Tag Archives: cancer

Salt and CancerWhen I was in the middle of my academic career during the mid to late 1990’s (I retired from Colorado State University in December 2013,) I had the great pleasure of corresponding with Birger Jansson, Ph.D. at the University of Texas, M.D. Anderson Cancer Center in Houston, Texas. Dr. Jansson was a Professor in the Department of Biomathematics at the M.D. Anderson Cancer Center and worked as a biomathematician for the National Large Bowel Cancer Project (NLBCP) between 1973 and 1983 when President Nixon launched his war against cancer in the early 1970s. Birger was known internationally for his brilliant mathematical modeling of all types of cancer, but today he is perhaps best known for his epidemiological and review publications demonstrating how a high salt (sodium) diet promotes all types of cancer, whereas a high potassium diet impedes cancer (1-8).

My correspondence with Dr. Jansson came about from my interest in the reported low incidence of all types of cancers in hunter-gatherers (9-17) who were essentially salt free populations. From animal and tissue experiments, I had long suspected that salt added to diet acted as a promoter of various cancers whereas a high potassium intake retarded cancer development. My correspondence with Birger further confirmed the evidence I had compiled.

Almost exactly 20 years ago in May of 1997 (see attached PDF file), Birger sent me his unpublished and unedited book entitled, Sodium: “NO!” Potassium: “Yes!” Sodium increases and potassium decreases cancer risks. This book represented Birger’s scientific work, from 1981 to 1997, documenting the relationship between dietary sodium and potassium (1-8). The data from his book includes hundreds of scientific references from 1) epidemiological studies, 2) animal studies, 3) tissue studies, and a limited number of 4) randomized controlled human trials with various disease endpoints and markers.

Unfortunately, my correspondence with Birger ceased shortly after he sent me his unpublished and unedited book manuscript on May 10, 1997. I only recently discovered that Birger died (May 23, 1998) about a year to the date after our last correspondence at age 77 as a Professor Emeritus at the University of Texas, M.D. Anderson Cancer Center.

I am in a unique position, in that I probably have one of the few copies of Dr. Jansson’s unpublished book in existence. The book runs about 350 pages in length and is comprised of 10 chapters. My copy clearly was produced as a Xeroxed copy of Birger’s hand typed manuscript (one sided, double spaced pages) and spiral bound with plastic. From my correspondence with Birger (May 10, 1997), you can see that he was contemplating publication of his book in the popular literature, but unfortunately it never happened with his untimely death in 1998.

I have always felt a debt to this great scientist, and after consultation with my colleague Anthony Sebastian (M.D.) at the University of California, San Francisco, we concluded that Birger would have been happy to see that his unpublished book was finally made known to the scientific and world communities.

In this blog I have included a single chapter (Chapter II of Birger’s book), entitled “Human Diet Before Modern Times” that I thought would be of interest to the “Paleo Community” and to worldwide scientists as well. Enjoy!

 

References

1. Jansson B. Potassium, sodium, and cancer: a review. J Environ Pathol Toxicol Oncol. 1996;15(2-4):65-73

2. Jansson B. Dietary, total body, and intracellular potassium-to-sodium ratios and their influence on cancer. Cancer Detect Prev. 1990;14(5):563-5

3. Jansson B. Intracellular electrolytes and their role in cancer etiology. In Thompson JR, Brown BW, eds. Cancer modeling. New York: Marcel Dekker 1987:1-59.

4. Jansson B. Geographic cancer risk and intracellular potassium/sodium ratios. Cancer Detect Prev. 1986;9(3-4):171-94

5. Jansson B, Jankovic J. Low cancer rates among patients with Parkinson’s disease. Ann Neurol. 1985 May;17(5):505-9

6. Newmark HL, Wargovich MJ, Bruce VR, Boynton AL, Kleine LP, Whitfield JF. Jansson B, Cameron IL. Ions and neoplastic development. In: Mastromarino AJ, Brattain MG, eds. Large bowel cancer. Clinical and basic science research. Cancer Research Monographs, Vol 3, New York: Praeger Publisher 1985:102-129.

7. Jansson B. Geographic mappings of colorectal cancer rates: a retrospect of studies, 1974-1984. Cancer Detect Prev. 1985;8(3):341-8

8. Jansson B. Seneca County, New York: an area with low cancer mortality rates. Cancer. 1981 Dec 1;48(11):2542-6

9. Bulkley JL. Cancer among primitive tribes. Cancer 1927; 4:289-295.

10. Henson, WW. Cancer in Kafirs: suggested cause. Guy’s Hospital Gazette, March 26, 1904, 131-133

11. Hearsey H. The rarity of cancer among the aborigines of British Central Africa. Brit Med J, Dec 1, 1906, 1562-63.

12. Hildes JA, Schaefer O. The changing picture of neoplastic disease in the western and central Canadian Arctic (1950-1980). Can Med Assoc J 1984; 130:25-32.

13. Rabinowitch IM. Clinical and other observations on Canadian Eskimos in the Eastern Arctic. Can Med Assoc J 1936; 34:487-501.

14. Renner W. The spread of cancer among the descendants of the liberated Africans or Creoles of Sierre Leone. Brit Med J, Sept 3, 1910, 587-589.

15. Riveros M. First observation of cancer among the Pampidos (Chulupi) Indians of the Paraguayan Chaco. Int Surg 1970; 53:51-55.

16. Stefansson V. Cancer: Disease of Civilization? Hill and Wang, NY, 1960.

17. Urquhart JA. The most northerly practice in Canada. Can Med Assoc J. 1935;33:193-196.

Red Meat | The Paleo Diet
As you probably already heard, earlier this week the International Agency for Research on Cancer (IARC), which is the World Health Organization’s (WHO) cancer agency, categorized processed meat as “carcinogenic” and unprocessed red meat as “probably carcinogenic.”1 What you might not have heard is that in an accompanying Q&A document, the IARC also said, “Eating meat has known health benefits.”2

Those who read the IARC’s statement and its Q&A document are likely to conclude that this story is nowhere near as dramatic and consequential as headlines from The Guardian, The New York Times, and other news outlets have implied:

  • “Processed meats rank alongside smoking as cancer causes – WHO” – The Guardian3

  • “Meat Is Linked to Higher Cancer Risk, W.H.O. Report Finds” – The New York Times4

Let’s see what the IARC actually said, then put things in context so we can determine what it means. The IARC evaluates chemicals, pollutants, biological agents, and other substances so as to determine whether or not they are carcinogenic. Agents are classified into one of several groups, ranging from “Group 1: the agent is carcinogenic to humans,” to “Group 4: the agent is probably not carcinogenic to humans.” The IARC does not determine how much any particular agent actually increases one’s risk of getting cancer. In its own words, the IARC explains,

“The classification indicates the weight of the evidence as to whether an agent is capable of causing cancer (technically called “hazard”), but it does not measure the likelihood that cancer will occur (technically called “risk”) as a result of exposure to the agent.”5

This is an essential point. Processed meats are now grouped into the same category as cigarettes and asbestos, but this doesn’t mean the risks associated with processed meats are anywhere near those of the latter two. Cigarette smoking, for example, increases one’s relative risk of getting lung cancer by 2,500%.6 Eating processed meat, according to the IARC, increases one’s risk of getting colorectal cancer by an estimated 18%.7 Given the frequency of colorectal cancer, this means that eating 50 grams of bacon every day over the course of your life would increase your risk of getting cancer from 5% to 6%.

Missing the Big Meaty Picture

Of course, all this talk of risk misses a bigger point – context is essential. For example, will those who smoke while eating healthy diets have the same chronic disease risks as those who smoke while eating unhealthy diets? Probably not. Red meat consumed within the context of a health-supportive Paleo diet is healthy. On the other hand, red meat consumed within the context of a junk-food diet might not be healthy, especially regarding poor-quality meat.

Dr. Cordain points out, “observational studies and even randomized controlled trials typically do not control for a variety of additional elements found in feedlot-raised red meats” and “only in the past 200 years of so have we ever consumed domesticated animals fed grains, injected with hormones, antibiotics, exposed to heavy metals and pesticides and sequestered in feedlots by the hundreds of thousands.” So when someone says meat is unhealthy, we should remember that meat is not a commodity; it ranges from poor to superior quality.

The Problem with Observational Studies

To assess carcinogenicity, the IARC analyzes observational studies. As Dr. Cordain and others have repeatedly pointed out, such studies alone cannot demonstrate causality. In response to the IARC announcement, Dr. Cordain noted, “In order to establish cause and effect between diet and disease, it takes more than just observational epidemiological evidence. There must also be what is referred to as ‘biological plausibility’ in which evidence gathered from tissue, animal and short-term human metabolic studies support causality.”8, 9

With respect to unprocessed red meat, the IARC’s “probably carcinogenic” determination is not even based on strong epidemiological evidence. It’s based on “limited evidence,” which according to the IARC, “means that a positive association has been observed between exposure to the agent and cancer but that other explanations for the observations (technically termed chance, bias, or confounding) could not be ruled out.”10

So the next time your vegetarian co-worker tells you that red meat causes cancer, remember the following four rebuttals:

  1. The IARC’s classification is based on observational studies, which cannot show causality.
  2. Evidence that unprocessed red meat could be carcinogenic is based on “limited evidence,” which means confounding factors could not be ruled out.
  3. The magnitude of risk for eating processed meat (and red meat if causality could be demonstrated) is nowhere near that of established risky behaviors, like smoking.
  4. Context matters – high-quality meat is healthy within the context of healthy diets, which include plenty of vegetables and other healthy foods.

Despite all the fanfare about increased cancer risk, at least the IARC acknowledges, “Eating meat has known health benefits.” It wouldn’t have been sensational, but this should have been the headline used by major news organizations.

References

1. World Health Organization, IARC. (October 26, 2015). IARC Monographs evaluate consumption of red meat and processed meat. Press Release Number 240. Retrieved from http://www.iarc.fr/en/media-centre/pr/2015/pdfs/pr240_E.pdf

2. World Health Organization, IARC. Q&A on the carcinogenicity of the consumption of red meat and processed meat. Retrieved from http://www.iarc.fr/en/media-centre/iarcnews/pdf/Monographs-Q&A_Vol114.pdf

3. Boseley, S. (October 26, 2015). Processed meats rank alongside smoking as cancer causes – WHO. The Guardian. Retrieved from http://www.theguardian.com/society/2015/oct/26/bacon-ham-sausages-processed-meats-cancer-risk-smoking-says-who

4. O’Connor, A. (October 26, 2015). Meat Is Linked to Higher Cancer Risk, W.H.O. Report Finds. The New York Times. Retrieved from http://www.nytimes.com/2015/10/27/health/report-links-some-types-of-cancer-with-processed-or-red-meat.html

5. World Health Organization, IARC. Q&A on the carcinogenicity of the consumption of red meat and processed meat. Retrieved from http://www.iarc.fr/en/media-centre/iarcnews/pdf/Monographs-Q&A_Vol114.pdf

6. U.S. Department of Health and Human Services. (2014). The Health Consequences of Smoking—50 Years of Progress: A Report of the Surgeon General. Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014.

