical hunger, glucose cannot pass through the sarcolemma because glucose is osmotic and GLUT4 shut off to protect the muscle cell damage done by a too high inner osmotic pressure. Insulin resistance happens after repeated excessive or unsolicited intake of any nutrient (directly when the patient overeats carbohydrates supplying foods, and indirectly when she overeats protein or fats supplying foods).²⁴
• On the other hand, when the patient eats too little, the high level of blood circulating free fatty acids increases the fat delivery to the muscles which increases sarcolemma density and membrane expression of GLUT4, inhibiting the glucose uptake by skeletal muscle cells and increasing the amount of fat deposited inside the muscle cell even in healthy subjects.²⁵ The result of an increased lipolysis does not equal fat loss. It equals an increase in circulating fatty acids, dyslipidemia and sometimes ectopic fat deposited inside the liver, the kidneys or the skeletal muscle.²⁶

So, insulin resistance can shut down fat loss by inhibiting lipolysis and by increasing hunger paralleled with decreased ability to perceive satiety. That is why it is so important to prevent or solve insulin resistance. But once insulin resistance has been decreased, patients still need all the other mechanisms to lose fat, and they need them to take place within the skeletal muscle cells because besides the skeletal muscle cells there are no other cells that can be physiologically influenced to increase the energy they use.

A daily minimal physical activity and the proper eating behavior can maintain the earned results obtained through breast cancer treatment, and they can also improve the life quality of the breast cancer patient.

References

1. Demark-Wahnefried, Wendy, et al. “Preventing sarcopenic obesity among breast cancer patients who receive adjuvant chemotherapy: results of a feasibility study.” Clinical Exercise Physiology 4.1 (2002): 44.
2. Demark-Wahnefried, Wendy, et al. “Preventing sarcopenic obesity among breast cancer patients who receive adjuvant chemotherapy: results of a feasibility study.” Clinical Exercise Physiology 4.1 (2002): 44.
3. Irwin, Melinda L., et al. “Changes in body fat and weight after a breast cancer diagnosis: influence of demographic, prognostic, and lifestyle factors.” Journal of Clinical Oncology 23.4 (2005): 774-782.
4. Messier, Virginie, et al. “Menopause and sarcopenia: a potential role for sex hormones.” Maturitas 68.4 (2011): 331-336.
5. Visovsky, Constance. “Muscle strength, body composition, and physical activity in women receiving chemotherapy for breast cancer.” Integrative cancer therapies 5.3 (2006): 183-191.
6. Laviano, Alessandro, et al. “Therapy insight: cancer anorexia–cachexia syndrome—when all you can eat is yourself.” Nature clinical practice Oncology2.3 (2005): 158-165.
7. Huebner, Jutta, et al. “Counseling Patients on Cancer Diets: A Review of the Literature and Recommendations for Clinical Practice.” Anticancer research 34.1 (2014): 39-48.
8. McEvoy, Claire T., Norman Temple, and Jayne V. Woodside. “Vegetarian diets, low-meat diets and health: a review.” Public health nutrition 15.12 (2012): 2287-2294.
9. Herbert, Victor. “The role of vitamin B12 and folate in carcinogenesis.” Essential Nutrients in Carcinogenesis. Springer US, 1986. 293-311.
10. Zoico, Elena, et al. “Adipose tissue infiltration in skeletal muscle of healthy elderly men: relationships with body composition, insulin resistance, and inflammation at the systemic and tissue level.” The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 65.3 (2010): 295-299.
11. Fielding, Roger A., et al. “The paradox of overnutrition in aging and cognition.” Annals of the New York Academy of Sciences 1287.1 (2013): 31-43.
12. Aapro, M., et al. “Early recognition of malnutrition and cachexia in the cancer patient: a position paper of a European School of Oncology Task Force.” Annals of Oncology (2014): mdu085.
13. Schmitz, Kathryn H., et al. “Safety and efficacy of weight training in recent breast cancer survivors to alter body composition, insulin, and insulin-like growth factor axis proteins.” Cancer Epidemiology Biomarkers & Prevention 14.7 (2005): 1672-1680.
14. Yarasheski KE. Managing sarcopenia with progressive resistance exercise training. The Journal of Nutrition, Health & Aging 2002; 6:  349-356
15. Kung, Thomas, et al. “Novel treatment approaches to cachexia and sarcopenia: highlights from the 5th Cachexia Conference: Barcelona, Spain, 5-8 December 2009.” Expert opinion on investigational drugs 19.4 (2010): 579-585.
16. Teixeira, Tatiana FS, et al. “Intestinal permeability parameters in obese patients are correlated with metabolic syndrome risk factors.” Clinical Nutrition 31.5 (2012): 735-740.
17. Viscarra, Jose Abraham, and Rudy Martin Ortiz. “Cellular mechanisms regulating fuel metabolism in mammals: role of adipose tissue and lipids during prolonged food deprivation.” Metabolism 62.7 (2013): 889-897.
18. Stenvinkel, Peter. “Obesity—a disease with many aetiologies disguised in the same oversized phenotype: has the overeating theory failed?.” Nephrology Dialysis Transplantation (2014): gfu338.
19. Tessitore, L., et al. “Leptin expression in colorectal and breast cancer patients.” International journal of molecular medicine 5.4 (2000): 421-427.
20. Yu, Y‐H., et al. “Metabolic vs. hedonic obesity: a conceptual distinction and its clinical implications.” Obesity Reviews (2015).
21. Ensling, Myriam, William Steinmann, and Adam Whaley-Connell. “Hypoglycemia: A possible link between insulin resistance, metabolic dyslipidemia, and heart and kidney disease (the Cardiorenal Syndrome).” Cardiorenal medicine 1.1 (2011): 67.
22. Borugian, Marilyn J., et al. “Insulin, macronutrient intake, and physical activity: are potential indicators of insulin resistance associated with mortality from breast cancer?.” Cancer Epidemiology Biomarkers & Prevention 13.7 (2004): 1163-1172.
23. Lu, Lin-jie, et al. “On the status of β-cell dysfunction and insulin resistance of breast cancer patient without history of diabetes after systemic treatment.” Medical Oncology 31.5 (2014): 1-5.
24. Rose, D. P., D. Komninou, and G. D. Stephenson. “Obesity, adipocytokines, and insulin resistance in breast cancer.” Obesity reviews 5.3 (2004): 153-165.
25. Boden, Guenther, et al. “Effects of acute changes of plasma free fatty acids on intramyocellular fat content and insulin resistance in healthy subjects.” Diabetes 50.7 (2001): 1612-1617.
26. Schaffer, Jean E. “Lipotoxicity: when tissues overeat.” Current opinion in lipidology 14.3 (2003): 281-287.
27. Yu, Yi-Hao, and Henry N. Ginsberg. “Adipocyte signaling and lipid homeostasis sequelae of insulin-resistant adipose tissue.” Circulation research 96.10 (2005): 1042-1052.

Articolul 2 weight gain mechanisms during breast cancer chemotherapy apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

Here is why you should lose weight if you were overweight or obese before diagnosis, or if you gained weight during breast cancer treatment:

a) Obesity decreases breast cancer treatment efficacy:

1. Triple negative patients without positive lymph nodes have a worst prognosis than normal weight patients.  – Bonsang-Kitzis si colab., 2015
2. Obesity decreases ER+/PR±/HER2+ breast cancer survival by diminishing Tamoxifen and Herceptin treatments efficacy. – Pande et al., 2014
3. Overweight and obese non-metastatic breast cancer patients have a lower response to neoadjuvant chemotherapy – Litton et al., 2008
4. Weight gain during chemotherapy increases the risks of recurrence and mortality – Thivat, 2010
5. The antiestrogenic treatment with aromatase inhibitors (Letrozole, Anastrozole or Exemestane) has less efficacy in postmenopausal obese breast cancer patients – Ioannides et al. 2014

b) Obesity increases the incidence and amplitude of breast cancer treatment side effects:

1. Obesity increases the risk of risk of persistent pain after breast cancer surgery. – Ding et al., 2017
2. Obesity is associated with a nearly 12-fold increased odds of a postoperative complication after elective breast procedures. – Chen et al., 2011
3. Obesity increases breast cancer secondary lymphedema risk. – DiSipio et al., 2013
4. Obesity increases radiotherapy skin toxicity. – Kraus-Tiefenbacher et al., 2012
5. Obesity associates an increased risk of depression – Ishii et al., 2016
6. Increased adiposity decreases vitamin D bioavailability – Parikh et al., 2004

c) Breast cancer patients obesity increases the risk of metastasis:

1. Obesity increases metastasis risk and decreases survival in  ER-/PR±/HER2+ breast cancer patients – Mazarella et al., 2013
2. Obesity increases the risk of lung and liver metastasis, and chemotherapy is less efficient in obese breast cancer patients – Osman and Hennessy, 2014
3. Obesity increases metastasis risk – Strong et al., 2015; Dowling et al., 2016
4. Obesity increases lung metastatis risk – Nagahashi et al., 2016
5. Obesity increases metastasis risk and decreases survival in  ER-/PR±/HER2± breast cancer patients – Wu et al., 2017

d) Obesity decreases breast cancer patients overall survival:

1. Obesity is an indepenedent factor that increases the risks of metastasis and breast cancer specific mortality, adjuvant therapies efficacy being lower in obese and overweight breast cancer patients – Ewertz et al., 2010
2. Obesity decreases overall survival independently of lymph node positivity – Kaviani et al., 2013
3. Obesity and diabetes have a negative impact on breast cancer survival – Jiralerspong et al., 2013
4. Obesity is an independent factor risk that decreases overall survival in ER+/PR±/HER2- postmenopausal breast cancer patients with lymph node involvment – Arce-Salinas et al., 2014; Scholtz et al., 2015
5. Obesity decreases overall survival in ER+ breast cancer patients younger than 40 years of age – Copson et al., 2015
6. Obesity increases breast cancer patients risk of mortality  – Chan and Norat, 2015

References:

Arce-Salinas, C., et al. “Overweight and obesity as poor prognostic factors in locally advanced breast cancer patients.” Breast cancer research and treatment 146.1 (2014): 183-188.

Bonsang-Kitzis, Hélène, et al. “Beyond axillary lymph node metastasis, BMI and menopausal status are prognostic determinants for triple-negative breast cancer treated by neoadjuvant chemotherapy.” PloS one 10.12 (2015): e0144359.

Chan, Doris SM, and Teresa Norat. “Obesity and breast cancer: not only a risk factor of the disease.” Current treatment options in oncology 16.5 (2015): 1-17.

