Tag Archives: obesity

Junk Food | The Paleo Diet

While the title of this article may at first seem implausible (and somewhat scary), a new scientific study seems to show that an inborn preference for junk food is not only possible – it may be affecting more of us than ever could have possibly been imagined. For the first time in history, researchers for Obesity Society have identified two genetic variants, which help to change how the brain responds to high-calorie foods.1 2 While this is potentially terrible news for those of us who struggle to resist highly processed and manufactured foods – it also means there is possibly a way to stop this genetic variant from controlling our dietary choices. This could include changing how the brain processes junk food, changing how much people crave these foods, and even altering the brain’s dopamine system. There are even more potential treatments using this new information – including using gut hormones to act on dopamine brain cells.

To delve into further detail, researchers specifically found that two genetic variants – FTO and DRD2 – influenced brain activity related to the reward system. This occurred when subjects simply looked at pictures of high-calorie foods. As I’ve written previously, this is far from the first time neuroscience (or other scientific studies) have shown that some of our brains respond differently, to rewarding foods.3 4 5 6 7 8 9 10 11 In early 2014, for example, a study was published which showed that not only did some people crave chocolate (while others did not) – but that there was literally different brain activity, in the two groups.12

Asmaro D, Liotti M. High-caloric and chocolate stimuli processing in healthy humans: an integration of functional imaging and electrophysiological findings. Nutrients. 2014;6(1):319-41.

In another, similar study, researchers found that by altering dopamine receptors (specifically D2 receptors) – they could cure binge eating.13 Unfortunately for us, that ground breaking study was done on rats – not humans. However, this is further evidence that our brain plays a fundamental role in overeating and cravings. In fact, it may be the excess stimulation of the nucleus accumbens (the ‘pleasure center’ of the brain) from junk food, which leads to obesity.14 15 16 17 18 19 20

How does this relate to our current world? Well, 70% of the United States is overweight, with 30% of us now being obese.21 What accounts for all these extra pounds? Certainly, as shown by research from Yale scientists, a hyper-stimulatory environment and excess advertisement of junk food – is a large part of the problem.22 23 24 But this data is compounded by other research, which shows that extended access to high-fat and high-sugar food, results in behavioral and physiological changes – which are similar to those caused by illegal drugs.25 [26] While a large portion of these corresponding studies were conducted on rats, this does not mean that the results will not translate to humans. Like many areas of scientific research, we simply need more data.

Baik JH. Dopamine signaling in food addiction: role of dopamine D2 receptors. BMB Rep. 2013;46(11):519-26.

As I’ve covered previously, the neurobiology of sugar addiction is fascinating as well.27 28 The brain is bombarded with an overwhelming amount of chemicals and reward, when you consume junk food.29 30 31 32 Over time, this leads to a higher quantity of junk food needing to be consumed, to achieve the same rewarding effect.33 34 35 So even for those of us who are not genetically susceptible to the temptations of junk food, we can alter our brain’s preferences and reward receptors, to become just as likely to crave it.36 37 38 39 40

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

The good side of all this bad news? Your brain can also be positively impacted by food.41 42 43 44 45 46 A Paleo diet, which is full of nutrient dense foods, will help keep you satiated, and keep your brain from craving high sugar, nutritionally empty choices. Be sure to load your plate with wild-caught fish (high in brain-friendly omega-3 fatty acids), healthy fats (like avocados) and complete sources of protein (like grass fed beef). You may indeed be hardwired for junk food – but that doesn’t mean you have to give in to temptation. Adopting a Paleo diet is associated with many different health benefits – many of which work to counteract the negative effects of junk food.47 48 49 50 What this means, is that you can improve your health drastically, by simply changing what’s on your plate. Start eating a Paleo diet today, and watch your health soar!

References

1. Available at: http://www.sciencedaily.com/releases/2015/11/151105103957.htm. Accessed November 23, 2015.

2. Available at: http://www.newswise.com/articles/are-you-hardwired-to-enjoy-high-calorie-foods-research-links-genes-to-heightened-brain-reward-responses-to-foods-high-in-fat-and-sugar. Accessed November 23, 2015.

3. Fortuna JL. The obesity epidemic and food addiction: clinical similarities to drug dependence. J Psychoactive Drugs. 2012;44(1):56-63.

4. Garber AK, Lustig RH. Is fast food addictive?. Curr Drug Abuse Rev. 2011;4(3):146-62.

5. Grimm O., Jacob M.J., Kroemer N.B., Krebs L., Vollstädt-Klein S., Kobiella A., Wolfensteller U., Smolka M.L. The personality trait self-directedness predicts the amygdala’s reaction to appetizing cues in fMRI. Appetite. 2012;58:1023–1029.

6. Macht M., Mueller J. Immediate effects of chocolate on experimentally induced mood states. Appetite.2007;49:667–674.

7. Kringelbach M.L. The human orbitofrontal cortex: Linking reward to hedonic experience. Nat. Rev. Neurosci. 2005;6:691–702.

8. Francis S.T., Head K., Morris P.G., Macdonald I.A. The effect of flavanol-rich cocoa on the fMRI response to a cognitive task in healthy young people. J. Cardiovasc. Pharm. 2006;47:S215–S220.

9. Small D.M., Zatorre R.J., Dagher A., Evans A.C., Jones-Gotman M. Changes in brain activity related to eating chocolate: From pleasure to aversion. Brain. 2001;124:1720–1733.

10. Kemmotsu N., Murphy C. Restrained eaters show altered brain response to food odor. Physiol. Behav.2006;87:323–329.

11.  Blechert J., Feige B., Hajcak G., Tuschen-Caffier B. To eat or not to eat? Availability of food modulates the electrocortical response to food pictures in restrained eaters. Appetite. 2010;54:262–268.

12. Asmaro D, Liotti M. High-caloric and chocolate stimuli processing in healthy humans: an integration of functional imaging and electrophysiological findings. Nutrients. 2014;6(1):319-41.

13. Halpern CH, Tekriwal A, Santollo J, et al. Amelioration of binge eating by nucleus accumbens shell deep brain stimulation in mice involves D2 receptor modulation. J Neurosci. 2013;33(17):7122-9.

14. Lawrence NS, Hinton EC, Parkinson JA, Lawrence AD. Nucleus accumbens response to food cues predicts subsequent snack consumption in women and increased body mass index in those with reduced self-control. Neuroimage. 2012;63(1):415-22.

15. Salamone JD, Cousins MS, Mccullough LD, Carriero DL, Berkowitz RJ. Nucleus accumbens dopamine release increases during instrumental lever pressing for food but not free food consumption. Pharmacol Biochem Behav. 1994;49(1):25-31.

16. Olausson P, Jentsch JD, Tronson N, Neve RL, Nestler EJ, Taylor JR. DeltaFosB in the nucleus accumbens regulates food-reinforced instrumental behavior and motivation. J Neurosci. 2006;26(36):9196-204.

17. Day JJ, Carelli RM. The nucleus accumbens and Pavlovian reward learning. Neuroscientist. 2007;13(2):148-59.

18. Pratt WE, Kelley AE. Nucleus accumbens acetylcholine regulates appetitive learning and motivation for food via activation of muscarinic receptors. Behav Neurosci. 2004;118(4):730-9.

19. Salamone JD, Correa M, Mingote S, Weber SM. Nucleus accumbens dopamine and the regulation of effort in food-seeking behavior: implications for studies of natural motivation, psychiatry, and drug abuse. J Pharmacol Exp Ther. 2003;305(1):1-8.