7. World Health Organization, IARC. Q&A on the carcinogenicity of the consumption of red meat and processed meat. Retrieved from http://www.iarc.fr/en/media-centre/iarcnews/pdf/Monographs-Q&A_Vol114.pdf

8. Flegal KM. (June 1999). Evaluating epidemiologic evidence of the effects of food and nutrient exposures. Am J Clin Nutr, 69(6):1339S-1344S.

9. Potischman N, Weed DL. (June 1999). Causal criteria in nutritional epidemiology. Am J Clin Nutr, 69(6):1309S-1314S.

10. World Health Organization, IARC. Q&A on the carcinogenicity of the consumption of red meat and processed meat. Retrieved from http://www.iarc.fr/en/media-centre/iarcnews/pdf/Monographs-Q&A_Vol114.pdf

Research Suggests Magnolia Flower Could Be the Cure To Cancer | The Paleo Diet

For many, the magnolia tree/shrub is known and grown for its beautiful, showy, sweet-smelling flowers. Yet, within this beauty, lays an even greater treasure, the cure to head and neck cancers.1 According to a breakthrough study by researchers in Alabama, a phytochemical honokiol, offers a chemotherapeutic effect on a form of cancers in this region known as head and neck squamous cell carcinomas. This means it stops the growth of cancerous tumors, and may be as effective as chemotherapy, without the rigors and harsh side effects.2

BACKGROUND

Head and neck squamous carcinomas (HNSCC) are common cancers seen globally,3 with an increased prevalence in men and people over the age of 50.4 Certain cancers in this region like the brain, eye, esophagus, thyroid gland, scalp, skin muscles, and bones are not usually classified as head and neck cancers.5 Alcohol and tobacco use are the biggest risk factors, but other factors include salted or preserved foods, poor oral health, human papillomavirus (HPV), and Chinese ancestry.6

CURRENT THERAPIES

While improved technology has revolutionized traditional therapies, this has not been reflected in the overall survival rate of HNSCC. For over the past 30 years, the mortality rate has stayed a constant 50%, with no sign of decreasing.7 Current forms of treatment include normal chemotherapy, as well as surgical resection, which remove the tumor.8 Notwithstanding these can be toxic to the body, increasing drug resistance, and impairing the individual’s ability to speak and swallow.9 Thus, seeking alternative and adjunct therapies is beneficial and a much needed necessity. A valuable treatment method should guarantee better patients’ outcomes, enhanced quality of life, as well as lower levels of drug toxicity.

Previous research has targeted epidermal growth factor receptor (EGFR).10 What exactly is EGFR you may ask? A protein found on the cell surface, which binds to epidermal growth factor (EGF), to stimulate cell growth, differentiation and maturation. Binding to EGFR brings on receptor dimerization and tyrosine autophosphorylation, basically undergoing mechanisms that result in cell proliferation.11 Overexpression of EGFR is seen in a large majority of HNSCC (90%), and has been linked with worsened clinical outcomes of patients with HNSCC.12 This makes sense as increased numbers of EGFR will provide ample amount of cancerous cell growth and proliferation. This has been the focus of both approved and investigational drugs, which have fared poorly as a result of drug toxicity and resistance.13 This has led to the search for natural and effective options that exist around us such as phytochemicals like honokiol.

WHAT IS HONOKIOL?

Honokiol comes from the bark and leaves of the Magnolia plant. Past studies explored its various biological and pharmacological behaviors, which include anti-inflammatory, antifungal, anti-oxidative and anti-carcinogenic.14 Basically, honokiol appears to be the perfect remedy for cancer. Previous work has indicated so for other types of cancers, such as skin, breast, melanoma, non-small cell lung cancer and prostate.15

BENEFITS OF HONOKIOL IN HNSCC

So what is all the hoopla about honokiol and HNSCC, you may be wondering. Well from the results of the study, increased dosage of honokiol resulted in decreased viability of HNSCC cells.16 Further reduction was seen over time in cells that had been treated with honokiol. Increased apoptosis or cell death was observed in HNSCC cells that received the honokiol treatment.17 Honokiol led to the decrease of cyclins and cdk, which are cell cycle regulations and enable the proliferation and growth of the HNSCC cells.18 Additionally honokiol led to the inhibition of the prized EGFR, and proved to be nontoxic on mice.19 Furthermore it inhibited the growth of HNSCC tumor xenograft cells in mice.20 Honokiol was also linked with lower levels of anti-apoptotic protein Bcl-xl and higher levels of pro-apoptotic protein Bax.21 In simple terms, honokiol is like the commander in the army, reducing the weaker members of the team and bringing out the best team to fight, destroy, and end the war.

CONCLUSION

One of the most convincing pieces of evidence not listed above is that honokiol had a much tighter bind with EGFR, when compared with Ceftuximab and getfitinib, which are widely used in treating HSNCC.22 This suggests the likelihood of better efficacy and a more improved chemotherapeutic effect, without the negative effects.

It is important to remember that while the results of this study is quite promising, it has not yet been proven in the human population. Nevertheless it will offer you much perspective the next time you observe the beauty of the Magnolia flower in nature. In addition, given the risk factors such as alcohol, tobacco use, and salted food, one cannot help but appreciate the huge benefit of healthy quality living that a Paleo lifestyle offers.

 

REFERENCES

[1] Singh, T., Nirzani, G., Xu, S., Prasad, R., Sadanandan, V., & Katiyar, S. (2015, May). Honokiol inhibits the growth of head and neck squamous cell carcinoma by targeting epidermal growth factor receptor. Oncotarget, 1-15.

[2] Ibid.

[3] Head and Neck Cancers. (2013, February 1). Head and Neck Cancers. Retrieved June 29, 2015, from National Cancer Institute: http://www.cancer.gov/types/head-and-neck/head-neck-fact-sheet

[4] Ibid.

[5] Ibid.

[6] Ibid.

[7] Singh, T., Nirzani, G., Xu, S., Prasad, R., Sadanandan, V., & Katiyar, S. (2015, May). Honokiol inhibits the growth of head and neck squamous cell carcinoma by targeting epidermal growth factor receptor. Oncotarget, 1-15.

[8] Gellrich, N., Schimming, R., Schramm, A., Schmalohr, D., Bremerich, A., & Kugler, J. (2002). Pain, function and psychologic outcome before, during, and after intraoral tumor resection. J Oral Maxillofac Surg, 60, 772-777.

[9] Ibid.

[10] Wheeler, S., Egloff, A., Wang, L., James, C., Hammerman, P., & Grandis, J. (2015, February 6). Challenges in EGFRvIII Detection in Head and Neck Squamous Cell Carcinoma. PLoS One, 10(2), 1-13. doi:10.1371/journal.pone.0117781

[11] Ibid.

[12] Grandis, J., Melhem, M., Gooding, W., Day, R., Holst, V., Wagener, M., . . . Tweardy, D. (1998). Levels of TGF-α and EGFR protein in head and neck squamous cell carcinoma and patient survival. J Natl Cancer Inst, 90, 824-832

[13] Leeman-Neill, R., Cai, Q., Joyce, S., Thomas, S., Bhola, N., Neill, D., . . . Grandis, J. (2010, May 1). Honokiol inhibits epidermal growth factor receptor signaling and enhances the antitumor effects of epidermal growth factor receptor. Clin Cancer Res, 16(9), 2571–2579. doi:10.1158/1078-0432.CCR-10-0333

[14] Singh, T., Nirzani, G., Xu, S., Prasad, R., Sadanandan, V., & Katiyar, S. (2015, May). Honokiol inhibits the growth of head and neck squamous cell carcinoma by targeting epidermal growth factor receptor. Oncotarget, 1-15.

[15] Leeman-Neill, R., Cai, Q., Joyce, S., Thomas, S., Bhola, N., Neill, D., . . . Grandis, J. (2010, May 1). Honokiol inhibits epidermal growth factor receptor signaling and enhances the antitumor effects of epidermal growth factor receptor. Clin Cancer Res, 16(9), 2571–2579. doi:10.1158/1078-0432.CCR-10-033.

[16] Singh, T., Nirzani, G., Xu, S., Prasad, R., Sadanandan, V., & Katiyar, S. (2015, May). Honokiol inhibits the growth of head and neck squamous cell carcinoma by targeting epidermal growth factor receptor. Oncotarget, 1-15.

[17] Ibid.

[18] Ibid.

[19] Ibid.

[20] Ibid.

[21] Ibid.

[22] Ibid.

Avocado's Cancer Fighting Fat | The Paleo Diet

If you’re eating avocados on a regular basis, you’re definitely on trend, but you may not be fully aware of their nutritional benefits and contents. Recently, brand new research revealed molecules derived from avocados could be effective in treating a specific form of Leukemia.1 Researchers filed a patent application for the use of avocation B, a compound found in avocados, to develop a lipid drug that combats acute myeloid leukemia (AML).

Fighting occurs via specific targeting of the root of the disease – leukemia stem cells. With the existing body of scientific literature linking fruit consumption (yes, the avocado is a fruit) and cancer, we must take an unbiased look at the salient research.2, 3, 4, 5 Even back in 2005, researchers found the avocado is a rich source of monounsaturated fatty acids, but also noted its bioactive substances were overlooked.6 This included carotenoids, which may help with cancer prevention.7, 8, 9

In 2009, researchers noted phytochemicals extracted from avocado into a chloroform partition selectively induced apoptosis in cancer cells.10 These experiments are conducted using extracts and are in much higher amounts than you would get from just eating avocados regularly. But, would it be a good idea to consume avocados regularly, as a potential preventative measure against cancer?

I would argue yes, since avocados have a plethora of other benefits as well.11, 12, 13 They are a great source of monounsaturated fatty acids, and also contain nearly 50% of your daily dose of pantothenic acid, among other nutrients.14, 15 As many who follow a Paleo diet know, the intake of fat along with carotenoids greatly improves their absorption.16, 17 When consuming a salad for example, without fat content present, absorption is hindered. So, employ a simple, inexpensive, and delicious fix by adding it to your vegetable medley!

Cancer is something we all fear, and it can be debilitating in the extreme. But if you exercise regularly, sleep plenty, and eat a nutrient rich Paleo diet – your cancer risk is lessened.18 While cancer research continues to only skim the surface, we do know increased vegetable consumption and healthy habits are associated with a decreased risk.19

Pile your plate high with vegetables, choosing options like kale and spinach, both known to have cancer combative properties. 20 Between leafy greens and cruciferous veggies, and healthy fats from avocados, these measures might be just the ticket to nip cancer in the bud.

 

REFERENCES

[1] Lee EA, Angka L, Rota SG, et al. Targeting Mitochondria with Avocatin B Induces Selective Leukemia Cell Death. Cancer Res. 2015;75(12):2478-88.

[2] Vainio H, Weiderpass E. Fruit and vegetables in cancer prevention. Nutr Cancer. 2006;54(1):111-42.

