Tag Archives: featured

Eating Disorder | The Paleo Diet

There are currently 30 million people in the United States alone who suffer from eating disorders,1 where the related science and mental health are overlooked in their diagnoses.2 3 A new study, published by the journal of Psychosomatic Medicine, found new evidence of an association between the gut microbiota and the eating disorder anorexia.4

Researchers (and more mainstream sources) are beginning to understand just how much impact our gut has on nearly everything in our body – including our brain.5 6 7 Since nearly 90% of the body’s serotonin is made in the digestive tract – what’s going on in your gut – may be causing what’s going on inside your brain.8

Montiel-castro AJ, González-cervantes RM, Bravo-ruiseco G, Pacheco-lópez G. The microbiota-gut-brain axis: neurobehavioral correlates, health and sociality. Front Integr Neurosci. 2013;7:70.

Holzer P, Farzi A. Neuropeptides and the microbiota-gut-brain axis. Adv Exp Med Biol. 2014;817:195-219.

The researchers’ findings were remarkable. Individuals suffering from anorexia nervosa have not only one of the highest mortality rates,9 but also have very different microbial populations residing inside their guts, compared with healthy populations.10 How does this relate to a Paleo diet? Quite simply – what you eat plays a huge role in influencing your microbial population.11

There are of course a host of other factors, excluding diet that can influence your microbiome, but for our purposes, think of it as a basic equation: Bad food = bad microbial population in your gut = depression and anxiety, among other conditions. Good food = the opposite.

This is certainly an over-simplification, but for practical purposes, it works well. I’ll preface this with the importance of keeping your health and wellness in perspective and go from one extreme to another. A Paleo approach is meant to guide your lifestyle, not consume it. Since a Paleo diet focuses upon food qualitynot calories – it is oftentimes a good antidote to those who have food restriction behaviors.

If you were to go back to the 1950s, and tell a scientist or member of the general populace that what we have in our guts, in terms of microbes, would affect our weight or behavior – they would have escorted you away to a psychiatric ward. But, in the fascinating world of present day modern science, studies have shown the gut microbiome is indeed linked to weight gain, behavior, and even attention deficit disorders like ADHD.12 13 14 15 It’s not all so farfetched after all.

In the context of eating disorders, the microbiome is basically that of a spiral. The worse you eat, the worse your microbe population becomes, and the worse your mood and behavior fairs. Again, this is an oversimplification, but the analogy works. In a life filled with constant stressors, unpredictability, and other problems, if you follow the simple paradigm to make positive changes to our health and lifestyle, we can take back control.

A Paleo diet will provide your body with a wide array of beneficial nutrients that allow your gut bacteria to thrive, not hurt you. The human microbiome is basically an interface between our genes and our history of environmental exposures. Eating a healthy diet can only positively influence your gut microbiome.16

The science is far from definitive yet, but explorations of our microbiome continue to provide the chance of providing new answers into our own neurodevelopment – and behavior. If you or a loved one are suffering from an eating disorder, know that you are not alone and that healing your relationship with food and your body is possible, and professional counseling to help you overcome it is available.

For general information on mental health and to locate treatment services in your area, call the Substance Abuse and Mental Health Services Administration (SAMHSA) Treatment Referral Helpline at 1‑877‑SAMHSA7 (1‑877‑726‑4727). SAMSHA also has a Behavioral Health Treatment Locator on its website that can be searched by location.

References

1. Wade, T. D., Keski-Rahkonen A., & Hudson J. Epidemiology of eating disorders. In M. Tsuang and M. Tohen (Eds.), Textbook in Psychiatric Epidemiology (3rd ed.). New York: Wiley, 2011. p. 343-360.

2. Bulik CM, Tozzi F. Genetics in eating disorders: state of the science. CNS Spectr. 2004;9(7):511-5.

3. Wilson GT. Eating disorders, obesity and addiction. Eur Eat Disord Rev. 2010;18(5):341-51.

4. Kleiman SC, Watson HJ, Bulik-sullivan EC, et al. The Intestinal Microbiota in Acute Anorexia Nervosa and During Renourishment: Relationship to Depression, Anxiety, and Eating Disorder Psychopathology. Psychosom Med. 2015.

5. Gareau MG. Microbiota-gut-brain axis and cognitive function. Adv Exp Med Biol. 2014;817:357-71.

6. Holzer P, Farzi A. Neuropeptides and the microbiota-gut-brain axis. Adv Exp Med Biol. 2014;817:195-219.

7. Montiel-castro AJ, González-cervantes RM, Bravo-ruiseco G, Pacheco-lópez G. The microbiota-gut-brain axis: neurobehavioral correlates, health and sociality. Front Integr Neurosci. 2013;7:70.

8. Kato S. Role of serotonin 5-HT₃ receptors in intestinal inflammation. Biol Pharm Bull. 2013;36(9):1406-9.

9. American Journal of Psychiatry, Vol. 152 (7), July 1995, p. 1073-1074, Sullivan, Patrick F.

10. Available at: //www.sciencedaily.com/releases/2015/10/151005121310.htm. Accessed October 8, 2015.

11. Conlon MA, Bird AR. The impact of diet and lifestyle on gut microbiota and human health. Nutrients. 2015;7(1):17-44.

12. Petra AI, Panagiotidou S, Hatziagelaki E, Stewart JM, Conti P, Theoharides TC. Gut-Microbiota-Brain Axis and Its Effect on Neuropsychiatric Disorders With Suspected Immune Dysregulation. Clin Ther. 2015;37(5):984-95.

13. Turnbaugh PJ, Ridaura VK, Faith JJ, Rey FE, Knight R, Gordon JI. The effect of diet on the human gut microbiome: a metagenomic analysis in humanized gnotobiotic mice. Sci Transl Med. 2009;1(6):6ra14.

14. Sweeney TE, Morton JM. The human gut microbiome: a review of the effect of obesity and surgically induced weight loss. JAMA Surg. 2013;148(6):563-9.

15. Sampson TR, Mazmanian SK. Control of brain development, function, and behavior by the microbiome. Cell Host Microbe. 2015;17(5):565-76.

16. Gonzalez A, Stombaugh J, Lozupone C, Turnbaugh PJ, Gordon JI, Knight R. The mind-body-microbial continuum. Dialogues Clin Neurosci. 2011;13(1):55-62.

Vitamin E | The Paleo Diet

Symptoms of vitamin E deficiency are rare, but according to at least four national surveys, most Americans consume less than the government’s Recommended Daily Allowance (RDA) of this essential nutrient.1 The authors of an August 2015 study published in PLOS-One call vitamin E a “shortfall nutrient” because over 90% of Americans consume insufficient quantities and because low vitamin E status has been linked to multiple health consequences, including increased total mortality.2

Vitamin E is clearly important, but can the Paleo diet provide adequate levels? After all, some of the most frequently cited “best dietary sources” aren’t Paleo compliant. Are supplements necessary? The RDA for males and females above 14 years of age is 15 mg daily. The following table shows vitamin E values for 100 grams of various foods and their corresponding RDAs.

