Tag Archives: Diet

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The subject of human evolution is both fascinating and complex. Human beings evolved from fairly primitive creatures to the most advanced species on the planet. How and why did this happen? It’s a question that scientists have pondered for hundreds, if not thousands, of years. In the exploration of this subject, many researchers have focused on the study of the human diet—that is particularly true at The Paleo Diet. Now, many mainstream outlets have started to ask the question: Did humans evolve to eat lower carbohydrate diets, and do those diets provide us with a better chance of survival and health?

When it comes to the science, a specific gene, AMY1, appears to have played an important role in our development and diet over the years. [1] The gene’s function in starch digestion begins in the mouth; [2] your saliva contains an enzyme encoded by AMY1, and it starts breaking down starch when you chew your food. [3] There is genetic variability, with regard to the quantity of copies of this specific gene, in humans. Interestingly, those with more copies break down starch faster. [4]

However, other primates do not possess that same genetic variability. [5] (Any scientist reading this article should be intrigued by that sentence.) That fact suggests the genetic variability seen in humans may have been an adaptation that helped the species rise to the top. In other words, our evolution may have been aided by our consumption of starchy foods. Furthermore, we may have developed more copies of this gene because it provided an evolutionary advantage.

However, there’s a scientifically surprising fact about the gene variation: Those with different levels of the gene all have different microbiomes. [6] Some research has even shown that weight gain is associated with variations in the gene, another scientifically intriguing suggestion. [7]

Other research has shown that people with fewer copies of AMY1 are almost 10 times more likely to gain weight, when compared to those with more copies of the gene. [8] This is a staggering fact, and one that may not only hold the key to understanding our evolution, but also potentially understanding obesity.

Other studies have shown that boys with lower numbers of the AMY1 gene are associated with having a higher body mass index (BMI). [9] In essence, the fewer numbers of the gene you possess, the more likely you are to be overweight. This research suggests that people can react differently to a particular type of food, and even to the same amount of that food. While one person may gain weight, another may not.

Which begs the question: For those people with fewer copies of the AMY1 gene, what foods should they limit to avoid gaining weight? In short, starchy foods. [10] A low-carb diet is a favorable choice.

 

Evolutionary Advantage?

Did consuming starch provide us with an evolutionary advantage? Not necessarily. Since the Paleolithic era lasted over 2 million years—far longer than the relatively short period of time that we’ve had to adapt to starchier diets (around 10,000 years)—it is much more likely that evolution may have occurred in response to non-starchy foods. [11] However, the question is still up for debate.

What does this mean from a more practical level? What foods are better to consume? Quite simply: tread carefully with the starches, including foods like potatoes, peas, corn, rice, grains, beans, and pasta. If you’re following a Paleo Diet, you are avoiding these foods already. It would be interesting to see if there is a connection between the level of success one sees on a Paleo Diet—which almost completely omits these foods—and the number of AMY1 gene copies a person carries.

What about those people with more copies of the AMY1 gene? They could, hypothetically, consume starchier foods and keep weight low. However, as the science of The Paleo Diet makes clear, these foods do not provide good nutrition and have a vast array of downsides. So, we recommend refraining from them regardless of your genetic makeup.

Is there, then, an evolutionary advantage to having fewer AMY1 genes? The research suggests those with fewer copies of the AMY1 gene can consume a low-starch diet based around our Paleolithic ancestors and see very favorable results. This scientific evidence supports the notion that eating foods low in starch may have actually driven human evolution. If, by extension, consuming a low-starch diet caused problems in any element of the population, then this would not have been an advantageous development. However, that is not the case.

Since starchy foods have very little nutritional content, very few upsides, and are now associated with increased obesity in a large percentage of the population who have fewer copies of the AMY1 gene, the question becomes: Why would humans continue to eat starchy foods? Economics are clearly one factor. Starchy foods are inexpensive. That’s part of why, for the first time in history, those in lower income brackets have higher rates of obesity. Unfortunately, while many people would love to eat healthier, they simply can’t afford to do so.

However, even if your budget is very tight, there are still small changes that can be made which will go a long way towards supporting your health. Reducing starchy foods—regardless of how many AMY1 genes you have—is a good start.

If you enjoyed this article, check out Casey’s new cookbook!

 

References

  1. Perry GH, Dominy NJ, Claw KG, et al. Diet and the evolution of human amylase gene copy number variation. Nat Genet. 2007;39(10):1256-60.
  2. Fernández CI, Wiley AS. Rethinking the starch digestion hypothesis for AMY1 copy number variation in humans. Am J Phys Anthropol. 2017;163(4):645-657.
  3. Carpenter D, Dhar S, Mitchell LM, et al. Obesity, starch digestion and amylase: association between copy number variants at human salivary (AMY1) and pancreatic (AMY2) amylase genes. Hum Mol Genet. 2015;24(12):3472-80.
  4. Mandel AL, Peyrot des gachons C, Plank KL, Alarcon S, Breslin PA. Individual differences in AMY1 gene copy number, salivary α-amylase levels, and the perception of oral starch. PLoS ONE. 2010;5(10):e13352.
  5. O’bleness M, Searles VB, Varki A, Gagneux P, Sikela JM. Evolution of genetic and genomic features unique to the human lineage. Nat Rev Genet. 2012;13(12):853-66.
  6. Parks BW, Nam E, Org E, et al. Genetic control of obesity and gut microbiota composition in response to high-fat, high-sucrose diet in mice. Cell Metab. 2013;17(1):141-52.
  7. Mejía-benítez MA, Bonnefond A, Yengo L, et al. Beneficial effect of a high number of copies of salivary amylase AMY1 gene on obesity risk in Mexican children. Diabetologia. 2015;58(2):290-4.
  8. Falchi M, El-sayed moustafa JS, Takousis P, et al. Low copy number of the salivary amylase gene predisposes to obesity. Nat Genet. 2014;46(5):492-7.
  9. Marcovecchio ML, Florio R, Verginelli F, et al. Low AMY1 Gene Copy Number Is Associated with Increased Body Mass Index in Prepubertal Boys. PLoS ONE. 2016;11(5):e0154961.
  10. Rukh G, Ericson U, Andersson-assarsson J, Orho-melander M, Sonestedt E. Dietary starch intake modifies the relation between copy number variation in the salivary amylase gene and BMI. Am J Clin Nutr. 2017;106(1):256-262.
  11. Luca F, Perry GH, Di rienzo A. Evolutionary adaptations to dietary changes. Annu Rev Nutr. 2010;30:291-314.

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Prostate cancer is the second most common type of cancer among men (skin cancer is the most common). In 2020, the American Cancer Society projects approximately 190,000 new cases of prostate cancer, with about 60 percent of cases diagnosed in men over 65 (the condition is rare in men under 40). [1]

Prostate cancer will affect one in nine men over their lifetime, and tragically, it is the second leading cause of cancer-death in males (second only to lung cancer,) killing one in every 41 men diagnosed. [2]

Fortunately, early screening and medical imaging advancements have resulted in a five-year survival rate of 100 percent, and a 10-year survival rate of 98 percent. While these tremendous advancements in modern medicine are impressive, prevention is still the best cure.

What can you do with respect to your diet, exercise, and lifestyle to help reduce your risk of developing prostate cancer? If you have been diagnosed, are there any strategies that may help protect you against recurrence? Let’s explore the research.

 

Lifestyle factors

What increases your risk of prostate cancer? Let’s take a look.