[3] Block G, Patterson B, Subar A. Fruit, vegetables, and cancer prevention: a review of the epidemiological evidence. Nutr Cancer. 1992;18(1):1-29.

[4] Chan JM, Wang F, Holly EA. Vegetable and fruit intake and pancreatic cancer in a population-based case-control study in the San Francisco bay area. Cancer Epidemiol Biomarkers Prev. 2005;14(9):2093-7.

[5] Benetou V, Orfanos P, Lagiou P, Trichopoulos D, Boffetta P, Trichopoulou A. Vegetables and fruits in relation to cancer risk: evidence from the Greek EPIC cohort study. Cancer Epidemiol Biomarkers Prev. 2008;17(2):387-92.

[6] Lu QY, Arteaga JR, Zhang Q, Huerta S, Go VL, Heber D. Inhibition of prostate cancer cell growth by an avocado extract: role of lipid-soluble bioactive substances. J Nutr Biochem. 2005;16(1):23-30.

[7] Wu K, Erdman JW, Schwartz SJ, et al. Plasma and dietary carotenoids, and the risk of prostate cancer: a nested case-control study. Cancer Epidemiol Biomarkers Prev. 2004;13(2):260-9.

[8] Gallicchio L, Boyd K, Matanoski G, et al. Carotenoids and the risk of developing lung cancer: a systematic review. Am J Clin Nutr. 2008;88(2):372-83.

[9] Slattery ML, Benson J, Curtin K, Ma KN, Schaeffer D, Potter JD. Carotenoids and colon cancer. Am J Clin Nutr. 2000;71(2):575-82.

[10] Ding H, Han C, Guo D, et al. Selective induction of apoptosis of human oral cancer cell lines by avocado extracts via a ROS-mediated mechanism. Nutr Cancer. 2009;61(3):348-56.

[11] Dreher ML, Davenport AJ. Hass avocado composition and potential health effects. Crit Rev Food Sci Nutr. 2013;53(7):738-50.

[12] Pieterse Z, Jerling JC, Oosthuizen W, et al. Substitution of high monounsaturated fatty acid avocado for mixed dietary fats during an energy-restricted diet: effects on weight loss, serum lipids, fibrinogen, and vascular function. Nutrition. 2005;21(1):67-75.

[13] Alvizouri-muñoz M, Carranza-madrigal J, Herrera-abarca JE, Chávez-carbajal F, Amezcua-gastelum JL. Effects of avocado as a source of monounsaturated fatty acids on plasma lipid levels. Arch Med Res. 1992;23(4):163-7.

[14] Dreher ML, Davenport AJ. Hass avocado composition and potential health effects. Crit Rev Food Sci Nutr. 2013;53(7):738-50.

[15] Yang M, Moclair B, Hatcher V, et al. A randomized, double-blind, placebo-controlled study of a novel pantothenic Acid-based dietary supplement in subjects with mild to moderate facial acne. Dermatol Ther (Heidelb). 2014;4(1):93-101.

[16] Ribaya-mercado JD. Influence of dietary fat on beta-carotene absorption and bioconversion into vitamin A. Nutr Rev. 2002;60(4):104-10.

[17] Widjaja-adhi MA, Lobo GP, Golczak M, Von lintig J. A genetic dissection of intestinal fat-soluble vitamin and carotenoid absorption. Hum Mol Genet. 2015;24(11):3206-19.

[18] Verhoeven DT, Goldbohm RA, Van poppel G, Verhagen H, Van den brandt PA. Epidemiological studies on brassica vegetables and cancer risk. Cancer Epidemiol Biomarkers Prev. 1996;5(9):733-48.

[19] Murillo G, Mehta RG. Cruciferous vegetables and cancer prevention. Nutr Cancer. 2001;41(1-2):17-28.

[20] Maeda N, Matsubara K, Yoshida H, Mizushina Y. Anti-cancer effect of spinach glycoglycerolipids as angiogenesis inhibitors based on the selective inhibition of DNA polymerase activity. Mini Rev Med Chem. 2011;11(1):32-8.

 

Eat Your Vegetables! | The Paleo Diet

There may not be a more agreed-upon nutritional choice, across the board, than daily intake of vegetables.1 From our parents, to our grandparents, we likely always heard “eat your vegetables” at every meal. It turns out that they were on to something.2 Researchers found a hugely protective effect of vegetable consumption for cancers of the stomach, esophagus, lung, oral cavity and pharynx, endometrium, pancreas, and colon.3, 4 Not too shabby. Unfortunately, the vast majority of us are not taking their time-honored advice. As researchers have found, there is a huge gap between the average consumption of vegetables in Americans compared with the amount actually recommended.5, 6

Eat Your Vegetables! | The Paleo DIet

Liu, Rui Hai. “Health-Promoting Components of Fruits and Vegetables in the Diet.” Advances in Nutrition 4.3 (2013): 384S–392S. PMC. Web. 17 Apr. 2015.

What may be further damning for our collective health, by not consuming enough vegetables, is how we miss out on a plethora of phytochemicals, which are not even yet fully understood by the scientific community.7 Bioactive compounds such as isothiocyanate erucin (found in cruciferous vegetables) have been studied in regards to potential anti-cancer effects.8, 9 Then there is sulforaphane, which is found in broccoli.10 This dietary component has been studied extensively across a wide range of conditions, from autism to cancer.11

Were you aware that you were missing out on all these important elements, by skipping out on your vegetables? I bet you weren’t. Vegetables even provide nutrients for our eye health.12 That may be a strange way to think of things, but most of us take our eye health completely for granted. Most startlingly, however, researchers found the more vegetables consumed, the less likely they are to die!13 Though there are no doubt other lifestyle factors at play in such studies, the overall pattern and trends associated with vegetable consumption cannot be ignored.14, 15

Eat Your Vegetables! | The Paleo Diet

Mark P. Mattson , Sic L. Chan , Wenzhen Duan “Modification of Brain Aging and Neurodegenerative Disorders by Genes, Diet, and Behavior” Physiological Reviews Published 7 January 2002 Vol. 82 no. 3, 637-672

I know it may not be “thrilling” or “sexy” to eat your vegetables (or even particularly fun), but it is perhaps the single best thing you can do, on a daily basis, for your long-term health.16, 17 The bottom line is, we all have to eat something. Since high-fat, refined sugar diets have been shown to reduce hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning – it makes more sense to go with the veggies.18 The scientific evidence has shown the positive influence of nutrients on specific molecular systems and mechanisms that maintain mental function.19 The detrimental effects of too much sugar are well documented – but there are very few – if any – downsides to eating too many vegetables.20 Loading up on these brain-enhancing foods will also take away room on your plate from poor nutritional choices – like pizza.

A Paleo Diet promotes eating lots of vegetables, as well as other healthy elements like omega-3 fatty acids, in addition to quality sources of protein. All of these help us to achieve our most-optimal state of health. Choosing anything else is simply a mistake, and should be avoided if at all possible. As we become a fatter and fatter planet, we must take our own health very seriously, and make smart choices. And nothing is smarter than eating a large amount of vegetables everyday – just like your mother said.

 

REFERENCES

[1] Wang X, Ouyang Y, Liu J, et al. Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies. BMJ. 2014;349:g4490.

[2] Liu RH. Health benefits of fruit and vegetables are from additive and synergistic combinations of phytochemicals. Am J Clin Nutr. 2003;78(3 Suppl):517S-520S.

[3] Steinmetz KA, Potter JD. Vegetables, fruit, and cancer prevention: a review. J Am Diet Assoc. 1996;96(10):1027-39.

[4] Van duyn MA, Pivonka E. Overview of the health benefits of fruit and vegetable consumption for the dietetics professional: selected literature. J Am Diet Assoc. 2000;100(12):1511-21.

[5] Liu RH. Health-promoting components of fruits and vegetables in the diet. Adv Nutr. 2013;4(3):384S-92S.

[6] Katz DL. Plant foods in the American diet? As we sow. Medscape J Med. 2009;11(1):25.

[7] W watson G, M beaver L, E williams D, H dashwood R, Ho E. Phytochemicals from cruciferous vegetables, epigenetics, and prostate cancer prevention. AAPS J. 2013;15(4):951-61.

[8] Melchini A, Traka MH, Catania S, et al. Antiproliferative activity of the dietary isothiocyanate erucin, a bioactive compound from cruciferous vegetables, on human prostate cancer cells. Nutr Cancer. 2013;65(1):132-8.

[9] Herz C, Hertrampf A, Zimmermann S, et al. The isothiocyanate erucin abrogates telomerase in hepatocellular carcinoma cells in vitro and in an orthotopic xenograft tumour model of HCC. J Cell Mol Med. 2014;18(12):2393-403.

[10] Singh K, Connors SL, Macklin EA, et al. Sulforaphane treatment of autism spectrum disorder (ASD). Proc Natl Acad Sci USA. 2014;111(43):15550-5.

[11] Li Y, Zhang T. Targeting cancer stem cells with sulforaphane, a dietary component from broccoli and broccoli sprouts. Future Oncol. 2013;9(8):1097-103.

[12] Sommerburg O, Keunen JE, Bird AC, Van kuijk FJ. Fruits and vegetables that are sources for lutein and zeaxanthin: the macular pigment in human eyes. Br J Ophthalmol. 1998;82(8):907-10.

[13] Genkinger JM, Platz EA, Hoffman SC, Comstock GW, Helzlsouer KJ. Fruit, vegetable, and antioxidant intake and all-cause, cancer, and cardiovascular disease mortality in a community-dwelling population in Washington County, Maryland. Am J Epidemiol. 2004;160(12):1223-33.

[14] Grant R, Bilgin A, Zeuschner C, et al. The relative impact of a vegetable-rich diet on key markers of health in a cohort of Australian adolescents. Asia Pac J Clin Nutr. 2008;17(1):107-15.

[15] Adams MR, Golden DL, Chen H, Register TC, Gugger ET. A diet rich in green and yellow vegetables inhibits atherosclerosis in mice. J Nutr. 2006;136(7):1886-9.

[16] Holt EM, Steffen LM, Moran A, et al. Fruit and vegetable consumption and its relation to markers of inflammation and oxidative stress in adolescents. J Am Diet Assoc. 2009;109(3):414-21.

[17] Slavin JL, Lloyd B. Health benefits of fruits and vegetables. Adv Nutr. 2012;3(4):506-16.

[18] Molteni R, Barnard RJ, Ying Z, Roberts CK, Gómez-pinilla F. A high-fat, refined sugar diet reduces hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning. Neuroscience. 2002;112(4):803-14.

[19] Gómez-pinilla F. Brain foods: the effects of nutrients on brain function. Nat Rev Neurosci. 2008;9(7):568-78.

[20] Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008;32(1):20-39.