Vitamin E

The foods highest in vitamin E are predominantly seeds/nuts and their oils. Seed oils are excluded from the Paleo diet, however, primarily because they contain excessive amounts of polyunsaturated fatty acids (PUFAs). Almonds, hazelnuts, and sunflower seeds are good Paleo vitamin E sources. Fruits and vegetables are also good, but they contain very low amounts. Those small amounts accumulate, however, so collectively they are indeed significant.

Probably the best Paleo vitamin E source is olive oil. One tablespoon packs 1.9 mg, which is 10% of the RDA. You can add a few tablespoons of olive oil on salads or cooked vegetables, or use it for cooking. Olive oil becomes even more attractive when you consider its relatively low levels of PUFAs.

We should note that vitamin E functions primarily as an antioxidant, which means it protects against cellular damage by scavenging for free radicals. PUFAs have a high propensity to oxidize and oxidation creates free radicals. Therefore, high levels of PUFAs can negate vitamin E’s benefits. If we refer back to our chart, we see that many foods rich in vitamin E are also PUFA-rich.

Back in 1988, Brazilian scientists theorized that total vitamin E content is not the best indicator of vitamin E activity for vegetable oils. Using high-pressure liquid chromatography, they analyzed various oils for vitamin E activity and determined that high PUFA content offsets vitamin E activity and that oil refinement causes vitamin E losses upwards of 22%, especially during steam deodorization.3 They proposed that for vitamin E, unrefined oils beat their refined counterparts and that the ratio of vitamin E to PUFA better indicates vitamin E potential compared to absolute vitamin E levels.

A British Journal of Nutrition study published this month (October 2015) reiterates the same point: “The vitamin E requirement will increase with an increase in PUFA consumption and with the degree of unsaturation of the PUFA in the diet.”4 Another just-published study is also raising interest about vitamin E, particularly for its conclusion that those who have metabolic syndrome (about one-third of the US population) don’t absorb vitamin E as effectively as those who are healthy.5 Lead author of this latter study, Richard Bruno, commented, “Dietary requirements of nutrients are generally defined only in the context of what a healthy person needs, but considering that two-thirds of Americans are overweight or obese, a healthy person might not be representative of our society. This work tells us that at least one-third of Americans have higher vitamin E requirements than healthy people.”6

With all this in mind, one might conclude that supplementation is the best way to maintain adequate vitamin E levels. In the 1980s, scientists began to understand how free radicals contribute to atherosclerosis, cancer, vision loss, and various other chronic conditions. This sparked interest in the preventative potential of antioxidant supplements, particularly vitamin E. Several observational studies, including the Nurses’ Health Study, suggested 20 – 40% reductions in heart disease risk among people taking vitamin E supplements.7

Follow-up randomized controlled trials, however, dampened enthusiasm for vitamin E supplements, both for heart disease and cancer prevention. One meta-analysis even concluded that high-dose vitamin E supplementation may increase all-cause mortality and should be avoided.8 For those who are interested, the Harvard School of Public Health has an excellent summary on the history of research on vitamin E supplementation.

In conclusion, supplementation may provide benefits for certain conditions, but food sources of vitamin E are widely considered to be superior. Many of the richest food sources, however, are high-PUFA seed oils. High levels of PUFAs counteract vitamin E’s antioxidant capacity. It’s best to eliminate vegetable seed oils from your diet. The Paleo Diet provides plenty of vitamin E via olive oil, small quantities of seeds and nuts, and large amounts of vegetables.

References

1. National Institutes of Health, Office of Dietary Supplements. (June 2013). Vitamin E Fact Sheet for Health Professionals.

2. McBurney, M., et al. (August 19, 2015). Suboptimal Serum α-Tocopherol Concentrations Observed among Younger Adults and Those Depending Exclusively upon Food Sources, NHANES 2003-2006. PLOS-One.

3. Desai, D., et al. (June 1988). Vitamin E content of crude and refined vegetable oils in Southern Brazil. The Journal of Food Composition and Analysis, 1(3).

4. Raederstorff, D., et al. (October 2015). Vitamin E function and requirements in relation to PUFA. British Journal of Nutrition, 114(8).

5. Mah, E., et al. (October 7, 2015). α-Tocopherol bioavailability is lower in adults with metabolic syndrome regardless of dairy fat co-ingestion: a randomized, double-blind, crossover trial. American Journal of Clinical Nutrition [epub ahead of print].

6. Caldwell, E. (October 7, 2015). Metabolic syndrome leads 1 in 3 Americans to need more vitamin E. Ohio State University (Press Release).

7. Institute of Medicine. (2000). Dietary reference intakes for vitamin C, vitamin E, selenium, and carotenoids. National Academies Press.

8. Miller, ER., et al. (January 4, 2005). Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Annals of Internal Medicine, 142(1).

Wheat | The Paleo Diet

Click Here to Start The Wheat Series from the Beginning!

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

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

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

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

Environmental factors ultimately pull the trigger.

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

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

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

It’s Not So Easy to Pull the Trigger

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

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

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

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

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

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

Building Up to It…

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

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

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

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

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

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

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

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

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

So what happens if the inflammation doesn’t end?

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

Chronic Inflammation – Putting the Gun to our Heads

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

Chronic Inflammation | The Paleo Diet

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

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

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

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

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

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

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

Gut Microbiota | The Paleo Diet

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

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

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

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

Why Aren’t More Guns Going Off?

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

So why aren’t we all sick?

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

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

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

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

Still, There Are a Lot of Bullets…

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

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

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

That amounts to a whole lot of genetic bullets.

