Tag Archives: paleo

The most important meal of the day is the most delicious meal of the day with this Paleo dish. The combination of meats, eggs, veggies, and spices will wake up your taste buds and keep you energized throughout the busy morning hours. This casserole is so impressive that it can be prepared for special occasions as well as casual get togethers. Best of all, it’s perfectly Paleo!


Paleo Breakfast Casserole

Breakfast Casserole

Breakfast CasseroleThe most important meal of the day is the most delicious meal of the day with this Paleo dish. The combination of meats, eggs, veggies, and spices will wake up your taste buds and keep you energized throughout the busy morning hours. This casserole is so impressive that it can be prepared for special occasions as well as casual get togethers. Best of all, it’s perfectly Paleo!

  • Author: Lorrie Cordain
  • Prep Time: 25 minutes
  • Cook Time: 65 minutes
  • Total Time: 1 hour 30 minutes
  • Yield: 4-6 People 1x
  • Category: Eggs/Meat
  • Cuisine: Breakfast


  • 12 slices pork bellies**
  • 1 tsp smoked paprika
  • 1 tsp cracked black pepper
  • 24 tbs coconut oil, divided
  • 2 large sweet potatoes peeled and sliced into ¼ inch rounds
  • 3 cups Brussels sprouts tops removed and quartered (or rough chopped)
  • 1 large onion, thinly sliced
  • 12 eggs
  • 1/31/2 cup full fat coconut milk
  • 1/2 tsp garlic powder
  • Black pepper to taste

**If necessary substitute 12-16 oz ground turkey or pork.


Preheat oven to 425°F. Grease a 9×13 inch casserole dish with coconut oil, making sure to cover bottom and sides of pan. Line a large baking sheet with parchment paper.

Cut the pork bellies into 1-inch pieces and sprinkle with paprika and pepper. Place in a large heavy skillet. Cook over medium high heat, stirring occasionally for even browning. Cook until pork pieces are crisp. If using ground meat, cook until well browned. Remove meat using a slotted spoon and place on paper towels. Set aside the pan containing the cooking remnants and oils.

In small saucepan, heat 1-2 tablespoons coconut oil until liquid. In a large mixing bowl, toss the sweet potato rounds with half of the coconut oil and spread evenly over the bottom of the casserole dish.

Toss brussel sprouts with remaining oil and arrange on the parchment lined baking sheet in a single layer. Place the sweet potatoes and brussels sprouts in the oven to roast. After 20 minutes, remove the brussels sprouts. Continue roasting the sweet potatoes for an additional 10 minutes. Remove from oven.

Reheat cooking pan used for pork bellies over low to medium heat. Add onions to pan, stirring occasionally, and cook for about 25 minutes until onions have carmelized. Remove from heat.

In a medium sized mixing bowl, whisk together the eggs, coconut milk, and garlic powder. Set aside.

Set oven to 400°F. To assemble the casserole, layer brussels sprouts over the sweet potato rounds in the casserole dish. Remove the caramelized onions with a slotted spoon and layer over the brussels sprouts, followed by the cooked meat. Pour the whisked egg mixture over the casserole to evenly cover.

Place on middle rack in the oven and bake for about 25 minutes until the center is set and edges begin to turn light brown.


Allow to cool for 10 minutes before cutting into desired serving sizes.



Breakfast Casserole

Keywords: paleo, breakfast, casserole, eggs, meat, bake, oven, autumn, fall

A favorite dish at The Paleo Diet® is this slow-cooked creation of meatballs with marinara sauce. Pair with your favorite Paleo veggie noodles or a fresh salad and you’ve got a nutritious and delicious meal to be enjoyed by all.  Leftovers can be served with eggs at breakfast, taken for a midday lunch on a busy workday, or heated up the next evening for dinner.  Better make double!


Paleo Slow Cooker Meatballs & Marinara

Paleo Meatballs

Paleo Meatballs

favorite dish at The Paleo Diet® is this slow-cooked creation of meatballs with marinara sauce. Pair with your favorite Paleo veggie noodles or a fresh salad and you’ve got a nutritious and delicious meal to be enjoyed by all.  Leftovers can be served with eggs at breakfast, taken for a midday lunch on a busy workday, or heated up the next evening for dinner.  Better make double!

  • Author: Lorrie Cordain
  • Prep Time: 15 minutes
  • Cook Time: 4 hours
  • Total Time: 4 hours 15 minutes
  • Yield: Serves 4 1x
  • Category: Dinner
  • Cuisine: Italian


For the meatballs: 

  • 1/4 cup blanched almond flour
  • 2 tsp onion powder
  • 1 tsp garlic powder
  • 1 tbsp salt-free Italian seasoning blend
  • generous pinch crushed red pepper adjust for spice preference
  • 2 lbs grass-fed beef, ground
  • 1 egg
  • 1 tbsp chopped fresh parsley – optional

For the sauce: 

  • 28 oz can salt-free crushed tomatoes with basil
  • 14 oz can salt-free diced tomatoes with basil and garlic
  • 16 oz can tomato paste
  • 1/2 medium onion chopped
  • 2 tbsp chopped fresh garlic
  • 2 tbsp chopped fresh oregano leaves
  • 2 bay leaves


To make the meatballs:

  1. In a small bowl, mix the almond flour, onion and garlic powder, Italian seasoning, and crushed red pepper.
  2. In a large bowl, add the ground beef, the egg and almond flour mix (plus parsley if adding) and gently mix with your hands until the mixture binds and is evenly distributed.
  3. It’s important not to work the meat too much or it becomes tough.
  4. Line a large baking sheet with parchment paper and preheat your broiler on low.
  5. Form the meat mixture into 20 meatballs and arrange on the baking sheet.
  6. Broil 2-4 minutes, just to lightly brown, and release a small amount of fat (this avoids an overly greasy sauce).
  7. Remove promptly.
  8. Add the meatballs to the slow cooker, leaving behind any rendered fat.
  9. Top the meatballs with all sauce ingredients and give a gentle stir, being careful not to break the meatballs.
  10. Cover and cook on low for 4 hours, or until meatballs are cooked through.

To make the sauce:

  1. Put crushed tomatoes in a bowl.
  2. While stirring, add in the remaining ingredients.


Paleo Meatballs Ingredients

Paleo Meatballs

Keywords: paleo, meatballs, marinara, slow cooker

Bucket of Fish


Anyone concerned about climate change should pay attention…and that means you…and you…and you too! Yes, we all must be concerned about climate change, regardless of whether it is a result of natural climatic cyclicality, or because of human activity.

OK, I’m going to get off of the fence on this one and say it’s man-made—caused by human activities. I usually try to stay neutral because I’m not a climatologist. But, as a scientist, I am compelled by recent evidence that strongly suggests the contribution of greenhouse gases to global warming and climate change.

And this problem is only accentuated by the fact that, because of increasing population, we will need more and more food to satisfy us. About 10 billion people will live on the planet in 2050—up from the current 7.5 billion1. So, a reasonable person would think, well, it’s one-third more people, so we need one-third more food. Not so.

The World Resources Institute paints a rather solemn picture of our dietary future in a recent report without action on our part1. Scarcity of food calories, insufficient land for agriculture, and a significant increase in greenhouse gas emissions are just some of the challenges we face.

According to a recent article on CNN2 and quoting calculations from the World Resources Institute, the demand for food will increase by more than 50 percent, given the higher average standard of living that is expected to exist in 30 years.

The article goes on to say that beef production accounts for 41 percent of livestock greenhouse emissions, and 14.5 percent of emissions overall. The suggestion in the article is that Americans need to eat less beef—and for that matter, dairy as well (you get dairy from cows; they all eat the same stuff.)

Well, I will put myself out on a limb here and say, the chance of that happening is about as likely as Americans giving up cars. It’s not going to happen! While per capita consumption may fall, total consumption will rise with the increasing population. As the advertising slogan says, “Beef: It’s what’s for dinner.”

Making things worse is all the space that cattle need and use. If we keep on the current path with beef, we will need additional space – the equivalent size of India to accommodate our tastes and demand1. That’s quite frightening, considering additional arable space of that magnitude simply does not exist!

Wait! There’s more bad news! (Spoiler alert: There’s good news at the end.)