 

Fight Inflammation with a Paleo Diet

Most athletes are well aware of a fun little word called “inflammation”.1 Tough workouts are a common cause of inflammation. Acute inflammation (the only kind most people are aware of) is actually beneficial.2, 3 But – and this is a big BUT – chronic inflammation is a killer. Literally.4, 5, 6 The difference here is important, and very misunderstood. One of the biggest health benefits of consuming a Paleo diet comes from its anti-inflammatory nature.7, 8, 9 By fixing the Standard American Diet (SAD) ratio of high omega-6 to low omega-3, nearly everyone sees improvements.10, 11 But before we proceed further, let’s specify and define acute inflammation and chronic inflammation.

Fight Inflammation with a Paleo Diet

Imai, Yumi, Anca D. Dobrian, Margaret A. Morris, and Jerry L. Nadler. “Islet Inflammation: A Unifying Target for Diabetes Treatment?” Science Direct. Trends in Endocrinology & Metabolism, July 2013. Web. 25 Mar. 2015.

Fight Inflammation with a Paleo Diet

Heneka, Michael T., Markus P. Kummer, and Eicke Latz. “Innate Immune Activation in Neurodegenerative Disease.” Immunology Reviews. Nature, 25 June 2014. Web. 25 Mar. 2015.

Acute inflammation is what occurs when you get a bruise, cut, experience stress, or go through a hard workout.12 I used to practice Brazilian Jiu Jitsu and CrossFit on a near-daily basis, and I became very familiar with inflammation! However, this is the good kind of inflammation, remember. Without acute inflammation, you would never heal. Think about that for a minute. Chronic inflammation, by contrast, is problematic for two reasons. One, it is much less noticeable. You likely won’t have a bruise, cut, or any obvious symptoms. And two, it is the cause behind most serious diseases – whether it be cancer, heart disease or other conditions.13, 14, 15

With regard to diet, inflammation also plays a bigger role than most are aware of. Take acne, for example. This is an inflammatory condition. Some have even surmised that inflammation plays a role in acne at a subclinical level.16 This is one of the many reasons why dairy should be avoided when consuming a Paleo Diet. Perhaps surprisingly to some, coconut oil has been shown to have components which help protect against acne.17 The lauric acid found in coconut oil has anti-bacterial and anti-inflammatory properties, and would therefore also be beneficial after a tough workout.18 Win-win.

Vegetables are another key component of an anti-inflammatory diet, and unsurprisingly, a healthy Paleo diet is largely comprised of vegetables!19, 20 So what should athletes be eating? Coconut oil, protein and vegetables! Of course you’ll also want some anti-inflammatory fats, like the omega-3 fatty acids found in wild-caught seafood.21 From strictly a scientific perspective, it is quite clear athletes should stick to a diet based upon these foods to provide you with the best results.

Fight Inflammation with a Paleo Diet

Dantzer, Robert et al. “From Inflammation to Sickness and Depression: When the Immune System Subjugates the Brain.” Nature reviews. Neuroscience 9.1 (2008): 46–56. PMC. Web. 25 Mar. 2015.

Another aspect of inflammation which many are unaware of is that it can occur (and often does occur) in your brain!22 If the brain’s barrier is opened, your glial cells will likely be activated.23 These are the cells that deal with immunity. Once activated, an inflammatory response in your brain occurs.24 This is not good. To add to the fun, your brain now has trouble communicating with your gut, creating more issues, specifically serotonin biosynthesis problems.25 And, the delicate HPA (hypothalamus, pituitary, adrenal) axis will now likely be off-balance, as well.26

So, what is the best way to avoid inflammation, of all kinds (except beneficial, acute inflammation)? Quite simply: eat a Paleo diet. By avoiding gluten (a huge instigator of inflammation throughout the body and brain) you will be doing yourself a huge favor.27, 28 And when we replace problematic proteins like gluten, with nutrient-dense foods rich in protein, antioxidants and anti-inflammatory compounds, we procure better health for ourselves.29 Your mom was right: eat your vegetables for better health and less inflammation.30 Stay the course with a Paleo Diet and optimal health sans inflammation is within reach.

 

REFERENCES

[1] Pinto A, Di raimondo D, Tuttolomondo A, Buttà C, Milio G, Licata G. Effects of physical exercise on inflammatory markers of atherosclerosis. Curr Pharm Des. 2012;18(28):4326-49.

[2] Pedersen BK. The anti-inflammatory effect of exercise: its role in diabetes and cardiovascular disease control. Essays Biochem. 2006;42:105-17.

[3] You T, Arsenis NC, Disanzo BL, Lamonte MJ. Effects of exercise training on chronic inflammation in obesity : current evidence and potential mechanisms. Sports Med. 2013;43(4):243-56.

[4] Osiecki H. The role of chronic inflammation in cardiovascular disease and its regulation by nutrients. Altern Med Rev. 2004;9(1):32-53.

[5] Peev V, Nayer A, Contreras G. Dyslipidemia, malnutrition, inflammation, cardiovascular disease and mortality in chronic kidney disease. Curr Opin Lipidol. 2014;25(1):54-60.

[6] Kelly E, Owen CA, Pinto-plata V, Celli BR. The role of systemic inflammatory biomarkers to predict mortality in chronic obstructive pulmonary disease. Expert Rev Respir Med. 2013;7(1):57-64.

[7] De punder K, Pruimboom L. The dietary intake of wheat and other cereal grains and their role in inflammation. Nutrients. 2013;5(3):771-87.

[8] Soares FL, De oliveira matoso R, Teixeira LG, et al. Gluten-free diet reduces adiposity, inflammation and insulin resistance associated with the induction of PPAR-alpha and PPAR-gamma expression. J Nutr Biochem. 2013;24(6):1105-11.

[9] Nowlin SY, Hammer MJ, D’eramo melkus G. Diet, inflammation, and glycemic control in type 2 diabetes: an integrative review of the literature. J Nutr Metab. 2012;2012:542698.

[10] Kowalski LM, Bujko J. [Evaluation of biological and clinical potential of paleolithic diet]. Rocz Panstw Zakl Hig. 2012;63(1):9-15.

[11] Jönsson T, Granfeldt Y, Lindeberg S, Hallberg AC. Subjective satiety and other experiences of a Paleolithic diet compared to a diabetes diet in patients with type 2 diabetes. Nutr J. 2013;12:105.

[12] Ryan GB, Majno G. Acute inflammation. A review. Am J Pathol. 1977;86(1):183-276.

[13] Holmes C, Cunningham C, Zotova E, et al. Systemic inflammation and disease progression in Alzheimer disease. Neurology. 2009;73(10):768-74.

[14] Mcmillan DC, Elahi MM, Sattar N, Angerson WJ, Johnstone J, Mcardle CS. Measurement of the systemic inflammatory response predicts cancer-specific and non-cancer survival in patients with cancer. Nutr Cancer. 2001;41(1-2):64-9.

[15] Gomes de lima KV, Maio R. Nutritional status, systemic inflammation and prognosis of patients with gastrointestinal cancer. Nutr Hosp. 2012;27(3):707-14.

[16] Tanghetti EA. The role of inflammation in the pathology of acne. J Clin Aesthet Dermatol. 2013;6(9):27-35.

[17] Huang WC, Tsai TH, Chuang LT, Li YY, Zouboulis CC, Tsai PJ. Anti-bacterial and anti-inflammatory properties of capric acid against Propionibacterium acnes: a comparative study with lauric acid. J Dermatol Sci. 2014;73(3):232-40.

[18] Huang WC, Tsai TH, Chuang LT, Li YY, Zouboulis CC, Tsai PJ. Anti-bacterial and anti-inflammatory properties of capric acid against Propionibacterium acnes: a comparative study with lauric acid. J Dermatol Sci. 2014;73(3):232-40.

[19] Watzl B. Anti-inflammatory effects of plant-based foods and of their constituents. Int J Vitam Nutr Res. 2008;78(6):293-8.

[20] Galland L. Diet and inflammation. Nutr Clin Pract. 2010;25(6):634-40.

[21] Wall R, Ross RP, Fitzgerald GF, Stanton C. Fatty acids from fish: the anti-inflammatory potential of long-chain omega-3 fatty acids. Nutr Rev. 2010;68(5):280-9.

[22] Dantzer R, O’connor JC, Freund GG, Johnson RW, Kelley KW. From inflammation to sickness and depression: when the immune system subjugates the brain. Nat Rev Neurosci. 2008;9(1):46-56.

[23] Prat A, Biernacki K, Wosik K, Antel JP. Glial cell influence on the human blood-brain barrier. Glia. 2001;36(2):145-55.

[24] Skaper SD, Facci L, Giusti P. Mast cells, glia and neuroinflammation: partners in crime?. Immunology. 2014;141(3):314-27.

[25] Spiller R. Serotonin, inflammation, and IBS: fitting the jigsaw together?. J Pediatr Gastroenterol Nutr. 2007;45 Suppl 2:S115-9.

[26] Morand EF, Leech M. Hypothalamic-pituitary-adrenal axis regulation of inflammation in rheumatoid arthritis. Immunol Cell Biol. 2001;79(4):395-9.

[27] Hansen CH, Krych L, Buschard K, et al. A maternal gluten-free diet reduces inflammation and diabetes incidence in the offspring of NOD mice. Diabetes. 2014;63(8):2821-32.

[28] Antvorskov JC, Fundova P, Buschard K, Funda DP. Dietary gluten alters the balance of pro-inflammatory and anti-inflammatory cytokines in T cells of BALB/c mice. Immunology. 2013;138(1):23-33.

[29] Halliwell B. Antioxidants in human health and disease. Annu Rev Nutr. 1996;16:33-50.

[30] Holt EM, Steffen LM, Moran A, et al. Fruit and vegetable consumption and its relation to markers of inflammation and oxidative stress in adolescents. J Am Diet Assoc. 2009;109(3):414-21.

Artificial Sweeteners | The Paleo Diet

Introduction: Evolutionary Perspective

It’s pretty clear that if we follow the example of our hunter gatherer ancestors, artificial sweeteners should not be part of contemporary Stone Age diets. In my book, The Paleo Diet Revised (2010)1 I warned against drinking artificially sweetened soft drinks and further strengthened my opposition to all artificial sweeteners in 2012 with The Paleo Answer.2 Over the past few years numerous epidemiological (population), animal, tissue and human studies have demonstrated the adverse health effects of these synthetic chemicals. A particularly powerful study just published in the October 2014 issue of Nature3 provides a convincing argument against the use of artificial sweeteners in our food supply. If you consume artificial sweeteners in the form of sodas or foods once in a blue moon, they will have little or no adverse effects upon your long term health. However, I would never recommend that you drink artificially sweetened beverages or foods on a daily or even weekly basis, as they may promote insulin resistance,3, 4 obesity in adults5-7, 30-33 and children,8-11, 32, 44 metabolic syndrome diseases,12-18, 33 migraine headaches,19-23 adverse pregnancy outcomes,24-26 childhood allergies,24 and certain cancers.27-29

Artificial Sweeteners

The table* below shows the five artificial sweeteners that the U.S. Food and Drug Administration (FDA) has approved for consumption.