1. Obesity

The more overweight or obese you are, the greater your likelihood of developing prostate cancer. [3] In fact, obesity increases risk of prostate mortality independent of other lifestyle or clinical factors. In the Physician’s Health Study (PHS), a body mass index (BMI) of greater than 30 kg/m2 —the classification for obesity—nearly doubles your risk of prostate cancer death. [3]

If you’ve already been diagnosed with prostate cancer, weight gain after diagnosis is also associated with a greater risk of prostate cancer recurrence and cancer-specific mortality. [4]

How does weight gain impact prostate cancer risk? Experts aren’t exactly sure, but some combination of excess insulin or insulin-like growth factor (IGF), altered sex hormones and/or adipokine (hormones secreted by fats cells) output seem to play a role in the disease progression. [5,6]

What all this means is that losing weight has a major protective effect on prostate cancer (if you’re overweight or obese).

2. Inactivity

Incorporating more movement and exercise into your life exerts a major protective effect against prostate cancer. The Health Professional Follow-Up Study (HPFS) examined 2,705 men with prostate cancer and found that men engaging in three or more hours of vigorous activity per week had approximately 60 percent lower risk of death from prostate cancer (compared to men exercising less than one hour per week). [7]

In particular, vigorous activity appears to be highly protective against prostate cancer, and most importantly, lethal prostate cancer. Anything that significantly ramps up your heart rate or sweat rate is classified as ‘vigorous’ activity, including jogging, cycling, swimming, and interval-based weight training—with short rest periods of 30-60 seconds between sets.

What if you can’t exercise vigorously at the moment?

Start incorporating more walking into your routine. Men who walked three or more hours per week at a brisk rate (greater than 3 mph) had a 57 percent lower risk of prostate cancer recurrence compared with men who walked less than three hours per week at an easy pace (less than 2 mph). [8] Furthermore, Swedish men who walked or cycled more than 20-minutes per day had a 36 percent reduced risk of prostate-cancer specific mortality. [9] Walking appears to support prostate health via positive changes in energy metabolism, inflammation, oxidative stress, and immunity.

3. Smoking

Smoking is harmful for your health and this also includes your prostate health, with research highlighting the fact that smoking is associated with more aggressive forms of the disease. [10,11] If you smoke, you’ll have a higher risk of progression of your prostate cancer, a 61 percent greater chance of recurrence, and prostate-cancer specific mortality, as well. [10] If you do smoke, you’ll need to abstain for 10 years before your prostate-cancer risk drops to the same rate as non-smokers. So, if you’re over 50, it’s time to think long and hard about the best strategy to kick the habit.

 

Nutrition factors

What foods may decrease your risk of prostate cancer?

1. Dietary fish intake

The data on fish consumption and prostate cancer suggests a significant association between omega-3-rich fish and reduced risk of clinically significant prostate cancer. [2] Association does not equal causation; however, it’s encouraging to see pooled data from multiple studies reporting a 63 percent reduction in prostate cancer death in those consuming the highest intake of fish per week. [12] Aim to include multiple servings of salmon, sardines, anchovies, mackerel, herring, among other species. in your diet every week.

2. Cruciferous vegetables

Eat your greens. You’ve likely heard this common refrain before, and when it comes to protecting your prostate, this sage advice also appears to be highly impactful. Research in animal models highlights the positive effects of isothiocyanates and indoles—compounds found in cruciferous vegetables—at detoxifying carcinogenic compounds and stopping the rapid growth and proliferation of cancer cells. [13] In humans, several studies have found the greater your consumption of cruciferous vegetable, the lesser your risk of prostate cancer, particularly the more aggressive forms. [14,15] Add more asparagus, broccoli, Brussels sprouts, cabbage, cauliflower, and kale to your plate to reduce your risk.

3. Tomatoes

Tomatoes are a rich source of the antioxidant lycopene, which has demonstrated the ability to inhibit prostate cancer growth and spread in some studies. [16] While many people incorrectly assume raw vegetables have greater nutrient bioavailability, cooking tomatoes and consuming them with oils (i.e. extra-virgin olive oil) increases lycopene absorption. [17] Men who consume the most tomato products, or tomato sauces, saw a 28 percent reduction in prostate cancer mortality compared to men who ate the least. [16] A simple way to increase your lycopene intake is to add more tomato-based soups and stews to your nutritional arsenal, as well as more tomato-based sauces to your protein and vegetables dishes. Of course, at The Paleo Diet, we recommend making your own tomato sauces and soups. Store-bought and canned tomato products are generally very high in both salt and added sugar. Nothing beats fresh tomatoes.

Can supplements help to protect against prostate cancer? There is limited data on whether supplements may provide a protective effect against prostate cancer or the progression of the disease. The Physician’s Health Study (PHS), in a randomized trial, did find a small but significant 8 percent reduction in total cancer risk in men who took a multi-vitamin daily. [18] More interestingly, of the subset of men with a history of previous cancers, there was a 27 percent reduction in total cancer. The available evidence does suggest a multi-vitamin is safe and may provide some benefit, however, no other supplements to date appear to provide any significant benefits. Also, while we understand that addressing a cancer diagnosis is a unique situation, in general we do not recommend multi-vitamins for improved health.

Modern medicine has come a long way in its ability to diagnose and treat prostate cancer. However, it remains one of the most common causes of cancer in men. A few simple modifications in your diet, exercise, and lifestyle can go a long way to protecting you from this disease. Be pro-active and take charge of your health.

 