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

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

References

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  3. Harris, K.M., A. Fasano, and D.L. Mann, Monocytes differentiated with IL-15 support Th17 and Th1 responses to wheat gliadin: implications for celiac disease. Clin Immunol, 2010. 135(3): p. 430-9.
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  5. Fasano, A., Physiological, Pathological, and Therapeutic Implications of Zonulin-Mediated Intestinal Barrier Modulation Living Life on the Edge of the Wall. American Journal of Pathology, 2008. 173(5): p. 1243-1252.
  6. Fasano, A., Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer. Physiol Rev, 2011. 91(1): p. 151-75.
  7. Ahlbom, A., et al., Cancer in twins: Genetic and nongenetic familial risk factors. Journal of the National Cancer Institute, 1997. 89(4): p. 287-293.
  8. Marenberg, M.E., et al., GENETIC SUSCEPTIBILITY TO DEATH FROM CORONARY HEART-DISEASE IN A STUDY OF TWINS. New England Journal of Medicine, 1994. 330(15): p. 1041-1046.
  9. Heward, J. and S.C.L. Gough, Genetic susceptibility to the development of autoimmune disease. Clinical Science, 1997. 93(6): p. 479-491.
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  16. Gonzalez-Quintial, R., et al., Systemic autoimmunity and lymphoproliferation are associated with excess IL-7 and inhibited by IL-7Ralpha blockade. PLoS One, 2011. 6(11): p. e27528.
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  53. Voo, K.S., et al., Identification of IL-17-producing FOXP3+ regulatory T cells in humans. Proc Natl Acad Sci U S A, 2009. 106(12): p. 4793-8.
  54. Shi, G., et al., Cell-cell interaction with APC, not IL-23, is required for naive CD4 cells to acquire pathogenicity during Th17 lineage commitment. J Immunol, 2012. 189(3): p. 1220-7.
  55. Bernardo, D., et al., Is gliadin really safe for non-coeliac individuals? Production of interleukin 15 in biopsy culture from non-coeliac individuals challenged with gliadin peptides. Gut, 2007. 56(6): p. 889-890.
  56. Evans, H.G., et al., In vivo activated monocytes from the site of inflammation in humans specifically promote Th17 responses. Proc Natl Acad Sci U S A, 2009. 106(15): p. 6232-7.
  57. Kamada, N., et al., Unique CD14 intestinal macrophages contribute to the pathogenesis of Crohn disease via IL-23/IFN-gamma axis. J Clin Invest, 2008. 118(6): p. 2269-80.
  58. Weng, X., et al., Clustering of inflammatory bowel disease with immune mediated diseases among members of a northern california-managed care organization. Am J Gastroenterol, 2007. 102(7): p. 1429-35.
  59. Holmes, G.K.T., Coeliac disease and Type 1 diabetes mellitus – the case for screening. Diabetic Medicine, 2001. 18(3): p. 169-177.
  60. Not, T., et al., Undiagnosed coeliac disease and risk of autoimmune disorders in subjects with Type I diabetes mellitus. Diabetologia, 2001. 44(2): p. 151-155.
  61. Valerio, G., et al., Severe clinical onset of diabetes and increased prevalence of other autoimmune diseases in children with coeliac disease diagnosed before diabetes mellitus. Diabetologia, 2002. 45(12): p. 1719-1722.
  62. Pohjankoski, H., et al., Diabetes, coeliac disease, multiple sclerosis and chronic arthritis in first-degree relatives of patients with juvenile idiopathic arthritis. Acta Paediatrica, 2012. 101(7): p. 767-771.
  63. Binus, A.M., et al., Associated comorbidities in psoriasis and inflammatory bowel disease. Journal of the European Academy of Dermatology and Venereology, 2012. 26(5): p. 644-650.
  64. Coussens, L.M. and Z. Werb, Inflammation and cancer. Nature, 2002. 420(6917): p. 860-867.
  65. Grivennikov, S.I., F.R. Greten, and M. Karin, Immunity, Inflammation, and Cancer. Cell, 2010. 140(6): p. 883-899.
  66. Hotamisligil, G.S., Inflammation and metabolic disorders. Nature, 2006. 444(7121): p. 860-867.
  67. Festa, A., et al., Chronic subclinical inflammation as part of the insulin resistance syndrome: the Insulin Resistance Atherosclerosis Study (IRAS). Circulation, 2000. 102(1): p. 42-7.
  68. Akiyama, H., et al., Inflammation and Alzheimer’s disease. Neurobiology of Aging, 2000. 21(3): p. 383-421.
  69. Libby, P., P.M. Ridker, and A. Maseri, Inflammation and atherosclerosis. Circulation, 2002. 105(9): p. 1135-1143.
  70. Linton, M.F. and S. Fazio, Macrophages, inflammation, and atherosclerosis. International Journal of Obesity, 2003. 27: p. S35-S40.
  71. Antvorskov, J.C., et al., Dietary gluten and the development of type 1 diabetes. Diabetologia, 2014. 57(9): p. 1770-1780.
  72. Sildorf, S.M., et al., Remission without insulin therapy on gluten-free diet in a 6-year old boy with type 1 diabetes mellitus. BMJ Case Rep, 2012. 2012.
  73. Shahbazkhani, B., et al., Non-Celiac Gluten Sensitivity Has Narrowed the Spectrum of Irritable Bowel Syndrome: A Double-Blind Randomized Placebo-Controlled Trial. Nutrients, 2015. 7(6): p. 4542-4554.

Sodium Levels | The Paleo Diet

For the majority of people, the problem with sodium is too much of it, not too little. National health organizations and the Paleo diet agree that high levels of dietary sodium should be avoided for healthy blood pressure levels and to reduce the risks of cardiovascular disease.1 However, diets too low in sodium are also dangerous, especially for athletes engaged in endurance sports.  Fortunately, it is possible for athletes to keep their sodium levels in check, without added processed foods, while still following the Paleo diet.

Understanding the Importance of Sodium in the Body

Although the Paleo diet is in inherently a low sodium lifestyle, dietary sodium, from naturally rich sodium foods and no common table salt, is necessary for everyday bodily functions.2 Muscles, including both the skeletal and cardiac types, need sodium to function properly. Twitches, cramps, spasms, and muscle weakness can occur when sodium levels are too low. The nervous system also uses electrolytes, such as ions of sodium, potassium and chloride, to transmit nerve impulses across cell membranes and to trigger muscle contractions.3 Sodium, in conjunction with potassium, is also necessary to maintain normal blood pressure, blood volume, and to balance bodily fluids.4 If that balance is disturbed, problems like heat-related illnesses and hyponatremia, low blood sodium (<130 mmol/L), may occur.5

Do Athletes Require More Dietary Sodium?

One major concern for athletes, especially those engaged in endurance activities, is that high sweat rates in athletes result in loss of both fluids and sodium.6 Low blood sodium can also occur in people who drink too much water, eat too little food, or take medications that deplete the body’s supply of water.7 Research indicates that the amount of sodium consumed in the days prior to exercise, might be more important in maintaining the proper levels during exercise, then in specific supplementation during the activity.8

Additionally, avoiding sodium rich beverages and foods during physical activity has been shown to not impact performance,9 ingesting sodium prior or during intense or prolonged physical activities is linked to an improved rate of absorption of water and carbohydrate in the small intestines.10 An athlete can encourage proper blood serum sodium levels by drinking for thirst and eating whole fruit, such as oranges, for a gradual fructose release.

