Tag Archives: diabetes

The increased abdominal fat that many women develop after menopause due to hormonal changes and the skin disorder psoriasis are divergent health concerns that would seem to have little in common. But two recently published studies found a common ground – chronic inflammation.

More importantly, the anti-inflammatory properties of the Paleo Diet were found to improve both [1, 2].

After menopause, women have a tendency to “redistribute” fat around the abdomen which increases the risk for metabolic disorders such as diabetes and cardiovascular disease [3, 4]. In the first study, which was published in Obesity, researchers placed 70 obese postmenopausal women on either a Paleo Diet or a “prudent control diet” (CD) for 24 months. The CD diet, also called the Diabetes diet, is recommended for people with diabetes or insulin resistance; it includes higher vegetable, fiber, whole-grain, and fruit consumption along with lower fat intake [5].

Women on both diets were able to reduce adipose tissue and improve their inflammatory markers. However, improvements in the Paleo Diet group were greater. Women in this group were also the only ones to lower two key inflammatory markers – MCP-1 and plasma C-reactive protein (figure 3). This led the researchers to suggest that the Paleo Diet produced “a more pronounced overall decrease in low-grade inflammation compared to the CD group.”

It’s worth pointing out that subjects on the Diabetes diet reported greater difficulty adhering to the diet and had a higher dropout rate [2]. The Diabetes diet differed from the Paleo Diet in only two major ways – unlike the Paleo Diet, it recommended whole grain consumption and it recommended reduced fat intake. The researchers pointed to the fatty acid profile of the Paleo diet as a potential reason for the better inflammatory profile.

The second study, out of the Department of Dermatology at the University of California, took a different tact. The researchers surveyed 1206 psoriasis patients through the National Psoriasis Foundation to determine specific foods and diets that may influence their condition [1].

Tables 4 and 5 below shows reported trigger foods, foods that may have improved symptoms, and diets that patients said helped their condition:

What is fascinating is that with only a few exceptions, the foods that worsened or helped the condition aligned very closely with Paleo Diet recommendations. Likewise, 69 percent of respondents who tried the Paleo Diet found it helped their condition. Many of the other diets on the list, including the Pangano diet (increased fruit and vegetables/decreased nightshades and junk food) have Paleo-like characteristics. In fact, the study reported that compared to controls in the large-scale NHANES 2009-2010 dataset, “respondents reported less daily intake of sugar, whole grain fiber, dairy products, and calcium.” A quote that could be used to describe someone starting a Paleo Diet.

A theme of the two studies was that chronic inflammation was considered both a cause and a major risk factor for co-morbidities. In fact, psoriasis is being increasingly recognized as a systemic inflammatory condition that is associated with a variety of cardiac and metabolic diseases [6-8].

Researchers of the psoriasis study proposed that a poor diet may change the microbiome and digestion leading to poor immune function. They specifically pointed to the consumption of simple carbohydrates (sugar) and nightshades.

Likewise, authors of the postmenopausal study discussed past research showing that fat deposits can increase inflammation and contribute to metabolic dysfunction.  But weight-loss alone did not resolve the inflammation in some of this past research [2, 9]. The authors pointed to the better fatty acid profile of the Paleo Diet – focused on monounsaturated and polyunsaturated fatty acids over saturated fats – as a potential explanation for the better inflammatory profile after both six and 24 months [2].

Perhaps most telling is that after including many diets in their survey, the authors of the psoriasis study specifically called out the Paleo Diet. They wrote the diet “can reduce the risk of cardiometabolic comorbidities in psoriasis which are a predominant cause of reduced life expectancy and an important aspect of disease management” [1].

 

References

  1. Afifi, L., et al., Dietary Behaviors in Psoriasis: Patient-Reported Outcomes from a U.S. National Survey. Dermatol Ther (Heidelb), 2017. 7(2): p. 227-242.
  2. Blomquist, C., et al., Attenuated Low-Grade Inflammation Following Long-Term Dietary Intervention in Postmenopausal Women with Obesity. Obesity (Silver Spring), 2017. 25(5): p. 892-900.
  3. Gaspard, U., Hyperinsulinaemia, a key factor of the metabolic syndrome in postmenopausal women. Maturitas, 2009. 62(4): p. 362-5.
  4. Kranendonk, M.E., et al., Inflammatory characteristics of distinct abdominal adipose tissue depots relate differently to metabolic risk factors for cardiovascular disease: distinct fat depots and vascular risk factors. Atherosclerosis, 2015. 239(2): p. 419-27.
  5. Jonsson, T., et al., Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study. Cardiovasc Diabetol, 2009. 8: p. 35.
  6. Takeshita, J., et al., Psoriasis and comorbid diseases: Implications for management. J Am Acad Dermatol, 2017. 76(3): p. 393-403.
  7. Coimbra, S., et al., Systemic inflammation and proinflammatory interleukin-17 signalling persist at the end of therapy in patients with metabolic syndrome and psoriasis, reducing the length of remission. Br J Dermatol, 2016. 174(2): p. 414-6.
  8. Reich, K., The concept of psoriasis as a systemic inflammation: implications for disease management. J Eur Acad Dermatol Venereol, 2012. 26 Suppl 2: p. 3-11.
  9. Magkos, F., et al., Effects of Moderate and Subsequent Progressive Weight Loss on Metabolic Function and Adipose Tissue Biology in Humans with Obesity. Cell Metab, 2016. 23(4): p. 591-601.

 

You Are When You Eat | The Paleo DietRenowned evolutionary biologist Theodosius Dobzhansky said “nothing in biology makes sense except in the light of evolution.”[1] Throughout our evolution, we have lived in daily cycles of light and dark. These cycles have led to the development of natural circadian rhythms that impact many aspects of our health and vitality.

Circadian rhythms are triggered by the bright light stimulus in the morning and darkness in the evening. The hypothalamus area of the brain – specifically the suprachiasmatic nucleus (SCN) – is the master regulator, synchronising the body’s circadian clock based on information it receives from photoreceptors in the eyes in response to light [2]. The impacts of circadian rhythm are wide-reaching;

Disruption of the circadian clock can have a big impact on the body’s ability to function optimally. Jet lag – that feeling of fatigue, disorientation and mental sluggishness after travelling through multiple time zones – is a classic example [3-6]

Unfortunately, the negative effects can be more serious than just a little sluggishness. The incidence of workplace injuries and traffic accidents increases when the clocks move forward in the spring [7, 8].