References

  1. https://www.cancer.org/cancer/prostate-cancer/about/key-statistics.html
  2. Peishch, S ,et al. Prostate cancer progression and mortality: a review of diet and lifestyle factors. World J Urol. 2017 June ; 35(6): 867–874.
  3. Ma J, Li H, Giovannucci E, Mucci L, Qiu W, Nguyen PL, et al. Prediagnostic body-mass index, plasma C-peptide concentration, and prostate cancer-specific mortality in men with prostate cancer: a long-term survival analysis. Lancet Oncol. 2008; 9:1039–1047.
  4. Joshu CE, Mondul AM, Menke A, Meinhold C, Han M, Humphreys EB, et al. Weight gain is associated with an increased risk of prostate cancer recurrence after prostatectomy in the PSA era. Cancer Prev Res (Phila). 2011; 4:544-551
  5. Margel D, Urbach DR, Lipscombe LL, Bell CM, Kulkarni G, Austin PC, et al. Metformin use and all-cause and prostate cancer-specific mortality among men with diabetes. J Clin Oncol. 2013; 31:3069–3075.
  6. Roberts DL, Dive C, Renehan AG. Biological mechanisms linking obesity and cancer risk: new perspectives. Annu Rev Med. 2010; 61:301–316.
  7. Kenfield SA, Stampfer MJ, Giovannucci E, Chan JM. Physical activity and survival after prostate cancer diagnosis in the health professionals follow-up study. J Clin Oncol. 2011;29:726–732.
  8. Richman EL, Kenfield SA, Stampfer MJ, Paciorek A, Carroll PR, Chan JM. Physical activity after diagnosis and risk of prostate cancer progression: data from the cancer of the prostate strategic urologic research endeavor. Cancer Res. 2011; 71:3889–3895
  9. Bonn SE, Sjolander A, Lagerros YT, Wiklund F, Stattin P, Holmberg E, et al. Physical activity and survival among men diagnosed with prostate cancer. Cancer Epidemiol Biomark Prev. 2015; 24:57–64.
  10. Kenfield SA, Stampfer MJ, Chan JM, Giovannucci E. Smoking and prostate cancer survival and recurrence. JAMA. 2011; 305:2548–2555.
  11. Rieken M, Shariat SF, Kluth LA, Fajkovic H, Rink M, Karakiewicz PI, et al. Association of cigarette smoking and smoking cessation with biochemical recurrence of prostate cancer in patients treated with radical prostatectomy. Eur Urol. 2015; 68:949–956.
  12. Szymanski KM, Wheeler DC, Mucci LA. Fish consumption and prostate cancer risk: a review and meta-analysis. Am J Clin Nutr. 2010; 92:1223–1233.
  13. Higdon JV, Delage B, Williams DE, Dashwood RH. Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis. Pharmacol Res. 2007; 55:224–236.
  14. Kolonel LN, Hankin JH, Whittemore AS, Wu AH, Gallagher RP, Wilkens LR, et al. Vegetables, fruits, legumes and prostate cancer: a multiethnic case–control study. Cancer Epidemiol Biomark Prev. 2000; 9:795–804.
  15. Richman EL, Carroll PR, Chan JM. Vegetable and fruit intake after diagnosis and risk of prostate cancer progression. Int J Cancer. 2012; 131:201–210.
  16. Zu K, Mucci L, Rosner BA, Clinton SK, Loda M, Stampfer MJ, et al. Dietary lycopene, angiogenesis, and prostate cancer: a prospective study in the prostate-specific antigen era. J Natl Cancer Inst. 2014; 106(2):djt430
  17. Gann PH, Ma J, Giovannucci E, Willett W, Sacks FM, Hennekens CH, et al. Lower prostate cancer risk in men with elevated plasma lycopene levels: results of a prospective analysis. Cancer Res. 1999; 59:1225–1230.
  18. Gaziano JM, Sesso HD, Christen WG, Bubes V, Smith JP, Mac-Fadyen J, et al. Multivitamins in the prevention of cancer in men: the Physicians’ Health Study II randomized controlled trial. JAMA. 2012; 308:1871–1880.

 

Man with alzheimers

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[This article discusses health improvements based, at least in part, on a ketogenic diet. Dr. Loren Cordain and many others, including The Paleo Diet editorial review board, don’t recommend or endorse long-term ketogenic dieting for the general public. They do acknowledge that it can be effective if used short-term and as a therapeutic measure for Alzheimer’s and other diseases.]

Peter Dredge’s book Beating Alzheimer’s, the enemy at the gate: turning despair into hope and action [1], recounts his wife Ann’s early-onset Alzheimer’s diagnosis and their intense struggle with both the disease and “conventional” medical treatment. They refused to accept what most of us believe; that Alzheimer’s is unstoppable, incurable, and irreversible (at one-point Ann was offered euthanasia.) Instead, they researched every nontraditional alternative.

They discovered the work of Dr. Mary Newport [2] and Dr. Dale Bredesen [3] and using that work as a guide, they achieved both short term relief from the worst symptoms, and measurable reversal of the condition. Ann, initially given only three months to live, is sometimes referred to as “probably the first New Zealander to come back from end-stage Alzheimer’s” [4].

Diet and supplementation contributed heavily to Ann’s progress. Drs. Newport and Bredesen, among many others, have exhaustively researched how the conventional Western diet, heavy in carbs, sugar, inflammatory oils and additives, can create a “perfect storm” in the brain. While food choices are not the only Alzheimer’s culprits, dietary changes can be pivotal in slowing—and even reversing—cognitive decline.

 

Dr. Newport and coconut oil

Dr. Newport’s husband Steve also suffered early-onset Alzheimer’s. Frustrated by conventional medicine’s lack of options, she began her own internet research. As passionately and painstakingly described in her book Alzheimer’s Disease – What If There Was A Cure? The Story of Ketones, [3] she discovered research on a prototype “medical food” (Ketasyn, a forerunner of Axona [5]) for dementia patients. The food was based on medium-chain triglycerides derived from coconut and palm kernel oil. Since the food itself was not yet available, Dr. Newport calculated the available MCT’s in coconut oil and added this to Steve’s diet.

Steve responded dramatically and immediately to coconut oil, and later MCT oil, consuming both regularly. His caregivers, including Dr. Newport, all noticed that he “was back,” with improved life and coping skills (dexterity, gait, personality,) better short-term memory, and measurably improved cognitive exam scores. Two years later, “stable” MRI results showed that there had been little, if any, additional brain atrophy during this oil-supplementation phase.

Steve did not experience a miracle cure, but rather measurable, intermittent relief from the worst symptoms of Alzheimer’s over fifteen years. Average life expectancy after diagnosis is 3-11 years [6]. During this time, the family diet was gradually modified along more classic ketogenic, or at least lower-carb lines. Steve also later used prototype “ketone esters,” then being developed by Dr. Richard Veech et al. [7]

Like Steve, Ann Dredge also responded quickly to a 60/40 MCT to coconut oil mixture. Four ounces each day, caused her daily, hour-long full-body twitching episodes to disappear. The same mixture could alleviate any rare recurrence. Dressing herself became much easier, and the oil mixture would also help calm Ann during what Peter calls “more-delusional episodes” of anxiety and confusion.

Ann also follows a ketogenic diet, exercises when possible, minimizes stress, and continues to use the oil mixture to this day. Symptoms often resume or intensify if she misses a dose. [1]

 

Ketones and the brain

Dr. Newport’s original 2008 case study [8], available on her website, succinctly introduces ketones, and ketosis, in the context of Alzheimer’s and other chronic diseases. Ketosis, the body’s use of fat-derived “ketone bodies” for energy (instead of glucose) has been widely popularized in the last few years due to the ketogenic diet craze.

As most keto dieters know, our bodies (and brains) come “factory equipped” to function in the absence of exogenous glucose. While we manufacture some glucose internally, due to our ability to survive on ketones, we don’t need to consume additional glucose in order to maintain bodily function. Keto texts, including Dr. Newport’s, often refer to starvation or fasting as a normal context for ketosis, but low-enough carbohydrate dieting produces the same result.

Interestingly, full ketosis is not the only way to increase available ketones—especially for use by the brain.

High fat foods and supplements like coconut or MCT oil can provide medium-chain triglycerides, which are readily converted to ketones. These become available immediately in the bloodstream. MCT oil supplementation, in particular, has been shown to increase bioavailable ketones even without reducing dietary carbohydrates [13]. The brain will preferentially use available ketones even if glucose is also present. That is, full ketosis is not required for the brain to take advantage of ketones [9]. One reason, or perhaps the main reason, for this is that ketones freely cross the blood-brain barrier.

Glucose, on the other hand, requires a more complex chemical process (involving insulin) to be made available to the brain.

Alzheimer’s is often characterized by insulin insensitivity in the brain and has been called “Type 3 Diabetes” by some researchers [10]. They theorize that the brain atrophies over time as glucose provides less and less available energy—even if ingested in prodigious amounts. They also note that the brain can develop this insensitivity even if the patient is not clinically “diabetic” [11].

 

Strong anecdotal evidence

Steve and Ann’s quick reactions to ingesting medium- and long-change triglycerides, metabolized into ketone bodies, appears to show that energy deprivation in the brain could be a major contributor to Alzheimer’s.