Beef cattle and all ruminant cattle have the nasty habit of the expelling methane gas as they digest their food. We continually hear about carbon dioxide (CO2) as the preeminent greenhouse gas that we need to control. But methane is 80 times more efficient at trapping heat in our atmosphere than carbon dioxide3.

Here’s how dire our situation may be. Two scientists actually propose turning atmospheric methane into carbon dioxide because of the beneficial trade-off in heat-trapping capability3. Under our current circumstances, that seems very reasonable. How freaky is that? This is the corner into which we have painted ourselves!

While I believe the total consumption of beef and dairy will continue to rise on an absolute basis, I do think per capita consumption will fall, based on what appears to be people’s “new-found” appetite for all things vegetarian, and the unwavering increase in demand for fish and seafood4. I want to focus on the second part of that equation.

We have known for a long time that fish and shellfish are the champs at converting food to edible flesh—better than chickens, better than hogs, and certainly better than cattle5. On average, finfish and shellfish convert feed at a rate of about 1.5 kg of feed for every kg of live fish. Chickens and other terrestrial livestock—especially cattle—don’t stand a chance of beating fish at this game. The best beef cattle can do is about 6 to 1 (usually worse at 8 or 10 to 1 or higher), and that’s horrible.

You probably wonder how fish make feed conversion look so easy. It all boils down to their environment. Finfish and shellfish “decided” evolutionarily that maintaining a constant body temperature is too difficult and too energetically costly in water. Only very large marine mammals with much smaller surface to volume ratios (heat loss occurs much more slowly) such as whales and seals can maintain body temperature and that requires the help of thick layers of insulating fat and blubber. Instead, finfish and shellfish have body temperatures at or very close to their surrounding aquatic environment. That means all the calories they consume can be spent on movement (a very small percentage) and growth, with virtually no consideration for heating or cooling.

Consider this as well. Seventy percent of the earth is covered in water. Why not use some of that space for food production? Land is becoming too precious for us to pasture cattle and other terrestrial livestock at low densities.

Food production in water also provides the added benefit of a three-dimensional space. Not only is the surface available, but the depths below the surface as well.

So, if you look at the situation objectively, it makes the most sense for us to focus our livestock efforts away from terrestrial species and toward aquatic species. In other words, aquaculture. This includes the production of aquatic plants—30 million metric tons in the year most recently reported4. Some marine macroalgae are directly consumed by people, such as nori for sushi, or “sea lettuce.” Other aquatic plants become fertilizer for terrestrial agriculture or cosmetics, and some provide protein and fat extracts for animal feeds6.

It’s time for us to develop our planet and the resources we require in more imaginative, innovative, and sustainable ways. In all likelihood, our long-term survival as a species depends on it.



1Searchinger, T., R. Waite, C. Hanson, and J. Ranganathan. 2018. Synthesis report: creating a sustainable food future: a menu of solutions to feed nearly 10 billion people by 2050. World Resources Institute, Washington, D.C. 92pp.

2Christensen, J. 2019. To help save the planet, cut back to a hamburger and a half per week. CNN. https://www.cnn.com/2019/07/17/health/beef-environment-resources-report/index.html

3Jackson, R., and P. Canadell. 2019. A crazy-sounding climate fix. Scientific American 321(2; August):10.

4FAO. 2018. FAO yearbook. Fishery and aquaculture statistics 2016. Food and Agriculture Organization of the United Nations. http://www.fao.org/3/i9942t/I9942T.pdf

5Anonymous. 2018. Feed conversion ratio. Wikipedia. https://en.wikipedia.org/wiki/Feed_conversion_ratio#Beef_cattle

6Chase, C. 2019. Veramaris opens USD 200 million algal oil facility. https://www.seafoodsource.com/news/aquaculture/veramaris-opens-usd-200-million-algal-oil-facility

Bill Manci is president of Fisheries Technology Associates, Inc., a Fort Collins, Colorado-based aquaculture, aquaponics, and fisheries consulting firm.

Man with alzheimers


[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.



  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.


Summer isn’t over yet, and what better time is there to be a cook, gardener, or just a food lover? Fresh vegetables are spilling out of every garden and farm, markets are stocked with fantastic fresh ingredients, and it’s warm enough to grill and eat outside. Summer is a great time to experiment with new ingredients and flavors, and on hot days you can turn a salad into a meal without turning on the oven.

If you’re following the Paleo Diet®, you can enjoy everything that summer has to offer. Your local farmers will have plenty of meat for the grill, and you can craft meals around your favorite seasonal vegetables. Here are a few summer recipe ideas (really more like meal blueprints) to whet your appetite:


 A New Take on Salad

Paleo Arugula Salad


If regular lettuce is getting repetitive, try spicing up your salads with different salad greens. Baby kale, arugula, mustard greens, and radicchio all make excellent salads with a bit of extra flavor and texture. Top your salad with radishes, herbs, microgreens, or even shredded beets for another layer of flavor, and finish it with your protein of choice (grilled skirt steak is a favorite). A simple dressing of olive oil and lemon juice completes your satisfying salad. As a bonus, these different salad greens can offer more nutritional benefits than plain lettuce.


 Salsa with a Twist

Cucumber Salsa


What could scream “summer!” more than spicy, tangy salsa? With some creativity, you can make a variety of different salsas with Paleo ingredients, and then use your creations to top all kinds of dishes. For a fruity salsa that’s great with fish, try combining finely chopped peaches, mangoes, melons, or pineapples with lime juice, cilantro, and a bit of jalapeno pepper. For more crunch, try a cucumber salsa: diced cucumber and sweet peppers mixed with red onion, cider vinegar, and your favorite hot peppers. You could add avocado pieces to either of these salsas to turn them into a heartier side dish.


 Go Beyond Steak on the Grill

Grilled Napa Cabbage


If you’re getting the grill fired up to cook some grass-fed steaks or lamb chops, why not make use of it for other dishes as well? While grilled eggplant, zucchini, and peppers are classic summer side dishes, you can get even more creative when cooking with fire. Have you ever tried grilled Napa cabbage? Slice a large cabbage in half, cover the cut sides in olive oil and herbs, then wrap each half in foil and grill until the cabbage is tender. This technique is also great with radicchio and escarole.


 Exotic Herbs

Herbs add a terrific punch of flavor to all kinds of dishes, and there’s a whole world of herbal ingredients you probably haven’t tried yet. Papalo, epazote, lemongrass, kaffir lime — they can all add a new twist to your salads, grilled meat, and vegetable dishes. As long as they haven’t been processed with non-Paleo ingredients (and you should use plain, fresh herbs for maximum flavor,) any herb you choose will be Paleo-friendly.


Summer Desserts

Fruit Salad

While the Paleo Diet doesn’t include processed sugar, there are some great desserts you can make with

fruit. For a cool treat that’s just as good as sorbet, freeze chunks of your favorite fruit and blend them until they’re the consistency of soft-serve ice cream. Banana, mango, and strawberry are all good choices for this dessert. A simple fruit salad can be livened up with fresh mint, crushed walnuts, and a squeeze of lime juice for a tasty post-meal treat.


With these basic ideas, let your imagination run wild and create a summer full of delicious, Paleo-friendly meals. We can help you find more fantastic recipes and learn more about the basics of the Paleo Diet.

Don’t let the color scare you away! There’s nothing childish about this Paleo Diet® twist on an old favorite. Deviled eggs are the perfect grab- and-go snack to have on hand for between meal nutrition. Make them ahead of time and store in the fridge for up to two days. Kids from one to one hundred will love this delicious, fun treat!


Recipe: Green Eggs and Ham Paleo Style

Avocado Deviled Eggs Close-Up

Avocado Deviled Eggs

Don’t let the color scare you away! There’s nothing childish about this Paleo Diet® twist on an old favorite. Deviled eggs are the perfect grab- and-go snack to have on hand for between meal nutrition. Make them ahead of time and store in the fridge for up to two days. Kids from one to one hundred will love this delicious, fun treat!


