Tag Archives: sugar

When it comes to humans, we’re all just victims of our own biochemistry. Our brains are controlled and ruled by chemicals – from what we eat; to how and when we sleep; even to who we choose as a life partner.[1] Biochemistry – or ‘biological chemistry’ – is concerned with all of the biochemical reactions which take place within our bodies and brains.[2] [3] This means that the simple act of eating a meal is actually composed of thousands of tiny reactions and interactions – on a biochemical level, at least.[4] [5]

Biochemistry is important because it helps us better understand how our bodies work. Biochemistry is most critical to understanding how and what foods to eat and remains a criminally overlooked component of both keeping weight off and maintaining a healthy lifestyle.[6] If we can better understand the reactions happening inside our body, we can better understand how to treat ourselves, overall.

 

The Biochemistry of our Morning Coffee

To better understand the biochemistry of our eating, it will help to look at how a few individual components of a diet affect our biochemistry. For many (if not all) of us, our day begins with the ingestion of a stimulant. Specifically, caffeine. From our morning cup of coffee onwards, many of us feel most energetic after our first dose of caffeine. This is simple to understand from a biochemical perspective – the caffeine is binding to our adenosine receptors, and simply removing our caffeine withdrawal.[7] [8]

Adenosine helps us stay calm and is even related to sleep.[9] Many do not know this, but caffeine binds to the receptors for adenosine. But this also means that it effectively blocks our body from functioning normally.[10] Our bodies love homeostasis, so if we consume large enough quantities of caffeine on a regular basis, they try to remain in balance by creating more and more adenosine receptors.[11] So – you guessed it – the more caffeine we consume, the more we need just to achieve the same mild ‘high’ we got when we first started drinking coffee.[12] Sadly, this is exactly how all drugs work and caffeine – though legal and widespread – is still a drug, biochemically speaking.[13]

 

The Enormous Impact of Sugar on our Biochemistry

Another huge element of the biochemistry of our food and drink is sugar. Sugar is definitely a drug. In fact, it’s probably the substance in our diet most obviously associated with drugs.[14] Scientific research has shown that sugar is addictive, it has no nutritional value, and it has hugely negative impacts on our health, especially when it’s consumed in excess.[15] To astute readers – or anyone who has been paying attention – this is not shocking news.

Sugar is fascinating from a biochemistry perspective because there is essentially no reason to consume it – especially in excess – or even in the amounts that we do in a typical western diet. Sugar consumption has gone up ten-fold, in the US and worldwide, since the invention of soda.[16] It is, quite literally, used solely by processed food manufacturers and surreptitiously added to everything (even bread) to make foods more addictive, to get us to crave their products, and buy more of them.[17]

While this sounds like a pretty stark reality, it is nonetheless reality. There is no need for sugar in almost any food. Sugar is only found in good ratios, in food that is organic and made by the earth naturally.[18] If you could only pick one thing to do to improve your healthy biochemistry, lowering or removing sugar from your diet should be it.

In John Yudkin’s classic book Pure, White, and Deadly, he goes over just how bad sugar’s effects are. And the miraculous thing is that he was saying this long before most of us had any concerns at all about too much sugar.[19] If there is one product or industry to blame for decreasing the quality of our diet and decreasing our nation’s health, it would be soda. There is literally no reason for soda to exist. And as Steve Jobs famously said; it’s just sugar water.

When we look at the biochemical makeup up of soda, that is quite literally almost all we find – water, and sugar. Disturbingly, soda is even worse than just this simple formula, as most of the sugar is in the form of fructose, which has been shown, in numerous studies, to have hugely negative impacts on both our liver and overall health.[20] From a biochemical standpoint, fructose is processed differently than glucose and has many disturbing parallels to alcohol in terms of how our bodies and brains are affected by it.[21]

In fact, NAFLD (non-alcoholic fatty liver disease), caused by excess fructose is in many ways the exact same disease as alcoholism.[22] As its name implies, fatty liver disease is usually caused by excess alcohol. However, pediatric endocrinologists are seeing an epidemic in obese children – and they only get this way by excess sugar (specifically fructose) consumption.[23]

So, what does the biochemistry of healthy eating look like? In short, it’s filled with protein, healthy (anti-inflammatory) fats, and complex carbohydrates.[24] These food choices all provide favorable reactions, biochemically, with no real downsides. When we eat a diet like the Paleo Diet® – our bodies and brains remain happy, and function optimally.[25]

Many do not understand that the toll a poor diet takes on us is great. We can lose our ability to process thoughts as quickly, lose our hair, gain weight, develop disease, and even die.[26] And yet many of us still choose to not eat properly. This is truly self-sabotage. By following the Paleo Diet template – all the hard work is done for you. You do not have to think about food choices or worry about the biochemistry of what you are eating. A Paleo Diet is perfectly proportioned to optimize our health, and to keep us lean, healthy, and happy.

 

References

[1] Granado-lorencio F, Hernández-alvarez E. Functional Foods and Health Effects: A Nutritional Biochemistry Perspective. Curr Med Chem. 2016;23(26):2929-2957.

[2] Winblad B, Hardy J, Bäckman L, Nilsson LG. Memory function and brain biochemistry in normal aging and in senile dementia. Ann N Y Acad Sci. 1985;444:255-68.

[3] Holden-dye LM, O’connor VM, Stephenson FA. Molecules of the mind: integrating synaptic biochemistry to understand brain function. Biochem Soc Trans. 2006;34(Pt 1):43-4.

