Archive for the “Good Science” Category
Here’s part two of my interview with Richard Nikoley, Tim “Tatertot” Steele and Grace Liu about resistant starch. Given how many questions I asked and the comprehensive answers, I decided to divide the interview into three parts.
Fat Head: What do you think of the high-maize resistant starch the corn refiners are promoting? From some of your comments, I get the feeling you consider it yet another industrial food we can do without.
Tim: I’m very disappointed in the direction that the makers of Hi-Maize have taken it. Here they have a substance with the potential to help billions, yet they only want to put it in bakery goods and snacks so they can promote them as “high fiber foods.” The people who make Hi-Maize are the same ones who make High Fructose Corn Syrup. Since that bubble burst, they are looking for ways to refill the coffers of the corn producers. The studies in which Hi-Maize, or High Amylose Maize Starch (HAMS) was used to show marked metabolic improvements required approximately 20-40g of RS per day. This level makes most people fart, so when they put it in food, they are very careful to get it in at a level that ensures nobody “squeaks one off” in church, God forbid. This fart-proof level is the same issue that inulin and other prebiotic supplement makers had to deal with. A level of RS that produces no farts in 90% of the consumers is a level that does no good for 100% of people eating it for its “high fiber” benefits.
Grace: Movies like Fat Head, and others — King Corn and Future of Our Food — brought awareness and enlightenment for me about the dangers of the greed and perversions of industry interests including USDA collusion and GMO Big Agriculture. Part of the reason industrialized nations have epidemic gut problems, many experts believe, is secondary to GMO foods in the food supply that make up 80-90% of the American SAD food pyramid: GMO grain and GMO Bt corn fed livestock (pork, poultry, beef), GMO grain crops, GMO Bt corn, GMO soy, GMO sugar beets, etc. We have moved away from sustainable, organic, heirloom and biodynamic farming and livestock production and all its abundant life, including the soil organisms and other gut-preserving probiotics that live on the roots, tubers, shoots, fruits and leaves of our crops.
Fat Head: Lower glucose levels are a nice benefit, but I wasn’t getting the high fasting glucose levels that you and other people have reported on a very low-carb diet – perhaps because I’m low-carb but not zero-carb, and I usually have a high-carb Saturday night meal. So reports of lower fasting glucose levels didn’t persuade me to run out and buy potato starch. But when you wrote several posts about resistant starch and gut bacteria, you got my attention. Describe how resistant starch affects our gut microbiome.
Tim: RS is ALL about the gut bugs –100%. The first studies on RS in the late ‘80s and early ‘90s didn’t take the gut microbiome into account, and lots of their studies made it look like RS was not all it was cracked up to be. However, give a person RS for a couple weeks and allow their gut bugs to grow and change, then try the same studies — big difference. If most people had really good gut flora and all that was lacking was some fermentable fiber, then RS would be HUGE on its own.
Unfortunately, with widespread overuse of antibiotics, sanitized food and living conditions, and a disconnect from the microbes that live in the dirt, most people just don’t have the right set of gut bugs to take full advantage of simply adding RS to their diet. Back in the ‘80s and ‘90s when they first started looking into prebiotic fibers, they noted that about 75% of test subjects could not tolerate RS or inulin over 30 or so grams per day, causing them excessive gas, bloating, and pain. Now I suspect it’s even higher. The folks who can’t tolerate RS are the ones who need it most! For them, a good program of probiotics and fermented food should get them back on track.
Richard: It’s really been quite a deal for me. Unlike you, Tom, I’d had high fasting numbers for years and recently had seen a post-meal spike as high as 194 after a carby meal. Thing is, as I already said, my carb intake was very sporadic. Now, someone’s gonna say “Well, then you’re diabetic, or pre-diabetic, by clinical definition.” Well, that’s the rub. I just did a post about the Inuit and how in three studies, 1928, 1936 and 1972, they found no ketosis in the Inuit (To Reiterate, Just In Case You Missed It: No Elevated Ketone Levels in the Inuit), even though they are low carb, about 55g per day on average, mostly from the glycogen in fresh, raw animals (liver, meat, skin and surprisingly enough, whale blubber—the most carby of all). So researchers give them a glucose tolerance test and they passed with flying colors, with max spikes right to about 140. Keep in mind that nowadays in LC forums and comment threads all over, people have convinced themselves that they literally cannot have carbs. Why? Because they have physiological insulin resistance, high fasting BG, and so when they go eat a piece of their kid’s birthday cake and get 160-180, they self diagnose as diabetic or pre-diabetic and the prophesy is self-fulfilled.
So then how come the Inuit eating low carb can handle a bolus dose of glucose? The secret is in two things: 1) all the prebiotic fibers they get from the glycans in fresh raw blood, organs and meat, so they have healthier guts than your average modern LC dieter and 2) they have a massive protein intake, 250g and up. Try eating 250g protein daily without drinking it. So, they had plenty of dietary protein to fuel gluconeogenesis without causing insulin resistance. But what happens if you fast them for 82 hours, putting them into no-shit ketosis and forcing physiological insulin resistance? Give them the same bolus dose of glucose and they spike to 280-300 and 3 hours later, they’re still above 230.
Interestingly enough, some negative reaction to that post focuses more on measuring methods for ketones, insisting that it’s a LCHF diet — missing the point that it’s the very high protein that’s making the difference — and for some inexplicable reason, continuing to insist that they just must have really been in ketosis in spite of three studies spanning 44 years finding no ketosis amongst Inuit eating their traditional LC diet. For some reason, perpetual, chronic ketosis just simply has to be a very healthful thing to do, beyond it being proven therapeutic for certain medical conditions, and in spite of the very unhealthful thing that happened to their BG numbers when there’s no dispute about them being in deep ketosis after an 82 hr fast.
There’s much work to be done.
Fat Head: You’ve written that living on a very-low-carb diet might even starve our gut bacteria in the long term. Is there evidence for that, or is it more of a concern that warrants more research?
Tim: Well, here’s my stance on that…a VLC diet, such as an Atkins induction-type keto diet, isn’t going to completely kill off all your gut bugs, but what will happen is that the ones that do all the “good stuff” we’ve been talking about — for instance, producing butyrate and stimulating gut health — will be relegated to the minority. The majority of your gut bugs on a VLC diet are ones that can eat any old plant matter, animal scraps, and the lining of your intestine — the mucus layer. A gut thus populated has a high pH, pathogens thrive, and colonocytes starve. The good gut bugs are more than likely still there, just hiding and waiting for enough food for them to once again flourish. These populations change fast, even on a “by-meal” basis. Long-term eating habits set up long-term health patterns. We can eat however we want in survival situations, or any short-term diet intervention, but in the long run, a colon with ample butyrate and populated with beneficial microbes such as those that eat RS and the ones that benefit from the RS feeding frenzy is best.