  • Author: Lorrie Cordain
  • Prep Time: 15 minutes
  • Cook Time: 10 minutes
  • Total Time: 25 minutes
  • Yield: Serves 6 1x
  • Category: Snack
  • Cuisine: American


  • 12 large eggs (hardboiled)
  • 2 avocados
  • ¼ cup fresh cilantro, finely chopped
  • 2 tablespoons fresh lime juice
  • 2 cloves garlic, finely chopped
  • ½ jalapeño pepper, stems and seeds removed, minced
  • ½ teaspoon cayenne
  • ¼ teaspoon ground, black pepper
  • ¼ cup chicharrones, no salt, preservatives or additives


  1. Hard boil the eggs and place in refrigerator to cool.
  2. Peel eggs and cut in half the long way.
  3. Remove yolks and place in mixing bowl.
  4. Set aside egg white halves on serving dish.
  5. Slice avocados in half, remove pits and remove insides from skins.
  6. Combine with egg yolks and mash until well blended.
  7. Add cilantro lime juice, garlic, jalapeño, cayenne, and pepper.
  8. Stir gently to combine.
  9. Fill each egg half with yolk and avocado mixture.
  10. Top with crushed chicharrones.


Avocado Deviled Eggs Ingredients


Avocado Deviled Eggs


Avocado Deviled Eggs Close-Up

Keywords: paleo, recipe, keto, deviled eggs, avocado


When it comes to brain fuel – glucose is king.[1] Glucose is the brain’s primary source of fuel and it is quite narrowly regulated inside our body as a result. This is referred to as glucose homeostasis.[2] There are two key players in this process – insulin and glucagon.[3] These two hormones are kept in balance so that our blood sugar remains stable. When we eat, the ratio of insulin to glucagon is high – which helps to facilitate many postprandial (after meal) processes in the body.[4]

The standard American diet is very high in glucose – meaning it’s high in carbohydrates like bread, pasta, baked goods, and juices.[5] While glucose is the king of brain (and body) fuel, we do also have the ability to fuel our brains with ketone bodies, which is part of why low carb diets are currently exploding in popularity.[6] Heck, even I got in on the action, and wrote a low carb cookbook. (Note that while the Paleo Diet is lower carbohydrate than the standard American diet, at www.thepaleodiet.com, Dr. Loren Cordain and the Editorial Board do not support extreme low-carbohydrate diets like the Ketogenic diet.)


How the Body Manages Glucose

The nuts and bolts of how our brain handles glucose is actually very fascinating. To easily explain a very complex situation, it is best to start by describing the various different metabolic states which bring about different activity in the body and brain. For example, when we lack carbohydrates, our liver glycogen stores are rapidly used and fatty acids are then shuttled (from stored fat,) to provide energy via a process called oxidation.[7] These changes rapidly makes the body less reliant on glucose as it addresses the shortage.

Fatty acid oxidation allows the limited supply of glucose to be conserved for the brain – likely a mechanism developed to prevent starvation in our ancestors, during times of food scarcity.[8]

Think of this as a backup fuel system. Our body knows when one fuel is running low or not available, and switches to another energy supply. Taken to an extreme, when carbohydrates are low enough, for long enough, we go into ketosis.[9] The ‘keto flu’ – where we don’t feel very good after removing carbohydrates from our diet – is directly related to this switch in fuel systems.

On the flip side, if we have plenty of carbohydrates, our bodies will choose to store fat and rely on glucose for fuel since our ability to store carbohydrates is limited. This is also why marathon runners carb-load. They want to maximize this limited store and make sure more glucose is available for their bodies to draw upon as they step outside of a normal human activity range. Glycogen stores can be increased temporarily this way, but if you do this repeatedly – without burning the energy – you are very likely to gain weight instead.[10]

But when we really get into the details; how exactly does our brain sense glucose? and why is this important?

Essentially, there are neurons which detect the presence of glucose, and send signals to our brain, alerting the brain to its presence.[11] Since our brain controls our energy balance (as well as our hunger and satiety signaling processes) – the neurons which detect glucose are critically important.[12] But interestingly, these neurons are located outside the blood-brain barrier – not where you might expect.


What Happens to the Brain when Glucose Balance is Disrupted?

When glucose gets out of balance, diseases, obesity, and other conditions develop. But how does this happen, if we have glucose sensing neurons? In some cases, cells such as these neurons, can die and this is tightly related to brain disorders and degenerative brain conditions.[13] Also, neurotransmitter synthesis requires glucose, and our brain will simply have extreme issues if glucose levels (or regulation of glucose sensing) is disrupted.[14]

Glucose is actually shuttled from the blood to the brain through GLUT1 transporters on the surface of the brain which allows glucose to cross the blood-brain barrier.[15] This transport is carefully regulated and can be disrupted if the glucose-sensing neurons aren’t functioning appropriately. This can lead to serious issues.

Most glucose in the brain is used for ‘thinking’ and ‘processing’. These are broad terms, but essentially mean that without enough glucose in the brain, we can’t think properly, or process information. This disruption is similar to what is seen when alcohol is consumed, for example.

These processes (and glucose) are very critical for both learning and memory, and one can quickly see how glucose disruption and cell malfunction or cell death can greatly impair our brain’s critical processes.[16]

Glucose is in fact even more critical for other functions. For example, glucose can be used to synthesize glutamate, glycine, aspartate, and other important compounds. This is critical, as these compounds normally cannot easily gain entry directly into the brain, without glucose being used to synthesize them.[17] Another example of the importance of glucose, is autophagy. Autophagy is a greatly important process that “cleans out” dying or misfunctioning cells. It can be disrupted by poor glucose metabolism. In the simplest terms, think of it as recycling – but for the body.[18] Just as we recycle to provide better results for the earth – our body has internal mechanisms of recycling, for our own well-being. Glucose is also critical for metabolic coupling – where compounds made in one cell, can be used by a neighboring cell.[19] Think of it as similar to your neighbor borrowing a cup of sugar from you (though hopefully as a Paleo Dieter, you’re not keeping big bags of sugar in your kitchen.)

About 50 percent of all glucose in the body is used by the brain – which helps explain the ‘hangry’ state that we all experience.[20] If there isn’t glucose in the brain – neurotransmitters are not produced. This means neurons can’t talk to each other and helps explain our confusion and foul mood when our blood sugar gets very low.

Interestingly, research has also shown a direct link between too much sugar (specifically fructose) – and premature aging. Other studies have shown that too much glucose can be linked to cognitive decline and memory issues.[21] This research is the most frequently cited when articles claim that ‘sugar can kill us’, or ‘sugar can cause Alzheimer’s’. Type 2 diabetes is of course known as the disease where our bodies simply become resistant to insulin – truly scary.

Glucose sensing in the brain is critically important, and a Paleo Diet® will keep glucose levels at normal, healthy levels – leading to much better brain health and a healthier life overall.