Experts are just starting to uncover the many potential ripple effects of circadian dysfunction on our health: from heart disease [9, 10] and cognitive decline [11, 12], to blood sugar dysfunction and increased diabetes risk [13]; to changes in body-fat storage and breakdown [14-16], reduced liver, pancreatic, and cardiac and skeletal muscle function [17-25].

 

Late-Night Eating & Circadian Rhythm

Today, there are many ancestral circadian mismatches with modern life. Late-night eating may be one of the most glaring incongruous elements. We’re in the midst of a weight gain and obesity epidemic with 70% of adults over the age of 20 in America are overweight or obese and 50% of the population now classified as pre-diabetic or diabetic.[26-27] A body of research is appearing showing that late-night eating may be a significant contributor [27-29].

A 2014 study of overweight and obese diabetics investigated the impacts of a late-night snack on their requirement for supplemental insulin. Subjects were divided into carbohydrate, whey protein, casein, or placebo groups. All groups required significantly more insulin after all late-night snacks, though the protein snack did compare more favourably to the carbohydrate snack [30]. These results confirmed a 2003 study on late-night eating and diabetics. This earlier study showed consistently higher blood sugar levels when snacking late at night, regardless of the macronutrient composition of the meal [31].

Why is late-night eating potentially so bad for us? One possible explanation is our circadian rhythms may prevent us from effectively managing food eaten later at night. There is evidence showing the thermic effect of food is reduced in the evening, due to the circadian regulation of insulin sensitivity, meaning your blood sugar and insulin response to carbs at night is more exaggerated than during the day [32].

 

Solutions for A Modern Circadian Mismatch

Our Paleolithic ancestors would’ve rarely (if ever) eaten after dark. Yet in today’s modern world, the light emitted from iPads, laptops, TVs and mobile devices make it far easier to stay up later at night. This presents a circadian mismatch to our evolutionary biological clocks which translates into more opportunity (and likelihood) to eat. If you’re struggling with weight gain, chronically high blood sugar, pre-diabetes or diabetes then shifting your focus to “meal-timing” can be a simple and highly effective part of the solution to improving your health.

To support a healthy circadian clock, implement the following “meal-timing” strategy:

  • Avoid eating late at night – consider abstaining from all food after 6:00 or 7:00 pm or ditch your late-night snacking while on the couch and try sipping on a herbal tea instead
  • Go for an evening walk, do some light stretching, or take a relaxing bath.

 

In my experience as a clinician, I see major progress in clients who decide to abstain from food in the evening. Once they get through the first few nights, the cravings plummet and it becomes much easier to ingrain the new habit.

Supporting your circadian clock with meal-timing strategies can be an “easy win” to restoring health and vitality [33]. It’s simple and highly effective. 

References

1. Gerhart-Hines, Z. and M.A. Lazar, Circadian metabolism in the light of evolution. Endocr Rev, 2015. 36(3): p. 289-304.
2. Guler, A.D., et al., Melanopsin cells are the principal conduits for rod-cone input to non-image-forming vision. Nature, 2008. 453(7191): p. 102-5.
3. Tapp, W.N. and B.H. Natelson, Circadian rhythms and patterns of performance before and after simulated jet lag. Am J Physiol, 1989. 257(4 Pt 2): p. R796-803.
4. Leloup, J.C. and A. Goldbeter, Critical phase shifts slow down circadian clock recovery: implications for jet lag. J Theor Biol, 2013. 333: p. 47-57.
5. Comperatore, C.A. and G.P. Krueger, Circadian rhythm desynchronosis, jet lag, shift lag, and coping strategies. Occup Med, 1990. 5(2): p. 323-41.
6. Vosko, A.M., C.S. Colwell, and A.Y. Avidan, Jet lag syndrome: circadian organization, pathophysiology, and management strategies. Nat Sci Sleep, 2010. 2: p. 187-98.
7. Coren, S., Daylight savings time and traffic accidents. N Engl J Med, 1996. 334(14): p. 924.
8. Varughese, J. and R.P. Allen, Fatal accidents following changes in daylight savings time: the American experience. Sleep Medicine, 2001. 2(1): p. 31-36.
9. Maemura, K., [Circadian rhythm and ischemic heart disease]. Nihon Rinsho, 2013. 71(12): p. 2124-9.
10. Marchant, B., Circadian rhythms and ischaemic heart disease. Br J Hosp Med, 1996. 55(3): p. 139-43.
11. Gehrman, P., et al., The relationship between dementia severity and rest/activity circadian rhythms. Neuropsychiatr Dis Treat, 2005. 1(2): p. 155-63.
12. Ancoli-Israel, S., et al., Variations in circadian rhythms of activity, sleep, and light exposure related to dementia in nursing-home patients. Sleep, 1997. 20(1): p. 18-23.
13. Afsar, B., Disruption of circadian blood pressure, heart rate and the impact on glycemic control in type 1 diabetes. Diabetes Metab Syndr, 2015. 9(4): p. 359-63.
14. Cincotta, A.H., et al., Circadian neuroendocrine role in age-related changes in body fat stores and insulin sensitivity of the male Sprague-Dawley rat. Chronobiol Int, 1993. 10(4): p. 244-58.
15. Wang, L. and S. Liangpunsakul, Circadian clock control of hepatic lipid metabolism: role of small heterodimer partner (Shp). J Investig Med, 2016. 64(7): p. 1158-61.
16. Gnocchi, D., et al., Lipids around the Clock: Focus on Circadian Rhythms and Lipid Metabolism. Biology (Basel), 2015. 4(1): p. 104-32.
17. Gerhart Hines, Z., et al., The nuclear receptor Rev-erbα controls circadian thermogenic plasticity. Nature, 2013. 503(7476): p. 410-413.
18. Bookout, A.L., et al., FGF21 regulates metabolism and circadian behavior by acting on the nervous system. Nat Med, 2013. 19(9): p. 1147-52.
19. Shostak, A., J. Meyer-Kovac, and H. Oster, Circadian regulation of lipid mobilization in white adipose tissues. Diabetes, 2013. 62(7): p. 2195-203.
20. Boden, G., et al., Evidence for a circadian rhythm of insulin secretion. Am J Physiol, 1996. 271(2 Pt 1): p. E246-52.
21. Degaute, J.P., et al., Quantitative analysis of the 24-hour blood pressure and heart rate patterns in young men. Hypertension, 1991. 18(2): p. 199-210.
22. Zambon, A.C., et al., Time- and exercise-dependent gene regulation in human skeletal muscle. Genome Biol, 2003. 4(10): p. R61.
23. Carter, R., et al., Non-alcoholic fatty pancreas disease pathogenesis: a role for developmental programming and altered circadian rhythms. PLoS One, 2014. 9(3): p. e89505.
24. Kettner, N.M., et al., Circadian Homeostasis of Liver Metabolism Suppresses Hepatocarcinogenesis. Cancer Cell, 2016. 30(6): p. 909-924.
25. Zhou, D., et al., Evolving roles of circadian rhythms in liver homeostasis and pathology. Oncotarget, 2016. 7(8): p. 8625-39.
26. CDC: Center for Disease Control & Prevention. Retrieved from – https://www.cdc.gov/nchs/fastats/obesity-overweight.htm
27. Menke, A., et al., Prevalence of and Trends in Diabetes Among Adults in the United States, 1988-2012. JAMA, 2015. 314(10): p. 1021-9.
28. Cleator, J., et al., Night eating syndrome: implications for severe obesity. Nutr Diabetes, 2012. 2: p. e44.
29. Gallant, A.R., J. Lundgren, and V. Drapeau, The night-eating syndrome and obesity. Obes Rev, 2012. 13(6): p. 528-36.
30. Colles, S.L., J.B. Dixon, and P.E. O’Brien, Night eating syndrome and nocturnal snacking: association with obesity, binge eating and psychological distress. International Journal of Obesity, 2007. 31(11): p. 1722-1730.
31. Kinsey, A.W., et al., Influence of night-time protein and carbohydrate intake on appetite and cardiometabolic risk in sedentary overweight and obese women. Br J Nutr, 2014. 112(3): p. 320-7.
32. Kalergis, M., et al., Impact of bedtime snack composition on prevention of nocturnal hypoglycemia in adults with type 1 diabetes undergoing intensive insulin management using lispro insulin before meals: a randomized, placebo-controlled, crossover trial. Diabetes Care, 2003. 26(1): p. 9-15.
33. Bo, S., et al., Is the timing of caloric intake associated with variation in diet-induced thermogenesis and in the metabolic pattern? A randomized cross-over study. Int J Obes (Lond), 2015. 39(12): p. 1689-95.
34. Mattson, M.P., et al., Meal frequency and timing in health and disease. Proc Natl Acad Sci U S A, 2014. 111(47): p. 16647-53.