20. Demos KE, Heatherton TF, Kelley WM. Individual differences in nucleus accumbens activity to food and sexual images predict weight gain and sexual behavior. J Neurosci. 2012;32(16):5549-52.

21. Available at: http://www.cdc.gov/nchs/fastats/obesity-overweight.htm. Accessed November 23, 2015.

22. Yokum S, Gearhardt AN, Harris JL, Brownell KD, Stice E. Individual differences in striatum activity to food commercials predict weight gain in adolescents. Obesity (Silver Spring). 2014;22(12):2544-51.

23. Udo T, Weinberger AH, Grilo CM, et al. Heightened vagal activity during high-calorie food presentation in obese compared with non-obese individuals–results of a pilot study. Obes Res Clin Pract. 2014;8(3):e201-98.

24. Gearhardt AN, Roberto CA, Seamans MJ, Corbin WR, Brownell KD. Preliminary validation of the Yale Food Addiction Scale for children. Eat Behav. 2013;14(4):508-12.

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

26. Stockburger J., Schmälzle R., Flaisch T., Bublatzky F., Schupp H.T. The impact of hunger on food cue processing: An event-related brain potential study. Neuroimage. 2009;47:1819–1829.

27. 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.

28. García-cáceres C, Tschöp MH. The emerging neurobiology of calorie addiction. Elife. 2014;3:e01928.

29. Norton P, Falciglia G, Gist D. Physiologic control of food intake by neural and chemical mechanisms. J Am Diet Assoc. 1993;93(4):450-4.

30. Wurtman RJ. Nutrients affecting brain composition and behavior. Integr Psychiatry. 1987;5(4):226-38.

31. Young SN. How to increase serotonin in the human brain without drugs. J Psychiatry Neurosci. 2007;32(6):394-9.

32. Wang GJ, Volkow ND, Telang F, et al. Exposure to appetitive food stimuli markedly activates the human brain. Neuroimage. 2004;21(4):1790-7.

33. Baik JH. Dopamine signaling in food addiction: role of dopamine D2 receptors. BMB Rep. 2013;46(11):519-26.

34. Lietti C.V., Murray M.M., Hudry J., le Coutre J., Toepel U. The role of energetic value in dynamic brain response adaptation during repeated food image viewing. Appetite. 2012;58:11–18.

35. Meule A. Are certain foods addictive?. Front Psychiatry. 2014;5:38.

36. Davis C, Curtis C, Levitan RD, Carter JC, Kaplan AS, Kennedy JL. Evidence that ‘food addiction’ is a valid phenotype of obesity. Appetite. 2011;57(3):711-7.

37. Reward systems and food intake: role of opioids. International Journal of Obesity. 2009;:S54.

38. Naleid AM, Grace MK, Chimukangara M, Billington CJ, Levine AS. Paraventricular opioids alter intake of high-fat but not high-sucrose diet depending on diet preference in a binge model of feeding. Am J Physiol Regul Integr Comp Physiol. 2007;293(1):R99-105.

39. Woolley JD, Lee BS, Fields HL. Nucleus accumbens opioids regulate flavor-based preferences in food consumption. Neuroscience. 2006;143(1):309-17.

40. Zhang M, Gosnell BA, Kelley AE. Intake of high-fat food is selectively enhanced by mu opioid receptor stimulation within the nucleus accumbens. J Pharmacol Exp Ther. 1998;285(2):908-14.

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

42. Bourre JM. Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients. J Nutr Health Aging. 2006;10(5):377-85.

43. Hill JO, Berridge K, Avena NM, et al. Neurocognition: the food–brain connection. Adv Nutr. 2014;5(5):544-6.

44. Armelagos GJ. Brain evolution, the determinates of food choice, and the omnivore’s dilemma. Crit Rev Food Sci Nutr. 2014;54(10):1330-41.

45. Galland L. The gut microbiome and the brain. J Med Food. 2014;17(12):1261-72.

46. Lachance L, Ramsey D. Food, mood, and brain health: implications for the modern clinician. Mo Med. 2015;112(2):111-5.

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

48. Konner M, Eaton SB. Paleolithic nutrition: twenty-five years later. Nutr Clin Pract. 2010;25(6):594-602.

49. Klonoff DC. The beneficial effects of a Paleolithic diet on type 2 diabetes and other risk factors for cardiovascular disease. J Diabetes Sci Technol. 2009;3(6):1229-32.

50. Frassetto LA, Schloetter M, Mietus-synder M, Morris RC, Sebastian A. Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet. Eur J Clin Nutr. 2009;63(8):947-55.

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.

 

Quit Sugar | The Paleo Diet

Sugar – is there a more popular word for dieticians and nutritionists? Interestingly, economists have also been talking about the pure white stuff – but in a different context than the standard ‘insulin and cravings’ discussions. A new piece in The Atlantic discussed just how much money is spent on selling Americans sugar, every single day of our lives.1

Though nothing truly shocks me anymore, in the sleazy world of processed food marketing, I was a bit taken aback to realize that Kellogg’s spent $32 million on advertising their (truly awful) Pop Tarts last year. With that money, we could be helping to fix the obesity pandemic we are all collectively in, instead.2 3 4 5 70% of Americans are now overweight, and 30% of us are obese – couldn’t we allocate these funds better? I think so.6

But, instead, we get a new flavor of the Franken-Food that absolutely no one (let alone developing children) should eat for breakfast. Or any other time of day, for that matter. But the depressing statistics don’t end there. Last year, Coca-Cola spent over $250 million advertising their flagship sugar water. And for a quick science detour, remember that sugar has been shown to demonstrate a set of behaviors and parallel brain changes that are characteristic of addictive drugs.7 8 9 10

Brain Glucose Metabolusm

(a) Averaged images for DA D2 receptors (measured with [11C]raclopride) in a group of (i) controls (n=10) and (ii) morbidly obese subjects (n=10). (b) Results from SPM identifying the areas in the brain where D2 receptors availability was associated with brain glucose metabolism; these included the OFC, the CG and the DLPFC (region not shown in sagittal plane). (c) Regression slopes between D2 receptor availability (measured in striatum) and brain glucose metabolism in (i) CG and (ii) OFC in obese subjects. 10

Back to the money spent on sugar. Pepsi seems almost saint-like by comparison here, as they only spent $150 million advertising Gatorade last year. Keep in mind that all of the products listed so far (we’re at a total of $432 million at this point) are just brightly colored versions of sugar. This would almost be comical, if it weren’t destroying our collective health.11 12 13 14

I hope you’ve buckled up, because this is where things turn truly depressing. Did you know that our own government (who – obviously – should be looking out for our collective health) spent less than 0.5% of all agricultural subsidies on production of fruits and vegetables? You read that right – that’s less than 1%. Should less than 1% of any food-related funding be going to fruits and vegetables? Shouldn’t the majority of funding be going to fruits and vegetables? I feel like we are all in a bad Twilight Zone episode here.

And, while I wholeheartedly believe in freedom, liberty, and a free market economy, when you have 70% of the population overweight, and one in three people obese, you need to make some changes, and you need to have some oversight. It doesn’t take an advanced college degree, or even a high school diploma to see the problem here. As the old saying goes, numbers don’t lie.

I will leave you with one more staggering fact, which shows how truly disconnected we have become, from our Paleo ancestors. Fruits and vegetables are the only foods, which all nutrition experts can agree upon; we should be eating, ad libitum. But do you know what classification they have, by our own U.S. Department Of Agriculture? Their classification is only a brief two words: ‘specialty crops’.

Hopefully in your own personal, ongoing scientific experiment (that is your life), fruits and vegetables are not ‘specialty crops’. They should be part of your main course. I hope I’ve given you some real things to think about here. And remember – our children and future grandchildren are the ones who will suffer the most from this ludicrous sugar economy we are allowing to persist. Not us.