Pre-and-Post Workout Meals

Pre-and-post workout meals can provide the necessary recovery nutrients rather than turning to processed supplements that are often sickeningly sweet, and contain many unnecessary additives and refined sugars. Surprisingly, they don’t contain exorbitant amounts of sodium. For example, a scoop of powdered electrolyte supplement contains 14 mg of sodium,11 compared to the 97mg available in a dash of table salt.12 An athlete concerned about maintaining adequate sodium levels during their exercise program can focus including naturally sodium-rich foods to their pre-workout meal, and focusing on the main principles of the Paleo diet. Our favorite sodium-rich and Paleo foods include:13

  • 1 large celery stalk (50 mg)
  • 1 beet (65 mg)
  • 4 oz. lamb chop (65 mg)
  • 4 oz. chicken breast (70 mg)
  • 4 oz. grass-fed ground beef (75 mg)
  • 1 cup of spinach (125 mg)
  • 1 cup of Swiss chard (300 mg)

By simply following a Paleo diet, focused on eating a wide variety of mineral rich vegetables, animal organs, and bone broth will supply the necessary nutrients to maintain adequate sodium levels, for both the weekend warrior and the elite endurance athlete under most training conditions. Traditional hunter-gathers participate in rigorous and demanding physical activities required by their hunting, gathering, and foraging lifestyles without needing to supplement their diets with table salt, or electrolyte supplements, to meet their sodium requirements. Dietary sodium is not quite the villain he has been made out to be. However, we don’t need to overcompensate with sodium-rich supplements when a regular Paleo diet offers enough of this essential nutrient to support most individuals, even those who are avid exercisers.

References

1. Mattes, R. D., and D. Donnelly. “Relative contributions of dietary sodium sources.” Journal of the American College of Nutrition 10.4 (1991): 383-393.

2. Centers for Disease Control and Prevention (CDC. “Usual sodium intakes compared with current dietary guidelines—United States, 2005-2008.” MMWR. Morbidity and mortality weekly report 60.41 (2011): 1413.

3. Brodal, Per. The central nervous system: structure and function. Oxford University Press, 2004.

4. Blaustein, M. P. “Sodium ions, calcium ions, blood pressure regulation, and hypertension: a reassessment and a hypothesis.” American Journal of Physiology-Cell Physiology 232.5 (1977): C165-C173.

5. Noakes, T. D., et al. “The incidence of hyponatremia during prolonged ultraendurance exercise.” Medicine and Science in Sports and Exercise 22.2 (1990): 165-170.

6. Godek, S. Fowkes, A. R. Bartolozzi, and J. J. Godek. “Sweat rate and fluid turnover in American football players compared with runners in a hot and humid environment.” British journal of sports medicine 39.4 (2005): 205-211.

7. Noakes, Timothy D. “The hyponatremia of exercise.” International journal of sport nutrition 2.3 (1992): 205-228.

8. Stofan, John R., et al. “Sweat and sodium losses in NCAA football players: a precursor to heat cramps?.” International journal of sport nutrition and exercise metabolism 15.6 (2005): 641.

9. Merson, Stuart J., Ronald J. Maughan, and Susan M. Shirreffs. “Rehydration with drinks differing in sodium concentration and recovery from moderate exercise-induced hypohydration in man.” European journal of applied physiology 103.5 (2008): 585-594.

10. Murray, Robert. “The effects of consuming carbohydrate-electrolyte beverages on gastric emptying and fluid absorption during and following exercise.” Sports Medicine 4.5 (1987): 322-351.

11. Available at: //nutritiondata.self.com/facts/beverages/9232/2. Accessed on October 7, 2015.

12. Avaialble at: //nutritiondata.self.com/facts/spices-and-herbs/216/2. Accessed on October 7, 2015.

13. //nutritiondata.self.com/

Paleo Recipe | The Paleo Diet

Hawaiian cuisine incorporates five distinct styles of food reflecting the diverse food history of settlement and immigration in the islands.1 Polynesian voyagers brought plants and animals to the islands, contributing to the local fish, taro (which were raised for poi), coconuts, sugarcane, sweet potatoes and yams, and meat, cooked in earth ovens.

Later, large plantations developed with the arrival of Europeans, Americans, missionaries, and whalers who introduced cuisine native to their homelands to Hawaii. In the late 1800s, migrant workers from China, Korea, Japan, the Philippines, and Portugal immigrated to meet the growing labor needs of the pineapple industry in Hawaii, bringing with them rich new foods and flavors that further influenced the region.

Can we say fusion cuisine? Try saying that five times!

When we think of a Paleo autumn recipe, most of us, myself included, don’t think tropical flavors from lands from afar. But since it is fall, and I happen to be writing to you from Kona, why not come up with a Hawaiian twist on a fall favorite?

The hardest part: deciding what type of preparation seems most fitting, captures Hawaiian tradition, but also stays true to the seasonal goodness packed with the wholloping punch of health-packing nutrients of any real Paleo recipe!

A trip to the farmer’s market on Ali’i Drive in downtown Kona2 was just the ticket. Freshly picked pineapple, Japanese sweet potato, sweet onion from Waimea, and locally grown basil were amongst the goodies I encountered. And, while a bit on the starchier and sweeter side than I’d recommend for day-to-day dining, in context of preparing for a long endurance event, absolutely perfect.

Hearty, tasty and ideal for preparing the body’s fuel stores for a day of intense physical activity to come, my Blue Sweet Potato and Pineapple ‘Poke’ is both easy to prepare and easy to enjoy.

Paleoista’s Blue Sweet Potato and Pineapple ‘Poke’

A play on the local island favorite, ‘Poke,’ is a raw salad served as an appetizer in Hawaiian cuisine. This recipe will fill your boots and ensure you’re ready to race or train hard!

Ingredients

  • 2 lbs boiled blue sweet potatoes, cubed into 1” pieces and cooled
  • 1 sweet onion, chopped
  • 1 small pineapple, cored, peeled and cut into 1” cubes
  • 1 small lime, juiced
  • ¼ cup coconut oil, melted
  • ½ cup freshly chopped basil, plus a few leaves for garnish

Instructions

  1. Combine all ingredients in large bowl
  2. Stir to combine
  3. Chill for one hour before serving
  4. Garnish with basil leaves

References

1. Wikipedia. Wikimedia Foundation, n.d. Web. 07 Oct. 2015

2. //www.konafarmersmarket.com

Paleo Sandwich | The Paleo Diet

What’s for lunch?  For at least 49% of the U.S., it’s a sandwich. The common sandwich components, such as yeasted grain breads, cheese, and cured meats, are among the top contributors not only to sodium (accounting for at least one-fifth of the total daily sodium intake), but also to excess caloric consumption in the diets of adult Americans.1 Fortunately, the Paleo diet avoids the sandwich components that are added sodium-rich and offer empty nutrients.

There’s no disputing that whether you are pack a lunchbox or grab a quick bite on your lunch hour, sandwiches are popular because they are quick-and-easy. Subscribing to the Paleo diet doesn’t mean you still can’t enjoy convenience or the flavor profiles offered at your favorite deli. Check out our ideas for ways to turn your pre-Paleo favorite into a new Paleo staple.