Dr. Newport carefully gathered numerous testimonials in her books, which she received during heroic efforts to raise awareness of Steve’s progress, both within and outside of the medical community. Not everyone responds as quickly or easily as Steve, or Ann Dredge, but even the slightest improvement can be welcome to the afflicted, as well as desperate family members or caregivers.

It should be noted that this “oil therapy” is not a cure but appears to slow, arrest and mitigate—sometime even reverse—multiple gross Alzheimer’s symptoms.

According to Dr. Dale Bredesen (a neurologist specializing in Alzheimer’s research,) insulin resistance is only one of several possible contributing co-factors to Alzheimer’s and other dementias. Nevertheless, his own protocol is also based on a ketogenic diet, including supplemental MCT or coconut oil. [3] His book also contains many corroborative case studies and testimonials.

Dr. Bredesen’s protocol will be examined in a subsequent article.

 

Lack of mainstream acceptance

The Dredges, Newports, and Dr. Bredesen have all experienced resistance on many levels as they explored or tried to promote awareness of these ideas.

Peter Dredge recounts repeated instances of vigorous opposition to the idea that Alzheimer’s could be treated. He has often been treated very negatively and was even threatened with legal proceedings to remove Ann from his care. His courageous refusal to accept conventional medicine’s death sentence on his beloved wife is a strong theme throughout his book. Ann is still with us.

Dr. Newport similarly describes being repeatedly stymied as she tried to follow conventional pathways to raise awareness of Steve’s modest recovery. Attempts to exhibit or speak at Alzheimer’s Association-sponsored events were denied or shut down, once with a public announcement that the Association “did not support” coconut oil research. She was also privately told that “extensive clinical trials” would be needed before her ideas could be publicly discussed.

As Dr. Bredesen’s book [3] shows, money for “extensive clinical trials” is controlled by various institutional review boards and hard to come by. His own protocol was denied funding as “too complicated,” despite many successful case studies [12].

Conventional medicine’s intransigence, especially when faced with effective but non-traditional methodologies, is well known to Paleo readers—many of whom have resolved serious health conditions by abandoning conventional dietary advice.

The stories of Peter and Ann Dredge, and the work of Drs. Newport and Bredesen, deserve much wider awareness.

 

REFERENCES:

  1. Beating Alzheimer’s, The Enemy at the Gate: Turning Despair into Hope and Action EBook: Peter Dredge: Gateway. https://www.amazon.com/Beating-Alzheimers-Enemy-Gate-Turning-ebook/dp/B07HH67GV3/ref=sr_1_4 crid=1OL2PXR69Y6EO&keywords=beating+alzheimers&qid=1560174789&s=gateway&sprefix=beating+al%2Caps%2C187&sr=8-4.
  2. Newport, Mary T. Alzheimer’s Disease: What If There Was a Cure?: The Story of Ketones. Second edition, Basic Health Publications, Inc, 2013.
  3. Bredesen, Dale E. The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline. Avery, an imprint of Penguin Random House, 2017.
  4. “Beating Alzheimer’s Disease? Anne Dredge’s ‘huge Improvements’ with Dale Bredesen Treatment.” RNZ, 21 Sept. 2018, https://www.rnz.co.nz/national/programmes/afternoons/audio/2018663546/beating-alzheimer-s-disease-anne-dredge-s-huge-improvements-with-dale-bredesen-treatment.
  5. Henderson, Samuel T., et al. “Study of the Ketogenic Agent AC-1202 in Mild to Moderate Alzheimer’s Disease: A Randomized, Double-Blind, Placebo-Controlled, Multicenter Trial.” Nutrition & Metabolism, vol. 6, 2009, p. 31. www.ncbi.nlm.nih.gov, doi:10.1186/1743-7075-6-31.
  6. “What to Know about the Stages of Alzheimer’s.” Mayo Clinic, https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/in-depth/alzheimers-stages/art-20048448.
  7. Kashiwaya, Yoshihiro, et al. “A Ketone Ester Diet Exhibits Anxiolytic and Cognition-Sparing Properties, and Lessens Amyloid and Tau Pathologies in a Mouse Model of Alzheimer’s Disease.” Neurobiology of Aging, vol. 34, no. 6, June 2013, pp. 1530–39. PubMed, doi:10.1016/j.neurobiolaging.2012.11.023.
  8. Newport, Mary. “What If There Was a Cure for Alzheimer’s Disease and No One Knew?  A Case Study by Dr. Mary Newport.” www.CoconutKetones.Com , Mary Newport, MD, 22 July 2008, http://coconutketones.com/wp-content/uploads/2016/09/whatifcure.pdf.
  9. Reger, Mark A., et al. “Effects of β-Hydroxybutyrate on Cognition in Memory-Impaired Adults.” Neurobiology of Aging, vol. 25, no. 3, Mar. 2004, pp. 311–14. DOI.org (Crossref), doi:10.1016/S0197-4580(03)00087-3.
  10. de la Monte, Suzanne M., and Jack R. Wands. “Alzheimer’s Disease Is Type 3 Diabetes–Evidence Reviewed.” Journal of Diabetes Science and Technology (Online), vol. 2, no. 6, Nov. 2008, pp. 1101–13.
  11. Schilling, Melissa A. “Unraveling Alzheimer’s: Making Sense of the Relationship between Diabetes and Alzheimer’s Disease 1.” Journal of Alzheimer’s Disease, vol. 51, no. 4, Jan. 2016, pp. 961–77. content.iospress.com, doi:10.3233/JAD-150980.
  12. Bredesen, Dale E. “Reversal of Cognitive Decline: A Novel Therapeutic Program.” Aging, vol. 6, no. 9, Sept. 2014, pp. 707–17. PubMed, doi:10.18632/aging.100690.
  13. Courchesne-Loyer, Alexandre, et al. “Stimulation of Mild, Sustained Ketonemia by Medium-Chain Triacylglycerols in Healthy Humans: Estimated Potential Contribution to Brain Energy Metabolism.” Nutrition, vol. 29, no. 4, Apr. 2013, pp. 635–40. ScienceDirect, doi:10.1016/j.nut.2012.09.009.

 

Anti-Aging Supplements | The Paleo Diet
Coenzyme Q10 (CoQ10) is one of the most widely consumed antioxidant supplements, but according to recently published research CoQ10 doesn’t function as commonly believed. Earlier this month, a team of researchers led by professor Siegfried Hekimi of McGill University (Canada) published their remarkable findings in Nature Communications.[1] Specifically, they demonstrated that CoQ10 doesn’t behave as antioxidant and, thus, shouldn’t be marketed as an anti-aging supplement.

This spells bad news for the rapidly growing CoQ10 market, but good news for people genuinely interested in improved health. A recently published market research report suggests the global CoQ10 market will nearly double by 2020, ballooning to an estimated $850 million. This money would be much better spent on healthy food, which provides plenty of antioxidants.

Professor Hekimi explained, “Our findings show that one of the major anti-aging antioxidant supplements used by people can’t possibly act as previously believed. Dietary supplements cost a lot of money to patients throughout the world—money that would be better spent on healthy food. What’s more, the hope for a quick fix makes people less motivated to undertake appropriate lifestyle changes.”[2]

CoQ10 is a lipid-like substance occurring naturally in all cells of the body. Cell mitochondria use CoQ10 to create energy from oxygen and various nutrients. In addition to this vital role, CoQ10 was also thought to behave as an antioxidant, hence being positioned as an anti-aging supplement.