While it is easy to be complacent, apathetic, and not do anything, you have a voice. And what is a democracy, if not simply a collection of individual voices? Make your voice be heard, and tell the world where you stand on the true price of sugar.

REFERENCES

1 Available at: http://www.theatlantic.com/health/archive/2015/09/the-money-spent-selling-sugar-to-americans-is-staggering/407350/. Accessed September 29, 2015.

2 Roth J, Qiang X, Marbán SL, Redelt H, Lowell BC. The obesity pandemic: where have we been and where are we going?. Obes Res. 2004;12 Suppl 2:88S-101S.

3 Swinburn BA, Sacks G, Hall KD, et al. The global obesity pandemic: shaped by global drivers and local environments. Lancet. 2011;378(9793):804-14.

4 Catenacci VA, Hill JO, Wyatt HR. The obesity epidemic. Clin Chest Med. 2009;30(3):415-44, vii.

5 Popkin BM, Adair LS, Ng SW. Global nutrition transition and the pandemic of obesity in developing countries. Nutr Rev. 2012;70(1):3-21.

6 Available at: http://www.toledoblade.com/Food/2015/06/23/70-of-Americans-overweight-or-obese-study-finds.html. Accessed September 29, 2015.

7 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.

8 Lustig RH. Fructose: it’s “alcohol without the buzz”. Adv Nutr. 2013;4(2):226-35.

9 Lustig RH. Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc. 2010;110(9):1307-21.

10 Volkow ND, Wang GJ, Fowler JS, Telang F. Overlapping neuronal circuits in addiction and obesity: evidence of systems pathology. Philos Trans R Soc Lond, B, Biol Sci. 2008;363(1507):3191-200.

11 Puhl R, Brownell KD. Bias, discrimination, and obesity. Obes Res. 2001;9(12):788-805.

12 Brownell KD, Kersh R, Ludwig DS, et al. Personal responsibility and obesity: a constructive approach to a controversial issue. Health Aff (Millwood). 2010;29(3):379-87.

13 Vartanian LR, Schwartz MB, Brownell KD. Effects of soft drink consumption on nutrition and health: a systematic review and meta-analysis. Am J Public Health. 2007;97(4):667-75.

14 Brownell KD, Warner KE. The perils of ignoring history: Big Tobacco played dirty and millions died. How similar is Big Food?. Milbank Q. 2009;87(1):259-94.

The Paleo Diet Skinny on Fat: White Fat Vs Brown Fat

Fat gets a bad rap. Our societal standards for attractiveness promotes lean body types, leading to eating disorders and body image disturbances for men and women1 alike, leading most people to prefer to have as little body fat as possible.2 Although we know obesity is a huge risk factor for numerous diseases and conditions,3 there’s more to adipose tissue than meets than eye. In fact, body fat isn’t the biggest villain if we maintain healthy levels and stimulate the best kind of it.

Adipose tissue is critical to our survival, and a body without any body fat could lead to decreased fecundity and premature death. 4 Fat has a critical evolutionary function to store calories safely and abundantly so the energy can be used when food is scarce. Adipose tissue is also an insulator to our internal organs and provides cushioning to protect us from the environment, such as having a nice plush landing pad when we fall. Scientists have discovered that stored fat does more than sit around waiting to be used, it also metabolically active – that’s right fat can burn calories. 5

Scientists classify adipose tissue as an endocrine organ6 that releases over 20 different hormones and bioactive substances that control metabolism. For example, adipose tissue produces one form of estrogen, as well as leptin, a hormone that helps regulate appetite and hunger. It also contains receptors for insulin, growth hormone, adrenaline, and cortisol.7 The dysregulation of the bioactive substances, called adipocytokines, contributes directly to obesity-related diseases, such as atherosclerosis and inflammatory conditions. 8

There are two distinct types of adipose tissue found within the body, with completely different functions from one another. White fat, which is the one we normally want to reduce to improve our appearance, and brown fat, which is the beneficial one (we probably didn’t even know about) that we want to create more of.  Brown fat is composed of several small lipid droplets, compared to the white fat’s single lipid droplet, and it contains a large number of iron-containing mitochondria and tiny blood vessels,9 combining to give this fat its brownish color.10 These mitochondria consume fat and glucose11 to produce heat to generate warmth for the body as needed, while also increasing the metabolism12 by oxidizing white fat, and burning calories, without producing much ATP. 13 This activity is similar to how muscle functions compared to that of white fat.

Scientists discovered that lean people tend to have more brown fat than obese people and they are investigating how to increase a person’s brown fat or stimulate it to be more active.  In addition to the benefit of burning white fat, people with higher levels of brown adipose tissue demonstrate an inverse relationship with developing non-alcoholic fatty liver disease.14 When people overeat and under-exercise, they not only increase their total amount of white fat into unhealthy levels, but also it is distributed in a way to leads to metabolic15 and inflammatory diseases.16 Further, this behavior results in brown fat becoming dysfunctional and in turn unable to burn calories. Recent studies on brown adipose tissue have shown that a defect and dysregulation in this tissue is one probable cause of obesity.17

So, how do you boost brown fat generation? Focus on the pillars of your Paleo lifestyle. Regular exercise, adequate high-quality sleep, and consistent exposure to cold temperatures, such as exercising outdoors in cold weather or keeping the heat turned down in your home, have all been shown to contribute to healthy functioning and increased levels of brown fat, meanwhile keeping you white fat in check.18

 

REFERENCES

[1] Thompson, J. Kevin, and Eric Stice. “Thin-ideal internalization: Mounting evidence for a new risk factor for body-image disturbance and eating pathology.” Current directions in psychological science 10.5 (2001): 181-183.

[2] Hellmich, Nanci. “Do thin models warp girls’ body image.” USA Today 26 (2006).

[3] Eckel, Robert H., and Ronald M. Krauss. “American Heart Association call to action: obesity as a major risk factor for coronary heart disease.” Circulation97.21 (1998): 2099-2100.

[4] Moitra, Jaideep, et al. “Life without white fat: a transgenic mouse.” Genes & development 12.20 (1998): 3168-3181.

[5] Addy, Carol, et al. “The acyclic CB1R inverse agonist taranabant mediates weight loss by increasing energy expenditure and decreasing caloric intake.”Cell metabolism 7.1 (2008): 68-78.

[6] Kershaw, Erin E., and Jeffrey S. Flier. “Adipose tissue as an endocrine organ.”The Journal of Clinical Endocrinology & Metabolism 89.6 (2004): 2548-2556.

[7] Kershaw, Erin E., and Jeffrey S. Flier. “Adipose tissue as an endocrine organ.”The Journal of Clinical Endocrinology & Metabolism 89.6 (2004): 2548-2556.

[8] Rosenow, Anja, et al. “Identification of novel human adipocyte secreted proteins by using SGBS cells.” Journal of proteome research 9.10 (2010): 5389-5401.

[9] Bartelt, Alexander, et al. “Brown adipose tissue activity controls triglyceride clearance.” Nature medicine 17.2 (2011): 200-205.

[10] Flatmark, Torgeir, Frank J. Ruzicka, and Helmut Beinert. “The pattern of iron—sulfur centers in brown adipose tissue mitochondria: Preponderance of ETF dehydrogenase and invariance with the thermogenic state.” FEBS letters 63.1 (1976): 51-55.

[11] Ouellet, Véronique, et al. “Brown adipose tissue oxidative metabolism contributes to energy expenditure during acute cold exposure in humans.” The Journal of clinical investigation 122.2 (2012): 545.