Chen, Catherine L., et al. “The impact of obesity on breast surgery complications.” Plastic and reconstructive surgery 128.5 (2011): 395e-402e.

Copson, E. R., et al. “Obesity and the outcome of young breast cancer patients in the UK: the POSH study.” Annals of Oncology 26.1 (2015): 101-112.

Ding, Yuan-Yuan, et al. “Body mass index and persistent pain after breast cancer surgery: findings from the women’s healthy eating and living study and a meta-analysis.” Oncotarget 8.26 (2017): 43332.

DiSipio, Tracey, et al. “Incidence of unilateral arm lymphoedema after breast cancer: a systematic review and meta-analysis.” The lancet oncology 14.6 (2013): 500-515.

Dowling, R. J. O., et al. “Abstract P2-02-09: Obesity associated factors are inversely associated with circulating tumor cells in metastatic breast cancer.” (2016): P2-02.

Ewertz, Marianne, et al. “Effect of obesity on prognosis after early-stage breast cancer.” Journal of Clinical Oncology 29.1 (2010): 25-31.

Ioannides, S. J., et al. “Effect of obesity on aromatase inhibitor efficacy in postmenopausal, hormone receptor-positive breast cancer: a systematic review.” Breast cancer research and treatment 147.2 (2014): 237-248.

Ishii, Shinya, et al. “The association between sarcopenic obesity and depressive symptoms in older Japanese adults.” PloS one 11.9 (2016): e0162898.

Kaviani, Ahmad, et al. “Effects of obesity on presentation of breast cancer, lymph node metastasis and patient survival: a retrospective review.” Asian Pac J Cancer Prev 14.4 (2013): 2225-9.

Kraus-Tiefenbacher, Uta, et al. “Factors of influence on acute skin toxicity of breast cancer patients treated with standard three-dimensional conformal radiotherapy (3D-CRT) after breast conserving surgery (BCS).” Radiation Oncology 7.1 (2012): 217.

Mazzarella, Luca, et al. “Obesity increases the incidence of distant metastases in oestrogen receptor-negative human epidermal growth factor receptor 2-positive breast cancer patients.” European Journal of Cancer 49.17 (2013): 3588-3597.

Nagahashi, M., et al. “Abstract P2-05-11: Sphingosine-1-phosphate signaling promotes metastatic niches and lung metastasis in obesity-related breast cancer.” (2016): P2-05.

Osman, Mohammed A., and Bryan T. Hennessy. “Obesity Correlation With Metastases Development and Response to First-Line Metastatic Chemotherapy in Breast Cancer.” Clinical Medicine Insights. Oncology 9 (2014): 105-112.

Parikh, Shamik J., et al. “The relationship between obesity and serum 1, 25-dihydroxy

Pande, Mala, et al. “Association between germline single nucleotide polymorphisms in the PI3K-AKT-mTOR pathway, obesity, and breast cancer disease-free survival.” Breast cancer research and treatment 147.2 (2014): 381-387.

Jiralerspong, S., et al. “Obesity, diabetes, and survival outcomes in a large cohort of early-stage breast cancer patients.” Annals of oncology (2013): mdt224.

Litton, Jennifer K., et al. “Relationship between obesity and pathologic response to neoadjuvant chemotherapy among women with operable breast cancer.” Journal of Clinical Oncology 26.25 (2008): 4072-4077.

Scholz, Christoph, et al. “Obesity as an independent risk factor for decreased survival in node-positive high-risk breast cancer.” Breast cancer research and treatment 151.3 (2015): 569-576.

Strong, Amy L., et al. “Leptin produced by obese adipose stromal/stem cells enhances proliferation and metastasis of estrogen receptor positive breast cancers.” Breast Cancer Research 17.1 (2015): 112.

Thivat, Emilie, et al. “Weight change during chemotherapy changes the prognosis in non metastatic breast cancer for the worse.” BMC cancer 10.1 (2010): 648.

Wu, Yong, et al. “Aberrant phosphorylation of SMAD4 Thr277-mediated USP9x-SMAD4 interaction by free fatty acids promotes breast cancer metastasis.” Cancer Research (2017): canres-2012.

Articolul Why should overweight and obese breast cancer patients lose weight? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

Friendly consideration: because the idea that milk is a carcinogenic has become as popular as the idea that we have to eat the fruit between meals so as not to ferment the bacteria that are non-existent in the stomach, it will be a loooooooooooooooooooong and scientifically detailed article.

If you just want to have fun reading a personal opinion about dairy products and cancer, close this article, it’s not for you.

For those who want to understand why we recommend cancer patients to continue to consume milk, fermented dairy and cheese during both treatment and the relapse prevention period, I will begin by answering in detail one of the written comments in response to first part.

And I think it’s important to do this because I think this commentary mirrors the ideas transmitted in a popular way from one patient to another and from benevolent people to the oncological patient:

– “Things are never simple. Let’s ask ourselves: Why did not Asian people consume dairy for 6,000 years? Dairy is known to be acid products. And in the Asian diet abounds vegetables”.

Ignoring the fact that the author of the comment does not know that blood alkalinisation is as dangerous to health as acidification, what I do not understand is how you can write a valid comment like “things are never easy” in the same phrase that you write that “Asian people dit not consume dairy for 6,000 years“.

– Which Asians have not consumed dairy for 6,000 years?

The fact that some believe the Asians do not consume dairy ignores how geographically Asia is, it is just a guess based on the popular image promoted by green grass fans on the other side of the fence – a kind of Utopian China where live mythical antioxidant survivors.

Here are two Chinese milk advertisements of the 1930s and 1933s respectively, the first describing the mother who feeds her healthy baby with milk, and the second – an elderly woman who says she is healthy because she drinks a glass of milk daily in the morning and in the evening.

– So, did Asians not consumed dairy for 6,000 years, and then the marketers decide to start to advertise in 1930 to introduce a new product to the Chinese market?

In the database used by researchers quoted by Campbell himself, the inhabitants of one of the 65 regions studied – Tuoli – consumed on average 865.5 g dairy/day, but not because milk ads were so effective as to persuade even the Asians who did not consume dairy 6,000 years ago to consume them, but simply because the Tuoli region looks like this:

According to this database, the inhabitants of Tuoli:

1) had an average daily consumption of:

• 865.5 g dairy products
• 371.6 g wheat flour products
• 121 g of meat.

2) consumed extremely rarely or not at all:

• Potatoes – 5-6 times a year
• Vegetables – twice a year
• Fruits – maximum once a year
• Legumes – never
• Nuts – never
• Eggs – never
• Fish – never
• Vegetable oil – never

So these Asians lived with dairy, bread and meat, most of them being shepherds.

Considering that milk has an average content of 80% casein and an average protein content of about 4 g/l, we can calculate that casein intake in the Tuoli region was 27.39 g/day.

ANow let’s compare the risk of mortality through cancer due to a daily intake of 27.39 g of casein and one of 0 g by comparing them to:

– vegans from Jiexiu, Jingsing, Huguan, Cangxi, or Songxian regions = average intake of 0 g casein/day

with
– omnivores from the Tuoli region = average intake of 27.39 g casein/day.

And I invite you to do this as a parallel to Campbell’s famous study in which mice fed 20% of casein –they say – have cancer.

And I write “they say” because you can read even in that study că that none of the mice actually did cancer, but only precancerous lesions, of which 95% were self-healing, the researchers assuming that the remaining 5 % will turn into cancer at some point.

Here are some graphs based on the data obtained by researchers who analyzed the food intake of the people in the 65 regions of China with a vegan or omnivorous diet:

Nevertheless, according to Campbell:

“People who ate the most animal-based foods got the most chronic disease. Even relatively small intakes of animal-based food were associated with adverse effects. People who ate the most plant-based foods were the healthiest”.

Simplier, Campbell argues that “people with the highest consumption of animal food were the most unhealthy, and those who fed plants were the healthiest“.

Now, look at the graphs above and judge with your own brain the validity of this statement.

This is just one of many examples of what Campbell’s quoted studies say and what Campbell says that these studies say.

So – leaving aside more or less famous personal opinions – let’s answer the following 3 questions based on the current scientific literature:

1. Are carcinogenic milk proteins?
2. Does milk or dairy daily consumption increase the risk of mortality in cancer patients?
3. Does milk or dairy daily consumption increase the risk of cancer in healthy people?

1) Are carcinogenic milk proteins?

Campbell’s famous statement that we can activate / inactivate “cancer” by simply lowering casein intake is another example of the difference between what the studies quoted by him say and what he says say these studies say:

“casein proved to be so powerful in its effect that we could turn on and turn off cancer growth simply by changing the level consumed”

It would be absolutely brilliant to treat cancer so easily!

Just as I wrote in the first part of this series of articles, the studies quoted or made by Campbell did not „prove“ the carcinogenicity of casein in any way, but rather that increased intake of casein increases the survival of mice exposed to a substance carcinogens such as aflatoxin.

Studies show that the casein intake:

1. prolongs survival – Engel and Copeland, 1952
2. has antimutagenic effect – Van Boekel et al., 1993
3. has anticancerogenic activity both in vitro and in vivo – Goeptar et al., 1997
4. stimulates the immune system – Parodi, 1998
5. stimulates the apoptosis of intestinal malignant cells – Perego et al., 2012

And other milk proteins:

1. provide anticarcinogenic protection in case of exposure to carcinogens – McIntosh et al., 1995
2. stimulate the immune system –  Meisel and FitzGerald, 2003
3. inhibit the growth of malignant cells – Meisel, 2004
4. have antimutagenic effect – Parodi, 2007
5. inhibit angiogenesis – Tung et al., 2013
6. support the efficacy of treatment and the healing of the patient with cancer – Chen et al., 2014 
7. improve prognosis of patients with advanced cancer (stage III, IV) – Engelen et al., 2015

2) Daily milk or dairy consumption increases the risk of mortality in cancer patients?