Another thing to consider, Tom, is your lifestyle on the farm … your close association with chickens, animals, dirt, trees and fresh foods give you a leg up compared to most people. Your gut is most likely populated with all the soil-based organisms and lactic acid producers that folks are paying dearly for. I’d guess that for you, a big slug of RS gave your gut bugs a real treat and they were trying to tell you something: FEED US! What do your chickens do when you miss a day of feeding them? They cluck and fuss and let you know they are hungry. When well fed, they lay eggs and grow big juicy breasts and drumsticks. It’s the same with your gut bugs. Treat them like your farm animals or crops, feed, fertilize, and treat them well and they will pay it back in spades.
Grace: I love VLC and LC diets. They will always have a place therapeutically and clinically, I believe. My problem is that for some or many, these diets compromise or will eventually compromise 1) the gut and 2) adrenal/thyroid/gonad health. In four different LC or VLC short-term studies, prominent core gut microbial populations were dramatically reduced. These gut populations are important for health because not only do they serve vital functions such as expelling pathogens, vitamin processing and production (A, K2, B) and maintaining healthy immunity, they are also huge butyrate factories, pumping out butyrate which keeps gut tight junctions tight, immunity intestinal integrity intact, pathogens low and insulin sensitivity appropriate via the GPR41/43 receptors.
In one study, the researchers examined the shifts in gut populations during an Atkins induction diet (24 g carb/day) for 4 wks. With the VLC diet, they observed an enormous drop in butyrate to a fraction (about one-quarter) of the maintenance diet level. Four very significant subpopulations of gut bugs were decimated by the VLC low fiber and RS-deficient diet: Bifidobacteria, Ruminococci, Roseburia, and F. prausnitzii.
The study groups ate salads, but this was not apparently enough to sustain the important core gut communities. Salads may provide about 10 grams of non-starch fiber, but zero RS or oligosaccharides for them to feed on. These prominent populations are also highly correlated to longevity and robustness in centenarian and aging studies. In more and more gut microbiota studies, these populations are found missing in disorders and disease, yet found in great abundance and diversity in the healthy. Their favorite substrate to feed on is resistant starch.
Strict paleo diets that eliminate legumes, GF grass grains, roots and tubers may also exert the same detrimental gut effects as RS-deficient Atkins because the gut has to contend with the same conflict: a deficiency of RS and soluble fibers from starchy ‘plant babies.’ Without RS and other fiber, fecal carcinogens are not diluted, N-nitroso compounds occur at higher amounts, stool pH increases (allowing more pathogenic growths), and microbial-derived antioxidants such as ferulate and other phenolic compounds decrease.
Fat Head: If we do starve our gut bacteria, what would be the negative health effects?
Tim: Look at America…the modern, dyspeptic gut we’ve created: Frequent heartburn, loose stools or constipation, indigestion, smelly gas, GERD, IBS, or worse. You may even have one of the many autoimmune diseases that are running rampant, diabetes, metabolic syndrome, or cancer. Digestive diseases affect over 70 million people in the US alone! These diseases required 48.3 million ambulatory care visits, 21.7 million hospitalizations, and caused 245,921 deaths in 2009. Total cost for digestive diseases was estimated at $141.8 billion in 2004. And, these stats are getting worse, not better. It’s estimated that over 90 million Americans use antacids or other digestive upset medicines. Upset stomachs are the number one cause of self-treatment. These are all caused by “hungry gut bugs.”
Richard: Most people actually have both E. coli and C. difficile in them, but they are kept at bay by our symbionts and commensals. C. difficile causes about a half million sicknesses annually in the US, hospitalizes 250,000 and kills 15,000. Guess when the most common time is for an infection to occur? Immediately following a round of antibiotics. Now, connect them dots.
[On that topic, folks, you may want to listen to this NPR interview about the effects of antibiotics on the gut microbiome -- Tom]
Fat Head: To experience the benefits of feeding our gut bacteria, we need gut bacteria to feed. Is it worth taking probiotics while adding resistant starch to the diet? Or do probiotic supplements just create expensive poop?
Richard: This was the last puzzle piece for me personally. I pounded three brands of soil-based organism probiotics that Grace recommends. I did this for a week or so but by about day three, it was very clear this was a huge benefit. Very notable was energy and sleep. Very interesting because I seemed to be relieved of this sort of regimented thing where you have to get 7-8 hours. It quickly became way different. Some nights 4-5 hours and others, 8-9 but less on average and when it was one of those 4-5 hour deals, I wasn’t just getting up at 4 a.m. because of insomnia. I was ready to hit it and felt great.
But the biggest deal of all was airborne allergies or, for all I know, food allergies. Anyway, I’ve had perpetual congestion, sneezing, runny nose and cough virtually all my life. Used to be on meds year round. LC Paleo did wonders for that initially. Got rid of the meds, felt a lot better. But it was creeping back and I’d always have to have tissue on hand, have to shoot Afrin some nights to get to sleep, and now and then, have to pop an OTC. Within 3 days on the SBO probiotics and for the first time ever, I’m breathing clearly through my nose 80-90% of the time. Seems to be getting even better, even though I’m down to just taking one or the other of those three products every day or two. They are pricey, so after pounding them the first week or two, I’d recommend stretching them out like that.
Lots of folks have now introduced these and many positive reports are beginning to come in. Clear breathing seems to be a common one.
Grace: Since you are a farmer, Tom, I am envious of the natural probiotics you and your family encounter daily! My family and I are suburbanites with no garden and the only healthy dirt I encounter is the few that rim our carrot tops or the little dusting on my organic greens that haven’t been blasted off by triple filtered water rinsing. Also I’ve had plenty of antibiotics in my lifetime which likely decimated my gut little did I know.
What I see anecdotally and clinically is that many people’s guts are missing core ancestral species (which is my AHS14 topic this year). Our gut bugs have taken a hit and the damage is immeasurable. By using functional medicine lab testing of stools and urine organic acids, I can see the damage. By talking to people, the damage is often evident as well. This is the same advanced testing that is bringing us rapid information about the gut microbiota over the last 10-15 years.
I can’t tell you how often I see Bifidobacter, Lactobacilli and other core ancestral species missing. I advocate a few good soil based organisms (SBO) probiotics such as Prescript Assist and AOR Probiotic-3, which do an excellent job of filling in nicely for now for the lack of soil exposures that our ancestors were immersed in, and we now have challenges in obtaining.
Modern, industrialized societies consume 100% of food, vegetables, and packaged beer that is sterile, dead, or hyper-hygienically clean. By contrast, our ancestral gut strains Bifidobacter, Lactobacilli, Clostridium, Bacilli, and wild yeasts all naturally co-exist on farm livestock, children, chickens, eggs, raw dairy, legumes, grass grains, tubers, roots and other plant sources.
Tim: In the ancient past, no one needed probiotics because we got all the new microbes we needed from dirty food, dirty fingers and a close connection with the Earth. In the more recent past, probiotics worked like migratory farm workers. As long as you used them, they gave you some benefits, but as soon as you stopped, they were gone because they had no incentive to stick around. With RS, that all changes. Probiotics now have a reason to stick around a while. If you are one of the 25% of people who cannot ferment RS, or even one of the 75% who can, you should take probiotics when first healing your gut or switching to a high RS diet. Most if not all of us are missing key gut bugs that are found in several probiotic supplements. In a diet filled with RS, inulin, glucomannan, and other prebiotics in the 20-40 gram per day range, these probiotics will not only survive, but kick ass on the pathogens and set the stage for stability and resilience in your gut’s ecosystem.