[12] Seale, Patrick, et al. “PRDM16 controls a brown fat/skeletal muscle switch.”Nature 454.7207 (2008): 961-967.

[13] Ouellet, Véronique, et al. “Brown adipose tissue oxidative metabolism contributes to energy expenditure during acute cold exposure in humans.” The Journal of clinical investigation 122.2 (2012): 545.

[14] Yilmaz, Y., et al. “Association between the presence of brown adipose tissue and non‐alcoholic fatty liver disease in adult humans.” Alimentary pharmacology & therapeutics 34.3 (2011): 318-323.

[15] Jensen, Michael D. “Role of body fat distribution and the metabolic complications of obesity.” The Journal of Clinical Endocrinology & Metabolism93.11_supplement_1 (2008): s57-s63.

[16] Lovejoy, Jennifer C., Steven R. Smith, and Jennifer C. Rood. “Comparison of Regional Fat Distribution and Health Risk Factors in Middle‐Aged White and African American Women: The Healthy Transitions Study.” Obesity research9.1 (2001): 10-16.

[17] Himms-Hagen, Jean. “Obesity may be due to a malfunctioning of brown fat.”Canadian Medical Association Journal 121.10 (1979): 1361.

[18] Ouellet, Véronique, et al. “Brown adipose tissue oxidative metabolism contributes to energy expenditure during acute cold exposure in humans.” The Journal of clinical investigation 122.2 (2012): 545.

 

Obesity | The Paleo Diet

Unfortunately, 70% of the United States is now overweight.1 And nearly half of that 70% is obese – a truly scary prospect for the future of our nation’s health.2 But despite this alarming obesity epidemic (technically it is a pandemic, because the entire world is suffering from this problem) there has never been more debate about what exactly is causing the issue.3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 While this article will cover specific transcription factors and antioxidant pathways, the big bullet points for preventing obesity are simple.26 27 28 29 30 31 32 33 34 35

For starters, we are eating too many calories.36 37 38 39 Secondly, we are eating too much sugar and not enough nutrients.40 41 42 43 44 45 46 47 48 49 50 Third, we are not getting enough exercise.51 52 53 And lastly, we are stressed like never before, and sleeping less than ever.54 55 56 57 58 59 In a way, the rest of the debate is just minutia, because until we fix these four problems, we are not going to be able to stop this boat from capsizing.

Booth FW, Laye MJ. Lack of adequate appreciation of physical exercise’s complexities can pre-empt appropriate design and interpretation in scientific discovery. J Physiol. 2009;587:5527–5539.

But if we are to delve into the details of obesity, there are two dichotomous factors, which are at play. As I mentioned, too much sugar is a cornerstone of our nation’s various health problems. The fructose transporter GLUT5 plays a specific role in this problem, since we are taking in far too much fructose in our collective diet.60 61 62 63 64 By contrast, if we were to eat more vegetables and other healthful foods, we would see better results via the Nrf2 pathway.65 66 67 68 69 70 Most of us are aware that free radicals are categorized as ‘bad’ and antioxidants as ‘good’.71 But the details behind these scientific terms remain elusive, for most of the population.

Evolution of the consumption of high-fructose corn syrup (HFCS) and sucrose in the United States between 1970 and present. HFCS has increased rapidly to replace 50% of the sucrose consumption. Over this period, not only total sugar consumption but also total calorie intake and total fat intake have increased significantly. (USDA)

[/one_half]

Fructose metabolism in liver cells. Fructose metabolism (grey arrows) differs from glucose (black arrows) due to 1) a nearly complete hepatic extraction and 2) different enzyme and reactions for its initial metabolic steps. Fructose taken up by the liver can be oxidized to CO2 and then converted into lactate and glucose; glucose and lactate are subsequently either released into the circulation for extrahepatic metabolism or converted into hepatic glycogen or fat. The massive uptake and phosphorylation of fructose in the liver can lead to a large degradation of ATP to AMP and uric acid.60

Summary of the potential mechanisms for fructose-induced insulin resistance.60

The research on fructose has been steamrolling the scientific community since the viral popularity of pediatric endocrinologist Robert Lustig’s lecture, a few years ago.72 73 74 75 Not surprisingly, the food and beverage industry is trying like mad to stop any bad publicity from arising from the scientific community, around their sugary cash cow.76 But the actual, unbiased data has been very damning.77 78 79 80 Take the following chart, which shows that fructose in beverages, which do not list it on the label, often contain quantities of fructose that surpass the amount of the substance in beverages which do list it on the label.

Fructose concentration and fructose-to-glucose (F:G) ratio: juices. Concentration of fructose (g/L) in juices is displayed on the left y axis (open bars) and the F:GAdjusted is shown on the right y axis (solid bars). * Products with high-fructose corn syrup listed as an ingredient on the label. F:GAdjusted, the F:G ratio adjusted for other detected disaccharides.

Walker, R.W.; Dumke, K.A.; Goran, M.I. Fructose content in popular beverages made with and without high-fructose corn syrup. Nutrition 2014, 30, 928–935.

In an evolutionary sense, this level of fructose consumption is out of control and unprecedented.81 82 83 We’ve known for thousands of years, humans consumed about 20g of fructose each day.84 85 Their intake came from fruit and honey,86  vastly different than more concentrated sources of fructose, like soda. For one thing – there is no fiber in soda, which might slow down hepatic absorption of fructose. Oh, and for those curious, we are now consuming about 80g of fructose per day, on average.87 88

Proposed pathways and mechanisms underlying the differential effects of fructose compared with glucose consumption on adipose deposition, postprandial lipid metabolism glucose tolerance/insulin sensitivity.

Stanhope, K. L., & Havel, P. J. (2010). Fructose consumption: Recent results and their potential implications. Annals of the New York Academy of Sciences, 1190, 15–24. doi:10.1111/j.1749-6632.2009.05266.x

But why is fructose so harmful, and how does the GLUT5 transporter factor into this issue? GLUT5 was successfully cloned around 20 years ago and was initially described as a glucose transporter, until it became clear that it was specifically related to fructose.89 The brain and kidneys have both shown levels of GLUT5 mRNA and/or protein.90 This (indirectly) means that by eating too much fructose, your brain processes might be impaired.91 92 93 Since we now know that high levels of HA1c correlate with dementia, this shouldn’t be shocking news.94

Your small intestine has the greatest amount of GLUT5, and it also controls the availability of fructose to other areas.95 Interestingly, intestinal GLUT5 mRNA levels and fructose transport rates are very low until fructose is introduced, or after a few weeks of development (this appears to be genomic).96 97 98 99 The problems start to arise when too much fructose is introduced (via processed foods, usually) too early, creating a baseline of consumption, which seems to need to be satisfied.100 101 102 103 Though the science is still out, this ‘created need’ may force children to overeat, and as a result, become overweight and/or obese.

The GLUT5 transporter has been linked to hypertension, and also to diabetes.104 105 Since the United States spends over $240 billion on diabetes annually, scientific research into the area of GLUT5 should be pushed to the forefront, with the hope being that by better understanding the transport and processing of fructose, we can help improve the rates of disease – if not prevent them entirely.106

For example, diabetes profoundly affects GLUT5 expression in the small intestine.107 By down-regulating GLUT5 protein levels in those with high blood sugar, we may have a mechanism to help diabetics. Of course, there are many potential areas of research, which could be interesting for the GLUT5 transporter. But for the brevity of this article, I will stop here.  I invite those further interested to research the GLUT5 transporter, via easily using a search engine to locate articles on PubMed relating to the topic.