1. Consumption of yoghurt and buttermilk can provide protection against breast cancer – van’t Veer et al., 1989
2. Consumption of 6 servings of dairy products per day is not detrimental to patients with rectal cancer – Karagas et al., 1998
3. Consumption of fermented dairy contributes to the preservation of intestinal integrity during radiotherapy – Salminen et al., 1998
4. Milk consumption during paclitaxel chemotherapy increases the effectiveness of treatment and decreases the incidence of side effects – Sun et al., 2011
5. Consumption of skimmed milk and dairy products does not increase the risk of mortality in patients with prostate cancer diagnosis – Petterson et al., 2012
6. Milk consumption lowers the risk of mortality in colon cancer patients – Yang et al., 2014
7. Consumption of milk and dairy products lowers the risk of mortality by cardiovascular disease, diabetes and cancer – Elwood et al., 2008
8. And, in general, it helps to counteract side effects of oncological treatment:

• anti-inflammatory and immunomodulatory effect – Mukhopadhya and Sweeney, 2016
• antihypertensive effect – Pepe et al., 2013
• supports type II diabetes prevention and sarcopenic obesity – McGregor and Poppitt, 2013
• associates a lower level of uric acid – Choi, Liu and Curhan, 2005
• improves hepatic transaminase levels and contributes to the reduction of total cholesterol and LDL-cholesterol – Nabavi et al., 2014

3) Daily milk or dairy consumption increases the risk of cancer in healthy people?

1. Moderate intake of milk and dairy products does not increase the risk of cancer – Davoodi, Esmaeili and Mortazavian, 2013
2. Men who consume milk frequently have a 60% lower risk of colon cancer than those who do not consume milk – Jing Ma et al., 2001
3. A low consumption of fermented dairy is associated with an increased risk of pancreatic cancer – De Mesquita et al., 1991
4. Consumption over two portions of dairy is associated with a lower risk of breast cancer ER + in menopausal women – McCullough et al., 2005
5. Increased intake of buttermilk and yogurt may lower the risk of bladder cancer – Larsson et al., 2008
6. Consumption of fermented dairy products lowers the risk of liver cancer – Rayes, El-Naggar and Mehanna, 2008
7. Consumption of milk and dairy products lowers the risk of colorectal cancer – Aune et al., 2012
8. Consumption of milk and dairy products does not increase the risk of lung cancer – Yu et al., 2016
9. Consumption of milk and dairy products is associated with a decrease in the risk of colon cancer, bladder cancer, gastric cancer and breast cancer – Thorning et al., 2016
10. The meta-analysis of 22 cohort studies that analyzed 1,566,940 people and 5 case studies that analyzed 33,372 Asian people over a 10-year period demonstrates that a minimum intake of over 400 ml of yogurt or dairy products per day is associated with a low risk of breast cancer – Zang et al., 2015
11. The meta-analysis of 10 population studies analyzing the eating habits of 534,536 people claims that daily intake of at least 250 ml of milk reduces the risk of colorectal cancer – Cho et al., 2004
12. The meta-analysis of 52 studies analyzing milk intake from the perspective of fat, growth hormones, IGF-1 and estrogen contaaining does not support the association between dairy consumption and breast cancer risk – Parodi, 2013
13. The meta-analysis of 45 studies that analyzes 26,769 cases does not support the epidemiological assumption that dairy intake would increase the risk of prostate cancer – Huncharek, Muscat, Kupelnick, 2008
14. The meta-analysis of 17 case studies and 6 population studies analyzing a total of 3,256 cases suggests that milk intake does not increase the risk of gastric cancer, dairy consumption lowering this risk – Guo et al., 2015
15. The meta-analysis of 19 studies examining the consumption of skimmed milk, whole milk, yoghurt and lactose does not support any association between the intake of these foods or lactose in particular and the risk of ovarian cancer – Liu et al., 2015
16. The meta-analysis of 32 studies of milk, yogurt, dairy and cheese consumption claims that the intake of these foods is not associated with an increased risk of lung cancer – Yang et al., 2016

Here are dozens of studies that claim that dairy products are not carcinogenic for healthy people and that milk and dairy intake decreases the risk of mortality and supports the effectiveness of oncology treatment.

If you are diagnosed with cancer and you are tempted to remove milk and meat from food, packed with various pseudo-treatments such as veganism, detox, bicarbonate, red beet juice, wonder mushrooms, and vitamin supplements C or other antioxidants instead of or with oncology, please think:

– How powerful should these malignant cells be that only 1, 2 or 5 cm from you endanger the survival of your entire body?

The malignant cell is the queen of survival, a real chameleon relaxed in front of such simplistic strategies, strategies that it will use to survive, evolve and multiply precisely because you deliver it on a platter:

1. has the ability to use antioxidants to inactivate free radicals that could prevent it from multiplying and damaging it by generating apoptosis – Seifried et al., 2003
2. has the ability to survive and develop without glucose when conditions become unfavorable – Alfarouk et al., 2011
3. is a black glucose hole – Kroemer and Pouyssegur, 2008;

• co-administration of antioxidant supplements reduces side effects, but decreases the effectiveness of radiotherapy – Bairati et al., 2005
• co-administration of antioxidant supplements decreases the effectiveness of chemotherapy and radiotherapy – Lawenda et al., 2008

I will write a more detailed article on the harmfulness of antioxidant supplementation during oncology treatment because the use of such pseudo-oncological products can even transform the cancers that are initially treatable into incurable cancers.

What I want to emphasize now is that by oncological nutrition we can only support the efficiency of allopathic treatment, not cure a disease like cancer!

Anyone who claims otherwise has no idea what he’s saying – on the money, the health and, unfortunately, sometimes even on the life of the oncological patient.

Utopical China painted in pink by Campbell sells cancer patients, through pseudo-oncological industry traders, high hopes elevates to a universal panacea.

„…that it is better to tell the cancer patient to eliminate milk and meat, drink red beet juice and take antioxidant supplements than leave it so confused without trying to help it with an advice!“

Quoted studies

1. Alfarouk, Khalid O., et al. “Evolution of tumor metabolism might reflect carcinogenesis as a reverse evolution process (dismantling of multicellularity).” Cancers 3.3 (2011): 3002-3017.
2. Aune, D., et al. “Dairy products and colorectal cancer risk: a systematic review and meta-analysis of cohort studies.” Annals of oncology 23.1 (2012): 37-45.
3. Bairati, Isabelle, et al. “Randomized trial of antioxidant vitamins to prevent acute adverse effects of radiation therapy in head and neck cancer patients.” Journal of Clinical Oncology 23.24 (2005): 5805-5813.
4. YF Chen, H., et al. “Potential clinical applications of multi-functional milk proteins and peptides in cancer management.” Current medicinal chemistry 21.21 (2014): 2424-2437.
5. Chen, Wanqing, et al. “Cancer statistics in China, 2015.” CA: a cancer journal for clinicians 66.2 (2016): 115-132.
6. Cho, Eunyoung, et al. “Dairy foods, calcium, and colorectal cancer: a pooled analysis of 10 cohort studies.” Journal of the National Cancer Institute 96.13 (2004): 1015-1022.
7. Choi, Hyon K., Simin Liu, and Gary Curhan. “Intake of purine‐rich foods, protein, and dairy products and relationship to serum levels of uric acid: the Third National Health and Nutrition Examination Survey.” Arthritis & Rheumatism 52.1 (2005): 283-289.
8. Davoodi, H., S. Esmaeili, and A. M. Mortazavian. “Effects of milk and milk products consumption on cancer: a review.” Comprehensive Reviews in Food Science and Food Safety 12.3 (2013): 249-264.
9. De Mesquita, H. Bueno, et al. “Intake of foods and nutrients and cancer of the exocrine pancreas: A population‐based case‐control study in the Netherlands.” International journal of cancer 48.4 (1991): 540-549.
10. Elwood, Peter C., et al. “The survival advantage of milk and dairy consumption: an overview of evidence from cohort studies of vascular diseases, diabetes and cancer.” Journal of the American College of Nutrition 27.6 (2008): 723S-734S.
11. Engel, R. W., and D. H. Copeland. “The influence of dietary casein level on tumor induction with 2-acetylaminofluorene.” Cancer research 12.12 (1952): 905-908.
12. Engelen, M. P. K. J., et al. “High anabolic potential of essential amino acid mixtures in advanced non-small cell lung cancer.” Annals of Oncology (2015): mdv271.
13. Goeptar, Arnold R., et al. “Impact of digestion on the antimutagenic activity of the milk protein casein.” Nutrition Research 17.8 (1997): 1363-1379.
14. Guo, Yanjun, et al. “Dairy consumption and gastric cancer risk: a meta-analysis of epidemiological studies.” Nutrition and cancer 67.4 (2015): 555-568.
15. Huncharek, Michael, Joshua Muscat, and Bruce Kupelnick. “Dairy products, dietary calcium and vitamin D intake as risk factors for prostate cancer: a meta-analysis of 26,769 cases from 45 observational studies.” Nutrition and cancer60.4 (2008): 421-441.
16. Karagas, Margaret R., et al. “Effects of milk and milk products on rectal mucosal cell proliferation in humans.” Cancer Epidemiology Biomarkers & Prevention 7.9 (1998): 757-766.
17. Kroemer, Guido, and Jacques Pouyssegur. “Tumor cell metabolism: cancer’s Achilles’ heel.” Cancer cell 13.6 (2008): 472-482.
18. Larsson, Susanna C., et al. “Cultured milk, yogurt, and dairy intake in relation to bladder cancer risk in a prospective study of Swedish women and men.” The American journal of clinical nutrition 88.4 (2008): 1083-1087.
19. Lawenda, Brian D., et al. “Should supplemental antioxidant administration be avoided during chemotherapy and radiation therapy?.” Journal of the national cancer institute 100.11 (2008): 773-783.
20. Liu, Jing, et al. “Milk, yogurt, and lactose intake and ovarian cancer risk: A meta-analysis.” Nutrition and cancer 67.1 (2015): 68-72.
21. Joint FAO/WHO Expert Committee on Food Additives (JECFA) . Toxicological evaluation of certain veterinary drug residues in food: Estradiol-17β progesterone and testosterone. WHO Food Additives Series.2000b;43
22. Ma, Jing, et al. “Milk intake, circulating levels of insulin-like growth factor-I, and risk of colorectal cancer in men.” Journal of the National Cancer Institute 93.17 (2001): 1330-1336.
23. McCullough, Marjorie L., et al. “Dairy, calcium, and vitamin D intake and postmenopausal breast cancer risk in the Cancer Prevention Study II Nutrition Cohort.” Cancer Epidemiology Biomarkers & Prevention 14.12 (2005): 2898-2904.
24. McGregor, Robin A., and Sally D. Poppitt. “Milk protein for improved metabolic health: a review of the evidence.” Nutrition & metabolism 10.1 (2013): 1.
25. McIntosh, Graeme H., et al. “Dairy proteins protect against dimethylhydrazine-induced intestinal cancers in rats.” Journal of Nutrition 125.4 (1995): 809-816.
26. Meisel, H., & FitzGerald, R. J. (2003). Biofunctional peptides from milk proteins: mineral binding and cytomodulatory effects. Current pharmaceutical design, 9(16), 1289-1296.
27. Meisel, Hans. “Multifunctional peptides encrypted in milk proteins.” Biofactors 21.1-4 (2004): 55-61.
28. Mukhopadhya, Anindya, and Torres Sweeney. “Milk Proteins: Processing of Bioactive Fractions and Effects on Gut Health.” MILK PROTEINS (2016): 83.
29. Nabavi, S., et al. “Effects of probiotic yogurt consumption on metabolic factors in individuals with nonalcoholic fatty liver disease.” Journal of dairy science 97.12 (2014): 7386-7393.
30. Parodi, Peter W. “A role for milk proteins in cancer prevention.” Australian journal of dairy technology 53.1 (1998): 37.
31. Parodi, P. W. “A role for milk proteins and their peptides in cancer prevention.” Current pharmaceutical design 13.8 (2007): 813-828.
32. Parodi, Peter W. “Impact of cows’ milk estrogen on cancer risk.” International dairy journal 22.1 (2012): 3-14.
33. Parodi, Peter W. “Dairy product consumption and the risk of breast cancer.” Journal of the American College of Nutrition 24.sup6 (2005): 556S-568S.
34. Pepe, Giacomo, et al. “Potential anticarcinogenic peptides from bovine milk.” Journal of amino acids 2013 (2013).
35. Perego, Silvia, et al. “Casein phosphopeptides modulate proliferation and apoptosis in HT-29 cell line through their interaction with voltage-operated L-type calcium channels.” The Journal of nutritional biochemistry 23.7 (2012): 808-816.
36. Pettersson, Andreas, et al. “Milk and dairy consumption among men with prostate cancer and risk of metastases and prostate cancer death.” Cancer Epidemiology Biomarkers & Prevention 21.3 (2012): 428-436.
37. Rayes, Amna AH, Sabah MM El-Naggar, and Nayra Sh Mehanna. “The effect of natural fermented milk in the protection of liver from cancer.” Nutrition & Food Science 38.6 (2008): 578-592.
38. Salminen, E., et al. “Preservation of intestinal integrity during radiotherapy using live Lactobacillus acidophilus cultures.” Clinical radiology 39.4 (1988): 435-437.
39. Seifried, Harold E., et al. “The antioxidant conundrum in cancer.” Cancer Research 63.15 (2003): 4295-4298.
40. Sun, Xueying, et al. “Dairy milk fat augments paclitaxel therapy to suppress tumour metastasis in mice, and protects against the side-effects of chemotherapy.” Clinical & experimental metastasis 28.7 (2011): 675-688.
41. Thorning, Tanja Kongerslev, et al. “Milk and dairy products: good or bad for human health? An assessment of the totality of scientific evidence.” Food & Nutrition Research 60 (2016).
42. Tung, Yu-Tang, et al. “Bovine lactoferrin inhibits lung cancer growth through suppression of both inflammation and expression of vascular endothelial growth factor.” Journal of dairy science 96.4 (2013): 2095-2106.
43. van’t Veer, Pieter, et al. “Consumption of fermented milk products and breast cancer: a case-control study in The Netherlands.” Cancer research 49.14 (1989): 4020-4023.
44. Yang, Baiyu, et al. “Calcium, vitamin D, dairy products, and mortality among colorectal cancer survivors: the Cancer Prevention Study-II Nutrition Cohort.” Journal of Clinical Oncology (2014): JCO-2014.
45. Yang, Yang, et al. “Dairy Product, Calcium Intake and Lung Cancer Risk: A Systematic Review with Meta-Analysis.” Scientific reports 6 (2016).
46. Yu, Yi, et al. “Dairy consumption and lung cancer risk: a meta-analysis of prospective cohort studies.” OncoTargets and therapy 9 (2016): 111.
47. Zang, Jiajie, et al. “The Association between Dairy Intake and Breast Cancer in Western and Asian Populations: A Systematic Review and Meta-Analysis.” Journal of breast cancer 18.4 (2015): 313-322.
48. Zeitoun, M. M., I. S. Salem, and S. M. Ahmed. “Evaluation of the Male and Female Sex Steroid Hormones Residues in Eggs, Milk and their Productsin Alqassim Region.” Journal of Agricultural and Veterinary Sciences 8.1 (2015).