 

 

 

Arthritis | The Paleo Diet
It’s often times a diagnosis of cancer, diabetes, multiple sclerosis (MS), or another disease which proves to be the pivot point for individuals to make significant changes to their eating and exercise habits. Whether the change stems from obvious reasons, like losing weight because obesity has been the causal agent for developing type 2 diabetes, or per the advice of their physicians to cut out gluten and dairy following an autoimmune diagnosis, these steps are reactive versus proactive.

If we were to exercise daily and eat foods that set us up for health, rather than sickness in the first place, would we be able to determine our destiny? Clearly, we can take preventative measures to lower our risk for obesity and type 2 diabetes by leading an active lifestyle, veering away from the typical, highly refined Standard American Diet (SAD), and implementing a Paleo diet.

But what about minimizing our risk for autoimmune diseases like rheumatoid arthritis (RA) with diet? Science suggests it’s looking quite promising.

Two studies presented at the American College of Rheumatology Annual Meeting in San Francisco show diet can significantly lower our chance for developing RA.1 RA is an autoimmune disease where the body’s immune system mistakenly attacks the joints, creating inflammation that causes the tissue lining of the joints to thicken, resulting in swelling and pain in and around the joint.2

For those following a Paleo regime, inflammation is hardly a foreign term, and you’re familiar with the notion that avoiding certain foods can help offset symptoms dramatically.3 But how does this scientifically factor into RA treatment or minimize risk altogether?

In the first study, researchers found “typical Western diets high in red meat, processed meat, refined grains, fried food, high-fat dairy, and sweets can increase a person’s risk of developing RA in comparison to Prudent diets (a diet low in total fat, saturated fat, trans fat, cholesterol and sodium which aid in lowering cholesterol and triglyceride blood levels and blood pressure)4 made mostly of fruit, vegetables, legumes, whole grains, poultry and fish.”

The second study found that “following the Dietary Guidelines for Americans can also lower one’s chances of developing the disease because they provide authoritative advice about consuming fewer calories, making informed food choices, and being physically active to attain and maintain a healthy weight, reduce risk of chronic disease, and promote overall health.”

How was this measured? By using the Alternate Healthy Eating Index, created to measure how well participants followed the Dietary Guidelines for Americans, researchers observed associations of the subjects’ diets and their likelihood of developing RA. The researchers noted those who best adhered to the Dietary Guidelines for Americans had a 33% reduced risk of developing RA when compared to those who did not follow the guidelines as closely. And, just as in the first study, the researchers noted that body mass index may be a modest intermediate factor linking diet and risk of RA.

A few questions arise. If the sole means of data collection was to review and analyze what the participants reported to eat, how accurate can the findings really be? Were findings measured upon accountability and how can we be sure participants didn’t take the liberty of “cleaning up” their food log entries, energy levels, or sleep patterns?

A colleague of mine joked in reference to a new client who’d touted the benefits of a new fad diet, “any eating plan is going to ‘work’ in comparison to what one did before, because before, they didn’t have one!”

Researchers state “the single-nutrient approach may be inadequate for taking into account complicated interactions among nutrients, and high levels of inter-correlation makes it difficult to examine their separate effects.” So grouping all foods into  one lump category (recall the list: “diets high in red meat, processed meat, refined grains, fried food, high-fat dairy, and sweets”) doesn’t differentiate between high quality, grass fed meats, from the corn-fed beef. Nor does the “diet made mostly of fruit, vegetables, legumes, whole grains, poultry and fish” distinguish the effects of antinutrients contained in legumes and grains,5 or the glycemic load of eating too much fruit.6

While I do agree that a healthy diet may prevent RA development, it’s a matter of deciphering what actually comprises a healthy diet. And from everything I’ve read and seen over the past decade, I certainly don’t need further convincing that a real Paleo diet can be the remedy to addressing a diagnosis of RA. By eating a diet rich in alkaline, anti-inflammatory foods, the body is armed with its best defenses and most equipped to stay diseases free for a healthy, long life!