[4] Mathes WF, Brownley KA, Mo X, Bulik CM. The biology of binge eating. Appetite. 2009;52(3):545-553.

[5] Imai S, Fukui M, Kajiyama S. Effect of eating vegetables before carbohydrates on glucose excursions in patients with type 2 diabetes. J Clin Biochem Nutr. 2014;54(1):7-11.

[6] Sikaris KA. The clinical biochemistry of obesity. Clin Biochem Rev. 2004;25(3):165-81.

[7] Ammon HP. Biochemical mechanism of caffeine tolerance. Arch Pharm (Weinheim). 1991;324(5):261-7.

[8] Nehlig A, Daval JL, Debry G. Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects. Brain Res Brain Res Rev. 1992;17(2):139-70.

[9] Shryock JC, Belardinelli L. Adenosine and adenosine receptors in the cardiovascular system: biochemistry, physiology, and pharmacology. Am J Cardiol. 1997;79(12A):2-10.

[10] Ribeiro JA, Sebastião AM. Caffeine and adenosine. J Alzheimers Dis. 2010;20 Suppl 1:S3-15.

[11] Urry E, Landolt HP. Adenosine, caffeine, and performance: from cognitive neuroscience of sleep to sleep pharmacogenetics. Curr Top Behav Neurosci. 2015;25:331-66.

[12] Meredith SE, Juliano LM, Hughes JR, Griffiths RR. Caffeine Use Disorder: A Comprehensive Review and Research Agenda. J Caffeine Res. 2013;3(3):114-130.

[13] Pardo lozano R, Alvarez garcía Y, Barral tafalla D, Farré albaladejo M. [Caffeine: a nutrient, a drug or a drug of abuse]. Adicciones. 2007;19(3):225-38.

[14] 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.

[15] Freeman CR, Zehra A, Ramirez V, Wiers CE, Volkow ND, Wang GJ. Impact of sugar on the body, brain, and behavior. Front Biosci (Landmark Ed). 2018;23:2255-2266.

[16] Anjum I, Jaffery SS, Fayyaz M, Wajid A, Ans AH. Sugar Beverages and Dietary Sodas Impact on Brain Health: A Mini Literature Review. Cureus. 2018;10(6):e2756.

[17] Rippe JM, Angelopoulos TJ. Relationship between Added Sugars Consumption and Chronic Disease Risk Factors: Current Understanding. Nutrients. 2016;8(11)

[18] Martínez steele E, Baraldi LG, Louzada ML, Moubarac JC, Mozaffarian D, Monteiro CA. Ultra-processed foods and added sugars in the US diet: evidence from a nationally representative cross-sectional study. BMJ Open. 2016;6(3):e009892.

[19] Yudkin J. Dietetic aspects of atherosclerosis. Angiology. 1966;17(2):127-33.

[20] Rizkalla SW. Health implications of fructose consumption: A review of recent data. Nutr Metab (Lond). 2010;7:82.

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

[22] Byrne CD, Targher G. NAFLD: a multisystem disease. J Hepatol. 2015;62(1 Suppl):S47-64.

[23] Basaranoglu M, Basaranoglu G, Bugianesi E. Carbohydrate intake and nonalcoholic fatty liver disease: fructose as a weapon of mass destruction. Hepatobiliary Surg Nutr. 2015;4(2):109-16.

[24] Sauberlich HE. Implications of nutritional status on human biochemistry, physiology, and health. Clin Biochem. 1984;17(2):132-42.

[25] 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.

[26] Leslie W, Hankey C. Aging, Nutritional Status and Health. Healthcare (Basel). 2015;3(3):648-58.

Paleo devotees are still waiting for mainstream nutritional science to recognize the demonstrated, profound anti-diabetic effects of their nutrient-dense, naturally low-carbohydrate diet.

Unfortunately, based on a recent meta-analysis by Professor Nita Forouhi et al [1] that surveyed diet-based diabetes therapies, they will have to wait a bit longer.

Researchers have once again sidestepped Ancestral living in favor of pills, surgery and crash dieting.

Part One of this series examined the study which showed a clear bias toward Western dietary norms, and concluded that weight loss is the best therapy for diabetesbased on bariatric surgery results.  

Forouhi et al explored other therapies that could challenge the mainstream, including low-carb diets, but declared them “controversial” or “difficult.” Instead, the study noted that bariatric surgery often normalizes blood glucose levels—and endorsed diets which mimic it including high-sugar liquid meal replacement “crash” diets.

Even worse, this idea has been taken to new extremes by a separate team of researchers, who are developing an oral medication intended to mimic bariatric surgery.

 

The surgery pill: eat your cake without having it

Published in the same month as the Forouhi study, a separate paper by Yuhan Lee et al [2] proposed going one step further—an oral medication that mimics bariatric surgery – for the same reasons: short term improvement in blood glucose markers.

The proposed “therapeutic luminal coating of the intestines” is being developed to “block glucose absorption” and also to deliver biologics and other medications to the lower intestine with less pre-digestion.

The authors claim their product “will emulate a critical part of bariatric surgery in a non-invasive way.”

As of this writing, the drug creates a transient paste that coats the intestines, blocking up to 43% of ingested glucose in the first hour, dropping to 25% after the third hour.  The paste takes three days to disperse.

Long-term side effects of its use are not explored in the paper.

 

Weight loss at any cost?