Let’s start on the outside and explore the options for keeping the contents of your sandwich together.  You can use any of these Paleo wrap ideas for a variety of classic fillings, such as Paleo chicken salad, ground bison burgers, or to reinvent last night’s leftover roast beef.

Leafy Greens

Large, flat green leaves make excellent wrappers for all kinds of fillings – such as tacos, burgers, or Asian-style lettuce cups. Collard greens can be lightly steamed so that a tight wrap can be made, while Swiss chard and romaine both work well in their raw form.

Grilled vegetable slabs

Portobello mushrooms, eggplant slices, and bell peppers can be grilled or lightly roasted to create a solid platform that supports the inside of your sandwich. Although, you may find that these are neater to eat with a fork and knife.

Cauliflower “Bread”

The Real Paleo Diet Cookbook has a recipe for Cauliflower Cups made using a muffin tin, this recipe can be transformed by baking as a flatbread in the oven on a parchment lined backing sheet.  It could be topped with roasted tomatoes and eggplant and a drizzle of olive oil and makes an impressive open-faced vegetable sandwich.

We have recreated many classic sandwich options below with the same hearty taste and flavors, but reinvented into healthy Paleo diet compliant versions.

The Paleo Nut Butter & Jelly

With or without the crust, peanut butter (a legume) is not part of the Paleo diet. Fortunately, other spreads, such as sunflower seed or almond butter, are available to layer between thinly sliced apples or pears to replicate the flavor and convenience of this kid-friendly staple.  Serve with a side of dehydrated beet chips.

The Paleo Chicken Parmesan

Combine grilled chicken thighs with your favorite dairy-free Paleo pesto, such as a puree of basil, kale, toasted pine nuts, and olive oil. Top with sun-dried tomatoes and sautéed shiitake mushrooms and set on a large romaine lettuce leaf for added crunch. Serve with crispy, oven roasted, thin slices of zucchini.

The Paleo Cuban Sandwich

There’s no Paleo substitute for cheese, but in our take of this traditional Latin dish you won’t miss it. Melt in your mouth warm, citrus marinated, grilled, pork shoulder butt (blade roast), combined with Paleo Dijon-style mustard, sliced cucumbers, shredded raw purple cabbage, and avocado served on butter lettuce leaves. Served with a side of homemade plantain chips cooked in coconut oil.

The Paleo Bánh mì

There’s a lot of variation with the type of protein used to make a Bánh mì. However, the key is to find the proper balance between the spice, crunch, and tang of this Vietnamese recipe. Start with Paleo mayo (recipe available in The Paleo Diet Cookbook), thinly sliced jalapeno pepper, cilantro, minced garlic, julienne carrots and cucumber, with roasted pork belly, and a smear of dairy-free chicken liver pâté. Tuck the ingredients onto a Belgian endive leaf.

The Paleo Turkey Sandwich

The best part of Thanksgiving is making a leftover turkey sandwich. Thinly slice the roasted breast meat, top with a dollop of tangy, homemade cranberry relish, and serve between two sweet potato pancakes. Serve with a side of roasted Brussels sprout chips.

What’s your favorite Paleo sandwich combination? Post ‘em below!

REFERENCES

[1] Sebastian, Rhonda S., et al. “Sandwiches Are Major Contributors of Sodium in the Diets of American Adults: Results from What We Eat in America, National Health and Nutrition Examination Survey 2009-2010.” Journal of the Academy of Nutrition and Dietetics 115.2 (2015): 272-277.

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.

Healthy Eating | The Paleo Diet

Anyone who follows the U.S. nutritional guidelines has almost certainly been frustrated at some point or another by the conflicting advice and sometimes hopelessly outdated marketing material – think the Food Pyramid that still graces the walls of many elementary school classrooms.

The frustration has reached the point that cries of government corruption and inappropriate influence of big food industry lobbyists are frequently heard. Case in point, the February 2015 draft of the U.S. Dietary Guidelines,1 published every five years, prompted over 29,000 public comments compared to a couple thousand in 2010. The outcry has been so strong it has led to a Congressional review to start in October.

And just last week journalist Nina Teicholz published a scathing review of the guidelines in the high impact factor journal BMJ.2

Teicholz accused the Dietary Guidelines Advisory Committee (DGAC) of not listing their conflicts of interest, of using reviews from industry influenced professional associations, and of overall “weak scientific standards.” Which is scary considering the importance of the 2015 Dietary Guidelines can’t be understated.

According to Teicholz, “the guidelines have a big influence on diet in the U.S., determining nutrition education, food labeling, government research priorities at the National Institutes of Health (NIH) and public feeding programs.”

So what did the Committee recommend? The overall body of evidence examined by the 2015 DAC identifies that a healthy dietary pattern is higher in vegetables, fruits, whole grains, low- or non-fat dairy, seafood, legumes, and nuts; moderate in alcohol (among adults); lower in red and processed meats; and low in sugar-sweetened foods and drinks and refined grains.

Certainly not a win for the Paleo community, but also not anything we haven’t heard from these agencies for a long time.

Dr Barbara Millen, the Chair of the Committee, published an immediate response in BMJ claiming that “the procedures used to develop the DGAC scientific report are expansive, transparent, and thoughtful, with multiple opportunities for public input.”1

Millen pointed out that the committee was nominated by their peers and rigorously reviewed. She even fired back at Teicholz saying that she was just one individual with a clear bias herself having written the book The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet.

The biggest point of contention, however, was the methods for selecting the research the recommendations were based on.

In 2010, the US Department of Agriculture established the Nutrition Evidence Library (NEL) to help ensure the quality of nutritional recommendations by establishing standards for identifying and selecting research.3

Teicholz contends that the DGAC “did not use NEL reviews for more than 70 percent of the topics” and instead selected studies ad hoc often relying on reviews by external professional associations.

Millen defended the committee claiming that “you don’t simply answer these questions on the basis of the NEL. On topics where there were existing comprehensive guidelines, we didn’t do them.” Millen also contended that the bulk of their research came from the NIH and other federal agencies.

To her credit, the Guidelines detail four methods of research selection, most of which involved at the least consulting the NEL.

Ultimately, it is the recommendations themselves that will determine the integrity of the report and Teicholz had issues with several of them, all of which are highly relevant to those of us in the Paleo world:

THE CONTESTED RECOMMENDATIONS

Teicholz addressed the recommendation for lower dietary saturated fats first, pointing out that no NEL review of the research on saturated fat from the past five years was conducted. She claimed many conflicting studies were omitted, in particular a large controlled clinical trial known as the Women’s Health Initiative (WHI). No benefits of a lower saturated fat diet were observed in a cohort of 49,000 women over seven years.4

Millen responded that the report states “dietary advice should put the emphasis on optimizing the types of dietary fat and not reducing total fat.”