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I should file my next few posts under Stuff I Got Wrong, or at least Stuff I Wish I Hadn’t Ignored. One is resistant starch. The other is “safe starch” as prescribed in Paul Jaminet’s Perfect Health Diet. Revisiting resistant starch led to me to revisit safe starch, so I’ll start with resistant starch.
I dismissed resistant starch because of how it came to my attention. Some articles hit the media praising resistant starch as a means of controlling blood sugar. Reading those articles, it was clear to me that resistant starch was being promoted by the makers of high-maize resistant starch – an industrial corn product. When I looked up the studies mentioned in the articles, it turned out researchers had replaced white flour with high-maize resistant starch in baked goods, and lo and behold, people who ate the resistant-starch versions ended up with lower blood sugar.
So it looked like the “Whole grains are good for you!” story all over again: replace total crap with less-than-total crap, and people have better health outcomes. That doesn’t mean less-than-total crap is good for you. If you want to convince me resistant starch lowers blood sugar, show me the studies where it’s added to the diet, not used to replace white flour.
Turns out those studies exist and have been around for decades. I only became aware of that after Richard Nikoley took up the subject of resistant starch with a vengeance on his Free The Animal blog. He’s become so passionate about the subject, he created a permanent, top-level page on the blog called A Resistant Starch Primer for Newbies.
That page includes this brief video, which offers a clear explanation of what resistant starch is, so give it a look:
Mark Sisson also wrote a nice summary of the benefits of resistant starch on Mark’s Daily Apple.
The bottom line is that despite being labeled as “starch,” resistant starch doesn’t turn to glucose in your body. It resists digestion (thus the term) until it reaches your colon, where it feeds your gut bacteria – and that’s where the benefits kick in. The good gut bacteria digest the resistant starch and release butyrate, a short-chain fatty acid, as a result. Yup, eating a “starch” produces good fats in your colon.
And although the exact biological mechanism isn’t known (at least according to the research I’ve read), something about the process increases insulin sensitivity and leads to lower blood sugar, both before and after meals. Let’s see … glucose control, insulin control, gut health … isn’t that what drew most of us to a low-carb paleo diet in the first place?
So after Nikoley had posted enough articles to overcome my resistance to the subject of resistant starch, I finally ordered some Bob’s Red Mill Potato Starch, which is almost pure resistant starch, and started experimenting. (I’ve since learned I can just buy the stuff at our local Whole Foods.)
I started out with two tablespoons per day and didn’t experience any of the explosive-gas problems some people reported on Nikoley’s blog, so I upped it to four. I just stir it into some warm water (warning: hot water will turn it into starch, not resistant starch) and drink it.
Like many of Nikoley’s readers, I found that my fasting glucose dropped, from around 100 in the morning to around 90. Not bad, but the more impressive result has been post-meal glucose levels. As an experiment, I ate about 3/4 cup of white rice without consuming any resistant starch for the preceeding 24 hours. My glucose peaked at 150. The next day, I swallowed two tablespoons of resistant starch around 10:00 AM and consumed the same amount of rice around noon. This time my glucose peaked at 118 and dropped to 95 an hour later. In another experiment, I pre-loaded with resistant starch and then had a baked potato with dinner. My glucose peaked at 126. Lots of Free the Animal readers have reported similar results.
I was early in the experimenting phase when Jimmy Moore invited me to participate in the 100th episode of Low-Carb Conversations, so that’s what I talked about: resistant starch. My part begins at around 1:27:00 into the episode.
Jimmy, in fact, has invited Richard Nikoley to host The Livin’ La Vida Low Carb show later this month and interview his partners in crime about resistant starch. The partners are Tim “Tatertot” Steele and Grace Liu, who together with Nikoley are writing a book on the subject.
I enjoy podcasts, but I’m also a fan of written interviews, so I asked all three of them if I could submit a long list of questions, and they graciously agreed. You’re probably familiar with Nikoley already. Here are brief bios on Steele and Liu before we get to the Q & A:
Tim Steele lives in the small town of North Pole, Alaska where he is the electrical systems supervisor of a local hospital. He retired from the Air Force in 2004 after 21 years of service as an electronics technician and combat engineer. In his spare time he hunts, fishes, gardens, and studies health and food science for simple solutions to modern problems.
Grace Liu, PharmD, AFMCP, is a functional medicine practitioner with an international functional medicine practice. In addition to hormone and digestive disorders, her clinical areas of interest are autoimmune disorders, diabesity, heart disease, cancer prevention, toxins, and nutrition. As science editor, she has an upcoming book being published on evolution, the gut microbiota and how to fuel it. She also writes about gut health and other topics on her AnimalPharm blog.
On to the interview. Like I said, I asked a lot of questions and the answers are very comprehensive, so I’ll post this in two or three parts.
Fat Head: Richard, you’ve become known as the resistant-starch blogger in the past year or so. In fact, most of your posts recently fall into one of three categories: 1) resistant starch, 2) people who piss me off, and 3) people who piss me off about resistant starch.
Richard: Heh, never really thought of it that way but it does have a nice ring to it. I suppose I might add to that, those entrenched about anything, where it becomes more about the entrenchment than whether it still makes complete sense. I’d use the word iconoclastic, but I think that’s something others call you and not something you call yourself — like being humble, or something. One just doesn’t say, “I’m so humble.”
Fat Head: True, if you call yourself humble, people tend not to believe you, especially if you’re proud of being humble. Anyway, as you’ve pointed out on your blog, research pointing to possible benefits of resistant starch has been around for 30 years. There was a bit of buzz about resistant starch three years ago, but since the articles hitting the media were about replacing white flour with high-maize resistant starch, most of us in the low-carb camp dismissed it as an attempt to sell more corn products. So what prompted you to take such a passionate interest in the subject last year?
Richard: It was also dismissed out of hand because it had the word “starch” in it, and but for Paul Jaminet — who was only coming online around that time as I recall — we’d probably still be entrenched against starch. One prominent member of the overall community even called resistant starch an “anti-nutrient,” and even though he has since admitted he was unaware of it and has expressed a willingness to look at it again, that post from way back was referenced dozens of times in various forums and comment threads all over as justification to not even bother looking.
I think that’s a bad thing and I hope I never see anything anywhere like “Well, Richard (or Tim, or Grace) said this, so that settles it for me.” Nobody deserves to be taken as an authority like that. On the other hand, take a guy like Mark Sisson who, in his Definitive Guide on Resistant Starch, just plain comes out and admits he was wrong and regrets not taking a harder look.