References

1. “Diet May Determine Your Risk for Rheumatoid Arthritis.” ScienceDaily. ScienceDaily, n.d. Web. 16 Nov. 2015

2. “What Is Rheumatoid Arthritis?” What Is Rheumatoid Arthritis? Arthritis Foundation, n.d. Web. 16 Nov. 2015

3. Wahls, Terry L., and Eve Adamson. The Wahls Protocol: How I Beat Progressive MS Using Paleo Principles and Functional Medicine. N.p.: n.p., n.d. Print

4. “What Is the Prudent Diet?” LIVESTRONG.COM. LIVESTRONG.COM, 30 June 2015. Web. 16 Nov. 2015

5. Stephenson, Nell. “Antinutrients, the Antithesis of True Paleo | The Paleo Diet.” The Paleo Diet. The Paleo Diet, 10 Mar. 2015. Web. 16 Nov. 2015

6. “Glycemic Index and Glycemic Load | The Paleo Diet | Dr. Loren Cordain.” The Paleo Diet. N.p., n.d. Web. 16 Nov. 2015

Diabetes | The Paleo Diet

The sea of candies and chocolates will continue to flood supermarket shelves from now through Valentine’s Day. Consumers often think, “It is only one day of the year, why not indulge?” The truth is it is not just one day of the year, but rather one of many days, including all holidays, birthdays, and anniversaries, that center around sweets and treats. Today’s food environments exploit people’s biological, psychological, social, and economic vulnerabilities, encouraging them to eat unhealthy foods.1 The obesity and type two diabetes pandemic prevails, with 23.6 million people in the United States, who struggle with Type 2 diabetes (non-insulin-dependent diabetes mellitus.2 A lackadaisical approach to nutrition continues to prove unsuccessful in achieving one’s best health.

We are embarking on the season of weight gain.3  On average, weight gain during the 6-weeks from Thanksgiving through New Year averages only 0.37 kg. However, weight gain is greater among individuals who are overweight or obese, with 14% gaining over 2.3 kg during the holidays.4 In addition, weight gain during the holiday season accounts for 51% of annual weight gain among individuals.5 It’s no wonder that so many people hope to lose their excess weight in the New Year, which turns out to be an ill-fated resolution.6 Be prudent this year and avoid adding weight during the holidays to maintain your long-term health and a smaller waistline.

The old school of thought many parents subscribed to suggested kids should be allowed to eat whatever they want because they don’t need to worry about their weight. Children are in fact not immune to the destructive nature of diets high in refined sugars and excess carbohydrates. Sadly, during the past two decades, the prevalence of obesity in children has risen greatly worldwide.7 Childhood obesity has contributed to an increased incidence of Type 2 diabetes mellitus and metabolic syndrome among children.8 Enjoying a few pieces of candy on Halloween isn’t the most detrimental to a child’s body, but eating a few pieces each day until it runs out won’t instill an understanding of the adverse effects of sugar and chemicals like high fructose corn syrup in your child.

We are constantly assaulted with processed, refined sugar containing foods from the fresh baked pastries lurking in the display while you order coffee to the snacks offered at your child’s soccer match. The Paleo Diet permits the 85:15 rule, which provides flexibility to make choices that work best for your modern lifestyle and palette. The challenge is how to limit yourself and your children to three non-Paleo compliant meals per week during the holiday season.

Practice Mindfulness

It’s easy to get distracted at holiday parties, leading many to make unhealthful food choices and indulge in too much food and alcohol. Research indicates mindful eating may be an effective approach for weight management and glycemic control.9 Make a conscious choice for what goes into your mouth – those chocolates won’t magically appear in your stomach. Take a few deep breaths listen to your body to recognize when you are about 80% full to avoid overeating.

Be Accountable

The frosted Halloween cupcakes and sugar cookies your co-workers brought to the breakroom sure are tempting. But how do you balance them with last night’s pasta dinner and tomorrow’s pizza and pumpkin beer party? Be honest with yourself about the choices you make and plan for what lies in the week ahead. Hold yourself accountable and if you need to deviate from a strict Paleo path, stay within three non-compliant meals per week. Keep in mind that you are faced daily with a slippery slope of options you may regret choosing.

Indulge Responsibly

The foundation of the Paleo diet is centered on consuming whole, real foods. However, it is not about restriction and suffering. During the holidays and special occasions you can enjoy your celebratory treats, especially when you stick to the 85:15 rule. Seek out the highest quality ingredients; preferably indulging in a Paleo-friendly, homemade sweet, that has the lowest glycemic load.

Cheers to your health as we embark upon the holiday season!

References

1. Batch, Jennifer A., and Louise A. Baur. “Management and prevention of obesity and its complications in children and adolescents.” The Lancet (2015).

2. Bliss, Amanda K., and Sanjay Gupta. “High fructose corn syrup.” Annals of Clinical Psychiatry 23.3 (2011): 228-229.

3. Bliss, Amanda K., and Sanjay Gupta. “High fructose corn syrup.” Annals of Clinical Psychiatry 23.3 (2011): 228-229.

4. Roberts, Susan B. “Holiday weight gain: fact or fiction?.” Nutrition reviews 58.12 (2000): 378-379.

5. Roberts, Susan B. “Holiday weight gain: fact or fiction?.” Nutrition reviews 58.12 (2000): 378-379.

6. Kassirer, Jerome P., and Marcia Angell. “Losing weight—an ill-fated New Year’s resolution.” New England Journal of Medicine 338.1 (1998): 52-54.

7. Ebbeling, Cara B., Dorota B. Pawlak, and David S. Ludwig. “Childhood obesity: public-health crisis, common sense cure.” The lancet 360.9331 (2002): 473-482.

8. Boney, Charlotte M., et al. “Metabolic syndrome in childhood: association with birth weight, maternal obesity, and gestational diabetes mellitus.” Pediatrics115.3 (2005): e290-e296.

9. Miller, Carla K., et al. “Comparative effectiveness of a mindful eating intervention to a diabetes self-management intervention among adults with type 2 diabetes: a pilot study.” Journal of the Academy of Nutrition and Dietetics112.11 (2012): 1835-1842.