Next, Teicholz addressed the report’s failure to endorse a low carbohydrate diet claiming critical research was left out including a meta-analysis and a critical review demonstrating a benefit of low carb diets for type 2 diabetes.5, 6 Millen simply replied that there is limited evidence of the long-term health effects.

One of the biggest shifts in the new guidelines was a stronger emphasis on plant-based diets with the recommendation to reduce meat particularly red meat. The draft 2015 Guidelines added for the first time a “Healthy Vegetarian Pattern” to their three recommended diets that also include a “Healthy Mediterranean-Style Pattern” and a “Healthy U.S.-Style Pattern.”

Teicholz contends that there has been no review by the NEL of the health effects of red meat. While an NEL review of a vegetarian diet does exist and states that the evidence is limited for its disease fighting power.7 Yet, Teicholz holds that the report arbitrarily upgraded the rating of the evidence. She also claimed that the Guidelines left out three contradictory NIH studies including one from the WHI that found no significant advantage of a diet high in fruit, vegetables and grains for weight loss, diabetes, heart disease, or cancer.8-11 Even the Guideline’s sole diagram addressing red meat, according to Teicholz, showed that diets high in red meat were equivocal with diets lower in red meat.

Millen did not address the question of red meat in her response, but the report stated that the three recommended dietary patterns reaffirmed the 2010 DGAC recommendations and aligned with the American Institute for Cancer Research (AICR) and the American Health Association (AHA).1

A MORE MUNDANE EXPLANATION

A friend of mine, who by her own admission had a “cushy” well-paid job at a large government nutrition agency, once gave me her impression of government nutrition.

Her job was to follow the current research and take her findings to the higher-ups. She was quickly frustrated by the all-too-common response. They would thank her for bringing it to their attention, then tell her they already knew about it and they weren’t going to do anything. Did she experience, first hand, government corruption or industry influence at play?

My friend had a much more mundane answer. In a government nutrition agency, she said, there’s one unforgivable sin – to make a recommendation contrary to the decades old accepted cannon and end up being wrong. So was something this mundane going on with the DGAC?

The Report starts by asserting it was motivated by the current state of public health in the United States, a lot of which was a result of poor dietary patterns. Half of U.S. adults have a chronic disease and two-thirds are obese. It goes on to say these patterns “adversely affected the health of the U.S. public for decades and raise the urgency for immediate attention and bold action.”1

Yet that “bold action” consists of recommendations that by their own admission are consistent with past DGAC reports.

The few new recommendations they offer – replacing refined grain products with whole grain products and the reduction of refined sugar and sodium in the diet – are neither novel nor in any way controversial within the nutrition community.

Even in the Paleo world, while we would say to bypass the grains altogether, if you’re going to eat them, we’re still generally going to recommend whole grain products over refined empty-calorie snacks.

Perhaps Teicholz’s most poignant criticism of the report was her pointing out “a reluctance by the committee behind the report to consider any evidence that contradicts the last 35 years of nutritional advice.” She goes on to say that with the failure of existing intervention strategies, they should be welcoming new views.

Nowhere is the aging nature of the report potentially more obvious than in its handling of omega-3 fatty acids. As mentioned above, Millen responded to Teicholz by stating that the committee focused more on types of fats than absolute quantity. Which would imply that omega-3 fats were a focus.

Yet omega-3s are mentioned only three times in the 571-page report. Once in the context of wild vs farm raised fish. One paragraph under mental health where they briefly review the vast research showing the benefits of omega-3 for the brain and finally to point out the single study that found an association between nutrients in the diet and type 2 diabetes because it differentiated types of fats.12

The broad ranging health benefits of consuming omega-3 fatty acids, and the ratio of omega-3 to omega-6 fatty acids in the diet are some of the most heavily researched topics currently in nutrition.13 Yet the report made no recommendations about omega-3s. Instead it focused on a decades-old concept of “achieving better saturated fat to polyunsaturated fat ratios.”

IS MUNDANE ANY BETTER?

Teicholz herself concludes by admitting the mundane may be more at play than conflict of interest or industry pressure – “nearly all nutrition scientists accept funding from industry. Of far greater influence is likely to be bias in favor of institutionalized hypothesis.”

Nonetheless, does this really make the end result any better?

The report may very well answer that question itself. It has long been accepted that there is a big difference between refined sugar, refined grain products, and whole grain products despite all being grain-based. The report is careful and thorough in making this distinction and providing very different recommendations for each.

The report also admits to a difficulty in defining meat – “there was variability across the food groupings and this was particularly apparent in the meat group.” Red meats were clumped together with processed meat and chicken, fish was grouped with eggs and sausage.

Yet, after admitting to this issue, the report still stuck with traditional lines. Where it was careful to distinguish different categories of grains and plant foods it still ultimately lumped almost all meat together in its recommendation.

That is with the exception of a small footnote that ultimately contradicted its own recommendations:

As lean meats were not consistently defined or handled similarly between studies, they were not identified as a common characteristic across the reviews. However, as demonstrated in the food patterns modeling of the Healthy US-style and Healthy Mediterranean-style patterns, lean meats can be a part of a healthy dietary pattern.

Whether it was industry influence, conflict of interest, or simply mundane adherence to nutritional cannon, when it came to their final recommendations, they were unable to see the important implications of a distinction they themselves made.

REFERENCES

  1. United States. Department of Agriculture., Dietary Guidelines Advisory Committee. Scientific Report. v.
  1. Teicholz, N., The scientific report guiding the US dietary guidelines: is it scientific? BMJ, 2015. 351: p. h4962.
  1. Library, N.E., Frequently Asked Questions. 2015.
  1. Howard, B.V., et al., Low-fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA, 2006. 295(6): p. 655-66.
  1. Feinman, R.D., et al., Dietary carbohydrate restriction as the first approach in diabetes management: critical review and evidence base. Nutrition, 2015. 31(1): p. 1-13.
  1. Ajala, O., P. English, and J. Pinkney, Systematic review and meta-analysis of different dietary approaches to the management of type 2 diabetes. Am J Clin Nutr, 2013. 97(3): p. 505-16.
  1. Library, N.E., How do the health outcomes of a vegetarian diet compare to that of a diet which customarily includes animal products?
  1. Beresford, S.A., et al., Low-fat dietary pattern and risk of colorectal cancer: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA, 2006. 295(6): p. 643-54.
  1. Knopp, R.H., et al., Long-term cholesterol-lowering effects of 4 fat-restricted diets in hypercholesterolemic and combined hyperlipidemic men. The Dietary Alternatives Study. JAMA, 1997. 278(18): p. 1509-15.
  1. Prentice, R.L., et al., Low-fat dietary pattern and risk of invasive breast cancer: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA, 2006. 295(6): p. 629-42.
  1. Prentice, R.L., et al., Low-fat dietary pattern and cancer incidence in the Women’s Health Initiative Dietary Modification Randomized Controlled Trial. J Natl Cancer Inst, 2007. 99(20): p. 1534-43.
  1. Fung, T.T., et al., A prospective study of overall diet quality and risk of type 2 diabetes in women. Diabetes Care, 2007. 30(7): p. 1753-7.
  1. Gomez-Candela, C., et al., The Role of Omega-3 Fatty Acids in Diets. J Am Coll Nutr, 2015. 34 Suppl 1: p. 42-7.