As for me, RS didn’t cross my radar back then, for whatever reason. I was probably too busy soaking in ice cold water whilst engaging in Internet warfare or something, and when at war, things get serious in a hurry. Pansy stuff like “resistant starch” just isn’t going to cross the attention threshold.
So, when I did begin blogging about this last April — so a year ago now, or nearly 100 blog posts and over 10,000 comments ago — it was a completely new thing for me. Tim Steele, a.k.a. “Tatertot,” brought it to me and we’d just had a pretty good run with “the potato hack,” where people were essentially doing Chis Voigt’s “20-Potatoes-a-Day” deal and virtually everyone was dropping weight very rapidly.
I tried it but stopped at about a week or so. I happen to love potatoes and don’t want that to ever change. But it was very instructive and once again, caused me to begin questioning entrenched “wisdom.” So Tim had creds with me and I heard him out. He shot me enough info to take it seriously, and there was this point where I thought that if half of this stuff is true, it’s going to be huge; and moreover, this goes way beyond resistant starch. This is about the human gut biome, so you have these news things you’re seeing every day and you have all these researchers studying resistant starch, but for the purposes of better livestock, or to help a big company get their franken-RS product into every baked good on the planet — but not for gut health, but because it’ll essentially lower GI and cause 1% fewer cases of diabetes, colo-rectal cancer, or both, or something.
But I knew the Ancestral community had a very good appreciation for gut health, was paying attention, knew why it was important, had the evolutionary context in terms of probiotics and prebiotics, and really, we’re just looking at another in a set of prebiotics. All I had to do was overcome the hurdle of the “S-word.” And that was tough. We were dismissed essentially by everyone. Ridiculed, etc. But of course, ridicule is like high-octane fuel for a true iconoclast…oops, there I go again, being all humble.
Fat Head: We appreciate your humility. For those who don’t already know, what is resistant starch? How is it different from other starches?
Tim: Normally when we think of “starch,” we think of the blood-glucose spiking stuff that is one step away from pure sugar. The “bad calories” of Good Calories, Bad Calories fame. Of course, Paul Jaminet made some of the starches “safe” for us in his Perfect Health Diet, but resistant starch is something entirely different. RS was discovered in the ‘80s when scientists were trying to measure fiber in food. Under microscopic examination of the effluent of human and animal small intestines, they kept finding a confounding element that they weren’t expecting—undigested starch granules. They termed these “resistant starch.” Resistant in this case meaning resistant to enzymes that digest food.
Grace: During my schooling and training for diabetes education, no one was aware of resistant starch or how it blunts blood sugar increases just as other fibers do — psyllium, pectin, hemicellulose, and oligosaccharides. Resistant starch is consumed by the vast majority of the ‘core members’ of the gut microbes. It is a core fuel for the core gut bugs. The evolutionary purposes of fiber and resistant starch may be threefold: 1) store carbohydrate energy from the sun and photosynthesis, 2) provide structure, and 3) act as anti-freeze and stress protectors to safeguard the plant and ‘plant babies’ against environmental extremes such as frost, acid, moisture, dryness, mold/fungi, pests, and pathogens.
What I mean by plant ‘babies’ are the progeny that contain genetic material that will be passed on to the next generation of plants: tubers, underground storage organs, legumes, grass grains, fruits, and seeds and nuts. All of these contain some degree or a lot of RS and oligosaccharides that resistant human digestion. By shielding the genetic material, the fiber and RS buffered and protected the tuber, root, legume and grain from freezing and bursting open. Plants and microbial bugs were here on Earth billions of years long before Homo sapiens emerged. It is actually speculated that the extreme Ice Ages are what largely shaped the carbohydrate and fiber content in plants and their survival. To us mammals, the vast majority of these carbohydrates are indigestible; however, for the gut critters, these carbs are their favorite feasts and fuel. Our co-evolution was inseparable. Now, perhaps our de-evolution is imminent because we are suspiciously lacking our co-evolved microbial appendages. Antibiotic over-utilization, C-sections, and phobic attempts to be sterile and super-sanitary has perhaps amputated our collective guts.
Resistant starch will not raise blood glucose, unlike starch. It behaves like other fiber. The plants that have more RS also have more protein (again protecting and nourishing future ‘plant babies’) and a lower glycemic index. All of these contribute to a lower impact on blood sugars.
Fat Head: If resistant starch isn’t digested and converted to glucose, what happens to it?
Tim: Resistant starch ends up in the large intestine where it gets fermented by gut bugs into fat (short chain fatty acids=SCFA). Sounds simple, but it’s anything but! RS is the substrate for fermentation by the prime gut bacterial players, but one of the few fibers that require numerous ‘actors’ to degrade it into its final end stages. The gut is truly an ecosystem and the apex predators take first dibs on the prime rib, then the bottom feeders and scavengers get their turns eventually. The byproducts of all these interactions feed other microbes and create an entirely different structure in the gut than when simpler fibers are eaten. Inulin, legume oligosaccharides, and glucomannan are other fibers that behave the same way. The fibers found in human breast milk (Human Milk Oligosaccharides or HMOs) also share this trait. Unfortunately, when we are weaned we usually never get a good taste of these type prebiotics again, except for the tiny bits found in a few foods and snacks.
Richard: What’s cool beyond this is that we live mostly in a symbiotic relationship with the vast majority of these gut microorganisms. Keep in mind we’re talking big numbers, 100 trillion to our 10 trillion human cells. About the size of a football if packed together. People can have up to about 1,000 different species, and while the human genome is comprised of about 25,000 genes, the total genome of all the different microbial lines in our gut are about 3 million, over 100 times more. There’s more. A human generation is about 30 years while on average, bacteria go through 6 generations in a day, and they’ve been evolving for 2 billion years longer than we have.
It makes you wonder in a chicken or egg kinda way, are we just a nice house that bacteria built for themselves? And then it takes on sci-fi alien invasion proportions when you consider that via the brain-gut connection—with more neurons outside the brain than anything, including the spinal cord—it influences behavior, mood, sleep, satiety and more. I’m just guessing, but I’ll throw out there that you want to keep your mind-control aliens well fed and content.
Fat Head: If we’re talking about NSA mind-control aliens, I’d rather keep them starved and cranky, but I see your point.
Grace: It’s great you bring up breast milk, Tim! Since the dawn of breasts and breast milk, babies have received carbs (lactose) and over 100 oligosaccharides (fiber) from mom’s milk. The lactose is for the baby, but the fiber feeds the neonate’s burgeoning societies of microbes colonizing its gut and other organs. Another misconception about breast milk was recently busted as well. Mom’s breast milk contains over 700 species of probiotics (entering the mammary glands via the gut lymph circulation). On Day One of life, our superorganism symbiosis starts. Richard loves the cyborg and Matrix motifs, and rightly so!
Fat Head: “The Dawn of Breasts” sounds like a movie I might have rented when I was single, but I digress. So as counter-intuitive as it sounds, when we consume resistant starch, the stuff is converted to short-chain fatty acids in our colons. What happens to those fatty acids? Do we burn them for energy, or do they mostly feed our gut bacteria?