 

Wheat | The Paleo Diet

Click Here to Start The Wheat Series from the Beginning!

It’s one of the most commonly used analogies in existence and it’s about a game that few want to play. A revolver is loaded with a single bullet. The hapless players take turns putting the gun to their heads and pulling the trigger. The analogy is often used to make a point about the high stakes of luck. Eventually someone gets a loaded chamber and pays the ultimate price.

There is a second side to the analogy, however that is frequently overlooked. Regardless of whether you have extremely good or bad luck, you first have to willingly pull the trigger.

We’ve known for a while that most chronic diseases such as cancer, autoimmune disease, and heart disease have a genetic component.1 – 10 Genetics are the loaded bullet that we sadly have no control over.

For celiac disease, the “bullet” is a genetic variant in HLA-DQ.11, 12 However, a large number of people with the variant never express the disease. Further, those who do develop the condition usually resolve it by removing gluten from their diet.13, 14 In other words, the bullet might be in the chamber, but often the gun is never fired.

Environmental factors ultimately pull the trigger.

In the first four parts of this series we talked about how wheat (and to a degree other gluten-containing grains such as rye and barley) is highly effective at dysregulating the immune system of our guts. In fact, it’s the only food we know of that affects all three pathways of dysregulation:

  1. Opening up the tight junctions of our gut (Part 2)
  2. Excess and chronic bacterial stress (Part 3)
  3. Harmful dietary antigens (Part 4)

In this final part, we’ll talk about how the resulting chronic inflammation leads to a pathological state that essentially “pulls the trigger” on disease. But just as importantly, we’ll discuss how there has to be a bullet in the chamber first. The genetic susceptibility has to be there.

It’s Not So Easy to Pull the Trigger

Our genetics have not changed in the last 100 years. Yet, chronic disease such as autoimmune conditions and cancer have risen dramatically. Faster than rate of population growth.

In other words, going with our analogy, the number of bullets hasn’t changed, but for some reason the trigger is getting pulled a lot more often. Which is surprising considering no one wants to pull it.

Imagine for a minute what it takes for a person to get to the point where they will voluntarily put a gun to their heads. None of us handed a revolver and told we have a five in six chance would exclaim “sure, those sound like good odds.”

From what little we understand, Russian Roulette players essentially have to build up to it, engaging in other risky behavior, and slowly desensitizing themselves. As it turns out, a lot of behavior altering substances help too.15

Likewise, our bodies have a lot of defenses to avoid ever pulling the trigger on disease, even when the bullet is there.

So, while we hopefully made the case in the previous four parts that wheat is not good for us, one piece of bread isn’t going to give you cancer. Despite all the dysregulation of our immune system caused by wheat, it still takes a lot to build up to the point of disease.16, 17

Building Up to It…

In fact, as we discussed in Part 1, all the inflammatory processes activated by wheat are both normal and necessary processes designed to deal with regular bacterial stress. Mice breed without these inflammatory responses suffer severe tissue damage and wasting disease.18, 19

Even the temporary shift in the balance between two critical immune cells – Tregs and TH17 cells – is a natural response to this inflammation. Let’s explore these two cells a little more.

In a healthy state, Tregs dominate. Their role is to suppress the immune system20 – 24 preventing it from damaging our own bodies. People unfortunate enough to have dysfunctioning Tregs suffer severe autoimmune diseas.25

TH17, on the other hand, have a murkier and less benign role. Only discovered in 2006, they solved an important puzzle for researchers. Scientists knew that T cells were involved in many conditions but none of the known T cells at the time fully explained disease development.26

With the discovery of TH17, they had their answer.26, 27

Proving to be highly inflammatory cells, TH17 effectively explained the damage in a multitude of chronic diseases16, 28 – 31 such as asthma,32 heart disease,33, 34 and most autoimmune conditions30, 35 including celiac disease,36, 37 type I diabetes,38, 39 Crohn’s disease,40, 41 rheumatoid arthritis,31, 42 and multiple sclerosis.43

A question remained, however: Why would our bodies produce such a self-destructive cell?

The reason lies in their role. It was believed that TH17 cells evolved to deal with harmful bacterial infections and effectively handling the invasion means doing some damage to our own bodies.19, 44, 45

This damage seems to be acceptable to our bodies and even part of a healthy immune response as long as one essential condition is met – the shift towards TH17 dominance is short-lived and ends. Once an infection is dealt with and the resulting inflammation quiets down, TH17 cells die off and Tregs return to dominating our immune system.24, 46

So what happens if the inflammation doesn’t end?

According to one emerging theory, the result is an out-of-control pathogenic form of the TH17 cell.10, 23, 24 In other words, if normal bacterial stress causes a little risky behavior by inciting beneficial TH17, chronic inflammation causes the buildup that leads to the pathogenic TH17 putting the gun to our heads and pulling the trigger.

Chronic Inflammation – Putting the Gun to our Heads

The diagram below shows the different responses between normal and chronic inflammation.30

Chronic Inflammation | The Paleo Diet

Kamada, N., et al., Role of the gut microbiota in immunity and inflammatory disease. Nat Rev Immunol, 2013. 13(5): p. 321-35.

Let’s explore this destructive shift a little more closely. Bear with me – this gets technical.

Under normal inflammation, the number of Treg cells increase alongside the TH17 cells allowing Tregs to continue controlling TH17’s destructive potential and maintain some balance.30, 47

But in chronic inflammation, a dramatic shift occurs. More and more innate immune cells such as dendritic cells and CD14+ macrophages (explained in Part 3) are activated or recruited to the digestive immune system.17, 28, 48, 49

Over time, these cells change the chemical milieu of the gut to one that is high inflammatory. Il-23 is released which both promotes the destructive form of TH17 and inhibits Tregs.27, 47, 50, 51 Newly recruited CD14+ macrophages also suppress Tregs.52

In fact, it gets worse. The chronic inflammation causes Tregs to “flip” and start behaving like TH17 contributing to the inflammation instead of preventing it.47, 52, 53

The result is that chronic inflammation breaks the Treg/ TH17 balance. Treg lose their ability to control the immune system and TH17, now uninhibited, take on a more destructive form traveling from the gut45 throughout the body pulling the trigger:30

Gut Microbiota | The Paleo Diet

Kamada, N., et al., Role of the gut microbiota in immunity and inflammatory disease. Nat Rev Immunol, 2013. 13(5): p. 321-35.