Healthy, sustainable improvements in body composition are certainly therapeutic for diabetes and many other ailments.  The benefits range from reduced inflammatory cytokines (secreted by excess adipose tissue) to simple relief on load-bearing joints.

However, surgery to promote weigh loss (or a “crash” low-calorie diet) are extreme steps—and not indicated, or sustainable, for most diabetics or healthy individuals.

These sudden, disruptive lifestyle changes (not to mention discomfort and possible surgical complications) should be a last resort—even if they produce short term results and temporarily improved blood glucose markers.

One follow-up study of bariatric surgical patients showed reasonable weight loss (77 percent after one year, dropping to 56 percent in five years) but diabetes remission was only 51 percent after one year, and 21 percent at five years. [3]

This short term success may justify surgery (and its risks) for the morbidly obese, but as Yuhan Lee et al point out in their paper on Therapeutic Luminal Coating of the Intestine, most diabetics are not surgical candidates to begin with.

Nor does the Lee paper examine diet. The focus is simply on inhibiting glucose uptake.

The issue is that surgery or ultra-low calorie diets (or intestinal paste) don’t address fundamental dietary issues.  Post-surgery dietary recommendations still include grains, cereals and processed foods (like “creamed soups”) [4]. Sugar is discouraged but not eliminated.  

As even new Paleo dieters realize, grains, sugars, seed oils and processed foods all contribute to inflammation, glucose insensitivity… and lead back to diabetes.

 

Surgery in a pill… is still a pill

While “coating the intestines to prevent glucose uptake” may have clinical applications, it also sidesteps the idea of healthy dietary changes.

Instead, it implies that we can eat whatever we like–and take yet another pill to protect us from our diet’s worst effects.

But how sustainable is reliance on medication to insulate us from lifelong, chronic intestinal permeability, systemic inflammation, and elevated blood glucose?

Not everyone thinks this is a good idea.

Dr. Fiona Godlee, is the editor-in-chief of The BMJ, an international medical online journal.  She addresses this issue in a penetrating article: Pills are not the answer to unhealthy lifestyles. [5]

Referencing the Forouhi study among others, she criticizes the multi-billion-dollar market for drugs aimed at lifestyle-based diseases like T2D, hypertension, and fatty liver disease.

Her conclusion:

…pills can’t be the answer to diseases caused by unhealthy living. As well as unsustainable cost for often marginal benefit, they always cause harm. Rather than medicating almost the entire adult population, let’s invest our precious resources in societal and lifestyle change, public health, and prevention. [Emphasis added.]

 

When unhealthy living is normal

Surgery. Unsustainable, non-satiating crash diets. Intestinal paste.

Temporary results.

These extreme, short term strategies all tiptoe around the idea that fundamental dietary change might workor at least be worth a try. They also highlight the deeply entrenched [6] nature of conventional dietary norms.

The Forouhi study acknowledges how hard it is for patients (or anyone) to adopt significant dietary changes. Elimination of unhealthy foods or food groups is dismaying or even threatening to many people.

Mainstream media often reinforces this perception.

Articles like The problems with elimination diets, by Paige Smathers, RD, [7] and Overwhelming thoughts about food can have a profound impact on overall health, by Devrie Pettit, RD.N [8] appear often. They make the case that “average dieters” can’t handle giving up certain foods—and shouldn’t be expected to do so.  

Both of these dietitians (and many others) claim the stress isn’t worth the health benefits.

But is it really that hard to stop eating unhealthy food?  

 

Paleo living: the common-sense alternative

Every Paleo dieter knows healthy dietary changes are possible—and well worth the effort. Thousands of Paleo converts permanently eliminate grains, sugars, dairy, seed oils, and processed foods every day.

They do all this without surgery or drugs—or the associated discomfort, lifestyle dislocation, and expense.  

They don’t panic over absent pasta.

Most don’t require medical supervision, except to reduce medications for ongoing ailments (like diabetes.)  Their nutrient-dense, highly satiating pre-agrarian diet is sustainable, enjoyable and promotes vibrant good health.

This writer (down 40 pounds) has been Paleo for almost three years, has had exactly one cold in that time, is no longer pre-diabetic, clinically obese or hypercholesterolemic…and will never go back.

 

REFERENCES

  1. “Dietary and nutritional approaches for prevention and management of type 2 diabetes,” 6/13/2018, published in The BMJ by professors Nita G. Forouhi, Anoop Misra, Viswanathan Mohan, Roy Taylor, and director William Yancy, retrieved
  2. “Therapeutic Luminal Coating of the Intestine,” 6/11/2018, published in Nature Materials by  Yuhan Lee, Tara E. Deelman, Keyue Chen, Dawn S.Y. Lin, Ali Tavakkoli & Jeffrey M. Karp, retrieved
  3. “Bariatric Surgery Patients See Weight Gain After ‘Honeymoon’ Period,” published on Healthline.com by Brian Krans, 8/5/2015, retrieved
  4. “Gastric bypass diet: What to eat after the surgery,” published on MayoClinic.org by Mayo Clinic Staff, 9/21/2018, retrieved
  5. “Pills are not the answer to unhealthy lifestyles,” published in The BMJ by Dr. Fiona Godlee, 7/12/2018, retrieved
  6. “The reality of food addiction,” published on ThePaleoDiet.com by Casey Thaler, B.A, NASM-CPT, FNS, 7/24/2014, retrieved here
  7. “The problems with elimination diets,” published on KSL.com by Paige Smathers, RD, 7/18/2017, retrieved
  8. “Overwhelming thoughts about food can have a profound impact on overall health,” published on KSL.com by Devrie Pettit, RDN, 9/11/2018, retrieved  

Paleo dieters often wonder when the rest of the world will catch up.