Artificial Sweeteners: Agents of Insulin Resistance, Obesity and Disease | The Paleo Diet

*Note that the artificial sweetener cyclamate was banned in the U.S. in 1969, but is still available in certain countries outside of the U.S.

In addition to these artificial sweeteners, the FDA has sanctioned a sugar substitute, stevia, as a dietary supplement since 1995. Stevia is a crystalline substance made from the leaves of a plant native to central and South America and is 100 to 300 times sweeter than table sugar. A concentrated derivative of stevia leaves called rebaudioside A was recently (2008) authorized by the FDA and goes by the trade names of Only Sweet, PureVia, Reb-A, Rebiana, SweetLeaf, and Truvia.

Since 1980 the number of people consuming artificially sweetened products in the U.S. has more than doubled.32, 33 Today, at least 46 million Americans regularly ingest foods sweetened by these chemicals – mainly in the form of soft drinks, or in a huge number of artificially sweetened products, including baby food.32, 33

Artificial Sweeteners and Obesity

If you were to ask most people why they drink artificially sweetened beverages, the resounding answer would be to enjoy a sweet drink without all the drawbacks of sugar laden sodas. Doesn’t everyone know that soft drinks sweetened with sugar promote obesity, type 2 diabetes and the Metabolic Syndrome (high blood pressure, high blood cholesterol and heart disease)? Of course, and the standard line of thought goes something like this, “if we remove refined sugars from our diets and replace them with artificial sweeteners, we would all be a lot healthier.” I can agree with the first and last parts of this argument, but not the second.

A number of large epidemiological studies5-7; 8-11, 44 and animal experiments34-43 indicate that artificially sweetened beverages may actually not be part of the solution to the U.S. obesity epidemic, but rather may be part of the problem.30-33 Unexpectedly, a series of large population based studies, including the San Antonio Heart Study6 examining 3,682 adults over a 7-8 year period; the American Cancer Society Study7 including 78,694 women; and the Nurses’ Health Study5 of 31,940 women have clearly demonstrated strong associations between increased intakes of artificial sweeteners and obesity. Alarmingly, these effects have been observed in children8, 11, 44 as well as in adults, and were utterly unanticipated because most artificial sweeteners were previously thought to be inert and not react with our gut or metabolism in an unsafe manner.30-33, 45

Laboratory Animal Experiments

In the course of the past few years, animal experiments have reversed these erroneous assumptions. Rats allowed to eat their normal chow consumed more food and gained more weight when artificial sweeteners were added to their diet.34-43 The best available evidence indicates that artificial sweeteners when consumed by either laboratory animals or humans promote weight gain by altering the normal gut bacterial biome3, 45 which in turn adversely affects glucose and insulin metabolism and consequently appetite. Who would have ever thought that a mass marketed product which supposedly was designed to help us lose weight may have actually caused exactly the opposite result? But wait, there is more.

Cancer

In 1958 the federal government deemed both saccharin and cyclamate as “generally recognized as safe (GRAS)” artificial sweeteners. Eleven years later the FDA banned cyclamate and announced its intention to ban saccharin in 1977 because of worries over increased cancer risks from both of these chemicals. Consumer protests eventually led to a moratorium from congress on the ban for saccharin, but unfortunately it is still with us today. Aspartame was sanctioned for use as a sweetener by the FDA in 1996, followed by sucralose (1999), neotame (2002), and acesulfame (2003). You may think that anytime chemical additives such as artificial sweeteners were permitted into our food supply, they would have been thoroughly tested and conclusively shown to be safe. Unfortunately, this is not always the case, and the potential toxicity of some of these sweetening compounds are widely disputed in the scientific community, particularly in light of newer, more carefully controlled animal studies.27-29

A series of more recent experiments29 from Dr. Soffritti’s laboratory in Bologna, Italy have shown that even low doses of aspartame given to rats over the course of their lives leads to increased cancer rates. This study is important, because many people may consume much higher concentrations of this chemical by drinking artificially sweetened beverages on a daily basis for years and years.

Migraines

Aspartame has also been shown to trigger migraine headaches in certain people because it breaks down into a compound called methanol (otherwise known as wood alcohol) in our bodies. And it’s not just aspartame that may prove dangerous to our health when we ingest these synthetic concoctions on a regular basis. Recent animal experiments27 have revealed that saccharin, acesulfame as well as aspartame caused DNA damage in mice bone marrow. Frequently, it is difficult to translate results from animal experiments into, meaningful recommendations for humans, because large epidemiological studies generally don’t show artificial sweeteners to be risk factors for cancer. Does this mean that these compounds are completely safe? Absolutely not.

Pregnancy

A 2010 prospective study25 of 59,334 pregnant women from Denmark showed for the first time that consumption of artificially sweetened soft drinks significantly increased the risk for pre-term delivery (less than 37 weeks). This condition shouldn’t be taken lightly, as it represents the leading cause of infant death. An interesting outcome of this study was that only artificially sweetened beverages increased the risk for pre-term delivery – and not sugar sweetened soft drinks. A follow-up study confirmed these results.26 Am I recommending that pregnant women consume sugary soft drinks? Emphatically no! But these studies indicate that sugar sweetened drinks may be less harmful to your developing fetus than are artificially sweetened soft drinks.

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

REFERENCES

1. Cordain L. The Paleo Diet. John Wiley & Sons, NY New York, 2010.

2. Cordain L. The Paleo Answer. John Wiley & Sons, NY New York, 2012

3. Suez J, Korem T, Zeevi D, Zilberman-Schapira G, Thaiss CA, Maza O, Israeli D, Zmora N, Gilad S, Weinberger A, Kuperman Y, Harmelin A, Kolodkin-Gal I, Shapiro H, Halpern Z, Segal E, Elinav E. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature. 2014 Oct 9;514(7521):181-6

4. Horwitz DL, McLane M, Kobe P. Response to single dose of aspartame or saccharin by NIDDM patients. Diabetes Care. 1988 Mar;11(3):230-4.

5. Colditz GA, Willett WC, Stampfer MJ, London SJ, Segal MR, Speizer FE. Patterns of weight change and their relation to diet in a cohort of healthy women. Am J Clin Nutr. 1990 Jun;51(6):1100-5

6. Fowler SP, Williams K, Resendez RG, Hunt KJ, Hazuda HP, Stern MP. Fueling the obesity epidemic? Artificially sweetened beverage use and long-term weight gain. Obesity (Silver Spring). 2008 Aug;16(8):1894-900.

7. Stellman SD, Garfinkel L. Artificial sweetener use and one-year weight change among women. Prev Med. 1986 Mar;15(2):195-202.

8. Blum JW, Jacobsen DJ, Donnelly JE. Beverage consumption patterns in elementary school aged children across a two-year period. J Am Coll Nutr. 2005 Apr;24(2):93-8.

9. Forshee RA, Storey ML. Total beverage consumption and beverage choices among children and adolescents. Int J Food Sci Nutr. 2003 Jul;54(4):297-307

10. Striegel-Moore RH, Thompson D, Affenito SG, Franko DL, Obarzanek E, Barton BA, Schreiber GB, Daniels SR, Schmidt M, Crawford PB. Correlates of beverage intake in adolescent girls: the National Heart, Lung, and Blood Institute Growth and Health Study.J Pediatr. 2006 Feb;148(2):183-7.

11. Brown RJ, de Banate MA, Rother KI. Artificial sweeteners: a systematic review of metabolic effects in youth. Int J Pediatr Obes. 2010 Aug;5(4):305-12

12. Nettleton JA, Lutsey PL, Wang Y, Lima JA, Michos ED, Jacobs DR Jr. Diet soda intake and risk of incident metabolic syndrome and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes Care. 2009 Apr;32(4):688-94.

13. Cohen L, Curhan G, Forman J. Association of sweetened beverage intake with incident hypertension. J Gen Intern Med. 2012 Sep;27(9):1127-34.

14. Gardener H, Rundek T, Markert M, Wright CB, Elkind MS, Sacco RL. Diet soft drink consumption is associated with an increased risk of vascular events in the Northern Manhattan Study. J Gen Intern Med. 2012 Sep;27(9):1120-6.

15. Dhingra R, Sullivan L, Jacques PF, Wang TJ, Fox CS, Meigs JB, D’Agostino RB, Gaziano JM, Vasan RS.Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community. Circulation. 2007 Jul 31;116(5):480-8.

16. Lutsey PL, Steffen LM, Stevens J. Dietary intake and the development of the metabolic syndrome: the Atherosclerosis Risk in Communities study. Circulation. 2008 Feb 12;117(6):754-61

17. Fagherazzi G, Vilier A, Saes Sartorelli D, Lajous M, Balkau B, Clavel-Chapelon F.
Consumption of artificially and sugar-sweetened beverages and incident type 2 diabetes in the Etude Epidemiologique aupres des femmes de la Mutuelle Generale de l’Education Nationale-European Prospective Investigation into Cancer and Nutrition cohort. Am J Clin Nutr. 2013 Mar;97(3):517-23

18. Greenwood DC, Threapleton DE, Evans CE, Cleghorn CL, Nykjaer C, Woodhead C, Burley VJ. Association between sugar-sweetened and artificially sweetened soft drinks and type 2 diabetes: systematic review and dose-response meta-analysis of prospective studies. Br J Nutr. 2014 Sep 14;112(5):725-34.

19. Abegaz EG, Bursey RG. Formaldehyde, aspartame, migraines: a possible connection. Dermatitis. 2009 May-Jun;20(3):176-7; author reply 177-9

20. Bigal ME, Krymchantowski AV. Migraine triggered by sucralose–a case report. Headache. 2006 Mar;46(3):515-7

21. Jacob SE, Stechschulte S. Formaldehyde, aspartame, and migraines: a possible connection. Dermatitis. 2008 May-Jun;19(3):E10-1.

22. Lipton RB, Newman LC, Cohen JS, Solomon S. Aspartame as a dietary trigger of headache. Headache. 1989 Feb;29(2):90-2

23. Newman LC, Lipton RB. Migraine MLT-down: an unusual presentation of migraine in patients with aspartame-triggered headaches. Headache. 2001 Oct;41(9):899-901.
Araújo JR, Martel F, Keating E. Exposure to non-nutritive sweeteners during pregnancy and lactation: Impact in programming of metabolic diseases in the progeny later in life. Reprod Toxicol. 2014 Sep 28;49C:196-201.

24. Maslova E, Strøm M, Olsen SF, Halldorsson TI. Consumption of artificially-sweetened soft drinks in pregnancy and risk of child asthma and allergic rhinitis.PLoS One. 2013;8(2):e57261.

25. Halldorsson TI, Strøm M, Petersen SB, Olsen SF. Intake of artificially sweetened soft drinks and risk of preterm delivery: a prospective cohort study in 59,334 Danish pregnant women. Am J Clin Nutr. 2010 Sep;92(3):626-33.