The researchers experimented with a strain of mice unable to produce adequate amounts of endogenous CoQ10 and, therefore, requiring supplements. As expected, absent supplementation, those mice suffered severe illnesses and early death due to CoQ10’s vital role in energy production. Surprisingly, however, the scientists observed no signs of elevated oxidative damage when supplementation was suspended. This lack of damage, they determined, was not due to deployment of other antioxidant strategies. Eventually, they concluded that CoQ10 is not an antioxidant.

This study underscores a larger, more important issue with respect to supplements, particularly antioxidant supplements. Besides simply being ineffective, as per CoQ10, antioxidant supplements (or those marketed as such) can actually damage your health. Dr. Cordain has written extensively about the numerous randomized controlled trials and meta-analyses showing these products actually increase all-cause mortality. For example, a 2007 meta-analysis spanning 67 random controlled trials (232,606 participants) determined that antioxidant supplementation with vitamin E or vitamin A increases overall death rates.[3]

For most people, the only supplements Dr. Cordain recommends (if any) are fish oil and vitamin D. And, whereas the recently published study shows CoQ10 is not an antioxidant, you might wonder whether it’s a worthwhile supplement based on CoQ10’s role in energy production. This is a valid question, but the answer is very simple and straightforward. By consuming a healthy Paleo diet, your cells will have all the CoQ10 they need. Dr. Cordain further points out that meat, poultry, and fish are concentrated sources of natural CoQ10.

Supplementation is a dangerous game because nutrients can easily be consumed excessively and in the wrong proportions with respect to other nutrients. Whole foods don’t have this problem. That’s why the Paleo diet emphasizes food while largely discouraging supplements.

Christopher James Clark, B.B.A.
@nutrigrail
Nutritional Grail
www.ChristopherJamesClark.com

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

 

REFERENCES

[1] Wang Y, et al. (Mar 2013). Mitochondrial function and lifespan of mice with controlled ubiquinone biosynthesis. Nature Communications, 6(6393).

[2] McGill University. (Mar 6, 2015). Popular antioxidant likely ineffective, study finds. ScienceDaily.

[3] Bjelakovic G, et al. (Feb 2007). Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis. JAMA, 297(8).

Hemp | The Paleo Diet

There’s no argument that eating protein is an essential component of the Paleo diet. Traditional hunter-gatherers consumed high amounts (45–65% of energy) of animal food, resulting in a macronutrient consumption ratio in which protein accounted for 19–35% of their energy intake.[1] Although there are many grass-fed, pastured, and wild animal sources for protein intake in modern times, consumers are still attracted to plant based options to meet their protein requirements.

One popular plant protein is sourced from hemp. Specifically, hemp protein powders have been marketed as a highly digestible, superior quality plant source, but should it be incorporated into your Paleo Diet? Let’s take a closer look at hemp.

Hemp is a plant, that has been cultivated for thousands of years in China, used for both its seed and fibers as a food and in textiles.[2] It is a high protein seed containing 20 amino acids, including all nine of the essential amino acids. Hemp seeds are rich in oil: 44% (by weight) is edible oil, containing about 80% essential fatty acids (EFAs); e.g., linoleic acid, omega-6(LA, 55%), alpha-linolenic acid, omega-3 (ALA, 22%), in addition to gamma-linolenic acid, omega-6 (GLA, 1–4%) and stearidonic acid, omega-3 (SDA, 0–2%).

Proteins (including edestin) comprise the other major component (33%). Hemp seed’s amino acid profile is comparable to other sources of protein such as meat, milk, and eggs.[3] Overall, it has a ratio of omega 3 to 6 fats at around a three to one ratio. Since, hemp seeds are high in polyunsaturated fats, they can easily go rancid and should be stored properly.

As a whole food, the shelled seeds (called hearts), oil, and even the fresh leaves can be eaten. You may notice hemp seed oil, hemp butter, hemp milk and even hemp flour on the grocery store shelves. Unlike other seeds, hemp doesn’t contain phytic acid viewed as an anti-nutrient in human diets as it binds with important minerals.[4]

Although hemp is a member of the same plant family (Cannabis sativa) as marijuana, there are distinct differences between the two. The most important is that hemp has less than 1% of the psychoactive substance THC, while marijuana can contain 20% or more.[5] (//thepaleodiet.com/habitual-marijuana-use-paleo-diet-long-strange-trip/)

Proteins from animal sources (i.e. eggs, milk, meat, fish and poultry) provide the highest quality rating of food sources due to the completeness of proteins from these sources.[6]  However, hemp seed protein is unique in that 65% of it is globulin edestin, the highest amount found in any plant.[7] Protein digestibility-corrected amino acid score (PDCAAS) evidence that hemp proteins have a PDCAAS equal to or greater than certain grains or nuts, 49-53% for whole hemp seed, 46-51% for hemp seed meal, and 63-66% for dehulled hemp seed.[8] It is clear that hemp seeds provide a concentrated amount of highly digestible protein. For example, one ounce of hemp seeds contains 10 grams of protein[9], compared to one ounce of steak with 6 grams of protein.[10]

However, are Hemp seeds Paleo?

Despite it’s apparent advantages, hemp in any whole food form, like any seed, should only be consumed moderately on the Paleo Diet. If you like the taste of shelled hemp seeds, you can sprinkle them over a green salad or add them to your homemade Paleo trail mix in addition to other nuts for a quick energy snack.

The best sources of protein still remain from wild, predominately grass-fed and wild animals. If you like to start your day with a vegetable-based smoothie, add a piece of previously cooked chicken or bison on the side to boost the protein content and steer clear of protein powders. Hemp protein powder is not recommended on the Paleo Diet.

Stephanie Vuolo
@primarilypaleo
Facebook
Website

Stephanie Vuolo | The Paleo Diet Team

Stephanie Vuolo is a Certified Nutritional Therapist, an American College of Sports Medicine Personal Trainer, and a Certified CrossFit Level 1 Coach. She has a B.A. in Communications from Villanova University. She is a former contributor to Discovery Communications/TLC Blog, Parentables.

Stephanie lives in Seattle, WA, where she is a passionate and enthusiastic advocate for how diet and lifestyle can contribute to overall wellness and longevity. She has been raising her young daughter on the Paleo Diet since birth. You can visit her website at www.primarilypaleo.com.

REFERENCES

[1] Cordain, Loren, et al. “Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets.” The American journal of clinical nutrition 71.3 (2000): 682-692.

[2] Bocsa, Ivan, and Michael Karus. The cultivation of hemp: botany, varieties, cultivation and harvesting. Hemptech, 1998.

[3] Callaway, J. C. “Hempseed as a nutritional resource: an overview.” Euphytica 140.1-2 (2004): 65-72.

[4] Lott, John NA, et al. “Phytic acid and phosphorus in crop seeds and fruits: a global estimate.” Seed Science Research 10.01 (2000): 11-33.

[5] Datwyler, Shannon L., and George D. Weiblen. “Genetic Variation in Hemp and Marijuana (Cannabis sativa L.) According to Amplified Fragment Length Polymorphisms*.” Journal of Forensic Sciences 51.2 (2006): 371-375.

[6] Campbell, Wayne W., et al. “Effects of an omnivorous diet compared with a lactoovovegetarian diet on resistance-training-induced changes in body composition and skeletal muscle in older men.” The American journal of clinical nutrition 70.6 (1999): 1032-1039.

[7] Osburn, Lynn. “Hemp seed: the most nutritionally complete food source in the world.” Part two: Hemp seed oils and the flow of live force. Hemp Line J 1.2 (1992): 12-13.