Most of all, they wonder when mainstream nutritional science will finally validate what they experience every day: safe and natural weight loss; freedom from chronic illness; vibrant energy all day long.

But mainstream nutritional researchers remain divided on basic diet and health issues and many factors inhibit progress—especially toward understanding non-conventional approaches like Paleo.

Freighted with years of conventional wisdom, torn by conflicting agendas, and (like scientists in all disciplines) too frequently impervious to new ideas, these savants often run in place. Covering new ground sometimes only moves a few inches a year.

A new study by Professor Nita G. Forouhi and colleagues provides some understanding of the lack of consensus when it comes to diabetes, and what drives it.

The study itself is an overview or meta-analysis of several current dietary therapies for type 2 diabetes (T2D).[1]

The authors discuss several interventions, including pros and cons from different camps within the nutritional field. Forouhi is not afraid to show both sides of each debate, especially regarding low-carbohydrate diets.

The analysis acknowledges that dietary interventions can mitigate or even reverse T2D but admits up front that these interventions are both “controversial and difficult.”  

Paleo readers will quickly note how conventional Western dietary wisdom underlies much of the controversy.

Some highlights:

 

Questions about data and dietary guidelines

Intriguingly, the study notes that basic scientific nutritional data is subject to manipulation:  

Moreover, lack of transparency in the development of guidelines and bias in the primary nutritional studies can undermine the development of reliable dietary guidelines; recommendations for their improvement must be heeded.

The study continues further down …more investment is needed in good quality research with a greater focus on overcoming the limitations of existing research.”

This frank admission is important in the context of what follows—including the discussions of unconventional therapies like low-carb and ultra-low calorie diets.

And bear in mind that entrenched conventional ideas do bias the analysis throughout including the diet-heart hypothesis (bias against saturated fat), and the traditional low-fat-high fiber agenda including a strong bias in favor of whole grains.

 

Unexpected disagreement on foods

Participants agree that patients should avoid processed meats, sodium, trans fats, refined grains and sugars, as well as sugary drinks.

Surprisingly, fruits and vegetables are dismissed by some as desirable but too expensive for low- to middle- income populations. Other researchers recommend them, but only in the context of weight loss.  

Diets that rely on vegetables for fiber (instead of whole grains) are discarded as “difficult without further discussion.

As an aside, the study stops short of endorsing unprocessed red meat (and even fish) claiming more research is needed.

 

The low carbohydrate conundrum

Low carbohydrate diets are discussed extensively, but not all researchers endorse them—even though the study admits that they work.

Macronutrient ratios (fat to carbohydrates to protein) are acknowledged as important, but no consensus exists on therapeutic ratios. The American Heart Association is cited as insisting that no population-wide recommendations can be made and that all advice should be individualized.

The research cited by Forouhi shows no real agreement on what constitutes low-carb, or what type of carbs are best. Reducing grains and legumes appears broadly acceptable but different factions disagree on fruit consumption.  Refined carbs are discouraged, but most researchers insist on including whole grains.

Carbohydrate percentages in the analysis vary from ketogenic levels to 40% of calories, or more.

Some researchers think low-carb diets arent sustainable (or desirable) because they think people will eat too much protein, or too much saturated fat.  

Others claim that low-carb diets have no affect at all on diabetesdirectly contradicting the studys premise that such diets are recognized as therapeutic.

The study concludes that low-carb is controversial, but candidly admits it deserves further study.

 

Weight loss

The study emphasizes weight loss as therapeutic, endorsing it as a cornerstone of diabetes treatment.

The study emphasizes the success that bariatric surgery patients have with T2D due to caloric reduction and the resulting normalization of glucose levels. It explores ultra-low calorie diets that mimic this sudden, dramatic drop in total calories.

However, these diets are acknowledged as hard to sustain over time, and often include heavily processed, high sugar, liquid meal-replacements. The study notes and accepts the high sugar component as a tradeoff for the overall reduction in calories.

Note: The drug industry has also taken note of this bariatric surgery effect and is developing a new pill that coats the intestines to prevent caloric uptake. The goal is to mimic the surgerys blood glucose results for T2D patients.

 

Looking beyond weight loss  

Something the Forouhi seems to miss is that while sudden weight loss improves blood glucose markers, this may not be the whole story. Focusing on weight loss alone ignores the central issue that whole grains affect blood glucose levels the same way refined grains do. [2]

Even if a whole grain-based diet promotes overall weight loss, with all its acknowledged positive effects, the grains themselves will still promote insulin resistance, intestinal permeability, overall systemic inflammationand diabetes.

Most diabetics are unlikely to choose drastic surgery, with its likelihood of complications, or highly processed, unsatisfying sugar-based liquid diets. Instead, they should consider an inexpensive, low-impact, health-promoting low-carb diet like Paleo.

 

Paleo: the original low-carb, weight loss diet  

Following a sustainable, satiating Paleo Diet is easy (compared to surgery) and addresses the study’s major concerns:

  • High fiber: anyone on the Paleo Diet for over 30 days knows that vegetables provide MORE fiber than any type of grains.
  • Lower calories:  well-planned Paleo Diets (approximately 2/3 vegetables by volume) provide satiety from protein and healthy fats (like coconut, avocado, and olive oils) without exceeding sensible caloric guidelines. (Anyone can overeat on any diet, but Paleo makes this far less likely.)
  • Low carbohydrates: Paleo carb calories come from healthy, low-glycemic sources like sweet potatoes, squash, and non-starchy colorful vegetables.