This is the point where you may want to remind me that this is the fifth part in a series about wheat. Where does wheat come into all of this?

Wheat, as we’ve shown in the previous parts, creates the chronic inflammation that sets off this cascade. In fact, in one study of mice, that tested many dietary antigens, wheat was the only one that could activate inflammatory TH17 cells.54

Put simply, wheat sets in motion the build-up that causes our bodies to ultimately put the gun to our heads and pull the trigger.

Why Aren’t More Guns Going Off?

The very sobering thought is that the chronic inflammation, which wheat is so effective at creating (in fact it took three parts to explain all the ways wheat can cause it,) appears to be common to everyone.17, 20, 55

So why aren’t we all sick?

This is where we need to flip things around and remember there are two parts to the Russian Roulette analogy. Wheat causes our immune system to put the gun to our heads and pull the trigger, but there still needs to be a bullet in the chamber. The genetic susceptibility has to be there.

Sure enough, a genetic susceptibility to chronic inflammation has been identified in many conditions. Often taking the form of a hyper-sensitivity to inflammation or a failure of the Treg system to suppress it.

CD14+ macrophages appear to be particularly potent in rheumatoid arthritis.56 Celiacs are hyper-sensitive to Il-15 – one of the key proteins used by wheat to produce inflammation.3 Much higher levels of inflammatory CD14+ macrophages exist in the guts of people with Irritable Bowel Disease (IBD).57 IBD sufferers also appear to be more responsive to IL-23.29 In type II diabetes, the immune cells that destroy the pancreas exist in healthy and afflicted subjects, but Treg cells appear to be less functional in diabetics.1, 2

Making a further case for the importance of genetics, people with one of these conditions are often more susceptible to the others.58-63

Still, There Are a Lot of Bullets…

The need for a “genetic bullet” in order for a disease to materialize has led many to breathe a sigh of relief. An example is the recent Washington Post article “For many, gluten isn’t the villain it gets cracked up to be.”

But the fact is that there are many chronic disease and they are all on the rise. A lot more guns are actually going off now.

Recent research is showing more and more that inappropriate chronic inflammation is at the heart of almost every “disease of civilization” including cancer,64, 65 metabolic disorders,66, 67 Alzheimer’s disease,68 most autoimmune conditions,30, 35 and heart disease where aberrant macrophages (immune cells) form the atherosclerotic plaques.69, 70

That amounts to a whole lot of genetic bullets.

While the research is still small, several of these conditions including celiac’s disease, diabetes, and     IBD are improved when wheat is removed from the diet.13, 14, 71 – 73

So feel free to do as the Washington Post article says, eat your bread, and trust your luck that the chamber is empty. But with that many potential bullets in the revolver and chronic inflammation – so effectively produced by wheat – ready to pull the trigger, I’m personally going to avoid putting the gun to my head.

References

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Keep It Simple: Doctors Say Sound Nutrition Should Replace Calorie-Counting and Pharmacotherapy | The Paleo Diet

When we think about enormously complex problems, like the social and economic burdens of chronic degenerative diseases, we sometimes presume that the solutions must also be complex. Complex problems, however, often have simple, straightforward solutions.

Imagine you’re an astronaut living on a space station powered by enormous solar-powered generators. Your worst-case scenario would be for those generators to break down and for you to be missing the tools required to fix them. In 2012, astronauts aboard the International Space Station found themselves in precisely this situation. One of the station’s power distributors went down, but when the astronauts ventured outside to assess the situation, they discovered that metal shaving had accumulated around several critical bolts.

NASA had equipped them with highly technical tools, but none of their tools could remove the shavings, and if the shavings remained in place, the generator could not be repaired. After a thwarted 8-hour repair attempt, the astronauts went back inside to brainstorm solutions. Finally, they improvised a makeshift tool consisting of an allen wrench and a toothbrush. It worked – a $3 toothbrush saved a $100 billion space station.1

Could the same graceful simplicity be applied to the cardiovascular disease and diabetes crises? The American Heart Association estimates that in 2011 the annual cost of cardiovascular disease and stroke in the US was $320 billion.2 Similarly, the cost of diabetes increased over 40% from 2007 to 2012 and now costs at least $245 billion annually in the US.3

In a new editorial published in Open Heart, Doctors Aseem Malhotra, James DiNicolantonio, and Simon Capewell argue that complex, expensive, and ultimately ineffective “solutions” are exacerbating the heart disease and diabetes crises while simple, relatively inexpensive, effective solutions are being overlooked.

Specifically, they argue, “An exaggerated belief in the (modest) benefits of pharmacotherapy, aggressively reinforced by commercial vested interests, can often mislead patients and doctors, and promotes overtreatment in chronic disease management, and may even distract from and undermine the benefits of simple lifestyle interventions.4

In short, our approach to chronic diseases is one of treating symptoms rather than addressing underlying disease causes. Likewise, our approach to food is one focusing on calorie-counting and energy balance rather than sound nutrition. The diet industry generates $58 billion annually the US but long-term follow-up studies show the vast majority of dieters regain the weight they lost during diet regimens.5

So what is the solution? In their Open Heart editorial, the doctors point to numerous randomized controlled trials in which simple dietary interventions resulted in dramatic disease risk reductions. In the DART trial, for example, the consumption of fatty fish among survivors of myocardial infarction resulted in a significant 29% reduction in all-cause mortality compared to control patients. Moreover, in an Italian study, the consumption of 1 daily gram of omega-3 fatty acids led to clinically important and statistically significant reductions in all-cause and cardiovascular disease mortality.

Higher-fat diets inclusive of nuts, olive oil, oily fish, as well as plenty of vegetables, consistently outperform the antiquated low-fat, high-carbohydrate diet recommended by the American Heart Association with respect to attenuating inflammation, atherosclerosis, and thrombosis. In their editorial, the doctors specifically endorse “a high-fat Mediterranean-type diet and lifestyle.” A high-fat Mediterranean-type diet has remarkable overlaps with the Paleo diet, as both emphasize sound nutritional principles and a widely varied, yet balanced diet. Our modern health problems are complex, but the solutions can be as simple as respecting and embracing the dietary traditions and nutritional wisdom of our ancestors.