Lustig RH. Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc. 2010;110(9):1307-21.

One of the many issues with fructose is that it helps to cause non-enzymatic glycation – in layman’s terms; fructose helps to age your liver.108 This shouldn’t be surprising. Remember – increased dietary intake of sugar was linked to dementia – premature aging/degradation of brain tissue usually due to excessive buildup of the beta amyloid protein.109

By contrast, activation of the Nrf2 pathway may help to stop aging – not just in your liver, but also throughout the body.110 The Nrf2 pathway helps in regulating over 500 cytoprotective genes, which give your cells multiple layers of protection.111 112 Interestingly, research has found that dietary flavonoids help to activate this pathway, and thus, your diet can truly determine whether you age quickly or slowly.113 It really is this simple. Sort of.

NRF2, p53 and FOXOs support complementary antioxidant pathways.

Gorrini, C., Harris, I. S. & Mak, T. W. Modulation of oxidative stress as an anticancer strategy. Nature Rev. Drug Discov. 12, 931–947 (2013).

You see, in science, one must resist the urge to oversimplify, and in this case we must remember to not forget all the other stressors to our cells. This means sleep quantity and quality, exercise, stress from work, genetics, epigenetics, pollution – it is truly a never ending list. However, we very much have control over what we put in our mouths.

Differential responses to rising oxidative stress.

Stefanson, A. L., & Bakovic, M. (2014). Dietary Regulation of Keap1/Nrf2/ARE Pathway: Focus on Plant-Derived Compounds and Trace Minerals. Nutrients, 6(9), 3777–3801. doi:10.3390/nu6093777

The Nrf2 pathway has been recently found to react to apigenin and luteolin (dietary phytochemical flavones) in a favorable way.114 The antioxidant pathway is activated upon ingestion of apigenin and luteolin, and the flavones may be responsible for vital anti-inflammatory effects.

Schematic representation depicting some of the various cytoprotective proteins that are upregulated by Nrf2. Flavonoid-mediated protection from ischemic/hemorrhagic stroke, traumatic brain injury, and/or other neuropathies may result in large part from Nrf2 regulation of these pathways.113

In fact, activation of the Nrf2 pathway is being studied fairly extensively, in regards to cancer prevention and treatment.115 Since dietary activation is very cheap (especially when compared to pharmaceutical drugs) this research could pave the way for widespread effective change in our world’s health. Mandatory spinach and kale consumption might be a potential guideline – if one was to hypothesize about potential ways this research could be implemented on a widespread basis.

Schematic representation depicting the potential mechanisms by which flavanol-mediated Nrf2 induction leads to activation of cytoprotective pathways after stroke, traumatic brain injury, and/or other neurodegenerative diseases. Flavanols may induce Nrf2 through binding to receptors seated on the plasma membrane and subsequent initiation of intracellular signaling cascades. Alternatively, passive diffusion or active transport through the plasma membrane may permit direct cytosolic dissociation of the Keap1/Nrf2 complex or activation of second messengers that regulate Nrf2 translocation into the nucleus. Upon nuclear translocation, Nrf2 binds to AREs on the promoter regions of cytoprotective genes to regulate heme/biliverdin, glutathione, NAD(P)H, and/or other protective pathways.113

So, if your diet is making you fat, old and sick, you now have some great motivation to affect change. What can be more powerful than that? By loading up on neuro-protective vegetables and healthy fats, as well as quality proteins (which contain essential amino acids) you will be helping to fight back against cellular aging, obesity and illness.

And good news – a Paleo Diet – by its very nature – eliminates all the bad choices for you, and emphasizes all the best foods. The work has already been done. It couldn’t get any easier. You have a path towards obesity, dementia and medication. You also have a path towards health, wellness and vitality. The choice is yours – so choose wisely.

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84 Douard V, Ferraris RP. The role of fructose transporters in diseases linked to excessive fructose intake. J Physiol (Lond). 2013;591(Pt 2):401-14.

85 Port AM, Ruth MR, Istfan NW. Fructose consumption and cancer: is there a connection?. Curr Opin Endocrinol Diabetes Obes. 2012;19(5):367-74.

86 Konner M, Eaton SB. Paleolithic nutrition. Nutr Clin Pract. 2010;25:594–602.

87 Gross LS, Li L, Ford ES, Liu S. Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment. Am J Clin Nutr. 2004;79(5):774-9.

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The Reality of Food Addiction: Recharged | The Paleo Diet

In one of my post popular articles, I dove deep into the mire of just why so many of us are addicted to food. This subject is fascinating on both a molecular and individual level.1, 2, 3, 4  There are so many factors which go into food addiction.5, 6, 7, 8, 9, 10, 11, 12, 13 And most of them go totally unnoticed, to most people.14, 15, 16, 17, 18, 19, 20, 21, 22 The pervasiveness of advertising, the purposely addictive nature of processed foods, and the stressful nature of modern life is just too much for most of us to stay healthy.23, 24, 25, 26, 27, 28, 29, 30, 31, 32 Of course, new research has emerged on this topic, since an entire calendar year has passed since I wrote my first piece on food addiction – and some of it is quite startling.33, 34, 35, 36, 37, 38, 39, 40,

The Reality of Food Addiction: Recharged | The Paleo Diet

Volkow, Nora D et al. “Overlapping Neuronal Circuits in Addiction and Obesity: Evidence of Systems Pathology.” Philosophical Transactions of the Royal Society B: Biological Sciences 363.1507 (2008): 3191–3200. PMC. Web. 7 Aug. 2015.

But perhaps most troublingly, many scientists are still trying to fight the notion that food addiction even exists.41, 42, 43 I’m alarmed, offended and angry about this continued hemming and hawing (no doubt influenced by industry) – and you should be too. In simplest terms, go ask the average person following a Standard American Diet (SAD) if they feel addicted to food. I would bet everything I own that their answer would be a resounding “yes.”44, 45 No one wants to be obese, and unquestionably some level of addiction is underlying our obesity pandemic.46, 47, 48, 49, 50, 51 52, 53, 54, 55 Certainly there are also other factors, which I’ve also written about, (like leptin resistance) that happen as a result of poor food choices compounded over time.56, 57, 58, 59, 60, 61, 62, 63, 64

The Reality of Food Addiction: Recharged | The Paleo Diet

Agrawal, Rahul, and Fernando Gomez-Pinilla. “‘Metabolic Syndrome’ in the Brain: Deficiency in Omega-3 Fatty Acid Exacerbates Dysfunctions in Insulin Receptor Signalling and Cognition.” The Journal of Physiology 590.Pt 10 (2012): 2485–2499. PMC. Web. 7 Aug. 2015.

The Reality of Food Addiction: Recharged | The Paleo Diet

Cai, Dongsheng, and Tiewen Liu. “Inflammatory Cause of Metabolic Syndrome via Brain Stress and NF-κB.” Aging (Albany NY) 4.2 (2012): 98–115. Print.

It is my generation who is now having to pay for all the poor choices made by prior ones, and now more than 66% of adults are overweight or obese.65 Four years ago researchers knew that “there are a number of shared neural and hormonal pathways…that may help researchers discover why certain individuals continue to overeat despite health and other consequences”.66 And yet, some scientists refuse to even acknowledge people are addicted to food! It is maddening.

The Reality of Food Addiction: Recharged | The Paleo Diet

Sturm, Roland, and Aiko Hattori. “Morbid Obesity Rates Continue to Rise Rapidly in the US.” International journal of obesity (2005) 37.6 (2013): 889–891. PMC. Web. 7 Aug. 2015.