Properly followed, Paleo is by definition a sustainable, low carb, high-fiber diet. Exactly what Forouhi’s analysis recommends and it has been demonstrated as therapeutic for Type 2 Diabetes many times [3].

 

REFERENCES:

  1. Dietary and nutritional approaches for prevention and management of type 2 diabetes, 6/13/2018, published in The BMJ by professors Nita G. Forouhi, Anoop Misra, Viswanathan Mohan, Roy Taylor, and director William Yancy, retrieved
  2. The Paleo Diet, Revised, by Loren Cordain, Ph.D., Professor Emeritus, copyright 2002, 2011, published by John Wiley & Sons, Hoboken, NJ; electronic edition, page 48
  3. The Paleolithic Diet is the best bet for diabetes and other diseases by Loren Cordain, Ph.D., Professor Emeritus, published in The Insider, Vol. 5, Issue 12, retrieved here

 

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: //www.sciencedaily.com/releases/2015/11/151105103957.htm. Accessed November 23, 2015.

2. Available at: //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: //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.

Sweet Sugar Coconut Fat | The Paleo Diet
If you’ve popped into your local Starbucks lately, you’ve already seen it. The Christmas red cups are here!  As someone who is admittedly an absolute Christmas fanatic, I must say that the hint of the season’s festivities in the air brings a smile to my face and that happy, and coaxes the warm holiday aura.

But one thing that doesn’t sit quite right is thinking about the sizeable number of syrupy sweet holiday drinks we’re consuming as a whole, let alone the sheer size of each individual drink has gone from 12 oz to 16 oz to… a 31 oz!1

A ‘Grande,’ 2% milk, peppermint latte is a whopping 54g of sugar from Starbucks.2 Thinking about supersizing to the mega 31 oz? That’s a whole heck of a lot of sugar (nearly double)!

But what if we want to enjoy a taste of the season? Is there a way to do so without wreaking havoc to our blood sugar, our mood, and our guts? Yes.

And it’s not about finding a ‘more Paleo’ sweetener. Instead of focusing on sweet, do yourself a favor and instead focus on fat. Without sugar, you can forget about the blood sugar spike, ensuing crash, and craving pangs for another.

Long before we ever knew about putting butter in coffee, in the lofty Himalayan mountains a few cups of yak butter tea, or po cha, was a welcome respite from the cold, thin air.[3] Since neither butter nor coffee are part of a strict Paleo diet, why not put a spin on the Tibetan model and brew a hot cup with a healthy, Paleo approved fat?

Can you say let’s go nuts with coconuts? Tasty, warming, and a with a fantastic creamy texture to boot, the Paleo recipe below will satisfy your palate and leave you feeling energized and ready to face the hectic holiday season… without ever feeling like you’ve had to deprive yourself!

Paleoista’s Holiday Coconut Tea

(Serves 2)

Ingredients

  • Herbal tea, your preference; try peppermint, cinnamon or ginger to create the holiday flavor profile
  • ¼ cup coconut butter, at room temperature
  • Ground cinnamon, to taste

Instructions

  1. Brew tea and let steep 3- 5 minutes.
  2. Remove tea leaves or bag and let cool slightly.
  3. Combine tea with coconut butter in blender and whiz to combine.
  4. Top with cinnamon and enjoy!

References

1. “Starbucks to Roll Out Biggest Drink Size Yet | Fox News.” Fox News. FOX News Network, 16 Jan. 2011. Web. 04 Nov. 2015.

2. “Peppermint Mocha.” Starbucks Coffee Company. Starbucks Coffee Company, n.d. Web. 04 Nov. 2015.

3. “Tea Tuesdays: Butter Up That Tea, Tibetan-Style.” NPR. NPR, n.d. Web. 04 Nov. 2015.

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: //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: //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.

Coca-Cola Sugar | The Paleo Diet

If your core business involves the mass production and distribution of sugary products with little nutritional value, times are tough. In the old days, prominent health institutions and regulatory governmental agencies looked upon sugar as relatively benign. Today, however, the science of sugar metabolism is much better understood and accordingly, those institutions and regulatory agencies are becoming increasingly fastidious regarding sugar.

The cat is out of the bag and it’s not going back. So if you’re in the sugar business, your most viable marketing strategies may well involve shifting consumer attention away from food and toward other aspects of healthy living, like exercise.

This seems to be the case with Coca-Cola, according to a story that broke earlier this week in The New York Times. A new nonprofit organization, the Global Energy Balance Network (GEBN), which collected $1.5 million in donations from Coke in 2014, promotes the idea that focusing on healthy food is the wrong approach to losing weight.1 Instead of food, dieters should be focusing on exercise.

In an astounding, you-have-see-it-for-yourself online video, GEBN’s vice president, Dr. Steven N. Blair, explains about obesity, “Most of the focus in the popular media and in the scientific press is that they’re eating too much, eating too much, eating too much, blaming fast food, blaming sugary drinks and so on. And there’s really virtually no compelling evidence that that in fact is the cause.”

While it’s true that no single food is solely responsible for obesity, the notion that sugar consumption doesn’t matter flies in the face of decades of nutritional science research. Even the big regulatory governmental agencies are now lining up against sugar and this isn’t happening for lack of “compelling evidence.”