P.S. Are laptele impact estrogenic?

Unele dintre pacientele cu cancer mamar cu care lucrez nu consumă lapte de teama impactului estrogenic.

– Conţine laptele estrogen?

– Evident da, chiar 17β-estradiol – cel mai activ tip de estrogen.

Doza maximă admisă de OMS (Organizaţia Mondială a Sănătăţii) este de 5 μg 17β-estradiol/kg corp.

De exemplu, o femeie de 60 kg poate avea un aport alimentar maxim 60 x 5 μg = 300 μg 17β-estradiol pe zi.

1 l lapte contine 0,1571 μg17β-estradiol – Zeitoun si colab., 2015

Dar 95% din estradiolul ingerat este inactivat gastro-intestinal – Parodi, 2012

Această inactivare gastro-intestinală a estradiolului ingerat face ca, din cele 0,1571 μg aduse de 1 l lapte, doar 0,007855 μg să ramână active.

Deci, cantitatea de lapte pe care ar trebui să o consume într-o zi o femeie de 60 kg pentru a genera impact estrogenic este de 38.192 litri.

Articolul „The China Study“ Part II – Are the dairy products carcinogenic? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

First of all, I would like to point out that there is no diet to cure cancer.

No diet, no dietary supplement and no plant remedy cures cancer. NONE.

Cancer is a piece of our own body that managed to become so adaptable, aggressive, and capable of camouflage like a chameleon – it knows all our defensive secrets inside out, it uses all our defense mechanisms against its own body.

As a patient – the belief that the natural healer can cure your cancer with antioxidants, mushrooms, teas, sins forgiveness, Karma cleanses, or ginseng powdered magic pills sprinkled with star dust can be understood based on the confusion and on the feeling that you just lost of control over your own life, feelings commonly associated with a cancer diagnosis.

But to promote that you – the “Carpathian quack” – can naturally cure cancer on your own equals either an incapacity to understand what you’re fighting with, or an equally callousness, both sold to desperate patients for hard earned money and end of life hopes.

A true pseudo-medical industry has flourished on the basis of the confusion and despair of oncological patients.

However, because of its high adaptability and aggressivity, cancer treatment requires one of the most multidisciplinary approaches possible. And, even so, the war with cancer is not won by default because the malignant cells are extraordinarily unpredictable.

By oncology nutrition we do not cure cancer, we only support the effectiveness of oncology treatment, counteracting side effects as much as possible and only when this is possible without influencing treatment efficacy.

Oncology nutrition means moderate consumption of high quality food of both vegetable and animal origin, consumption carefully adapted to the body weight, body composition, appetite impairment, any other non-oncological associated pathologies the individual patient might have, and to the actual oncology treatment stage and its side effects.

Extremes such as “you can eat everything” are just as damaging as the extremes “don’t drink milk (1), don’t eat meat (2), or take a waggon of antioxidants” (3).

Firstly, I would like to underline that oncology nutrition is just highly personalised clinical nutrition simply because we cannot starve cancer. There are many mechanisms behind this avoidance extreme dietary recommendation, but the main ones are the following:

• malignant cells are a true “black hole” for glucose because they have much more glucose transporters than any normal cell could ever have (4) – and it simply doesn’t matter if this glucose is obtained by the tumour from consuming glucose from rice, corn, potatoes, pasta, bread, sweets, fruits, honey; or from the glucose produced inside the body from amino acids or glycerol when glucose intake is restricted
• malignant cells can use antioxidants to survive despite treatment administration, which is exactly why the antioxidant co-administration can decrease the efficacy of oncological treatment (5).

But the fact that we recommend moderate consumption of meat, fish, eggs and dairy products during oncological treatment – besides the moderate consumption of fruits, vegetables and whole grains – does not mean that we recommend the consumption of roasted eggs, donuts, bacon, fried cheese or soda drinks.

Even Campbell himself said that such simplistic thinking is idiotic:

“Everything in food works together to create health. The more we think that a single chemical characterises a whole food, the more we stray into idiocy”.

(“The China Study”, page 106)

Secondly, I would also like to underline that:

1. Epidemiology studies results are correlations, not causality evidence.
2. And correlations are invalid if the issue at hand can be generated by other bias factors that have not been taken into account by the researches that did that particular study.

So, despite the popularity, the book entitled “The China Study” at most raises hypotheses, it does not bring any causal evidence about the link between foods and cancer.

The main findings associated with a cancer risk presented in this book – findings listed on the Cornell University website – are the following:

• Plasma cholesterol in the 90-170 milligrams per deciliter range is positively associated with most cancer mortality rates. Plasma cholesterol is positively associated with animal protein intake and inversely associated with plant protein intake.
• Breast cancer is associated with dietary fat (which is associated with animal protein intake) and inversely with age at menarche (women who reach puberty at younger ages have a greater risk of breast cancer).
• For those at risk for liver cancer (for example, because of chronic infection with hepatitis B virus) increasing intakes of animal-based foods and/or increasing concentrations of plasma cholesterol are associated with a higher disease risk.
• Colorectal cancers are consistently inversely associated with intakes of 14 different dietary fiber fractions (although only one is statistically significant). Stomach cancer is inversely associated with green vegetable intake and plasma concentrations of beta-carotene and vitamin C obtained only from plant-based foods.
• Western-type diseases, in the aggregate, are highly significantly correlated with increasing concentrations of plasma cholesterol, which are associated in turn with increasing intakes of animal-based foods.

Before we discuss about the fact that the increased risk of cancer associated by Campbell to animal-based foods can be at most be interfered indirectly through hypercholesterolemia potentially associated with the fat contained by such foods as no conclusive association “animal protein” is made.

Thus, it would be logical to ask ourselves some questions:

– What is the essential difference between “animal protein” and “vegetable protein”?

– Why would vegetable protein intake be protective while animal protein intake harmful?

– And doesn’t categorising all animal-based foods’ as “bad” based on the inferred impact of a single isolated substance increases the risk of idiocy, according to Campbell’s own words?

Leaving aside the fact that there is a multitude of animal proteins and a multitude of vegetable proteins, their simplistic definition of as “animal protein” or “vegetable protein” can only be made on the basis of their essential amino acid content.