 

REFERENCES

[1] Garber, M. (September 6, 2012). “Behold, the Toothbrush That Just Saved the International Space Station,” The Atlantic.

[2] Mozaffarian, D., et al. (December 17, 2014). “Heart Disease and Stroke Statistics – 2015 Update,” Circulation 2015, 131.

[3] American Diabetes Association. (April 2013). “Economic costs of diabetes in the U.S. in 2012.” Diabetes Care, 36(4).

[4] Malhortra, A., et al. (August 26, 2015). “It is time to stop counting calories, and time instead to promote dietary changes that substantially and rapidly reduce cardiovascular morbidity and mortality,” Open Heart, 2(1).

[5] Strohacker, K., et al. (January 2010). “Influence of obesity, physical inactivity, and weight cycling on chronic inflammation,” Frontiers in Bioscience, 2.

Extra Virgin Olive Oil: The Magic Pill for Healthy Living? | The Paleo Diet
The tremendous benefits of extra virgin olive oil (EVOO) cannot be overstated. Most significantly it has long been associated with keeping the heart healthy.1 This is one of the many reasons why it is recommended for Paleo, and well living. Scientific studies have already shown the possible link between EVOO and stroke prevention.2 EVOO has also been shown to play a key role in preventing diabetes, through some unclear mechanisms. Based on this, do you need any more reasons why you need to cook with EVOO?

Well actually to a recent study published in the prominent Nature journal, there is another reason to add to the list. Researchers in Italy recently described how EVOO improves post-prandial (after eating a meal) blood glucose, and low-density lipoprotein cholesterol (LDL-c).1 Basically individuals who ate meals prepared with EVOO experienced greatly improved levels of lower blood glucose, and cholesterol, when compared to those with corn oil. Now before buying stock in EVOO companies, it is important to understand the whys, whats and hows.

THE STUDY

In the study of 25 subjects, there were two objectives using a Mediterranean-type meal, with the first one including extra virgin olive oil (EVOO), while the second used corn oil. After consumption of the meal with EVOO, participants experienced significantly decreased levels of blood glucose, dipeptidyl-peptidase-4 (DPP-4) protein, lipoprotein cholesterol (LDL-C), oxidized LD (ox-LDL)L, as well as higher levels of  insulin, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP).1 In the second part of the study, EVOO was shown to lead to better improvement in glycemic and lipid profile compared to corn oil. The meal with EVOO compared to the one with corn oil resulted in significantly smaller increase of glucose, DPP-4 protein and activity, as well as increased levels of insulin, and GLP-1. Additionally, eating meals with EVOO resulted in lower amounts of LDL-C and ox-LDL.

WHAT DOES THIS ALL MEAN?

Well, while the Mediterranean diet does not agree with all the principles of a Paleo diet, the study insinuates that the wonderful health benefits attributed to the Mediterranean diet, stem from the intake of extra virgin olive oil (EVOO). These benefits include antiatheroslerotic effect, which preventing the development of stroke, and the start of new-onset diabetes.3 The speculation was that EVOO contains antioxidants, which are beneficial for oxidative stress, given evidence of a link between oxidative stress and beta cells dysfunction.4 Since beta cells are responsible for the release of insulin in the pancreas, then this dysfunction may result in diabetes. In addition oxidative stress is thought to activate DPP-4, ultimately decreasing the release of insulin. The latter helps decrease levels of blood glucose, so this further compounds the issue with oxidative stress, and increased blood glucose.

DECREASING THE RISK OF ALZHEIMER’S DISEASE, PARKINSON’S DISEASE, CANCER, AND MORE

Now this is where it gets even more interesting. In addition to atherosclerosis, stroke and diabetes, oxidative stress, the latter being the overproduction of free oxygen radical molecules. Its toxicity is linked with other neurodegenerative diseases such as cancer, aging damage, Alzheimer’s, Parkinson’s, rheumatoid arthritis, and other cardiovascular diseases. Does this mean that extra virgin olive oil could decrease the risk of developing a wide myriad of conditions? Possibly.

Several studies have shown that oleuropein aglycone, which is a natural phenol widely found in EVOO, is protective and therapeutic against Alzheimer’s disease.5 Furthermore other studies also indicate that this same compound could provide protective and therapeutic effects against a number of conditions including obesity, non-alcoholic hepatitis and type 2 diabetes.5 Additionally studies have shown neuroprotective effects against other critical conditions such as cerebral ischemia, multiple sclerosis, peripheral neuropathy and spinal cord injury.6 HIV has an increased inflammatory process, and so bring on the EVOO! It only makes sense why we recommend extra virgin olive oil.

In summary, the truth is there is no magic pill for healthy living. There is a scientific basis behind the extra virgin olive oil recommendation, and the long list of potential benefits keeps growing. Preventative care is always the best form of medicine, and you can play your part in making the right and healthy choice.

 

REFERENCES

[1] Violi, F., Loffredo, L., Pignatelli, P., Angelico, F., Bartimoccia, S., C, N., . . . Carnevela, R. (2015, June 2015). Extra virgin olive oil use is associated with improved post-prandial blood glucose and LDL cholesterol in healthy subjects. Nutrition & Diabetes, 5(e172). doi:10.1038/nutd.2015.23

[2] Melnick, M. (2011, June 16). Can Olive Oil Help Prevent Stroke? Retrieved from Time.

[3] Martínez-González, M., Dominguez, L., & Miguel Delgado, R. (2014). Olive oil consumption and risk of CHD and/or stroke: a meta-analysis of case–control, cohort and intervention studies. British Journal of Nutrition, 112(2), 248-259.

[4] Uttara, B., Singh, A., Zamboni, P., & Mahajan, R. (2009). Oxidative Stress and Neurodegenerative Diseases: A Review of Upstream and Downstream Antioxidant Therapeutic Options. Current Neuropharmacology, 7(1), 65-74.

[5] Luccarini, I., Grossi, C., Rigassi, S., Coppi, E., Pugliese, A., Pantano, D., . . . Casamenti, F. (2015). Oleuropein aglycone protects against pyroglutamylated-3 amyloid-ß toxicity: biochemical, epigenetic and functional correlate. Neurobiol Aging, 36(2).