After sitting on the sidelines for decades, both the U.S. and the U.K. governments are now aligning themselves with the published scientific literature and indicating that official warnings against excessive sugar consumption are forthcoming.

Last month in the U.K., the Scientific Advisory Committee on Nutrition (SACN), which advises Public Health England and other government agencies on nutrition, suggested that daily intake of sugar should be halved, from 10% to 5% of total calories, to reduce obesity and improve dental health.2

Here in the U.S., the USDA’s Dietary Guidelines for Americans are due for revision this year. The Dietary Guidelines Advisory Committee has already met and, after reviewing the published scientific literature, has determined that sugar should account for no more than 10% of total calories.3 Previously, the guidelines recommend against consuming “too much” sugar, but failed to quantify upper limits.

Finally, in March of this year, the World Health Organization issued an official communiqué stating that sugar should account for no more than 10% of total calories and that 5% would confer even greater health benefits.4 According to Dr. Francesco Branca, Director of WHO’s Department of Nutrition for Health and Development, “We have solid evidence that keeping intake of free sugars to less than 10% of total energy intake reduces the risk of overweight, obesity and tooth decay.”

Americans are drinking fewer soft drinks every year. In March, The Wall Street Journal reported that U.S. soft drink sales have declined every year for the past 10 years, representing a 14% decline since 2004.5 Are beverage giants trying to lull the public into believing that sugar plays no part in obesity?

Coca-Cola insists they partner with “the foremost experts in the fields of nutrition and physical activity,” but it’s curious that they seem to avoid funding groups that warn about sugar. In fact, since 2008, they have given upwards of $5.5 million to projects organized by two of GEBN’s founders, Dr. Blair and Gregory A. Hand, dean of the West Virginia University School of Public Health.6]

This story serves as a dramatic example of how corporate money can influence public opinion through purportedly independent, nonprofit organizations. We at The Paleo Diet would like to emphasize that exercise is indeed an important component of healthy lifestyles, but unfortunately exercise cannot compensate for unhealthy diets, particularly those high in processed, sugary foods.

REFERENCES

1 O’Connor, Anahad. (August 9, 2015). Coca-Cola Funds Scientists Who Shift Blame for Obesity Away From Bad Diets. The New York Times. Retrieved from //well.blogs.nytimes.com/2015/08/09/coca-cola-funds-scientists-who-shift-blame-for-obesity-away-from-bad-diets/?_r=0

2 The BBC. (July 17, 2015). Scientific experts: Sugar intake ‘should be halved’. Retrieved from //www.bbc.com/news/health-33551501

3 O’Connor, Anahad. (February 19, 2015). Nutrition Panel Calls for Less Sugar and Eases Cholesterol and Fat Restrictions. The New York Times. Retrieved from //well.blogs.nytimes.com/2015/02/19/nutrition-panel-calls-for-less-sugar-and-eases-cholesterol-and-fat-restrictions/?_r=1

4 Press Release. (March 4, 2015). WHO calls on countries to reduce sugars intake among adults and children. The World Health Organization. Retrieved from //www.who.int/mediacentre/news/releases/2015/sugar-guideline/en/

5 Esterl, Mike. (March 26, 2015). Soft Drinks Hit 10th Year of Decline. The Wall Street Journal. Retrieved from //www.wsj.com/articles/pepsi-cola-replaces-diet-coke-as-no-2-soda-1427388559

6 O’Connor, Anahad. (August 9, 2015). Coca-Cola Funds Scientists Who Shift Blame for Obesity Away From Bad Diets. The New York Times. Retrieved from //well.blogs.nytimes.com/2015/08/09/coca-cola-funds-scientists-who-shift-blame-for-obesity-away-from-bad-diets/?_r=0

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 .

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

 

 

REFERENCES

[1] Avena NM, Bocarsly ME, Hoebel BG. Animal models of sugar and fat bingeing: relationship to food addiction and increased body weight. Methods Mol Biol. 2012;829:351-65.

[2] Avena NM, Rada P, Hoebel BG. Sugar bingeing in rats. Curr Protoc Neurosci. 2006;Chapter 9:Unit9.23C.

[3] Rada P, Avena NM, Hoebel BG. Daily bingeing on sugar repeatedly releases dopamine in the accumbens shell. Neuroscience. 2005;134(3):737-44.

[4] Blum K, Thanos PK, Gold MS. Dopamine and glucose, obesity, and reward deficiency syndrome. Front Psychol. 2014;5:919.

[5] Berridge KC. ‘Liking’ and ‘wanting’ food rewards: brain substrates and roles in eating disorders. Physiol Behav. 2009;97(5):537-50.

[6] Wise RA. Role of brain dopamine in food reward and reinforcement. Philos Trans R Soc Lond, B, Biol Sci. 2006;361(1471):1149-58.

[7] Murray S, Tulloch A, Gold MS, Avena NM. Hormonal and neural mechanisms of food reward, eating behaviour and obesity. Nat Rev Endocrinol. 2014;10(9):540-52.

[8] Blum K, Gardner E, Oscar-berman M, Gold M. “Liking” and “wanting” linked to Reward Deficiency Syndrome (RDS): hypothesizing differential responsivity in brain reward circuitry. Curr Pharm Des. 2012;18(1):113-8.

[9] Swiecicki L, Scinska A, Bzinkowska D, et al. Intensity and pleasantness of sucrose taste in patients with winter depression. Nutr Neurosci. 2014.