Humans do not feed with proteins, but with foods that are digested up to amino acids to be absorbed through the intestinal wall.

The only difference between “animal protein” and “vegetal protein” is that the vegetal  protein does not contain all the essential amino acids.

– So, if the “animal protein” is somehow carcinogenic because it has all the essential amino acids, why would the combination of vegetal protein recommended to the vegans to ensure the proper essential amino acid intake be as carcinogenic as the intake of meat?

Because, basically, if we consider not only the generic concept of “protein intake”, but also the fact that the eaten food must be digested up to amino acids in order to pass through the intestinal wall, all we have after protein digestion are:

• all essential amino acids – after digesting proteins of animal origin
• only a part of them – after digesting proteins of plant origin
• all essential amino acids – after digesting a mixed meal composed of plant proteins with complementary amino acid intake

But nowhere in this book called “study” is it demonstrated that animal protein intake feeds cancer, increases cancer risk or that it decreases in any way the survival of cancer patients. Paradoxically, the mentality behind the nutritional recommendations in “The China study” is completely unrelated to any protein, being inferred from fats not from proteins:

But there are a lot of BUTs.

The database used by Campbell to draw these conclusions did not belong to him, the “evidence” behind his book being published in 1990 by Zhongguo by Shan Shi, Sheng Huo Fang Shi He Si Wang and Junshi Chen in Diet, Life-Style, and Mortality in China: A Study of the Characteristics of 65 Chinese Counties.

And, despite the opinion of many natural healing gurus, this database is not about the fact that due to the traditional Chinese diet China’s population has a lowed risk of cancer or a lower cancer related mortality. Not even close.

Unfortunately, China occupies one of the leading positions in cancer statistics, and the rural residents of China have a much higher cancer incidence and mortality than those living in the cities (6).

The study on which Campbell’s book is based is an epidemiological study based on a questionnaire in which respondents were asked to check boxes of pre-filled tables with various foods and written fixed quantities – the foods they had consumed in the last 3 days, followed by blood and urine analysis. Then the statical results obtained from this questionnaire were correlated with the cancer related mortality calculated for that particular area 10 years prior to the study.

Junshi Chen and his colleagues chose to do this epidemiological study because the rural Chinese people of the 1980s used to live their entire life in the same region without altering their lifestyle and diet, and because of the vast geographical areas there are very large differences in lifestyle and nutrition from one Chinese region to another: the inhabitants of some areas being traditionally almost vegan, while the inhabitants of other regions traditionally consuming ± 1 kg of dairy products per day simply because they were shepherds.

But these researchers quoted by Campbell found only a mild correlation with no statistical significance between animal protein intake and cancer (+ 3% overall risk for mortality due to any type of cancer) and a slightly higher correlation for vegetable protein intake and cancer (+ 12% overall risk for mortality due to any type of cancer):

• Risk of cancer mortality correlated to the animal protein intake

Lymphoma: -18
Bladder cancer: -9
Colorectal cancer: -8
Leukemia: -5
Nasopharyngeal cancer: -4
Cervical cancer: -4
Liver cancer: -3
Cancer of esophagus: +2
Breast cancer: +12

• Risk of cancer related mortality correlated with vegetable protein intake

Lymphoma: -4
Bladder cancer: -3
Colorectal cancer: +19
Leukemia: +15
Nasopharyngeal cancer: -40*
Cervical cancer: +12
Liver cancer: +12
Cancer of esophagus: +18
Breast cancer: +1

But correlations without * are not statistically valid and the obtained values increase in statistical significance when they have two or three asterixes (p<0.05 = * statistically significant; p<0.001 = ** more statistically significant; p<0.0001 = *** very statistically significant).

Also, in order to be able to raise a risk factor hypothesis, we must take into account any other confounding factors that can also be correlated with the particular risk we are trying to evaluate.

For example, for breast cancer – besides non-statistical correlations generated by the consumption of proteins, be it animal or vegetable  – there are other correlations, some significant, some not:

• Hyperglycemia: +36**
• Wine consumption: +33*
• Alcohol consumption: +31*
• Fruit intake: +25
• Workplace in industry (as opposed to agriculture): +24
• Sweets and flour products intake: +20
• Beer intake: +19
• Legumes intake: +17

I underline again that these are “correlations” – either positive = risk factor, either negative = protective factor; either statistically valid if they have *, either with no statistical significance if they do not have *. Correlations are not causal evidence.

And Junshi Chen and his collaborators have not found any statistically significant correlations between animal protein intake and cancer risk or with cancer related mortality.

For instance, their respondents from one of the areas with the highest animal-protein intake (Tuoli) had lower rates of cancer related mortality risks than those from areas with almost zero animal protein intake (Huguan).

So 1: Ignore the fact that Campbell nutritional recommendations are contradicted by the very researchers he quoted as proof.

These were other researchers.

Despite the fact that a researcher like Campbell quoted their correlations as arguments in support of his conclusions, these other researchers might have been wrong.

It seems incredible, however, that he used his 1983 study to prove that the “animal protein” feeds malignant cells by “activating” cancer, because – unlike popular opinion believed by many – the results of his own study was not that 20% casein-fed mice developed tumours, and that mice fed with 5% lived happily ever after, learning their grandchildren about the benefits of veganism (7).

His own study protocol was as follows:

1. two groups of mice were fed for 2 weeks with either 5% casein or 20% casein while administered aflatoxin.
2. then each group was divided into two, and each of the two new subgroups was fed either with 5% casein or with 20% casein for another 12 weeks.

And please keep in mind that aflatoxin was the carcinogen in this whole story, not casein (8).

You can see the results in Tables 1 and 2 of the picture below (with the mention that you can read the entire English study by clicking on the link to the study quoted under No. 7).

So, Campbell’s own results were the following:

• The group fed with 5% casein during the administration of the aflatoxin carcinogen developed severe hepatic lesions (hepatomegaly, cholangiofibrosis, and bile duct proliferation)
• The group fed with 20% casein on the duration of the aflatoxin carcinogen developed only rare moderate hepatic lesions (no colangiofibrosis or bile duct proliferation)

And this was no surprise for him, Campbell demonstrating in another of his earlier studies that aflatoxin is far more carcinogenic in case of insufficient protein intake (9).

– And I would sometimes like to ask those who advise cancer patients to become vegans: Do you understand that you basically advise these poor sick people to adhere to a diet that increases the toxicity of carcinogens?

Nowhere in this study, Campbell has shown that mice fed with 20% casein have cancer or those with 5% did not. What his study demonstrates is that hepatic lesions developed by 5% casein fed mice are different and more severe than those developed by mice fed with 20% casein.

Campbell points out that:

• biliary duct hyperplasia and cholangiofibrosis are not pre-neoplastic lesions;
• the lesions developed in 20% casein-fed mice “probably have a higher tendency towards tumour growth”;
• although in the next paragraph he writes that most of these lesions regress, transforming back into normal tissue, and that only a few of them persist, probably generating tumours.

None of the mice in the Campbell’s study died of even developed cancer, regardless of their diet.

– How does that sound as a scientific evidence that animal protein intake is carcinogenic?

As I write above, using such a study to support the casein harm looks unbelievable. And it looked unbelievable also to the Indian researchers Mathur and Nayak, who tried in 1989 to recreate Campbell’s results using the same aflatoxin protocol while feeding 5% and 20% casein monkeys, not mice (10).

The results of this study demonstrated once again what Campbell had actually obtained = a higher casein intake provides hepatic protection and increased survival even in the presence of aflatoxin exposure:

• most monkeys fed with 5% casein died before 70 weeks before they started developing liver tumors
• monkeys fed with 5% casein that survived for more than 90 weeks developed preneoplastic liver lesions
• monkeys fed with 20% casein did not develop any preneoplastic hepatic injury (the exact words of the researchers are: “The animals in the high protein group surviving even beyond 90 weeks do not show any preneoplastic / neoplastic lesions”.)

Thus, unlike Campbell – whose study showed the same protective effect of casein, but who chose ignore his own study results in order to present his his own personal view – Mathur and Nayak concluded that the protein-caloric malnutrition combined with the intake of aflatoxin contaminated foods explain the increased incidence of liver cancer in areas where these two factors co-exist.

I will explain more about casein and aflatoxin in particular and about the importance of dairy intake during oncological treatment generally in the part II of this article.

So 2: Please ignore the fact that a higher intake of casein protects the liver and increases survival even when exposed to a carcinogen as strong as aflatoxin.

Furthermore, the correlation between hypercholesterolemia and an increased risk of cancer is very far-fetched (11).

At nowadays’ hypercholesterolemia incidence, we could perorate bizarre correlations like:

• The school is carcinogenic because it keeps children nailed down in school benches for long, long hours – sedentariness increases cholesterol, so attending school increases the risk of cancer.
• Pokemon reduces the risk of cancer because the egg has to be walked 10 km – so when you play Pokemon you are no longer sedentary, thus playing Pokemon lowers your cholesterol, thus playing Pokemon reduces the risk of cancer.

Jokes aside, even if we accept that hypercholesterolemia would be so carcinogenic as Campbell paints it to be – despite the fact that current scientific literature does not support this hypothesis – to conclude that foods of animal origin increase the cancer risk because their intake might generate hypercholesterolemia is scientifically incredible.

The hypothesis that “the intake of foods of animal origin is the cause of hypercholesterolemia:

– puts under the same label:

• Fried schnitzels and steaks of lean meat baked in the oven – simply calling them both “meat” (12);
• Fried oil with extra virgin olive oil – simply calling them both “vegetable oil” (13);
• Fried potatoes or chips with baked or boiled potatoes – simply calling “potatoes” (14).

– does not take into account that we can make cholesterol inside the body from carbohydrates consumed in excess (15).

Of course, we can educate people with the Dr. Google, but researchers should not allow even researchers like Campbell to ignore any other lifestyle factors that can lead to hypercholesterolemia or any other pathologies or medications that can potentially increase both cholesterol and the cancer risk.

For example, it seems to be common sense to believe that increased fiber intake protects against colon cancer (16).

But – leaving common sense aside because it’s no longer that common these days – many of the respondents of the Junshi Chen study quoted by Campbell were infected with schistosomia – a risk factor for both hypercholesterolemia and colon and bladder cancer (17, 18).

Thus – because this parasite can cause both hypercholesterolemia and cancer – it would be logical to exclude schistosomia infected respondents from a population you study in order to draw a valid scientific conclusion about risk factors that can cause cancer.

But Campbell did not exclude them, hiding under the carpet also the fact that schistosomia increases the hypercholesterolemia and cancer risk.