[8] House, James D., Jason Neufeld, and Gero Leson. “Evaluating the quality of protein from hemp seed (Cannabis sativa L.) products through the use of the protein digestibility-corrected amino acid score method.” Journal of agricultural and food chemistry 58.22 (2010): 11801-11807.

[9]  Available at: //nutritiondata.self.com/facts/custom/629104/2. Accessed on January 8, 2015.

[10] Available at: //nutritiondata.self.com/facts/beef-products/10525/2. Accessed on January 8, 2015.

USNWR Cherry Picks Diets | The Paleo Diet

Just as surely as the swallows make their annual return to Mission San Juan Capistrano, U.S. News and World Report (USNWR) embarrasses not only itself, but the scientific and nutritional communities via its annual (January) subjective ratings of various popular, not so popular, and virtually unknown diets. As I and others have previously pointed out in 2014’s Rebuttal and 2013’s Rebuttal, these listings have no basis in objective science, but simply represent tallied subjective ratings by a group of experts, cherry picked by an unknown process, presumably by non-scientists at USNWR. I recognize a number of colleagues and good scientist in the expert list and am dismayed that they would participate in such a baseless and non-scientific process. Surely they did not participate in analyzing the data, because it is statistically inappropriate.

Sound nutritional science should not be about people’s opinions, but rather should employ the scientific method in which hypotheses are tested and conclusions drawn using replicable data that is statistically analyzed. Clearly, these procedures were not even remotely followed for this report, consequently the data USNWR has compiled is virtually meaningless. A better use of resources would be for USNWR to actually experimentally test one or more diets against any other diet for the seven end points of concern in this report. Or, at the very least, the panel of experts should be required to read, tabulate and analyze peer review publications of the diets rated in this report. This objective undertaking would be virtually impossible as more than half of the diets have never been written up in peer review scientific journals, much less experimentally tested against one another.

Evidently, a non-scientist at USNWR, not versed in statistics, compiled these results. Let me explain. The panel of 22 experts were asked to give each diet a 1, 2, 3, 4 or 5 ranking for each of the seven categories of interest (short term weight loss, long term weight loss, easy to follow, nutrition, safety, diabetes, heart health). When data is correctly analyzed, one of the first decisions is to determine the level (nominal, ordinal, interval or ratio) of the data. The expert panel’s 1 to 5 rankings represents ordinal data and not higher level interval or ratio data.  Accordingly, it is statistically incorrect to calculate a mean score from ordinal data for each of the seven categories as USNWR has done. Rather a frequency distribution displaying the totals, for each of the 5 rankings, is required for all seven categories to more accurately display this data. But why even bother, as this subjective information, even if analyzed correctly, has zero objective merit when making any logical decisions about diet.

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

Mid-Victorian Diet, How Far Have We Come? | The Paleo Diet

Review of: An unsuitable and degraded diet? Part one: public health lessons from the mid-Victorian working class diet (Clayton and Rowbotham, 2014)

Context: Early Victorian era was plagued with starvation; this was corrected, technically, during the late Victorian era, but at what cost?

Dietary changes in the late 19th century in Britain reduced malnutrition and starvation-induced morbidity and mortality, but were far from optimal.

Refined flour, fresh and tinned meat, canned fruit preserved in heavy syrups, and evaporated milk became readily available to the public. In turn, sugar consumption increased exponentially.

Reduced starvation? The population at large became weaker and frailer, their teeth rotted, albeit they were less starved.

Previously, their diet included healthier foods like onions, cherries and apples, bones, dripping, offal, and meat scraps. The study authors inevitably concluded the malnourishment abated because the food got cheaper (less starvation), not healthier.

Another factor in reduced starvation was the fact that physical activity markedly declined in this period, so people simply needed fewer calories to survive. Combine that with sugar-laden confectionaries and otherwise junk food and you have a recipe for disaster.

In other words, they went from a Paleo-template to a Western diet in just a few years. The nutrient density, fibre, potassium, and omega-3 fatty acids were diluted with processed grains and refined flour. And so a sad state of health was born: diets low in fresh fruits and veggies, and rich in high glycemic index foods like potato products, breakfast cereals, confectioneries, and refined baked foods.  And low physical activity.  They call it “Type B Malnutrition.”  The cause?  Sedentary lifestyle and cheap junk food… in other words, “not Paleo.”

History has repeated itself.  Now that we are in a state where healthy food prices are comparable to junk food, we should be striving to get back to our dietary roots.  A diet rich in whole foods, more similar to an early Victorian or otherwise Paleo template.  That is a necessary prerequisite to curb the rising rate of non-communicable diseases.  “It’s too expensive” is no longer a valid excuse.

William Lagakos, Ph.D.
@caloriesproper
CaloriesProper

William Lagakos, Ph.D.Dr. William Lagakos received a Ph.D. in Nutritional Biochemistry and Physiology from Rutgers University where his research focused on dietary fat assimilation and integrated energy metabolism. His postdoctoral research at the University of California, San Diego, centered on obesity, inflammation, and insulin resistance. Dr. William Lagakos has authored numerous manuscripts which have been published in peer-reviewed journals, as well as a non-fiction book titled The Poor, Misunderstood Calorie which explores the concept of calories and simultaneously explains how hormones and the neuroendocrine response to foods regulate nutrient partitioning. He is presently a nutritional sciences researcher, consultant, and blogger.

Fad Diets vs. Long-Term Lifestyles for Weight Loss | The Paleo Diet

A new study, published in Circulation: Cardiovascular Quality and Outcomes, compares four popular diets—Atkins, the Zone, the South Beach Diet, and Weight Watchers—in terms of weight loss and cardiovascular disease risk factors. Researchers analyzed 26 randomized controlled trials involving 3,575 subjects, the majority of whom were young, white, obese women. Men and people with body mass indices (BMI) less than 30 kg/m2 were poorly represented in these trials.

Based on the available evidence, the researchers concluded, “Our results suggest that all 4 diets are modestly efficacious for short-term weight loss, but that these benefits are not sustained long-term.”1 Long-term, in this study, is defined as just 24 months. Do these results also apply to people with BMI scores less than 30? Can moderately overweight people expect sustained, long-term weight loss? Unfortunately, for lack of data, this study cannot answer these questions.

Curiously, the study’s discussion focuses mostly on weight loss rather than cardiovascular disease risk factors, even though elsewhere the authors comment, “Long-term RCTs comparing Atkins to usual care showed significant improvements in high-density lipoprotein cholesterol and, to a lesser extent, triglyceride levels at 12 and 24 months; there was no evidence of a low-density lipoprotein cholesterol increase.”2 Usual care refers to traditional weight loss approaches, including low-fat diets, behavioral weight loss intervention, and nutritional counseling.