Grace: The SCFAs made are butyrate, propionate (metabolized by the liver) and acetate (muscle, kidney, heart and brain). Approximately 30% of butyrate is burned for host energy and the remaining 70% is rapidly absorbed to feed the intestinal cells, which are as enormous in surface area as that of a tennis court. The gut also houses a hidden brain which is innervated by over 100 million neurons, bigger than our spinal cord. Additionally the entire gastrointestinal tube is lined by immune cells; therefore, the gut is one long lymphoid organ. For an extremely large and often overlooked organ, studies demonstrate what happens when it is not properly fueled or fed. In sterile, germ-free animals, their immunity and immune organs are blunted and intestinal organs atrophied when the gut bugs are absent.
Richard: Another thing to keep in mind is that you basically have three types of these critters: 1) the symbionts, i.e., we cut a deal and it’s win-win, 2) the commensals, those who do nothing for us, but don’t harm us, either, and 3) the parasites or pathogens. The commensals are an interesting lot, because while they may not do anything directly for us and so don’t fit technically the definition of symbiosis, some do stuff for the symbionts who do, such as produce stuff they need to eat.
Keeping the whole thing in balance by feeding them fermentable fibers, primarily, is the ideal way to keep the pathogens in check. It’s chemical warfare down there, and it’s far better to have a specifically targeted antibiotic, manufactured in a 3 billion-year-old chemical plant, than to have to resort to carpet bombing or nuking the whole thing with broad spectrum antibiotics.
Tim: The end-result with the biggest impact does seem to be the creation of SCFAs, especially butyrate. A colon flooded with butyrate has a lower pH and healthier colonocytes. The lowered pH creates an environment that favors beneficial over pathogenic microbes and the increased butyrate serves as fuel for the special cells that line the colon. When these cells are fueled by butyrate, they behave normally, self-destructing when they need to and regrowing as they should. Colonocytes can also run off glucose, but when fueled by glucose, they behave completely differently. They don’t self-destruct and they are at higher risk for cancer. A low carb/high fat diet for you is a low fat/high carb diet for your gut.
Fat Head: When the makers of high-maize resistant starch sent out press releases announcing that resistant starch doesn’t raise glucose levels, my thought was “Whoop-de-do. Neither does cardboard, but that doesn’t mean eating it will improve my health.” But resistant starch doesn’t just have a neutral effect on blood glucose; it seems to have actual positive effects. Describe what you’ve heard from people about how resistant starch affects their fasting blood sugar levels.
Tim: If you replace 50% of the wheat in white bread with sawdust, the glycemic index will be cut in half! — this is how most people read those reports. But with RS, it’s a bit different. Some of the immediate blunting of blood-sugar spikes is definitely from the same action as in the sawdust and cardboard analogies, but RS is also acting as a powerful prebiotic in your large intestine, making long-term changes that affect hormones that stimulate insulin among others. Usually within a few days, many people who have type 2 diabetes or prediabetes notice lower fasting blood glucose in the morning and post-prandial spikes that are lower than normal after a carby meal.
Some really neat experiments were done by Steve Cooksey (the Diabetes Warrior) involving a dose of RS before exercising, and he clearly demonstrates that RS increased his insulin sensitivity while exercising — which is something that diabetics struggle with continuously. RS has been shown to increase whole body insulin sensitivity … that’s huge!
Richard: For me personally, RS alone wasn’t enough to get me all the way there. For some low carbers, even clinically diabetic ones, RS just works like a champ, right off. Steve Cooksey, as Tim mentioned, is one of those. Then there are others for whom it seemingly does nothing, or works for a while then nothing. I was in the middle. So, instead of 110-120 fasting, it brought me to 100-110. And in terms of post meal, I was seeing spikes maybe 20 points less but still in the 140-160 range, often.
But I had been so used to eating low carb so much of the time that it was difficult, and I had to really force myself to eat the rice, potatoes or legumes with almost every meal. As it turns out, I now prefer a bowl of my pinto beans with a couple of over-easy eggs on top to my bacon and eggs; and anyway, I was getting pretty tired of the most Paleo food on the planet: bacon. It began tasting like a salt lick to me (just guessing) a long time ago, but I digress. So, yeah, some days it’s the beans and eggs, some days “refried wok potatoes” from previously baked and tossed in the fridge to form retrograde RS that resists degradation with mild reheating.
Long story short, by getting my starchy carbs (“safe” in every sense) up to the 100-200 range, maybe 150 average, BANG!, my BG normalized, both in terms of fasting and post meal. I understand that this is hugely inconvenient for a lot of folks to hear, entrenched in low carb doctrines, but it is nonetheless true, and I’m far from the only one to report it.
Grace: What is impressive to me is how RS and other fibers improve insulin sensitivity anecdotally and in clinical trials. We have seen a huge number of improvements in fasting BGs reported at Free the Animal. If a person has noticed fasting BGs > 125 mg/dl in the mornings, then with consumption of RS, they may report that their fasting glucoses return to the 80s range. Many of these folks at FTA noticed trending of higher glucose readings the longer that they were adapted to chronic VLC. With no other changes to diet, they noted that after eating RS, their BGs began to shift downwards. It’s not uncommon to see high fasting sugars in regards to VLC diets. It is related to normal feedback mechanisms of the body to preserve circulating glucose for the high energy organs — liver, brain and muscles — by ratcheting up insulin resistance in peripheral tissues. Under perceived starvation, insulin resistance can occur at even the muscle level — exactly where you don’t want it. If one is trying to lose body fat, this physiological insulin resistance may strongly hinder your efforts. The best ways to improve insulin sensitivity in my opinion is to not starve insulin-regulating organs of what they need (gut, fiber + RS; muscles, carbs) and use the organs that use insulin — muscles. Studies demonstrate that weight loss can depend on the glycemic index of diet, but even more predominantly the insulin-resistant status of the individual.
Fat Head: People are also reporting that if they consume resistant starch, they get less of a rise in glucose levels after eating starchy foods like beans or rice or potatoes. Is there a timing issue involved? Do we need to consume resistant starch shortly before consuming other starches for that blunting effect to occur?
Richard: It was actually first called “the lentil effect” because they noted that legumes yielded less of a spike in glucose than one would expect for the amount of carbohydrate ingested, and that the blunting persisted, often into the next day, for other starches or sugars a person ate. They had unwittingly discovered what RS and other fermentable fibers do when the gut critters get fed.
Tim: What you are referring to is the “second-meal effect.” This has been studied for many years and is a normal part of our physiology. When you embark on a diet that incorporates RS at every meal or at least every day, then every meal is a ‘second meal’ and you see long term reductions in HgbA1C as well as postprandial glucose spikes.
Grace: This effect is one of the coolest side benefits. It appears to last 2-4 hours depending on the study. Many other fibers like glucomannan, psyllium and pectin have it as well. In a way it provides even further shielding from potential high-glucose damage, because one study demonstrated for a high glycemic meal with sufficient fiber and resistant starch, glucose tolerance was maintained at the next meal. Ultimately what impacts the second meal effect is the fermentability of the indigestible carbohydrates and fiber, and this is contigent upon the right species being located in the gut, which ultimately do the magic.