So 3: If you agree to consider animal protein carcinogenic because animals have cholesterol and plants don’t, please ignore any other possible causes of hypercholesterolemia.

In marketing, there is a principle that sells well and can even make blackened bananas go viral:

Keep

It

Simply

Stupid

Congruently, Campbell keeps it as simple and as stupidly possible:

„Hypercholesterolemia increases the cancer risk.

Foods of animal origin contain cholesterol, thus their intake increase cholesterol, thus their intake increases cancer risk.

Foods of plant origin don not contain cholesterol, thus their intake does not increase cholesterol, thus their intake decreases cancer risk.

– So what if the researchers you are quoting concluded that plant protein intake is correlated with a higher cancer mortality risk?

– So what if you name casein a carcinogenic despite your own studies results?

– So what if hypercholesterolemia is not considered carcinogenic?

– So what if the patients whose cancer you claim to be caused by animal protein intake also had schistosomia?

Despite your very own scientific evidence, you are Campbell and you decided to follow marketing guidelines and to keep things simply stupid: „Consumption of any quantity of animal food increases the cancer risk and mortality through cancer“.

– Why should anyone use their logic when a biochemistry professor makes clinical recommendations based on extrapolations contradicted by the quoted epidemiological data and by his very own results?

Quoted studies

(1) McCullough, Marjorie L., et al. “Dairy, calcium, and vitamin D intake and postmenopausal breast cancer risk in the Cancer Prevention Study II Nutrition Cohort.” Cancer Epidemiology Biomarkers & Prevention 14.12 (2005): 2898-2904.

(2) Gilsing, A. M. J., et al. “Vegetarianism, low meat consumption and the risk of lung, postmenopausal breast and prostate cancer in a population-based cohort study.” European journal of clinical nutrition 70.6 (2016): 723-729.

(3) Seifried, Harold E., et al. “The antioxidant conundrum in cancer.” Cancer Research 63.15 (2003): 4295-4298.

(4) Szablewski, Leszek. “Expression of glucose transporters in cancers.” Biochimica et Biophysica Acta (BBA)-Reviews on Cancer 1835.2 (2013): 164-169.

(5) D’Andrea, Gabriella M. “Use of antioxidants during chemotherapy and radiotherapy should be avoided.” CA: a cancer journal for clinicians 55.5 (2005): 319-321.

(6) Chen, Wanqing, et al. “Cancer statistics in China, 2015.” CA: a cancer journal for clinicians 66.2 (2016): 115-132.

(7) Appleton, B. Scott, and T. Colin Campbell. “Effect of high and low dietary protein on the dosing and postdosing periods of aflatoxin B1-induced hepatic preneoplastic lesion development in the rat.” Cancer research 43.5 (1983): 2150-2154.

(8) Svoboda, D. O. N. A. L. D., H. Jo Grady, and J. O. H. N. Higginson. “Aflatoxin B1 injury in rat and monkey liver.” The American journal of pathology 49.6 (1966): 1023.

(9) Campbell, T. Colin, and J. R. Hayes. “The effect of quantity and quality of dietary protein on drug metabolism.” Federation Proceedings. Vol. 35. No. 13. 1976.

(10) Mathur, Meera, and N. C. Nayak. “Effect of Low Protein Diet on Low Dose Chronic Aflatoxin B1 Induced Hepatic Injury in Rhesus Monkeys.” Journal of Toxicology: Toxin Reviews 8.1-2 (1989): 265-273.

(11) Kritchevsky, S. B., and D. Kritchevsky. “Serum cholesterol and cancer risk: an epidemiologic perspective.” Annual review of nutrition 12 (1992): 391.

(12) Omojola, A. Babatunde, et al. “Effect of cooking methods on cholesterol, mineral composition and formation of total heterocyclic aromatic amines in Muscovy drake meat.” Journal of the Science of Food and Agriculture 95.1 (2015): 98-102.

(13) Wang, Y., et al. “Effects of frying conditions on the formation of heterocyclic amines and trans fatty acids in grass carp (Ctenopharyngodon idellus).” Food chemistry 167 (2015): 251-257.

(14) Furrer, Amber N., Mohammad Chegeni, and Mario G. Ferruzzi. “Impact of Potato Processing on Nutrients, Phytochemicals and Human Health.” Critical reviews in food science and nutrition just-accepted (2016): 00-00.

(15) Parks, Elizabeth J., and Marc K. Hellerstein. “Carbohydrate-induced hypertriacylglycerolemia: historical perspective and review of biological mechanisms.” The American journal of clinical nutrition 71.2 (2000): 412-433.

(16) Park, Yikyung, et al. “Dietary fiber intake and risk of colorectal cancer: a pooled analysis of prospective cohort studies.” Jama 294.22 (2005): 2849-2857.

(17) Ishii, A., et al. “Parasite infection and cancer: with special emphasis on Schistosoma japonicum infections (Trematoda). A review.” Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 305.2 (1994): 273-281.

(18) Mostafa, Mostafa H., S. A. Sheweita, and Peter J. O’Connor. “Relationship between schistosomiasis and bladder cancer.” Clinical Microbiology Reviews 12.1 (1999): 97-111.

Articolul „The China Study“ – part I – How to make a big deal out of nothing? apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

Cancer is an extreme diagnosis with a strong psychological and social impact on both the patient and his / her family and entourage. Many people feel the need to give advice to the patient, but despite good intentions, most of these tips are based on personal ideas that feel like common sense rather than on in-depth understanding of the:

• malignant cell biochemistry: the Warburg effect (1), the Crabtree effect (2),
• metabolic impact of the treatment: dysbiosis (3), dyslipidemia (4), leptin resistance (5),
• metabolic impact of the disease: low adiponectin (6), high insulin ± insulin resistance (7), sarcopenia (8), and so on.

Despite good intentions, eliminating meat, dairy, eggs or other food of animal origin on the grounds that “the cancer cell feeds animal protein” is neither necessary nor useful for cancer patients for at least two reasons:

1. there is no human cell that feeds on animal protein

I want to warn any cancer patient that a person who argues that the “malignant cell feeds animal protein” probably did not take a class of physiology or biochemistry in his life, or his mind wondered on Facebook while he was in class because there is no human cell that feeds on proteins, any proteins – be it animal or vegetable.

Scientifically, we can say that “cells can also feed on amino acids”.

But absolutely no cell can feed on proteins, be it vegetal or animal.

In starvation conditions, where blood glucose falls below 50-60 mg/dl, glucagon helps us survive by nourishing the cells of internal organs, brain and blood with glucose obtained with ATP energy expenditure from the muscles constitutive aminoacids (a process called “gluconeogenesis”). But even under such extreme conditions, we do not feed ourselves with proteins, but with amino acids either converted to glucose, either integrated into the Krebs cycle.

Ingested proteins should be digested completely to pass through the intestinal wall without generating allergies (9). Moreover, proteins are not meant to be used to feed anything, being nutrients for other functions and not for energy supply.

Only after being used for all the functions they are meant to do inside the body, and only if some amino acids still remain unused, and only if there are no monosaccharides or fatty acids available – then and only then amino acids can be used to “feed” some types of cells.

Claiming that the “malignant cell feeds on animal protein” is like sticking a label on your forehead that “Intestinal protein digestion does not exist”. 

Because after intestinal digestion, there are only amino acids of any origin in the portal blood.

The only thing important is that in this portal blood we have all the 9 essential amino-acids.

If those 9 essential amino acids are absent or if they were in suboptimal proportions, the body will take them directly from muscle proteins, because:

• it cannot work without them,
• it cannot make them from other non-essential amino acids, from carbohydrates or from fats,
• it cannot store them, because amino acids are the only nutrients that cannot be stored in the body

And strictly from the point of view of the essential amino acid content, foods we eat from animals contain all the essential amino acids in optimal proportions for the human body.

Now leaving aside the essential amino acid content of the plants we eat, the main amino acid involved in the malignant cell metabolism is glutamine (10).

But glutamine exists in all food sources of proteins:

• meat, dairy and eggs,
• beans, peas, lentils, soybean, chickpeas,
• spinach, parsley, cabbage, red beet (fruit and vegetable freshly squeezed juices being one of the best sources of glutamine).

And if we were to remove all the glutamine food sources:

• it would be in vain, because glutamine is not an essential amino acid = the body can synthesise it without any food intake, being one of the most abundant amino acids in the body
• it would be harmful, because glutamine is involved in:
  • preventing weight gaining during chemotherapy by preventing dysbiosis and sarcopenia (11,12)
  • preservation of neurophysiological functions (mood, concentration, memory) (13)
  • prevention of anemia (14)

Healthy people do not need additional food intake of glutamine.

But in people with low immunity, intense stress or after surgery, glutamine should be supplemented by intake of foods rich in protein (for example meat, dairy, eggs, beans, peas, lentils) and vegetables (15).

And vegetable proteins foods are no better than animal proteins foods because:

• they also contain nitrates (16), fertilizers and fungicides that can be either as harmful (17) or more harmful (18) than the non-metabolised trace of antibiotics and hormones that might be found in some types of low quality meat or poultry (19)
• vegetable proteins also contain glutamine, just like animal proteins

The latest oncological nutrition meta-analyses of the available studies show that only processed meat (sausage, roasted meat) associates an increased risk of cancer, not meat per se.  (20).

So, we do not need to remove from the diet or diminish the intake of protein, neither vegetal nor animal food, from the diet of oncological patients, but to ensure that the protein intake is optimal to keep the patient’s health during oncological treatment (21,22).

1. all human cells, including the malignant ones, prefer to feed on glucose

For many people, to recommend moderate consumption of lean meat, dairy products and eggs may seem blasphemy when it comes to oncological patients. But nutrition is not about what people are taught to think, is about physiology. The body works as it works either if you agree with it or not. And most often than not most people have no idea about how the body actually works, making all sorts of assumptions that sound like common sense.

But, the physiology of the malignant cell is far, far, far from common sense: cancer cells do not feed on animal proteins or any proteins for that matter.

As any other cells in the human body, malignant cells prefer to use carbohydrates.

And foods of vegetable origin are predominant sources of carbohydrates directly usable by the malignant cell for survival and proliferation (23).

Of course, that does not mean going to the other extreme – from recommending the avoidance of foods of animal origin, to recommending the avoidance of foods of the plant origin. Not eating food sources of glucose – either by fasting or by ketogenic diets – brings no benefit for a cancer patient because when you take out glucose you get ketones. And ketones stimulate tumor growth and metastasis (24).