Thus far, the popular press has also focused almost exclusively on the long-term weight loss prospects of “fad diets,” largely ignoring the cardiovascular disease aspect and failing to ask whether or not these diets improve health, irrespective of weight loss. In response to the study, Dr. Barry Sears, creator of the Zone, stressed that improved health, as opposed to weight loss, is indeed the goal, including better control of insulin and better control of inflammation.3

You can carry a few extra pounds and still be metabolically healthy, but you can’t have chronic, systemic inflammation and expect the same. Health improves when we stop looking at diets as temporary interventions and start adopting them as lifestyles. “You need to pick a way of life,” says Sears, “and stick with it, and a way of life that gives the greatest health for the longest period of time.”4

FAD DIETS

In an accompanying editorial, published in the same journal, Dr. David Katz questions the rational for comparing three carbohydrate-restricted diets (Atkins, Zone, South Beach) with one calorie-restricted diet (Weight Watchers). “The choices,” says Katz “are rather odd if the objective here was to examine the full expanse of competing dietary claims, which readily extends from vegan to Paleo.”5

The Circulation study only scrutinized four diets, but you wouldn’t know this by reading the headlines. The media’s all-encompassing “fad diet” pejorative casts doubt on all diets bearing particular names and espousing particular philosophies. This is unfortunate, especially for lifestyle diets, as opposed to diets based on strict calorie counting or rigid macronutrient requirements.

The Paleo Diet, of course, is a lifestyle diet encompassing movement, sleep, food choices, and much more. In other words, the Paleo Diet is a holistic approach to wellness, which draws upon the wisdom of our ancestors. It allows for customization, emphasizes whole foods, and encourages traditional practices, like nose to tail eating. To curb obesity, the Circulation study’s authors recommend lifestyle interventions with “dietary, behavioral, and exercise components.”6 Diets will always fail so long as they remain just diets. Only when they become lifestyles can they truly yield long-term results.

Christopher James Clark, B.B.A.

@nutrigrail
Nutritional Grail
www.ChristopherJamesClark.com

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

REFERENCES

[1] Atallah, R, et al. Long-Term Effects of 4 Popular Diets on Weight Loss and Cardiovascular Risk Factors: A Systematic Review of Randomized Controlled Trials. Circulation: Cardiovascular Quality & Outcomes. Published online November 11, 2014, doi: 10.1161/CIRCOUTCOMES.113.000723

[2] Ibid, Atallah.

[3] Fox, M, et al. (November 12, 2014). ‘Overcooked Baloney’: Diets Don’t Work for Long, Review Shows. NBCNews.com. Retrieved from //www.nbcnews.com/health/diet-fitness/overcooked-baloney-diets-dont-work-long-review-shows-n246331

[4] Ibid, Fox.

[5] Katz, D. Diets, Diatribes, and a Dearth of Data. Circulation: Cardiovascular Quality & Outcomes. Published online November 11, 2014. doi: 10.1161/CIRCOUTCOMES.114.001458

[6] Atallah, R, et al. Long-Term Effects of 4 Popular Diets on Weight Loss and Cardiovascular Risk Factors: A Systematic Review of Randomized Controlled Trials. Circulation: Cardiovascular Quality & Outcomes. Published online November 11, 2014, doi: 10.1161/CIRCOUTCOMES.113.000723

Media’s Botched Coverage of Long Term Weight Loss | The Paleo Diet

A study recently published online in The Lancet Diabetes & Endocrinology journal compares rapid and gradual weight loss diets.1 We’ll examine this study, but first let’s fast-forward to its conclusions. Study author Katrina Purcell said contrary to widespread recommendations for gradual weight loss, “our results show that achieving a weight loss target of 12.5% is more likely, and drop-out is lower, if losing weight is done quickly.”2

In an editorial published in the same journal, scientists Corby Martin and Kishore Gadde expressed modern, crash-diet products are well-formulated, provide adequate nutrition, and are “safe if used under expert supervision.”3 They added that for weight loss, “a slow and steady approach does not win the race, and the myth that rapid weight loss is associated with rapid weight regain is no more true than Aesop’s fable.”4

The popular press swallowed this pro-crash diet slant and swiftly regurgitated it for readers touting:

  • “Crash diets might not be so bad in beating fat after all, suggests new study”5The Independent
  • “Does it matter if you lose weight quickly or gradually? Apparently not.”6 CNN
  • “Fast Weight Loss May Be More Effective, Study Says.”7 Men’s Fitness
  • “Crash diets may be most effective weight-loss technique, U.K. study suggests.”8The Telegraph
  • “Another Diet Myth Exploded: Gradual Weight Loss No Better Than Rapid Weight Loss”9 Forbes

What’s going on here? On the surface, based on comments from the study’s authors, an editorial published alongside the study, and sensational headlines spewed across the web, this study seems like fantastic news for crash-diet product manufacturers. Keep this in mind.

THE STUDY

This was a two-phase study involving 204 participants, whom all had BMI (body mass index) scores between 30 and 45. In other words, the study involved only obese participants. Do its conclusions also apply to those only slightly overweight and in better metabolic health than the participants? We cannot say, but the discussion around this study has avoided this question, taking a more “crash diets work for everyone” tone.

During phase 1, participants were randomly assigned either a rapid weight loss (RWL) or gradual weight loss (GWL) program. Here’s where it gets interesting. RWL participants consumed only 450 to 800 calories daily for 12 weeks, subsisting solely on Nestlé’s Optifast products. GWL participants consumed an energy-reduced diet based on the Australian Guide to Healthy Eating (AGHL) and with one or two Optifast meal replacements daily.

The AGHL is nearly identical to the USDA’s MyPlate as both are high-carbohydrate, grain-centric diets. Additionally, both encourage dairy, discourage saturated fat, and promote vegetable oils. Nestlé’s Optifast products are heavily processed, featuring ingredients ranging from hydrogenated oils to soy protein isolate, high fructose corn syrup, aspartame, and other nutritional abominations. Additionally, these products contain little to no fiber and low amounts of vitamins and minerals. The ingredients and nutritional information for three Optifast products are pictured below.

Media’s Botched Coverage of Long Term Weight Loss | The Paleo Diet

“OPTIFAST HP® Shake Mix.” OPTIFAST HP Shake Mix. N.p., n.d. Web. 13 Nov. 2014.

Media’s Botched Coverage of Long Term Weight Loss | The Paleo Diet

OPTIFAST 800® Bar.” OPTIFAST 800 Bar. N.p., n.d. Web. 13 Nov. 2014.

Media’s Botched Coverage of Long Term Weight Loss | The Paleo DIet

“OPTIFAST 800® Soup Mix.” OPTIFAST 800 Soup Mix. N.p., n.d. Web. 13 Nov. 2014.

Of the 204 participants who completed phase 1, only 104 completed phase 2. The authors explained, “The main reason given for withdrawal in both groups was difficulty adhering to the diet.”10

At the end of phase 1 (12 weeks), 81% of RWL participants achieved 12.5% or more weight loss, whereas only 50% of GWL participants achieved such results.

For phase 2, participants were placed on individualized diets based on the AGHL. At the end of phase 2 (144 weeks), RWL participants regained 71.2% of the weight they lost, whereas GWL participants regained 70.5% of the weight they lost.

CONCLUSION

This study shows that neither grain-centric diets, nor crash diets are effective for long-term weight loss and neither are health supportive. The headlines should have highlighted this. Instead, many of them read like Optifast advertisements, focusing on crash diets being slightly more effective than grain-heavy diets for short-term weight loss. Interestingly, Joseph Proietto, the study’s lead author, “was Chair of the Optifast Medical Advisory Committee for Nestlé Healthcare Nutrition Australia Ltd from 2005 to 2010,” as fully disclosed in the study’s Declaration of Interest.11

The Paleo Diet is a nutrient-dense template delivering optimal nutrition for sustainable, long-term health. The Paleo Diet is wholly unlike both the Nestlé crash diet and the U.S. / A.U. government-endorsed, grain-centric diets. Unfortunately, irresponsible reporting around this study is sending the message that all diets fail long-term, but at least short-term benefits can be enjoyed through crash diets consisting of synthetic, heavily processed products. We see this as a grave error and encourage people to consume nutrient-dense, natural foods, in accordance with the Paleo Diet, for both short-term and long-term health.