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

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

[12] Caffaro CE, Hirschberg CB. Nucleotide sugar transporters of the Golgi apparatus: from basic science to diseases. Acc Chem Res. 2006;39(11):805-12.

[13] Willett WC, Ludwig DS. Science souring on sugar. BMJ. 2013;346:e8077.

[14] Grant JE, Potenza MN, Weinstein A, Gorelick DA. Introduction to behavioral addictions. Am J Drug Alcohol Abuse. 2010;36(5):233-41.

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

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

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

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

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

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

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

[22] 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.

[23] Popkin BM, Nielsen SJ. The sweetening of the world’s diet. Obes Res. 2003;11(11):1325-32.

[24] 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.

[25] Sharma LL, Teret SP, Brownell KD. The food industry and self-regulation: standards to promote success and to avoid public health failures. Am J Public Health. 2010;100(2):240-6.

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

[27] Copinschi G. Metabolic and endocrine effects of sleep deprivation. Essent Psychopharmacol. 2005;6(6):341-7.

[28] Harris JL, Bargh JA, Brownell KD. Priming effects of television food advertising on eating behavior. Health Psychol. 2009;28(4):404-13.

[29] Knutson KL, Spiegel K, Penev P, Van cauter E. The metabolic consequences of sleep deprivation. Sleep Med Rev. 2007;11(3):163-78.

[30] Andreyeva T, Long MW, Brownell KD. The impact of food prices on consumption: a systematic review of research on the price elasticity of demand for food. Am J Public Health. 2010;100(2):216-22.

[31] Gearhardt AN, White MA, Potenza MN. Binge eating disorder and food addiction. Curr Drug Abuse Rev. 2011;4(3):201-7.

[32] Davis C, Levitan RD, Kaplan AS, Kennedy JL, Carter JC. Food cravings, appetite, and snack-food consumption in response to a psychomotor stimulant drug: the moderating effect of “food-addiction”. Front Psychol. 2014;5:403.

[33] Dimitrijević I, Popović N, Sabljak V, Škodrić-trifunović V, Dimitrijević N. Food addiction-diagnosis and treatment. Psychiatr Danub. 2015;27(1):101-6.

[34] Schulte EM, Avena NM, Gearhardt AN. Which foods may be addictive? The roles of processing, fat content, and glycemic load. PLoS ONE. 2015;10(2):e0117959.

[35] Meule A, Hermann T, Kübler A. Food addiction in overweight and obese adolescents seeking weight-loss treatment. Eur Eat Disord Rev. 2015;23(3):193-8.

[36] Hardman CA, Rogers PJ, Dallas R, Scott J, Ruddock HK, Robinson E. “Food addiction is real”. The effects of exposure to this message on self-diagnosed food addiction and eating behaviour. Appetite. 2015;91:179-84.

[37] Schulte EM, Joyner MA, Potenza MN, Grilo CM, Gearhardt AN. Current considerations regarding food addiction. Curr Psychiatry Rep. 2015;17(4):563.

[38] Piccinni A, Marazziti D, Vanelli F, et al. Food addiction spectrum: a theoretical model from normality to eating and overeating disorders. Curr Med Chem. 2015;22(13):1631-8.

[39] Pedram P, Sun G. Hormonal and dietary characteristics in obese human subjects with and without food addiction. Nutrients. 2015;7(1):223-38.

[40] Karlsson HK, Tuominen L, Tuulari JJ, et al. Obesity is associated with decreased μ-opioid but unaltered dopamine D2 receptor availability in the brain. J Neurosci. 2015;35(9):3959-65.

[41] Hebebrand J, Albayrak Ö, Adan R, et al. “Eating addiction”, rather than “food addiction”, better captures addictive-like eating behavior. Neurosci Biobehav Rev. 2014;47:295-306.

[42] Ziauddeen H, Fletcher PC. Is food addiction a valid and useful concept?. Obes Rev. 2013;14(1):19-28.

[43] Barry D, Clarke M, Petry NM. Obesity and its relationship to addictions: is overeating a form of addictive behavior?. Am J Addict. 2009;18(6):439-51.

[44] Ogden J, Clementi C. The experience of being obese and the many consequences of stigma. J Obes. 2010;2010

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

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

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

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

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

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

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

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

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

[54] Lustig RH, Schmidt LA, Brindis CD. Public health: The toxic truth about sugar. Nature. 2012;482(7383):27-9.

[55] 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.

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

[57] Yates KF, Sweat V, Yau PL, Turchiano MM, Convit A. Impact of metabolic syndrome on cognition and brain: a selected review of the literature. Arterioscler Thromb Vasc Biol. 2012;32(9):2060-7.

[58] Singh RB, Gupta S, Dherange P, et al. Metabolic syndrome: a brain disease. Can J Physiol Pharmacol. 2012;90(9):1171-83.

[59] Tiehuis AM, Van der graaf Y, Mali WP, et al. Metabolic syndrome, prediabetes, and brain abnormalities on mri in patients with manifest arterial disease: the SMART-MR study. Diabetes Care. 2014;37(9):2515-21.

[60] Mauro C, De rosa V, Marelli-berg F, Solito E. Metabolic syndrome and the immunological affair with the blood-brain barrier. Front Immunol. 2014;5:677.

[61] Agrawal R, Gomez-pinilla F. ‘Metabolic syndrome’ in the brain: deficiency in omega-3 fatty acid exacerbates dysfunctions in insulin receptor signalling and cognition. J Physiol (Lond). 2012;590(Pt 10):2485-99.