  1. Mergenthaler P, Lindauer U, Dienel GA, Meisel A. Sugar for the brain: the role of glucose in physiological and pathological brain function. Trends Neurosci. 2013;36(10):587-97.
  2. Tups A, Benzler J, Sergi D, Ladyman SR, Williams LM. Central Regulation of Glucose Homeostasis. Compr Physiol. 2017;7(2):741-764.
  3. Kalra S, Gupta Y. The Insulin:Glucagon Ratio and the Choice of Glucose-Lowering Drugs. Diabetes Ther. 2016;7(1):1-9.
  4. Kalra S, Gupta Y. The Insulin:Glucagon Ratio and the Choice of Glucose-Lowering Drugs. Diabetes Ther. 2016;7(1):1-9.
  5. Sartorius K, Sartorius B, Madiba TE, Stefan C. Does high-carbohydrate intake lead to increased risk of obesity? A systematic review and meta-analysis. BMJ Open. 2018;8(2):e018449.
  6. Laffel L. Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes. Diabetes Metab Res Rev. 1999;15(6):412-26.
  7. Purdom T, Kravitz L, Dokladny K, Mermier C. Understanding the factors that effect maximal fat oxidation. J Int Soc Sports Nutr. 2018;15:3.
  8. Houten SM, Wanders RJ. A general introduction to the biochemistry of mitochondrial fatty acid β-oxidation. J Inherit Metab Dis. 2010;33(5):469-77.
  9. Miller VJ, Villamena FA, Volek JS. Nutritional Ketosis and Mitohormesis: Potential Implications for Mitochondrial Function and Human Health. J Nutr Metab. 2018;2018:5157645.
  10. Ma Y, Olendzki B, Chiriboga D, et al. Association between dietary carbohydrates and body weight. Am J Epidemiol. 2005;161(4):359-67.
  11. Burdakov D, Luckman SM, Verkhratsky A. Glucose-sensing neurons of the hypothalamus. Philos Trans R Soc Lond, B, Biol Sci. 2005;360(1464):2227-35.
  12. Routh VH. Glucose sensing neurons in the ventromedial hypothalamus. Sensors (Basel). 2010;10(10):9002-25.
  13. Hotchkiss RS, Strasser A, Mcdunn JE, Swanson PE. Cell death. N Engl J Med. 2009;361(16):1570-83.
  14. Bak LK, Schousboe A, Sonnewald U, Waagepetersen HS. Glucose is necessary to maintain neurotransmitter homeostasis during synaptic activity in cultured glutamatergic neurons. J Cereb Blood Flow Metab. 2006;26(10):1285-97.
  15. Morgello S, Uson RR, Schwartz EJ, Haber RS. The human blood-brain barrier glucose transporter (GLUT1) is a glucose transporter of gray matter astrocytes. Glia. 1995;14(1):43-54.
  16. Mergenthaler P, Lindauer U, Dienel GA, Meisel A. Sugar for the brain: the role of glucose in physiological and pathological brain function. Trends Neurosci. 2013;36(10):587-97.
  17. Hertz L, Rothman DL. Glucose, Lactate, β-Hydroxybutyrate, Acetate, GABA, and Succinate as Substrates for Synthesis of Glutamate and GABA in the Glutamine-Glutamate/GABA Cycle. Adv Neurobiol. 2016;13:9-42.
  18. Glick D, Barth S, Macleod KF. Autophagy: cellular and molecular mechanisms. J Pathol. 2010;221(1):3-12.
  19. Steinman MQ, Gao V, Alberini CM. The Role of Lactate-Mediated Metabolic Coupling between Astrocytes and Neurons in Long-Term Memory Formation. Front Integr Neurosci. 2016;10:10.
  20. Mergenthaler P, Lindauer U, Dienel GA, Meisel A. Sugar for the brain: the role of glucose in physiological and pathological brain function. Trends Neurosci. 2013;36(10):587-97.
  21. Calsolaro V, Edison P. Alterations in Glucose Metabolism in Alzheimer’s Disease. Recent Pat Endocr Metab Immune Drug Discov. 2016;10(1):31-39.


If you’re following the Paleo Diet®, your grocery list is largely made up of fresh vegetables, grass-fed or pasture-raised meat, and free-range eggs. While your body benefits from this way of eating, your wallet might be hurting – these high-quality foods can have a high price tag! It can also be a challenge to find good sources for locally-grown produce and grass-fed meat. The offerings at your local grocery store might not cut it and there may not be a convenient farmers market in your area.

Community Supported Agriculture (CSA) could be a great solution for making your Paleo lifestyle work. While CSA models vary, the general principle is that customers support a specific farm or group of farms by buying “shares” of their products. In exchange for paying at least part of the season’s cost up front, customers usually receive a slight discount off the equivalent retail costs, or they receive special items not available in regular retail outlets.

CSA started as a model primarily for vegetable sales, but now all kinds of farms are getting in on the action. In some areas, farms have formed cooperative CSAs that offer a wider variety of products. By joining a CSA run by a local farm or cooperative, you can ensure you’re getting the freshest produce and properly raised meat at a reasonable cost.


How does it work?

How it works varies with each CSA, but most will ask for some sort of commitment at the beginning of each season. You might be asked to pay for the entire CSA share up front or make a deposit. However, some CSAs will offer weekly or monthly payment options.

Your farm will tell you how to pick up your CSA share – some farms only offer onsite pickup, while others deliver to several locations in the area or even offer home delivery. Pickups will usually be on a set schedule: Just keep in mind that CSAs aren’t quite like Fresh Direct or other grocery delivery services and depends on the farm’s harvest schedule.

Your farm should give you plenty of information about what to expect in your share. Many CSAs offer little to no choice; the farmer plans out the shares based on how the harvest is going. But many farms respond to customer demand and let CSA members have some say about what they want in their shares. Meat and eggs are often available as an add-on to a vegetable share, although some meat producers have their own CSAs.


How can I find one?

There are a number of websites that can help you find the right CSA in your area. A few good places to start include:

Sometimes areas with a lot of farms have CSA fairs where you can meet the farmers and learn more about the CSA options available to you.

If you’re strictly following the Paleo Diet, make sure to ask the farmer how often they plan to give you items like potatoes or green beans in the vegetable share, and what your options are for swapping those out for more Paleo-friendly ingredients. Some CSAs might let you make the switch in advance, and some have a “swap box” where members can deposit produce they don’t want and select something else.

The bottom line is that if you’re committed to the Paleo lifestyle, you might want to try committing to a local farm too. Joining a CSA might introduce you to new vegetables or cuts of meat that could expand your palette, and you’ll save some money while getting high-quality local food.

If you’ve joined a CSA and are looking for some good recipes for all that fresh food, check out our collection of Paleo Diet recipes.

There’s nothing like fresh peaches to sweeten up the end of summer! At The Paleo Diet®, we count the days until this incredible treat begins showing up at our local farmer’s markets and grocery stores. The taste difference between peaches that have been sitting in cold storage waiting to be ripened and the just-picked ripe and ready fruits makes the waiting and anticipation well worth it. Once fresh peaches arrive, it’s important to eat them within a day or two. Our team loves to top off our dinner menu with this delectable treat. The best part is that it’s fast and easy to prepare, so no long hours sweating away in the kitchen.


Paleo Peach Cobbler (Vegan)

Paleo Peach Cobbler Ready To Eat

There’s nothing like fresh peaches to sweeten up the end of summer! At The Paleo Diet®, we count the days until this incredible treat begins showing up at our local farmer’s markets and grocery stores. The taste difference between peaches that have been sitting in cold storage waiting to be ripened and the just-picked ripe and ready fruits makes the waiting and anticipation well worth it. Once fresh peaches arrive, it’s important to eat them within a day or two. Our team loves to top off our dinner menu with this delectable treat. The best part is that it’s fast and easy to prepare, so no long hours sweating away in the kitchen.

  • Author: Lorrie Cordain
  • Prep Time: 15 minutes
  • Cook Time: 40 minutes
  • Total Time: 55 minutes
  • Yield: Serves 6-8 1x
  • Category: Dessert
  • Cuisine: American


For the Filling:

  • 6 fresh and ripe peaches
  • 2 tablespoon coconut oil, melted
  • 1 teaspoon cinnamon
  • 2 teaspoons unsweetened, organic apple juice concentrate
  • 1 teaspoon arrowroot starch
  • 1 teaspoon vanilla extract

For the Crust:

  • ¾ cup pecans
  • 2 tablespoons coconut oil, melted
  • 1/3 cup almond flour
  • ½ teaspoon cinnamon
  • 12 tablespoons unsweetened, organic apple juice concentrate
  • ¼ cup unsweetened, shredded coconut
  • 2 tablespoons ground flax


  1. Preheat oven to 350 degrees F.
  2. Wash and slice peaches into ½ inch slices.
  3. Place in large bowl and add remaining filling ingredients.
  4. Gently combine all ingredients until peach slices are evenly coated.
  5. Pour filling mixture into 9-10 inch skillet or 8×8 baking dish.
  6. Prepare crust by pulsing pecans in food processor for 10-20 seconds.
  7. Add remaining crust ingredients and pulse again until well blended.
  8. Pour crust over the top of the filling, distributing evenly.
  9. Bake for 40 minutes until topping is golden brown and crispy.




Paleo Peach Cobbler Ready To Eat

Keywords: paleo, vegan, peach, cobbler, dessert

Introduction and Historical Perspective

Almost all of us are familiar with hot sauces – who among us hasn’t encountered a bottle of Tabasco, Cholula, Crystal, Tapatío or Sriracha hot sauces at our favorite Mexican Restaurant? Hot sauces represent condiments which are almost universally offered at Mexican and fast food restaurants in the U.S. and elsewhere. Later, I will get into the specific formulations of popular hot sauces, but for now, let it be known that most are mixtures of hot chili peppers, salt and vinegar among other ingredients.