Fat Head: Do researchers understand how resistant starch ends up lowering glucose levels? What’s the mechanism?
Tim: Well, it’s not so much that it lowers glucose, it’s more about increasing insulin sensitivity. Remember all those hormones that people have been talking about…Peptide YY, Glucagon-like Peptide-1, Ghrelin, and Leptin? These are all modulated by the microbes in your gut. When the right microbes are present and they are being fed enough fermentable fiber such as RS, they start producing these hormones that act together with them to increase insulin sensitivity.
Grace: In the gut, pancreas and immune system are fatty acid receptors called GPRs 41 and 43. The selective fats that bind these are the SCFAs (butyrate, etc.) made from the gut microbes metabolizing RS, oligosaccharides and other indigestible complex carbohydrates.
When GPR41/43 are activated by butyrate, they decrease body fat, increase satiety (PYY), increase insulin sensitivity and other anti-diabetic effects, reduce inflammation, power immunity, suppress and shrink cancer cells, divert oxidative DNA damage, maintain tight barrier and gut function, and many other beneficial host activities. We even double our butyrate from the gut microbiota with exercise.
Butyrate from microbial production also binds the ketone receptors known as GPR109a (formerly known as HM74A in humans and PUMA-G in animals). This was a surprising and recent discovery. I suspected butyrate would bind it, but no confirmatory studies occurred until recently. It makes sense, no? We are cyborgs and controlled in symbiosis with our microbes. Microbes maketh who we are and what we burn and store. Earlier the research showed only niacin (vitamin B3), nicotinic acid, and ketone bodies could bind HM74A with fidelity and duration. Therefore many of the health benefits that short-term ketosis affords overlaps with what is achieved by optimal gut health. This is what I observe clinically as well as anecdotally at my blog Animal Pharm and Richard’s blog Free the Animal.
Tim: Thanks, Grace…you had to go there didn’t you? As if this stuff isn’t boring enough! Now you kind of see our problem, Tom: this stuff is just so complex that everyone’s eyes sort of glaze over when we talk about the magic of RS. These GPRs that Grace talks about are an incredible piece of the puzzle, but just so hard to work into conversation or even write about. GPR stands for G Protein-coupled Receptors (the G doesn’t even seem to stand for anything). And, we haven’t even mentioned Peyer’s patches, Treg cells, and defensins! Seriously, you could write an entire book on the deep science of RS. People spend their entire lives studying it, but sometimes it’s best if we answer questions like this with, “It just works…who cares how?”
Okay, I admit it: Tim’s right — my eyes did glaze over a bit with all the chemical names. I don’t like words without vowels. But I agree … if it works, it works. So far it’s working nicely for me.
More Q & A in my next post. We have a ways to go yet.
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In a post last week, I wrote about why I believe most New Year’s resolutions to lose weight fail: those resolutions are based on the notion that shedding pounds is a matter of character … i.e., if you just have enough discipline to eat less and spend more time on the treadmill, you’ll lose weight.
As someone who tried simply eating less and spent many hours on a treadmill (I even bought one for my apartment) without getting leaner, I don’t believe losing weight is about character. I believe it’s (mostly) about chemistry, which is why weight-loss plans that rely on changing a fat person’s character are bound to fail.
I’ll have more to say on that later. For now, I just want to share some bits from an old study (1960) that I apparently downloaded some time ago and then forgot to read.
The handful of subjects in the study fell into three categories: 1) naturally thin people, 2) fat people who had previously demonstrated that they could lose weight by restricting calories, and 3) fat people whom the researchers labeled as the “resistant obese.” They wrote this about the “resistant obese”:
All had very small appetites, and none of these subjects lost weight even during observation in the hospital for prolonged periods of time.
By contrast, one of the naturally lean subjects was described as:
… a twenty-five year-old woman who is healthy, but literally unable to gain weight despite an excellent appetite.
The question the researchers wanted to answer was whether fat people and thin people release and burn fatty acids at similar rates if they’re fasting. So they had all the subjects fast from dinner until the next morning, then measured the concentration of free fatty acids in their blood. Then they extended the fast for a full 24 hours and took the same measurement at various intervals.
Here’s what they found: in the morning, the fat people generally had higher levels of fatty acids in their blood than the thin people did. But over the course of fasting for 24 hours, the naturally thin people experienced a sharp rise in the level of fatty acids in their bloodstreams. The fat people who’d previously demonstrated they could lose weight by restricting calories experienced a milder rise in the level of fatty acids in their bloodstreams. The “resistant obese” people experienced almost no rise at all in the level of fatty acids in their bloodstreams.
The researchers noted that in an earlier study, naturally thin subjects who were restricted to a high-fat diet of 1,000 calories per day showed a sharp rise in blood ketones over the next week, while obese subjects on the same diet showed a much lower rise in ketones. Ketones, as you know, are a by-product of burning fat for fuel.
So taken together, here’s what those two studies suggest (at least about the subjects who were studied): when naturally-thin people eat very little or not at all, they release a lot more fatty acids from their fat cells, and they burn those fatty acids for fuel. “Resistant obese” people, on the other hand, don’t release extra fatty acids when they eat less or not at all, and therefore don’t make up for the calorie deficit by tapping and burning their body fat — at least not to nearly the degree the thin people do.
Remember that in describing the “resistant obese” subjects, the researchers noted that they had small appetites and failed to lose weight even under observation in a hospital. In a discussion among several researchers included at the end of the paper, the leader researcher makes this statement:
This phenomenon of people who do not lose weight is really the most tantalizing thing that confronts physicians. There are these people who can live on 600 calories and not lose any weight. On what are they surviving? If we measure their basal metabolism in terms of calories, we get figures in excess of 600 calories per twenty-four hours. It would seem that on this diet they are in a caloric deficit all time, but still are not losing any weight. I am still an admirer of the laws of thermodynamics, but these people seem to be thermodynamic paradoxes.
Small appetites. Couldn’t lose weight even while under observation at a hospital. Didn’t release or burn more fatty acids (not to any significant degree) even while fasting for 24 hours. Able to live on 600 calories per day without losing weight, causing a researcher who worked with them to label them as “thermodynamic paradoxes.”
Meanwhile, the naturally-lean people released lots of fatty acids and burned them for fuel soon after they stopped eating – including that twenty-five year-old woman who couldn’t gain weight in spite of her “excellent” appetite.
Does anyone believe the fat people in this study just needed more discipline and character in order to become thin? Or does this sound like a problem rooted in chemistry?
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I was already impressed by Dr. Doug McGuff, but now I’m even more so.
Dr. McGuff’s book Body by Science (co-written with trainer John Little) is one of the best I’ve read on exercise and fitness. It’s a how-to guide for high-intensity resistance training, but also a nice primer on the science of how your muscles work, adapt and grow.