[62] Cai D, Liu T. Inflammatory cause of metabolic syndrome via brain stress and NF-κB. Aging (Albany NY). 2012;4(2):98-115.

[63] Buijs RM, Kreier F. The metabolic syndrome: a brain disease?. J Neuroendocrinol. 2006;18(9):715-6.

[64] Zhu S, St-onge MP, Heshka S, Heymsfield SB. Lifestyle behaviors associated with lower risk of having the metabolic syndrome. Metab Clin Exp. 2004;53(11):1503-11.

[65] Available at: //www.niddk.nih.gov/health-information/health-statistics/Pages/overweight-obesity-statistics.aspx. Accessed July 29, 2015.

[66] Zhang Y, Von deneen KM, Tian J, Gold MS, Liu Y. Food addiction and neuroimaging. Curr Pharm Des. 2011;17(12):1149-57.

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

[68] Sturm R, Hattori A. Morbid obesity rates continue to rise rapidly in the United States. Int J Obes (Lond). 2013;37(6):889-91.

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

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

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

[72] Blumenthal DM, Gold MS. Neurobiology of food addiction. Curr Opin Clin Nutr Metab Care. 2010;13(4):359-65.

[73] 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.

[74] Levy A, Salamon A, Tucci M, Limebeer CL, Parker LA, Leri F. Co-sensitivity to the incentive properties of palatable food and cocaine in rats; implications for co-morbid addictions. Addict Biol. 2013;18(5):763-73.

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

[76] 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.

[77] Chen L, Appel LJ, Loria C, et al. Reduction in consumption of sugar-sweetened beverages is associated with weight loss: the PREMIER trial. Am J Clin Nutr. 2009;89(5):1299-306.

[78] Drewnowski A, Bellisle F. Liquid calories, sugar, and body weight. Am J Clin Nutr. 2007;85(3):651-61.

[79] Malik VS, Pan A, Willett WC, Hu FB. Sugar-sweetened beverages and weight gain in children and adults: a systematic review and meta-analysis. Am J Clin Nutr. 2013;98(4):1084-102.

[80] Cantley LC. Cancer, metabolism, fructose, artificial sweeteners, and going cold turkey on sugar. BMC Biol. 2014;12:8.

[81] Suez J, Korem T, Zeevi D, et al. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature. 2014.

[82] Anton SD, Martin CK, Han H, et al. Effects of stevia, aspartame, and sucrose on food intake, satiety, and postprandial glucose and insulin levels. Appetite. 2010;55(1):37-43.

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

[84] Direct and indirect cellular effects of aspartame on the brain. European Journal of Clinical Nutrition. 2008;62(4):451.

[85] Zhiping P. Pang et al. Endogenous Glucagon-like Peptide-1 Suppresses High-Fat Food Intake by Reducing Synaptic Drive onto Mesolimbic Dopamine Neurons. Cell Reports, July 2015.

[86] Zumoff B. Hormonal abnormalities in obesity. Acta Med Scand Suppl. 1988;723:153-60.

[87] Wren AM. Gut and hormones and obesity. Front Horm Res. 2008;36:165-81.

[88] Nadia Micali, Alison E. Field, Janet L. Treasure, David M. Evans. Are obesity risk genes associated with binge eating in adolescence? Obesity, 2015; 23 (8): 1729.

[89] Stice E, Yokum S, Zald D, Dagher A. Dopamine-based reward circuitry responsivity, genetics, and overeating. Curr Top Behav Neurosci. 2011;6:81-93.

[90] Grimm ER, Steinle NI. Genetics of eating behavior: established and emerging concepts. Nutr Rev. 2011;69(1):52-60.

[91] Barry D, Clarke M, Petry NM. Obesity and its relationship to addictions: is overeating a form of addictive behavior?. Am J Addict. 2009;18(6):439-51.

[92] Fawcett KA, Barroso I. The genetics of obesity: FTO leads the way. Trends Genet. 2010;26(6):266-74.

[93] Gearhardt AN, Corbin WR. The role of food addiction in clinical research. Curr Pharm Des. 2011;17(12):1140-2.

[94] Pursey KM, Stanwell P, Gearhardt AN, Collins CE, Burrows TL. The prevalence of food addiction as assessed by the Yale Food Addiction Scale: a systematic review. Nutrients. 2014;6(10):4552-90.

[95] Kasim-karakas SE, Almario RU, Cunningham W. Effects of protein versus simple sugar intake on weight loss in polycystic ovary syndrome (according to the National Institutes of Health criteria). Fertil Steril. 2009;92(1):262-70.

[96] Van itallie TB. Dietary fiber and obesity. Am J Clin Nutr. 1978;31(10 Suppl):S43-52.

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

[98] 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.

[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 , second only to corn, which amounted to 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). PLOS One, 10(7).

[2] University of California – Riverside. (2015, July 22). ScienceDaily.

[3] CEP/Imperial College, Luc Pelkmans, VITO and Arnaldo Walter, UNICAMP for IEA Bioenergy Task 40.

[4] Haspel, T. (February 18, 2014). The Washington Post.

[5] Blasbalg, TL, et al. (March 2011). The American Journal of Clinical Nutrition, 93(5).

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

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

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

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

Affiliates and Credentials
https://tmtravel.com.ua

medicaments-24.net

https://steroid-pharm.com