Obviously, the most important component of fiery hot sauces is their chili peppers. All worldwide farmed chili peppers were first grown from wild seeds indigenous to present day Mexico and dated to about 7,000 to 8,500 years before present (B.P.) (1-4). These chili pepper plants were eventually domesticated by about 900 BC (2). Hence, chili peppers were never consumed by humans until our species migrated from Asia to the Americas roughly 15,000 years B.P. Consequently, chili peppers represent a very recent dietary addition for our genus (Homo), which originated at least 2.0 million years ago in Africa. Clearly, numerous North and South American plant foods also represent unique dietary additions for humans as we migrated from Asia to the western hemisphere. So, at least upon initial glance, chili peppers characterize just one of hundreds of novel plant foods that humans encountered as our species made our way into North and South America about 15,000 years B.P.

Nevertheless, chili peppers are nutritionally unique because they are the only plant species in the world which produce capsaicinoids (5, 6). Capsaicinoids are the molecular compounds which give chili peppers their pungent taste and burning sensation when consumed – the higher the capsaicinoids concentration, the greater we perceive the feeling of “heat”. Two major biochemical forms of capsaicinoids exist: capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide) and dihydrocapsaicin (8-methyl-N-vanillynonanamide) which represent about 77-98 percent of the capsaicinoids present in chili peppers (7). Other minor capsaicinoids within chili peppers include nordihydrocapsaicin, homocapsaicin, homodihydrocapsaicin and nonivamide among more than 20 similar compounds (7).

All five domesticated species of chili peppers (Capsicum annuum, Capsicum frutenscens, Capsicum chinense, Capsicum pubescens and Capsicum baccatum) originated in the Americas (1-4). On the 15th of January, 1493, during Columbus’ first voyage back to Spain from the new world, he recorded in his diary that large quantities of chili peppers (which he called “axi, ques su piiento”) were harvested on Hispaniola (now the islands of Haiti and the Dominican Republic) by the native Americans (2). Shortly, after his return to Spain from Hispaniola (on the 3d of April, 1493), Columbus presented chili peppers to King Ferdinand and Queen Isabella of Spain who commented that “axi” burned their tongues (2). Diego Alvarez Chanca, a physician on Columbus’ second voyage to the West Indies in 1493-1496 also brought chili peppers back to Spain (8). In the ensuing 200 years, hot chili peppers then rapidly made their way to India, East Asia, and Southeast Asia (2) where they have become integral parts of the cuisines of these regions.

Although only five species of domesticated chili peppers are commonly consumed, numerous cultivars of these species are frequently eaten, and each cultivar maintains widely varying concentrations of capsaicinoids. The “heat” or relative pungency of any species or cultivars of chili peppers is measured by the concentration of capsaicinoids which it contains. These concentrations are most accurately determined by high performance liquid chromatography (HPLC) procedures (9), but most frequently are measured using Scoville Heat Units (SHU), a subjective human measurement of “heat” or spiciness (9). For instance, the cultivar we all know as “green bell peppers” are a member of Capsicum annuum and maintain a Scoville Heat Unit of “0 -100”; meaning that this pepper has little or no perception of spiciness or “heat” (10-39). On the other hand, jalapeno peppers which also belong to the same species, Capsicum annuum, are considerably hotter than green bell peppers and have SHU ratings between 2,500 to 8,000 (10-39). The hottest of all peppers belong to the species, Capsicum chinense (the cultivars of this species are also known as ghost, habanero, datil, Scotch bonnet, naga, fatalli and bhut jolokia among other peppers) and maintain SHU rating between 272,897 and 1,037,305 (10-39). Intermediate to Capsicum annuum and Capsicum chinense chilies are members of the pepper species, Capsicum frutescens, which includes Tabasco, Thai, Piri Piri, Malagueta and Malawian Kambuzi peppers with SHU values ranging from 109,508 to 487,619 (10-39).

The race to produce a “hotter” hot sauce with the highest SHU rating of course makes for an interesting story on the internet, social media, and daily newspapers (40). As hotter hot sauces burn your tongue and make you sweat, few of us consider the health implications of regular capsaicinoid ingestion.


Fiery Hot Sauces: The Good

Table 1 below shows the sodium content, the Scoville Heat Units (SCU), the caloric density, the price and type of peppers found in 33 widely available hot sauces. Note that several hot sauces are manufactured without any added salt, and many brands contain very little sodium (< 35 mg/tsp) including the bestselling McIIhenny’s Tabasco (Original Red) Sauce. Because most hot sauces primarily contain salt, water, vinegar and chili peppers; they are uniformly low in calories (0-10 kcal per teaspoon; Table 1). Accordingly, these two nutritional characteristics (low sodium, low calories) can be viewed as “Good” from a health perspective. The USDA recommended sodium intake is 2,300 mg per day for adults and 1,500 mg per day for people with high blood pressure. Hence, a few hot sauces commonly available at grocery stores (Cholula, Tapatio, Crystal, Franks Red Hot Original and Louisiana Hot Sauce) represent condiments with higher concentrations of salt and therefore should be consumed cautiously for people wanting to reduce their sodium intake.

Table 1. The sodium (Na+) content, Scoville Heat Units, energy (kcal), price and type of chili peppers in 33 brands of hot sauces (10-39).



Many people are unaware that most hot chili pepper sauces are fermented foods. For instance, one of the original hot sauces, McIllhenny’s Tabasco Sauce (Original Red) is produced by grinding fresh peppers into a mash and then soaking the mash in a salt solution inside covered white oak barrels for up to three years (41). The mash is then strained of skins and seeds and mixed with vinegar for a month to produce the final sauce (41). This process (soaking in salt and then vinegar under anerobic [without oxygen] conditions) promotes growth of anaerobic bacteria which allow the food (mashed chili peppers) to ferment but not to spoil and putrefy. Salt encourages the growth of halophilic (salt loving) anaerobic bacteria. Vinegar increases the environmental acidity (lowering the pH) of the mixture which also boosts anaerobic, fermentive, bacterial growth.

Accordingly, the use of salt, vinegar, and covered containers epitomizes a universal and traditional formula to ferment food, thereby preventing its spoilage (42). Hence, fermented plant food contained within covered containers along with salt and vinegar produces a powerful anti-pathogenic effect causing the rapid disappearance of putrefying and disease producing bacteria in the fermented concoction including: Staphylococcus aureus; Salmonella typhymurium; Listeria monocytogenes; Escherichia coli; Clostridium perfringens and Vibrio parahaemolyticus (42, 43).

The anaerobic bacteria and other microorganisms causing the fermentation of vegetables including chili peppers produce metabolic byproducts which are released into the fermented vegetable mixture. Bacteria which ferment plant foods including sauerkraut (fermented cabbage,) pickles (fermented cucumbers,) kimchi (all Korean fermented plant food including cabbage, radishes, cucumbers, chili peppers, mustard leaves, and Welsh onion leaves) (42) encourage further growth of anaerobic bacteria (42, 44). Olives also are fruits produced by their fermentation in salt and vinegar. A less appreciated fermented food is chocolate (the fermented fruit of Theobroma cacao; the South American chocolate tree) which does not require either salt or vinegar for its fermentation.

Many fermented foods contain similar anaerobic bacteria and microorganisms, hence the fermented foods we regularly consume (cheeses, salami, sauerkraut, pickles, olives, kimchi, chili peppers, and chocolate) maintain similar bacterial nutrients derived from the microorganisms and bacteria responsible for their fermentation.

The bacterial compounds infused into fermented foods have seldom been recognized as therapeutic nutritional agents. In part, because nutritionists have not specifically measured these bacterially produced nutrients in fermented foods. For instance, pork has only recently (2016) been demonstrated to be a rich source of short (MK-4) and long chain menaquinones (MK-9 to MK-11) or vitamin K2 (45). Long-chain menaquinones can only enter the human food chain through bacterial contamination (spoilage/fermentation) of the normal fresh food which we eat.

Swine are notorious consumers of rotten, putrid and fermented food (46). Hence it is not surprising that pig tissues should represent a concentrated source of the bacterial nutrients which they consume such as the fat-soluble menaquinones (MK4, MK-9 to MK-11) or vitamin K2. Specifically, long-chain bacterially derived menaquinones are concentrated in the fat tissues of swine (45). A long-term evolutionary function of menaquinones (vitamin K2) is to act as lipid soluble antioxidants for anaerobic bacterial species (47-49).