The results of food addiction are happening here and now.67, 68 We see them every day on the way to work, at the store, in society, and even glamorized in popular media. Certainly, no one should be ‘fat shamed’ – but we shouldn’t be celebrating obesity either. Food addiction is just as sad as drug addiction – it is just destructive over a longer period of time, rather than acutely.69, 70, 71 As science shows, the same neurobiological pathways that are implicated in drug abuse also modulate food consumption.72, 73

The Reality of Food Addiction: Recharged | The Paleo Diet

Volkow, Nora D et al. “Overlapping Neuronal Circuits in Addiction and Obesity: Evidence of Systems Pathology.” Philosophical Transactions of the Royal Society B: Biological Sciences 363.1507 (2008): 3191–3200. PMC. Web. 7 Aug. 2015.

The Reality of Food Addiction: Recharged | The Paleo Diet

Volkow, Nora D et al. “Overlapping Neuronal Circuits in Addiction and Obesity: Evidence of Systems Pathology.” Philosophical Transactions of the Royal Society B: Biological Sciences 363.1507 (2008): 3191–3200. PMC. Web. 7 Aug. 2015.

The Reality of Food Addiction: Recharged | The Paleo Diet

Baik, Ja-Hyun. “Dopamine Signaling in Food Addiction: Role of Dopamine D2 Receptors.” BMB Reports 46.11 (2013): 519–526. PMC. Web. 7 Aug. 2015.

Or how about the scientific paper which showed that Oreo cookies were as addictive as cocaine?74 Again, you will find some scientists hemming and hawing, but the reality, the way the science translates into our everyday lives, shows clear addiction. Do you feel like you need to eat the whole bag of broccoli? Obviously not. For most, vegetables are a chore. But it sure is easy to eat a whole box of Oreos! In fact, many find it hard not to.75 Does this sound addictive to you?

Then we have the case of researchers “curing binge eating” by modulating dopamine receptors.76 Why is this notable? Because by altering the brain’s response to rewarding food, we can stop the cravings/addiction! This really hammers home the point that food can be addictive, and that it is not just an innocent bystander that some people (66% of all adults, if you’re keeping track) can’t seem to stop consuming. If you wants to know more of the deep molecular mechanisms and psychology behind eating, I have also written on this very subject.

The Reality of Food Addiction: Recharged | The Paleo Diet

Green, Erin, and Claire Murphy. “Altered Processing of Sweet Taste in the Brain of Diet Soda Drinkers.” Physiology & behavior 107.4 (2012): 560–567. PMC. Web. 7 Aug. 2015.

And what is one of the most addictive, and least healthy habits in the world? Soda. The less soda you drink, the great weight loss you see.77, 78, 79 Even artificial sweeteners have shown rewarding mechanisms in the brain.80, 81, 82, 83, 84 Interestingly, new research has shown that a hormone deficiency in the brain may also be causing overeating.85, 86, 87 This is in addition to new research which shows that ‘bad’ genes may also play a role in overconsumption.88, 89, 90, 91, 92

Clearly, food addiction is a real problem, which needs to be fixed as soon as possible.93, 94 The future of (a healthy) human world…sort of depends on it. A Paleo diet is one of the best ways to go cold turkey, and stop food addiction in its tracks. By eating nutrient dense foods, sleeping soundly, and managing stress, we are taking proactive steps to avoiding food addiction and obesity.95, 96 97, 98, 99, 100

 

 

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[99] Boers I, Muskiet FA, Berkelaar E, et al. Favourable effects of consuming a Palaeolithic-type diet on characteristics of the metabolic syndrome: a randomized controlled pilot-study. Lipids Health Dis. 2014;13:160.

[100] Konner M, Eaton SB. Paleolithic nutrition: twenty-five years later. Nutr Clin Pract. 2010;25(6):594-602.

Soy, Sugar's Cohort in Causing Obesity | The Paleo Diet

Since the 1930s, the US government has been heavily subsidizing corn, soy, wheat, and other so-called staple crops. Subsequently, these foods have remained artificially cheap for decades, leading to enormously increased consumption.

For a new study, just published in PLOS One, scientists at UC Riverside compared the effects of diets high in soybean oil with those high in fructose and/or coconut oil. They concluded that soybean oil, when consumed at typical American consumption levels, causes significant liver damage and promotes obesity and diabetes even more so than fructose.1

“This was a major surprise for us—that soybean oil is causing more obesity and diabetes than fructose—especially when you see headlines everyday about the potential role of sugar consumption in the current obesity epidemic,” said Poonamjot Deol, the study’s lead scientist.2

This study is believed to be the first comparing the effects of unsaturated fat, saturated fat, and fructose on obesity, diabetes, insulin resistance and nonalcoholic fatty liver disease. While excessive sugar consumption has rightfully been criticized during the past several years, this study shows that industrial seed oils, particularly soybean oil, can be just as dangerous.

Soybean oil features prominently in many processed foods, especially margarine, salad dressings, and snack foods. It’s also the preferred cooking oil throughout the restaurant industry. In 2007, around 80 million tons of edible vegetable oils were produced globally, about half of which was soybean oil.3

Just how much money goes into keeping soy cheap and plentiful? Between 1995 and 2012, US soy subsidies totaled an astounding $27.8 billion, second only to corn, which amounted to $84.4 billion for the same period. In 2014, the US government replaced direct payments to farmers with Price Loss Coverage (PLC) and Agricultural Risk Coverage (ARC), but these new programs still cost taxpayers two-thirds as much as the direct payments did.4

Annual consumption of soybean oil increased from a miniscule 0.01 kg per person in 1909 to 11.2 kg in 1999.5 So what has been the impact on health? The UC Riverside scientists fed mice diets with 40% of calories coming from fat and supplemented those diets with fructose. Diet 1 consisted of 36 kcal% from coconut oil and 4 kcal% from soybean oil. Diet 2 consisted of 21 kcal% from coconut oil and 19 kcal% from soybean oil. These diets were formulated to mimic American consumption patterns with respect to saturated fat, soybean oil, and fructose.

Mice on Diet 2, the high soybean oil diet, exhibited increased weight gain, adiposity, fatty liver, insulin resistance, and diabetes, compared to mice on Diet 1. The scientists believe the mechanisms behind these outcomes involve changes in gene expression. Diet 2, for example, caused significant global dysregulation of several genes, particularly cytochrome P450, related to diabetes, obesity, lipid metabolism, and cancer.

Fructose had less severe metabolic effects than did soybean oil, which was a surprise to the scientists. More importantly, they determined that fructose combined with soybean oil works synergistically to undermine health.

Fructose induced neither diabetes nor insulin resistance in this study, although it did induce obesity. The scientists point out that fructose and its metabolic impact are very hotly debated within the nutrition science community. Further research will yield a more evolved perspective on fructose, but this study stresses the importance of dietary context. In other words, fructose seems to be much more damaging when paired with unhealthy oils compared to healthy sources of fat.

Many people within the Paleo community are concerned about fructose, even going so far as to completely eliminate fruit from their diets. While this might be appropriate for some people, it’s probably unnecessary for others. The fat in the Paleo diet comes mostly from high-quality sources of saturated and monounsaturated fat, with minimal amounts of high-quality polyunsaturated fat. The current study shows how foods interact and why a holistic approach to diet is essential. If America is serious about reversing degenerative diseases, soybean oil must share the spotlight with sugar during the many ongoing national discussions about nutrition.

 

REFERENCES

[1] Deol, P., et al. (July 2015). Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver. PLOS One, 10(7).

[2] University of California – Riverside. (2015, July 22). Soybean oil causes more obesity than coconut oil, fructose: Scientists found mice on high soybean oil diet showed increased levels of weight gain, diabetes compared to mice on a high fructose diet or high coconut oil diet. ScienceDaily.