[6] Khalatbary, A. (2013). Olive oil phenols and neuroprotection. Nutritional Neuroscience, 243-249. Retrieved Aug 5, 2015, from http://www.maneyonline.com/doi/full/10.1179/1476830513Y.0000000052

Sugar and Alcohol: Your Liver Can’t Tell The Difference

Dr. David Unwin, Fellow of the Royal College of General Practitioners (FRCGP) together with fellow researchers recently completed a study showing low carb diets significantly reduce fatty liver, weight and blood sugar. Trialing a low carb approach over a year, they found rapid improvements in liver function among other positive effects.

“My interest in abnormal liver, and particularly GGT blood results began when I noticed that in our family practice of 9,000 patients well over a 1,000 had an abnormal GGT result,” said Dr. Unwin. “I could predict which patients would have lost weight -before they came into my consulting room from the improvement in GGT blood results alone- so began to wonder about raised GGT levels, Diabetes and non-alcoholic fatty liver disease (NAFLD): Was dietary carbohydrate a link?”

Before we get to the summary, let’s breakdown some of the statistics.

  • Approximately 30 million children and adults have diabetes in the United States. Out of that number, nearly 95% have type 2 diabetes according to the American Diabetes Association.1
  • The National Conference of State Legislatures (NCSL) reports obesity affects more than one-third of adults and 17% of youth in the United States. This equates to 78 million adults and 12 million children suffering from the obesity epidemic. As adopters of the Paleo diet well know, obesity increases risk for heart disease, type 2 diabetes, and cancer among other debilitating health conditions, like non-alcoholic fatty liver disease (NAFLD).2
  • The American Liver Foundation reports (NAFLD) affects up to 25% of Americans, where risk is directly correlated to being overweight or obese, having diabetes, high cholesterol or high triglycerides.3

As the cost of health care continues to skyrocket, Dr. Unwin has decreased his prescribing budget £15,000-£30,000 a year by prescribing a low carb diet to patients who in two years’ time decreased average blood sugar by 10% and is now below the national average in the UK4 and US.

“I would say sugar is definitely rather like alcohol for the liver, and would point out that starchy foods like bread and pasta are a rich source of glucose,” said Dr. Unwin.

Well, thankfully the Paleo diet is devoid of breads, pastas, grains, pseudo grains, and processed sugars. When we focus upon lean meats, fish, poultry, veggies, and fruits, nuts, and seeds in moderation, a Paleo prescription is the best, cost effective investment you can make for your health.

Summary* presented ahead of publication in Diabetes in Practice September 15, 2015.

Unwin DJ1, Cuthertson DJ2, Feinman R3, Sprung VS2 (2015) A pilot study to explore the role of a low-carbohydrate intervention to improve GGT levels and HbA1c. Diabesity in Practice 4 [in press]

1Norwood Surgery, Norwood Ave, Southport. 2Department of Obesity and Endocrinology, Institute of Ageing & Chronic Disease, University of Liverpool, UK. 3Professor of biochemistry and medical researcher at State University of New York Health Science Center at Brooklyn, USA.

Working title: Raised GGT levels, Diabetes and NAFLD: Is dietary carbohydrate a link?  Primary care pilot of a low carbohydrate diet

Abnormal liver function tests are often attributed to excessive alcohol consumption and/or medication without further investigation. However they may be secondary to non-alcoholic fatty liver disease (NAFLD). NAFLD is now prevalent in 20-30% of adults in the Western World. Considering the increased cardiovascular and metabolic risk of NAFLD, identification and effective risk factor management of these patients is critical.

Background Excess dietary glucose leads progressively to hepatocyte triglyceride accumulation (non-alcoholic fatty liver disease-NAFLD), insulin resistance and T2DM. Considering the increased cardiovascular risks of NAFLD and T2DM, effective risk-factor management of these patients is critical. Weight loss can improve abnormal liver biochemistry, the histological progression of NAFLD, and diabetic control. However, the most effective diet remains controversial.

Aim We implemented a low-carbohydrate (CHO) diet in a primary health setting, assessing the effect on serum GGT, HbA1c levels (as proxies for suspected NAFLD and diabetic control), and weight.

Design  69 patients with a mean  GGT of 77 iu/L (NR 0-50) and an average BMI of 34.4Kg/m2 were recruited opportunistically and advised on reducing total glucose intake (including starch), while increasing intake of  natural fats, vegetables and protein.

Method Baseline blood samples were assessed for GGT levels, lipid profile, and HbA1c. Anthropometrics were assessed and repeated at monthly intervals. The patients were provided monthly support by their general practitioner or practice nurse, either individually or as a group.

Results After an average of 13 months on a low-CHO diet there was a 46% mean reduction in GGT of 29.9 iu/L (95% CI= -43.7, -16.2; P<0.001), accompanied by average reductions in weight [-8.8Kg (95% CI= -10.0, -7.5; P<0.001)],and HbA1c [10.0mmol/mol (95% CI= -13.9, -6.2; P<0.001)].

Conclusions We provide evidence that low-carbohydrate, dietary management of patients with T2DM and/or suspected NAFLD in primary care is feasible and improves abnormal liver biochemistry and other cardio-metabolic risk factors. This raises the question as to whether dietary carbohydrate plays a role in the etiology of diabetes and NAFLD, as well as obesity. Over the study period and given a choice not a single patient opted to start antidiabetic medication, losing weight instead. This helps explain why our practice is the only one in the Southport and Formby CCG to have static diabetes drug costs for three years running.

*Note: The summary displayed above is not the official abstract from Diabetes in Practice.

David Unwin | The Paleo Diet

David Unwin is the senior partner and GP trainer at the Norwood Surgery, Southport, a seaside resort in the North West of England. He is an expert clinical adviser in diabetes for the Royal College of General Practitioners, and has a special interest in the Solution Focused psychological approach to the consultation. David lives on a farm with his wife, son and their sheep, turkeys, hens -and a very large pig!

 

 

REFERENCES

[1] http://www.diabetes.org/diabetes-basics/statistics/infographics.html?loc=db-slabnav

[2] http://www.ncsl.org/research/health/obesity-statistics-in-the-united-states.aspx

[3] http://www.liverfoundation.org/abouttheliver/info/nafld/

[4] http://diabetesdietblog.com/2015/07/15/you-only-need-one-arrow-dr-unwin-proves-it-again/

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

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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.
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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.

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