A wide range of bacterial species have been found with the spontaneous fermentation of Jalapeno chili peppers in a saline environment including the anaerobic lactic acid bacteria (LAB) Lactobacillus plantarum, Leuconostoc citreum, Weissella cibaria and Lactobacillus paraplantarum (50). Further, these same genera (Leuconostoc, Lactobacillus, Weissella) and others Lactococcus and Pediococcus are key players in kimchi fermentation (51).

The crucial point here is not to become overly engaged in the microbiology of specific bacterial species which cause fermentation of chili peppers and other vegetables and fruits, but to realize that common bacterial species are associated with the fermentation of almost all plant foods. These common anaerobic LAB bacterial species, during the fermentation process, synthesize nutrients which have the capacity to serve as lipid soluble antioxidants capable of defusing the toxic ROS produced by the mitochondria in aerobic cells.

Currently, the menaquinone concentrations in bacterial species of LAB are either unknown or obscure; further these lipid soluble antioxidants have rarely or never been measured in fermented chili peppers or other fermented foods except soybeans. Other bacterially produced, important lipid soluble antioxidants which have been shown to improve health such as melatonin (52), pyrroloquinoline quinone (PQQ) (53) and CoQ10 (54) and CoQ9 have not or have barely been measured in fermented foods such as spicy hot sauces, despite the knowledge that fermented peppers and fermented vegetables may contain bacterial species capable of producing these lipid soluble antioxidant compounds.

Numerous studies have suggested that capsaicinoid containing foods may have positive and therapeutic health promoting effects (55-65). In humans, the biological receptor for capsaicin is called the transient receptor potential vanilloid subtype 1 (TRPV1) which is widely expressed in brain, sensory nerves, bladder, gut and blood vessels. TRPV1 is activated by multiple environmental stimuli including exogenous chili pepper capsaicin ingestion, heat, low pH (<5.9) and certain endogenous lipid molecules (63). TRPV1 plays essential roles in inflammation, oxidative stress, and pain sensation (66). Accordingly, capsaicinoids derived from the consumption of hot chili peppers and fiery hot sauces likely have therapeutic functions in the prevention of cardiovascular disease (62-64), diabetes (62, 64), pain (62, 66) and certain autoimmune diseases (65).

Nevertheless, an infrequently recognized downside to consumption of chili peppers is their ability to disrupt the intestinal barrier function (67-78).


Summary (The Good, The Bad)

So, to summarize. Fiery hot sauces are low in calories, frequently (but not always) low in sodium and often contain mashes of chili peppers with bacterially fermented by products and their residues that may have therapeutic health effects together with the beneficial effects of the capsaicinoids present in chili themselves.


Fiery Hot Sauces: The Ugly

Exogenous dietary capsaicinoids from chili peppers represent unique biochemical compounds which the human genome did not encounter until very recently from an evolutionary perspective. As previously demonstrated, Columbus and his crew brought chili peppers to Europe in 1493, and they then spread worldwide in the ensuing 200 years. Accordingly, our species has had little or no time to evolve genetic adaptations to an exogenous plant substance (capsaicinoids) which fundamentally interact with our physiologies via the TRPV1 receptor and other cellular mechanisms.

One of the unexpected health consequences of worldwide chili pepper consumption is its adverse effect upon the human gut, particularly with chili pepper species and cultivars which maintain higher capsaicinoid concentrations and hence higher SHU values. The notion that chili pepper consumption could increase intestinal permeability was unknown until 1994 when Hashimoto and colleagues (67) demonstrated that a vegetable extract only found in sweet peppers (of 32 vegetables analyzed) impaired the intercellular tight junction (TJ) barrier through the paracellular pathway. The authors noted that these changes would, “bring about an invasion of allergenic molecules from the intestinal lumen to the serosal region, which may cause food allergy.” In their 1997 follow-up study (68), Hashimoto and co-workers identified that the active substances in the purified sweet pepper extract which increased intestinal permeability were capsianosides (capsaicins). The authors suggested that, “capsianosides would be useful to enhance the permeability for drugs or other biologically important hydrophilic substances across the intestinal mucosa.”

One year later in 1998 Jensen-Jarolim and colleagues (69) demonstrated that paprika and cayenne pepper spices increased intestinal macromolecular permeability. The authors noted that this event might be of pathophysiological importance, particularly with respect to food allergy and intolerance.

One mechanism underlying capsaicin’s ability to increases intestinal permeability was further examined by Isoda, Han, and colleagues in a series of papers (69-71). These investigators demonstrated that capsaicin’s intestinal permeability impairment resulted partially from capsaicin’s ability to bind the TRPV1 receptor in the gut which directly altered tight junction opening characteristics partially via increasing calcium influx in intestinal cells (70, 71).

One of the implications about capsaicin ingestion from chili peppers is this compound’s ability to promote drug (71), macromolecule and intestinal luminal content (allergens) movement across the intestinal barrier (67-69). A molecule of potential interest from capsaicin’s increase in gut permeability is LPS, a pro-inflammatory residue from gut bacteria. Current studies suggest that capsaicin induces an anti-inflammatory profile that inhibits LPS-induced IL-1β, IL-6 and TNF-α production in a time- and dose-dependent manner (79) that sensitizes the TRPV1 receptor activation (80).

Given this information and the prior data suggesting that capsaicin does not promote autoimmune disease (65), which clearly has an increased gut permeability element, it appears that capsaicin’s ability to increase gut permeability may not be associated with increased inflammation (79) or autoimmunity (65). An important caveat to the autoimmune data associated with capsaicin consumption is a recent study suggesting that hot chili pepper consumption may cause the cellular events leading to disease symptoms in IgA nephropathy patients (81).



Regular consumption of hot chili peppers may have numerous health promoting effects, and its pungent taste adds to the cuisine of worldwide cultures. People trying to lower their sodium intake can choose fiery pepper sauces with lower salt formulations. People with food allergies and certain autoimmune diseases may benefit by limiting pepper sauce consumption or ingesting sauces and chili peppers with lower capsaicin concentrations.



1. Kraft KH, Brown CH, Nabhan GP, Luedeling E, Luna Ruiz Jde J, Coppens d’Eeckenbrugge G, Hijmans RJ, Gepts P. Multiple lines of evidence for the origin of domesticated chili pepper, Capsicum annuum, in Mexico. Proc Natl Acad Sci U S A. 2014 Apr 29;111(17):6165-70.

2. Halikowski Smith S. In the shadow of a pepper-centric historiography: Understanding the global diffusion of capsicums in the sixteenth and seventeenth centuries. J Ethnopharmacol. 2015 Jun 5; 167:64-77

3. Perry L, Dickau R, Zarrillo S et al. Starch fossils and the domestication and dispersal of chili peppers (Capsicum spp. L.) in the Americas. Science. 2007 Feb 16;315(5814):986-8.

4. Perry L, Flannery KV. Precolumbian use of chili peppers in the Valley of Oaxaca, Mexico. Proc Natl Acad Sci U S A. 2007 Jul 17;104(29):11905-9

5. Arce-Rodríguez ML, Ochoa-Alejo N. Biochemistry and molecular biology of capsaicinoid biosynthesis: recent advances and perspectives. Plant Cell Rep. 2019 Apr 2. doi: 10.1007/s00299-019-02406-0.

6. Popelka P, Jevinová P, Šmejkal K, Roba P. Determination of capsaicin content and pungency level of different fresh and dried chilli peppers, Folia Veterinaria. 2017 61(2): 11-16.

7. Barbero GF, Ruiz AG, Liazid A, Palma M, Vera JC, Barroso CG. Evolution of total and individual capsaicinoids in peppers during ripening of the Cayenne pepper plant (Capsicum annuum L.) Food Chem. 2014 Jun 15; 153:200-6.

8. Bosland PW, Votava EJ. Peppers: Vegetable and Spice Capsicums. New York: Cabi, 2000.

9. Kachoosangi RT, Wildgoose GG, Compton RG. Carbon nanotube-based electrochemical sensors for quantifying the ‘heat’ of chilli peppers: the adsorptive stripping voltammetric determination of capsaicin. Analyst. 2008 Jul;133(7):888-95

10. http://www.scottrobertsweb.com/scoville-scale/

11. Othman ZA, Ahmed YB, Habila MA, Ghafar AA. Determination of capsaicin and dihydrocapsaicin in Capsicum fruit samples using high performance liquid chromatography. Molecules. 2011 Oct 24;16(10):8919-29

12. Ananthan R, Subhash K, Longvah T. Capsaicinoids, amino acid and fatty acid profiles in different fruit components of the world hottest Naga king chilli (Capsicum chinense Jacq). Food Chem. 2018 Jan 1;238:51-57.