26. Englund-Ögge L1, Brantsæter AL, Haugen M, Sengpiel V, Khatibi A, Myhre R, Myking S, Meltzer HM, Kacerovsky M, Nilsen RM, Jacobsson B. Association between intake of artificially sweetened and sugar-sweetened beverages and preterm delivery: a large prospective cohort study. Am J Clin Nutr. 2012 Sep;96(3):552-9.

27. Bandyopadhyay A, Ghoshal S, Mukherjee A. Genotoxicity testing of low-calorie sweeteners: aspartame, acesulfame-K, and saccharin. Drug Chem Toxicol. 2008;31(4):447-57

28. Belpoggi F, Soffritti M, Padovani M, Degli Esposti D, Lauriola M, Minardi F. Results of long-term carcinogenicity bioassay on Sprague-Dawley rats exposed to aspartame administered in feed. Ann N Y Acad Sci. 2006 Sep;1076:559-77.

29. Soffritti M, Belpoggi F, Tibaldi E, Esposti DD, Lauriola M. Life-span exposure to low doses of aspartame beginning during prenatal life increases cancer effects in rats. Environ Health Perspect. 2007 Sep;115(9):1293-7

30. Ferreira AV1, Generoso SV, Teixeira AL. Do low-calorie drinks ‘cheat’ the enteral-brain axis? Curr Opin Clin Nutr Metab Care. 2014 Sep;17(5):465-70.

31. Swithers SE, Martin AA, Davidson TL. High-intensity sweeteners and energy balance. Physiol Behav. 2010 Apr 26;100(1):55-62

32. Yang Q. Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings: Neuroscience 2010. Yale J Biol Med. 2010 Jun;83(2):101-8.

33. Swithers SE. Artificial sweeteners produce the counterintuitive effect of inducing metabolic derangements. Trends Endocrinol Metab. 2013 Sep;24(9):431-41.

34. Swithers SE, Davidson TL. A role for sweet taste: calorie predictive relations in energy regulation by rats. Behav Neurosci. 2008 Feb;122(1):161-73.

35. Swithers SE, Baker CR, Davidson TL. General and persistent effects of high-intensity sweeteners on body weight gain and caloric compensation in rats. Behav Neurosci. 2009 Aug;123(4):772-80

36. Swithers SE, Martin AA, Clark KM, Laboy AF, Davidson TL. Body weight gain in rats consuming sweetened liquids. Effects of caffeine and diet composition. Appetite. 2010 Dec;55(3):528-33

37. Feijó Fde M1, Ballard CR, Foletto KC, Batista BA, Neves AM, Ribeiro MF, Bertoluci MC. Saccharin and aspartame, compared with sucrose, induce greater weight gain in adult Wistar rats, at similar total caloric intake levels. Appetite. 2013 Jan;60(1):203-7.

38. Swithers SE, Sample CH, Davidson TL. Adverse effects of high-intensity sweeteners on energy intake and weight control in male and obesity-prone female rats. Behav Neurosci. 2013 Apr;127(2):262-74.

39. Pierce WD, Heth CD, Owczarczyk JC, Russell JC, Proctor SD. Overeating by young obesity-prone and lean rats caused by tastes associated with low energy foods. Obesity (Silver Spring). 2007 Aug;15(8):1969-79.

40. von Poser Toigo E, Huffell AP, Mota CS, Bertolini D, Pettenuzzo LF, Dalmaz C.
Metabolic and feeding behavior alterations provoked by prenatal exposure to aspartame. Appetite. 2014 Dec 24. pii: S0195-6663(14)00774-0.

41. Polyák E, Gombos K, Hajnal B, Bonyár-Müller K, Szabó S, Gubicskó-Kisbenedek A, Marton K, Ember I. Effects of artificial sweeteners on body weight, food and drink intake. Acta Physiol Hung. 2010 Dec;97(4):401-7

42. Malaisse WJ, Vanonderbergen A, Louchami K, Jijakli H, Malaisse-Lagae F. Effects of artificial sweeteners on insulin release and cationic fluxes in rat pancreatic islets. Cell Signal. 1998 Nov;10(10):727-33

43. Swithers SE, Laboy AF, Clark K, Cooper S, Davidson TL. Experience with the high-intensity sweetener saccharin impairs glucose homeostasis and GLP-1 release in rats. Behav Brain Res. 2012 Jul 15;233(1):1-14

44. Berkey CS, Rockett HR, Field AE, Gillman MW, Colditz GA. Sugar-added beverages and adolescent weight change. Obes Res. 2004 May;12(5):778-88.

45. Schiffman SS. Rationale for further medical and health research on high-potency sweeteners. Chem Senses. 2012 Oct;37(8):671-9.

 

Fighting Cancer, Autism, and Neurodegenerative Diseases One Molecule at a Time | The Paleo DietWe know eating our vegetables is good for us, but few are familiar with the copious benefits of the molecules that are contained within each vegetable.1, 2, 3 Take for example, sulforaphane, a molecule within the isothiocyanate group of organosulfur compounds.4, 5, 6 Broccoli, Brussels sprouts, and cabbage all contain sulforaphane,7 among others including kale, cauliflower, radishes, broccoli raab, mustard, turnips, bok choy, collards, kohlrabi, arugula, and watercress.8 9 This molecule is currently being studied for its potential antioxidant properties, and how it relates to autism,10, 11, 12, 13, 14 neurodegenerative disorders, and cancers.15, 16, 17, 18

Fighting Cancer, Autism, and Neurodegenerative Diseases One Molecule at a Time | The Paleo Diet

Boddupalli, Sekhar et al. “Induction of Phase 2 Antioxidant Enzymes by Broccoli Sulforaphane: Perspectives in Maintaining the Antioxidant Activity of Vitamins A, C, and E.” Frontiers in Genetics 3 (2012): 7. PMC. Web. 20 Jan. 2015.

Fighting Cancer, Autism, and Neurodegenerative Diseases One Molecule at a Time | The Paleo Diet

Boddupalli, Sekhar et al. “Induction of Phase 2 Antioxidant Enzymes by Broccoli Sulforaphane: Perspectives in Maintaining the Antioxidant Activity of Vitamins A, C, and E.” Frontiers in Genetics 3 (2012): 7.

In fact, one of the most interesting studies regarding sulforaphane was released just a few months ago.19 The authors of this study concluded that sulforaphane activates the Nrf2 pathway, which helps many inflammatory conditions, after looking specifically at sulforaphane’s effects on autism. With regard to other conditions, recent research into the effects of sulforaphane on cancer stem cells has drawn tremendous interest.20 Sulforaphane has also proven to be an effective chemoprotective agent in cell culture, in carcinogen-induced and genetic animal cancer models, as well as in xenograft models of cancer.21

Other studies have looked at sulforaphane’s potential effects on Alzheimer’s disease. Researchers have found that sulforaphane significantly increased the numbers of 5-bromo-2′-deoxyuridine-positive neurons in the subventricular and subgranular zones.22 Though the molecule is not yet a definitive cure for any condition, the preventive potential of sulforaphane remains high, and should provide enough incentive to prioritize a healthy, Paleo diet rich in vegetables.

Sulforaphane has also shown a protective effect on the kidney mitochondrial complex,23 where damage is often induced by a high-fat diet. It is, however, worth mentioning that when researchers use the term ‘high-fat,’ they usually are referring to a high-fat, as well as a high-sugar diet. In addition to this kind of protection, a wide variety of acute and chronic neurodegenerative diseases, including ischemic/traumatic brain injury, Alzheimer’s disease, and Parkinson’s disease, share common characteristics. These characteristics include: oxidative stress, misfolded proteins, excitotoxicity, inflammation, and neuronal loss. Sulforaphane has been shown to help combat nearly all of these characteristics.24 In essence, by eating kale and making other healthy food choices, you will not only avoid damage caused by a poor diet, but also simultaneously protect yourself against potential neurological conditions.

Fighting Cancer, Autism, and Neurodegenerative Diseases One Molecule at a Time | The Paleo Diet

Tarozzi, Andrea et al. “Sulforaphane as a Potential Protective Phytochemical Against Neurodegenerative Diseases.” Oxidative Medicine and Cellular Longevity 2013 (2013): 415078. PMC. Web. 20 Jan. 2015.

Fighting Cancer, Autism, and Neurodegenerative Diseases One Molecule at a Time | The Paleo Diet

Boddupalli, Sekhar et al. “Induction of Phase 2 Antioxidant Enzymes by Broccoli Sulforaphane: Perspectives in Maintaining the Antioxidant Activity of Vitamins A, C, and E.” Frontiers in Genetics 3 (2012): 7. PMC. Web. 20 Jan. 2015.

So, it seems that when your mother told you to eat your vegetables, she may have been more right than either of you realized. The sheer idea that by simply consuming broccoli, you may be helping to protect your brain against neurodegenerative disorders, or potentially even against cancer, is both a tantalizing prospect, and one more reason to eat a healthy, balanced diet. Though one molecule may not protect you against everything, consuming a diet rich with nutrients is arguably the best thing you can do to protect your own health.25, 26, 27 A Paleo Diet, which is rich with vegetables, high quality sources of protein, and healthy fats, will keep your body and mind in the best shape possible. Eat up!

REFERENCES

[1] This H. Food for tomorrow? How the scientific discipline of molecular gastronomy could change the way we eat. EMBO Rep. 2006;7(11):1062-6.

[2] Rao MB, Tanksale AM, Ghatge MS, Deshpande VV. Molecular and biotechnological aspects of microbial proteases. Microbiol Mol Biol Rev. 1998;62(3):597-635.

[3] Pandey KB, Rizvi SI. Plant polyphenols as dietary antioxidants in human health and disease. Oxid Med Cell Longev. 2009;2(5):270-8.

[4] Hwang ES, Jeffery EH. Induction of quinone reductase by sulforaphane and sulforaphane N-acetylcysteine conjugate in murine hepatoma cells. J Med Food. 2005;8(2):198-203.

[5] Wang LI, Giovannucci EL, Hunter D, Neuberg D, Su L, Christiani DC. Dietary intake of Cruciferous vegetables, Glutathione S-transferase (GST) polymorphisms and lung cancer risk in a Caucasian population. Cancer Causes Control. Dec 2004;15(10):977-85.

[6] Cornblatt BS, Ye L, Dinkova-Kostova AT, et al. Preclinical and clinical evaluation of sulforaphane for chemoprevention in the breast. Carcinogenesis. 2007 Jul;28(7):1485-90.

[7] Egner PA, Chen JG, Wang JB, et al. Bioavailability of Sulforaphane from two broccoli sprout beverages: results of a short-term, cross-over clinical trial in Qidong, China. Cancer Prev Res (Phila). 2011;4(3):384-95.

[8] Wang L, Liu D, Ahmed T, Chung FL, Conaway C, Chiao JW. Targeting cell cycle machinery as a molecular mechanism of sulforaphane in prostate cancer prevention. Int J Oncol. 2004;24(1):187-92.

[9] Ho E, Clarke JD, Dashwood RH. Dietary sulforaphane, a histone deacetylase inhibitor for cancer prevention. J Nutr. 2009;139(12):2393-6.