Christopher James Clark, B.B.A.

@nutrigrail
Nutritional Grail
www.ChristopherJamesClark.com

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

REFERENCES

[1] Purcell, K, et al. The effect of rate of weight loss on long-term weight management: a randomised controlled trial. The Lancet Diabetes & Endocrinology, Early Online Publication, 16 October 2014, doi:10.1016/S2213-8587(14)70200-1

[2] The Lancet. (2014, October 15). Gradual weight loss no better than rapid weight loss for long-term weight control. ScienceDaily. Retrieved from www.sciencedaily.com/releases/2014/10/141015190832.htm

[3] Martin, CK and Gadde, KM. Weight loss: slow and steady does not win the race. The Lancet Diabetes & Endocrinology, Early Online Publication, 16 October 2014, doi:10.1016/S2213-8587(14)70153-6

[4] Martin, CK and Gadde, KM. Weight loss: slow and steady does not win the race. The Lancet Diabetes & Endocrinology, Early Online Publication, 16 October 2014, doi:10.1016/S2213-8587(14)70153-6

[5] Cooper, C. (October 16, 2014). Crash diets might not be so bad in beating fat after all, suggests new study. The Independent. Retrieved from //www.independent.co.uk/life-style/health-and-families/health-news/crash-diets-might-not-be-so-bad-after-all-suggests-new-study-9796651.html

[6] Kimball, H and Ryan, D. (October 17, 2014). Slow and steady may not win the weight-loss race. CNN. Retrieved from //edition.cnn.com/2014/10/17/health/five-studies/

[7] Fox, K. (October 16, 2014). Fast weight loss may be more effective, new study says. Men’s Fitness. Retrieved from //www.mensfitness.com/weight-loss/burn-fat-fast/fast-weight-loss-may-be-more-effective-new-study-says

[8] Knapton, S. (October 16, 2014). Crash diets may be most effective weight-loss technique, U.K. study suggests. The Daily Telegraph. Retrived from //www.telegraph.co.uk/science/science-news/11164914/Crash-dieting-more-effective-than-gradual-weight-loss-study-suggests.html /

[9] Husten, L. (October 15, 2014). Another Diet Myth Exploded: Gradual Weight Loss No Better Than Rapid Weight Loss. Forbes. Retrieved from //www.forbes.com/sites/larryhusten/2014/10/15/another-diet-myth-exploded-gradual-weight-loss-no-better-than-rapid-weight-loss/

[10] Purcell, K, et al. The effect of rate of weight loss on long-term weight management: a randomised controlled trial. The Lancet Diabetes & Endocrinology, Early Online Publication, 16 October 2014, doi:10.1016/S2213-8587(14)70200-1

[11] Purcell, K, et al. The effect of rate of weight loss on long-term weight management: a randomised controlled trial. The Lancet Diabetes & Endocrinology, Early Online Publication, 16 October 2014, doi:10.1016/S2213-8587(14)70200-1

Schizophrenia and The Paleo Diet

If you have a loved one who suffers from the debilitating mental condition of schizophrenia, the quality of life is often very low.1, 2 With a growing rate of schizophrenia worldwide, any measures that may help improve this, should be considered.3, 4

Even more sadly, sometimes improvements in symptoms do not necessarily equate to a better quality of life.5 Cognitive impairment, however, can be correlated with perceived quality of life, where improved cognition could potentially lead to a better life in schizophrenics.6, 7, 8

Scientifically, it seems mental disorders, like schizophrenia, may be an issue of glutamatergic transmission.9, 10 Researchers note the deletion at the SLC1A1 glutamate transporter gene,11 which has also been shown in sufferers of obsessive-compulsive disorder.12 Glutamatergic theories of schizophrenia are based on the ability of N-methyl-aspartate receptor (NMDAR) antagonists to induce schizophrenia-like symptoms.13

Schizophrenia and Diet

(As Seen In: Zhou Y, Danbolt NC. GABA and Glutamate Transporters in Brain. Front Endocrinol (Lausanne). 2013;4:165.)

If the glutamatergic hypothesis is indeed correct, it stands to reason that altering one’s diet may result in cognitive improvements.14 Couple this with the fact that schizophrenia has been shown to present with intestinal permeability.15 Also of note, schizophrenics are 50 times more likely to have celiac disease,16 a correlation that is very intriguing, if somewhat unsurprising.

We have discussed gluten’s negative cognitive effects previously in Gluten and the Brain, 17, 18 but besides gluten, deficiencies in vitamin C, niacin and folate may worsen symptoms of schizophrenia.19 As researchers noted in 2003, a growing body of evidence implicates GABA (an important inhibitory neurotransmitter) in the pathogenesis of schizophrenia.20, 21 Schizophrenics, especially when eating an unhealthy diet, may have altered GABA synthesis.22 Researchers found that a low carbohydrate, ketogenic diet, may be useful in treating schizophrenic patients.23 This is thought to partially be from the increased synthesis of GABA in the brain.24

Schizophrenia and Diet

(As Seen In: Gordon JA. Testing the glutamate hypothesis of schizophrenia. Nat Neurosci. 2010;13(1):2-4.)

Schizophrenia and Diet


(As Seen In: Schwartz TL, Sachdeva S, Stahl SM. Glutamate neurocircuitry: theoretical underpinnings in schizophrenia. Front Pharmacol. 2012;3:195.)

The Paleo Diet is rich in “brain foods,” that are shown to have positive effects on cognition.25 These foods include docosahexaenoic acid (DHA), which can be found in wild-caught fish.26 It also includes flavonoids, which have been shown to help with cognitive decline.27 Choline is also an overlooked essential nutrient. It can be found in egg yolks.28 In fact, lower amounts of choline acetyltransferase in the pontine tegmentum of schizophrenic patients suggests involvement of pontine cholinergic neurons in the disorder.29
Schizophrenia and Diet

 

Schizophrenia and Diet

If you, or a loved one, are diagnosed with a debilitating mental disorder like schizophrenia, it’s important to try any and all methods, in hopes that quality of life can be improved. A Paleo Diet that is low in carbohydrate, and removes problematic proteins like gluten, would be a good start. Couple this with a regimen that is high in vitamins and minerals, and great results are likely be seen. The formula is simple: If improving the quality of food, can help improve the quality of life, what have you got to lose?

References

1. Cardoso CS, Caiaffa WT, Bandeira M, Siqueira AL, Abreu MN, Fonseca JO. Factors associated with low quality of life in schizophrenia. Cad Saude Publica. 2005;21(5):1338-40.

2. Solanki RK, Singh P, Midha A, Chugh K. Schizophrenia: Impact on quality of life. Indian J Psychiatry. 2008;50(3):181-6.

3. Bray I, Waraich P, Jones W, Slater S, Goldner EM, Somers J. Increase in schizophrenia incidence rates: findings in a Canadian cohort born 1975-1985. Soc Psychiatry Psychiatr Epidemiol. 2006;41(8):611-8.

4. Burns JK, Tomita A, Kapadia AS. Income inequality and schizophrenia: increased schizophrenia incidence in countries with high levels of income inequality. Int J Soc Psychiatry. 2014;60(2):185-96.

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