When you read this book, you’ll learn about the different types of muscle fibers and how they’re recruited during exertion. You’ll learn why there’s really no such thing as “cardiovascular fitness.” (All fitness comes down to muscular fitness. Your vascular system doesn’t become “fit.”) You’ll understand why you will never – no matter how hard you work – develop eye-popping muscles like a body-builder or professional athlete unless you’ve been blessed with an unusual ratio of fast-twitch vs. slow-twitch muscle fibers. That’s the bad news. The good news is that you’ll also learn how to become as fit and as strong as you can be by lifting weights correctly during brief but intense workouts.
I’ve also seen Dr. McGuff give a couple of speeches on diet, exercise and health that I thought were excellent. The man knows his stuff on those topics. I expected that.
I didn’t expect him to be equally impressive speaking about economics, but he is. (Any doctor who can talk intelligently about Milton Friedman’s spending quadrant is cool in my book.) After last week’s debate in the comments about insurance and ObamaCare, a reader sent me a link to this speech Dr. McGuff gave in 2012 titled Fitness, Health and Liberty. It’s more than an hour long, but worth the watch if you want to understand the economics of how and why our medical system got so screwed up in the first place. (Hint: products and services rarely become prohibitively expensive as a result of too much freedom.)
As an emergency-room physician, Dr. McGuff has seen what happens when people wind up in the medical system, which he calls “the belly of the beast.” I’d suggest paying close attention to the end of the speech, when he offers advice on how to avoid winding up in an emergency room in the first place.
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Here’s a journal article the anti-fat hysterics at the USDA, American Heart Association, American Diabetes Association, etc. all should read. (Of course if they did, they’d dismiss it.) The article, published in Advances in Nutrition, is titled Dietary Fats and Health: Dietary Recommendations in the Context of Scientific Evidence. Let’s look at some quotes:
Although early studies showed that saturated fat diets with very low levels of PUFAs increase serum cholesterol, whereas other studies showed high serum cholesterol increased the risk of coronary artery disease (CAD), the evidence of dietary saturated fats increasing CAD or causing premature death was weak.
The evidence was weak because the anti-fat hysterics relied on teleoanalysis: saturated fat raises cholesterol (in some people) and cholesterol is associated with heart disease, therefore saturated fat must cause heart disease. Bad logic leads to bad theories.
Numerous reports and reviews in recent years have begun to call the perceived pernicious effects of dietary saturated fatty acids (SFAs) into question.
And yet few of those reports have changed the thinking of your average health reporter … not to mention the goofballs who write those annoying Eat This, Not That books and articles.
The purpose of this review is to summarize the scientific understanding as it relates to dietary fats in health and disease, particularly with regard to the innocuous nature of SFAs and the physiological effects that have implicated PUFAs in numerous disorders and diseases. The role of dietary fats in cardiovascular disease (CVD) and many other diseases is complex, yet there is a powerful inertia that has allowed the saturated fat doctrine to endure.
I don’t think powerful inertia is the correct phrase here. More like powerful vested interests.
Human food preferences tend to favor foods with both fats and sugars, which complicates any attempts to correlate saturated fats with disease.
Well, that should complicate any attempts at correlation, but the geniuses at the American Heart Association and other promoters of arterycloggingsaturatefat! hysteria found a simple solution: if people who eat saturated fats mixed with sugars get heart disease, blame the fat. (After all, you can’t blame sugar and still put your seal of approval on boxes of Cocoa Puffs.)
Because dietary saturated fats do not promote inflammation, it may be wiser to minimize omega-6 PUFAs and consume more SFAs to reduce various types of inflammation.
But … but … but the American Heart Association says corn oil is good for you.
Investigators often seem to have a particular bias against saturated fats.
That’s a polite way of saying “Scientists are freakin’ liars.”
Campaigns were waged against tropical oils (palm and coconut oils) in the early 1980s because of their high levels of SFAs, even though palm oil contains about as much MUFAs acids as SFAs and has an ample amount of PUFAs to keep serum cholesterol low …. Claims that tropical oils with a high SFA content increase the risk of CAD lack clear scientific evidence to that effect. Indeed, countries with high intake of tropical oils have some of the lowest rates of heart disease in the world.
Quick, somebody call The Guy From CSPI. He was behind those campaigns waged against tropical oils, which caused coconut oil to be replaced with trans fats – which he declared safe at the time. Given the success (ahem, ahem) of his campaigns, I’d like him to comment on that last paragraph.
Many of the shorter chain fatty acids found in milk fat and coconut oil have beneficial health effects. The shorter chain SFA in milk (C4–C12) are not only metabolized rapidly for energy in infants, but have been found to have important antiviral, antimicrobial, antitumor, and immune response functions. Lauric acid, which is present in milk and the most abundant fatty acid in coconut oil, is effective in preventing tooth decay and plaque buildup. Diets rich in coconut oils have also been shown to lower other risk factors for CAD, such as tissue plasminogen activator antigen and Lp(a).
Aren’t you glad the USDA has decided kids in school can’t drink whole milk, but sugar-laden skim milk is fine and dandy?
It should not be surprising that substitution of carbohydrates (starches) for saturated fats in the diet has relatively little effect on serum lipids. Excess carbohydrates are converted to fats for efficient energy storage, and the human body synthesizes primarily SFAs from excess carbohydrates, although MUFAs are also formed. Consequently, from a physiological viewpoint, there is no reason to believe that replacing fat in the diet with carbohydrate at a constant caloric intake will improve the serum lipid profile significantly. Indeed, a low-fat, high-carbohydrate diet causes an increase in serum triglycerides and small, dense LDL particles, which are more strongly associated with CAD than serum total cholesterol or LDL-C.
So skip the bacon and eggs and eat your Cheerios. The American Heart Association says those processed grains are good for your heart.
The meager effect that saturated fats have on serum cholesterol levels when modest but adequate amounts of polyunsaturated oils are included in the diet, and the lack of any clear evidence that saturated fats are promoting any of the conditions that can be attributed to PUFA makes one wonder how saturated fats got such a bad reputation in the health literature. The influence of dietary fats on serum cholesterol has been overstated, and a physiological mechanism for saturated fats causing heart disease is still missing.
No, no, no … I’ve heard nutritionists, doctors and dietitians on TV insisting that thousands of studies prove that saturated fat causes heart disease. Thousands!
It is time to reevaluate the dietary recommendations that focus on lowering serum cholesterol and to use a more holistic approach to dietary policy.
Well, the USDA dietary experts reevaluate their dietary recommendations every five years. Then, acting like the division of Monsanto the USDA has become, they recommend even less natural saturated fat and more mutant grains. But give them another 50 years or so, and they may actually pay attention to the science.
And another 50 years after that, the American Heart Association may do the same.
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A reader asked me for some information on cancer and sugar, so I pulled up some items from my research database. As long as I had the articles in front of me, I thought I’d share them.
Nothing listed here proves absolutely that sugars drive cancer or that a ketogenic diet will prevent cancer, but taken together, the articles do paint a picture. Let’s take a look.