Oncology nutrition does not mean hearing one piece of information with one ear getting it out on the other ear with a diametrically opposed sense.

Oncology nutrition means:

• continuously adapting patient’s diet to the physiological needs of the body undergoing each stage of the oncological treatment
• and moderation in absolutely everything – „everything“ that includes even giving nutritional advice to cancer patients by people – medically trained or not – who know not what really happens to food after the food passes their mouth

Oncology nutrition practice requires one of the highest levels of nutrition training there is, health care personnel without a solid background in nutrition just giving general, common sense advice just like any other untrained people.

This is because – in order to make proper oncology nutrition recommendations – we need to understand how and what the malignant cells use to obtain energy for survival and proliferation, unlike the healthy cell, the complexity of the tumor’s biology and the metabolic impact of the treatment applied on patients with different health statuses.

The main features of malignant cells that influence what they prefer to use as main nutrients involve:

• changes in the surface of the cell membrane
• changes in the use of glucose in the presence of oxygen, exactly as in hypoxic conditions (“aerobic glycolysis”) (25).

Thus, when it comes to oncological nutrition, GLUT proteins (especially 1, 3, 4 and 12) are small stumps that break down the big cart of the common sense of people without real nutrition studies (26).

Because cell membranes are impermeable to glucose, cells use GLUT transmembrane transporters to introduce glucose and fructose into cells.

Healthy cells have only one type of transmembrane glucose transporter,  neurons such as GLUT 3, striated muscle cell – GLUT 4, red blood cells – GLUT 1, and hepatocyte and pancreas cell having GLUT 2.

But the malignant cell has 4 types of transmembrane glucose transporters: GLUT 1, GLUT 3, GLUT 4, and GLUT 12 – acting like black holes, absorbing glucose from any possible source, be it external (from food) or internal (from gluconeogenesis) (27).

And:

• not only does the malignant cells “absorb” more blood glucose than any normal cell could ever do because of the abundance of GLUT transporters (28, 29),
• but it also uses it inefficiently, continuously depriving healthy cells from this essential nutrient (30).

This energy-inefficient way to use glucose under aerobic conditions (with oxygen in the cell) using glucose as a normal cell under anaerobic conditions (no oxygen in the cell) is called the Warburg effect.

Otto Heinrich Warburg demonstrated in 1924 that malignant cells use glycolysis instead of oxidative phosphorylation (the Krebs cycle), despite the presence of oxygen in the cell. This effect can be objectively demonstrated by increasing the level of lactate dehydrogenase (LDH) (31).

But not all malignant cells get into Warburg effect.

And it seems that the malignant cells that enter aerobic glycolysis do not do this to hurt healthy cells by depriving them of essential food (or not only for that reason), but because of the biochemical reactions chains of aerobic glycolysis they get the substances they need for accelerated proliferation (32).

In addition, in order to demonstrate the capacities of maximum survival and adaptability, the malignant can stop aerobic glycolysis when necessary – and hence temporarily stop their growth and proliferation – and just sit there and survive without any problems until the resumption of favorable conditions, just like a chameleon, by switching back to the use of glucose in the Krebs cycle as a normal cell (Crabtree effect) (33).

The ability to procure the necessary biomass for proliferation through aerobic glycolysis (Warburg effect = proliferation) alternatively with the ability to stop doing so (Crabtree effect = survival by temporarily stopping proliferation) influences cancer treatment efficacy, the new therapies targeting inhibition of aerobic glycolysis being ineffective in completely eradicating some malignant cells that can survive through these alternative mechanisms, increasing the risk of post-treatment recurrence (34).

These effects have been known for over 80 years, and people who still claim that the “malignant cell feeds on animal protein” either have not heard of intestinal protein digestion and malignant cells biochemistry, or they are trying to sell you something.

The effects of Warburg, reverse Warburg and Crabtree, entosis, ketogenesis, gluconeogenesis, and de novo lipogenesis are the small stumps that overturn the great cart of common sense of the people that without a solid background in oncology nutrition nutrition and without a solid clinical practice with cancer patients (35,36).

Removing “animal proteins” from a cancer patient’s diet and feeding him only with vegetables, fruits, kernels, beans and other foods of vegetable origin brings a high intake of glucose easy to use by malignant cells, packed with a lower satiety and a lower ability to overcome oncology treatments’ side effects (37).

Unfortunately:

• cancer is an extremely unpredictable disease, the shallow elimination of the “animal proteins” not affecting the survival malignant cells, but the survival of the healthy cells
• perfect food does not exist; vegetables, fruits, vegetables, and cereals that are truly organic still contain substances that can be as harmful or more harmful than those as meat, dairy or eggs;
• the malignant cell is more adaptable and more unpredictable than people who recommend veganism as universal panacea can conceive (38).

Biochemically, malignant cells that thrive despite the more or less vague or argumentative personal opinions of self-proclaimed nutrition experts.

Quoted studies 

(1) Vander Heiden, Matthew G., Lewis C. Cantley, and Craig B. Thompson. “Understanding the Warburg effect: the metabolic requirements of cell proliferation.” science 324.5930 (2009): 1029-1033.

(2) Redman, Emily K., Paul S. Brookes, and Marcin K. Karcz. “Role of p90RSK in regulating the Crabtree effect: implications for cancer.” Biochemical Society transactions 41.1 (2013): 124.

(3) Schwabe, Robert F., and Christian Jobin. “The microbiome and cancer.” Nature Reviews Cancer 13.11 (2013): 800-812.

(4) Emaus, Aina et al. “Metabolic profile, physical activity, and mortality in breast cancer patients.” Breast cancer research and treatment 121.3 (2010): 651-660.

(5) Garofalo, Cecilia, and Eva Surmacz. “Leptin and cancer.” Journal of cellular physiology 207.1 (2006): 12-22.

(6) Dalamaga, Maria, Kalliope N. Diakopoulos, and Christos S. Mantzoros. “The role of adiponectin in cancer: a review of current evidence.” Endocrine reviews33.4 (2012): 547-594.

(7) Arcidiacono, Biagio et al. “Insulin resistance and cancer risk: an overview of the pathogenetic mechanisms.” Experimental diabetes research 2012 (2012).

(8) Argilés, Josep M., et al. “Muscle wasting in cancer and ageing: cachexia versus sarcopenia.” Sarcopenia–Age-Related Muscle Wasting and Weakness. Springer Netherlands, 2011. 9-35.

(9) Bannon, Gary A. “What makes a food protein an allergen?.” Current Allergy and Asthma Reports 4.1 (2004): 43-46.

(10) Zhao, Y., E. B. Butler, and M. Tan. “Targeting cellular metabolism to improve cancer therapeutics.” Cell death & disease 4.3 (2013): e532.

(11) Souba, Wiley W. et al. “Oral glutamine reduces bacterial translocation following abdominal radiation.” Journal of Surgical Research 48.1 (1990): 1-5.

(12) Klimberg, V. Suzanne et al. “Glutamine-enriched diets support muscle glutamine metabolism without stimulating tumor growth.” Journal of Surgical Research 48.4 (1990): 319-323.

(13) Ziegler, Thomas R. “Glutamine supplementation in cancer patients receiving bone marrow transplantation and high dose chemotherapy.” The Journal of nutrition 131.9 (2001): 2578S-2584S.

(14) Oburoglu, Leal et al. “Glucose and glutamine metabolism regulate human hematopoietic stem cell lineage specification.” Cell stem cell 15.2 (2014): 169-184.

(15) Moynihan, Paula J. “The role of diet and nutrition in the etiology and prevention of oral diseases.” Bulletin of the World Health Organization 83.9 (2005): 694-699.

(16) Hord, Norman G., Yaoping Tang, and Nathan S. Bryan. “Food sources of nitrates and nitrites: the physiologic context for potential health benefits.” The American journal of clinical nutrition 90.1 (2009): 1-10.

(17) Türkdoğan, M. Kürsad et al. “Heavy metals in soil, vegetables and fruits in the endemic upper gastrointestinal cancer region of Turkey.” Environmental Toxicology and Pharmacology 13.3 (2003): 175-179.

(18) Paro, Rita et al. “The fungicide mancozeb induces toxic effects on mammalian granulosa cells.” Toxicology and applied pharmacology 260.2 (2012): 155-161.

(19) Ghidini, Sergio et al. “16 Chemical Residues in Organic Meats Compared to Conventional Meats.” Organic Meat Production and Processing 53 (2012).

(20) Mourouti, Niki et al. “Meat consumption and breast cancer: A case-control study in women.” Meat science 100 (2015): 195-201.

(21) Paddon-Jones, Douglas et al. “Protein, weight management, and satiety.” The American journal of clinical nutrition87.5 (2008): 1558S-1561S.

(22) Capuron, Lucile, and Robert Dantzer. “Cytokines and depression: the need for a new paradigm.” Brain, behavior, and immunity 17.1 (2003): 119-124.

(23) Greiner, Erich F., Michael Guppy, and Karl Brand. “Glucose is essential for proliferation and the glycolytic enzyme induction that provokes a transition to glycolytic energy production.” Journal of Biological Chemistry 269.50 (1994): 31484-31490.

(24) Martinez-Outschoorn, U. E., Lin, Z., Whitaker-Menezes, D., Howell, A., Sotgia, F., & Lisanti, M. P. (2012). Ketone body utilization drives tumor growth and metastasis. Cell cycle, 11(21), 3964-3971.

(25) Ganapathy, Vadivel, Muthusamy Thangaraju, and Puttur D. Prasad. “Nutrient transporters in cancer: relevance to Warburg hypothesis and beyond.”Pharmacology & therapeutics 121.1 (2009): 29-40.

(26) Barron, Carly, Evangelia Tsiani, and Theodoros Tsakiridis. “Expression of the glucose transporters GLUT1, GLUT3, GLUT4 and GLUT12 in human cancer cells.” BMC Proceedings. Vol. 6. No. Suppl 3. BioMed Central Ltd, 2012.

(27) Calvo, Moisés Blanco et al. “Potential role of sugar transporters in cancer and their relationship with anticancer therapy.” International journal of endocrinology2010 (2010).

(29) Hsu, Peggy P., and David M. Sabatini. “Cancer cell metabolism: Warburg and beyond.” Cell 134.5 (2008): 703-707.

(30) Calvo, Moisés Blanco et al. “Potential role of sugar transporters in cancer and their relationship with anticancer therapy.” International journal of endocrinology2010 (2010).