Bone Health | The Paleo Diet

Did you know that exercise works to strengthen your bones, just as it works to strengthen your muscles? Research shows that regular exercise, mimicking our hunter-gatherer ancestors,1 is critical to the health of our skeletal system. These exercise patterns include endurance activities; as well as weight-bearing, high intensity cross training with adequate rest for complete recovery. Physical activity has been shown to maintain bone mass and reduce age-related bone loss. Further, it preserves muscle strength and postural stability that reduces the risk of falls and fractures, both of which can be deadly.2  

Engaging in exercise that promotes strong, dense bones is an important consideration. Osteoporosis, diagnosed with a bone mineral density at the hip of 2.5 standard deviations below the average value for young adults,3 remains a major modern health problem.4  Worldwide, one in two women and up to one in four men age 50 and older will break a bone due to osteoporosis.5 Other kinds of bone disease, like osteopenia and osteomalacia,6 make bones prone to fractures and can lead to osteoporosis if untreated.

There are many factors that contribute to a healthy skeletal system. Deciphering the interactions between various permutations of elements helps us to understand the complexity of the development of bone disease and create strategies to maintain the integrity of our bones.7 Some are static and cannot be changed, such as age, gender, and genetics. Others, specifically lifestyle habits that can be controlled, which include physical activity type and intensity and dietary nutrient status, have been shown to play a large role in dense, well-functioning bones.

Bone health begins early in life,8 with consistent exercise during growth and young adulthood linked to reduced fracture risk in later decades.9 You can still take advantage at any age that the skeletal system operates as a metabolically activity organ that undergoes continuous remodeling, with typically about 2-4% being rebuilt annually.10

HOW TO EXERCISE FOR BONE HEALTH

Exercise leads to improvements in skeletal development and maintenance, because weight bearing during exercise plays a crucial role in improving the mechanical properties of bone. 11 Due to the sedentary nature of our modern lifestyle, exercise adds the necessary challenges to alter the normal daily pattern of bone bending and strain through the application of force. The bone tissues responds to the load applied through the movement patterns by increasing formation that encourages increases mass, size, and moment of inertia to resist the altered bending.12

Different types of exercise benefit skeletal mechanical properties in different ways.13  Studies have found that the bone mineral density of young endurance runners is consistently lower than that of sprinters, gymnasts or ball sports athletes. In fact, those engaged in endurance and non-weight-bearing activities sometimes have weaker bones and a greater risk of fractures, both while actively competing and later in life, than their inactive peers.14 Those engaged in endurance activities should also do cross-training, involving weight lifting to maximize bone strength.15

As important as physical activity is for a fully functioning skeletal tissue, so is planned rest from load bearing, force-applying movements. Load induced bone formation is improved by periods of rest, stressing the importance of adequate recovery periods as part of any training program geared towards bone health.16  As no‐loading periods are lengthened, such as with 24 hours of rest, bone formation and restoration is further enhanced. 17

A proper exercise regime is one factor, in addition to the Paleo diet, in our control for supporting the health of our skeletal tissue. Follow a consistent fitness program that focuses on cross training, combing weight lifting and high intensity activities, with time to recover between exercise sessions. Our favorite ways to build bone strength include incorporating movements that add resistance and force to the entire skeletal system, such as barbell weight training, hanging and brachiating movements, push-ups/ pull-ups, and plank holds.

REFERENCES

1 O’Keefe, James H., et al. “Exercise like a hunter-gatherer: a prescription for organic physical fitness.” Progress in cardiovascular diseases 53.6 (2011): 471-479.

2 Beck, Belinda R., and Christine M. Snow. “Bone health across the lifespan—exercising our options.” Exercise and sport sciences reviews 31.3 (2003): 117-122.

3 Siris, E., and P. D. Delmas. “Assessment of 10-year absolute fracture risk: a new paradigm with worldwide application.” Osteoporosis International 19.4 (2008): 383-384.

4 Cole, Zoe A., Elaine M. Dennison, and Cyrus Cooper. “Osteoporosis epidemiology update.” Current rheumatology reports 10.2 (2008): 92-96.

5 Cummings, Steven R., and L. Joseph Melton. “Epidemiology and outcomes of osteoporotic fractures.” The Lancet 359.9319 (2002): 1761-1767.

6 Rodan, Gideon A., and T. John Martin. “Therapeutic approaches to bone diseases.” Science 289.5484 (2000): 1508-1514.

7 Ilich, Jasminka Z., and Jane E. Kerstetter. “Nutrition in bone health revisited: a story beyond calcium.” Journal of the American College of Nutrition 19.6 (2000): 715-737.

8 Beck, Belinda R., and Christine M. Snow. “Bone health across the lifespan—exercising our options.” Exercise and sport sciences reviews 31.3 (2003): 117-122.

9 Turner C H, Robling A G. Designing exercise regimens to increase bone strength. Exerc Sport Sci Rev200331(1)45–50.50

10 Hadjidakis, Dimitrios J., and Ioannis I. Androulakis. “Bone remodeling.” Annals of the New York Academy of Sciences 1092.1 (2006): 385-396.

11 Carter, Dennis R. “Mechanical loading history and skeletal biology.” Journal of biomechanics 20.11 (1987): 1095-1109.

12 Cullen, D. M., R. T. Smith, and M. P. Akhter. “Time course for bone formation with long-term external mechanical loading.” Journal of Applied Physiology 88.6 (2000): 1943-1948.

13 Huang, T. H., et al. “Effects of different exercise modes on mineralization, structure, and biomechanical properties of growing bone.” Journal of Applied Physiology 95.1 (2003): 300-307.

14 Scofield, Kirk L., and Suzanne Hecht. “Bone health in endurance athletes: runners, cyclists, and swimmers.” Current sports medicine reports 11.6 (2012): 328-334.

15 Santos-Rocha, Rita Alexandra, Carla Sofia Oliveira, and António Prieto Veloso. “Osteogenic index of step exercise depending on choreographic movements, session duration, and stepping rate.” British journal of sports medicine 40.10 (2006): 860-

16 Turner, Charles H., and Alexander G. Robling. “Designing exercise regimens to increase bone strength.” Exercise and sport sciences reviews 31.1 (2003): 45-50.

17 Turner, Charles H., and Alexander G. Robling. “Designing exercise regimens to increase bone strength.” Exercise and sport sciences reviews 31.1 (2003): 45-50.