[10] Fahey JW, Talalay P. Antioxidant functions of sulforaphane: a potent inducer of Phase II detoxication enzymes. Food Chem Toxicol. 1999;37(9-10):973-9.

[11] Boddupalli S, Mein JR, Lakkanna S, James DR. Induction of phase 2 antioxidant enzymes by broccoli sulforaphane: perspectives in maintaining the antioxidant activity of vitamins a, C, and e. Front Genet. 2012;3:7.

[12] Riedl MA, Saxon A, Diaz-sanchez D. Oral sulforaphane increases Phase II antioxidant enzymes in the human upper airway. Clin Immunol. 2009;130(3):244-51.

[13] Singh K, Connors SL, Macklin EA, et al. Sulforaphane treatment of autism spectrum disorder (ASD). Proc Natl Acad Sci USA. 2014;111(43):15550-5.

[14] Niculescu MD, Lupu DS. Nutritional influence on epigenetics and effects on longevity. Curr Opin Clin Nutr Metab Care. 2011;14(1):35-40.

[15] Zhang R, Miao QW, Zhu CX, et al. Sulforaphane Ameliorates Neurobehavioral Deficits and Protects the Brain From Amyloid β Deposits and Peroxidation in Mice With Alzheimer-Like Lesions. Am J Alzheimers Dis Other Demen. 2014;:1533317514542645.

[16] Vauzour D, Buonfiglio M, Corona G, et al. Sulforaphane protects cortical neurons against 5-S-cysteinyl-dopamine-induced toxicity through the activation of ERK1/2, Nrf-2 and the upregulation of detoxification enzymes. Mol Nutr Food Res. 2010;54(4):532-42.

[17] Xu T, Ren D, Sun X, Yang G. Dual roles of sulforaphane in cancer treatment. Anticancer Agents Med Chem. 2012;12(9):1132-42.

[18] Zhang C, Su ZY, Khor TO, Shu L, Kong AN. Sulforaphane enhances Nrf2 expression in prostate cancer TRAMP C1 cells through epigenetic regulation. Biochem Pharmacol. 2013;85(9):1398-404.

[19] Singh K, Connors SL, Macklin EA, et al. Sulforaphane treatment of autism spectrum disorder (ASD). Proc Natl Acad Sci USA. 2014;111(43):15550-5.

[20] Li Y, Zhang T. Targeting cancer stem cells with sulforaphane, a dietary component from broccoli and broccoli sprouts. Future Oncol. 2013;9(8):1097-103.

[21] Clarke JD, Dashwood RH, Ho E. Multi-targeted prevention of cancer by sulforaphane. Cancer Lett. 2008;269(2):291-304.

[22] Zhang R, Zhang J, Fang L, et al. Neuroprotective effects of sulforaphane on cholinergic neurons in mice with Alzheimer’s disease-like lesions. Int J Mol Sci. 2014;15(8):14396-410.

[23] Xue H, Li Y, Liang B, Wang S. [Protective effects of sulforaphane on the oxidative damage of kidney mitochondria complex in obese rats induced by high-fat diet]. Zhonghua Yu Fang Yi Xue Za Zhi. 2014;48(11):1007-11.

[24] Tarozzi A, Angeloni C, Malaguti M, Morroni F, Hrelia S, Hrelia P. Sulforaphane as a potential protective phytochemical against neurodegenerative diseases. Oxid Med Cell Longev. 2013;2013:415078.

[25] Pandey KB, Rizvi SI. Plant polyphenols as dietary antioxidants in human health and disease. Oxid Med Cell Longev. 2009;2(5):270-8.

[26] Habauzit V, Morand C. Evidence for a protective effect of polyphenols-containing foods on cardiovascular health: an update for clinicians. Ther Adv Chronic Dis. 2012;3(2):87-106.

[27] Dreher ML, Davenport AJ. Hass avocado composition and potential health effects. Crit Rev Food Sci Nutr. 2013;53(7):738-50.

Paleo Diet Linked to Decreased Colorectal Cancer | The Paleo Diet

According to research recently conducted at Emory University in Atlanta, adherence to the Paleo Diet may significantly slash colorectal cancer rates.1 For their study, published online last month in the American Journal of Epidemiology, researchers examined the dietary habits of 2,301 men and women, 30 to 74 years old. Participants were categorized based on how closely their diets resembled the Paleo Diet. Overall, 564 participants developed colorectal adenoma, a benign tumor of the colon or rectum. Scientists classify colorectal adenoma as a precursor to colorectal cancer.2 For women with diets most closely resembling the Paleo Diet, tumor rates fell 29 percent compared to control groups. For men, Paleo Diet benefits were even more pronounced, with tumor rates falling 51 percent.

For those who study and follow the Paleo lifestyle, these results are hardly surprising. As the Paleo Diet becomes increasingly popular, however, it’s also more frequently misrepresented. Just last week, for example, Janet Helm of US News & World Report wrote about Paleo, “I don’t support this restrictive, meat-heavy diet that bans so many nutritious foods, such as dairy, grains and beans.”3 The Paleo Diet, of course, includes healthy animal foods, but disparagingly calling it “meat-heavy,” ignores the fact that it’s very vegetable-heavy. Could the Paleo Diet’s high vegetable level explain its protective effects against colorectal cancer?

Vegetables, of course, contain fiber and Western diets contain far less fiber than those of our Paleolithic ancestors. Whereas mean daily fiber intakes in the US range from 10 to 18 grams, our Paleolithic ancestors consumed upwards of 100 grams daily.4, 5 Some 40 years ago, an Irish surgeon named Denis Burkitt introduced the theory that increased consumption of dietary fiber decreases colorectal cancer risks.6 Burkitt’s theory gained traction and was eventually accepted as common knowledge, but a number of cohort studies and randomized controlled trials in recent decades have strongly challenged his contention.7 Although many prominent institutions, including the Harvard School of Public Health, no longer accept Burkitt’s theory, it may be premature to conclude that fiber consumption and colorectal cancer are unrelated.8

In an article published in the European Journal of Clinical Nutrition, anthropologist Jeff Leach points out that fiber levels in studies challenging Burkitt’s theory, even for participants in the uppermost quintiles, are still far below evolutionary standards.9 We should also acknowledge fiber’s beneficial effects with respect to gut microbiome health. Increased fiber consumption promotes decreased intestinal inflammation, decreased body weight, and decreased obesity-induced chronic inflammation.10 While the causes of colorectal cancer are not entirely known, the Mayo Clinic lists inflammatory intestinal conditions, insulin resistance, obesity, smoking, heavy alcohol consumption, and sedentary lifestyle all as factors that may increase colorectal cancer risks.11

So what does this new research associating the Paleo Diet with decreased colorectal cancer really tell us? Does the Paleo Diet’s vegetable-heavy, and thus fiber-heavy, aspect account for this benefit? We cannot say so definitively. We can say, however, that the Paleo Diet is more than just a diet. It’s a lifestyle that promotes wellness and prevents disease. Most diseases, especially cancer, have multiple roots, the combination of which eventually grows into disease. This recent research is a testament to the holistic nature of the Paleo Diet and Paleo lifestyle, encompassing many informed decisions, which likely collectively protect against colorectal cancer.

Christopher James Clark, B.B.A.

@nutrigrail
Nutritional Grail
www.ChristopherJamesClark.com

Christopher James Clark | The Paleo Diet TeamChristopher James Clark, B.B.A. is an award-winning writer, consultant, and chef with specialized knowledge in nutritional science and healing cuisine. He has a Business Administration degree from the University of Michigan and formerly worked as a revenue management analyst for a Fortune 100 company. For the past decade-plus, he has been designing menus, recipes, and food concepts for restaurants and spas, coaching private clients, teaching cooking workshops worldwide, and managing the kitchen for a renowned Greek yoga resort. Clark is the author of the critically acclaimed, award-winning book, Nutritional Grail.

REFERENCES

1 Whalen, K., et al. (2014). Paleolithic and Mediterranean Diet Pattern Scores and Risk of Incident, Sporadic Colorectal Adenomas. American Journal of Epidemiology. Retrieved from http://aje.oxfordjournals.org/content/early/2014/10/17/aje.kwu235.abstract

2 Srivastava, S., et al. (May 2001). Biomarkers for early detection of colon cancer. Clinical Cancer Research, 7(5). Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11350874

3 Helm, Janet. (November 5, 2014). 8 Positive Outcomes of the Paleo Trend. US News & World Report. Retrieved from https://www.yahoo.com/health/8-positive-outcomes-of-the-paleo-trend-101439975577.html

4 Clemens, R., et al. (July 2012). Filling America’s Fiber Intake Gap: Summary of a Roundtable to Probe Realistic Solutions with a Focus on Grain-Based Foods. Journal of Nutrition, 142(7). Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/22649260

5 Leach, JD. (January 2007). Evolutionary perspective on dietary intake of fibre and colorectal cancer. European Journal of Clinical Nutrition, 61(1). Retrieved from Evolutionary perspective on dietary intake of fibre and colorectal cancer

6 Burkitt, DP. (July 1971). Epidemiology of cancer of the colon and rectum. Cancer, 28(1). Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/5165022

7 Lawlor, DA, and Ness, AR. (2003). Commentary: The rough world of nutritional epidemiology: Does dietary fibre prevent large bowel cancer? International Journal of Epidemiology, 32(2). Retrieved from http://ije.oxfordjournals.org/content/32/2/239.full

8 Nutrition Source, Harvard School of Public Health. Fiber and Colon Cancer: Following the Scientific Trail. Retrieved from http://www.hsph.harvard.edu/nutritionsource/fiber-and-colon-cancer/

9 Ibid, Burkitt

10 Kuo, SM. (January 2013). The Interplay Between Fiber and the Intestinal Microbiome in the Inflammatory Response. Advances in Nutrition, 4(1). Retrieved from http://advances.nutrition.org/content/4/1/16.full

11 Mayo Clinic Staff. (August 2013). Diseases and Conditions: Colon Cancer: Risk Factors. Retrieved from http://www.mayoclinic.org/diseases-conditions/colon-cancer/basics/risk-factors/con-20031877

Sugar Is Killing Us

It’s no surprise a vast majority of the world recognizes sugar is destroying our health and ruining our lives.1, 2, 3, 4 Over the last 30 years, we’ve seen disease rates skyrocket, alongside our climbing intake of sugar.5, 6, 7, 8, 9 Our concern for this creeping information wavers and takes a backseat to social media, “selfies” and celebrities.10, 11

The growing concern around sugar deserves not only immediate attention, but immediate action.12, 13, 14 Unfortunately, the roadblocks are endless.15, 16 The least of which, is the food industry itself.17 Take, for example, the makers of orange juice, a product which contains a whopping 21g of sugar in a mere 8oz glass,18 and is traditionally the standard American breakfast beverage.

The addictive properties of sugar are well-documented, as are the risks of consuming too much.19, 20 And yet, we can’t seem to stop ourselves.21, 22 Sugar is often added to products surreptitiously, without our consent.23 It is also marketed – quite heavily – towards children.24, 25 We must put a stop to this. Our children are our future, and if they are obese, cognitively impaired, and sick – how much of a future do they really have?