(31) Schwartzenberg-Bar-Yoseph, Fabiana, Michal Armoni, and Eddy Karnieli. “The tumor suppressor p53 down-regulates glucose transporters GLUT1 and GLUT4 gene expression.” Cancer research 64.7 (2004): 2627-2633.

(32) Walenta, Stefan, and Wolfgang F. Mueller-Klieser. “Lactate: mirror and motor of tumor malignancy.” Seminars in radiation oncology. Vol. 14. No. 3. WB Saunders, 2004.

(33) Feron, Olivier. “Pyruvate into lactate and back: from the Warburg effect to symbiotic energy fuel exchange in cancer cells.” Radiotherapy and oncology92.3 (2009): 329-333.

(34) Diaz-Ruiz, Rodrigo, Michel Rigoulet, and Anne Devin. “The Warburg and Crabtree effects: On the origin of cancer cell energy metabolism and of yeast glucose repression.” Biochimica et Biophysica Acta (BBA)-Bioenergetics 1807.6 (2011): 568-576.

(35) DeBerardinis, Ralph J. et al. “The biology of cancer: metabolic reprogramming fuels cell growth and proliferation.” Cell metabolism 7.1 (2008): 11-20.

(36) Kim, Jung-whan, and Chi V. Dang. “Cancer’s molecular sweet tooth and the Warburg effect.” Cancer research 66.18 (2006): 8927-8930.

(37) Jones, Russell G., and Craig B. Thompson. “Tumor suppressors and cell metabolism: a recipe for cancer growth.” Genes & development 23.5 (2009): 537-548.

(38) Ernst, Edzard, and Barrie R. Cassileth. “Cancer diets: fads and facts.” Cancer Prevention International 2.3-4 (1996): 181-187.

Articolul Animal proteins & oncology nutrition apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.

Here I want to mention 5 simple habits that – applied daily – can help us prevent breast cancer.

1. Spend at least 30′ a day outside.

In the modern world we all live in today, where we move from home to the car, from car to the office, and from office back into the car and back home, many of us do not spend even a quarter of an hour in sunlight during some days.

Which means our vitamin D3 level risk to be insufficient to keep us healthy.

Related to breast cancer, studies show that vitamin D3 deficiency is associated with an increased risk of breast cancer and that the deficiency is present in more than 74% of patients diagnosed with breast cancer (1,2).

Of course, besides practicing outdoor activities for a minimum of 30′ every day – consuming foods (like whole milk, egg yolk, fatty fish, various extra virgin oils and raw seeds and seeds), and supplements can help maintain an proper level of vitamin D3 in the blood – ~30 ng/ml –, but optimally the supplement dose should be calculated based on the blood test result of D3 and not on a presumed defficit (3).

2. Practice sports regularly.

Sedentariness affects more and more of us. If we add 8-10 hours daily in the office, 1-2 hours driving in the car, 2-3 hours in bed or on the couch watching TV, and 6-8 hours in bed sleeping, there is very little time left for physical exercise.

The modern living style encourages sedentariness, the risk of breast cancer being much higher in “civilised” countries (4).

We move less and less, we take the car even to the corner of the street. And the less we move, the greater the risk of breast cancer, paralleled with the increased risk of many other diseases (5).

Compliance with World Health Organisation recommendations – 150′ of mild or moderate physical activity or 75′ of intense physical activities / week – may sometimes make the difference between health and illness (6).

3. Do not exceed 1 alcoholic or soft drink  per day.

Alcoholic and soft drinks, either sweetened with HFCS (“artificial fructose”) or with aspartame or with other artificial sweeteners, have a metabolic and carcinogenic impact.

Drinking alcohol has been associated in many observational studies with an increased risk of breast cancer (7).

It is not a single glass of red wine occasionally drunk, but occasional consumption of large amounts of alcohol. Many people drink alcohol only once a week, but when they do they consume well over the one drink recommended for cardiovascular protection (equivalent to 10 ml of alcohol / beverage in women and double for men), increasing their breast cancer risk (8).

Compared to people with compulsive consumption of alcohol, abstinent people or those who limits themselves to one single drink a day have a lower risk of breast cancer  (9).

Regarding the consumption of soft drinks as a behaviour, many people associate them with social events or with jumping over meals.

Many studies in recent years have shown that HFCS-sweetened soft drinks associate an increased cancer risk, especially for ER+/ PR+ breast cancer subtypes (10).

Studies on the link between soft drinks sweetened with artificial sweeteners and the risk of breast cancer are inconclusive, but some have raised questions about the intake of artificial sweeteners and the risk of bladder, stomach, pancreas and endometrial cancers (11,12).

Consumption of water, green tea and coffee per day seems to be neutral in the prevention of breast cancer, although we have some epidemiological data showing a protective effect for green tea and coffee (13).

4. Try to eat only when hungry.

As long as you are healthy and don’t have specific dietary needs to particular health issues, eating only when hungry will keep you safe both from obesity and from the increased cancer risk associated with obesity.

The nutrients within the food you consume when not hungry will only replenish glycogen stores if there is something to replenish. If you are sedentary and if you usually eat regardless of hunger you will only eat more and more filling up your liver, kidney, adipose tissue and, finally, even your muscles with fat (14).

Now, about the quality of the eaten foods, many studies show that hydrogenated fat are involved in the development of many cancers. On the other hand, a lot of people think that if they eat low fat foods, it lowers cholesterol or triglycerides. But consuming foods in which these natural fats replenished with carbs won’t help as in the absence of these fats intake the human body can make fats from the excessive consumption of carbohydrates (15).

So “excessive” consumption is the problem.

And it is about too much of anything, including too much fruits at the expense of quality protein foods (16).

Every time we eat without being hungry, we interfere massively with all the hormones regulating and maintaining satiety. The main satiety hormone – leptin, abundantly secreted by adipose tissue – will become more and more ineffective in stopping the hunger and becoming more effective in disrupting immunity and estrogen secretion (17). For this reason, especially in estrogenic cancers, such as ER+/PR+ breast cancer subtypes, the respect for physical hunger and satiety is absolutely essential for preventing such diseases (18).

Before you eat anything, physically check whether you are hungry or not.

And check your stomach, not your clock.

5. Cook as often as you can and try to eat at home with your family as often as you can.

Although we learned, strangely enough, to reject everything all that’s Romanian, we still have natural food in Romania and we still cook at home.

Foreign people coming to Romania fall in love with the flavour of our homemade dishes and of Romanian fruits and vegetables. Maybe we should follow this instead of following their example they are applying when they return to their native countries – to cook less and less, to eat “in the city” more and more often.

Food cooked at home is missing from many meals in the “civilised” world because in the civilised world cooking is no longer in fashion.

Maybe also for this reason, highly civilised and modern countries such as Netherlands, France or England are among the countries with the highest incidences of breast cancer in Europe (19).

Quoted studies

(1) Garland, Cedric F. et al. “Vitamin D and prevention of breast cancer: pooled analysis.” The Journal of steroid biochemistry and molecular biology 103.3 (2007): 708-711.

(2) Crew, Katherine D. et al. “High prevalence of vitamin D deficiency despite supplementation in premenopausal women with breast cancer undergoing adjuvant chemotherapy.” Journal of Clinical Oncology 27.13 (2009): 2151-2156.

(3) Garland, Cedric F. et al. “Vitamin D and prevention of breast cancer: pooled analysis.” The Journal of steroid biochemistry and molecular biology 103.3 (2007): 708-711.

(4) Jemal, Ahmedin et al. “Global cancer statistics.” CA: a cancer journal for clinicians 61.2 (2011): 69-90.

(5) Guimarães, Guilherme Veiga, and Emmanuel Gomes Ciolac. “Physical activity: practice this idea.” American journal of cardiovascular disease 4.1 (2014): 31.

(6) Physical activity. World Health Organization; 2014.

(7) Park, Song‐Yi et al. “Alcohol consumption and breast cancer risk among women from five ethnic groups with light to moderate intakes: The Multiethnic Cohort Study.” International Journal of Cancer 134.6 (2014): 1504-1510.

(8) Chen, Wendy Y. et al. “Moderate alcohol consumption during adult life, drinking patterns, and breast cancer risk.” Jama 306.17 (2011): 1884-1890.

(9) Scoccianti, Chiara et al. “Female Breast Cancer and Alcohol Consumption: A Review of the Literature.” American journal of preventive medicine 46.3 (2014): S16-S25.

(10) Cordain, Loren, Michael R. Eades, and Mary D. Eades. “Hyperinsulinemic diseases of civilization: more than just Syndrome X.” Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 136.1 (2003): 95-112.

(11) Yılmaz, Serkan, and Aslı Uçar. “A review of the genotoxic and carcinogenic effects of aspartame: does it safe or not?.” Cytotechnology (2014): 1-7.

(12) DE CHINCHÓN, D. E. C. L. A. R. A. C. I. Ó. N., DECÁLOGO SOBRE EDULCORANTES SIN Y. BAJOS, and EN CALORÍAS. “Chinchón declaration; decalogue on low-and no-calorie sweeteners (LNCS).” Nutr Hosp 29.4 (2014): 719-734.

(13) Ganmaa, Davaasambuu et al. “Coffee, tea, caffeine and risk of breast cancer: A 22‐year follow‐up.” International journal of cancer 122.9 (2008): 2071-2076.

(14) Stoll, Basil A. “Western diet, early puberty, and breast cancer risk.” Breast Cancer Research and Treatment 49.3 (1998): 187-193.

(15) Schwarz, Jean-Marc et al. “Hepatic de novo lipogenesis in normoinsulinemic and hyperinsulinemic subjects consuming high-fat, low-carbohydrate and low-fat, high-carbohydrate isoenergetic diets.” The American journal of clinical nutrition 77.1 (2003): 43-50.

(16) Borugian, Marilyn J. et al. “Insulin, macronutrient intake, and physical activity: are potential indicators of insulin resistance associated with mortality from breast cancer?.” Cancer Epidemiology Biomarkers & Prevention 13.7 (2004): 1163-1172.

(17) Rose, D. P., D. Komninou, and G. D. Stephenson. “Obesity, adipocytokines, and insulin resistance in breast cancer.” Obesity reviews 5.3 (2004): 153-165.

(18) Rock, Cheryl L. et al. “Eating pathology and obesity in women at risk for breast cancer recurrence.” International Journal of Eating Disorders 27.2 (2000): 172-179.

(19) Estimated incidence, mortality & prevalence, 2012

Articolul 5 habits that help prevent breast cancer apare prima dată în Nutrition Services | Nutritionist Dr. Diana Artene.