[3] Rosillo-Calle, F. (2009). A global overview of vegetable oils, with reference to biodiesel. CEP/Imperial College, Luc Pelkmans, VITO and Arnaldo Walter, UNICAMP for IEA Bioenergy Task 40.

[4] Haspel, T. (February 18, 2014). Farm bill: Why don’t taxpayers subsidize the foods that are better for us? The Washington Post.

[5] Blasbalg, TL, et al. (March 2011). Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. The American Journal of Clinical Nutrition, 93(5).

Lose Weight and Keep It Off? | The Paleo Diet

Besides winning the lottery, there may not be a more universally shared goal than losing body weight and keeping it off.1 If this is a goal you are after, you may not want to read the rest of today’s piece! That is because brand new research has pointed out that the odds of going from obese to a normal weight and staying there – are vanishingly slim.2, 3 For men, the odds are 1 in 210, and for women the odds are 1 in 124. That’s less than 1% – no matter what gender you are.

So how do we beat these (very depressing) odds? Quite simply, by following a Paleo diet! By consuming foods that are high in satiety and nutrients, we keep hunger at bay, and our body and brain happy.4, 5, 6, 7 Satiety and nutrition are both absolutely vital if long term, sustainable weight loss is one’s goal. As has been seen in scientific studies, a Paleo diet works better than even condition-specific diets (like those seen in patients with diabetes).8 One study sums it up thusly: “The Paleolithic diet might be the best antidote to the unhealthy Western diet.”9

Combining a great diet with a smart exercise routine (like CrossFit) is a great recipe to start stacking these odds in one’s favor.10 As the CrossFit Games are in full swing, we get to see professional athletes at their absolute peak – hopefully inspiring us to spend less time on the couch and more time at the gym. But you do not need to be a CrossFit Games competitor to enjoy a healthy exercise routine. If you are sedentary, just start walking around your neighborhood every day after work. Get your head in the game with baby steps, you’ll feel the difference.11 Once you’ve mastered that, you can progress to higher feats of fitness.

Lose Weight and Keep It Off? | The Paleo Diet

Erickson, Kirk I. et al. “Exercise Training Increases Size of Hippocampus and Improves Memory.” Proceedings of the National Academy of Sciences of the United States of America 108.7 (2011): 3017–3022. PMC. Web. 27 July 2015.

And even more than exercise, make sure you get plenty of sleep! This overlooked factor allows many to work extremely hard, eat right and still not keep the pounds off. Scientific researchers have known this for years.12 Sleep is an important modulator of neuroendocrine function and glucose metabolism.13 Both are usually disrupted when a person becomes obese, so getting them back in line requires eating well, exercise, and plenty of shuteye!

Sleep loss has also been shown to result in metabolic and endocrine alterations, including decreased glucose tolerance, decreased insulin sensitivity, increased evening concentrations of cortisol and increased levels of ghrelin.14 Bottom line: With all of this at play, our chances of losing weight and keeping it off are very slim! We want our body to be insulin sensitive, cortisol lower in the evening, and to express low levels of ghrelin (a key hunger hormone).

Lose Weight and Keep It Off?  | The Paleo Diet

Beccuti, Guglielmo, and Silvana Pannain. “Sleep and Obesity.” Current opinion in clinical nutrition and metabolic care 14.4 (2011): 402–412. PMC. Web. 27 July 2015.

Lose Weight and Keep It Off? | The Paleo Diet

Patel, Sanjay R., and Frank B. Hu. “Short Sleep Duration and Weight Gain: A Systematic Review.” Obesity (Silver Spring, Md.) 16.3 (2008): 643–653. PMC. Web. 27 July 2015.

Finally, sleep loss leads to decreased levels of leptin (one of the main satiety hormones) and increased hunger and appetite.15 So, the longer you go without sleep, the hungrier you get. Stop the cycle by hitting the pillow earlier.

With our world in an ever-increasing obesity pandemic, think of all the healthy ways you can lose weight and keep it off.16, 17, 18, 19, 20 Put your mind to it, don’t let anything stand in your way, and you’ll be on your way, to a leaner, healthier you!

 

REFERENCES

[1] Why Do You Say You Want to Lose Weight But Then Don’t Do It | Psychology Today. (n.d.). Retrieved from https://www.psychologytoday.com/blog/shrink/201208/why-do-you-say-you-want-lose-weight-then-don-t-do-it

[2] Available at: http://www.sciencedaily.com/releases/2015/07/150716180913.htm. Accessed July 21, 2015.

[3] Fildes A, Charlton J, Rudisill C, Littlejohns P, Prevost AT, Gulliford MC. Probability of an Obese Person Attaining Normal Body Weight: Cohort Study Using Electronic Health Records. Am J Public Health. 2015;:e1-e6.

[4] Westerterp-plantenga MS, Lemmens SG, Westerterp KR. Dietary protein – its role in satiety, energetics, weight loss and health. Br J Nutr. 2012;108 Suppl 2:S105-12.

[5] Paddon-jones D, Westman E, Mattes RD, Wolfe RR, Astrup A, Westerterp-plantenga M. Protein, weight management, and satiety. Am J Clin Nutr. 2008;87(5):1558S-1561S.

[6] Leidy HJ, Carnell NS, Mattes RD, Campbell WW. Higher protein intake preserves lean mass and satiety with weight loss in pre-obese and obese women. Obesity (Silver Spring). 2007;15(2):421-9.

[7] Soenen S, Westerterp-plantenga MS. Proteins and satiety: implications for weight management. Curr Opin Clin Nutr Metab Care. 2008;11(6):747-51.

[8] Jönsson T, Granfeldt Y, Ahrén B, 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;8:35.

[9] Klonoff DC. The beneficial effects of a Paleolithic diet on type 2 diabetes and other risk factors for cardiovascular disease. J Diabetes Sci Technol. 2009;3(6):1229-32.

[10] Curioni CC, Lourenço PM. Long-term weight loss after diet and exercise: a systematic review. Int J Obes (Lond). 2005;29(10):1168-74.

[11] Erickson KI, Voss MW, Prakash RS, et al. Exercise training increases size of hippocampus and improves memory. Proc Natl Acad Sci USA. 2011;108(7):3017-22.

[12] Patel SR, Hu FB. Short sleep duration and weight gain: a systematic review. Obesity (Silver Spring). 2008;16(3):643-53.

[13] Van cauter E, Knutson KL. Sleep and the epidemic of obesity in children and adults. Eur J Endocrinol. 2008;159 Suppl 1:S59-66.

[14] Knutson KL. Impact of sleep and sleep loss on glucose homeostasis and appetite regulation. Sleep Med Clin. 2007;2(2):187-197.

[15] Pejovic S, Vgontzas AN, Basta M, et al. Leptin and hunger levels in young healthy adults after one night of sleep loss. J Sleep Res. 2010;19(4):552-8.

[16] Roth J, Qiang X, Marbán SL, Redelt H, Lowell BC. The obesity pandemic: where have we been and where are we going?. Obes Res. 2004;12 Suppl 2:88S-101S.

[17] Swinburn BA, Sacks G, Hall KD, et al. The global obesity pandemic: shaped by global drivers and local environments. Lancet. 2011;378(9793):804-14.

[18] Catenacci VA, Hill JO, Wyatt HR. The obesity epidemic. Clin Chest Med. 2009;30(3):415-44, vii.

[19] James PT, Leach R, Kalamara E, Shayeghi M. The worldwide obesity epidemic. Obes Res. 2001;9 Suppl 4:228S-233S.