13. Antonious GF, Jarret RL. Screening Capsicum accessions for capsaicinoids content. Journal of Environmental Science and Health Part B. 2006 Aug 1;41(5):717-29.

14. Canto-Flick A, Balam-Uc E, Bello-Bello JJ, Lecona-Guzmán C, Solís-Marroquín D, Avilés-Viñas S, Gómez-Uc E, López-Puc G, Santana-Buzzy N, Iglesias-Andreu LG. Capsaicinoids content in habanero pepper (Capsicum chinense Jacq.): hottest known cultivars. HortScience. 2008 Aug 1;43(5):1344-9.

15. Cisneros-Pineda O, Torres-Tapia LW, Gutiérrez-Pacheco LC, Contreras-Martín F, González-Estrada T, Peraza-Sánchez SR. Capsaicinoids quantification in chili peppers cultivated in the state of Yucatan, Mexico. Food Chemistry. 2007 Jan 1;104(4):1755-60.

16. Deng M, Wen J, Zhu H, Zou X. The hottest pepper variety in China. Genetic resources and crop evolution. 2009 Aug 1;56(5):605-8.

17. Dong MW. Instruments & Applications How Hot Is That Pepper? Quantifying capsaicinoids with chromatography. Today’s Chemist at Work. 2000;9(5):17-22.

18. Duelund L, Mouritsen OG. Contents of capsaicinoids in chillies grown in Denmark. Food Chem. 2017 Apr 15; 221:913-918.

19. Dyah JS, Oen LH, Winarno FG. Capsaicin content of various varieties of Indonesian chilies. Asia Pacific J Clin Nutr 1997;6: 99-101.

20. Gahungu A, Ruganintwali E, Karangwa E, Zhang X, Mukunzi D. Volatile compounds and capsaicinoid content of fresh hot peppers (Capsicum chinense) scotch bonnet variety at red stage. Adv. J. Food Sci. Technol. 2011 Jun 6;3(3):211-8.

21. Giuffrida D, Dugo P, Torre G, Bignardi C, Cavazza A, Corradini C, Dugo G. Characterization of 12 Capsicum varieties by evaluation of their carotenoid profile and pungency determination. Food Chemistry. 2013 Oct 15;140(4):794-802.

22. Gnayfeed MH, Daood HG, Biacs PA, Alcaraz CF. Content of bioactive compounds in pungent spice red pepper (paprika) as affected by ripening and genotype. Journal of the Science of Food and Agriculture. 2001 Dec;81(15):1580-5.

23. Islam MA, Sharma SS, Sinha P, Negi MS, Neog B, Tripathi SB. Variability in capsaicinoid content in different landraces of Capsicum cultivated in north-eastern India. Sci Hort 183 (2015) 66-71.

24. Korkutata NF, Kavaz A. A comparative study of ascorbic acid and capsaicinoid contents in red hot peppers (Capsicum annum L.) grown in southeastern Anatolia region. International journal of food properties. 2015 Apr 3;18(4):725-34.

25. Lang Y, Kisaka H, Sugiyama R, Nomura K, Morita A, Watanabe T, Tanaka Y, Yazawa S, Miwa T. Functional loss of pAMT results in biosynthesis of capsinoids, capsaicinoid analogs, in Capsicum annuum cv. CH‐19 Sweet. The Plant Journal. 2009 Sep;59(6):953-61.

26. Mathur R, Dangi RS, Dass SC, Malhotra RC. The hottest chilli variety in India. Current science. 2000;79(3):287-8.

27. Nwokem CO, Agbaji EB, Kagbu JA, Ekanem EJ. Determination of capsaicin content and pungency level of five different peppers grown in Nigeria. New York Science Journal. 2010;3(9):17-21.

28. Ogawa K, Murota K, Shimura H, Furuya M, Togawa Y, Matsumura T, Masuta C. Evidence of capsaicin synthase activity of the Pun1-encoded protein and its role as a determinant of capsaicinoid accumulation in pepper. BMC plant biology. 2015 Dec;15(1):93.

29. Perucka I, Oleszek W. Extraction and determination of capsaicinoids in fruit of hot pepper Capsicum annuum L. by spectrophotometry and high-performance liquid chromatography. Food Chemistry. 2000 Nov 1;71(2):287-91.

30. Pino J, Sauri-Duch E, Marbot R. Changes in volatile compounds of Habanero chile pepper (Capsicum chinense Jack. cv. Habanero) at two ripening stages. Food chemistry. 2006 Feb 1;94(3):394-8.

31. Popelka P, Jevinova P, Smejkal K, Roba P. Determination of capsaicin content and pungency level of different fresh and dried chilli peppers. Folia Veterinaria, 61, 2: 11-16, 2017.

32. Sanatombi K, Sharma GJ. Capsaicin content and pungency of different Capsicum spp. cultivars. Notulae Botanicae Horti Agrobotanici Cluj-Napoca. 2008;36(2):89-90.

33. Schmidt A, Fiechter G, Fritz EM, Mayer HK. Quantification of capsaicinoids in different chilies from Sustria by a novel UHPLC method. J Food Comp Analysis, 60, (2017. 32-37.

34. Sganzerla M, Coutinho JP de Melo AMT2, Godoy HT. Fast method for capsaicinoids analysis from Capsicum chinense fruits. Food Res Int. 2014 Oct; 64:718-725.

35. Sora GT, Haminiuk CW, da Silva MV, Zielinski AA, Gonçalves GA, Bracht A, Peralta RM. A comparative study of the capsaicinoid and phenolic contents and in vitro antioxidant activities of the peppers of the genus Capsicum: an application of chemometrics. Journal of food science and technology. 2015 Dec 1;52(12):8086-94.

36. Thomas BV, Schreiber AA, Weisskopf CP. Simple method for quantitation of capsaicinoids in peppers using capillary gas chromatography. Journal of Agricultural and Food Chemistry. 1998 Jul 20;46(7):2655-63.

37. Topuz A, Ozdemir F. Assessment of carotenoids, capsaicinoids and ascorbic acid composition of some selected pepper cultivars (Capsicum annuum L.) grown in Turkey. Journal of Food Composition and Analysis. 2007 Nov 1;20(7):596-602.

38. Wahyuni Y, Ballester AR, Sudarmonowati E, Bino RJ, Bovy AG. Metabolite biodiversity in pepper (Capsicum) fruits of thirty-two diverse accessions: Variation in health-related compounds and implications for breeding. Phytochemistry. 2011 Aug 1;72(11-12):1358-70.

39. Ziino M, Condurso C, Romeo V, Tripodi G, Verzera A. Volatile compounds and capsaicinoid content of fresh hot peppers (Capsicum annuum L.) of different Calabrian varieties. Journal of the Science of Food and Agriculture. 2009 Mar 30;89(5):774-80.

40. https://www.nytimes.com/2018/09/24/dining/anarchy-of-chilies-book.html

41. https://en.wikipedia.org/wiki/Tabasco_sauce

42. Rhee SJ, Lee JE, Lee CH. Importance of lactic acid bacteria in Asian fermented foods. In Microbial Cell Factories 2011 Dec (Vol. 10, No. 1, p. S5). BioMed Central.

43. Lee CH. Fermentation Technology in Korea. Korea University Press, 2001.

44. Zhang L,Xiang WL, Zeng ZS et al. Separation, identification and direct vat set (DVS) development of bacteria from fermented chili pepper. Food Sci 2013;21:242-247.

45. Fu X, Shen X, Finnan EG, Haytowitz DB, Booth SL. Measurement of multiple vitamin k forms in processed and fresh-cut pork products in the U.S. Food Supply. J Agric Food Chem. 2016 Jun 8;64(22):4531-5

46. https://www.reviewjournal.com/news/new-pig-farm-consuming-las-vegas-strips-leftovers-1535210/

47. Brooijmans R, Smit B, Santos F, van Riel J, de Vos WM, Hugenholtz J. Heme and menaquinone induced electron transport in lactic acid bacteria. Microb Cell Fact. 2009 May 29;8:28

48. Søballe B, Poole RK. Ubiquinone limits oxidative stress in Escherichia coli. Microbiology. 2000 Apr;146 (Pt 4):787-96.