So why sugar is so detrimental? The biochemistry says it all.20 As sugar enters the bloodstream, insulin is secreted.26 The more sugar you eat, the more insulin you secrete. High sugar diets can lead to insulin resistance.27 This condition is one of the hallmarks of obesity and overweight humans everywhere.28 If you consume too much sugar, you’re bound to experience hypoglycemia, commonly referred to as your “sugar crash.”29 This leaves your body craving more sugar – and the addictive process perpetuates.30

Sugar is Killing Us | The Paleo Diet

Sagittal, Coronal and Axial Representations of Glucose-related Regional Grey (A) and White (B) Matter Volumes.
doi:10.1371/journal.pone.0073697.g002

It’s a simple model, but one which we are all familiar with.36 Stress also leads us to overeat.31, 37 And we do not over-consume just any calories, but rather we eat neurologically-rewarding foods.38 This means foods that are either: high in sugar, or foods high in sugar and fat.39 In a study from 2010, researchers showed a disruption of sensitivity to brain-stimulation reward (BSR) from eating high fat and/or high carbohydrate food.40 So you become accustomed to the rewards of these foods, and crave them more.41

The rates of diabetes both nationally, and worldwide, have skyrocketed.42 This is not debatable. Guess what else has skyrocketed, in conjunction with diabetes rates? You guessed it: sugar consumption. There are now obese newborns.43, 44

All of these problems and conditions can be linked directly to sugar intake, and yet, you may be blindsided by how much sugar you’re consuming in the first place. A recent study showed food manufacturers not disclosing the actual values of fructose corn syrup on their product labels.45 Does this bother you? It should.

Sugar is Killing Us | The Paleo Diet

Besides the physiologic effects of too much sugar, there are vast and damning economic effects.32 Take, for example, that diabetes alone costs the United States $245 billion per year.46 This is a rise of 41% in a mere five years. That is an absolutely terrifying figure. Have I scared you yet?

How about the fact that higher glucose levels are associated with lower memory and reduced hippocampal microstructure?47 Or, how about the study from the New England Journal of Medicine, which showed that higher glucose levels may be a risk factor for dementia.48 What was interesting (and alarming) about this finding, was that this was the risk for those without diabetes. This means that you can be taking in “normal” amounts of sugar, not exhibit symptoms of diabetes, and still be risking dementia. Act and don’t turn a blind eye. Save your health.

Sugar is Killing Us | The Paleo Diet

N Engl J Med. Aug 8, 2013; 369(6): 540–548.

Other studies have shown, unsurprisingly, that sugar consumption promotes weight gain in children and adults.33 All behaviors have a biochemical basis. ADHD, ADD, et al, are all likely partially due to a poor diet.49, 50 A diet that, almost always, is high in sugar.51, 52 Since studies have shown that intense sweetness surpasses cocaine reward, it is not surprising that many Americans cannot stop consuming sugar.53 But, in order to help stop alarmingly rising healthcare costs, they must stop their gluttonous consumption, and re-focus their diet on whole, real foods, all part of a Paleo Diet.

Other studies have shown that most US adults consume more added sugar than is recommended,34 and that this overconsumption leads to increased risk for cardiovascular disease mortality.54 This is literally the smoking gun that shows that sugar is killing us. Other studies have shown that higher levels of sugar also lower fitness.55 And another interesting study showed that junk food alone made rats lazy.56 Does this give you food for thought? Perhaps you should prioritize a change to your diet?

Insulin, which is secreted in order to deal with sugar in the bloodstream, blocks leptin signaling.35 Leptin is the “satiety” hormone, which helps to tell our hypothalamus to stop eating.57 Since we are now secreting 2-3 times the amount of insulin than we used to, you can see, directly, how this has resulted in disastrous consequences for our world’s health.58 And why are we secreting more insulin? Quite simply, to deal with all the sugar we are over-consuming. It is not a complicated formula, but it is a formula that is bankrupting our nation, and making so many sick and overweight.

Prevention is paradigm. Avoid a high-sugar diet, become leaner, think faster, and feel better. There is not a single better thing you can do, diet-related, that will help you to improve your health. A Paleo Diet, which is intrinsically low in sugar, high in nutrient-dense foods, and filled with micronutrients, is the best path to wellness.

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References

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4. Moreira PI. High-sugar diets, type 2 diabetes and Alzheimer’s disease. Curr Opin Clin Nutr Metab Care. 2013;16(4):440-5.

5. Ford ES, Giles WH, Mokdad AH. Increasing prevalence of the metabolic syndrome among u.s. Adults. Diabetes Care. 2004;27(10):2444-9.

6. Seaquist ER. Addressing the burden of diabetes. JAMA. 2014;311(22):2267-8.

7. Available at: http://www.cdc.gov/nchs/data/databriefs/db122.htm. Accessed September 13, 2014.

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9. Johnson RK, Appel LJ, Brands M, et al. Dietary sugars intake and cardiovascular health: a scientific statement from the American Heart Association. Circulation. 2009;120(11):1011-20.

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18. Available at: http://www.orangejuicefacts.com/nutrition.html. Accessed September 13, 2014.

19. Ahmed SH, Guillem K, Vandaele Y. Sugar addiction: pushing the drug-sugar analogy to the limit. Curr Opin Clin Nutr Metab Care. 2013;16(4):434-9.

20. Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008;32(1):20-39.

21. Gearhardt A, Roberts M, Ashe M. If sugar is addictive…what does it mean for the law?. J Law Med Ethics. 2013;41 Suppl 1:46-9.

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25. Lythgoe A, Roberts C, Madden AM, Rennie KL. Marketing foods to children: a comparison of nutrient content between children’s and non-children’s products. Public Health Nutr. 2013;16(12):2221-30.

26. Daly M. Sugars, insulin sensitivity, and the postprandial state. Am J Clin Nutr. 2003;78(4):865S-872S.

27. Musselman LP, Fink JL, Narzinski K, et al. A high-sugar diet produces obesity and insulin resistance in wild-type Drosophila. Dis Model Mech. 2011;4(6):842-9.

28. Gallagher EJ, Leroith D, Karnieli E. Insulin resistance in obesity as the underlying cause for the metabolic syndrome. Mt Sinai J Med. 2010;77(5):511-23.

29. Hofeldt FD. Reactive hypoglycemia. Endocrinol Metab Clin North Am. 1989;18(1):185-201.

30. Yang Q. Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings: Neuroscience 2010. Yale J Biol Med. 2010;83(2):101-8.

31. Oliver KG, Huon GF, Zadro L, Williams KD. The role of interpersonal stress in overeating among high and low disinhibitors. Eat Behav. 2001;2(1):19-26.

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33. Malik, Vasanti S., Matthias B. Schulze, and Frank B. Hu. “Intake of sugar-sweetened beverages and weight gain: a systematic review.” The American journal of clinical nutrition 84.2 (2006): 274-288.

34. Yang Q, Zhang Z, Gregg EW, Flanders WD, Merritt R, Hu FB. Added sugar intake and cardiovascular diseases mortality among US adults. JAMA Intern Med. 2014.

35. Kellerer M, Lammers R, Fritsche A, et al. Insulin inhibits leptin receptor signalling in HEK293 cells at the level of janus kinase-2: a potential mechanism for hyperinsulinaemia-associated leptin resistance. Diabetologia. 2001;44(9):1125-32.

36. Available at: http://www.huffingtonpost.co.uk/2013/07/26/why-is-sugar-so-addictive_n_3643965.html. Accessed October 2, 2014.

37. Greeno CG, Wing RR. Stress-induced eating. Psychol Bull. 1994;115(3):444-64.

38. Available at: http://www.cnn.com/2012/02/08/health/healthy-eating-tips-stress/. Accessed October 2, 2014.

39. Torres SJ, Nowson CA. Relationship between stress, eating behavior, and obesity. Nutrition. 2007;23(11-12):887-94.

40. Epstein DH, Shaham Y. Cheesecake-eating rats and the question of food addiction. Nat Neurosci. 2010;13(5):529-31.

41. Johnson PM, Kenny PJ. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nat Neurosci. 2010;13(5):635-41.

42. Weeratunga P, Jayasinghe S, Perera Y, Jayasena G, Jayasinghe S. Per capita sugar consumption and prevalence of diabetes mellitus–global and regional associations. BMC Public Health. 2014;14:186.

43. Soubry A, Murphy SK, Wang F, et al. Newborns of obese parents have altered DNA methylation patterns at imprinted genes. Int J Obes (Lond). 2013.

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45. Walker RW, Dumke KA, Goran MI. Fructose content in popular beverages made with and without high-fructose corn syrup. Nutrition. 2014;30(7-8):928-35.

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47. Kerti L, Witte AV, Winkler A, Grittner U, Rujescu D, Flöel A. Higher glucose levels associated with lower memory and reduced hippocampal microstructure. Neurology. 2013;81(20):1746-52.

48. Crane PK, Walker R, Hubbard RA, et al. Glucose levels and risk of dementia. N Engl J Med. 2013;369(6):540-8.

49. Millichap JG, Yee MM. The diet factor in attention-deficit/hyperactivity disorder. Pediatrics. 2012;129(2):330-7.

50. Johnson RJ, Gold MS, Johnson DR, et al. Attention-deficit/hyperactivity disorder: is it time to reappraise the role of sugar consumption?. Postgrad Med. 2011;123(5):39-49.

51. Kanoski SE, Davidson TL. Western diet consumption and cognitive impairment: links to hippocampal dysfunction and obesity. Physiol Behav. 2011;103(1):59-68.

52. Crescenzo R, Bianco F, Coppola P, et al. Fructose supplementation worsens the deleterious effects of short-term high-fat feeding on hepatic steatosis and lipid metabolism in adult rats. Exp Physiol. 2014;99(9):1203-13.

53. Lenoir M, Serre F, Cantin L, Ahmed SH. Intense sweetness surpasses cocaine reward. PLoS ONE. 2007;2(8):e698.

54. Schmidt LA. New unsweetened truths about sugar. JAMA Intern Med. 2014;174(4):525-6.

55. Ruff JS, Suchy AK, Hugentobler SA, et al. Human-relevant levels of added sugar consumption increase female mortality and lower male fitness in mice. Nat Commun. 2013;4:2245.

56. Blaisdell AP, Lau YL, Telminova E, et al. Food quality and motivation: a refined low-fat diet induces obesity and impairs performance on a progressive ratio schedule of instrumental lever pressing in rats. Physiol Behav. 2014;128:220-5.

57. Myers MG, Cowley MA, Münzberg H. Mechanisms of leptin action and leptin resistance. Annu Rev Physiol. 2008;70:537-56.

58. Larsson H, Ahrén B. Glucose intolerance is predicted by low insulin secretion and high glucagon secretion: outcome of a prospective study in postmenopausal Caucasian women. Diabetologia. 2000;43(2):194-202.

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