[20] Pan WH, Lee MS, Chuang SY, Lin YC, Fu ML. Obesity pandemic, correlated factors and guidelines to define, screen and manage obesity in Taiwan. Obes Rev. 2008;9 Suppl 1:22-31.

Not So (Artifically) Sweet | The Paleo Diet

I have had countless clients try to replace their sugar-laden diets with ones rich with artificial sweeteners. While this may work in the short term, it definitely does not work in the long term.1 2 And, the reasons for this are countless.3,

New research shows sugars specifically activate six neurosecretory cells in the brain, which produce Dh44, a homolog of the mammalian corticotropin-releasing hormone.4, 5 Artificial sweeteners do not activate these same cells – possibly leaving the brain in a half-finished reward state – potentially leading to more calories being taken in.6, 7

Not So (Artificially) Sweet | The Paleo Diet

Yang, Qing. “Gain Weight by ‘going Diet?’ Artificial Sweeteners and the Neurobiology of Sugar Cravings: Neuroscience 2010.” The Yale Journal of Biology and Medicine 83.2 (2010): 101–108. Print.

Another issue with artificial sweeteners is they are typically much, much sweeter than sugar. Just how much sweeter are these manmade creations? Most artificial sweeteners are 200-400 times sweeter than regular table sugar!8 Many researchers argue this leaves the brain expecting a plethora of calories, and also disrupts the brain’s natural reward mechanisms.9

While followers of the Paleo diet will certainly know that artificial sweeteners have no place in a healthy lifestyle, many who are trying to change their eating habits rely on artificial sweeteners for brief time periods. Not a great idea. As the scientific literature suggests, artificial sweeteners (because they are sweet) encourage sugar craving and sugar dependence.10

Even stevia, which many will argue is a healthier alternative to most artificial sweeteners, is 100-300 times sweeter than table sugar!11 It is certainly not a good idea to be consuming something that sweet on a regular basis – whether it contains sugar or not. Furthermore, artificial sweeteners are typically packaged in foods or drinks that have a laundry list of other negative substances and artificial ingredients.12

Salient scientific studies clearly show how in repeatedly exposing ourselves to sugar, we help to train our flavor preference. In short – the more sweet we eat, the more we crave and expect it. Many studies have shown lowering fat and/or salt intake, over several weeks, leads to less craving of these elements. This is exactly how you should treat sugar and artificial sweeteners.

Not So (Artificallyy) Sweet | The Paleo Diet

Sclafani, Anthony. “Sweet Taste Signaling in the Gut.” Proceedings of the National Academy of Sciences of the United States of America 104.38 (2007): 14887–14888. PMC. Web. 7 July 2015.

On a granular level, T1R2 and T1R3 sweet taste receptors are found in taste cells in the mouth and enteroendocrine cells in the gut.13 Stimulation of the T1R2 and T1R3 receptors in the mouth by sugars and artificial sweeteners activates intracellular signaling elements, which trigger peripheral taste nerves and brain gustatory pathways. This is one way in which artificial sweeteners actually have a similar effect to sugar – which is not a good thing.

Moreover, research shows substituting sucrose-sweetened drinks for diet drinks does not reduce total energy intake – and may even result in a higher intake during the following day.14 Artificial sweeteners are not the answer.

Even back in 1986, researchers concluded that the data do not support the hypothesis that long-term artificial sweetener use either helps weight loss or prevents weight gain.15

Not So (Artifically) Sweet | The Paleo Diet

Fernstrom, John D. et al. “Mechanisms for Sweetness.” The Journal of Nutrition 142.6 (2012): 1134S–1141S. PMC. Web. 7 July 2015.

So why are artificial sweeteners still used? Well, quite simply: money and industry.

Artificial sweeteners are beneficial to the food industry for a variety of reasons. One – they are cheap, and can help make poor quality foods taste ‘better’. Two – it makes it seem like they care. They sell you the sugar-laden stuff, and then – if you are ‘health conscious’ – you can buy their artificially sweetened product instead. Either way – they win.

I may be preaching to the converted here on The Paleo Diet, but often times even the most disciplined of us slowly let little ‘cheats’ into our diet – without realizing the long term impacts these seemingly innocuous choices may be having on our bodies and brains. If we have any hope of getting out of the current obesity pandemic we currently find ourselves in, it starts with removing all the sweetness (artificial or not) from our collective diet.16, 17, 18, 19, 20, 21 Your health (and waistline) will thank you for it!

 

REFERENCES

[1] Feijó Fde M, Ballard CR, Foletto KC, et al. Saccharin and aspartame, compared with sucrose, induce greater weight gain in adult Wistar rats, at similar total caloric intake levels. Appetite. 2013;60(1):203-7.

[2] Bellisle F, Drewnowski A. Intense sweeteners, energy intake and the control of body weight. Eur J Clin Nutr. 2007;61(6):691-700.

[3] Suez J, Korem T, Zeevi D, et al. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature. 2014;514(7521):181-6.

[4] Available at: http://www.endocrinologyadvisor.com/neuroendocrinology/sugar-artificial-sweeteners-satiety/article/423644/. Accessed July 5, 2015.

[5] Dus M, Lai JS, Gunapala KM, et al. Nutrient Sensor in the Brain Directs the Action of the Brain-Gut Axis in Drosophila. Neuron. 2015;87(1):139-51.

[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;16(8):1894-900.

[7] Blundell JE, Hill AJ. Paradoxical effects of an intense sweetener (aspartame) on appetite. Lancet. 1986;1(8489):1092-3.

[8] Pandurangan M, Park J, Kim E. Aspartame downregulates 3T3-L1 differentiation. In Vitro Cell Dev Biol Anim. 2014;50(9):851-7.

[9] Fernstrom JD, Munger SD, Sclafani A, De araujo IE, Roberts A, Molinary S. Mechanisms for sweetness. J Nutr. 2012;142(6):1134S-41S.

[10] 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.

[11] Goyal SK, Samsher, Goyal RK. Stevia (Stevia rebaudiana) a bio-sweetener: a review. Int J Food Sci Nutr. 2010;61(1):1-10.

[12] Kellett GL, Brot-laroche E, Mace OJ, Leturque A. Sugar absorption in the intestine: the role of GLUT2. Annu Rev Nutr. 2008;28:35-54.

[13] Sclafani A. Sweet taste signaling in the gut. Proc Natl Acad Sci USA. 2007;104(38):14887-8.

[14] Lavin JH, French SJ, Read NW. The effect of sucrose- and aspartame-sweetened drinks on energy intake, hunger and food choice of female, moderately restrained eaters. Int J Obes Relat Metab Disord. 1997;21(1):37-42.

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

[16] Swinburn BA, Sacks G, Hall KD, et al. The global obesity pandemic: shaped by global drivers and local environments. Lancet. 2011;378(9793):804-14.

[17] Soeliman FA, Azadbakht L. Weight loss maintenance: A review on dietary related strategies. J Res Med Sci. 2014;19(3):268-75.

[18] Lustig RH. Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc. 2010;110(9):1307-21.

[19] Isganaitis E, Lustig RH. Fast food, central nervous system insulin resistance, and obesity. Arterioscler Thromb Vasc Biol. 2005;25(12):2451-62.

[20] Lustig RH, Sen S, Soberman JE, Velasquez-mieyer PA. Obesity, leptin resistance, and the effects of insulin reduction. Int J Obes Relat Metab Disord. 2004;28(10):1344-8.

[21] Lustig RH. The neuroendocrinology of obesity. Endocrinol Metab Clin North Am. 2001;30(3):765-85.

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