Inuit | The Paleo Diet

The Inuit have long been used as a shining example that low carbohydrate approaches to diet can work.1 2 3 4 In fact, traditionally they consumed very little vegetables or any other typically Western foods, and subsisted mainly on fish, sea mammals, and land animals.5 And despite this diet (which would horrify most mainstream dieticians) the Inuit traditionally had very low rates of disease.6

By contrast, the traditional Western diet has been correlated with a plague of health issues.7 8 9 As a further example of just how nutritionally poor the Western diet can be, one third of all cancer deaths have been linked to continued intake of low quality foods – which are everyday staples of the Western diet.10

Interestingly, when consumed in a very low carbohydrate version, a Paleo Diet looks very similar – if not identical – to the traditional Inuit diet. Since this way of eating is higher in fat than most North American diets, it is commonly presumed (erroneously) that high fat diets must somehow be “bad.”11 12 What gets (purposely) left out of these arguments is the fact that the type of fat consumed is very important.13 14 15 16 17 Consuming omega-3 fatty acids is highly beneficial for health – while consuming industrial trans fat is pretty much the worst thing you can do for your health.18

To bring all this background knowledge to a head, new research published last week, showed that the Inuit have special mutations in genes involved in fat metabolism.19 These genetic mutations may allow them to thrive on their very low carbohydrate diet. This is thought provoking because these genetic mutations are found in nearly 100% of the Inuit. By contrast, only a mere 2% of Europeans exhibit the same mutations. This means that those of us from European ancestry may synthesize omega-3 polyunsaturated fatty acids differently than the Inuit.

While the initial buzz of this paper was high, in practice it really doesn’t change anything we know about consuming a healthy Paleo Diet. Omega-3 fatty acids, like those found in wild-caught fish, are still extremely beneficial for our health. In fact, researchers have found that omega-3 fatty acids have widely beneficial anti-inflammatory properties.20 This proves beneficial for inflammatory and autoimmune diseases, in addition to maintaining good health for those without specific health conditions. The advice to consume omega-3 fatty acids is great for mitigating coronary heart disease, depression, aging, and cancer.21

Beyond this, arthritis, Crohn’s disease, ulcerative colitis and lupus erythematosis are autoimmune diseases which may be helped by adequate omega-3 consumption.22 Of the omega-3 fatty acids available, DHA (docosahexaenoic acid) is the best, for a variety of reasons.23 24 Look for foods naturally high in DHA (such as wild-caught fish) and avoid inflammatory seed oils – like those commonly used by most major restaurants. This crucial step will help you stay healthy in the long term – no matter what genes and ancestry you may have.

REFERENCES

[1] Dewailly E, Mulvad G, Sloth pedersen H, Hansen JC, Behrendt N, Hart hansen JP. Inuit are protected against prostate cancer. Cancer Epidemiol Biomarkers Prev. 2003;12(9):926-7.

[2] Bjerregaard P, Dewailly E, Young TK, et al. Blood pressure among the Inuit (Eskimo) populations in the Arctic. Scand J Public Health. 2003;31(2):92-9.

[3] Mulvad G, Pedersen HS, Hansen JC, et al. The Inuit diet. Fatty acids and antioxidants, their role in ischemic heart disease, and exposure to organochlorines and heavy metals. An international study. Arctic Med Res. 1996;55 Suppl 1:20-4.

[4] O’keefe JH, Harris WS. From Inuit to implementation: omega-3 fatty acids come of age. Mayo Clin Proc. 2000;75(6):607-14.

[5] Kuhnlein HV. Nutrition of the Inuit: a brief overview. Arctic Med Res. 1991;Suppl:728-30.

[6] Stefansson V. The friendly arctic. The MacMillan Co, NY. 1921.

[7] Manzel A, Muller DN, Hafler DA, Erdman SE, Linker RA, Kleinewietfeld M. Role of “Western diet” in inflammatory autoimmune diseases. Curr Allergy Asthma Rep. 2014;14(1):404.

[8] Myles IA. Fast food fever: reviewing the impacts of the Western diet on immunity. Nutr J. 2014;13:61.

[9] Simopoulos AP. The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomed Pharmacother. 2002;56(8):365-79.

[10] American Cancer Society. Cancer facts & figures 2004. Atlanta: American Cancer Society, 2004.

[11] Guldstrand MC, Simberg CL. High-fat diets: healthy or unhealthy?. Clin Sci. 2007;113(10):397-9.

[12] Schwingshackl L, Hoffmann G. Comparison of effects of long-term low-fat vs high-fat diets on blood lipid levels in overweight or obese patients: a systematic review and meta-analysis. J Acad Nutr Diet. 2013;113(12):1640-61.

[13] Abumrad NA, Piomelli D, Yurko-mauro K, Merrill A, Clandinin MT, Serhan CN. Moving beyond “good fat, bad fat”: the complex roles of dietary lipids in cellular function and health: session abstracts. Adv Nutr. 2012;3(1):60-8.

[14] Simopoulos AP. Omega-3 fatty acids in health and disease and in growth and development. Am J Clin Nutr. 1991;54(3):438-63.

[15] Daley CA, Abbott A, Doyle PS, Nader GA, Larson S. A review of fatty acid profiles and antioxidant content in grass-fed and grain-fed beef. Nutr J. 2010;9:10.

[16] Loef M, Walach H. The omega-6/omega-3 ratio and dementia or cognitive decline: a systematic review on human studies and biological evidence. J Nutr Gerontol Geriatr. 2013;32(1):1-23.

[17] Swanson D, Block R, Mousa SA. Omega-3 fatty acids EPA and DHA: health benefits throughout life. Adv Nutr. 2012;3(1):1-7.

[18] Ip C. Review of the effects of trans fatty acids, oleic acid, n-3 polyunsaturated fatty acids, and conjugated linoleic acid on mammary carcinogenesis in animals. Am J Clin Nutr. 1997;66(6 Suppl):1523S-1529S.

[19] Fumagalli M, Moltke I, Grarup N, et al. Greenlandic Inuit show genetic signatures of diet and climate adaptation. Science. 2015;349(6254):1343-7.

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

[21] Harris WS, Dayspring TD, Moran TJ. Omega-3 fatty acids and cardiovascular disease: new developments and applications. Postgrad Med. 2013;125(6):100-13.

[22] Robinson DR, Knoell CT, Urakaze M, et al. Suppression of autoimmune disease by omega-3 fatty acids. Biochem Soc Trans. 1995;23(2):287-91.

[23] Horrocks LA, Yeo YK. Health benefits of docosahexaenoic acid (DHA). Pharmacol Res. 1999;40(3):211-25.

[24] Conquer JA, Holub BJ. Dietary docosahexaenoic acid as a source of eicosapentaenoic acid in vegetarians and omnivores. Lipids. 1997;32(3):341-5.

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