Cancer cells slurp up fructose, US study finds
Pancreatic tumor cells use fructose to divide and proliferate, U.S. researchers said on Monday in a study that challenges the common wisdom that all sugars are the same.
Tumor cells fed both glucose and fructose used the two sugars in two different ways, the team at the University of California Los Angeles found.
They said their finding, published in the journal Cancer Research, may help explain other studies that have linked fructose intake with pancreatic cancer, one of the deadliest cancer types.
“These findings show that cancer cells can readily metabolize fructose to increase proliferation,” Dr. Anthony Heaney of UCLA’s Jonsson Cancer Center and colleagues wrote.
“They have major significance for cancer patients given dietary refined fructose consumption, and indicate that efforts to reduce refined fructose intake or inhibit fructose-mediated actions may disrupt cancer growth.”
I found some suggested meal plans on the USDA’s official My Plate site, which I’ll share in another post. Whole milk isn’t on the meal plan for breakfast, but orange juice and strawberry-flavored (i.e., sugary) skim milk are. Remind me again … which of those drinks contains fructose and which doesn’t?
Compound That Blocks Sugar Pathway Slows Cancer Cell Growth
Scientists at Johns Hopkins have identified a compound that could be used to starve cancers of their sugar-based building blocks. The compound, called a glutaminase inhibitor, has been tested on laboratory-cultured, sugar-hungry brain cancer cells and, the scientists say, may have the potential to be used for many types of primary brain tumors.
The Johns Hopkins scientists, inventors on patent applications related to the discovery, caution that glutaminase inhibitors have not been tested in animals or humans, but their findings may spark new interest in the glutaminase pathway as a target for new therapies.
Glutaminase is an enzyme that controls how glucose-based nutrients are converted into the carbon skeleton of a cell. Additional enzymes that help construct the so-called “bricks” of the carbon skeleton are controlled by a gene called IDH1. In some brain cancer cells, IDH1 is mutated and the resulting enzyme grinds up the bricks into nutrients that feed cancer cells.
Yes, yes, I know what you’re thinking: if blocking the glucose pathway slows cancer growth, why not just tell people to stop eating foods that spike glucose? Well, I’m pretty sure the answer lies in the fact that scientists have applied for patents. You can’t patent dietary advice, but you can patent a drug.
Diabetes Medication May Get New Life as Cancer Treatment
The drug metformin, a mainstay of diabetes care for 15 years, may have a new life as a cancer treatment, researchers said.
In a study in mice, low doses of the drug, combined with a widely used chemotherapy called doxorubicin, shrank breast-cancer tumors and prevented their recurrence more effectively than chemotherapy alone.
The findings add to a growing body of evidence that metformin, marketed as Glucophage by Bristol-Myers Squibb Co. and available in generic versions, could be a potent antitumor medicine.
In the report, being published in the Oct. 1 edition of Cancer Research, a journal of the American Association for Cancer Research, researchers said the combination of metformin and doxorubicin killed both regular cancer cells and cancer stem cells.
In contrast, doxorubicin alone had limited effect on the stem cells.
Mice that grew tumors generated from human breast-cancer cells have remained tumor-free for nearly three months on the combined treatment, while tumors have recurred in those not given the diabetes remedy.
Researchers said the results have potentially broad implications for cancer treatment.
Hmmm, now why would a drug given to type 2 diabetics be effective against cancer? You have to read pretty far down the article to find out:
How metformin affects cancer isn’t certain, but one possibility is that it deprives tumor cells of sugar.
“Cancer cells are gluttons for glucose,” said George Prendergast, president and chief executive officer of Lankenau Institute for Medical Research, Wynnewood, Pa. “It is likely that metformin is taking advantage of this gluttony of the cancer cell in order to attack it.”
Cancer cells are gluttons for glucose … I’ll be sure to think about when I’m drinking my USDA-approved skim milk with added sugar.
Dietary glycemic load and colorectal cancer risk
The link above is to an observational study based on food questionnaires, so it doesn’t exactly meet the gold standard for research. Nonetheless, here’s the conclusion:
The positive associations of glycemic index and load with colorectal cancer suggest a detrimental role of refined carbohydrates in the etiology of the disease.
The next time some vegan zealot trots out an observational study showing a weak association between meat and cancer, you can reply with this one and explain that since glycemic load is strongly associated with colorectal cancer, you’re sticking with a low-glycemic diet – meat included. If the vegan zealot starts quoting the China Study, you can reply with this (sort of) China study of Chinese Americans:
Carbohydrates and colorectal cancer risk among Chinese in North America
Here’s the conclusion:
These data indicate that increased eCarb (non-fiber carb) and total carbohydrate consumption are both associated with increased risk of colorectal cancer in both sexes, and that among women, relative risk appears greatest for the right colon, whereas among men, relative risk appears greatest for the rectum.
So get T. Colin Campbell’s high-carb diet out of my face.
Effects of a ketogenic diet on tumor metabolism
This one isn’t a study; it’s a case report from 1995 of two pediatric cancer patients put on ketogenic diets. Here are some quotes from the abstact:
OBJECTIVE: Establish dietary-induced ketosis in pediatric oncology patients to determine if a ketogenic state would decrease glucose availability to certain tumors, thereby potentially impairing tumor metabolism without adversely affecting the patient’s overall nutritional status.
So all the way back in 1995, at least some doctors suspected that depriving cancers of glucose might help. Sheesh. Anyway …
RESULTS: Within 7 days of initiating the ketogenic diet, blood glucose levels declined to low-normal levels and blood ketones were elevated twenty to thirty fold. Results of PET scans indicated a 21.8% average decrease in glucose uptake at the tumor site in both subjects. One patient exhibited significant clinical improvements in mood and new skill development during the study. She continued the ketogenic diet for an additional twelve months, remaining free of disease progression.
Improvements in mood and skill development? No, no, no … low-carb diets make you depressed and irritable. I know that’s true, because I read it on Yahoo Health.
Glucose deprivation activates feedback loop that kills cancer cells
Compared to normal cells, cancer cells have a prodigious appetite for glucose, the result of a shift in cell metabolism known as aerobic glycolysis or the “Warburg effect.” Researchers focusing on this effect as a possible target for cancer therapies have examined how biochemical signals present in cancer cells regulate the altered metabolic state.
Now, in a unique study, a UCLA research team led by Thomas Graeber, a professor of molecular and medical pharmacology, has investigated the reverse aspect: how the metabolism of glucose affects the biochemical signals present in cancer cells.
In research published June 26 in the journal Molecular Systems Biology, Graeber and his colleagues demonstrate that glucose starvation — that is, depriving cancer cells of glucose —activates a metabolic and signaling amplification loop that leads to cancer cell death as a result of the toxic accumulation of reactive oxygen species, the cell-damaging molecules and ions targeted by antioxidants like vitamin C.
Hey, I don’t care if it’s an amplification loop that does the job or if the cancer cells just die off from a lack of fuel. The point is, once again we see that depriving cancer cells of sugars can kill them.
Keep starving those cancer cells, folks.
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