49. Vido K, Diemer H, Van Dorsselaer A, Leize E, Juillard V, Gruss A, Gaudu P. Roles of thioredoxin reductase during the aerobic life of Lactococcus lactis. J Bacteriol. 2005 Jan;187(2):601-10.

50. González-Quijano GK1, Dorantes-Alvarez L, Hernández-Sánchez H, Jaramillo-Flores ME, de Jesús Perea-Flores M, Vera-Ponce de León A, Hernández-Rodríguez C. Halotolerance and survival kinetics of lactic acid bacteria isolated from jalapeño pepper (Capsicum annuum L.) fermentation. J Food Sci. 2014 Aug;79(8):M1545-53. doi: 10.1111/1750-3841.12498. Epub 2014 Jul 17.

51. Jeong SH, Lee HJ, Jung JY, Lee SH, Seo HY, Park WS, Jeon CO. Effects of red pepper powder on microbial communities and metabolites during kimchi fermentation. Int J Food Microbiol. 2013 Jan 1;160(3):252-9.

52. Reiter RJ, Rosales-Corral S, Tan DX, Jou MJ, Galano A, Xu B. Melatonin as a mitochondria-targeted antioxidant: one of evolution’s best ideas. Cell Mol Life Sci. 2017 Nov;74(21):3863-3881

53. Wu JZ, Huang JH, Khanabdali R, Kalionis B, Xia SJ, Cai WJ. Pyrroloquinoline quinone enhances the resistance to oxidative stress and extends lifespan upon DAF-16 and SKN-1 activities in C. elegans. Exp Gerontol. 2016 Jul; 80:43-50.

54. Mortensen SA, Rosenfeldt F, Kumar A, Dolliner P, Filipiak KJ5 Pella D6 Alehagen U7 Steurer G, Littarru GP; Q-SYMBIO Study Investigators. The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure: results from Q-SYMBIO: a randomized double-blind trial. JACC Heart Fail. 2014 Dec;2(6):641-9.

55. Palma J.M.et al. Physiology of pepper fruit and the metabolism of antioxidants: chloroplasts, mitochondria and peroxisomes. Ann. Bot. 2015; 116: 627-636

56. Spiller F. et al. Anti-inflammatory effects of red pepper (Capsicum baccatum) on carrageenan- and antigen-induced inflammation. J. Pharm. Pharmacol. 2008; 60: 473-478

57. Bogusz S. et al. Brazilian Capsicum peppers: capsaicinoids content and antioxidant activity. J. Sci. Food Agric. 2018; 98: 217-224

58. Chapa-Oliver A., Mejía-Teniente L. Capsaicin: from plants to a cancer-suppressing agent. Molecules. 2016; 21: 931

59. Varghese S. et al. Chili pepper as a body weight-loss food. Int. J. Food Sci. Nutr. 2017; 68: 392-401

60. Hardy G. Nutraceuticals and functional foods: introduction and meaning. Nutrition. 2000; 16: 688-689

61. Anand P., Bley K. Topical capsaicin for pain management: therapeutic potential and mechanisms of action of the new high-concentration capsaicin 8% patch. Br. J. Anaesth. 2011; 107: 490-502.

62. Srinivasan K. Biological Activities of Red Pepper (Capsicum annuum) and its pungent principle capsaicin: a review. Crit Rev Food Sci Nutr. 2016 Jul 3;56(9):1488-500.

63. Sun F, Xiong S, Zhu Z. Dietary capsaicin protects cardiometabolic organs from dysfunction. Nutrients. 2016 Apr 25;8(5). pii: E174. doi: 10.3390/nu8050174

64. Kwon Y, Apostolidis E, Shetty K. Evaluation of pepper (Capsicum annuum) for management of diabetes and hypertension. Journal of Food Biochemistry. 2007 Jun;31(3):370-85.

65. Deng Y, Huang X, Wu H, Zhao M, Lu Q, Israeli E, Dahan S, Blank M, Shoenfeld Y.

Some like it hot: The emerging role of spicy food (capsaicin) in autoimmune diseases. Autoimmun Rev. 2016 May;15(5):451-6

66. Mózsik G. Capsaicin as new orally applicable gastroprotective and therapeutic drug alone or in combination with nonsteroidal anti-inflammatory drugs in healthy human subjects and in patients. In Capsaicin as a Therapeutic Molecule 2014 (pp. 209-258). Springer, Basel.

67. Hashimoto K, Matsunaga N, Shimizu M. Effect of vegetable extracts on the transepithelial permeability of the human intestinal Caco-2 cell monolayer. Bioscience, biotechnology, and biochemistry. 1994 Jan 1;58(7):1345-6.

68. Hashimoto K, Kawagishi H, Nakayama T, Shimizu M. Effect of capsianoside, a diterpene glycoside, on tight-junctional permeability. Biochimica et Biophysica Acta (BBA)-Biomembranes. 1997 Jan 31;1323(2):281-90.

69. Jensen-Jarolim E, Gajdzik L, Haberl I, Kraft D, Scheiner O, Graf J. Hot spices influence permeability of human intestinal epithelial monolayers. J Nutr. 1998 Mar;128(3):577-81.

70. Isoda H, Han J, Tominaga M, Maekawa T. Effects of capsaicin on human intestinal cell line Caco-2. Cytotechnology. 2001 Jul;36(1-3):155-61.

71. Han J, Isoda H, Maekawa T. Analysis of the mechanism of the tight-junctional permeability increase by capsaicin treatment on the intestinal Caco-2 cells. Cytotechnology. 2002 Nov;40(1-3):93-8.

72. Nagumo Y, Han J, Arimoto M, Isoda H, Tanaka T. Capsaicin induces cofilin dephosphorylation in human intestinal cells: the triggering role of cofilin in tight-junction signaling. Biochem Biophys Res Commun. 2007 Apr 6;355(2):520-5

73. Komori Y, Aiba T, Nakai C, Sugiyama R, Kawasaki H, Kurosaki Y. Capsaicin-induced increase of intestinal cefazolin absorption in rats. Drug Metab Pharmacokinet. 2007 Dec;22(6):445-9.

74. Tsukura Y, Mori M, Hirotani Y, Ikeda K, Amano F, Kato R, Ijiri Y, Tanaka K. Effects of capsaicin on cellular damage and monolayer permeability in human intestinal Caco-2 cells. Biol Pharm Bull. 2007 Oct;30(10):1982-6.

75. Nagumo Y, Han J, Bellila A, Isoda H, Tanaka T. Cofilin mediates tight-junction opening by redistributing actin and tight-junction proteins. Biochem Biophys Res Commun. 2008 Dec 19;377(3):921-5

76. Shiobara T, Usui T, Han J, Isoda H, Nagumo Y. The reversible increase in tight junction permeability induced by capsaicin is mediated via cofilin-actin cytoskeletal dynamics and decreased level of occludin. PLoS One. 2013 Nov 18;8(11):e79954. doi: 10.1371/ journal. pone.0079954

77. Duan L, Yan Y, Sun Y, Zhao B, Hu W, Li G. Contribution of TRPV1 and multidrug resistance proteins in the permeation of capsaicin across different intestinal regions. Int J Pharm. 2013 Mar 10;445(1-2):134-40

78. Prakash UN, Srinivasan K. Enhanced intestinal uptake of iron, zinc and calcium in rats fed pungent spice principles–piperine, capsaicin and ginger (Zingiber officinale). J Trace Elem Med Biol. 2013 Jul;27(3):184-90

79. Tang J, Luo K, Li Y, Chen Q, Tang D, Wang D, Xiao J. Capsaicin attenuates LPS-induced inflammatory cytokine production by upregulation of LXRα. International immunopharmacology. 2015 Sep 1;28(1):264-9.

80. Diogenes A, Ferraz CC, Akopian AA, Henry MA, Hargreaves KM. LPS sensitizes TRPV1 via activation of TLR4 in trigeminal sensory neurons. Journal of dental research. 2011 Jun;90(6):759-64.

81. Shao J, Peng Y, He L, Liu H, Chen X, Peng X. Capsaicin induces high expression of BAFF and aberrantly glycosylated IgA1 of tonsillar mononuclear cells in IgA nephropathy patients. Hum Immunol. 2014 Oct;75(10):1034-9

Affiliates and Credentials